Title of Invention

"A N-6 SUBSTITUTED 7-DEAZAPURINE COMPOUND"

Abstract

The present invention relates to a N-6 substituted 7-deazapurine having the structure: (Formula Removed) wherein when R3 is phenyl, R1NR2 together form a ring having the structure: (Formula Removed) or R1 is H and R2 is: (Formula Removed) or R1 is H and R2 is: (Formula Removed) R5 is H, or substituted or unsubstituted alkyl or alkylaryl, when R3 is: (Formula Removed) together form a ring having the structure: (Formula Removed) R5 is phenyl or (Formula Removed)

Full Text

Field of the Invention The present invention relates to a N-6 Substituted 7-Deazapurine Compound. Background of the Invention Adenosine is an ubiquitous modulator of numerous physiological activities, particularly within the cardiovascular and nervous systems. The effects of adenosine appear to be mediated by specific cell surface receptor proteins. Adenosine modulates diverse physiological functions including induction of sedation, vasodilation, suppression of cardiac rate and contractility, inhibition of platelet aggregability, stimulation of gluconeogenesis and inhibition of lipolysis. In addition to its effects on adenylate cyclase, adenosine has been shown to open potassium channels, reduce flux through calcium channels, and inhibit or stimulate phosphoinositide turnover through receptor-mediated mechanisms (See for example, C. E. Muller and B. Stein "Adenosine Receptor Antagonists: Structures and Potential Therapeutic Applications" Current Pharmaceutical Design, 2: 501 (1996) and C. E. Muller "A1-Adenosine Receptor Antagonists," Exp. Opin. Ther. Patents 7 (5): 419 (1997)). Adenosine receptors belong to the superfamily of purine receptors which are currently subdivided into Pl (adenosine) and P2 (ATP, ADP, and other nucleotides) receptors. Four receptor subtypes for the nucleoside adenosine have been cloned so far from various species including humans. Two receptor subtypes (A, and A2a) exhibit affinity for adenosine in the nanomolar range while two other known subtypes A2b and A3 are low-affinity receptors, with affinity for adenosine in the low-micromolar range. Ax and A3 adenosine receptor activation can lead to an inhibition of adenylate cyclase activity, while A2a and A2b activation causes a stimulation of adenylate cyclase. A few A, antagonists have been developed for the treatment of cognitive disease, renal failure, and cardiac arrhythmias. It has been suggested that A2a antagonists may be beneficial for patients suffering from Morbus Parkinson (Parkinson's disease). Particularly in view of the potential for local delivery, adenosine receptor antagonists may be valuable for treatment of allergic inflammation and asthma. Available information (for example, Nyce & Metzger "DNA antisense Therapy for Asthma in an Animal Model" Nature (1997) 385: 721-5)indicates that in this pathophysiologic context, Aj antagonists may block contraction of smooth muscle underlying respiratory epithelia, while A2b or A3 receptor antagonists may block mast cell degranulation, mitigating the release of histamine and other inflammatory mediators. A-,b receptors have been discovered throughout the gastrointestinal tract, especially in the colon and the intestinal epithelia. It has been suggested that A:b receptors mediate cAMP response (Strchmeier ec al. , J. Bio. Chem. (1995) 270:2387-94). Adenosine receptors have also been shown to exist on the retinas of various mammalian species including bovine, porcine, monkey, rat, guinea pig, mouse, rabbit and human (See, Blazynski et al., Discrete Distributions of Adenosine Receptors in Mammalian .Retina, Journal of Neurochemistry, volume 54, pages 648-655 (1990); Woods et al., Characterization of Adenosine A,-.Receptor Binding Sites in Bovine Retinal Membranes, Experimental Eye Research, volume 53, pages 325-331 (1991); and Braas et al . , Endogenous adenosine and adenosine receptors localized to ganglion cells of the retina, Proceedings of the National Academy of Science, volume 84, pages 3906-3910 (1987)). Recently, Williams reported the observation of adenosine transport sites in a cultured human retinal cell line (Williams et al., Nuclecside Transport Sites in a Cultured Human Retinal Cell Line Established By SV-40 T Antigen Gene, Current Eye Research, volume 13, pages 109-118 (1994)). Compounds which regulate the uptake of adenosine uptake have previously been suggested as potential therapeutic agents for the treatment of retinal and optic nerve head damage. In U.S. Patent No. 5,780,450 to Shade, Shade discusses the use of adenosine uptake inhibitors for treating eye disorders. Shade doe's not disclose the use of specific A3 receptor inhibitors. The entire contents of U.S. Patent No. 5,780,450 are hereby incorporated herein by reference. Additional adenosine receptor antagonists are needed as pharmacological tools and are of considerable interest as drugs for the above-referenced disease states and/or conditions. Qt tfre Invention The present invention is based on compounds which select -ve'v bind to adenosine A- receptor, thereby treating a disease associated with Aa adenosine receptor in a subiect bv » ^ * administering to the subject a therapeutically effective amount of such compounds. The disease to be treated are associated with cognitive disease, renal failure, cardiac arrhythmias, respiratory epithelia, transmitter release, sedation, vasoccnstriction, bradycardia, negative cardiac inotropy and dromotropy, branchoconstriction, neucropil chemotaxis, reflux condition, or ulcerative condition. The present invention is based, at least in part, on the discovery that certain N-6 substituted 7-deazapurines, described infra, can be used to treat a N-6 substituted 7- deazapurine responsive state. Examples of such states include those in which the activity of the adenosine receptors is increased, e.g.. bronchitis, gastrointestinal disorders, or asthma. These states can be characterized in that adenosine receptor activation can lead to the inhibition or stimulation of adenylate cyclase activity. Compositions and methods of the invention include enantiomerically or diastereomerically pure N-6 substituted 7-deazapurines. Preferred N-6 substituted 7-deazapurines include those which have an acetamide, carboxamide, substituted cyclohexyl, e.g., cyclohexanol, or a urea moiety attached to the N-6 nitrogen through an alkylene chain. The present invention pertains -.o methods for modulating an adenosine receptor (s) in a mammal by administering to the mammal a therapeutically effective amount of a N-6 substituted 7-deazapurine , such that modulation of the adenosine receptor's activity occurs. Suitable adenosine receptors include the families of Aj , A2/ or A3 In a preferred embodiment, the N-6 substituted 7-deazapurine is a adenosine receptor antagonist . The invention further pertains to methods for treating N-6 substituted 7-deazapurine disorders, e.g., asthma, bronchitis, allergic rhinitis, chronic obstructive pulmonary disease, renal disorders, gastrointestinal disorders, and eye disorders, in a mammal by administering to the mammal a theraoeutically effective amount of a N-6 substituted 7-deazapunne, such that treatment of the disorder in the mammal occurs. Suitable N-6 substituted 7 deazapunnes include those illustrated by the general formula I.- (Figure Remove) and pharmaceutically acceptable salts thereof. Rl and R2 are each independently a hydrogen atom or a substituted or unsubstituted alkyl, aryl, or alkylaryl moiety or together form a substituted or unsubstituted heterocyclic ring. R3 is a substituted or unsubstituted alkyl, aryl, or alkylaryl moiety. R4 is a hydrogen atom or a substituted or unsubstituted alkyl, aryl, or alkylaryl moiety. R5 and R6 are each independently a halogen atom, e.g., chlorine, fluorine, or bromine, a hydrogen atom or a substituted or unsubstituted alkyl, aryl, or alkylaryl moiety, or R§ is carboxyl, esters of carboxyl, or carboxamides, or R4 and R$ or R5 and R§ together form a substituted or unsubstituted heterocyclic or carbocyclic ring. In certain embodiments, Rl and R2 can each independently be a substi-uted or unsubstituted cycloalkyl or heteroarylalkyl moieties. In other embodiments, R3 is a hydrogen atom or a substituted or unsubstituted heteroaryl moiety. in still other embodiments, R,., R; and Rc- car. each be independentiv 3 heteroaryl moieties. In a preferred embodiment, RL is 5 hydrogen atom, R- is a cyclchexancl, e.z.. trans-cyciohexanol, R, is phenyl, R (Figure Remove) R-, is phenyl, R4 is a hydrogen atom and R5 and R6 are methyl groups. The invention further pertains to pharmaceutical compositions for treating a N-6 substituted 7-deazapurine responsive state in a mammal, e.g., asthma, bronchitis, allergic rhinitis, chronic obstructive pulmonary disease, renal disorders, gastrointestinal disorders, and eye disorders. The pharmaceutical composition includes a therapeutically effective amount of a N-6 substituted 7-deazapurine and a pharmaceutically acceptable carrier. The present invention also pertains to packaged pharmaceutical compositions for treating a N-6 substituted 7-deazapunne responsive state in a mammal. The packaged pharmaceutical composition includes a container holding a therapeutically effective amount of at least one N-6 substituted 7-deazapurine and instructions for using the N-6 substituted 7-deazapurine for treating a N-6 substituted 7-deazaourine resoonsive state in a mammal. The invention further pertains to compounds of wherein Fo is hydrogen; R2 is substituted or unsubstituted cycioaikyl, substituted or unsubstituted alkyl, cr R1 and R2 together fern- a substituted or unsubstituted heterocyclic ring; R3 is unsubstituted or substituted aryl; R4 is hydrogen; and Ri and R6 are each independently hydrogen or alkyl, and pharmaceutically acceptable salts thereof. The deazapunnes cf this embodiment may advantageously be selective A- receptor antagonists. These compounds may be useful for numerous therapeutic uses such as, for example, the treatment of asthma, kidney failure associated with heart failure, and glaucoma. In a particularly preferred embodiment, the deazapurine is a water soluble prodrug that is capable cf being metabolized in vivo to an active drug by, for example, esterase catalyzed hydrolysis. In yet another embodiment, the invention features a method for inhibiting the activity of an adenosine receptor (e.g., Aj) in a cell, by contacting the cell with .N-6 substituted 7-deazapurine (e.g., preferably, an adenosine receptor antagonist). In another aspect, the invention features a method for treating damage to the eye of an animal (e.g., a human) by administering to the animal an effective amount of an N-6 substituted 7-deazapurine of formula I. Preferably, the N-6 substituted 7-deazapurine is an antagonist of A; adenosine receptors in cells of the animal. The damage is to the retina or the optic nerve head and may be acute or chronic. The damage may be the result of, for example, glaucoma, edema, ischemia, hypoxia or trauma. The invention also features a pharmaceutical ccmcositior. comprising a N-6 substituted compound cf formula I. Preferably, the pharmaceutical preparation is an ophthalmic formulation (e.g., an periocular, retrobulbar or intraocular injection formulation, a systemic formulation, or a surcioal irrigating solution). In yet another embodiment, the invention features a compound having the formula II: (Figure Remove) wherein X is N or CR6; R± and R; are each independently hydrogen, or substituted or unsubsticuted alkoxy, aminoalkyl, alkyl, aryl, or alkylaryl, or together form a substituted or unsubstituted heterocyclic ring, provided that both R1 and R2 are both not hydrogen; R3 is substituted or unsubstituted alkyl, arylalkyl, or aryl; R4 is hydrogen or substituted or unsubstituted Cl- C6 alkyl; L is hydrogen, substituted or -unsubstituted alkyl, or R proviaec tnat i: R;. is pyrrcucinc, methyl. The invention also pertains to w* p- 3 •»-• k-*4O._ i acceptable salts and prodrucs cf the c: invention. In an advantageous embodiment, X is CR$ and C is CH:, C, S, or NH in formula II, wherein Rr is as defined above. In another embodiment cf formula II, X is N. The invention further pertains to a method for inhicitinc the activity cf an adenosine receptor (e.g., an A:b adencsine receptor) in a cell by contacting the cell with a compound of the invention. Preferably, the compound is an antagonist of the receptor. The invention also pertains to a method for treating a gastrointestinal disorder (e.g., diarrhea) or a respiratory disorder (e.g., allergic rhinitis, chronic obstructive pulmonary disease) in an animal by administering to an animal an effective amount of a compound of formula II (e.g., an antagonist of A:r) . Preferably, the animal is a human. This invention also features a compound having the structure: (Figure Remove) wherein R: is trans-4-hydrcxy cyclohexyl, 2-methylamino carbonylamino cyclohexyl, 2-methylamino carbonylamino cyclohexyl, acetamido ethyl, or methylamino carbonylamino ethyl; wherein at is a substituted cr unsubstituted four to six membered ring. In one embodiment of the compound, Ar is pher.yi, pyrrole, thicphene, furan, thiazcle, imidazole, pyratrle, 1,2,4- triazole, pyridine, 2(1H)-pyxidone, 4 (IK)-pyricone, pyratine, pyrimidine, pyridazine, isothiazcle, isoxazole, oxazcle, tetrazoie, naphthalene, tetralin, naphthyridine, benzofurar., benzothiophene, indole, 2,3-dihydrcindcle, iH-indole, indoline, benzopyrazole, 1,3-benzodioxole, benzoxazole, purine, coumarin, chromone, guinoline, tetrahydrcquinoline, isocruincline, ber.zimidazole, guinazoline, pyrido[2,3- b]pyrazine, pyrido [3,4-b]pyrazine, pyrido[3,2-cjpyridazine, purido [3,4-b]-pyridine, IK-pyrazole[3,4-d]pyrimidine, pteridine, 2 (1H)-quinolone , 1(2H)-isoquinclone, 1,4-benzisoxazine, benzothiazcle, guinoxaline, quincline-N-oxide, isoguinolme-N-oxide, guinoxaline-N-oxide, guinazoline-N-oxide, benzoxazine, phthalazine, cinnoline, or having a structure: (Figure Remove) wherein Y is carbon or nitrogen,- wherein R: and R:' are independently H, substituted or unsubstituted alkyl, substituted cr unsubstituted aryl, halogen, methcxy, methyl amino, or methyl thio; wherein rj is K, alkyl, substituted alkyl, aryl, arylalkyl, amino, substituted aryl, wherein said substituted alkyl is -C(R-) (Ri)XR:. wherein X is 0, S, or NR wherein R*. is H, alkyl, substituted alkyl, cycloalkyl; cr a pharmaceuticaily acceptable salt, cr a crcdruc derivative, or a biologically active metabolite; with the proviso that when R: is acetylamino ethyl, Ar is not 4-pyndyl. This invention also pertains structure : to a compound havinc the (Figure Remove) wherein R: is aryl, substituted aryl, or heteroaryl; wherein R: is H, alkyl, substituted alkyl, or cycloalkyl; wherein R; is H, alkyl, substituted alkyl, aryl, arylalkyl, amino, substituted aryl, wherein said substituted alkyl is -C(Ri) (RONR;Rf, wherein Rt and R-> are each H cr alkyl, wherein R; and Rs are each alkyl or cycloalkyl, or R* R; and the nitrogen together form a ring system of between 4 and 7 members. This invention also features a method for inhibiting the activity of an Ai adenosine receptor in a cell, which comprises contacting said cell with the above-mentioned comoounds. Detailed Descriptipa The features and other details of the inventicr. will now oe mere particularly described and pointed out in the claims. It will be understood that the particular embodiments of the invention are shown by way of illustration and not as limitations of the invention. The principle features of this invention can be employed in various embodiments without departing from the scope of the invention. The present invention pertains to methods for treating a N-6 substituted 7-deazapunne responsive state in a mammal. The methods include administration of a therapeutically effective amount of a N-6 substituted 7-deazapurine, described infra, to the mammal, such that treatment of the N-6 substituted 7-deazapurine responsive state in the mammal occurs. The language "N-6 substituted 7-deazapurine responsive state" is intended to include a disease state or condition characterized by its responsiveness to treatment with a N-6 substituted 7-deazapurine of the invention as described infra, e.g., the treatment includes a significant diminishment of at least one symptom or effect of the state achieved with a N-6 substituted 7-deazapurine of the invention. Typically such states are associated with an increase of adenosine within a host such that the host often experiences physiological symptoms which include, but are not limited to, release of toxins, inflammation, coma, water retention, weight gain or weight loss, pancreatitis, emphysema, rheumatoid arthritis, osteoarthritis, multiple organ failure, infant and adult respiratory distress syndrome, allergic rhinitis, chronic obstructive pulmonary disease, eye disorders, gastrointestinal disorders, skin tumor promotion, immunodeficiency and asthma. (See for example, C.£. Muller and B. Stein "Adenosine Receptor Antagonists: Structures and Potential Therapeutic Applications," Current Pharmaceutical Design, 2:501 (1996) and C.E. Muller "A^-Adenosine Receptor Antagonists," Exp. Opin. Thsr. Patents 7(5):41S (1997) and I. Feoktistcve. =. Polosa, S. T. Kolgate and I. Eiaggicr.i "Ader.osine A;c receptors: a novel therapeutic target in asthma?" Ti?S 19; 148 (1996)). The effects often associated with such syr.pt or.s include, but are not limited to, fever, shortness of'breath, nausea, diarrhea, weakness, headache, and even death. In one embodiment, a N-6 substituted 7-deazapurine resconsive state includes those disease states which are mediated by stimulation of adenosine receptors, e.g., A: , A-a, n-,^, A-, etc., such that calcium concentrations in cells and/or activation of PLC (phospholipase C) is modulated. In a preferred embodiment, a N-6 substituted 7-deazapurine responsive state is associated with adenosine receptor (s), e.g., the N-6 substituted 7-deazapurine acts as an antagonist. Examples of suitable responsive states which can be treated by the compounds of the invention, e.g., adenosine receptor subtypes which mediate biological effects, include central nervous system (CNS) effects, cardiovascular effects, renal effects, respiratory effects, immunological effects, gastro-intestinal effects and metabolic effects. The relative amount of adenosine in a subject can be associated with the effects listed below,- that is increased levels of adenosine can trigger an effect, e.g., an undesired physiological response, e.g., an asthmatic attack. CNS effects include decreased transmitter release (Ai), sedation (Aj), decreased locomotor activity (A2a) , anticonvulsant activity, chemoreceptor stimulation (A2) and hyperalgesia. Therapeutic applications of the inventive compounds include treatment of dementia, Alzheimer's disease and memory enhancement. Cardiovascular effects include vasodilaticn (A2a) , (A2b) and (A3), vasoccnstriction (A:) , bradycardia (Aj), platelet inhibition (A2i), negative cardiac inotropy and dromotropy !A:), arrhythmia, tachycardia and angiogenesis. Therapeutic applications of the inventive compounds include, for exa-rl-e, prevention of ischaemia-induced impairment of the r.eart and cardiotonics, myocardial tissue protection and restoration of cardiac function. Renal effects include decreased GFR (Af/ , mesansial cell contraction (A:), antidiuresis (A,) and inhibition of renir. release (A,) . Suitable therapeutic applications of the inventive compounds include use of the inventive compounds as diuretic, natriuretic, potassium-sparing, kidney-protective/prevention of acute renal failure, antihypertensive, anti-oedematous and anti-nephritic agents. Respiratory effects include bronchodilation (A2), bronchoconstriction (A:), chronic obstructive pulmonary disease, allergic rhinitis, mucus secretion and respiratory depression (A2). Suitable therapeutic applications for the compounds of the invention include anti-asthmatic applications, treatment of lung disease after transplantation and respiratory disorders. Immunological effects include immunosuppression (A:) , neutrophil chemotaxis (Aj) , neutrophil superoxide generation (A2a) and mast cell degranulation (A:b and A3) Therapeutic applications of antagonists include allergic and non allergic inflammation, e.g., release of histamine and other inflammatory mediators. Gastrointestinal effects include inhibition of acid secretion (A:) therapeutic application may include reflux and ulcerative conditions Gastrointestinal effects also include colonic, intestinal and diarrheal disease, e.g., diarrheal disease associated with intestinal inflammation (A:o) . Eye disorders include retinal and optic nerve head injury and trauma related disorders (A,). In a preferred embodiment, the eye disorder is glaucoma. Other therapeutic applications of the compounds cf the invention include treatment cf obesity (lirciytir properties), hypertension, treatment cf depression, sedative. anxiclytic, as antileptics and as laxatives, e.g.. effecting motility without causing diarrhea. The term "disease state" is intended to include tnose conditions caused by or associated with unwanted levels of adencsine, adenyiyl cyclase activity, increased pr.ysiciogical activity associated with aberrant stimulation cf adenosine receptors and/or an increase in cAMP. In one embodiment, the disease state is, for example, asthma, chronic obstructive pulmonary disease, allergic rhinitis, bronchitis, renal disorders, gastrointestinal disorders, or eye disorders. Additional examples include chronic bronchitis and cystic fibrcsis. Suitable examples of inflammatory diseases include non-lymphocytic leukemia, myocardial ischaemia, angina, infarction, cerebrovascular ischaemia, intermittent claudication, critical limb ischemia, venous hypertension, varicose veins, venous ulceration and arteriosclerosis. Impaired reperfusion states include, for example, any post-surgical trauma, such as reconstructive surgery, thrombolysis or angioplasty. The language "treatment of a N-6 substituted 7-deazapurine responsive state" or "treating a N-6 substituted 7-deazapurine responsive state" is intended to include changes in a disease state or condition, as described above, such that physiological symptoms in a mammal can be significantly diminished or minimized. The language also includes control, prevention or inhibition of physiological symptoms or effects associated with an aberrant amount of adencsine. In one preferred embodiment, the control of the disease state or condition is such that the disease state or condition is eradicated. In another preferred embodiment, the control is selective such that aberrant levels of adenosine receptor activity are controlled while other physiologic systems and parameters are unaffected. The term "N-6 substif and is intended to in -tec 7-deazapunne" is art re: .ude those compounds havir.= the I: (Figure Remove) "N-substituted 7-deazapurine" includes pnarmaceutically acceptable salts thereof, and, in one embodiment, also includes certain N-S substituted purines described herein. In certain embodiments, the N-6 substituted 7-deazapurine is not N-6 benzyl or N-6 phenylethyl substituted. In other embodiments, R4 is not benzyl or phenylethyl substituted. In preferred embodiments, Ri and R2 are both not hydrogen atoms. In still other preferred embodiments, R^ ^s noc a hydrogen atom. The language "therapeutically effective amount" of an N-6 substituted 7-deazapurine, described infra, is that amount of a therapeutic compound necessary or sufficient to perform its intended function within a mammal, e.g., treat a N-6 substituted 7-deazapurine responsive state, or a disease state in a mammal. An effective amount of the therapeutic compound can vary according to factors such as the amount of the causative agent already present in the mammal, the age, sex, and weight cf the mammal, and the ability of the therapeutic compounds of the present invention to affect a N-S substituted 7-deazapurine responsive state in the mammal. One cf ordinary skill in -he art would be able tc study tr.f aforementioned farters and make a determination resardir.c the effective amount cf the therapeutic compound without undu= experimentation. An in vi zro or in \-ivc assay alsc oar. oe used to determine an "effective amount" cf the therapeutic compounds described infra. The ordinarily skilled artisar. would select an appropriate amount of the therapeutic compound for use in the aforementioned assay or as a therapeutic treatment. A therapeutioally effective amount preferably diminishes at D least one symptom or effect associated with the N-substituted 7-deazapurine responsive state or condition being treated by at least about 20%, (more preferably by at least about 40%, even more preferably by at least about 60V, and still more preferably by at least about 80%) relative to untreated subjects. Assays can be designed by one skilled in the art to measure the diminishment of such symptoms and/or effects. Any art recognized assay capable of measuring such parameters are intended to be included as part of this invention. For example, if asthma is the state being treated, - then the volume of air expended from the lungs of a subject can be measured before and after treatment for measurement cf increase in the volume using an art recognized technique. Likewise, if inflammation is the state being treated, then the area which is inflamed can be measured before and after treatment for measurement of diminishment in the area inflamed using an art recognized technique. The term "cell" includes both prokaryctic and eukaryotic cells. The term "animal" includes any organism with adenosine receptors or any organism susceptible to a N-6-substituted 7-deazapurine responsive state. Examples of animals include yeast, mammals, reptiles, and birds. It also includes transoenic animals. The term "mammal" is art recognized and is intended to include an animal, mere preferably a warm-blooded ar.ir.al, most preferably cattle, sheep, pigs, horses, doss, cats, rats, mice, and humans. Mammals susceptible tc a N-c substituted 7-deazapurine responsive state, ir.f lar.maticr., emphysema, asthma, central nervous system conditions, or acute respiratory distress syndrome, for example, are included as part of this invention. In another aspect, the present invention pertains to methods for modulating an adenosine receptor(s) in a mammal by administering to the mammal a therapeutically effective amount of a N-6 substituted 7-deazapurine, such that modulation of the adenosine receptor in the mammal occurs. Suitable adenosine receptors include the families of A:, A;, or A, _ In a preferred embodiment, the N-6 substituted 7-deazapurine is an adenosine receptor antagonist. The language "modulating an adenosine receptor" is intended to include those instances where a compound interacts with an adenosine receptor(s), causing increased, decreased or abnormal physiological activity associated with an adenosine receptor or subsequent cascade effects resulting from the modulation of the adenosine receptor. Physiological activities associated with adenosine receptors include induction of sedation, vasodilation, suppression of cardiac rate and contractility, inhibition of platelet aggregbility, stimulation of gluconeogenesis, inhibition of lipolysis, opening of potassium channels, reducing flux of calcium channels, etc. The terms "modulate", "modulating" and "modulation" are intended to include preventing, eradicating, or inhibiting the resulting increase of undesired physiological activity associated with abnormal stimulation of an adenosine receptor, e.g., in the context of the therapeutic methods of the invention. In another embodiment, the term modulate includes antagonistic effects, e.g., dimir.ishment cf th^ activity or production of mediators of allergy and allerrir inflammation which results from the overstimulaticr. cf adenosine receptor(s). For example, the therapeutic deazapunnes of the invention can interact with an adenosine receptor to inhibit, for example, adenylate cyciase activity. The language "condition characterized by aberrant adenosine receptor activity" is intended to include those diseases, disorders or conditions which are associated with aberrant stimulation of an adenosine receptor, in that the stimulation cf the receptor causes a biochemical and or physiological chain of events that is directly or indirectly associated with the disease, disorder or condition. This stimulation of an adenosine receptor does not have to be the sole causative agent of the disease, disorder or condition but merely be responsible for causing some of the symptoms typically associated with the disease, disorder, or condition being treated. The aberrant stimulation of the receptor can be the sole factor or at least one other agent can be involved in the state being treated. Examples of conditions include those disease states listed supra, including inflammation, gastrointestinal disorders and those symptoms manifested by the presence of increased adenosine receptor activity. Preferred examples include those symptoms associated with asthma, allergic rhinitis, chronic obstructive pulmonary disease, emphysema, bronchitis, gastrointestinal disorders and glaucoma. The language "treating or treatment of a condition characterized by aberrant adenosine receptor activity" is intended to include the alleviation of or diminishment of at least one symptom typically associated with the condition. The treatment also includes alleviation or diminishment of more than one symptom. Preferably, the treatment cures, e.g., substantially eliminates, the symptoms associated with the condition. The present invention pertains to compounds, N-c subs 7-deazapurines, having the formula I: (Figure Remove) wherein R^ and R2 are each independently a hydrogen atom or a substituted or unsubstituted alkyl, aryl, or alkylaryl moiety or together form a substituted or unsubstituted heterocyclic ring; R3 is a hydrogen atom or a substituted or unsubstituted alkyl, aryl, or alkylaryl moiety; R4 is a hydrogen atom or a substituted or unsubstituted alkyl, aryl, or alkylaryl moiety. R5 and Rg are each independently a halogen atom, e.g., chlorine, fluorine, or bromine, a hydrogen atom or a substituted or unsubstituted alkyl, aryl, or alkylaryl or moiety or R4 and and R§ together form a substituted or unsubstituted heterocyclic or carbocyclic ring. Also included, are pharmaceutically acceptable salts of the N-6 substituted 7-deazapurines . In certain embodiments, R^ and R2 can each independently be a substituted or unsubstituted cycloalkyl or heteroarylalkyl moieties. In other embodiments, R-% is a hydrogen atom or a substituted or unsubstituted heteroaryl moiety. In still other embodiments, R4 , R5 and R6 can each be independently a heteroaryl moiety. In one embodiment, Ri is a hydrogen atom, R2 is a substituted cr unsubstituted cyclohexane, cyclopentyl, cyclobutyl or cyclopropane mciety, R3 is a substituted or ur.substituted phenyi mciety, R4 is a hydrogen atom and Rs and R^ are be ti­me thy 1 croups. another In anoter embodiment, R2 is a cyclohexar.cl . a cyclohexanediol, a cyclohexylsulf onamide , a cyclchexanamde , a cyclchexylester, a cyclohexene, a cyclcpentancl cr a cyclopentanediol and R3 is a phenyi moiety. In still another embodiment, Rj is a hydrogen atom, R- is a cyclohexanol, R3 is a substituted or unsubstituted phenyi, pyridine, furan, cyclopentane, or thiophene moiety, R4 is a hydrogen atom, a substituted alkyl, aryl cr arylalkyl moiety, and Rj and R6 are each independently a hydrogen atom, or a substituted or unsubstituted alkyl, aryl, or alkylaryl moiety. In yet another embodiment, R^ is a hydrogen atom, R2 is substituted or unsubstituted alkylamine, arylamine, or alkylarylamine, a substituted or unsubstituted alkylamide, arylamide or alkylarylamide, a substituted or unsubstituted alkylsulfonamide , arylsulfonamide or alkylarylsulfonamide, a substituted or unsubstituted alkylurea, arylurea or alkylarylurea, a substituted or unsubstituted alkylcarbamate, arylcarbamate or alkylarylcarbamate, a substituted or unsubstituted alkylcarboxylic acid, arylcarboxylic acid or alkylarylcarboxylic acid, R3 is a substituted or unsubstituted phenyi moiety, R4 is a hydrogen atom and R5 and R6 are methyl groups. In still another embodiment, R2 is guanidine, a modified gxianidine, cyanoguanidine, a thiourea, a thioamide or an amidine. (Figure Remove) In one embodiment , can be wherein R2a~*2c are eac-'1 independently a hydrogen atom cr a saturated or unsaturated alkyl, aryl or alkylaryl moiety and R2d is a hydrogen atom or a saturated cr unsaturated alkyl, aryl, or alkylaryl moiety, NR2eR?f, or OR2=, wherein R-6-R2c are each independently a hydrogen atom or a saturated cr unsaturated alkyl, aryl or alkylaryl moieties. Alternatively, R2a and R2b together can form a carbocyclic or heterocyclic ring having a ring size between about 3 and 6 members, e.g., cyclopropyl, cyclopentyl, cyclohexyl groups. In one aspect of the invention, both R5 and R6 are not methyl groups, preferably, one of R5 and R6 is an alkyl group, e.g., a methyl group, and the other is a hydrogen atom. In another aspect of the invention, when R4 is 1-phenylethyl and Rj is a hydrogen atom, then R3 is not phenyl, 2-chlorophenyl, 3-chlorophenyl, 4-chlorophenyl, 3,4-dichlorophenyl, 3-methoxyphenyl or 4-methoxyphenyl or when R4 and Ri are 1-phenylethyl, then R3 is not a hydrogen atom or when R4 is a hydrogen atom and R3 is a phenyl, then R^ is not phenylethyl. In another aspect of the invention, when R$ and R6 together form a carbocyclic ring, e.g., (Figure Remove) or pyrimido[4,5-6]indole, then R3 is not phenyl when R4 is 1-(4-methylphenyl)ethyl, phenylisopropyl, phenyl or 1-phenylethyl or when R3 is not a hydrogen atom when R4 is 1-phenylethyl. The carbocyclic ring formed by R5 and R6 can be either aromatic or aliphatic and can have between 4 and 12 carbon atoms, e.g., naphthyl, phenylcyclohexyl, etc.. preferably between 5 and 7 carbon atoms, e.g., cyclcpsr.tyl cr cyclohexyl. Alternatively, R; and Rc- together car. fcrr. a heterocyclic ring, such as those disclosed below. Typical heterocyclic rings include between 4 and 12 carocr. atoms, preferably between 5 and 7 carbon atoms, and car. be either aromatic or aliphatic. The heterocyclic ring car. oe further substituted, including substitution of one or mere carbon atoms of the ring structure with one or more heteroatoms . In still another aspect of the invention, R1 and R-. form a heterocyclic ring. Representative examples include, but are not limited to, those heterocyclic rings listed below, such as morpholino, piperazine and the like, e.g., 4- hydroxypiperidines, 4 -aminopiperidines . Where R^ and r£ together form a piperazino group, (Figure Remove) wherein R7 can be a hydrogen atom or a substituted or unsubstituted alkyl, aryl or alkylaryl moiety. In yet another aspect of the invention R4 and Rs together can form a heterocyclic ring, e.g., (Figure Remove) wherein the heterocyclic ring can be either aromatic or aliphatic and can form a ring having between 4 and 12 carbon atoms, e.g., naphthyi, phenylcyclohexyl, etc. and can be either aromatic or aliphatic, e.g., cyclohexyl, cyclopentyl. The heterocyclic ring can be further substituted, includir.c substitution of carbon atoms of the ring structure with cne or more heteroatoms. Alternatively, R_. and R^ together car. form a heterocyclic ring, such as tnose disclosed below. In certain embodiments, the N-6 substituted 7-deazacurine is not N-6 benzyl or N-6 phenylethyl substituted. In ctner embodiments, R^ is not benzyl or phenylethyl substituted. In preferred embodiments, Rj and R2 are both not hydrogen atoms. In still other preferred embodiments, R-, is not H. The compounds of the invention may comprise water-soluble prodrugs which are described in WO 99/33815, International Application No. PCT/US98/04595, filed March 9, 1998 and published July 8, 1999. The entire content of WO 99/33815 is expressly incorporated herein by reference. The water-soluble prodrugs are metabolized in vivo to an active drug, e.g., by esterase catalyzed hydrolysis. Examples of potential prodrugs include deazapurines with, for example, R2 as cycloalkyl substituted with -OC(0) (Z)NH2, wherein Z is a side chain of a naturally or unnaturally occurring amino acid, or, analog thereof, an a, B, y. or u amino acids, or a dipeptide. Preferred amino acid side chains include those of glycine, alanine, valine, leucine, isoleucine, lysine, a-methylalanine, aminocyclopropane carboxylic acid, azetidine-2-carboxylic acid, 3-alanine, Y-aminobutyric acid, alanine-alanine, or glycine-alanine. In a further embodiment, the invention features deazapurines of the formula (I), wherein R^ is hydrogen; R2 is substituted or unsubstituted cycloalkyl, substituted or unsubstituted alkyl, or R, and R2 together form a substituted or unsubstituted heterocyclic ring; R3 is unsubstituted or substituted aryl,- R4 is hydrogen; and R5 and R6 are each independently hydrogen or alkyl, and pharmaceutically acceptable salts thereof. The deazapurines of this embodiment may potentially be selective A3 receptor antagonists. In one embodiment, R2 is substituted (e.g.. hydrcxy substituted) cr unsubstituted cycloalkyl. In ar. advantageous subembodiment, R-, and R4 are hydrogen, R-. is unsubstituted cr substituted phenyl, and Re, and R£ are each alkyl. Preferably R2 is mono-hydroxycyclopentyl or mono-hydroxycyclcr.exyl. R-, also may be substituted with -NK-C(=0)E, wherein E is substituted or unsubstituted C^C^ alkyl (e.g., alkylatr.ine, e.g., ethylamine . ) . rt^ and R2 may also together form a substituted or unsubstituted heterocyclic ring, which may be substituted with an amine or acetamido group. In another aspect, R: may be -A-NHC(=0)B, wherein A is unsubstituted C^-C, alkyl (e.g., ethyl, propyl, butyl), and B is substituted or unsubstituted C:-C aminoalkyl, e.g., aminomethyl or aminoethyl, alkylamino, e.g., methylamino, ethylamino), preferably when R1 and R4 are hydrogen, R3 is unsubstituted cr substituted phenyl, and R5 and Rg are each alkyl. B may be substituted or unsubstituted cycloalkyl, e.g., cyclopropyl or 1-amino-cyclopropyl. In another embodiment, R3 may be substituted or unsubstituted phenyl, preferably when R5 and R6 are each alkyl. Preferably, R, may have one or more substituents (e.g., o-, m- or p- chlorophenyl, o-, m- or p- fluorophenyl). Advantageously, R3 may be substituted or unsubstituted heteroaryl, preferably when Rs and Rg are each alkyl. Examples of heteroaryl groups include pyridyl, pyrimidyl, pyridazinyl, pyrazinyl, pyrrolyl, triazolyl, thioazolyl, oxazolyl, oxadiazolyl, furanyl, methylenedioxyphenyl and thiophenyl. Preferably, R3 is 2-pyridyl, 3-pyridyl, 4-pyridyl, 2-pyrimidyl or 3- pyrimidyl. Preferably in one embodiment, Re and R^ are each hydrcser.. In another, Re and R^ are each methyl. In a particularly preferred embodiment, the deazapurines cf the invention are water-soluble prodrugs t.iat car. be metabolized in vivo to an active drug, e.g. by esterase catalyzed hydrolysis. Preferably the prodrug comprises ar. R7 croup which is cycloalkyl substituted with -OC(0) (Z)NK-, wherein Z is a side chain of a naturally or unnaturally occurring amino acid, an analog thereof, an a, i?, y, or w amino acid, or a dipeptide. Examples of preferred side chains include the side chains of glycine, aianine, valine, leucine, isoleucine, lysine, a-methylalanine, aminocyclcpropane carboxylic acid, azetidine-2-carboxylic acid, £-alanine, y-anunobutyric acid, alanine-alanine, or glycine-alanine. In a particularly preferred embodiment, Z is a side chain of glycine, R2 is cyclohexyl, R3 is phenyl, and Re and R6 are methyl. In another emcodiment, the deazapurine is 4-(cis-3-hydroxycyclopentyl)amino-5,6-dimethyl-2-phenyl-7H-pyrrolo [2,3d]pyrimidine. In another embodiment, the deazapurine is 4-(cis-3-(2-aminoacetoxy) cyclopentyl)amino-5,6-dimethyl-2-phenyl-7H-pyrrclo[2,3d] pyrimidine triflucroacetic acid' salt. In another embodiment, the deazapurine is 4-(3-acetamido) piperidinyl-5, 6-dimethyl-2-phenyl- 7H-pyrrolo [2,3d] pyrimidine. In another embodiment, the deazapurine is 4-(2-N'-methylureapropyl) amino-5 , 6-dimethyl-2-phenyl- 7H-pyrrolo [2 , 3d] pyrimidine . In another embodiment, the deazapurine is 4- , I-acetamidcbutyl) ammo-5 , 6-dimethyl-2 -phenyl- 7H-cyrrrlo (2 , !-d.' pyrinudme. In another embodiment, the deazapurine is 4-;~-N'-methylureabutyl) ammo-5 , 6 -dimethyl -2 -phenyl- 7H-pyrrole [2 , 3d] pyrimidine. In another embodiment, the deazapurine is 4-;2-aminocyolopropylacetamidoethyl)amino-2-phenyl-7H-pyrrole [2 ,3d]pyrimidine . In another embodiment, the deazapurine is 4-(trans-4-hydrcxycyclchexyi ) amino-2 - (3-chlorcphenyl) - 7H-pyrrole- (2 , 3d] pyrimidine . In another embodiment, the deazapurine is 4-(crans-4-hydroxycyclohexyl)amino-2-(3-fluorophenyl)-7H-pyrrole[2,3d] pyrimidine. In another embodiment, the deazapurine is 4-(trans-4-hydroxycyclonexyl)amino-2-(4-pyridyl)-7H-pyrrole[2,3d] pyrimidine. In yet another embodiment, the invention features a method for inhibiting the activity of an adenosine receptor (e.g., A:, A;A, A:B/ or, preferably. A,) in a cell, by contacting the cell with N-6 substituted 7-deazapurine (e.g., preferably, an adenosine receptor antagonist). In another aspect, the invention features a method for treating damage to the eye of an animal (e.g., a. human) by administering to the animal an effective amount of an N-6 substituted 7-deazapurine. Preferably, the N-6 substituted 7-deazapurine is an antagonist of A;. adenosine receptors in cells cf the animal. The damage is ~c the retina cr tne optic nerve head and may be acute or chronic. The damage may be the result of, for example, glaucoma, edema, ischemia, hypoxia cr trauma. In a preferred embodiment, the invention features a deazapurine having the formula II, supra, wherein X is N cr CR6; R: and R: are each independently hydrogen, or substituted cr unsubstituted alkoxy, aminoalkyl, alkyl, aryl, or alkylaryl, or together form a substituted or unsubstituted heterocyclic ring, provided that both R: and R: are both not hydrogen; R3 is substituted or unsubstituted alkyl, arylalkyl, cr aryl; R In one embodiment, in compounds of formula II, X is CR6 and Q is CK2, 0, S, or NH. In another embodiment, X is N. In a further embodiment of compounds of formula II, W is substituted or unsubstituted aryl, 5- or 6- member heteroaryl, or biaryl. W may be substituted with one or more substituents. Examples of substituents include: halogen, hydroxy, alkoxy, ammo, aminoalkyl, aminocarboxyamide, CN, CF3/ CO:Re, CONHRj, CONReR9, SORB, SO:R8, and SC:NR5R9/ wherein RB and R9 are each independently hydrogen, or substituted or unsubstituted alkyl, cycioalkyl, aryl, or arylalkyl. Preferably, W may be substituted or unsubstituted phenyl, e.g., methylenedioxyphenyl. W also may be a substituted or unsubstituted 5-membered heteroaryl ring, e.cr., cyrrole, pyrazole, oxazole, imidazoie, triazcle, retrazcle, furan, thiophene, thiazcie, and oxadiazole. Preferably, W may ce a 6-member heteroaryl ring, e.g., pyridyl, pyrimidyl, pyridazinyl, pyrazinal, and thicphenyl. In a preferred embodiment, W is 2-pyridyl, 3- pyridyl, 4-pyridyl, 2-pyrimidyl, 4-pyrimidyl, or 5-pyrimidyl. In one advantageous embodiment of compounds of formula II, Q is Nrl and W is a 3-pyrazolo ring which is unsubstituted or N-substituted by substituted or unsubstituted alkyl, cycioalkyl, aryl, or arylalkyl. In another embodiment of compounds of formula II, 0 is oxygen, and W is a 2-thiazoio ring which is unsubstituted or substituted by substituted or unsubstituted alkyl, cycloalkyl, aryl, or arylalkyl. In- another embodiment of compounds of formula II, W is substituted or unsubstituted alkyl, cycloalkyl e.g., cyclopentyl, or arylalkyl. Examples of substituents include halogen, hydroxy , substituted or unsubstituted alkyl, cycloalkyi, aryl, arylalkyl, or NHR10, wherein R10 is hydrogen, or substituted or unsubstituted alkyl, cycloalkyl, aryl, or arylalkyl. In yet another embodiment, the invention features a deazapurine of formula II wherein W is - (CK;) a-C (=O) Y or - (CH:) ,-C (=S) Y, and a is an integer from 0 to 3, Y is aryl, alkyl, arylalkyl, cycloalkyl, heteroaryl, alkynyl, NHRUR12, or, provided that Q is NH, OR13, wherein R:i, Ri: and R13 are each independently hydrogen, or unsubstituted or substituted alkyl, aryl, arylalkyl, or cycloalkyl. Preferably, Y is a 5-cr 6- member heteroaryl ring. Furthermore, W may be -(CH:) t-S(-0).Y, wherein j is 1 or 2, b is 0, 1, 2, cr 3, Y is aryl, alkyl, arylalkyl, cycloalKyl. aikynyl, heteroaryl, NHR; In another embodiment, R, is selected from the croup consisting of substituted and unsubstituted phenyl, pyridyl, pyrimidyl, pyridazinyl, pyrazinal, pyrrolyl, triazciyl, thioazolyl, oxazolyl, oxadiazolyl, pyrazolyl, furanyl, methylenedioxyphenyl, and thiophenyl. When R. is phenyl, it may be substituted with, for example, hydroxyl, alkoxy (e.g., methoxy) , alkyl (e.g., tolyl), and halogen, (e.g., c-, n>-, or p- flucrophenyl or o-, m-, or p- chlcrophenyl) . Advantageously, R, may be 2-, 3-, or 4- pyridyl or 2- or 3-pyrimidyl. The invention also pertains to a deazapurine wherein R6 is hydrogen or C:-C2 alkyl. Preferably, R6 is hydrogen. The invention also includes deazapurines wherein R: is hydrogen, and R, is substituted or unsubstituted alkyl or alkoxy, substituted or unsubstituted alkylamine, arylamine, or alkylarylamine, substituted or unsubstituted aminoalkyl, amino aryl, or aminoalkylaryl, substituted or unsubstituted alkylamide, arylamide or alkylarylamide, substituted or unsubstituted alkylsulfonamide, arylsulfonamide or alkylarylsulfonamide, substituted or unsubstituted alkylurea, arylurea or alkylarylurea, substituted cr unsubstituted alkylcarbamate, arylcarbamate or alkylarylcarbamate, or substituted or unsubstituted alkylcarboxylic acid, arylcarboxylic acid or alkylarylcarboxyllc acid. Preferably, R, is substituted or unsubstituted cycloalkyl, e.g., mono- cr dihydroxy-substituted cyclohexyl or cyclopentyl (preferably, monohydroxy-substituted cyclohexyl cr mcnchydroxy-substituted cyclopentyl). Advantageously, R2 may be cf the following formula (Figure Remove) wherein A is C:-C; alkyl, C:.-O, cycloalkyl, a chair. cf one to seven acorns, or a ring of three to seven acorns, optionally substituted with C:-Cf alkyl, halogens, hydroxyl, carboxyl, thiol, or amino groups .- wherein B is methyl, N(Me)a, N(Et)2, NHMe, NKEt, (CH:) .NH3+ , NH (CK,) .CH3 , (CH2).NH;, (CK: ) rCHCK,NK: , (CH:)rNHMe, (CH:).OH, CH:CN, (CH:)rCO;K, CKR19RI?, or CHMeOH , wherein r is an integer from 0 to 2, m is l or 2, Rii is alkyl, R:5. is NH:» or CO:H or Rie and R1? together are-. (Figure Remove) wherein p is 2 or 3; and R17 is C:-C6 alkyl, C3-C7 cyclcalkyl, a chain of one to seven atoms, or a ring of three to seven atoms, optionally substituted with C^-C^ alkyl, halogens, hydroxyl, carboxyl, thiol, or amino groups . Advantageously, A is unsubstituted or substituted Cj-C6 alkyl. B may be unsubstituted or unsubstituted C:-C6 alkyl. In a preferred embodiment, R: is of the formula -A-NHC{=O)B. In a particularly advantageous embodiment, A is -CH:CH2- and B is methyl. The compounds of the invention may comprise water-soluble prodrugs which are metabolized in vivo to an active drug, e.g., by esterase catalyzed hydrolysis. Examples of potential prodrugs include deazapurines with, for example, ^2 as cycloalkyl substituted with -OC(0) (2)NH2. wherein 2 is a side chain cf a naturally or unnaturally occurring ar.inc acid, or analog thereof, an q, E, v, or w aminc acid, cr a dipeptide. Preferred amino acid side chains include those cf glycine, alanine, valine, leucine, isoleucine, lysine, cr-methylalanine, aminocyclcpropane carboxylic acid, azetidine-2-carboxylic acid, B-alanine, v-amincbutyric acid, alar.ine-alanine, cr glycine-alanine. In another embodiment, R: and R: together are: wherein n is 1 or 2, and wherein the ring may be optionally substituted with one or more hydroxyl, amino, thiol, c-arboxyl, halogen, CH,OH, CH2NKC (-0) alkyl, or CJ4;NHC (=0)NHalkyl groups. Preferably, n is 1 or 2 and said ring is substituted with -NHC(=0)alkyl. In one advantageous embodiment, R: is hydrogen, R: is substituted or unsubstituted C;-C6 alkyl, R, is substituted or unsubstituted phenyl, R4 is hydrogen, L is hydrogen or substituted or unsubstituted C:-C& alkyl, Q is 0, S or NR-,, wherein R7 is hydrogen or substituted or unsubstituted C;-C6 alkyl, and W is substituted or unsubstituted aryl. Preferably, R: is -A-NHC(=0)B, wherein A and B are each independently unsubstituted or substituted Cj-C, alkyl. For example, A may be CH:CH:. B may be, for example, alkyl (e.g., methyl), or aminoalkyl (e.g., aminomethyl). Preferably, R3 is unsubstituted phenyl and L is hydrogen. R6 may be methyl or preferably, hydrogen. Preferably, Q is O, S, or NR7 wherein R7 is hydrogen or substituted or unsubstituted Cj- C6 alkyl, e.g., methyl. W is unsubstituted or substituted phenyl (e.g., alkoxy, halogen substituted). Preferably, W is p-f lucrcphenyl, p-chlcrophenyl, or p-methoxyphenyl. w ~a\-also be heteroaryl. e.g., 2-pyridyi. In a particularly preferred embodiment, the dearapurine is 4-(2-acetylaminoethyl) amino-6-phenoxymethyl-2-phenyl - 7H-pyrrolo [2,3d] pyrimidine. In a particularly preferred embodiment, the deazapurine is 4-(2-acetylaminoethyl} amino-6-(4-fluorophenoxy)methyl-2-phenyl-7#-pyrrole[2,3d]pyrimidine. In a particularly preferred embodiment, the deazapurine is 4-(2-acetylaminoethyl) amino-6-(4-chlorophenoxy)methyl-2-phenyl-7H-pyrrole[2,3d]pyrimidine. In a particularly preferred embodiment, the deazapurine is 4-(2-acetylaminoethyl) amino-6-(4-methoxyphenoxy)methyl-2-phenyl-7H-pyrrolo[2,3d]pyrimidine. In a particularly preferred embodiment, the deazapurine is 4-(2-acetylaminoethyl} amino-6-(2-pyridyloxy)methyl-2-phenyl-7H-pyrrole[2,3d]pyrimidine. In a particularly preferred embodiment, the deazapurine is 4-(2-acetylaminoethyl) amino-6-(N-phenylamino)methyl-2-phenyl-7H-pyrrolo[2,3d]pyrimidine. In a particularly preferred embodiment, the deazapurine is 4-(2-acetylaminoethyl) amino-6- (N-methyl-N-pher.ylamino) methyl-2-phenyl-7H-pyrrolo[2 , 3d]pyrimidine. In a particularly preferred embodiment, the deazapurine is 4-(2-N1-methylureaethyl) amino-6-phenoxymethyl-2-phenyl-7H- pyrrolo[2,3d]pyrimidine. The invention further pertains to a method for inhibiting the activity cf an adenosine receptor (e.g., an A^, ader.csir.e receptor) in a cell by contacting the cell with a compound cf the invention. Preferably, the compound is an antagonist cf the receptor. The invention also pertains to a method for treating a gastrointestinal disorder (e.g., diarrhea) in an animal by administering to an animal an effective amount cf a compound of the invention (e.a., an antaaonist of AO . Preferably —* •• t>- + • the animal is a human. In another embodiment, the invention relates to a pharmaceutical composition containing an N-6 substituted 7-deazapunne cf the invention and a pharmaceutically acceptable carrier. The invention also pertains to a method for treating a N-6 substituted 7-deazapurine responsive state in an animal, by administering to a mammal a therapeutically effective amount of a deazapurine of the invention, such that treatment of a N-6 substituted 7-deazapurine responsive state in the animal occurs. Advantageously, the disease state may be a disorder mediated by adenosine. Examples of preferred disease states include: central nervous system disorders, cardiovascular disorders, renal disorders, inflammatory disorders, allergic disorders, gastrointestinal disorders, eye disorders, and respiratory disorders. The term "alkyl" refers to the radical of saturated aliphatic groups, including straight-chain alkyl groups, branched-chain alkyl groups, cycloalkyl (alicyclic) groups, alkyl substituted cycloalkyl groups, and cycioalkyl substituted alkyl groups. The term alkyl further includes alkyl groups, which can further include oxygen, nitrogen, sulfur or phosphorous atoms replacing one or more carbons of the hydrocarbon backbone, e.g., oxygen, nitrogen, sulfur or phosphorous atoms. In preferred embodiments, a straight chain or branched chain alkyl has 30 or fewer carbon atoms in its backbone (e.g., C-.-C^Q for straight: chair., C^-C-j fcr branched chain), and more preferably 20 or fewer. likewise, preferred cycloalkyls have from 4-10 carbon atoms in their ring structure, and more preferably have 5, 6 or " carbons ir. the ring structure. Moreover, the term alkyl as used throughout the specification and claims is intended to include both "unsubstitutec alkyls" and "substituted alkyls", the latter of which refers to alkyl moieties having substituents replacing a hydrogen on one or more carbons of the hydrocarbon backbone. Such substituents can include, for example, halogen, hydroxyl, alkylcarbonyloxy, arylcarbonyloxy, alkoxycarbonyloxy, aryloxycarbonyloxy, carboxylate, alkylcarbonyl, alkoxycarbonyl, aminocarbonyl, alkylthiocarbonyl, alkoxyl, phosphate, phosphonato, phosphinato, cyano, amino (including alkyl amino, dialkylamino, arylamino, diarylamino, and alkylarylamino), acylamino (including alkylcarbonylamino, arylcarbonylamino, carbamoyl and ureido), amidino, imino, sulfhydryl, alkylthio, arylthio, thiocarboxylate, sulfates, sulfcnato, sulfamoyl, sulfonamido, nitro, trifluoromethyl, cyano, azido, heterocyclyl, alkylaryl, or an aromatic or heteroarcmatic moiety. It will be understood by those skilled in the art that the moieties substituted on the hydrocarbon chain can themselves be substituted, if appropriate. Cycloalkyls can be further substituted, e.g., with the substituents described above. An "alkylaryl" moiety is an alkyl substituted with an aryl (e.g., phenylmethyl (benzyl)). The term "alkyl" also includes unsaturated aliphatic groups analogous in length and possible substitution to the alkyls described above, but that contain at least one double or triple bond respectively. The term "aryl" as used herein, refers to the radical of aryl groups, including 5- and 6-membered single-ring aromatic groups that may include from zero to four heteroatoms, for example, benzene, pyrrole, furan, thiophene, benzcxazoie, benzothiazole, criazole, tetrazcle, pyrazrle, pyridine, pyrazine, pyridazine and pyrimdine , and the like. Aryl croups also include polycyclic fused aromatic croucs such as naphchyl, quinolyl, indolyl, and the like. Those aryl groups having heceroacoms in the ring structure may also be referred to as "aryl hecerocycles", "heteroaryls" or "heteroaromaca.es". The aromatic ring can be substituted at one or more ring positions with such substituents as described above, as for example, halogen, hydroxyl, alkoxy, alkylcarbonyloxy, arylcarbonyloxy, alkoxycarbonyloxy, aryloxycarbonyloxy, carboxylate, alkylcarbonyl, alkoxycarbonyl, aminocarbonyl, alkylthiocarbonyl, phosphate, phosphonato, phosphinato, cyano, amino (including alkyl aminc, dialkylamino, arylamino, diarylamino, and alkylarylamino), acylamino (including alkylcarbonylamino, arylcarbonylamino, carbamoyl and ureido), amidino, imino, sulfhydryl, alkylthio, arylthio, thiocarboxylate, sulfates, sulfonato, sulfamoyl, sulfonamido, nitro, trifluoromethyl, cyano, azido, heterocyclyl, alkylaryl, or an aromatic or heteroaromatic moiety Aryl groups can also be fused or bridged with alicyclic or heterocyclic rings which are not aromatic so as to form a polycycle (e.g., tetralin). The terms "alkenyl" and "alkynyl" refer to unsaturated aliphatic groups analogous in length and possible substitution to the alkyls described above, but that contain at least one double or triple bond respectively. For example, the invention contemplates cyano and propargyl groups. Unless the number of carbons is otherwise specified, "lower aikyl" as used herein means an alkyl group, as defined above, but having from one to ten carbons, more preferably from one to six carbon atoms in its backbone structure, even more preferably one to three carbon atoms in its backbone structure. Likewise, "lower alkenyl" and "lower alkynyl" have similar chain lengths. The terms "alkoxyalkyl", "polyaminoalkyl" ar.d "thioalkoxyalkyl" refer to alkyl groups, as described above, which further include oxygen, nitrogen or sulfur atoms replacing, one or more carbons of the hydrocarbon backbone, e.g., oxygen, nitrogen or sulfur atoms. The terms "polycyclyl" or "polycyclic radical" refer to the radical of two or more cyclic rings (e.g., cycloalkyls, cycloalkenyls, cycloalkynyls, aryls and/or heterocyclyls) in which two or more carbons are common to two adjoining rings, e.g., the rings are "fused rings". Rings that are joined through non-adjacent atoms are termed "bridged" rings. Each of the rings of the polycycle can be substituted with such substituents as described above, as for example, halogen, hydroxyl, alkylcarbonyloxy, ary1carbonyloxy, alkoxycarbonyloxy, aryloxycarbonyloxy, carboxylate, alky 1carbonyl, alkoxycarbony1, aminocarbonyl, alkylthiocarbonyl, alkoxyl, phosphate, phosphonato, phosphinato, cyano, amino (including alkyl amino, dialkylamino, arylamino, diarylamino, and alkylarylamino), acylamino (including alkylcarbonylamino, arylcarbonylamino, carbamoyl -and ureido), amidino, imino, sulfhydryl, alkylthio, arylthio, thiocarboxylate, sulfates, sulfonato, sulfamoyl, sulfonamido, nitro, trifluoromethyl, cyano, azido, heterocyclyl, alkyl, alkylaryl, or an aromatic or heteroaromatic moiety The term "heteroatom" as used herein means an atom of any element other than carbon or hydrogen. Preferred heteroatoms are nitrogen, oxygen, sulfur and phosphorus. The term "amino acids" includes naturally and unnaturally occurring amino acids found in proteins such as glycine, alanine, valine, cysteine, leucine, isoleucine, serine, threonine, methionine, glutamic acid, aspartic acid, giutamine, asparagine, lysine, arginine, proline, histidine, phenylalanine, tyrosine, and tryptophan. Amino acid analogs include amino acids with lengthened or shortened side chains cr variant side chains with appropriate functions! groups. Ammo acids also include D and L stereoiscmers of an arr.inc acid when the structure of the ammo acid admits of stereoisomeric fcrms. The term "dipeptide" includes two cr more amino acids linked together. Preferably, dipeptides are two amino acids linked via a peptide linkage. Particularly preferred dipeptides include, for example, alar.ine-alani.ne and glycine-alanine. It will be noted that the structure of some of the compounds of this invention includes asymmetric carbon atoms and thus occur as racemates and racemic mixtures, single enantiomers, diastereomeric mixtures and individual diastereomers. Ail such isomeric forms of these compounds are expressly included in this invention. Each stereogenic carbon may be of the R or S configuration. It is to be understood accordingly that the isomers arising from such asymmetry (e.g., all enantiomers and diastereomers) are included within the scope of this invention, unless indicated otherwise. Such isomers can be obtained in substantially pure form by classical separation techniques and by stereochemically controlled synthesis. The invention further pertains to pharmaceutical compositions for treating a N-6 substituted 7-deazapurine responsive state in a mammal, e.g., respiratory disorders (e.g.. asthma, bronchitis, chronic obstructive pulmonary disorder, and allergic rhinitis), renal disorders, gastrointestinal disorders, and eye disorders. The pharmaceutical composition includes a therapeutically effective amount of a N-6 substituted 7-deazapurine, described supra, and a pharmaceutically acceptable carrier. It is to be understood, that all of the deazapurines described above are included for therapeutic treatment. It is to be further understood that the deazapurines of the invention can be used alone or in combination with other deazapurines of the invention or in combination witr. acciticnal tnerapeutic compounds, sucn a: antibiotics, antiinflammatories, cr anr.icar.cer agents, fei example. The term "antibiotic" is art recognized and is intended tc include these substances produced by growing mere-organisms and synthetic derivatives thereof, which eliminate or inhibit growth of pathogens and are selectively toxic to the pathcger while producing minimal or no deleterious effects upon the infected host subject. Suitable examples of antibiotics include, but are not limited to, the principle classes of aminoglyccsides, cephaicsporins, chlcramphenicols, fuscidic acids, macrclides, penicillins, polymixins, tetracyclines and streptomycins. The term "antiinfiammatcry" is art recognized and is intended to include those agents which act on body mechanisms, without directly antagonizing the causative agent of the inflammation such as clucoccrticoids, aspirin, ibuprofen, NSAIDS, etc. The term "anticancer agent" is art recognized and is intended to include those agents which diminish, eradicate, or prevent growth of cancer cells without, preferably, adversely affecting ether physiological functions. Representative examples include cisplatin and cyclophosphamide. When the compounds of the present invention are administered as Pharmaceuticals, to humans and mammals, they can be given per se or as a pharmaceutical composition containing, for example, 0.1 to 99.5% (more preferably, 0.5 to 90%) of active ingredient in combination with a pharmaceutically acceptable carrier. The phrase "pharmaceutically acceptable carrier" as used herein means a pharmaceutically acceptable material, composition or vehicle, such as a liquid or solid filler, diluent, excipient, solvent or encapsulating material, involved in carrying or transporting a compound (s) of the present invention within cr to the subject such tr.at it can performs its intended function. Typically, such compounds are carried or transported from one organ, cr portion cf the body, to another crgan, or portion cf the body. Each carrier must be "acceptable" in the sense cf being compatible with the other ingredients of the formulation and not injurious to the patient. Some examples of materials which can serve as pharmaceutically acceptable carriers include: sugars, sue.-, as lactose, glucose and sucrose; starches, such as corn starch and potato starch; cellulose, and its derivatives, such as sodium carboxymethyl cellulose, ethyl cellulose and cellulose acetate; powdered tragacanth; malt; gelatin,- talc; excipients, such as cocoa butter and suppository waxes,- oils, such as peanut oil, cottonseed oil, safflower oil, sesame oil, olive oil, corn oil and soybean oil; glycols, such as prcpylene glycol; pclycls, such as glycerin, scrbitol, manr.itol and polyethylene giycoi; esters, such as ethyl cleats and ethyl laurate; agar,- buffering agents, such as magnesium hydroxide and aluminum hydroxide; alginic acid; pyrogen-free water; isoconic saline; Ringer's solution; ethyl alcohol; phosphate buffer solutions; and other non-toxic compatible substances employed in pharmaceutical formulations. As set out above, certain embodiments of the present compounds can contain a basic functional group, such as amino cr alkylamino, and are, thus, capable of forming pharmaceuticaliy acceptable salts with pharmaceutically acceptable acids. The term "pharmaceutically acceptable salts" in this respect, refers to the relatively non-toxic, inorganic and organic acid addition salts of compounds of the present invention. These salts can be prepared in situ during the final isolation and purification of the compounds cf the invention, cr by separately reacting a purified compound of the invention in its free base form with a suitable organic or inorganic acid, and isolating the salt thus formed. Representative salts include the hydrofaromide, hydrochloride, sulfate, bisulfate, phosphate, nitrate. acetate, valerate, cleate, palmitate, stesrate, laurate. ber.zoate, lactate, phosphate, tosylate, citrate, rr.aleare. fumarate, succinate, tartrate, napthylate, rr.esylste, clucoheptonate , lactobicnate , and lauryisulphc~ate salts and the like. (See, e.g., Berge ec aJ . -(1577) "Pharmaceutical Salts", J. Phann. Sci . 66:1-19). In other 'cases, the compounds of the present invention may contain one or more acidic functional groups and, thus, are capable of forming pharmaceutically acceptable salts with pharmaceuticaily acceptable bases. The terir. "pharmaceutically acceptable salts" in these instances refers to the relatively non-toxic, inorganic and organic base addition salts of compounds of the present invention. These salts can likewise be prepared in sizu during the final isolation and purification of the compounds, or by separately reacting the purified compound in its free acid form with a suitable base, such as the hydroxide, carbonate or bicarbonate of a pharmaceutically acceptable metal cation, with ammonia, or with a pharmaceutically acceptable organic primary, secondary or tertiary amine . Representative alkali or alkaline earth salts include the lithium, sodium, potassium, calcium, magnesium, and aluminum salts and the like. Representative organic amines useful for the formation of base addition salts include ethylamine, diethylamine , ethylenediamine , ethanolamine , diethanolamine , piperazine and the like. The term "pharmaceutically acceptable esters" refers to the relatively non-toxic, esterified products of the compounds of the present invention. These esters can be prepared in situ during the final isolation and purification of the compounds, or by separately reacting the purified compound in its free acid form or hydroxyl with a suitable esterifying agent. Carboxylic acids can be converted into esters via treatment with an alcohol in the presence of a catalyst. Hydroxyl containing derivatives can be converted into esters via treatment with ar. estenfying agent such as alkanoyl halides. The term is further intended to include lower hydrocarbon groups capable of being solvated under physiological conditions, e.g., alkyl esters, methyl, ethyl and propyl esters. (See, for example, Berge et a.1 . , supra.} The invention further contemplates the use of prcdrugs which are converted in vivo to the therapeutic compounds of the invention (see, e.g., R.B. Silverman, 1992, "The Organic Chemistry of Drug Design and Drug Action", Academic Press, Chapter 8) . Such prodrugs can be used to alter the biodistribution (e.g., to allow compounds which would not typically enter the reactive site of the protease) or the pharmacokinetics of the therapeutic compound. For example, a carboxylic acid group, can be esterified, e.g., with a methyl group or an ethyl group to yield an ester. When the ester is administered to a subject, the ester is cleaved, enzymatically or non-enzymatically, reductively or hydrolytically, to reveal the anionic group. An anionic group can be esterified with moieties (e.g., acyloxymethyl esters) which are cleaved to reveal an intermediate compound which subsequently decomposes to yield the active compound. In another embodiment, the prodrug is a reduced form of a sulfate or sulfonate, e.g., a thiol, which is oxidized in vivo to the therapeutic compound. Furthermore, an anionic moiety can be esterified to a group which is actively transported in vivo, or which is selectively taken up by target organs. The ester can be selected to allow specific targeting of the therapeutic moieties to particular reactive sites, as described below for carrier moieties. Wetting agents, emulsifiers and lubricants, such as sodium lauryl sulfate and magnesium stearate, as well as coloring agents, release agents, coating agents, sweetening, flavoring and perfuming agents, preservatives and antioxidants can also be present in the compositions. Examples of pharmaceutically acceptable anticxidar.ts include: water soluble anticxidants, such as asccrbic acid, cysteine hydrochlcride, sodium bisulfate, scdiurr, metabisulfite, sodium sulfite and the like; oil-soluble antioxidants. such as asccrbyl palmitate, butylated hydroxyaniscle (3HA: , butylated hydrcxytoluene (BHT) , lecithin, prcpyl gallate,' alpha-tocopherol, and the like; and metal chelating ager.ts, such as citric acid, ethylenediamine tetraacetic acid (E27A) , scrbitcl, tartaric acid, phosphoric acid, and the like. Formulations of the present invention include those suitable for oral, nasal, topical, transdermal, buccal, sublingual, rectal, vaginal and/or parenteral administration. The formulations may conveniently be presented in unit dosage form and may be prepared by any methods well known in the art of pharmacy. The amount of active ingredient which can be combined with a carrier material to produce a single dosage form will generally be that amount of the compound which produces a therapeutic effect. Generally, out of one hundred per cent, this amount will range from about 1 per cent to about ninety-nine percent of active ingredient, preferably from about 5 per cent to about 70 per cent, most preferably from about 10 per cent to about 30 per cent. Methods of preparing these formulations or compositions include the step of bringing into association a compound of the present invention with the carrier and, optionally, one or more accessory ingredients. In general, the formulations are prepared by uniformly and intimately bringing into association a compound of the present invention with liquid carriers, or finely divided solid carriers, or both, and then, if necessary, shaping the product. Formulations cf the invention suitable for oral administration may be in the form of capsules, cachets, pills, tablets, lozenges (using a flavored basis, usually sucrose and acacia or tragacanth), powders, granules, or as a solution or a suspension in an aqueous or non-aqueous liquid, or as an cil-in-water cr water-ir.-cil liquid emulsion, cr as ar. elixir cr syrup, cr as pastilles lusi.ng an inert base, such as gelatin and glycerin, cr sucrose and acacia) and/or as mouth washes and the like, each containing a predetermined amount of a compound of the present invention as an active ingredient. A compound of the present invention may also be administered as a bolus, electuary or paste. In solid dosage forms of the invention for oral administration (capsules, tablets, pills, dragees, powders, granules and the like) , the active ingredient is mixed with one or more pharmaceutically acceptable carriers, such as sodium citrate or dicalcium phosphate, and/or any of the following: fillers cr extenders, such as starches, lactose, sucrose, glucose, mannitol, and/or silicic acid; binders, such as, for example, carboxymethylcellulose, alginates, gelatin, polyvinyl pyrrolidone, sucrose and/or acacia; humectants, such as glycerol; disintegrating agents, such as agar-agar, calcium carbonate, potato or tapioca starch, alginic acid, certain silicates, and sodium carbonate; solution retarding agents, such as paraffin; absorption accelerators, such as quaternary ammonium compounds,- wetting agents, such as, for example, cetyl alcohol and glycerol mcnostearate; absorbents, such as kaolin and bentonite clay; lubricants, such a talc, calcium stearate, magnesium stearate, solid polyethylene glycols, sodium lauryl sulfate, and mixtures thereof; and coloring agents. In the case of capsules, tablets and pills, the pharmaceutical compositions may also comprise buffering agents. Solid compositions of a similar type may also be employed as fillers in soft and hard-filled gelatin capsules using such excipients as lactose cr milk sugars, as well as high molecular weight polyethylene glyccls and the like. A tablet may be made by compression or molding, optionally with one or more accessory ingredients. Compressed tablets may be prepared using binder (for example, gelatin or hydroxypropylmethyl cellulose), lubricant, inert diluent, preservative, disintegrant (for example, sodium search glycclate or cross-linked sodium carboxymethyl cellulose', surface-active or dispersing agent. Molded tablets may be made by molding in a suitable machine a mixture cf the powdered compound moistened with an inert liquid diluent. The tablets, and other solid dosage forms of the pharmaceutical compositions of the present invention, such as dragees, capsules, pills and granules, may optionally be scored or prepared with coatings and shells, such as enteric coatings and other coatings well known in the pharmaceutical -formulating art. They may also be formulated so as to provide slow or controlled release of the active ingredient therein using, for example, hydroxypropylmethyl cellulose in varying proportions to provide the desired release profile, other polymer matrices, liposomes and/or microspheres. They may be sterilized by, for example, filtration through a bacteria-retaining filter, or by incorporating sterilizing agents in the form of sterile solid compositions which can be dissolved in' sterile water, or some other sterile injectable medium immediately before use. These compositions may also optionally contain opacifying agents and may be of a composition that they release the active ingredient(s) only, or preferentially, in a certain portion of the gastrointestinal tract, optionally, in a delayed manner. Examples of embedding compositions which can be used include polymeric substances and waxes. The active ingredient can also be in micro-encapsulated form, if appropriate, with one or more of the above-described excipients. Liquid dosage forms for oral administration of the compounds of the invention include pharmaceutically acceptable emulsions, microemulsions, solutions, suspensions, syrups and elixirs. In addition to the active ingredient, the liquid dosage forms may contain inert dilutents commonly used in the art, such as, for example, water or other solvents, solubilizing agents and emulsifiers, such as ethyl alcohol, iscpropyl alcohol, ethyl carbonate, ethyl acetate, benzyl alcohol, benzyl benzoate, propylene glycoi, 1, 3-butyler.e glycol, oils (in particular, cottonseed, groundnut, corn, germ, olive, castor and sesame oils), glycerol, tetrahydrofuryl alcohol, polyethylene clycols and fatty acid esters of sorbitan, and mixtures thereof. Besides inert dilutents, the oral compositions can also include adjuvants such as wetting agents, emulsifying and suspending agents, sweetening, flavoring, coloring, perfuming and preservative agents. Suspensions, in addition to the active compounds, may contain suspending agents as, for example, ethoxylated isostearyl alcohols, polyoxyethylene sorbitol and sorbitan esters, miorocrystalline cellulose, aluminum metahydroxide, bentonite, agar-agar and tragacanth, and mixtures thereof. Formulations of the pharmaceutical compositions of the invention for rectal or vaginal administration may be presented as a suppository, which may be prepared by mixing one or more compounds of the invention with one or more suitable n~nirritating excipients or carriers comprising, for example, c oa butter, polyethylene glyccl, a suppository wax or a salicylate, and which is solid at room temperature, but liquid at body temperature and, therefore, will melt in the rectum or vaginal cavity and release the active compound. Formulations of the present invention which are suitable for vaginal administration also include pessaries, tampons, creams, gels, pastes, foams or spray formulations containing such carriers as are known in the art to be appropriate. Dosage forms for the topical or transdermal administration of a compound of this invention include powders, sprays, ointments, pastes, creams, lotions, gels, solutions, patches and inhalants. The active compound may be mixed under sterile conditions with a pharmac-eutically acceptable carrier, and with any preservatives, buffers, or propellants which may be required. The ointments, pastes, creams and gels may contain, in addition 'to an active compound of this invention, excipients, such as animal and vegetable fats, oils, waxes, paraffins, starch, tragacanth, cellulose derivatives, polyethylene glycols, silicones, bentonites, silicic acid, talc and tine oxide, or mixtures thereof. Powders and sprays can contain, in addition to a compound of this invention, excipients such as lactose, talc, silicic acid, aluminum hydroxide, calcium silicates and polyamide powder, or mixtures of these substances. Sprays can additionally contain customary propellar.es, such as chlcrcfluorchydrocarbons and volatile unsubstituted hydrocarbons, such as butane and propane. Transdermal patches have the added advantage of providing controlled delivery of a compound of the present invention to the body. Such dosage forms can be made by dissolving or dispersing the compound in the proper medium. Absorption enhancers can also be used to increase the flux of the compound across the skin. The rate of such flux can be controlled by either providing a rate controlling membrane or dispersing the active compound in a polymer matrix or gel. Ophthalmic formulations, eye ointments, powders, solutions and the like, are also contemplated as being within the scope of this invention. Preferably, the pharmaceutical preparation is an ophthalmic formulation (e.g., an periocular, retrobulbar or intraocular injection formulation, a systemic formulation, or a surgical irrigating solution). The ophthalmic formulations of the present invention may include one or more deazapurines and a pharmaceutically acceptable vehicle. Various types of vehicles may be used. The vehicles will generally be aqueous in nature. Aqueous solutions are generally preferred, based on case of formulation, as wel. as a patient's anility to easi.y administer such compositions by means of instilling one tr two drops of the solutions in the affected eyes. However, the deazapunnes of the present invention nay also be readily incorporated into other types of compositions, such as suspensions, viscous or semi-viscous gels or other types of solid or semi-solid compositions. The ophthalmic compositions of the present invention may also include various other ingredients, such as buffers, preservatives, co-solvents and viscosity building agents. An appropriate buffer system (e.g., sodium phosphate, sodium acetate or sodium borate) may be added to prevent pH drift under storage conditions. Ophthalmic products are typically packaged in multidose form. Preservatives are thus required . to prevent microbial contamination during use. Suitable preservatives include: benzalkonium chloride, thimerosal, chlorobutanol, methyl paraben, propyl paraben, phenylethyl alcohol, edetate disodium, sorbic acid, polyquaternium-1, or other agents known to those skilled in the art. Such preservatives are typically employed at a level of from 0.001 to 1.0% weight/volume ("% w/v") . When the deazapurines of the present invention are administered during intraocular surgical procedures, such as through retrobulbar or periocular injection and intraocular perfusion or injection, the use of balanced salt irrigating solutions as vehicles are most preferred. ESS® Sterile Irrigating Solution and BSS Plus® Sterile Intraocular Irrigating Solution (Alcon Laboratories, Inc., Fort Worth, Texas, USA) are examples of physiologically balanced intraocular irrigating solutions. The latter type of solution is described in U.S. Pat. No. 4,550,022 (Garabedian, ec al.} , the entire contents of which are hereby incorporated in the present specification by reference. Retrcbulbar and periocular inactions are known to those skilled in the art and are described in numerous publications including, fcr example, Ophthalmic Surgery: Principles of Practice, Ed., C-. L. Spaeth. W. B. Sanders Co., Philadelphia, Pa., U.S.A., pages 85-87 (1990). As indicated above, use of deazapunnes to prevent cr reduce damage to retinal and optic nerve head tissues at the cellular level is a particularly important aspect of one embodiment of the invention. Ophthalmic conditions which may be treated include, but are not limited to, retinopathies, macular degeneraticn, ocular ischemia, glaucoma, and damage associated with injuries to ophthalmic tissues, such as ischemia reperfusion injuries, photochemical injuries, and injuries associated with ocular surgery, particularly injuries to the retina or optic nerve head by exposure to light cr surgical instruments. The compounds may also be used as an adjunct to ophthalmic surgery, such as by vitreal or subconjunctival injection following ophthalmic surgery. The compounds may be used for acute treatment of temporary conditions, or may be administered chronically, especially in the case of degenerative disease. The compounds may also be used prophyiactically, especially prior to ocular surgery or noninvasive ophthalmic procedures, or other types of surgery. Pharmaceutical compositions of this invention suitable for parenteral administration comprise one or more compounds of the invention in combination with one or more pharmaceutically acceptable sterile isotonic aqueous or ncr.aqueous solutions, dispersions, suspensions or emulsions, or sterile powders which may be reconstituted into sterile injectable solutions or dispersions just prior to use, which may contain antioxidants, buffers, bacteriostats, solutes which render the formulation isotonic with the blood of the intended recipient cr suspending or thickening agents. Examples of suitable aqueous and nonaqueous carriers which may be emplcyed in the pharmaceutical compositions of the invention include water, ethanol, polyols (such as glycerol, propylene glycol, polyethylene glyccl, and the like! , ar.d suitable mixtures thereof, vegetable oils, such as clive:cil, and injectable organic esters, such as ethyl cleate. Proper fluidity can be maintained, for example, by the use of coating materials, such as lecithin, by the maintenance of the required particle size in the case of dispersions, and by the use of surfactants. These compositions may also contain adjuvants such as preservatives, wetting agents, emulsifying agents and dispersing agents. Prevention of the action of microorganisms may be ensured by the inclusion of various antibacterial and antifungal agents, for example, paraben, chlorobutanol, phenol scrbic acid, and the like. It may also be desirable to include isotonic agents, such as sugars, sodium chloride, and the like into the compositions. In addition, prolonged absorption of the injectable pharmaceutical form may be brought about by the inclusion of agents which delay absorption such as aluminum monostearate and gelatin. In some cases, in order to prolong the effect of a drug, it is desirable to slow the absorption of the drug from subcutaneous or intramuscular injection. This may be accomplished by the use of a liquid suspension of crystalline or amorphous material having poor water solubility. The rate of absorption of the drug then depends upon its rate of dissolution which, in turn, may depend upon crystal size and crystalline form. Alternatively, delayed absorption of a parer.terally-administered drug form is accomplished by dissolving or suspending the drug in an oil vehicle. Injectable depot forms are made by forming microencapsule matrices of the subject compounds in biodegradable polymers such as pclylactide-polyglycolide. Depending on the ratio of drug to polymer, and the nature of the particular polymer employed, the rate of drug release can be controlled. Examples of other biodegradable polymers include polyicrthoesters) and poly(anhydrides). Depot injectable formulations are also prepared by entrapping the drug ir. liposomes or microemuisions which are compatible with body tissue. The preparations of the present invention may be given orally, parenterally, topically, or rectally. They are of course given by forms suitable for each administration route. For example, they are administered in tablets or capsule form, by injection, inhalation, eye lotion, ointment, suppository, etc. administration by injection, infusion or inhalation; topical by lotion or ointment; and rectal by suppositories. Oral administration is preferred. The phrases "parenteral administration" and "administered parenterally" as used herein means modes of administration other than enteral and topical administration, usually by injection, and includes, without limitation, intravenous, intramuscular, intraarterial, intrathecal, intracapsular, intraorbital, intracardiac, intradermal, intraperitoneal, transtracheal, subcutaneous,, subcuticular, intraarticular, subcapsular, subarachnoid, intraspinal and intrasternal injection and infusion. The phrases "systemic administration," "administered systematically," "peripheral administration" and "administered peripherally" as used herein mean the administration of a compound, drug or other material other than directly into the central nervous system, such that it enters the patient's system and, thus, is subject to metabolism and other like processes, for example, subcutaneous administration. These compounds may be administered to humans and other animals for therapy by any suitable route of administration, including orally, nasally, as by, for example, a spray, rectally, intravaginally, parenterally, intracisternally and topically, as by powders, ointments or drops, including buccaily and sublingually. Reaardless of the rcute of administration selectee, the compounds of the present invention, which may be used in a suitable hydrated form, and/or the pharmaceutical compositions of the present invention, are formulated into pharmaceutically acceptable dosage forms by conventional methods known to those of skill in the art. Actual dosage levels of the active ingredients in the pharmaceutical compositions of this invention nay be varied so as to obtain an amount of the active ingredient which is effective to achieve the desired therapeutic response for a particular patient, composition, and mode of administration, without being toxic to the patient. The selected dosage level will depend upon a variety of factors including the activity of the particular compound of the present invention employed, or the ester, salt or amide thereof, the route of administration, the time of administration, the rate of excretion of the particular compound being employed, the duration of the treatment, other drugs, compounds and/or materials used in combination with the particular compound employed, the age, sex, weight, condition, general health and prior medical history of the patient being treated, and like factors well known in the medical arts. A physician or veterinarian having ordinary skill in the art can readily determine and prescribe the effective amount of the pharmaceutical composition required For example, the physician or veterinarian could start doses of the compounds of the invention employed in the pharmaceutical composition at levels lower than that required in order to achieve the desired therapeutic effect and gradually increase the dosage until the desired effect is achieved. In general, a suitable daily dose of a compound of the invention will be that amount of the compound which is the lowest dose effective to produce a therapeutic effect. Such an effective dose will generally depend upon the facicrs described above. Generally, intravenous and subcutaneous doses of the compounds of this invention for a patient, when used for the indicated analgesic effects, will range from about O.OOC1 to about 200 mg per kilogram of body weight per day, more preferably from about 0.01 to about 150 mg per kg per day, and still more preferably from about 0.2 to about 140 mg per kg per day. If desired, the effective daily dose of the active compound may be administered as two, three, four, five, six or more sub-doses administered separately at appropriate intervals throughout the day, optionally, in unit dosage forms. While it is possible for a compound of the present invention to be administered alone, it is preferable to administer the compound as a pharmaceutical composition. The present invention also pertains to packaged pharmaceutical compositions for treating a N-6 substituted 7 deazapurine responsive state, e.g., undesirable increased adenosirre receptor activity in a mammal. The packaged pharmaceutical compositions include a container holding a therapeutically effective amount of at least one deazapurine as described supra and instructions for using the deazapurine for treating the deazapurine responsive state in the mammal. The deazapurines of the invention can be prepared using standard methods for organic synthesis. Deazapurines can be purified by reverse phase HPLC, -chromatography, recrystallization, etc. and their structures confirmed by mass spectral analysis, elemental analysis, IR and/or NMR spectroscopy. Typically, synthesis of the intermediates as well as the deazapurines of the invention is performed in solution:. The addition and removal of one or more protecting group is also tycical practice and is known to those skilled ir. the art . Typical synthetic schemes for the preparation of deazapurir.e intermediates of the invention are outlined below ir. Scheme I. This invention further provides a compound having the structure (IV): (Figure Remove) wherein R: is trans-4-hydroxy cyclohexyl, 2-methylamino carbcnylamino cyclohexyl, acetylamino ethyl, or methylamino carbonylamino ethyl; wherein Ar is a substituted or unsubstituted four to six nembered ring, phenyl, pyrrole, thiophene, furan, thiazcle, imidazole, pyrazole, 1,2,4 -triazole, pyridine, 2(IK)-pyridone, 4(1H)-pyridone, pyrazine, pyrimidine, pyridazine, isothiazole, isoxazole, cxazoie, tetrazole, naphthalene, tetralin, naphthyridine, benzofuran, benzothiophene, indole, 2,3-dihydroindole, IH-indole, indoline, benzopyrazole, 1,3-benzodioxole, benzoxazole, purine, coumarin, chromone, quinoline, tetrahydroquinoline, isoguinoline, . benzimidazole, quinazoline, pyrido[2,3-b]pyrazine, pyrido[3,4- b]pyrazine, pyrido[3,2-c]pyridazine, purido[3,4-b]- pyridine, IK-pyrazole[3,4-d]pyrimidine, pteridine, 2(1H)-quinolone, 1(2H)-isoquinolone, 1, 4-benzisoxazine, benzothiazole, quinoxaline, quinoline-N-oxide, isoc[uinoline-N-oxide, guinoxaline-N-oxide. quinazoline-N-oxide, benzcxazine, phthalazine, cinnoline, or having a structure: (Figure Remove) wherein Y is carbon or nitrogen; wherein R: and R: ' are independently H, substituted or unsubstituted alkyl, substituted or unsubstituted aryl, halogen, methoxy, methyl amino, or methyl thio; wherein R: is K, alkyl, substituted alkyl, aryl, arylalkyl, amino, substituted aryl, wherein said substituted alkyl is -CfR?) (Rr)XR:, wherein X is 0, S, or NRC, wherein R-and R; are each independently H or alkyl, wherein R; and Re are each independently alkyl or cycloalkyl, or NRsRs is a substituted or unsubstituted ring of between 4 and 7 members,- wherein R In one embodiment of the compound having structure IV, NRsRt is a substituted or unsubstituted ring of between 4 and 7 members which is selected from the group consisting of: (Figure Remove) wherein Y is carbon or nitrogen; wherein R: is H, or halogen, -0-alkyl group, amine group, or sulfide group; wherein Fb is H, alkyl, substituted alkyl, aryl, arylalkyl, amino, substituted aryl, wherein said substituted alkyl is -C(R->) (RsJNRiRe, wherein R~ and rb are each independently H or alkyl, wherein R: and Riare each independently alkyl or cycloalkyl, or Rs, Rt, and the nitrogen together form a substituted or unsubstituted ring of between 4 and 7 members. I In another embodiment of the compound, Y is carbon. In another embodiment of the compound, R: is hydrogen. In another embodiment of the compound, R« is hydrogen. In another embodiment of the compound, R: is hydrogen. In another embodiment of the compound, rj and R* are each methyl. In another embodiment of the compound, rj is -C(R-) (Rs)NRsRt, wherein Ri and Rt are each independently H or alkyl, wherein Rs and Re are each independently alkyl cr cycloalkyl, cr R , R and the nitrogen together form a substituted or unsubstituted ring of between 4 and 7 members. In another embodiment of the compound, R: is halogen. In another embodiment of the compound, Y is nitrogen. In yet another embodiment of the compound, R; is hydrogen. In a further embodiment of the compound, R: and R. are each hydrogen. This invention also provides a compound having the structure (V) : (Figure Remove) V wherein R: is aryl, substituted aryl, or heteroaryl; wherein Rz is H, alkyl, substituted alkyl, or cycloalkyl; wherein R: is H, alkyl, substituted alkyl, aryl, arylalkyl, amino, substituted aryl, wherein said substituted alkyl is -C(Rt) (Ri)NR In one embodiment of the compound having structure V, R^. and R- are each K; wherein R« is K and Rs is -Ri:C (=0} R::-. In another embodiment of the compound having structure V, R4 and R- are each K; wherein the ring system is rr.orpholino, thicmorpholino, N-4-substituted piperazino, 2-substituted piperazine, or Re substituted pyrrolldino, piperadine, wherein Ra is H, OH, CJfcOK, -C (=0) NRsRio, NRu, wherein Rn is -C(=O)CH3, -S02Me. In another embodiment of the compound, the compound has the following structure: (Figure Remove) (Compound 706) In another embodiment of the compound, the compound has the structure : (Figure Remove) In another embodiment of the compound, the compound has the structure: (Figure Remove) (Compound 1318-a) In another embodiment of the compound, the compound has the (Compound 1318-b) structure: (Figure Remove) wherein R2 is a 5-6 membered aromatic ring; wherein R:. and R In one embodiment of the compound, the compound has the structure: (Figure Remove) wherein R: is a substituted 5-6 membered aromatic ring; wherein R:, and R In one embodiment of the compound, the compound has the structure: (Figure Remove) wherein R: is a 5-6 membered aromatic ring; wherein X is oxygen, or sulfur. In one embodiment of the compound, the compound has the structure: (Figure Remove) This invention further provides a method for treating a disease associated with Ai adenosine receptor in a subject, comprising administering to the subject a therapeutically effective amount of a compound having the formula IV, V, VI, VII, VIII, IX, or X. In one embodiment of the method, the subject is a mammal. In another embodiment of the method, the mammal is a human. In another embodiment of the method, the Ai adenosine receptor is associated with cognitive disease, renal failure, cardiac arrhythmias, respiratory epithelia, transmitter release, sedation, vasoconstriction, bradycardia, negative cardiac inotropy and dromotropy, branchoconstriction, neutropil chemotaxis, reflux condition, or ulcerative condition. This invention also provides a combination therapy for asthma, comprising compounds IV and V, and a steroid, P2 agonist, glucocoticoid, lucotriene antagonist, or anticolinegic agonist. Diseases associated with adenosine Ai, A2a, A2b and A3 receptors are disclosed in WO 99/06053 and WO-09622465, WO-09705138, WO-09511681, WO-09733879, JP-09291089, PCT/US98/16053 and U.S. Patent No. 5,516,894, the entire content of which are fully incorporate herein by reference. This invention also provides a water-soluble prodrug of a compound having the structures IV, V, VI, VII, VIII, IX, or X, wherein said water-soluble prodrug that is metabolized in vivo to an active drug which selectively inhibit Ai adenosine receptor. In one embodiment of the prodrug, said prodrug is metabolized in vivo by esterase catalyzed hydrolysis. This invention also provides a pharmaceutical composition comprising the prodrug and a pharmaceutically acceptable carrier. This invention further provides a method for inhibiting the activity of an Ai adenosine receptor in a ceil, which comprises contacting said cell with a compound having the structures IV, V, VI. VII, VIII, IX, or X. In one embodiment of the method, the compound is an antagonist of said Ai adenosine receptor. This invention also provides for a method for treating a gastrointestinal disorder in an subject, comprising administering to the an effective amount of a compound having the structures IV, V, VI, VII, VIII, IX, or X. In one embodiment of the method, said disorder is diarrhea. In another embodiment of the method, the subject is a human. In another method of the method, the compound is an antagonist of A: adenosine receptors. This invention also provides a method for treating respiratory disorder in a subject, comprising administering to the subject an effective amount of a compound having the structures IV, V, VI, VII, VIII, IX, or X. In one embodiment of the method, said disorder is asthma, chronic obstructive pulmonary disease, allergic rhinitis, or an upper respiratory disorder. In another embodiment of the method, the subject is a human. In another embodiment of the method, said compound is an antagonist of Ai adenosine receptors. This invention further provides a method for treating damage to the eye of a subject which comprises administering to said subject an effective amount of a compound having the structures IV, V, VI, VII, VIII, IX, or X. In one embodiment of the method, said damaoe comprises retinal or optic nerve head damage. In another embodiment of the method, said damage is acute cr chronic. In another embodiment of the method, wherein said damage is the result of glaucoma, edema, ischemia, hypoxia cr trauma. In another embodiment of the method, the subject is a human. In another embodiment of the method, the compound is an antagonist of aj adenosine receptors. This invention also provides a pharmaceutical composition comprising a therapeutically effective amount of a compound having the structures IV, V, VI, VII, VIII, IX, or X, and a pharmaceutically acceptable carrier. In another embodiment of the pharmaceutical composition, said therapeutically effective amount is effective to treat a respiratory disorder or a gastrointestinal disorder. In another embodiment of the pharmaceutical composition, said gastrointestinal disorder is diarrhea. In another embodiment of the pharmaceutical composition, said respiratory disorder is asthma, allergic rhinitis, or chronic obstructive pulmonary disease. In another embodiment of the pharmaceutical composition, said pharmaceutical composition is an ophthalmic formulation. In another embodiment of the pharmaceutical composition, said pharmaceutical composition is an periocular, retrobulbar or intraocular injection formulation. In yet another embodiment of the pharmaceutical composition, said pharmaceutical composition is a systemic f orrr.ulatior.. In a further embodiment of the pharmaceutical preparation, said pharmaceutical composition is a surgical irrigating solution. This invention also provides a packaged pharmaceutical composition for treating a disease associated with Al adenosine receptor in a subject, comprising: (a) a container holding a therapeutically effective amount of an adenosine Al specific compound; and (b) instructions for using said compound for treating said disease in a subject. As used herein, "A compound is A: selective." means that a compound has a binding constant to adenosine Al receptor of at least ten time higher then that to adenosine A:a, A;b or A3. This invention also provides a method of preparing the compound having structure IV, comprising the steps of (Figure Remove) wherein R; is trans-4-hydroxy cyclohexyl, 2-methylamino carbonylamino cyclohexyl, acecylamino ethyl, or methylamino carfaonylamino ethyl; wherein Ar is a substituted or unsubstituted four to six metnbered ring; wherein R This invention also provides a method of preparing the compound having structure V, comprising the steps of (Figure Remove) wherein R: is aryl, substituted aryl, heteroaryl; wherein R: is H, alkyl, substituted alkyl, or cycloalkyi; wherein Rz is H, alkyl, substituted alkyl, aryl, arylalkyl, amino, substituted aryl, whereir. said substituted alkyl is -C(Rt) (R-)NR;R;, wherein Rb and R- are each H or alkyl, wherein R Compounds represented by formula VI, VII, and VIII can be synthesized by any of the Schemes I-VIII. Compounds represented by formula IX, and X can be prepared by Scheme IX. The invention is further illustrated by the following examples which in no way should be construed as being further limiting. The contents of all references, pending patent applications and published patent applications, cited throughout this application, including those referenced in the background section, are hereby incorporated by reference. It should be understood that the models used throughout the examples are accepted models and that the demonstration of efficacy in these models is predictive of efficacy in humans. This invention will be better understood from the Experimental Details which follow. However, one skilled in the art will readily appreciate that the specific methods and results discussed are merely illustrative of the invention as described more fully in the claims which follow thereafter. EXPERIMENTAL DETAILS The deazapurines of the invention can be prepared using standard methods for organic synthesis. Deazapurines can be purified by reverse phase KPLC, chromatography, recrystallization, etc. and their structures confirmed by mass spectral analysis, elemental analysis, IR and/or NMR spectroscopy. Typically, synthesis of the intermediates as well as the deazapurines of the invention is performed in solution. The addition and removal of one or more protecting group is also typical practice and is known to those skilled in the art. Typical synthetic schemes for the preparation of deazapurine intermediates of the invention are outlined below in Scheme (Figure Remove) wherein R3, R5 and R6 are as defined above. In general, a protected 2-amino-3-cyano-pyrrole can be treated with an acyl halide to form a carboxyamido-3-cyanc-pyrrole which can be treated with acidic methanol to effect ring closure to a pyrrolo [2, 3d] pyrimidine-4 (3H)-one (Muller, C.E. et aJ. J. Med. Chem. 40:4396 (1997)). Removal of the pyrrolo protecting group followed by treatment with a chlorinating reagent, e.g., phosphorous oxychloride, produced substituted or unsubstituted 4-chloro-7H-pyrrolo [2, 3d] pyrimidines . Treatment of the chloropyrimidine with amines afforded 7-deazapurines. For example, as shown in Scheme I/ a N-(l-dl-phenylethyl)-2- amino-3-cyano-pyrrole was treated with an acyl halide in pyridine and dichloromethane. The resultant N-(l-dJ- phenylethyl)-2-phenylcarboxyamido-3-cyano-pyrrole was treated with a 10:1 mixture of methanol/sulfuric acid to effect ring closure, resulting in a dI-7H-7-(l- phenylethyl)pyrrolo[2,3d]pyrimidine-4(3H)-one. Removal of the phertylethyl group by treatment of the pyrimidine with polyphosphoric acid (PPA) followed by POC13 afforded a key intermediate, the 4-chloro-7H-pyrrolo[2,3d]pyrimidine. Further treatment of the 4-chloro-7H-pyrrolo[2,3d]pyrimidine with various amines listed in Table 1 gives compounds of formula (I) and (II). (Figure Remove) A general approach to prepare 6-substituted pyrroles is depicted in the following scheme (Scheme II). (Figure Remove) Transesterification and alkylation of. ethyl cyanoacetate with an a-haloketone affords a ketomethylester. Protection of the ketone followed by treatment with an amidine (e.g., alkyl, aryl or alkylaryl) hydrochloride produced the resultant ketal protected pyrimidine. Removal of the protecting group, followed by cyclization and treatment with phosphorous cxychloride afforded the -hloride intermediate which could be further treated with ;i amine to afford an amine 6- substituted pyrrole. Additionally, alkylation of the pyrrcle nitrogen can be achieved under art recognized conditions. A general approach to prepare 5-substituted pyrroles is depicted in the following scheme (Scheme III). (Figure Remove) wherein R]_ through Rg are defined as above and R is a removable protecting group. Condensation of malononitrile and an excess of a ketone followed by bromination of the product afforded a mixture of starting material, monobrominated and dibrominated products which were treated with an alkylamine, arylamine or alkylarylamine. The resultant amine product was acylated with an acid chloride and the monacylated pyrrole was cyclized in the presence of acid to afford the corresponding pyrimidine. The pyrrole protecting group was removed with polyphosphoric acid and treated with phosphorous cxychlcride to produce a chlorinated product. The chlorinated pyrrole could subsequently be treated with an amine to produce an ammo 5-substituted pyrrole. Alkylation of the pyrrole nitrogen can be achieved under art recognized conditions. Schemes IV and V depict methods for preparing the deazapurines 1 and 2 of the invention. (Figure Remove) wherein R$ and R§ are as described above, e.g., CH3. Specifie Preparation of 6-methvl pyrrolopyrimidinea: The key reaction toward 6-methylpyrrolopyrimidines (I) CH3] was cyclization of a cyanoacetate with benzamidine to a pyrimidine. It was believed methyl cyanoacetate would cyclize more efficiently with benzamidine to a pyrimidine than the corresponding ethyl ester. Therefore, transesterification and alkylation of ethyl cyanoacetate in the presence of NaOMe and an excess of an a-haloacetyl moiety, e.g., chloroacetone, gave the desired methyl ester (3) in 79V yield (Scheme IV) . The ketoester (3) was protected as the acetal (4) in 81V yield. A new' cyclization method to the pyrimidine (5) was achieved with an amidine hydrochlcride, e.g., benzamidine hydrochloride, with 2 equivalents of DBU to afford the 5 in 54V isolated yield. This method improves the yield from 20% using the published conditions, which utilizes NaOMe during the cyclization with guanidine. Cyclization to the pyrrole-pyrimidine (6) was achieved via deprotection of the acetal in aqueous HCl in 78% yield. Reaction of (6) with phosphorous oxychloride at reflux gave the corresponding 4-chloro derivative (7) . Coupling with trans-4-aminocyclohexanol in dimethyl sulfoxide at 13 5 "C gave (1) in 57% from (7) . One skilled in the art will appreciate that choice of reagents allows for great flexibility in choosing the desired substituent R5. (Figure Remove) Seific Prea.ra- a Knoevengel condensation of maloncnitrile and an excess kecone, e.g., acetone in refluxing benzene gave 8 in 50% yield after distillation. Bromination of 8 with N- bromosuccinimde in the presence of benzoyl peroxide in chloroform yielded a mixture of starting material, mono- (9), and ci-brominated products (5/90/5) after distillation (70%) . The mixture was reacted with an a-methylalkylamine or o-methylarylamine, e.g., a-methylbenzylamine, to deliver the aminopyrrole (10) . After passing through a short silica gel column, the partially purified amine (31% yield) was acylated with an acid chloride, e.g., benzoyl chloride to deliver mono- (11), and diacylated (12) pyrroles, which were separated by fla;'- chromatography. Acid hydrolysis of the disubstituted pyrrole (12) generated a combined yield of 29V for the acylpyrrole (11) . Cyclization in the presence of concentrated sulphuric acid and DMF yielded (13) (23V), which was deprotected with polyphosphoric acid to (14). Reaction of (14) with phosphorous oxychloride at reflux gave the corresponding 4-chloro derivative (15). Coupling with trans- 4 -aminocyclohexanol in dimethyl sulf oxide at 135°C gave (2) [R6 = CH3] in 30V from (14) (See Scheme V) . One skilled in the art will appreciate that choice of reagents allows for great flexibility in choosing the desired substituent Rt. (Figure Remove) Alternative Synthetic Route to rc- Substituted Pyrroles, e.g.. 5 -methvl This alternative route to Rg-substituted pyrroles, e.g., 5- methylpyrrolopyrimidines, involves transesterif ication and alkylation of ethyl cyanoacetate to (16) (Scheme VI) . The condensation of (16) with benzamidine hydrochlonde with 2 equivalents of DBU affords the pyrimidine (17) . Cyclization to the pyrrole-pyrimidine (14) will be achieved via deprotection of the acetal in aqueous HCl . Reaction of (14) with phosphorous oxychloride at reflux gave the corresponding 4-chloro derivative (15). Coupling with crans-4- aminocyclohexanol in dimethyl sulfoxide at 135°C gives 2. This procedure reduces the number of synthetic reactions to the target compound (2) from 9 to 4 steps. Moreover, the yield is dramatically improved. Again, one skilled in the art will appreciate that choice of reagents allows for great flexibility in choosing the desired substituent R6 . (Figure Remove) A general approach to prepare des-methyl pyrrole is depicted in the following scheme (Scheme VII) (Figure Remove) wherein Rj through R3 are defined as above. Alkylation of an alkyl cyanoacetate with a diethyl acetal in the presence of a base afforded a cyano diethyl acetal which was treaced wich an amidine sale to produce a methyl pyrrclopyrimidine precursor. The precursor was chlorinated and treated with an amine to form the des-methyl pyrrolopyrimidine target as shown above. For example, Scheme VIII depicts the synthesis of compound (18) . (Figure Remove) Commercially available methyl cyanoacetate was alkylated with bromoacetaldehyde diethyl acetal in the presence of potassium carbonate and Nal to yield (19). Cyclization to the pyrimidine (20) was achieved in two steps. Initially, the pynrr.idine-acetal was formed via reaction of (19) with benzamidine hydrochloride with 2 equivalents of DBU. The resultant pyrimidine-acetal was deprotected without purification with aqueous 1 N HCl and the resultant aldehyde cyclized to the pyrrolo-pyrimidine (20), which was isolated by filtration. Reaction of (20) with phosphorous oxychloride at reflux afforded the corresponding 4-chloro derivative (21). Coupling of the chloro derivative with crans-4- aminocyclohexanol in DMSO at 135°C gave compound- (18) from compound (21). Schemes II-VIII demonstrate that it is possible to functionalize the 5- and 6-position of the pyrrolopyrimidine ring. Through the use of different starting reagents and slight modifications of the above reaction schemes, various functional groups can be introduced at the 5- and 6-positions in formula (I) and (II) . Table 2 illustrates some examples. Table 2. Selected pyrrolopyrimidines. (Figure Remove) list of 5- and 6-substituted A skilled artisan will know that metabolism of the compounds disclosed herein in a subject produces certain biologically active metabolites which can serve as. drugs. The invention is further illustrated by the following examples which in no way should be construed as being further limiting. The contents of all references, pending patent applications and published patent applications, cited throughout this application, including those referenced in the background section, are hereby incorporated by reference. It should be understood that the models used throughout the examples are accepted models and that the demonstration of efficacy in these models is predictive of efficacy in humans. Preparation 1: A modification of the alkylation method of Seela and Lupke was used. To an ice-cooled (OeC) solution of ethyl cyanoacetate (6.58 g, 58.1 mmol) in MeOH (20 mL) was slowly added a solution of NaOMe (25% w/v; 58.1 mmol) . After 10 min, chloroacetone (5 mL; 62.8 mmol) was slowly added. After 4 h, the solvent was removed. The brown oil was diluted the EtOAc (100 mL) and washed with H20 (100 mL) . The organic fraction was dried, filtered, and concentrated to a brown oil (7.79 g; 79V). The oil (3) (Scheme IV) was a mixture of methyl/ethyl ester products (9/1), and was used without further purification. XH NMR (200 MHz, CDC13) 5_4.24 (q, J = 7.2 Hz, OCK2), 3.91 (dd, 1H, J = 7.2, 7.0 Hz, CH) , 3.62 (s, 3H, OCH3), 3.42 (dd, 1H, J. 15.0, 7.1 Hz, 1 x CH2) ; 3.02 (dd, IK, J * 15.0, 7.0 Hz, 1 X CH2) ; 2.44 (s, 3H, CH3), 1.2€ (t, J - 7.1 Hz, ester-CH3) . :Seela, F.; Lupke, U. Chem. Ber. 1977, HO, 1462-1469. Preparation 2: The procedure of Seela and Lupke was used. Thus, protection of the ketone (3) (Scheme IV; 5.0 g, 32.2 mmol) with ethylene glycol (4 mL, 64.4 mmol) in the presence of TsOH (100 mg) afforded (4) as an oil (Scheme IV; 5.2 g, 81.0) after flash chromatography (Si02; 3/7 EtOAc/Hex, Rf 0.35). Still contains ~5V ethyl ester: XH NMR (200 MHz, CDC13) 6_4.24 (q, J « 7.2 Hz, OCH2), 3.98 (s, 4H, 2 x acetal-CH2), 3.79 (s, 3H, OCH3), 3.62 (dd, 1H, J = 7.2, 7.0 Hz, CH) , 2.48 (dd, 1H, J = 15.0. 7.1 HZ, 1 X CH2), 2.32 (dd, 1H, J = 15.0, 7.0 Hz, 1 X CH2) ; 1.35 (S, 3H, CH3), 1.26 (t, J - 7.1 Hz, ester-CH3); MS (ES): 200.1 (M' + l) . :Seela, F.; Lupke, U. Chem. Ber. 1977, HO, 1462-1469. Preparation 3: A solution of acetal (4) (Scheme IV, 1 g, 5.C2 mmci;, benzamidine (786 mg, 5.02 mmol), and DBU (1.5 mL. 10.04 mmol) in dry DMF (15 mL) was heated to 85°C for 15 h. The mixture was diluted with CHC13 (30 mL) and washed with 0.5 K NaOK (10 mL) and H20 (20 mL) . The organic fraction was dried, filtered and concentrated to a brown oil. Flash chrornatography (SiO->; 1/9 EtOAc/CH2Cl2, Rt 0.35) was attempted, but material crystallized on the column. The silica gel was washed with MeOH. Fractions containing the product (5) (Scheme IV) were concentrated and used without further purification (783 mg, 54.3V): 1H NMR (200 MHz, CDC13) 6 8.24 (m, 2H, Ar-H), 7.45 (m, 3H, Ar-H). 5.24 (br s, 2H, NH2), 3.98 (s, 4H, 2 x acetal-CH2), 3.60-3.15 (m, 2H, CH2) , 1.38 (s, 3H, CH3); MS (ES): 288.1 (M'+l) . Preparation of compound (20) (Scheme VIII): A solution of acetal (19) (4.43 g, 20.6 mmol)1, benzamine hydrochloride (3.22 g, 20.6 mmol), and DBU (6.15 mL, 41.2 mmol) in dry DMF (20 mL) was heated to 85°C for fifteen hours. The mixture was diluted with lOOmL of CHC1,, and washed with H:0 (2 x 50 mL) . The organic fraction was dried, filtered, and concentrated to a dark brown oil. The dark brown oil was stirred in IN HC1 (100 mL) for 2 hours at room temperature. The resulting slurry was filtered yielding the HCl salt of (20) as a tan solid (3.60 g, 70.6V); 1H NMR (200 MHz, DMSO-d6) 11.92 (s 1H) , 8.05 (m, 2H, Ar-H), 7.45 (m, 3H, Ar-H), 7.05 (s, 1H, pyrrole- H) ; MS(ES) : 212.1 (M' + l) . Preparation 4: A solution of acetal (5) (700 mg, 2.44 mmol) in 1 N HCl (40 mL) was stirred for 2 h at RT. The resultant slurry was filtered yielding the HCl salt of 2-phenyl-6-methyl-7H- pyrrolo [2,3d] pyrimidin-4 (3H) -one as a tan solid (498 mg, 78.0V): :H NMR (200 MHz, DMSO-d6) 6 11.78 (s. 1H) . 8.05 (m, 2H, Ar-H), 7.45 (m, 3H, Ar-H), 6.17 (s, 1H, pyrrole-H), 2.25 (S, 3H, CH3) ; MS (ES) : 226.1 (M"«-l). Preparation 5: A modification of the Chen et al. eye li ration method was used.1 To an ice-cooled (0°C) solution of bror.ide (9), (Scheme V; 20.0 g, 108 mmol; 90V pure) in isoprcpyl alcohol (60 mL) was slowly added a solution of a-methylber.zylamine (12.5 mL, 97.3 mmol). The black solution was allowed to warm to RT and stir for 15 h. The mixture was diluted with EtOAc (200 mL) and washed with 0.5 N NaOH (50 mL) . The organic fraction was dried, filtered, and concentrated to a black tar (19.2 g,- 94V). The residue was partially purified by flash chromatography (Si02; 4/96 MeOH/C^C^, Rf 0.35) to a black solid (6.38 g, 31V) as the compound dl-l-(1-phenylethyl)-2- amino-3-cyano-4-methylpyrrole: MS (ES): 226.1 (M"*l). :Chen, Y. L. ; Mansbach, R. S. ; Winter, S. M.; Brooks, E.; Collins, J.; Corman, M. L. ; Dunaiskis, A. R.; Faraci, W. S.; Gallaschun, R. J. ,• Schmidt, A.; Schulz, D. w. j. Med. Chem. 1997, 40, 1749-1754. Preparation 6: To a solution of dl-l- (1-phenylethyl)-2-amino-3-cyano-4,5- dimethylpyrroie1 (14.9 g, 62.5 mmol) and pyridine (10.0 mL) in dichioromethane (50.0 mL) was added benzoyl chloride (9.37 g, 66.7 mmol) at O'C. After stirring at 0°C for 1 hr, hexane (10.0 mL) was added to help precipitation of product. Solvent was removed in vacuo and the solid was recrystallized from EtOH/H:0 to give 13 . 9 g (65V) of dl-l-(1-phenylethyl)-2- phenylcarbonylamino-3-cyano-4 , 5-dimethylpyrrole. mp 218-221°C; •H NMR (200 MHz, CDC1J 6_1.72 (s, 3H), 1.76 (d, J » 7.3 Hz, 3H) , 1.98 (s, 3H) , 5.52 (q, J = 7.3 Hz, 1H) , 7.14-7.54 (m, 9H) , 7.68-7.72 !dd, J « 1.4 Hz, 6.9 Hz , 2H) , 10.73 (s, 1H) ; MS (ES) -. 344 .4 (M'+l) . : Liebigs Ann. Chem. 1986, 1485-1505. The following compounds were obtained in a similar manner. Preparation 6A: dl-l- (1-phenylethyl) -2- (3-pyridyl) carbonylamino-3-cyano-4 . 5-dimethylpyrrole. *H NMR (200 MHz, CDC13) 6_1.63 (d, J =.6.8 Hz, 3H) , 2.02 (s. 3H) , 2.12 (s, 3H) , .5.50 (q, J * 6.8 Hz, IK), 7.14-7.42 (m, 5H) , 8.08 (m, 2H) , 8.75 (m, 3H) ; MS (ES) : 345.2 (M'+l)- dl-I-(1-phenylethyl)-2-(2-fury 1)carbonylamino-3-cyano-4,5- dimethylpyrrole. 1H NMR (200 MHz, CDC1,) 6 1.84 (d, J = 7.4 Hz, 3H) , 1.92 (s, 3H) , 2.09 (s, 3H) , 5.49 (q, J * 7.4 Hz, 1H) , 6.54 (dd, J » 1.8 Hz, 3.6 Hz, 1H) , 7.12-7.47 (m, 7H) ; MS (ES): 334.2 (M'+l), 230.1. dl-I-(1-phenylethyl)-2-(3-furyl)carbonylamino-3-cyano-4,5- dimethylpyrrole. :H NMR (200 MHz, CDCl,) 6 1.80 (d, J « 7 Hz 3H), 1.89 (s, 3H), 2.05 (s, 3H), 5.48 (q, J = 7 Hz, 1H). 6.59 (S, 1H) , 7.12-7.40 (m, 6H) , 7.93 (s, 1H) ; MS (ES): 334.1 (M'*l), 230.0. dl-I- (1-phenylethyl) -2-cyclopentylcarbonylamino-3-cyano-4 , 5- dimethylpyrrole. "H NMR (200 MHz, CDC1J 6 1.82 (d, J = 7.4 Hz, 3H) , 1,88 (s, 3H) , 2.05 (s, 3H) , 1.63-1.85 (m, 8H) , 2.63 (m, 1H), 5.43 (q, J = 7.4 Hz, 1H). 6.52 (s, 1H), 7.05-7.20 (m, 5H) ; MS (ES) : 336.3 (M' + l) . dl-I-(1-phenylethyl)-2-(2-thieyl)carbonylamino-3-cyano-4,5- dimethylpyrrole, ;H NMR (200 MHz, CDC13) 6 1.82 (d, J = 6.8 Hz, 3H) , 1.96 (s, 3H) , 2.09 (s, 3H) , 5.49 (q, J- 6.8 Hz, 1H) , 7.05-7.55 (m, 8H); MS (ES): 350.1 (M'*l), 246.0. dl-I- (1-phenylethyl) -2- (3-thienyl) carbonylamino-3-cyano-4 , 5- dimethylpyrrole. *H NMR (200 MHz, CDCl,) 5 1.83 (d, J = 7.0 Hz, 3H) , 1.99 (s, 3H) , 2.12 (s, 3H) , 5.49 (q, J = 7.0 Hz, 1H) , 6.90 (m, 1H) , 7.16-7.36 (m, 6H), 7.79 (m, 1H); MS (ES): 350.2 (M'-l), 246.1. dl-1- (1-phenylethyl) -2- (4-f luorophenyl) carbonylamino-3-cyar.c- 4 , 5-dimethylpyrrole. 1H NMR (200 MHz, CDC10 6 1.83 (d, J = 7.4 Hz, 3K) , 1.96 (s, 3H), 2.08 (s, 3H), 5.51 (q, J = 7.4 Hz, 1H), 7.16-7.55 (m, 9H) ; MS (ES) : 362.2 (M' + l). 258.1. dl-1- {1-phenylethyl)-2-(3-fluorophenyl) carbonylamino-3-cyano- 4,5-dimethylpyrrcle. :H NMR (200 MHz, CDCl,) 6 1.83 (d, J = 7.4 Hz 3H) , 1.97 (s, 3H), 2.10(s, 3H), 5.50 (q, J = 7.4 Hz, 1H), 7.05-7.38 (m, 7 H) , 7.67-7.74 (m, 2H) ; MS (ES): 362.2 (M'-l), 258.1. dl-1-(1-phenylethyl)-2-(2-fluorophenyl) carbonylamino-3-cyano- 4,5-dimethylpyrrole. :H NMR (200 MHz, CDC13) 6 1.85 (d, J = 7.2 Hz, 3H) , 1.94 (s, 3H) , 2.11 (s, 3H) , 5.50 (q, J = 7.2 hz. 1H) , 7.12-7.35 (m, 6H) , 7.53 (m, 1H) , 7.77 (m, 1H) , 8.13 (m, 1H) ; MS (ES) : 362.2 (M' + D , 258.0. dl-1-(1-phenylethyl)-2-isoproylcarbonylamino-3-cyano-4,5- dimethylpyrrole.-H NMR (200 MHz, CDC13) 6 1.19 (d, J = 7.0 Hz, 6H) , l,82(d, J « 7.2 Hz, 3H) , 1.88 (s, 3H) , 2.06 (s, 3H) , 2.46 (m, 1H) , 5.39 (m, J = 7.2 Hz, 1H) , 6.64 (s, 1H) , 7.11-7.36 (m, 5H); MS (ES): 310.2 (M'+l), 206.1 . In the case of acylation of dl-1-(1-phenylethyl)-2-amino-3-cyano-4-methylpyrrole, monoacylated dl-1-(1-phenylethyl)-2- benzoylamino-3-cyano-4-dimethylpyrrole and diacylated pyrrole dl -1 - (l-phenylethyl)- 2-dibenzoylamino-3 -cyano-4-methylpyrrole were obtained. Monoacylated pyrrole: *H NMR (200 MHz, CDC13) 6_7.69 (d, 2H, J = 7.8 Hz, Ar-H) , 7.58-7.12 (m, 8H, Ar-H) , 6.18 (s, 1H, pyrrole-H) , 5.52 (q, 1H, J = 7.2 Hz, CH-CH3), 2.05 (s, 3H, pyrrole-CH3) , 1.85 (d, 3H, J» 7.2 Hz, CH-CH3); MS (ES) : 330.2 (M'+l); Diacylated pyrrole: :H NMR (200 MHz, CDC13) 6_7.85 (d, 2H, J - 7.7 Hz, Ar-H), 7.74 (d. 2H, J = 7.8 Hz, Ar-H), 7.52-7.20 (m, 9H, Ar-H), 7.04 (m, 2H, Ar-H), 6.21 (s, 1H, pyrrole-H), 5.52 (q, 1H, J. 7.2 Hz, CH-CH3), 1.77 (d. 3H, J« 7.2 H2, CK-C23), 1.74 (s, 3K, pyrrole-CK3); MS iESi: 434.1 (M'fl) . Preparation 7: To a solution of dl-l- {1-phenylechyl)-2-phenylcarboxyamido-3-cyano-4,5-dimethylpyrrole (1.0 g, 2.92 mmol) in methanol (10.0 mL) was added concentrated sulfuric acid (1.0 mL) at 0CC. The resulted mixture was refluxed for 15 hr and cooled down to room temperature. The precipitate was filtered to give 0.48 g (48%) of dI-5,6-dimethyl-2-phenyl-7H-7-(1 - phenylethyl)pyrrolo (2, 3d]pyrimidin-4 (3#) -one. :H NMR (200 MHz. CDC13) 6_2.02 (d, J = 7.4 Hz, 3H) , 2.04 (s, 3H) , 2.41 (s, 3H) , 6.25 (q, J * 7.4 Hz, 1H), 7.22-7.50 (m, 9H), 8.07-8.12 (dd, J = 3.4 Hz, 6.8 Hz, 2H) , 10.51 (s, 1H) ; MS (ES) : 344.2 (M' + l) . The following compounds were obtained in a similar manner as that of Preparation 7 .- di - 5 ,6-dimethyl-2-(3-pyricyl)-7H-7-(l-phenylechyl) pyrrolo [2,3d]pyrimidin-4(3H)-one. :H NMR (200 MHz, CDC13) 6_2.03 (d, J = 7.2 Hz, 3H) , 2.08 (s, 3H) , 2.42 (s, 3H) , 6.24 (q, J = 7:2 Hz, 1H) , 7.09-7.42 (m, 5H) , 8.48 (m, 2H) , 8.70 (m, 3H) ; MS (ES) : 345.1 (M' + l) . dJ-5, 6-dimethyl-2- (2-furyl) -7H-7- (l-phenylethyl) pyrrolo [2, 3d] pyrimidin-4 (3tf) -one. 'H NMR (200 MHz, CDC13) 6 1.98 (d, J = 7.8 Hz, 3H) , 1.99 (s, 3H) . 2.37 (s, 3H) , 6.12 (q, J = 7.8 Hz, 1H), 6.48 (dd, J-1.8 Hz, 3.6 Hz, 1H), 7.17-7.55 (m, 7H), 9.6 (s, 1H); MS (ES): 334.2 (M'+l). dJ-5,6-dimethy1-2-(3-fury1) -7H-7-(l-phenylethyl)pyrrolo [2, 3d] pyrimidin-4 (3H)-one. ;H NMR (200 MHz, CDC13) 6 1.99 (d, J . 7 HZ, 3H) , 2.02 (S, 3H) , 2.42 (s, 3H) , 6.24 (q, J = 7 Hz, 1H) , 7.09 (s, 1H) , 7.18-7.32 (m, 5H) , 7.48 (s, 1H) , 8.51 (S, 1H1 ; MS (ES) : 334.2 (M"*l) . cfJ-5, 6-dimethyl-2-cyclopentyl-7H-7- (l-phenylethyl) pyrrolo [2,3d] pyrimidin-4 (3#) -one. :H NMR (200 MHz, CDClj' 6 1.95 (d, J = 7.4 Hz, 3H), 2.00 (s, 3H), 2.33 (s, 3H), l.Se- 1.88 (m, 8H) , 2.97 (m, 1H) . 6.10 (q, J = 7.4 Hz, IK), 7.16-7.30 (m, 5H) , 9.29 (s, 1H); MS (ES): 336.3 (M'-l). dl-5 . 6-dimethyl-2- (2-thienyl) -7H-7- (l-phenylethyl) pyrrolo [2, 3d] pyrimidin-4 (3H)-one. :H NMR (200 MHz, CDC1}) 6 2.02(d, J = 7.2 Hz, 3H) , 2.OS (s, 3H) , 2.41 (s, 3H) , 6.13 (q, J = 7.2 HZ, 1H), 7.12 (dd, J = 4.8, 2.8 Hz, 1H), 7.26-7.32 (m, 5H) , 7.44 (d, J = 4.8 Hz, 1H) , 8.01 (d, J = 2.8 Hz, IK) 11.25 (s, 1H); MS (ES): 350.2 (M'+l). dl-5 , 6-dimethyl-2- (3-thienyl) -7H-7- (1-phenylechyl) pyrrolo [2, 3d] pyrimidin-4 (3H)-one. ;H NMR (200 MHz, CDC13) 6 2.00 (d, J « 7.4 Hz, 3H) , 2.05 (s, 3H) , 2.43 (s, 3H) , 6.24(q, J = 7.4 Hz, 1H), 7.24-7.33 (m, 5H), 7.33-7.39 (m, 1H), 7.85 (m, 1H), 8.47 (m, 1H), 12.01 (s, 1H); MS (ES): 350.2 (M'+l). dl-5,6-dimechyl-2-(4-fluorophenyl)-7H-7-(l-phenylethyl) pyrrolo[2,3d]pyrimidin-4(3H)-one. :H NMR (200 MHz, CDC13) 6 2.01 (d, "J = 6.8 Hz, 3H) , 2.05 (s, 3H) , 2.42 (s, 3H) , 6.26 (q, J = 6.8 Hz, 1H) , 7.12-7.36 (m, 7H) , 8.23-8.30 (m, 2H) , 11.82 (S, 1H); MS (ES): 362.3 (M'+l). dl-5, 6-dimethyl-2-(3 -fluorophenyl) -7H-7- (l-phenylethyl) pyrrolo [2,3d]pyrimidin-4(3tf)-one. :H NMR (200 MHz, CDC1,) 6 2.02 (d, J - 7.4 Hz, 3H) , 2.06 (s, 3H) , 2.44 (s, 3H) , 6.29 (q, J = 7.4 Hz, 1H) , 7.13-7.51(m, 7H) , 8.00-8.04 (m, 2H) , 11.72 (s, 1H); MS (ES): 362.2 (M'+l). dl-5. 6-dimethyl-2- (2 - fluorophenyl) -7H-7- (l-phenylethyl) pyrrclo [2, 3d] pyrimidin-4 (3tf) -one. :H NMR (200 MHz, CDC13) 6 2.00(d, J = 7.2 Hz, 3H) , 2.05 (s, 3H) , 2.38 (s, 3H) , 6.24 (q, J . 7.2 Hz, 1H) , 7.18 - 7.45 (m, 8 H) , 8.21 (m, 1H) , 9.54 (s, 1H); MS (ES): 362.2 (M**l). dI-5 , 6-dimethyl-2-isopropyl-7£-7-(1-phenyiethyl)pyrrole [2,3d] pyrimidin-4 (3H) -one. :H NMR (200 MHz, CDC1:.) b 1.30 (d, J = 6.8 Hz, 3H! , 1.32 (d, J = 7.0 HZ, 3H) , 2.01 (s, 3H) , 2.34 (s, 3H) , 2.90 (m, IK), 6.13 (m, 1H) , 7.17-7.34 (m, 5H) , 10.16 (S, 1H) ; MS (ES) : 310.2 (M'fl). Preparation 8: A solution of d2-l- (1-phenylethyl)-2-benzoylamino-3-cyano-4-dimethylpyrrole (785 mg, 2.38 mmol) with concentrated H->S04 (1 mL) in DMF (13 mL) was stirred at 130°C for 48 h. The black solution was diluted with CHC13 (10° "^ and washed with 1 N NaOH (30 mL), and brine (30 mL) . The organic fraction was dried, filtered, concentrated, and purified by flash chromatography (Si02; 8/2 EtOAc/Hex, Rf 0.35) to a brown solid (184 mg, 24%) as dl -5-methyl-2-phenyl-7H-7-(1 -phenylethyl)pyrrolo[2,3d]pyrimidin-4(3H) -one. :H NMR (200 MHz, CDG13) 6_8.18 (m, 2H, Ar-H). 7.62-7.44 (m, 3H, Ar-H), 7.40-7.18 (m, 5H, Ar-H), 6.48 (s, 1H, pyrrole-H), 6.28 (q, 1H, J - 7.2 Hz, CH-CH3), 2.18 (s, 3H, pyrrole-CH3)> 2.07 (d, 3H, J « 7.2 Hz, CH-CH3); MS (ES) : 330.2 (M* + 1). Preparation 9: A mixture of dl-l-(1-phenylethyl)-2-amino-3-cyano-4,5- dimethylpyrrole (9.60 g, 40.0 mmol) and of formic acid (50.0 mL, 98%) was refluxed for 5 hr. After cooling down to room temperature and scratching the sides of flask, copious precipitate was formed and filtered. The material was washed with water until washings showed neutral pH to give dI-5,6- dimethyl-7H-7-(i-phenylethyl)pyrrolo[2,3d]pyrimidin-4(3H)- one. :K NMR (200 MHz, CDC1J 6 1.96 (d, J = 7.4 hz, 3H) , 2.00 (S, 3H) , 2.38 (s, 3HJ , 6.21 (q, J = 7.4 Hz, 1H) , 7.11-7.35 (m, 5H), 7.81 (s, 1H), 11.71 (s, 1H); MS (ES): 268.2 (M'+l). Preparation 10: dl -5 , 6-dimethyl-2-phenyl-7H-7-(1-phenylethyl) pyrrclc [2 , 3d] pyrimidin-4 (3H)-one (1.0 g, 2.91 mrnol) was suspended in polyphosphoric acid (30.0 mL) . The mixture was heated at 100'C for 4 hr. The hot suspension was poured onto ice water, stirred vigorously to disperse suspension, and basified to pK 6 with solid KOK. The resulting solid was filtered and collected to give 0.49 g (69V) of 5,6-dimethyl-2-phenyl-7H- pyrrolo [2,3d]pyrimidin-4(3H)-one. :H NMR (200 MHz, DMSO-dJ 6_2.17 (s, 3H) , 2.22 Is, 3H), 7.45 (br, 3H) , 8.07 (br, 2H,) , 11.49 (S, 1H), 11.82 (S, 1H); MS (ES): 344.2 (M'+l). The following compounds were obtained in a similar manner as that of Preparation 10: 5-methyl-2-phenyl-7#-pyrrolo[2,3d]pyrimidin-4(3H) -one. MS (ES) : 226.0 (M'+l) . 5,6-dimethyl-2-(3-pyridyl)-7H-pyrrolo[2, 3d]pyrimidin-4(3H) -one. MS (ES) : 241.1 (M' + l) . 5, 6-dimethyl-2- (2-furyl) -7H-pyrrolo [2, 3d] pyrimidin-4 (3#) -one. :H NMR (200 MHz, DMSO-df) 5 2.13 (s. 3H) , 2.18 (s, 3H) , 6.39 (dd, J = 1.8, 3.6 Hz, 1H) , 6.65 (dd, J = 1.8 Hz. 3.6 Hz, 1H) , 7.85 (dd, J * 1.8, 3.6 Hz, 1H, ) , 11.45 (s, 1H) , 11.60 (s, 1H) ; MS (ES) : 230.1 (M' + l) . 5, 6-dimethyl-2- (3-furyl) -7H-pyrrolo [2 , 3d] pyrimidin-4 (3H) -one. •H NMR (200 MHz, DMSO-d€) 6 2.14 (S, 3H) , 2.19 (s, 3H) , 6.66 (s, 1H) , 7.78 (s, 1H) , 8.35 (s, 1H) , 11.3 (s, 1H) , 11.4 (s, IHJ ; MS (ES) : 230.1 (M' + l) . 5,6-dimethyl-2-eyelopentyl-7H-pyrrolo[2,3d]pyrimidin-4 (3#) - one. :H NMR (200 MHz, DMSO-dt) 6 1.57-1.91 (m, 8 H) , 2.12 (s, 3H) , 2.16 (s, 3H) , 2.99 (m, 1H) , 11.24 (s, 1H) , 11.38 (S, IK) ; MS (ES) : 232.2 (M'«-l) . 5, 6 -dimethyl -2- (2-thienyl) -7H-pyrrolo [2, 3d] pyrimidir.-4 ;3-r- - one. JH NMR (200 MHz, DMSO-dJ 6 2.14 (s, 3H) , 2.19 (s, 3H), 7.14 (dd, J = 3.0, 5.2 Hz, 1H), 7.70 (d, J = 5.2 Hz 1H), 6.10 (d, J=3.0 Hz, 1H) , 11.50 (S, 1HJ ; MS (ES): 246.1 (M'-l). 5,6-dimethyl-2-(3-thienyl)-7tf-pyrrolo[2,3d]pyrimidin-4(3H)- one. :H NMR (200 MHz, DMSO-dJ 6 2.17 (s, 3H) , 2.21(s, 3H) , 7.66(m, 1H) , 7.75 (m, 1H) , 8.43 (m, 1H) , ,11.47 (s, 1H) , 11.69 (S, 1H) ; MS (ES) : 246.1 (M* + l) . 5,6-dimethyl-2-(4 -fluorophenyl)-7H-pyrrclo [2,3d]pyrinudin-4(3H)-one. :H NMR (200 MHz, DMSO-dJ 5 2.17 (s, 3H) , 2.21 (s, 3H) , 7.31 (m, 2H) , 8.12 (m, 2H) , 11.47 (s, 1H) ; MS (ES): 258.2 (M'i-1). 5,6-dimethyl-2-(3-fluorophenyl)-7H-pyrrolo [2,3d]pyrimidin-4(3#)-one. :H NMR (200 MHz, DMSO-dJ 6 2.18 (S, 3H) , 2.21 (s, 3H) , 7.33 (m, 1H), 7.52 (m, 1H) , 7.85-7.95 (m, 2H) , 11.56 (s, 1H), 11.80 (s, 1H); MS (ES): 258.1 (M'+l). 5,6-dimethyl-2-(2-fluorophenyl)-7H-pyrroio[2,3d]pyrimidin-4(3H)-cne. *H NMR (200 MHz, DMSO-dJ 6 2.18 (s, 3H) , 2.22 (s, 3H) , 7.27-7.37 (m, 2H) , 7.53 (m 1H) , 7.68 (m, 1H) , 11.54 (s, 1H), 11.78 (s. 1H); MS (ES): 258.1 (M'+l). 5 , 6-dimethyl-2-isopropyl-7H-pyrrolo [2,3d] pyrimidin-4 (3#) -one . 1H NMR (200 MHz, DMSO-dJ 6 1.17 (d, J» 6.6 Hz, 6H) , 2.11 (s, 3H) , 2.15 (s, 3H) , 2.81 (m, 1H) , 11.20 (s, 1H) , 11.39 (s, 1H) ; MS (ES) : 206.1 (M**l) . 5,6-dimethyl-7H-pyrrolo[2,3d]pyrimidin-4 (3H) -one. 1H NMR (200 MHz, DMSO-dJ 6 2.13 (s, 3H), 2.17 (s, 3H), 7.65 (S, 1H); MS (ES) : 164.0 (M"*l) . Preparation 11: A solution of 5,6-dimethyl-2-phenyl-7H-pyrrolo[2,3d] pyrimidin-4 (3H) -one (1.0 g, 4.2 mmol) in phosphorus oxychloride (25.0 mL) was refluxed for 6 hr and then concentrated in vacua to dryness. Water was added to the residue to induce crystallization and the resulting solid was filtered and collected to give 0.90 g (83V) of 4-chlcro-5.6-dimethyl - 2-phenyl-7H-pyrrolo [2, 3d] pyrimidine. JK NMR (200 MHz, DMSO-d«) 5_2.33 (s, 3H) , 2.33 {s, 3H) , 7.46-7.49 (m, 3K) , 8.30-8.35 (m, 2H) , 12.20 (s, 1H) ; MS (ES) : 256.1 (M'+l). The following compounds were obtained in a similar manner as that of Preparation 11: 4-chloro-5-methyl-2-phenyl-7H-pyrrolo[2 , 3d]pyrimidine. MS (ES) : 244.0 (M" + l) . 4-chloro-6-methyl-2-phenyl-7H-pyrrolo [2,3d] pyrimidine . MS (ES): 244.0 (M'+l). 4-chlcro-2-phenyl-7Jj-pyrrolo [2, 3d] pyrimidine. 'K NMR (200 MHz, DMSO-d6) 8.35 (2, 2H) , 7.63 (br s, 1H) , 7.45 (m, 3H) , 6.47 (br S, IK); MS (ES) : 230.0 (M* + l). 4-chloro-5, 6-dimethyl-2- (3-pyridyl) -7H-pyrrolo[2,3d] pyrimidine, MS (ES): 259.0 (M'+l). 4-chloro-5,6-dimethyl-2-(2-furyl) -7H-pyrrolo[2, 3d]pyrimidine. :H NMR (200 MHz, DMSO-d6) 6 2.35 (s, 3H) , 2.35 (s, 3H) , 6.68 (dd, J - 1.8, 3.6 Hz, 1H) , 7.34 (dd, J = 1.8 Hz, 3.6 Hz, 1H) , 7.89 (dd, J = 1.8, 3.6 Hz, 1HJ; MS (ES): 248.0 (M*+l). 4-chioro-S, 6-dimethyl-2- (3-furyl) -7H-pyrrolo [2 , 3d] pyrimidine . 'H NMR (200 MHz, DMSO-d«) 6 2.31 (s, 3H) , 2.31 (s, 3H) , 6.62 (S, 1H) , 7.78 (s, 1H) , 8.18 (S, 1H) , 12.02 (s, 1H) ; MS (ES) : 248.1 (M"+l)- 4-chioro-5,s-dimethyl-2-cyclopentyl-7H-pyrrolo[2,3d] pyrimidine. 'H NMR (200 MHz, DMSO-dJ 6 1.61- 1.96 (m, 8H) , 2.27 (s, 3H) , 2.27 (s, 3H) , 3.22 (m, 1H) , 11.97 (s, IK); MS (ES) : 250.1 (M'*l) . 4-chloro-5,6-dirnethyl-2-(2-thienyl)-7H-pyrrolo[2,3d] pyrimidine. :H NMR (200 MHz, DMSO-dt) -6 2.29 (s, 3H) , 2.31 (s, 3H) , 7.14 (dd, J = 3.1 Hz, 4.0 Hz , 1H), 7.33 (d, J = 4.9 Hz, 1H) , 7.82 (d, J » 3.1 Hz, 1H) , 12.19 (s, 1H) ; MS ( ES ) : 264 .1 4-chloro-5,6-dimethyl-2- (3-thienyl) -7H-pyrrolo[2,3d] pyrimidine. :H NMR (200 MHz, DMSO-dJ 6 2.32 (s, 3H) , 2.32 (s, 3H) , 7.62 (dd, J = 3.0, 5.2 Hz, 1H) , 7.75 (d, J = 5.2 Hz, 1H) , 8.20 (d, J = 3.0 Hz, 1H) ; MS (ES): 264.0 (M' + l). 4 -chloro-5, 6 -dimethyl -2- (4 -f luorophenyl ) -7H-pyrrolo [2,3d] pyrimidine. 'H NMR (200 MHz, DMSO-d4) 6 2.33(s, 3H) , 2.33 (s, 3H) , 7.30 (m, 2K) , 8.34 (m, 2H) , 12.11 (s, 1HJ ; MS (ES): 276 .1. (M' + l) . 4 -chloro-5, 6 -dimethyl -2- ( 3 - f luorophenyl ) -7H-pyrrolo (2, 3d] pyrimidine. :H NMR (200 MHz, DMSO-dJ 6 2.31(s, 3H) , 2.33 (s, 3H) , 7.29(m, 1H) , 7.52 (m, 1H) , 7.96 (m, 1H) , 8.14(m, 1H) . 11.57 (s, 1H) ; MS (ES): 276.1 (M*+l). 4-chloro-5, 6 -dimethyl -2- (2-f luorophenyl ) -7H-pyrrolo [2,3d] pyrimidine. 'H NMR (200 MHz, DMSO-dJ 6 2.34 (s, 3H) , 2.34 (s, 3H) , 7.33 (m, 2H) , 7.44 (m, 1H) , 7.99 (m, 1H) , 12.23 (s, 1H) ; MS (ES) : 276.1 (MVl) . 4 -chloro-5, 6-dimethyl-2-isopropyl-7H-pyrrolo [2, 3d] pyrimidine . 'H NMR (200 MHz, DMSO-dJ 5 1.24 (d, J = 6.6 Hz, 6H) , 2.28 (s, 3H) , 2.28 (s, 3H) , 3.08 (q, J = 6.6 Hz, 1H) , 11.95 (s, 1H) ; MS (ES) : 224 .0 (M' + l) . 4-chlcro-5, 6 -dimethyl -7H-pyrrolo [2, 3d] pyrimidine . :H NMR (200 MHz, DMSO-d4) 5 2.31 (s, 3H) , 2.32 (s, 3H) , 8.40 (s, 1H) ; MS (ES) : 182.0 (M"«-l) . dI-4-chloro-5,6-dimethyl-2-phenyl-7#-7-(i-phenylethyl)pyrrclr [2,3d]pyrimidine. Preparation 12: To a solution of dl-l,2-diaminopropane (1.48 g, 20.0 rr.mol) and sodium carbonate (2.73 g, 22.0 mmol) in dioxane (100.0 ruL) and water (100.0 mL) was added di- cerc-dicarbonate (4.80 g, 22.0 mmol) at room temperature. The resulted mixture was stirred for 14 hr. Dioxane was removed in vacua. The precipitate was filtered off and the filtrate was concentrated in vacuo to dryness. The residue was triturated with EtOAc and then filtered. The filtrate was concentrated in vacuo to dryness to give a mixture of dl-1-amino-2-(1,1- dimethylethoxy)carbonylamino-propane and dl-2-anuno-l- (1,1- dimethylethoxy)carbonylamino-propane which were not separable by normal chromatography method. The mixture was used for the reaction in Example 8. Preparation 13: To solution of Fmoc-3-Ala-OH (1.0 g, 3.212 mmol) and oxalyl chloride (0.428 g, 0.29 mL, 3.373 mmol) in dichloromethane (20.0 mL) was added a few drops of N,N-dimethylformamide at 0"C. The mixture was stirred at room temperature for 1 hr followed by addition of cycloprcpylmethylamine (0.229 g, 0.28 mL, 3.212 mmol) and triethylamine (0.65 g, 0.90 mL, 6.424 mmol) . After 10 min, the mixture was treated with 1 M hydrochloride (10.0 mL) and the aqueous mixture was extracted with dichloromethane (3 x 30.0 mL) . The organic solution was concentrated in vacuo to dryness. The residue was treated with a solution of 20% piperidine in N,N-dimethylforamide (20.0 rnL) for 0.5 hr. After removal of the solvent in vacuo, the residue was treated with 1 M hydrochloride (20.0 mL) and ethyl acetate (20.0 mL). The mixture was separated and the aqueous layer was basified with solid sodium hydroxide to pH = 8. The precipitate was removed by filtration and the aqueous solution was subjected to ion exchange column eluted with 20% pyridine to give 0.262 g (57%; cf N-cycloprcpylmethyl 0-alanine amide. ;K NMR (200 MHz, C23cr: 6_0.22 (m, 2H) , 0.49 (m, '2H> , 0.96 (m, 2H) , 2.40 (t, 2K) , 2.92 (t, 2H) , 3.05 (d, 2H) ; MS (ES) : 143.1 (M^l). Preparation 14: N- cerc-butoxycarbonyl-crans-1,4-cyclohexyldiamine . crans-1,4-cyclonexyldiamine (6.08 g, 53.2 mmol) was dissolved in dichloromethane (lOOmL) . A solution cf di-t-butyldicarbonate (2.32 g, 10.65 mmol in 40 mL dichloromethane) was added via cannula. After 20 hours, the reaction was partitioned between CHCl, and water. The layers were separated and the aqueous layer was extracted with CHCl, (3x) . The combined organic layers were dried over MgSO,, filtered and concentrated to yield 1.20 g of a white solid (53%). ;H-NMR (200MHz, CDClj) : 6 1.0-1.3 (m, 4H) , 1.44 (s, 9H) , 1.8 -2.1 (m, 4H) , 2.62 (brtn, 1H) , 3.40 (brs. 1H) , 4.37 (brs, 1HO; MS (ES): 215.2 (M' + l). 4-(N-acetyl)-N-cerc-butoxycarbonyl-crans-1,4-cyclohexyl diamine. , N-cerc-butoxycarbonyl-crans-1,4-cyclohexyldiamine (530 mg, 2.47 mmol) was dissolved in dichloromethane (20 mL) . Acetic anhydride (250 mg, 2.60 mmol) was added dropwise. After 16 hours, the reaction was diluted with water and CHC13. The layers were separated and the aqueous layer was extracted with CHCl; (3x) . The combined organic layers were dried over MgSO,, filtered and concentrated. Recrystallization (EtOH/H:0) yielded 190 mg of white crystals (30%) . ;H NMR (200 MHz, CDC1J : 6 0.9 - 1.30 (m, 4H), 1.43 (s, 9H), 1.96-2.10 (m, 7H) , 3.40 (brs, 1H) , 3.70 (brs, 1H) , 4.40 (brs, 1H) , 4.40 (brs, IK); MS (ES): 257.2 (M' + l), 242.1 (M' - 15), 201.1 (M" - 56) . 4-(4 -crans-acetamidocyclohexyl)amino-5,6-dimethyl-2-phenyl- 7H-(1-phenylethyl) pyrroio[2,3d]pyrimidine. 4- (N-acetyl) -N-cerc-butoxycarbonyl- crans-1, 4- cyclohexyldiamine (190 mg, 0.74 mmol) , was dissolved ir. dichloromethane (5 mL) and diluted with TFA (6 ml) . After lr hours, the reaction was concentrated. The crude solid, DMSC (2mL), NaHCOi (200 mg, 2.2 mmol) and 4-chloro-5,6-dimethyl - 2-phenyl-7K-pyrrolo [2,3d] pyrimidine (35 mg, 0.14 mmol) were combined in a flask and heated to 130 °C. After 4.5 hours, the reaction was cooled to room temperature and diluted with EtOAc and water. The layers were separated and the aqueous layer was extracted with EtOAc (3x). The combined organic layers were dried over MgSO,, filtered and concentrated. Chromatography (silica preparatory plate; 20:1 CHCl?:EtOK) yielded 0.3 mg of a tan solid (1% yield). MS (ES) .- 378.2 (M' + l) . 4- (N-methanesulfonyl)-N-tert-butoxycarbonyl- trans-1,4- cyclohexyldiamine. trans-1,4-cyclohexyldiamine (530 mg, 2.47 mmol) was dissolved in dichloromethane (20 ml) and diluted with pyridine (233 mg, 3,0 mmol). Methanesulfonyl chloride (300 mg, 2.60 mmol) was added dropwise. After 16 hours, the reaction was diluted with water and CHC1;. The layers were separated and the aqueous layer was extracted with CHC13 (3x). The combined organic layers were dried over MgSO4, filtered and concentrated, recrystallization (EtOH/H:0) yielded 206 mg of white crystals (29%). 'H-NMR (200MHz, CDC1,) : 6 1.10-1.40 (m, 4H) , 1.45 (s, 9H), 2.00-2.20 (m, 4H) , 2.98 (s, 3H), 3.20-3.50 (brs, 2H) , 4.37 (brs, 1H) ; MS (ES) 293.1 (M' + D. 278.1 (M'-15) , 237.1 (NT-56) . 4 -(4 -crans-methanesulfamidocyclohexyl)amino-5,6-dimethyl-2- phenyl-7H- (1-phenylethyl) pyrrolo [2 , 3d] pyrimidine . 4- (N-sulfonyl) - N- cerc-butoxycarbonyl- trans-1, 4 - cyclohexyldiarnine (206 mg, 0.71 mmol), was dissolved in dichlcromethane (5ml) and diluted with TFA (6 ml). 'After 16 hours, the reaction was concentrated. The crude reaction mixture, DMSO (2 ml), NaHCO, (100 mg, 1.1 mmol) and 1-chloro- 5 , 6 -dimethyl- 2 -phenyl - 7H-pyrrolo [2 , 3d] pyrimidine were combined in a flask and heated to 130 °C. After 15 hours, the reaction was cooled to room temperature, and diluted with EtOAc (3x). The combined organic layers were dried over MgSO,, filtered and concentrated. Chromatography (silica preparatory plate, 20:1 CHCl3/EtOH) yielded 2.6 mg of a tan solid (5V yield). MS (ES): 414.2 (M'»l). Example 1: A solution of 4-chloro-5,6-dimethyl-2-phenyl-7H-pyrrolo[2,3d] pyro-midine (0.50 g, 1.94 mmol) and 4 - trans-hydroxy cyclohexylanune (2.23 g, 19.4 mmol) in methyl sulfoxide (10.0 mL) was heated at 130°C for 5 hr. After cooling down to room temperature, water (10.0 mL) was added and the resulted aqueous solution was extracted with EtOAc (3 xlO.O mL) . The combined EtOAc solution was dried (MgSOJ and filtered, the filtrate was concentrated in vacuo to dryness, the residue was chromatographed on silica gel to give 0.49 g (75%) of 4-(4 - trans-hydroxycyclohexyl)amino-5,6-dimethyl-2-phenyl-7#- pyrrolo[2,3d]pyrimidine. mp 197-199°C; ;H NMR (200 MHz, CDC13) 6_1.25-1.59 (m, 8H) , 2.08 (s, 3H) , 2.29 (s, 3H) , 3.68-3.79 (m, 1H) , 4.32-4.38 (m, 1H) , 4.88 (d, J = 8 Hz, IK), 7.26-7.49 (m, 3H) , 8.40-8.44 (dd, J = 2.2, 8 Hz, 2H) , 10.60 (s, 1H) ; MS (ES) : 337.2 (M' + l) . The following compounds were obtained in a similar manner to that of Example 1: 4 - (4 -crans-hydroxycyclohexyl)amino-6-methyl - 2-phenyl-7H- pyrrclo[2,3d]pyrimidine.XH NMR (200 MHz, CDC13) 6_11.37 (s, 1H, pyrrole-NH), 8.45 (m, 2H, Ar-H), 7.55 (m, 3H. Ar-H), 6.17 (s, 1H, pyrrole-H) , 4.90 (br d, 1H, NH) , 4.18 (m, 1H, CH-O) , 3.69 (m, 1H, CH-N) , 2.40-2.20 (m, 2H) , 2.19-1.98 (m, 2H) , 2.25 (S, 3H, CK3) 1.68-1.20 (m, 4H); MS (ES): 323.2 (M'+l). 4 -(4 -crans-hydroxycyclohexyl)amino-5-methyl-2-phenyl-7H-pyrrolo[2,3d]pyrimidine.:H NMR (200 MHz, CDC13) 6_11.37 (s, IK, pyrrole-NH), 8.40 (m, 2H, Ar-H), 7.45 (m, 3H, Ar-H), 5.96 (s, 1H. pyrrole-H) , 4.90 (br d. 1H, NH) , 4.18 (m, IK, CH-C» . 3.69 (m, 1H, CK-N) , 2.38-2.20 (m, 2H) , 2.18-1.98 (m, 2H) , 2.00 (s, 3H, CH3) 1.68-1.20 (m, 4H); MS (ES): 323.2 (M'+l). 4- (4 - trans-hydroxycyclohexyl) amino-2-phenyl-7H-pyrrclo [2 . 3d] pyrimidine. mp 245.5-246.5°C; 'H NMR (200MHz, CD7OD) 6 8.23im, 2H, Ar-H) , 7.42 (m, 3H, Ar-H) , 7.02 (d, 1H, J = 3.6 Hz, pyrolle-H), 6.53 (d, 1H, J=3.6 Hz. pyrolle-H), 4.26 (m, 1H, CH-0) , 3.62 (m,lH, CH-N) , 2.30-2.12 (m, 2H) , 2.12-1.96 (m, 2H) , 1.64-1.34 (m, 4H) ; MS, M+l*309.3; Anal (C,,K:,N;0) C, H, N. 4- (4-trans-hydroxycyclohexyl)amino-5,6-dimethyl-2- (3 -pyridyl)-7H-pyrrolo [2, 3d] pyrimidine. :H NMR (200 MHz, CDCl,) 6_1.21-1.54 (m, 8H) ; 2.28 (s, 3H) ; 2.33 (s, 3H) ; 3.70 (m, 1H) , 4.31(m, 1H) , 4.89 (d, 1H) , 7.40 (m, 1H) , 8.61 (m, 2H) , 9.64 (m, 1H) ,- MS (ES) : 338.2 (M'+l). 4--(4- traus-hydroxycyclohexyl) amino-5, 6-dimethyl-2- (2-furyl) -7H-pyrrolo[2,3d]pyrimidine. :H NMR (200 MHz, CDCl,) 6 1.26- 1.64(m, 8H), 2.22 (S, 3H), 2.30 (s, 3H), 3.72(m, 1H), 4.23 (m, 1H) , 4.85 (d, 1H), 6.52(m, 1H) , 7.12 (m, 1H) , 7.53 (m, 1H) , 9.28 (s, 1H) ; MS (ES) : 327.2 (M" + l). 4- (4- trans-hydroxycyclohexyl) amino-5, 6-dimethyl-2- (3-furyl) -7tf-pyrrolo[2,3d]pyrimidine. ;H NMR (200 MHz, CDCl,) 6 1.25- 1.63 (m, 8 H) , 2.11 (s, 3H) , 2.27 (s, 3H) , 3.71(m, 1H) , 4.20 (m, 1H) , 4.84 (d, 1H) , 7.03 (m, 1H) , 7.45(m, 1H) , 8.13(m, 1H), 10.38 (m, 1H); MS (ES): 327.2 (M' + l). 4-(4-trans-hydroxycyclohexyl)amino-5,6-dimethyl-2-cyclopentyl-7H-pyrrolo[2,3d]pyrimidine. :H NMR (200 MHz, CDCl,) 5 1.26-2.04 (m, 16 H) , 2.26 (s, 3H) , 2.27 (s, 3H) , 3.15(m, 1H) , 3.70 (m, 1H) , 4.12 (m, 1H) , 4.75(d, 1H) ; MS (ES) : 329.2 (M' + l) . 4-(4-trans-hydroxycyclohexyl) amino-5 , 6-dimethyl-2-\2-thier.yl• -7H-pyrrolo [2,3d]pyrimidin-4-amine. 4H NKR (200 MHz, CDC13) 5 1.28-1.59 (m, 8H), 2.19 (s. 3H), 2.29 (s, 3K), 3.74 (m, IK). 4.19 (m, 1H) , 4.84 (d, 1H) , 7.09 (m. 1H) , 7.34 (m, 1H), 7.63 (m, 1H), 9.02 (s, IK); MS (ES): 343.2 (M"*l). 4 - (4-trans-hydroxycyclohexyl)amino-5,6-dimechyl-2- ( 3 -thaenyl) -7H- pyrrole [2, 3d] pyrimidine. 'H NMR (200 MHz, CDClj} 6 1.21-1.60 (m, 8H) , 1.98 (s, 3H) , 2.23 (s, 3H) , 3.66 [m, 1H) , 4.22 (m, 1H) , 7.27 (m, 1H) , 7.86 {m, 1H) , 8.09 (m, 1H) , 11.23 (S, 1H); MS (ES): 343.2 (M'+l). 4 - (4 - trans-hydroxycyclohexyl)amino-5,6-dimethyl-2- (4 -fluorcphenyl)-7H-pyrrolo[2,3d]pyrimidine. !H NMR (200 MHz, CDC13) 6 1.26- 1.66 (m, 8H), 1.94 (s, 3H), 2.28 (s, 3H), 3.73 (m, IK), 4.33 (m, 1H) , 4.92 (d, 1H) , 7.13 (m, 2H) , 8.41 (m, 2H), 11.14 (S, 1H); MS (ES): 355.2 (M'+l). 4 - (4 - trans-hydroxycyclohexyl)amino-5,6-dimethy1-2- ( 3 -fluorophe'nyl)-7H-pyrrolo [2, 3d] pyrimidine. :H NMR (200 MHz, CDClj) 6 1.26-1.71 (m, SH), 2.06 (s, 3H), 2.30 (s, 3H), 3.72 (m, IK), 4.30 (m, 1H), 4.90 (d, 1H), 7.09 (m, 1H), 7.39 (m, 1H) , 8.05 (m, 1H) , 8.20 (m, 1H) , 10.04 (s. IK); MS (ES): 355 .2 (M" + l) . 4- (4-trans-hydroxycyclohexyl)amino-5,6-dime thy1-2- (2 -fluorcphenyl)-7H-pyrrolo[2, 3d]pyrimidine. ;H NMR (200 MHz, CDCl,) 5 1.30-1.64 (m, 8H), 2.17 (s, 3H). 2.31 (s, 3H), 3.73 (m, 1H), 4.24 (m, 1H), 4.82 (d, 1H), 7.28 (m, 2H), 8.18 (m, 1H), 9.02 (m, 1H), 12.20 (s, 1H); MS (ES): 355.3 (M**l). 4- (4 - trans-hydroxycyclohexyl) amino-5 , 6 - dimethyl-2 - isopropyl- 7H-pyrrolo [2,3d] pyrimidine :H NMR (200 MHz, CDClj) 6 1.31 (d, J = 7.0 Hz, 6H) , 1.30-1.65 (m, 8H) , 2.27 (s, 3H) , 2.28 (s, 3H) , 3.01 (m, J = 7.0 Hz, 1H) , 3.71 (m, 1H) , 4.14 (m, 1H) , 4 .78 (d, 1H) ; MS (ES) : 303 .2. dl-4 - (2-crans-hydroxycyclohexyl)amino-5,6-dimethyl -:-isopropyl-7H-pyrrolo[2,3d]pyrimidine 'H NMR (200 MHz, crci3) d 1.31-1.42 (br, 4H) . 1.75-1.82 (br, 4K), 2.02 is, 3H) , 2.2S (S, 3H) , 3.53 (m, 1H) , 4.02 (m, 1H) , 5.08 (d, IK), 7.41-7.46 (m, 3H), 8.30 (m, 2H), 10.08 (s, IK); MS (ES): 337.2- (K*-l). 4- (3 , 4- crans-dihydroxycyclohexyl) amino-5, 6 -dimethyl -2 -phenyl-7#-pyrrolo[2,3d]pyrimidine. MS (ES): 353.2 (M*»l). 4- (3 , 4-cis-dihydroxylcyclohexyl) amino-5, 6-dimethyl-2-phenyl-7H-pyrrolo[2,3d]pyrimidine. MS (ES): 353.2 (M~*l). 4 -(2-acetylaminoethyl)amino-5,6-dimethyl-2-phenyl-7#- pyrrclo[2,3d]pyrimidine. mp 196-199°C; :HNMR (200 MHz, CDC1,) 6_1.72 (s, 3H) , 1.97 (s, 3H), 2.31 (s, 3H) , 3.59 (m, 2H) , 3.96 (m, 2H) , 5.63 (br, 1H) , 7.44-7.47 (m, 3H) , 8.36-8.43 (dd, J = 1 Hz, 7 Hz, 2H) , 10.76 (S, 1H) ; MS (ES) : 324.5 (M' + l) . dJZ-4- (2- crans-hydroxycyclopentyl) amino-5, 6-dimethyl-2-phenyl- 7/f-pyrrolo [2, 3d] pyrimidine . • •H NMR (200 MHz, CDC1?) 6_1.62 (m, 2H) , 1.79 (br, 4H) , 1.92 (s, 3H), 2.29 (s, 3H), 4.11 (m, 1H), 4.23 (m, 1H), 5.28 (d, 1H) , 7.41-7.49 (m, 3H) , 8.22 (m, 2H) , 10.51 (s, 1H) ; MS (ES) : 323 .2 (M' + l) . : For preparation of 2-crans-hydroxycyclopentylamine, see PCT 9417090. dJ-4- (3- crajis-hydroxycyclopentyl) amino-5, 6-dimethyl-2-phenyl-7H-pyrrole[2,3d]pyrimidine. • •H NMR (200 MHz, CDC1J 6_1.58-1.90 (br, 6 H,), 2.0S'(s, 3H) , 2.29 (s, 3H) , 4.48-4.57 (m, 1H) , 4.91-5.01 (m, 2H) , 7.35-7.46 (m, 3H) , 8.42-8.47 (m, 2H) , 10.11 (s, 1H) ; MS (ES) : 323.2 (M'-l). 1 For preparation of 3- trans-hydroxycyclopentylamine, see E?> A-322242. d2-4- (3 -cis-hydroxycyclopentyl) amino-5 , 6-dimethyl -2-pher.yl-7H-pyrrolo[2,3d]pyrimidine.' :H NMR (200 MHz, CDC1,) 6_1.82-2.28 (br, 6H) , 2.02 Is, 3H), 2.30 (s, 3H), 4.53-4.60 (m, 1H), 4.95-5.08 (m, 1H). 5.85-5.93 (d, 1H) , 7.35-7.47 (m, 3H) , 8.42-8.46 (m, 2H) , 10.05 Is, IK) ; MS (ES) : 323.2 (M' + l) - • For preparation of 3-cis-hydroxycyclopentylamine, see EP-A- 322242. 4-(3,4-crans-dihydroxycyclopentyl)amino-5,6-dimethyl-2-phenyl -7H-pyrrolo[2,3d]pyrimidine.1 :H NMR (200 MHz, CDC1:.) 6_1.92- 1.99 (br, 2H) , 2.14 (s, 3H) , 2.20 (br, 2H) , 2.30 (s, 3H) , 2.41-2.52 (br, 2H) , 4.35 (m, 2H) , 4.98 (m, 2H) , 7.38-7.47 (m, 3H) , 8.38-8.42 (m, 2H) , 9.53 (s, 1H) ; MS (ES) : 339.2 (M' + l). • For preparation of 3 , 4 - crajis-dihydroxycyclopentylamine, see PCT 9417090. 4-(3-amino-3-oxopropyl)amino-5,6-dimethyl-2-phenyl-7H- pyrrolo[2,3d]pyrimidine. :H NMR (200MHz, CDC10 6_2.02 (s, 3H), 2.29 (s, 3H), 2.71 (t, 2H) , 4.18 (m, 2H) , 5.75-5.95 (m, 3H) , 7.38-7.48 (m, 3H) , 8.37-8.41 (m, 2H), 10.42 (s, 1H); MS (ES): 310.1 (M'*l). 4-(3-N-cyclopropylmethylamino-3-oxopropyl)aminc-5,6-dimethy1-2-phenyl-7H-pyrrolo[2, 3d] pyrimidine. :H NMR (200 MHz, CD.OD) 6_0.51 (q, 2H), 0.40 (q, 2H), 1.79-1.95 (br, 1H), 2.36 (s, 3H) , 2.40 (s, 3H) , 2.72 (t, 2H) , 2.99 (d, 2H) , 4.04 (t, 2H) , 7.58-7.62 (m, 3H), 8.22-8.29 (m, 2H); MS (ES): 364.2 (M'*l). 4-(2-amino-2-oxoethyl)amino-5,6-dimethyl-2-phenyl-7H- pyrrolo [2,3d] pyrimidine :H NMR (200 MHz, CD7OD) 6 2.31 (s, 3H) , 2.38 (s, 3H) , 4.26 (s,'2H), 7.36 (m, 3H) , 8.33 (m, 2H) ; MS (ES) : 396.1 (M'»l) . 4- (2-N-methylamino-2-oxoethyl) ammo-5, 6-dimethyl-2-pher.yl-7.~- pyrrole [2,3d] pyrimidine. :H NMR (200 MHz, CDCl,) 5_l.?r ;s. 3H) , 2.17 .(s, 3H) , 2.82 (d, 3H) , 4.39 (d, 2H) , 5.76 {-, 1H! , 6.71 (br, 1H) , 7.41-7.48 (m, 3H) , 8.40 (m, 2K) , 1C. 66 ts. 1H) ; MS (ES) : 310.1 (M'+l) . 4- (3- cerc-butylcxyl-3-oxopropyl) ammo-5, 6-dimethyl-2-phenyl-7A'-pyrrolo [2,3d] pyrimidine. :H NMR (200 MHz, CDCl:) c_1.45 is, 9H) , 1.96 (S, 3H) , 2.29 (s, 3H) , 2.71 (t, 2H), 4.01 (q, 2H) , 5.78 (t, 1H) , 7.41-7.48 (m, 3H) , 8.22-8.29 (m, 2H) ; MS i£S): 367.2 (M'+l). 4-(2-hydroxyethyl)amino-5,6-dimethyl-2-phenyl-7H- pyrrolo [2,3d] pyrimidine. 'H NMR (200 MHz, CDC1;.) 6 1. 92 (s, 3H) , 2.29 (s, 3H) , 3.81-3.98 (br, 4H) , 5.59 (t, 1H) , 7.39-7.48 (m, 3H) , 8.37 (m, 2H) , 10.72 (s, 1H) ; MS (ES): 283.1 (M' + l) . 4-(3-hydroxypropyl)amino-5,6-dimethyl-2-phenyl-7H- pyrrclo [2, 3d] pyrimidine. :H NMR (200 MHz, CDC1:.) 5 1.84 (m, 2H) , 1.99"(s, 3H) , 2.32 (s, 3H) , 3.62 (t, 2H) , 3.96 (m, 2H) , 3.35 (t, 1H) , 7.39-7.48 (m, 3H) , 8.36 (m, 2H) , 10.27 (s, 1H) ; MS (ES) : 297.2 (M' + l) . 4 - (4-hydroxybutyl)amino-5,6-dimethy1-2 -pheny1-1H-pyrrolo [2,3d] pyrimidine. 'H NMR (200 MHz, CDCl,) 6 1.71-1.82 (m, 4H) , 1.99 (s, 3H) , 2.31 (s, 3H) , 3.68-3.80 (m, 4H) , 5.20 (t, 1H) , 7.41-7.49 (m, 3H) , 8.41(m, 2H) , 10.37 (s, 1H) ; MS (ES): 311.2 (M'-l) . 4-(4-crans-acecylaminocyclohexyl) amino-5,6-dimethyl-2-phenyl-7H-pyrrole[2,3d]pyrimidine. 4- (4- crans-meuhylsulfonylaminocyclohexyl) amino-5, 6-dimethyl-2-phenyl-7#-pyrrcio[2,3d]pyrimidine. 4 - (2-acetylaminoethyl) amino-5 , 6-dimethyl-2-phenyl -1H- ~ - '. - -phenylethyl)pyrrole[2,3d]pyrimidine. 4- (4 - trans-hydoxycyciohexyl) amino-5, 6-dimethyl-2-phenyl -7K-1-phenylethyl)pyrrole[2,3d]pyrimidine. 4 - (3-pyridylmethyl)amino-5,6-dimethyl-2-phenyl-7H-7- (1 -phenylethyl)pyrrolo[2,3d]pyrimidine. 4- (2-methylpropyl)amino-5,6-dimethyl-2-phenyl-7H-7 - (i-phenylethyl) pyrrolo [2 , 3d] pyrimidine'. Example 2: To a stirred suspension of triphenylphosphine (0.047 g, 0.179 mmol) and benzoic acid (0.022 g, 0.179 mmol) in THF (1.0 mL) cooled to 0°C was added 4- (4- trans-hydroxycyclohexyl)amino- 5, 6-dimethyl-2-phenyl-7H-pyrrolo[2,3d]pyrimidine (0.05 g, 0.149 mmol) at 0°C. Diethyl azodicarboxylate (0.028 ml, 0.179 mmol) was then added drcpwise over 10 minutes. The reaction was then allowed to warm to room temperature. After reaction was complete by TLC the reaction mixture was quenched with aqueous sodium bicarbonate (3.0 mL). The aqueous phase was separated and extracted with ether (2 X 5.0 mL) . The organic extracts were combined, dried, and concentrated in vacua to dryness. To the residue was added ether (2.0 mL) and hexane (5.0 mL) whereupon the bulk of the triphenylphosphine oxide was filtered off. Concentration of the filtrate gave a viscous oil which was purified by column .chromatography (hexane:ethyl acetate=4:l) to give 5.0 mg (7.6V) of 4-(4-cis-benzoyloxycyclohexyl)amino-5,6-dimethyl-2-phenyl-7 H- pyrrol.o [2,3d] pyrimidine. MS (ES) : 441.3 (M' + l). The reaction also produced 50.0 mg (84%) of 4 - (3-cyclohexenyl)amino-5,6-dimethyl-2-phenyl-7H-pyrrolo [2, 3d] pyrimidine. MS (ES) : 319.2 Example 3 : To a solution of 4 - (4-cis-benzoyloxycyciohexyl) arr.ir.o- 5 . The following compounds were obtained in a similar manner as that of Example 3: 4- (3-N,N-dimethyl-3-oxopropyl) amino-5, 6-dimethyl-2-phenyl -7H- pyrrolo [2,3d] pyrimidine. :H NMR (200 MHz, CDC1;.) 6 2.01 (s. 3H) , 2.31 (s. 3H), 2.73 (t, 2H) , 2.97 (s, 6H) , 4.08 (m, 2H) , 6.09 (t, 1H) , 7.41-7.48 (m, 3H) , 8.43 (m, 2H) . 10.46 (s, 1H) ; MS (ES) :.. 338.2 (M' + l) . 4 - (2 -formy1 aminoethyl)amino-5 , 6-dimethyl-2-phenyl-7#- pyrrolo [2,3d] pyrimidine. :H NMR (200 MHz, CDC1:.) 5 2.26 (s, 3H) , 2.37 (s, 3H) , 3.59-3.78 (m, 2H) , 3.88-4.01 (m, 2H) , 5.48-5.60 (m, 1H) . 7.38-7.57 (m, 3H) , 8.09 (s, 1H) , 8.30-8.45 (m, 2H) , 8.82 (S, 1H) ; MS (ES): 310.1 (M' + l). 4-(3-acetylaminopropyl)amino-5,6-dimethyl-2-phenyl-7H-pyrrolo[2,3d]pyrimidine. MS (ES): 338.2 (M"+l). Example 4: 4- (3 - terc-butyloxy-3-oxopropyl) amino-5, 6-dimethyl-2-pher.yl -7H-pyrrolo [2,3d]pyrimidine (70.0 mg, 0.1S1 mmol)) was dissolved in trifluoroacetic acid:dichlcromethane (1:1, 5.0 mL) . The resulting solution was stirred at' room temperature for 1 hr. and then refluxed for 2 hr. After cooling down to room temperature, the mixture was concentrated in vacua to dryness. The residue was subjected to preparative thin layer chromatography (EtOAc:hexane: AcOH=7:2.5:0.5) to give 40.0 mg (68V) of. 4-(3-hydroxy-3 -oxopropyl)amino-5,6-dimethyl- 2-phenyl-7H-pyrrolo[2,3d] pyrimidine. ;H NMR (200 MHz, CD:OD) 6 2.32 (s, 3H) , 2.38 (s. 3H) , 2.81 (t, 2H) , 4.01 (t, 2H) , 7.55 (m, 3H) , 8.24 (m, 2H) ,-MS (ES) : 311.1 (M' + D . The following compound was obtained in a similar manner as that of Example 4: 4- (3-aminopropyl)amino-5, 6-dimethyl-2-phenyl-7#-pyrrolo [2, 3d] pyrimidine. MS (ES) : 296.1 (M' + l) , 279.1 (M"-NH3) . Example 5: 4 - (3 -hydroxy- 3 -oxopropyl) amino-5 , 6-dimethyl - 2-phenyl-7H- pyrrolo[2,3d]pyrimidine (50.0 mg, 0.161 mmol) was dissolved in a mixture of N,N-dimethylformamide (0.50 mL), dioxane (0.50 mL) and water(0.25 mL) . To this solution was added methylamine (0.02 mL, 40% wt in water, 0.242 mmol), triethylamine (0.085 mL) and N,N, N'N1-tetramethyl uroniutn tetrafluoroborate (61.2 mg, 0.203 mmol). After stirring at room temperature for 10 min, the solution was concentrated and the residue was subjected to preparative thin layer chromatography (EtOAc) to give 35.0 mg (67%) of 4 - (3 -N-methyl-3-oxopropyl) amino-5, 6 -dimethyl -2 -phenyl-7#- pyrrolo [2,3d] pyrimidine. :H NMR (200 MHz, CDClj) 5 1.92 (s, 3H) , 2.30 (s, 3H) , 2.65 (t, 2H) , 4.08 (t, 2H) , 5.90 (t, 1H) , 6.12 (m, 1H) , 7.45 (m, 3H) , 8.41 (m, 2H) , 10.68 (s, 1H) ; MS (ES) : 311.1 (M**l) . The following compounds were obtained in a similar manner as that of Example 5: 4-(2-cyclopropanecarbonylaminoethyl)anuno-5, 6-dimethyl- 2-phenyl-7H-pyrrolo[2,3d] pyrimidine. MS (ES) : 350.2 IM"»D . 4-(2-iscbutyrylaminoethyl)amino-5,6-dimethyl-2-phenyl-7H-pyrrolo[2,3d]pyrimidine. MS (ES): 352.2 (M'+l). 4-(3-propionylaminopropyl)amino-5,6-dimethyl-2-phenyl-7.v- pyrrolo[2,3d]pyrimidine. :H NMR (200 MHz, CDCl:) 5 l.00-1.08 (t, 3K) , 1.71-2.03 (m, 4H) , 2.08 (s, 3H) , 2.37 (s, 3K) , 3.26- 3.40 (m, 2H), 3.79-3.96 (m, 2H), 5.53-5.62 (m, IK),_6.17-6.33 (m, IK), 7.33-7.57 (m, 3H) , 8.31-8.39 (m, 2H) , 9.69 (s, 1H) ; MS (ES) : 352.2 (M' + U . 4-(2-methylsulfonylaminoethyl)amino-5,6-dimethyl-2-phenyl-7H- pyrrolo [2,3d] pyrimidine. "'H NMR (200 MHz, CDClJ 5 2.18 (s, 3H), 2.27 (s, 3H), 2.92 (s, 3H). 3.39-3.53 (m, 2H), 3.71-3.88 (m, 2HJ , 5:31-5.39 (m, 1H) , 6.17-6.33 (m, 1H) , 7.36-7.43 (m, 3H) , 8.20-8.25 (m, 2H) , 9.52 (s, 1H) ; MS (ES) : 360.2 (M' + l) . Example 6: A mixture of 4-chloro-5,6-dimethyl-2-phenyl-7K-pyrrolo[2,3d] pyrimidine (0.70 g, 2.72 mmol) and 1,2-diaminoethane (10.0 ml, 150 mmol) was refluxed under inert atmosphere for 6 hr. The excess amine was removed in vacuo, the residue was washed sequentially with ether and hexane to give 0.75 g (98%) of 4-(2-aminoethyl)amino-5,6-dimethyl-2-phenyl-7H- pyrroiol 2,3d]pyrimidine. MS (ES) ; 282.2 (M'*l) . 265.1 (M"-NH3). Example 7: To a solution of 4-(2-aminoethyl)amino-5,6-dimethyl-2-phenyl-TH-pyrrolo[2,3d]pyrimidine (70.0 mg, 0.249 mmol) and tnethylamine mL) was added propionyl chloride (25.6 mg, O.C24 rr.L, :.2~-. mmol) at 0CC. After 1 hr, the mixture was concentrated _r. vacuo and the residue was subjected to preparative thin layer chromatography (EtOAc) to give 22,0 mg (26%) cf 4-(2-propionylaminoethyl)amino-5,6-dimethyl-2-pher. yl-7.v-pyrrolo[2,3d]pyrimidine. MS (ES): 338.2 (M'-i). The following compounds were obtained in a similar manner as that of Example 7: 4-(2-N1-methylureaethyl)amino-5,6-dimethyl - 2-phenyl-7/s-pyrrolo [2 , 3d]pyrimidine. :H NMR (200 MHz, CDC1J 5 2.13 (s, 3H) , 2.32 (s, 3K) , 3.53 (d, 3H) , 3.55 (m, 2H) , 3.88 (m, 2H) , 4.29 (m, 1H) , 5.68 (t, 1H) , 5.84 (m, 1H), 7.42 (m, 3H) , 8.36 (dd, 2H). 9.52 (S, 1H); MS (ES): 339.3 (M" + l). 4-(2-N1-ethylureaethyl)amino-5,6-dimethyl-2-phenyl-7H-pyrrolo[2,3d]pyrimidine. MS (ES): 353.2 (M'+l). Example 8: To a soTution of 1-(3-dimethylaminopropyl)-3-ethylcarbodi-imide hydrochloride (41.1 mg, 0.215 mmol), dimethylamino-pyridine (2.4 mg, 0.020 mmol) and pyruvic acid (18.9 mg, 0.015 mL, 0.215 mmol) in dichloromethane (2.0 mL) was added 4 - (2-aminoethyl) amino-5, 6-dimethyl-2-phenyl-7H-pyrrolo [2, 3d] pyrimidine (55.0 mg, 0.196 mmol). The mixture was stirred at room temperature for 4 hr. Usual workup and column chromatography (EtOAc) then gave 10.0 mg (15%) of 4-(2'-pyruvylamidoethyl)amino-5,6-dimethyl-2-phenyl-7#- pyrrolo(2,3d]pyrimidine.. MS (ES): 352.2 (M'-l). Exaaple 9: To a solution of 4 -(2-aminoethyl)amino-5,6-dimethyl-2-phenyl- 7W-pyrrolo[2,3d]pyrimidine (60.0 mg, 0.213 mmol) in dichloromethane (2.0 mL) was added N-trimethylsilyl isocyanace (43.3 mg, 0.051 mL, 0.320 mmol). The mixture was stirred at room temperature for 3 hr followed by addition c: aqueous sodium bicarbonate. After filtration through small amount of silica gel, the filtrate was concentrated in varuc to dryness to give 9.8 mg (14%) of 4-(2-ureaethyi ) arr.ino-5 , 6 -dimethyl - 2 -phenyl-7#-pyrrolo [2 , 3d] pyrimidine . MS (£S) -. 225.2 (M' + l) . The following compounds were obtained in a similar manner as that of Example 9: dl-4 -(2-acetylaminopropyl)amino-5 ,6-dimethy1-2-phenyl-7H- pyrrolo [2,3d]pyrimidine. :H NMR (200 MHz, CDClJ 6 1.28-1.32 (d, J = 8 Hz, 3 H), 1-66 (s, 3H) , 1.96 (s, 3H) , 2.30 (s, 3H) 3.76-3.83 (m, 2H) , 4.10-4.30 (m, 1H) , 5.60-5.66 (t, J=6 Hz, 1H) , 7.40-7.51(m, 3H) , 8.36-8.43 (m, 2H) , 10.83 (s, 1H) ; MS (ES) : 338.2 (M' + l) . (R)-4-(2-acetylaminopropyl)amino-5,6-dimethyl-2-phenyl-7H-pyrrolo [2,3d] pyrimidine. :H NMR (200 MHz, CDC13) 5 1.31 (d, 3H) , 1.66 (s, 3H) 1.99 (s, 3H), 2.31 (R) -4- (1-methyl-2-acetylaminoethyl)amino-5,6-dimethy1-2-phenyl-7K-pyrrolo[2,3d]pyrimidine. :H NMR (200 MHz, CDC1,) 6 1.41 (d, 3H) , 1.68 (S, 3H) , 2.21 (s, 3H) , 2.34 (s, 3H) , 3.46-3.52 (br, m, 2H) , 4.73 (m, IK), 5.22 (d, 1H) , 7.41-7.46 (m, 3H) , 8.36-8.40 (m, 2H) , 8.93 (s, 1HJ ; MS (ES): 338.2 (M' + l). (S)-4 -(2-acetylaminopropyl)amino-5,5-dimethyl-2 -phenyl-7H-pyrrolo [2,3d] pyrimidine. :H NMR (200 MHz, CDClJ 6 1.31 (d, 3H), 1.66 (s, 3H) 2.26 (s, 3H), 2.35 (s, 3H), 3.78-3.83 (m, 2H) , 4.17-4.22 (m, 1H) , 5.67 (t, 1H) , 7.38-7.5 (m, 3H) , 8.39 (m, 2H), 8.S7(s, 1H); MS (ES): 338.2 (M'+l). (S) -4 - (1 -methyl -2-acetylaminoethyl)amino-5,6-dimethyl-2-phenyl-7K-pyrrolo [2.3d] pyrimidine. ;H NMR (200 MHz, CDC1.) 6 1.41 (d, 3H) , 1.68 (s, 3K) , 2.05 (s, 3H) , 2.32 is, 3H' , 3.4c-3.52 (m. 2H) , 4.73 (m, IK), 5.22 (d, IK) , 7.41-7.46 itn, 3H' , 8.36-8.40 (m, 2H), 10.13 (s, 1H); MS !ES): 338.2 (M'-l). Example 10: Reaction of 4-chloro-5,6-dimethyl-2-phenyl-7K-pyrrcio [2,3d] pyrimidine with the mixture of dl-l-amino-2-(1,1-dimethyl ethcxy)carbonylamino-propane and dl-2-amino-1-(1,1-dimethyl ethoxy) carbonylamino-propane was run in a similar manner as that of Example 1. The reaction gave a mixture of d!-4-(l- methyl-2-(1,1-dimethylethoxy)carbonylamino)ethylammo-5,6-dimethyl-2-phenyl-7H-pyrrolo[2,3d]pyrimidine and dJ-4-(2- methyl-2- (1,1-dimethylethoxy)carbonylamino)ethylamino-5,6 -dimethyl-2-phenyl-7H-pyrrclo[2,3d] pyrimidine which were separated by column chromatography (EtOAc:hexanes = l:3) . The first fraction was dl-4-(l-methyl-2-(1,1-dimethylethoxy) carbonylaminoethyl)amino-5,6-dimethyl-2-phenyl-7H-pyrrolo [2,3d) pyrimidine: JK NMR (200 MHz, CDCl,) 6 1.29 - 1.38 (m, 12 K) , 1.95 (s, 3H) , 2.31 (s, 3H) 3.34-3.43 (m, 2H) , 4.62-4.70 (m, 1H) , 5.36-5.40 (d, J=8 Hz, IK), 5.53 (br, 1H) , 7.37-7.49" (m, 3H) , 8.37-8.44(m, 2H) , 10.75 '(s, 1H) . MS 396.3 (M"*l); The second fraction was dl-4 -(2-(1,1- dimethyiethoxy)carbonylaminopropyl) amino-5,6-dimethyl- 2 -phenyi-7H-pyrrolo (2,3d]pyrimidine: :H NMR (200 MHz, CDCl,) 6 1.26-1.40 (m, 12 H) , 2.00 (s, 3H) , 2.31 (s, 3H) 3.60-3.90 (m, 2H) , 3.95-4.10 (m, 1H) , 5.41-5.44 (d, J-6.0 Hz, 1H) , 5.65(br, 1H) , 7.40-7.46(m, 3K) , 8.37-8.44(m, 2H) , 10.89 (s, 1H) ; MS (ES): 396.2 (M'+l). The following compounds were obtained in a similar manner as that of Example 10: (S,S! -4-(2-acetylaminocyclohexyl)amino-5,6-dimethyl-2-phenyl-7H-pyrrolo [2,3d] pyrimidine. ;H NMR (200 MHz, CDClj) 6_1.43 (m, 4 H) , 1.60 (s, 3 H) , 1.83 (m, 2 H) , 2.18 (S, 3 H) , 2.30 (m, 2 H) , 2.32 (s, 3 H) , 3.73 (br, 1H) , 4.25 (br, 1H), 5.29 (d, 1H) , 7.43-7.48 (m, 3H) , 8.35-8-40 (m, 2H) , 9.05 (s, 1 H) . 4 - (2 -methyl-2-acetylaminoprcpyl) amino-5 , 6-dimethyl-2-pher.yl -7H-pyrrolo [2,3d]pyrimidine. :H NMR (200 MHz, CDC1;.) £_l.5l (s, 6H) , 1.56 (s, 3H) , 2.07 (s, 3H) , 2.36 (s, 3H) , 3.76 (d, 2H! , 5.78 (t, 1H), 7.41-7.48 (m, 3H), 7.93 (s, 1H), 8.39 im, 2HJ, 10.07 (S, 1H); MS (ES): 352.3 (M'+l). Example 11: dI-4-(l-methyl-2-(1,1-dimethylethoxy) carbonyl aminoechyl) amino-5, 6-dimethyl-2-phenyl-7H-pyrrolo [2,3d] pyrirrudine (60.6 mg, 0.153 mmol) was treated with trifluoroacetic acid (0.5 mL) in dichloromethane (2.0 mL) for 14 hr. The organic solvent was removed in vacuo to dryness. The residue was dissolved in N,N-dimethylformamide (2.0 mL) and triethylamine (2.0 mL) . To the solution at 0°C was added acetic anhydride (17.2 mg, 0.016, 0.169 mmol). The resulted mixture was stirred at room temperature for 48 hr and then concentrated in vacuo to dryness. The residue was subjected to preparative thin layer chromatography (EtOAc) to give 27.0 mg (52%) of dl- 4 - (1 - methyl -2-acetylaminoethyl)amino-5,6-dimethyl-2- phenyl-7H-pyrrolo [2,3d] pyrimidine. :H NMR (200 MHz, CDC13) 6 1.38-1.42 (d, J=8 Hz, 3 H) , 1.69 (s, 3H) , 2.01 (s, 3H) , 2.32 (s, 3H) "3.38-3.60 (m, 2H) , 4.65-4.80 (m, 1H) , 5.23-5.26 (d, J=6 Hz, 1H) , 7.40-7.51(m, 3H) . 8.37-8.43(m, 2H) , 10.44 (s, 1H) ; MS (ES) : 338.2 (M'+l) . Example 12: (R,R)-4 -(2-aminocyclohexyl)amino-5 , 6-dimethyl-2-phenyl-7H- pyrrolo[2,3d]pyrimidine, prepared in a similar manner as that of Example 1 from 4-chloro-5,6-dimethyl-2-phenyl-7H- pyrrolo[2,3d]pyrimidine (0.15 g, 0.583 mmol) and (1R, 2R)-(-) -1,2-diaminocyclohexane (0.63 g, 5.517 mmol), was treated with triethylamine (0.726 g, 7.175 mmol) and acetic anhydride (0.325 g, 3.18 mmol) in N,N-dimethylformamide (10.0 mL) at rocrn temperature for 2 hr. After removal of solvent in vacuo, ethyl acetate (10.0 mL) and water (10.0 mL) were added to the residue. The mixture was separated and the aqueous layer was extracted with ethyl acetate (2 x 10.0 mL) . The corriir.ed ethyl acetate solution was dried (MgS04) and filtered. Tr.e filtrate was concentrated in vacuo to dryness and the residue was subjected to column chromatography (EtOAc:Hexane = l: 1) tc give 57.0 mg (26V) of (R, R) -4 - (2-acetylaminocyclohexyl) atr.ino-5,6-dimethyl-2-phenyl-7H-pyrrolo[2,3d]pyrimidine. :K NMR (200 MHz. CDClj) 5_1.43 (m. 4 H) , 1.60 (s, 3 K) , 1.84 (m, 2 H) , 2.22 (s, 3 H), 2.30 (m, 2 H) , 2.33 (s, 3 H) , 3.72 (br, 1H) , 4.24 (br, 1H) , 5.29 (d. 1H) , 7.43-7.48 (m, 3H) , 8.35-8.39 (m, 2H), 8.83 (S, 1 H); MS (ES): 378.3 (M'+l). Example 13: To a solution of 4-(2-hydroxyethyl)amino-5,6-dimethyl-2-phenyl-7H-pyrrolo[2,3d]pyrimidine (40.0 mg, 0.141 mmol) in pyridine (1.0 mL) was added acetic anhydride (0.108 g, 1.06 mmol) at 0CC. The mixture was stirred at room temperature for 4 hr and the solvent was removed in vacuo. The residue was subjected to preparative thin layer chromatography (EtOAc:hexane = l :1) to give 32.3 mg (71%) of 4-(2-acetyloxyethyl)amino-5, 6-dimethyl-2-phenyl-7H-pyrrolo[2,3d] pyrimidine. :H NMR (200 MHz, CDC13) 6_1.90 (s, 3H) , 2.08 (S, 3H) , 2.31 (s, 3H) , 4.05 (m, 2H) , 4.45 (t, 2H) , 5.42 (m, 1H) , 7.41-7.49 (m, 3H) , 8.42(m, 2H) , 11.23 (s, 1H) . Example 14: A solution of Fmoc-S-Ala-OH (97.4 mg, 0.313 mmol) and oxalyl chloride (39.7 mg, 27.3 p.L, 0.313 mmol) in dichloromethane (4.0 mL) with 1 drop of N, N-dimethylf ormamide was stirred at 0°C for 1 hr followed by addition of 4 -(2-aminoethyl)amino-5,6-dimethyl-2-phenyl-7H-pyrrolo[2,3d]pyrimidine (80.0 mg, 0.285 mmol) and triethylamine (57.6 mg, 79.4 fj.L, 0.570 mmol) at 0SC. After 3 hr, the mixture was concentrated in vacuo and the residue was treated with the solution of 20V piperidine in N,N-dimethylforamide (2.0 mL) for 0.5 hr. After removal of the solvent in vacuo. the residue was washed with diethyl ether:hexane (1:5) to give 3 . 0 mg (3V) of 4 -(6-amino-3-aza-4 - oxohexyl) amino-5, 6 - dimethyl - 2 -phenyl - 7H- pyrrole [I . 3d! pyrimidine. MS (ES) : 353.2 (M%1). Example 15: A solution of 4- (2-aminoethyl) amino-5, 6 -dimethyl- 2 -pher.yl -7H-pyrrolo [2, 3d] pyrimidine (70.0 mg, 0.249 mmoi) and succir.ic anhydride (27.0 mg, 0.274 mmol) in dichloromethane (4.0 ml! with 1 drop of N,N-dimethylf ormamide was stirred at room temperature for 4 hr. The reaction mixture was extracted with 20% sodium hydroxide (3 x 5.0 mL) . The aqueous solution was acidified with 3 M hydrochloride to pH = 7.0. The whole mixture was extracted with ethyl acetate (3 x 10 mL) . The combined organic solution was dried (MgSOJ and filtered. The filtrate was concentrated in vacuo to dryness to give 15.0 mg (16%) of 4- (7-hydroxy-3 -aza-4 , 7-dioxoheptyl ) amino-5 , 6-dimethyl-2-phenyl-7H-pyrrolo [2 , 3d] pyrimidine . MS (ES) : 382.2 Example 16: To 10 mL of dimethylformamide (DMF) at room temperature were added 700 mg of 4 - cis-3 -hydroxycyclopentyl ) amino-2 -phenyl - 5, 6 -dimethyl -7H-pyrrolo [2, 3d] pyrimidine followed by 455 mg of N-Boc glycine, 20 mg of N,N-dimethylaminopyridine (DMAP) , 293 mg of hydroxybenzotriazole (HOST) and 622 mg of l-(3-dimethylaminopropyl) -3-ethylcarboiimide hydrochloride (EDCl) . The reaction mixture was left stirring overnight. DMF was then removed under reduced pressure and the reaction mixture was partitioned between 20mL of ethyl acetate and 50mL of water. The aqueous portion was extracted further with 2x20mL of ethyl acetate and the combined organic portions were washed with brine, dried over anhydrous sodium sulfate, filtered and concentrated. Purification on silica gel, eluting with ethyl acetate/hexane gave 410 mg of the desired product : 4- (cis-3- (N-t -butoxycarbonyl - 2 - aminoacetoxy) cyclopentyl) amino-2 -phenyl- 5, 6, -dimethyl- 7H-pyrrolo [2, 3d] pyrimidine, MS (ES) (M"»l) =480 . 2 . The ester was then treated with 5 mL of 20% trifluoroacetic acid in dichloromethane at room temperature, left over night and then concentrated. Trituration with ethyl acetate gave 300 mg of an off white solid; 4- (cis-3- (2-aminoacetoxy) cyclopentyl) aminc-5, 6- dime thy 1-2-phenyl-7H-pyrrolo[2,3d] pyrimidine trifluoroacetic acid salt, MS (ES) (M'*l}-380.1. One skilled in the art will appreciate that the following compounds can be synthesized by the methods disclosed above: 4 -(cis-3-hydroxycyclopentyl)amino-5,6-dimethyl-2-phenyl-7H-pyrrolo[2,3d] pyrimidine MS (ES) (M' + D- 323.1. 4 -(cis-3-(2-aminoacetoxy)cyclopentyl)amino-5,6-dimethyl-2-phenyl-7H-pyrrolo[2,3d] pyrimidinetrifluoroacetic acid salt MS (ES) (M'*l)« 380.1. 4- (3-acetamido)piperidinyl-5, 6-dimethy1-2-phenyl-7H-pyrrolo[2,3d]pyrimidine MS (ES) (M"*l)« 364.2. 4 - (2-N'~-methylureapropyl) amino-5 , 6-dimethyl-2-phenyl - 7H-pyrrolo [2, 3d] pyrimidine, MS (ES) (M't-1) =353 . 4 . 4-{2-acetamidobutyl)amino-5,6-dimethyl-2-phenyl-7H-pyrrolo[2,3d]pyrimidine, MS (ES) (M' + l)» 352.4. 4 - (2-N'-methylureabutyl)amino-5 , 6-dimethyl-2-phenyl-7H- pyrrolo[2, 3d]pyrimidine MS (ES) (M' + l)= 367.5 4 - (2 -amlnocyclopropylacetamidoethyl)amino-2-phenyl-7H-pyrrclo [2, 3d] pyrimidine MS (ES) (M' + D* 309.1. 4 -(crans-4-hydroxycyclohexyl)amino-2-(3-chlorophenyl)-7H- pyrrolo[2,3d] pyrimidir.e MS (ES) (M'*I) =342 . 8 . 4 - (rra^s-4-hydroxycyciohexyl)amino-2-(3-fluorcphenyl! - "H-pyrrole [2,3d] pyrimidine MS (ES) (M'-l)=327.2 . 4- (c.razi£-4-hydroxycyclohexyl)amino-2- (4-pyridyI) - TH-pyrrcio [2 . 3d] pyrimidine MS (ES) (M~»l) =310.2 . Example 17 Scheme IX (Figure Remove) The pyrrole nitrogen of. (7) (Scheme IX) was protected with di-c-butyldicarbonate unds : basic conditions to yield the corresponding carbamate (22) . Radical bromination of (22) proceeded regioselectively to yield bromide (23). In general, compound (23) served as a key electrophilic intermediate for various nucleophilic coupling partners. Displacement of the alkyl bromide with sodium phenolace trihydrate yielded compound (24). Subsequent displacement of N-Bromosuccinimide (508 mg, 2.86 mrnol) and AIBN (112 tng, mmol) were added to a solution containing (22) (935 mg, 2.71 mmol) and CCl, (50 mL) . The solution was heated to reflux. After 2 h the reaction was cooled to room temperature 'and concentrated in vacua to yield a white solid. Flash chromatography (Si02; 1/1 CH:Cl:/Hexanes, Re 0.30) yielded 960 mg (84%)of a white solid (23). 1H NMR (200 MHz. CDC1:J 5_6.52 (m, 2H, Ar-H), 7.48 (m, 3H, Ar-H) , 6.76 (s, IK, pyrrole-H), 4.93 (s, 2H, pyrrole - CH,Br), 1.79 (s, 9H, carbamate-CH:) ; MS, M * 1 « 423.9; Mpt = 155-157°C. (Figure Remove) Sodium phenoxide trihydrate (173 mg, 1.02 mmol) was added in one portion to a solution of bromide (23) (410 mg, 0.97 mmol) dissolved in CH:C1; (5 mL) and DMF (10 mL) . After 2 h the reaction solution was partitioned between CH:C1: and water. The water layer was extracted with CH:C1:. The combined CH:C1: layers were washed with water, dried over MgSO4, filtered and concentrated to yield a yellow solid. Flash chromatography (Si02; 1/6 EtOAc/Hexanes, Rf 0.30) yielded 210 mg (50%) of a white solid (24). 1H NMR (200 MHz, CDC13) 6_8.53 (m, 2H, Ar- H) , 7.48 (m, 3H, Ar-H), 7.34 (m, 2H, Ar-H), 7.03 (m, 3H, Ar- H) , 6.83 (s, 1H, pyrrole-H), 5,45 (s, 2H, ArCH:0) , 1.76 (s, 9H, carbamate-CH-.) ; MS. M" - 436.2. the aryl chloride and removal of the t -butyl carca-sre protecting group occurred in one step yielding des.red comound (25 ). Detailed Synthesis of Compounds (22) -(25) in Accordance with Scheme IX (Figure Remove) Di-t-butyl dicarbonate (5.37 g, 24.6 mmol) and dimethyl aminopyridine (1.13 g, 9.2 mmol) were added to a solution containing (7) (1.50 g, 6.15 mmol) and pyridine (30 mL) . After 20 h the reaction was concentrated and the residue was partitioned between CH:C1: and water. The CH:Cl: layer was separated, dried over MgSO,, filtered and concentrated to yield a black solid. Flash chromatography (Si02; 1/9 EtOAc/Hexanes, Rf 0.40) yielded 1.70 g (80V) of a white solid (22). 1E NMR (200 MHz, CDC13) 5_8.50 (m, 2H, Ar-H), 7.45 (m, 3H, Ar-H), 6.39 (s, 1H, pyrrole-H), 2.66 (s, 3H,pyrrole- CH3) , 1.76 (s, 9H, carbamate-CHj) ; MS, M * 1 = 344.1; Mpt = 175-177°C. (Figure Remove) A solution containing (24) (85 mg, 0.20 mmol), N-acetylethylenediamine (201 mg, 1.95 mmol) and DMSO (3 mL) was heated to 100'C. After 1 h the temperature was raised to 130CC. After 3 h the reaction was cooled to room temperature and partitioned between EtOAc and water. The water layer was extracted with EtOAc (2x) . The combined EtOAc layers are washed with water, dried over MgSO., filtered and concentrated. Flash chromatography (Si02; 1/10 EtOH/ CHCl;., Rf 0.25) yielded 73 mg (93%)of a white foamy solid (25). 1U NMR (200 MHz, DMSO-d6) 5 11.81 (br s, 1H, N-H), 8.39 (m, 2H, Ar-H), 8.03 (br t, 1H, N-H), 7.57 (br t, 1H, N-H), 7.20 -7.50 (m, 5H, Ar-H), 6.89 - 7.09 (m, 3H, Ar-H), 6.59 (s, 1H, pyrrole-H) , 5.12 (s, 2H, ArCH.,0) , 3.61 (m, 2H, NCH-) , 3.36 (m, 2H, NCH-) , 1.79 (S, 3H.COCH:); MS, M* 1 = 402.6 The following compounds were obtained in a manner similar to that of Example 17: 4-(2-acetylaminoethyl)amino-6-phenoxymethyl-2-phenyl-7H-pyrrolo[2,3d]pyrimidine. mp 196-197°C; MS (ES): 401.6 (M* •*-!). 4- ;2-acetyIaminoethyl)amino-6-(4-fluorophenoxy)methyl-2-phenyl-7n-pyrrolo[2 , 3d]pyrimidine. MS(ES): 420.1 (M' + l) - 4 - ( 2 -acetylamnoethyl) amino- 6 - (4 - chlorcphencxy : methyl - : -phenyl-7H-pyrrclo[2,3d]pyrimidine. MS(ES): 436.1 iM'-l'. 4 - ( 2 -acetylaminoethyl) amino-6 - (4 -methoxyphencxy) methyl -2-phenyl-7H-pyrrolo[2,3d]pyrimidine. MS(ES): 432.1 ;M'-1!. 4-(2-acetylaminoethyl)amino-6-(N-pyridin-2-cne!methyl-2-phenyl-7H-pyrrcio[2,3d]pyrimidine. MS(ES): 403.1 (M'^l) . 4 -(2-acetylaminoethyl)amino-6-(N-phenylamino)methyl- 2-phenyl -7~-pyrrolo [2, 3] pyrimidine. MS(ES): 400.9 (M'-ri:. 4 - (2-acetyiaminoethyl)amino-6-(N-methyl-N-phenylamino)methyl -2-phenyl-7H-pyrrole[2,3d]pyrimidine. MS(ES): 414.3 (M'-l). 4 - (2-N'-methylureaethyl)amino-6-phenoxymethyl-2-phenyl-7H-pyrrolo [2, 3d] pyrimidine. MS (ES) : 416.9 (M"+l). Example 18: Synthesis of adenosine Aa Antagonists. Compound 1319 and Compound 1320 (Table 13 below) can be synthesized by the general procedures herein. (Figure Remove) Compound 1319 (81%) 'H-NMR (d^-DMSO) d 1.37 (m, 4H), 1.93 (m, 2H), 2.01 (m, 2H), 4.11 (brs, 1H), 4.61 (d, 1H, J = 4.4 Hz), .59 (m, IK), 7.09 (m, 1H), 7.21 (m, 2H), 7.49 (dd, 1H, J = 8Kz, 14H2), 8.03 (m, 1H), 8.18 (d, 1H. J - 8 Hz), 11.55 (brs, 1H) . MS (ES) : 327.0 (M'*l) . Compound 1320 (21%) MS (ES): 342.1 (M'+l). Example 19: Synthesis of adenosiae Aj Antagonist. Compound 1321 (Table 13 below) can be synthesized by the general procedures given below. (Figure Remove) Compound 28 (10.939, 50.76 mmol) was dissolved in DMF (67 mL) . 4-Amidinopyridine hvdrochloride (B.Og, 50.76 mmol) and DBU (15.4 g, 101.5 mmol) were added sequentially and the reaction was heated to 85°C. After 22 hours, the reaction was cooled to room temperature and the DMF was removed in vacuo. The dark oil was diluted with 2M HCl (80 mL) . The reaction was allowed to stand. After 2 hours, the solution was cooled to 1C°C and filtered. The solid was washed with cold water and dried to yield 7.40g of a yellow solid, Compound 29 (69%). -K-NMR (200MHz, d,-DMSO) d 6.58 (s, 1H) , 7.27 (s, 1H) , 8.53 (d, 2H, J = 5.6), 9.00 (d, 2K, J = 5.2Hz). 12.35 (brs, 1H) . MS (ES) : 212.8 (M' + l) . Compound 29 (7.4 mmol, 29.8 mmol) was diluted .with POC1? and heated to 105°C. After 18 hours, the reaction is cooled to room temperature and the POC13is removed in vacuo. The thick dark oil is diluted with MeOK (75mL) followed by ether (120mL). The amorphous red solid is filtered and washed with ether to yield 3.82 g of a red solid. The crude solid is apprcximately 80% pure and used without further purification in tne next reaction. MS (ES): 230.7 (M"+l). Compound 1321 'H-NMR (15%) (200MH, d.-DMSO) d 1.38 trr.. 4H . 1.92 (brs, 2K) , 2.C2 (brs, 2H), 3.44 (brs, 1HJ. 4.14 ibrs, 1H), 4.56 (d, IK, J = 4 Hz), 6.63 (m, IK;. 7.15 (m, 1H), ~.32 (d, 1H, J = 6.2 Hz), 8.20 (d, 2K, J = 4.4 Hz), 8.65 (d, 2H, J = 4.4HZ), 11.67 (brs, 1H). MS (ES): 310.2 (M'-ll. Compound 1501 (Table 15 below) :K-NMR (70V) (200MHz, CD,OD^ d 1.84 (s, 3H), 3.52 it, 2K, J = 6.0 Hz), 3.83, t, 2K, J = 6.C Hz), 6.51 (d, IK, J = 3.4HZ), 7.06 (d, IK, J = 3.8 Hz), 7.42 (m, 3H) , 8.36 (m, 2H) . MS (ES) : 296.0 (M%1). Compound 1502 (Table 15 below) MS (ES): 345.0 (M'*l). Compound 1500 (Table 15 below) 'K-NMR (200MHz, CDClj) d 1.40 - 1.80 (m, SH) , 1.85 - 2.10 (m, 2H) , 2.18 (s, 3H) , 2.33 (s, 3H) , 2.50 (d, 3H) , 3.90 - 4.10 (m, 2H) , 4.76 (m, 1H) , 5.50 (d, 1H) , 6.03 (m, 1H) , 7.40 (m, 3H) , 8.37 (m, 2H) , 9.15 (brs, 1H) . MS (ES) : 393 .3 (M' + l) . Example 20: Synthesis of adenosine Aj Antagonist. Compound 1504 (Table 15 below) can be synthesized by the general procedures given below. (Figure Remove) Compound 31 (200 mg, 0.47 mmol) was dissolved in DCM (4 mL) . Triethylamine (51 mg, O.Smmol) and thiomorpholine (52 mg, O.Smmol) were added sequentially. The solution was mixed for several minutes and allowed to stand for 72 hours. The reaction was diluted with DCM and H:0 and the layers were separated. The aqueous layer was extracted with DCM. The combined DO; layers were dried over MgSO«, filtered and concentrated. Ethyl ether was added to the crude sample ar.d the resulting solid was filtered to yield lOOmg of a white solid, 32 (€2%). :HNMR (200MHz, CDClj) d 1.75 is, 9K) , 2.6c (brs, 2H) , 2.79 (brs, 2H1 . 3.86 (s, 2H) , 7.46 ir, 3H) , 6.50 (m, 2K). Compound 32 was combined with DMSO !3ir.L) and trans-4-aminocyclohexanol (144mg, 1.25 mmcl) and heated to 13Q°C for 4 hours. The reaction was cooled to room temperature, and diluted with EtOAc and K:0. The layers were separated and the aqueous layer was extracted with EtOAc (2x) . The combined organic layers were washed with H_-0 and brine, dried over MgS04, filtered and concentrated. Chromatograpny (silica, 8:1 CHCl3/EtOH) yields 32 mg of a tan oil. Ethyl ether was added and the resulting solid was filtered to yield 5 mg of a white solid (9%) .OSIC-14S265 : •K-NMR (200MHz, CD,OD) : d 1.44 (brm, 4H) , 2.03 (brm, 2H) , 2.21 (farm, 2H), 2.70 (farm, 8H), 3.63 (m, 4H), 3.92 (m, 1H), 4.26 (brs, 1H) , 6.42 (s, IK), 7.42 (m, 3H) , 8.33 (m, 2H) . Example 21: Synthesis of adenosine Aj Antagonist. Compound 1503 (Table 15 below) can be synthesized by the general procedures given below. (Figure Remove) The bromide, compound 31 (220 mg, 0.47 mmol) was dissolved in 1:1 DMF:Dichloromethane (5 mL) . To this was added K:CO- (71 mg, 0.52 mmol) and morpholine (0.047 mL, 0.47 mmol) . The mixture was allowed to stir at room temperature overnight. Solvents were removed in vacuo and the residue was partitioned between H:0 and dichlcromethane. The organic layer was dried with MgSO,, filtered, and concentrated to give ar. off white solid which upon trituration with ether/hexanes gave 175mg of a white solid, 33 (84%). :K-NMR (200MHz, CDC1;) : ( 1.9 OH, s) , 2.54 (4H, s) , 3.65 (4H, s), 3.85 {IK. s) , 6-59 (1H, s), 7.45 (3H, m),8.5 (2H, m). Compound 33 (50 mg, 0.11 mmol) and trans-4-aminocyciohexanol (105 mg, 0.91 mmol) were taken up in DMSO (2mL). The resultant solution was sparged with N: and then heated to 10CTC in an oil bath and stirred overnight. The crude reaction mixture was poured into water and extracted twice with ethyl acetate (50rnL) . The combined organic layers were washed with H:0. After drying with MgSO, and filtering, the organic layer was concentrated in vacuo to give an orange solid. Chromatography (silica, 10% CH,OH in CH?C1:) yielded 15mg (33V). 'K-NMR ( 200 MHz, CDClj) : ( 1.24 - 1.62 (4H, m) , 1.85 (2K, m) , 2.10 (2H, m) , 2.26 (4H, m) , 3.53 (4K, m) , 4.22 (1H, m) , 4.73 (IK, m) , 5.85 (1H, d) , 6.15 (1H, s), 7.25 (3H, m) , 8.42 (2H, M), 10.0 (1H, s). MS (ES): 408 (M' + 1). Compounds 1500, 1501, and 1502 can be synthesized using similar preparation steps of Example 20 by treating compound 32 with -an appropriately substituted amine. Yeast fc-Galactosidase reporter gene assays for human adenosine A: and A2. receptor: Yeast strains (S. cerevisiae.' were transformed with human adenosine A: (A:R; CADUS strain CY126SO) or human A2a (A2a; CADUS strain CYS362! and the addition of a lacZ(3-Galactosidase) reporter gene tc utilize as a functional readout. A complete description of the transformations is listed below (see Yeast Strains). NECA (5'-N-ethylcarboxamidoadenosine), a potent adenosine receptor agonist with similar affinity for A: and a:i receptors, was used as a ligand for all assays. Test compounds were examined at 8 concentrations (0.1 - 10,000 nM) for ability to inhibit NECA-induced B-Galactosidase activity by CY12660 or CY8362. Preparation of Yeast Stock Cultures: Each of the respective yeast strains, CY12660 and CY8362, were streaked onto an LT agar plate and incubated at 30°C until colonies were observed. Yeast from these colonies were added to LT liquid (pH 6.8) and grown overnight at 30°C. Each yeast strain was then diluted to an OD60c = 1.0-2.0 (approximately 1-2 X l(f cells/ml), as determined spectrophotometrically (Molecular Devices VMAX). For each 6 ml of yeast liquid culture, 4 ml of 40V glycerol (1:1.5 volrvol) was added ("yeast/glycerol stock") . From this yeast/glycerol stock, ten 1 ml aliquots were prepared and stored at -80°C until required for assay. Yeast A, R and A2aR Assay: One vial each of CY8362 and CY12660 yeast/glycerol stock was thawed and used to inoculate Supplemented LT liquid media, pH 6.8 (92 ml LT liquid, to which is added: 5 ml of 40% glucose, 0.45 ml of 1M KOH and 2.5 ml of Pipes, pH 6.8). Liquid cultures were grown 16-18 hr (overnight) at 30°C. Aliquots from overnight cultures were then diluted in LT media, containing 4U/ml adenosine deaminase (Type VI or VII from calf intestinal mucosa, Sigma), to obtain OD,OC = 0.15 (1.5 X 10£ cells/ml) for CYB362 (A2aR) and OD(0& =0.50 (5X10* cells/ml) for CY12660 (A,R) . Assays were conducted with a final volume of 100 ul in 96-' well rr.icrctiter places, such that a final concentration cf 2'-, DMSO was achieved in all wells. For primary screening, 1-2 concentrations of test compounds were utilized (10 uM, iuM ) . For compound profiling, B concentrations were tested (1000C, 1000, 500, 100, 50, 10, 1 and 0.1 nM) . To each rr.icrotiter plate, 10 ul of 20% DMSO was added to "Control" and "Total" wells while 10 ul cf Test Compound (in 20% DMSO) was added to "Unknown" wells. Subsequently, 10 ul of NECA (5 uM for A;R, 1 uM for A;aR) were added to "Total" and 'Unknown" wells; 10 ul of PBS was added to the "Control" wells. In the final addition, 80 ul of yeast strain, CY8362 or CY12660, were added to all wells. All plates were then agitated briefly (LabLine orbital shaker 2-3 min) and allowed to incubate for 4 hrs. at 30CC in a dry oven. 3-Galactosidase activity can be guantitated using either cclcrimetnc (e.g., ONPG, CPRG) , luminescent (e.g., Galacton-Star) or fluorometric substrates (e.g., FDG, Resorufin) substrates. Currently, fluorescence detection is preferred on the basis of superior signal:noise ratio, relative freedom from interference and low cost. Fluorescein digalactopyranoside (FDG, Molecular Probes or Marker Gene Technologies), a fluorescent 3-Galactosidase substrate, was added to all wells at 20 ul/well (final concentration = 80 uM). Plates were shaken for 5-6 sec (LabLine orbital shaker) and then incubated at 37°C for 90 min (95% 0:/5% C0: incubator). At the end of the 90 min incubation period, 0-Galactosidase activity was stopped using 20 ul/well of 1M Na:CO, and all plates shaken for 5-6 sec. Plates were then agitated for 6 sec and relative fluorescence intensity determined using a fluorometer (Tecan Spectrafluor; excitation = 485 nm, emission = 535 nm). Calculations: Relative fluorescence values for "Control" wells were interpreted as background and subtracted from "Total" and "Unknown" values. Compound profiles were analyzed via logarithmic transformation (x-axis: compound concentration) followed by one site competition curve fitting to calculate 1C.- values (GraphPad Prism) . Yeast strains: Saccharomyces cerevisiae strains CY126oO [farl*1442 tbtl-1 fusl-HIS3 canl ste!4 : : crpl: :LYS2 ste3*H5c gpal (41)-Gai3 Iys2 ura3 Ieu2 crpl: his3; LEU2 PGKp- MfaiLeader-hAlR-?H05term 2mu-orig REP3 Ampr] and CY8362 [gpalp-rGasElOK farl*1442 tbtl-1 fusl-KIS3 canl sce!4::trpl: LYS2 ste3*1156 Iys2 ura3 Ieu2 trpl his3; LEU2 PGKp-hA2aR 2mu- ori REP3 AmprJ were developed. LT Media: LT (Leu-Trp supplemented) media is composed of lOOg DIFCO yeast nitrogen base, supplemented with the following: 1. Og valine, 1. Og aspartic acid, 0.75g phenylalanine, 0 . 9g lysine, 0.45g tyrosine, 0.45g isoleucine, 0. 3g methionine, 0.6g adenine, 0.4g uracil, 0.3g serine, 0.3g proline, 0.3g cysteine, 0.3g arginine, 0 . 9g histidine and 1.Og threonine. Construction of Yeast Strains Expressing Human Ax Adenosine Receptor In this example, the construction of yeast strains expressing a human A, adenosine receptor functionally integrated into the yeast pheromone system pathway is described. I. Expression Vector Construction To construct a yeast expression vector for the human AA adencsine receptor, the A: adenosine receptor cDNA was obtained by reverse transcriptase PCR of human hippocampus mRNA using primers designed based on the published sequence of the human A: adenosine receptor and standard techniques. The PCR product was subcloned into the Ncol and Xbal sites of the yeast expression plasmid pMPiS. The pMPIS plasmid was created from pLPXt as follows: The Xbal site of YEP51 (Broach, J.R. et al. (1983) "Vectors for high-level, inducible expression of cloned genes in yeast" p. 83-117 in M. Inouye (ed.), Experimental Manipulation of Gene Expression. Academic Press, New York) was eliminated by diaestion, end-fill and religacicn to create YepriNccCXba. Another Xbal site was created at the BamHI site by digesticr. with BamHI, end-fill, linker (New England Biolabs, £ 1081) ligation, Xbal digestion and re-ligation to generate YEPBlNccXt. This plasmid was digested with EspSl and NccI and ligated to Leu2 and PGKp fragments generated by PCR. The 2 kb Leu2 PCR product was generated by amplification from YEPSlNco using primers containing Esp31 and Bglll sites. The 660 base pair PGKp PCR product was generated by amplification from pPGKas (Kang, Y.-S. et al. (1990) Mol. Cell. Biol. i£:25S2-2590) with PCR primers containing Bglll and Ncol sites. The resulting plasmid is called pLPXt. pLPXt was modified by inserting the coding region of the a-factor pre-pro leader into the Ncol site. The prepro leader was inserted so that the Ncol cloning site was maintained at the 3' end of the leader, but not regenerated at the 5' end. In this way receptors can be cloned by digestion of the plasmid with Ncol and Xbal. The resulting plasmid is called pMP15. The pMPIS plasmid into which was inserted the human A: adenosine receptor cDNA was designated p5095. In this vector, the receptor cDNA is fused to the 3' end of the yeast a-factor prepro leader. During protein maturation the prepro peptide sequences are cleaved to generate mature full-length receptor. This occurs during processing of the receptor through the yeast secretory pathway. This plasmid is maintained by Leu selection (i.e., growth on medium lacking leucine) . The sequence of the cloned coding region was determined and found to be equivalent to that in the published literature (GenBank accession numbers S4S235 and S56143). II. Yeast Strain Construction To create a yeast strain expressing the human A: adenosine receptor, yeast strain CY7967 was used as the starting parental strain. The genotype of CY7967 is as follows: MATQ gpaDll63 gpal(41)Gai3 farlD1442 tbt-1 FUS1-HIS3 canl ste!4: :trpl: :LYS2 ste3D1156 iys2 ura3 lev:2 his3 The genetic markers are reviewed below: MATa Mating type a. gpalD1163 The endogenous yeast G-protein G?A1 has been deleted. groal (41) Gai3 gpal (41)-Gai3 was integrated into the . . yeast genome. This chimeric Ga protein is composed of the first 41 amino acids of the endogenous yeast Ga subunit GPA1 fused to the mammalian G-protein Gai3 in which the cognate N-terminal amino acids have been deleted. farlD1442 FAR1 gene (responsible for cell cycle arrest) has been deleted (thereby preventing cell cycle arrest upon activation of the pheromone response pathway). tbt-1 strain with high transformation efficiency by electroporation. FUS1-HIS3 a fusion between the FUS1 promoter and the KIS3 coding region (thereby creating a pheromone inducible HIS3 gene). can 1 arginine/canavinine permease. ste!4::trpl::L gene disruption of STE14, a C-farnesyl YS2.... methyltransferase (thereby lowering basal signaling through the pheromone pathway) . ste3DI156 endogenous yeast STR, the a factor pheromone receptor (STE3) was disrupted. Iys2 defect in 2-aminoapidate reductase, yeast need lysine to grow. ura3 defect in orotidine-5'-phosphate decarboxylase, yeast need uracil to grow Ieu2 defect in b-isopropylmalate dehydrogenase, yeast need leucine to grow. trpl defect in phosphoribosylanthranilate, yeast need tryptophan to grow. his3 defect in imidazoleglycerolphosphate dehydrogenase, yeast need histidine to grow. Two piasmids were transformed into strain CYT?£~ ry electroporation: plasmid p50S5 (encoding human A: aaenosine receptor; described above) and plasmid pl584, which is a FUSl-3-galactosidase reporter gene plasmid. Plasmid pi584 was derived from plasmid pRS426 (Christiansen, 7.W. et ai. (19S2) Gene ii£:119-1122). Plasmid pRS426 contains a polylinker site at nucleotides 2004-2016. A fusion between the FUS1 promoter and the 0-galactosidase gene was inserted at the restriction sites EagI and Xhol to create plasmid p!584. The p!584 plasmid is maintained by Trp selection (i.e., growth on medium lacking leucine). The resultant strain carrying pS095 and p!5B4, referred to as CY12660, expresses the human A: adenosine receptor. To grow this strain in liquid or on agar plates, minimal media lacking leucine and tryptophan was used. To perform a growth assay on plates (assaying FUS1-HIS3), the plates were at pH 6.8 and contained 0.5-2.5 mM 3-amino-1,2,4-triazole and lacked leucine, tryptophan and histidine. As a, control for specificity, a comparison with one or more other yeast-based seven transmemfarane receptor screens was included in all experiments. Construction of Yeast Strains Expressing Human A2a Adenosine Receptor In this example, the construction of yeast strains expressing a human A2a adenosine receptor functionally integrated into the yeast pheromone system pathway is described. I. Expression Vector Construction To construct a yeast expression vector for the human A2a adenosine receptor, the human A2a receptor cDNA was obtained from Dr. Phil Murphy (NIH) . Upon receipt of this clone, the A2a receptor insert was sequenced and found to be identical to the published sequence (GenBank accession # S46950) . The receptor cDNA was excised from the plasmid by PCR with VENT polymerase and cloned into the plasmid pLPBX, which drives receptor expression by a constitutive Phosphoglycerate Kinase (PGK) promoter in yeast. The sequence of the entire insert was once again sequenced and found to be identical with the published sequence. However, by virtue of the cloning strategy employed there were three amino acids appended to the carboxy-terminus of the receptor, GlySerVal. II. Yeast Strain Construction To create a yeast strain expressing the human A2a adenosine receptor, yeast strain CY8342 was used as the starting parental strain. The genotype of CY8342 is as follows: MATa fariD1442 tbtl-1 Iys2 ura3 Ieu2 trpl his3 fusl-HIS3 canl ste3D1156 gpaD1163 ste!4::trpl::LYS2 gpalp-rGas£10K (or gpalp-rGasD229S or gpalp-rGasE10K+D229S) The genetic markers are as described in Example 1, except for the G-protein variation. For human A2a receptor-expression, yeast strains were utilized in which the endogenous yeast G protein GPA1 had been deleted and replaced by a mammalian Gas. Three rat GQS mutants were utilized. These variants contain one or two point mutations which convert them into proteins which couple efficiently to yeast by- They are identified as G,.E10K (in which the glutamic acid at position ten is replaced with lysine) , Ga.D229S (in which the aspartic arid a- position 229 is replaced with serine) and G,.E10KO225S (whicr. contains both point mutations). Strain CY8342 (carrying one of the three mutar.t rat Gas proteins) was transformed with either the parental vector pL?3X (Receptor") or with pLPBX-A2a (Receptor"). A plasmid with the FUS1 promoter fused to (3-galactosidase coding sequences (described in above) was added to assess the magnitude of activation of the pheromone response pathway. Functional Assay using Yeast Strains Expressing Human A-Adenosine Receptor In this example, the development of a functional screening assay in yeast for modulators of the human A: adenosine receptor is described. I. Ligands Used in Assay Adenosine, a natural agonist for this receptor, as well as two other synthetic agonists were utilized for development of this assay. Adenosine, reported to have an ECiC of approximately 75 nM, and (-)-N6- (2-phenylisopropyl)-adenosine (PIA) with a reported affinity of approximately 50 nM were used in a subset of experiments. 5'-N-etnylcarboxamido-adenosine (NECA) was used in all growth assays. To prevent signaling due to the presence of adenosine in the growth media, adenosine deaminase (4U/ml) was added to all assays. II. Biological Response in Yeast The ability of the A: adenosine receptor to functionally couple in a heterologous yeast system was assessed by introducing the A: receptor expression vector (p5095, described above) into a series of yeast strains that expressed different G protein subunits. The majority of these transformants expressed G0 subunits of the Gai or Gao subtype. Additional Ga proteins were also tested for the possible identification of promiscuous receptor-Ga protein coupling. In various strains, a STE18 or a chimeric STE18- Gy2 construct was integrated into the genome cf the yeast. The yeast strains harbored a defective KIS3 gene and ar. integrated copy of FUS1-HIS3, thereby allowing for selection in selective media containing 3-amino-l, 2 , 4-tnazole (tested at 0.2, 0.5 and 1.0 mM) and lacking histidine. Transfcrmar.ts were isolated and monolayers were prepared or. media containing 3-amino-1,2,4-triazole, 4 U/ml adenosine deaminase and lacking histidine. Five microliters of various concentrations of ligand (e.g., NECA at 0, 0.1, 1.0 and 10 mM) was applied. Growth was monitored for 2 days. Ligand-dependent growth responses were tested in this manner in the various yeast strains. The results are summarized in Table 1 below. The symbol (-) indicates that ligand-dependent receptor activation was not detected while (») denotes ligand-dependent response. The term "LIRMA" indicates ligand indeoendent receotor mediated activation. (Table Remove) As indicated in Table 3, the most robust signaling was found to occur in a yeast strain expressing the GPA: (41) -Gai3 chimera. III. fusl-LacZ Assay To characterize activation of the pheromone response pathway mere fully, synthesis of 0-galactosidase through fuslLacZ in response to agonist stimulation was measured. To perform the S-calactosidase assay, increasing concentrations of ligand were added to mid-log culture of human A: adenosine receptor expressed in a yeast strain co-expressing a Stel6-Gv2 chimera and GPA4}-GQ13. Trans f ormants were isolated and growr. overnight in the presence of histidine and 4 U/tr.l adencsir.e deaminase. After five hours of incubation with 4 U/ml adenosine deaminase and ligand, induction of 5-gaiactosidase was measured using CPRG as the substrate for 3-galactcside . 5 x 10 cells were used per assay. The results obtained with NECA stimulation indicated that at _ p a NECA concentration of 10 M approximately 2-fold stimulation of 3-galactosidase activity was achieved. Moreover, a stimulation index of approximately 10-fold was observed at a NECA concentration of 10~ M. The utility of this assay was extended by validation of the activity of antagonists on this strain. Two known adenosine antagonist, XAC and DPCPX, were tested for their ability to compete against NECA (at 5 mM) for activity in the (J-galactosidase assay. In these assays, (3-galactosidase induction was measured using FDG as the substrate and 1.6 x 10" cells per assay. The results indicated that both XAC and DPCPX served as potent antagonists of yeast-expressed A-. adenosine receptor, with IC50 values of 44 nM and 49 nM, respectively. In order to determine if this inhibitory effect was specific to the A: subtype, a series of complementary experiments were performed with the yeast-based A2a receptor assay (described in Example 4). Results obtained with the A2a yeast-based assay indicated that XAC was a relatively effective A2a receptor antagonist, consistent with published reports. In contrast, DPCPX was relatively inert at this receptor, as expected from published reports. IV. Radioligand Binding The A: adenosine receptor assay was further characterized by measurement of the receptor's radioligand binding parameters. Displacement binding of [ H]CPX by several adenosine receptor reference compounds, XAC, DPCPX, and CGS, was analyzed usir.c membranes prepared from yeast expressing the human A: adenosine receptor. The results with yeast membrar.es expressing the human Aj adenosine receptor were compared to those from yeast membranes expressing the human A2a adenosine receptor or the human A3 receptor to examine the specificity of binding. To perform the assay, fifty mg of membranes were incubated with 0.4 nM [~H]C?X and increasing concentrations of adenosine receptor ligands. Incubation was in 50 mM Tris-HC1, pH 7.4, 1 mM EDTA, 10 mM MgCl2, 0.25 V BSA and 2 U/ml adenosine deaminase in the presence of protease inhibitors for 60 minutes at room temperature. Binding was terminated by addition of ice-cold 50 mM Tris-HCl, pH 7.4 plus 10 mM MgCl2, followed by rapid filtration over GF/B filters previously soaked with 0.5 V polyethyenimine, using a Packard 96-well harvester. Data were analyzed by nonlinear least square curve fitting procedure using Prism 2.01 software. The IC5o values obtained in this experiment are summarized in Table 4, below: (Table Remove) These data indicate that the reference compounds have affinities consistent with those reported in the literature. The data further indicate that the yeast-based assays are of sufficient sensitivity to discriminate receptor subtype specificity. Functional Assay using Yeast Strains Expressing Human Ala Adenosine Receptor In this example, the development of a functional screening assay in yeast for modulators of the human A: adenosine receptor is described. I. Ligande Used in Assay The natural ligand adenosine, as well as other thoroughly characterized and commercially available ligands were used for study of the human A2a receptor functionally expressed in yeast. Three ligands have been used in the establishment of this assay. They include.- T.lgand Reported £1 Function Adenosine 500 nM agonist 5'-N-ethylcarboxamidoadenosine 10-15 nM agonist (NECA) (-)-N6-(2- phenylisopropyl)-adenosine 100-125 nM agonist (PIA) To prevent signaling due to the presence of adenosine in the growth media, adenosine deaminase (4U/ml) was added to all assays.' II. Biological Response in Yeast A2a receptor agonists were tested for the capacity to stimulate the pheromone response pathway in yeast transformed with the A2a receptor expression plasmid and expressing either GQSE10K, GQSD229S or GQSE10K*D229S. The ability of ligand to stimulate the pheromone response pathway in a receptor dependent manner was indicated by an alteration in the yeast phenotype. Receptor activation modified the phenotype from histidine auxotrophy to histidine prototrophy (activation of fusl-HIS3). Three independent transformants were isolated and grown overnight in the presence of histidine. Cells were washed to remove histidine and diluted to 2 x 10° cells/ml. 5 m! of each transformant was spotted onto nonselective media (including histidine) or selective media (1 mM AT) in the absence or presence cf 4 adenosine deaminase. Plates were grown at 30 :C hours. In the presence of histidine both Receptor" (R~) and Receptor" (R~) strains were capable of growth. However, in the absence of histidine only R* cells grew. Since no ligand had been added to these plates two explanations were possible for this result. One possible interpretation was that the receptor bearing yeast were at a growth advantage due to Ligand Independent Receptor Mediated Activation (LIRMA). Alternatively the yeast could have been synthesizing the ligand adenosine. To distinguish between these two possibilities, an enzyme which degrades the ligand, adenosine deaminase (ADA), was added to the growing yeast and plates. In the presence of adenosine deaminase R* cells no longer grew in the absence of histicine, indicating that the yeast were indeed synthesizing ligand. This interpretation was confirmed by an A2a growth assay in liquid. In this experiment R* yeast (a GQSE10K strain expressing the A2a receptor) were inoculated at three densities (1 x 10° cell/ml; 3 x 105 cells/ml; or 1 x 105 cells/ml) in the presence or absence of adenosine deaminase (4 U/mll. The stringency of the assay was enhanced with increasing concentrations (0, 0.1, 0.2 or 0.4 mM)of 3-amino-1,2,4-triazole (AT), a competitive antagonist of imidazoleglycerol-P dehydratase, the protein product of the KIS3 gene. In the presence of adenosine deaminase and 3-amino-1,2,4-triazole yeast grew less vigorously. However in the absence of 3-amino-1,2,4 -triazole, adenosine deaminase had little effect. Thus adenosine deaminase itself had no direct effect upon the pheromone response pathway. An alternative approach to measuring growth and one that can be miniaturized for high throughput screening is an A2a receptor ligand spot assay. A GasE10K strain expressing the A2a receptor (A2aRt-) or lacking the receptor (R-) was grown overnight in the presence of histidine and 4 U/ml adenosine deaminase. Cells were washed to remove histidine and diluted to 5 x 10 cells/ml. 1 x 10 cells were spread or.tr selective plates containing 4 U/ml adenosine deaminase and 0.5 or 1.0 mM 3-amino-l,2,4-triazole (AT) and allowed to dry for 1 hour. 5 m! of the following reagents were applied to the monolayer: 10 mM adenosine, 38.7 mM histidine, dimethylsulfcxide (DMSO) , 10 mM PIA or 10 mM NECA. Cells were grown 24 hours at 30°C. The results showed that cells without receptor could only grow when histidine was added to the media. In contrast, R* cells only grew in areas where the A2a receptor ligands PIA and NECA had been spotted. Since the plates contained adenosine deaminase, the lack of growth where adenosine had been spotted confirmed that adenosine deaminase was active. III. fusl LacZ Assay To guantitate activation of the yeast mating pathway, synthesis of 0-galactosidase through fuslLacZ was measured. Yeast strains expressing G3JE10K, G,,SD229S or G.,SE10K*D229S were transformed with a plasmid encoding the human A2a receptor (Rt-) or with a plasmid lacking the receptor (R-). Transformants were isolated and grown overnight in the presence of histidine and 4 U/ml adenosine deaminase. 1 x 10 cells were diluted to 1 x 10 cells/ml and exposed to increasing concentrations of NECA for 4 hours, followed by determination of the S-galactosidase activity in the cells. The results demonstrated that essentially no 3-galactosidase activity was detected in R- strains, whereas increasing amounts of 0-galactosidase activity were detected in Re­strains expressing either G3,E10K, G.,5D229S or GaJE10K+D229S as the concentration of NECA increased, indicating a dose dependent increase in units of B-galactosidase detected in response to exposure to increased ligand concentration. This dose dependency was only observed in cells expressing the A2a receptor. Furthermore the most potent G01 construct for the A2a receptor was GOSE10K. The G0,D229S construct was the second-most potent GOJ construct for the A2a receptor, while the G.,,E10KTD229S construct was the least potent of the three G3S constructs tested. although even the G,.E10K-z;Zr = construct stimulated readily detectable amounts cf (3-galactosidase activity. For a further description of the assays identified, see U.S. Application Serial No. 09/088985, entitled "Functional Expression of Adenosine Receptors in Yeast", filed June 2, 1958 (Attorney Docket No. CPI-093), the entire contents cf which are hereby incorporated herein by reference . Pharmacological Characterization of the Human Adenosine Receptor Subtypes Material and Methods Materials. [~H] -DPCPX [Cyclopentyl-1 , 3-dipropylxantine, 8- [dipropyl-2,3-3H(N)] (120.0 Ci/mmol) ; [3H] -CGS 21680, [carboxyethyl-3H (N) ] (30 Ci/mmol) and [:"l] -AB-MECA ( [* I]-4 -Aminobenzyl-5 ' -N-Methylcarboxamideoadenosine } (2,200 Ci/mrnol) were purchased from New England Nuclear (Boston, MA). XAC (Xantine amine congener); NECA (5'-N-Ethylcarboxamidoadenosine) ; and IB-MECA from Research Biochemicals International (RBI, Natick, MA). The Adenosine Deaminase and Complete protease inhibitor cocktail tablets were purchased from Boehringer Mannheim Corp. (Indianapolis, IN) . Membranes from KEK-293 cells stably expressing the human Adenosine 2a [RB-HA2a] ; Adenosine 2b [RB-HA2b] or Adenosine 3 [RB-HA3] receptor subtypes, respectively were purchased from Receptor Biology (Beltsville, MD) . Cell culture reagents were from Life Technologies (Grand Island, NY) except for serum that was from Hyclone (Logan, UT) . yeast strains.- Saccharomyces cerevisiae strains CY12660 [farl'1442 tbtl-1 fusl-HIS3 canl ste!4 : : trpl : : LYS2 ste3*1156 gpal (41) -Gai3 Iys2 ura3 Ieu2 trpl: his3 ; LEU2 PGKp-MfalLeader-hAlR-PHOSterm 2mu-orig REP3 Ampr] and CY8362 [gpalp-rGasElOK farl*1442 tbtl-l fusl-HIS3 canl ste!4::trpl: LYS2 ste3*ll56 Iys2 ura3 Ieu2 trpl his3; LEU2 PGKp-hA2aR 2mu- ori ?*E?3 Ampr] were developed as described above. yeast culture: Transformed yeast were grown in leu-Trp [IT] media (pH 5.4} supplemented with 2't glucose. For the preparation of membranes 250 ml of LT medium were inoculated with start titer of 1-2 x 10 cells/ml from a 30 ml overnight culture and incubated at 30°C under permanent oxygenaticn by rotation. After 16 h growth the cells were harvested by centrifugation and membranes were prepared as described below. Mammalian Tissue Culture: The HEK-293 cells stably expressed human Adenosine 2a receptor subtype (Cadus clone # 5) were grown in Dulbeco's minimal essential media (DMEM) supplemented with 10V fetal bovine serum and IX penicillin/streptomycin under selective pressure using 500 mg/ml G418 antibiotic, at 37°C in a humidified 5% C02 atmosphere. yeast Cell Membrane Preparations: 250 ml cultures were harvested after overnight incubation by centrifugation at 2,000 x g" in a Sorvall RT6000 centrifuge. Cells were washed in ice-cold water, centrifuged at 4°C and the pellet was resuspended in 10 ml ice-cold lysis buffer [5 mM Tris-HCl, pH 7.5; 5 mM EDTA; and 5 mM EGTA] supplemented with Protease inhibitor cocktail tablets (1 tablet per 25 ml buffer). Glass beads (17 g; Mesh 400-600; Sigma) were added to the suspension and the cells were broken by vigorous vortexing at 4°C for 5 min. The homogenate was diluted with additional 30 ml lysis buffer plus protease inhibitors and centrifuged at 3,000 x g for 5 min. Subsequently the membranes were peleted at 36,000 x g (Sorvall RC5B, type SS34 rotor) for 45 min. The resulting membrane pellet was resuspended in 5 ml membrane buffer [50 mM Tris-HCl, pH 7.5; 0.6 mM EDTA; and 5 mM MgCl2] supplemented with Protease inhibitor cocktail tablets (1 tablet per 50 ml buffer) and stored at -80 °C for further experiments. Mammalian Cell Membrane Preparations: KEK-293 cell membranes were prepared as described previously (Duric £ e: si . .• J. Biol. Chem. , 267, 9844-9851, 1992} Briefly, cells were washed with PBS and harvested with a rubber policeman. Cells were pelted at 4CC 200 x g in a Sorvall RT6000 centrifuge. The pellet was resuspended in 5 ml/dish of lysis buffer at 4~C (5 mM Tris-HCl, pH 7.5; 5 mM EDTA; 5 mM EGTA; 0.1 mM Phenylmethylsulf onyl fluoride, 10 mg/ml pepstatin A; and 10 mg/ml aprotinin) and homogenized in a Dounce homogenizer. The cell lysate was then centrifuged at 36,000 x g (Sorvall RC5B, type SS34 rotor) for 45 min and the pellet resuspended in 5 ml membrane buffer [50 mM Tris-HCl, pH 7.5; 0.6 mM EDTA; 5 mM MgCl2; °-1 "^ Phenylmethylsulf onyl fluoride, 10 mg/ml pepstatin A; and 10 mg/ml aprotinin) and stored at -80 °C for further experiments. The Bio-Rad protein assay kits, based on the Bradford dye-binding procedure, (Bradford, M. : Anal . Biochem. 72:248 (1976)) were used to determine total protein concentration in yeast and mammalian membranes. Adenosine 1 receptor subtype saturation and competition radioligand binding: Saturation and competition binding on membranes from yeast cell transformed with human Aj receptor subtype were carried out using antagonist [ H] DPCPX as a radioactive ligand. Membranes was diluted in binding buffer [50 mM Tris-HCl, pH 7.4; containing 10 mM MgCl2; 1 . 0 mM EDTA; 0.25% ESA; 2 U/ml adenosine deaminase and 1 protease inhibitor cocktail tablet/50 ml] at concentrations of 1.0 mg/ml . In saturation binding membranes (50 ng/vell) were incubate with increasing concentrations of ["H] DPCPX (0.05 - 25 nM) in a final volume of 100 m! of binding buffer at 25°C for 1 hr in the absence and presence of 10 nM unlabeled XAC in a 96-well microtiter plate. In competition binding membranes (50 /ig/weli) were incubate with [2H] DPCPX (1.0 nM) in a final volume of 100 r.l cf binding buffer at 25°C for 1 hr in the absence and presence of 10 mm unlabeled XAC or increasing concentrations of competing compounds in a 96-well microtiter plate. Adenosine 2a receptor subtype competition radicligand binding: Competition binding on membranes from KEK293 cell stably expressing the human A2a receptor subtype were carried out using agonist [~H] CGS-21680 as a radioactive ligand. Membranes was diluted in binding buffer [50 mM Tris-HCl, pH 7.4; containing 10 mM MgCl2; 1.0 mM EDTA; 0.25V BSA; 2 U/ml adenosine deaminase and 1 protease inhibitor cocktail tablet/50 ml] at concentrations of 0.2 mg/ml. Membranes (10 Mg/well) were incubate with [ H] CGS-21680 (100 nM) in a final volume of 100 ml of binding buffer at 25°C for 1 hr in the absence and presence of 50 ^M unlabeled NECA or increasing concentrations of competing compounds in a 96-well microtiter plate. Adenosine 3 receptor competition radioligand binding: Competition binding on membranes from HEK293 cell stably expressing the human A3 receptor subtype were carried out i ? s. using agonist [" -I] AB-MECA as a radioactive ligand. Membranes was diluted in binding buffer [50 mM Tris-HCl, pH 7.4; containing 10 mM MgCl2; 1.0 mM EDTA; 0.25% BSA; 2 U/ml adenosine deaminase and 1 protease inhibitor cocktail tablet/50 ml] at concentrations of 0.2 mg/ml. Membranes (10 Mg/well) were incubate with [i25I] AB-MECA (0.75 nM) in a final volume of 100 m! of binding buffer at 25°C for 1 hr in the absence and presence of 10 MM unlabeled IB-MECA or increasing concentrations of competing compounds in a 96-well microtiter plate. At the end of the incubation, the Aj, A2a and A3 receptor subtypes radioligand binding assays was terminated by the addition cf ice-cold 50 mM Tris-HCl (pH 7.4) buffer supplemented with 10 mM MgCl2 Adenosine 2b receptor subtype competition radioligand binding: Competition binding on membranes from KEK293 cell stably expressing the human A2b receptor subtype were carried out using A, receptor antagonist [3H] DPCPX as a radioactive ligand. Membranes was diluted in binding buffer [10 mM Hepes-KOH, pK 7.4; containing 1.0 mM EDTA; 0.1 mM Benzamidine and 2 U/ml adenosine deaminase] at concentrations of 0.3 mg/ml. Membranes (15 ^g/well) were incubate with [3H] DPCPX (15 nM) in. a final volume of 100 pi of binding buffer at 25°C for 1 hr in the absence and presence of 10 ^M unlabeled XAC or increasing concentrations of competing compounds in a 96-well microtiter plate. At the end of the incubation, the assay was terminated by the addition of ice-cold 10 mM Hepes-KOH (pH 7.4) buffer followed by rapid filtration over glass fiber filters (96-well GF/C UniFilters, Packard) previously presoaked in 0.5% pclyethylenimine in a Filtermate 196 cell harvester (Packard). The filter plates were dried coated with 50 ^I/well scintillation fluid (MicroScint-20, Packard) and counted in a TopCount (Packard). Assays were performed in triplicate. Non-specific binding was 14.3 ± 2.3% of the total binding. Specific binding of [3H] DPCPX; [3H] CGS-21680 and [125I] AB-MECA was defined as the difference between the total binding and non-specific binding. Percent inhibition of the compounds was calculated against total binding. Competition data were analyzed by iterative curve fitting to a one site model, and Kr values were calculated from ICiQ values (Cheng and Pruscf. Eiochem. Pharmacol. 22, 3099-310S, 1S73) using the GraphPad Prizni 2.01 software. Results A primary function of certain cell' surface receptors is to recognize appropriate ligands. Accordingly, we determined ligand binding affinities to establish the functional integrity of the Adenosine 1 receptor subtype expressed in yeast. Crude membranes prepared from Saccharomyces cerevisiae transformed with human Adenosine l receptor subtype construct exhibited specific saturable binding of [ H] DPCFX with a KD of 4.0 ± 0.19 nM. The KD and Bmax value were calculated from the saturation isotherm and Scatchard transformation of the data indicated a single class of binding sites. The densities of adenosine binding sites in the yeast membrane preparations were estimated to 716.8 * 43.4 fmol/mg membrane protein. The pharmacological subtype characteristics of the recombinant yeast cells transformed with human Aa receptor subtype - were investigated with subtype selective adenosine ligands (XAC, DPCPX; CGS-15943; Compound 600; Compound 1002; NECA, (R)-PIA,- IB-MECA and Alloxazine) that competed with [ H] DPCPX in the expected rank order. Displacement curves recorded with these compounds show the typical steepness with all the ligands, and the data for each of the ligands could be modeled by a one-site fit. The apparent dissociation constants estimated for the individual compound from the curves (Table 5) are consistent with value published for the receotor obtained from other sources. Table 5 Ki values for membranes from yeast cells transformed with human A: receptor subtype (Table Remove) Tables 6 through 12 demonstrate the efficacy and structure activity profiles of deazapurines of the" invention. Tables 13 and 14 demonstrate selectivity can be achieved for human adenosine receptor sites by modulation of the functionality about the deazapurine structure. Table 14 also demonstrates the surprising discovery that the compounds set forth therein have subnanomolar activity and higher selectivity for the A;b receptor as compared to the compounds in Table 13. (Table Remove) Summary of the Invention The present invention is also base:: or. ccmpr-unas wr.icr. selectively bind tc adenosine A2a receptor, thereby treating a disease associated with A:a adenosine receptor in a suriect by administering tc the subject a therapeutical1y effective amount of. such compounds. The disease to be treated are associated with, for example, a central nerve;.s system disorder, a cardiovascular disorder, a renal disorder, an inflammatory disorder, a gastrointestinal disorder, an eye disorder, an allergic disorder or a respiratory disorder. ;is invention also features a compounc having tne structure (Figure Remove) (VI wherein NR.R- is a substituted or unsuostituted 4-8 membered r i n g ; wherein Ar is a substituted or ur.subs tituted four to six membered rina; wherein R, is H, alkyl, substituted alkyl, aryl, arylalkyl, aminc, substituted aryl, wherein said substituted alkyl is -C (Rs) (R=.) XRt, wherein X is 0, S, or NR-, wherein R- and R-, are each independently H or alkyl, wherein rl and R- are each independently alkyi or cycloaikyi, or R<: r- and the r.itrccer. together forrr a substituted or unsubst i tuted ring of between members.> wherein R. is wherein ?,; is H, alkyi, substituted aikyl, cr cyclealkyl; with the proviso that NR:R: is not 3-acetamido piperadino, 3-hydroxy pyrrciidinc, 3-methyloxy carbonylmethyi pyrrolidi.no, 3-a.Tiinccarbonylrrtethyl, or pyrrolidino; with the proviso that NR:R; is 3-hydroxymethyl piperadino only wher. Ar is 4-pyndyi. This invention also features a method for inhibiting the activity of an A2a adenosine receptor in a ceil, which comprises contacting said cell with the above-mentioned compounds. This invention -also provides a compounr. having the structure (Figure Remove) wherein NR,R: is a substituted or unsubstituted 4-8 membered ring; wherein Ar is a substituted or unsubstituted four to six memDerec ring; wherein R; is H, aikyl, substituted ai.-:yl, ary_, arylalkyl, aminc, subscitutec aryi, wr.erein said substituted aikyi is -C(Re) (R?)XRc, wherein X is G, S, or NR-;, wherein Re and R-- are each independently H or aikyl, wherein Re and R-; are each independently aikyl or cycl substituted or unsubstituted ring of between 4 and 7 members. wherein Ri is H, aikyl, substituted aikyl, or cycloalkyl; with the proviso that NRiR: is not 3-acetamido piperadino, 3-hydroxy pyrrclidino, 3-methyioxy caroonylmethyl pyrroiidino, 3-aminocarbonylmethyl, or pyrrolidino; with the proviso that NRiR: is 3-hydroxymethyi piperadino only when Ar is 4-pyridyl. In one embodiment of the compound, Ar is a substituted or unsubstituted four to six membered ring, phenyl, pyrrole, thiophene, furan, thiazole, imidazole, pyrazole, 1,2,4-triazole, pyridine, 2 (1H)-pyridone, 4 (IF.)-pyridone, pyrazine, pyrimidine, pyridazine, isothiazole, isoxazole, oxazole, tetrazole, naphthalene, tetralin, naphthyridine, benzofuran, benzothiophene , indole, 2 , 3-dihydroindole, IH-indole, indoline, benzopyrazole, 1,3-benzodioxole, benzoxazole, purine, coumarin, chrorr.one, quinoline, tetrahydrocuinoline, isoquinoline, benzimidazole, quinazoline, pyrido[2,3-b]pyrazine, pyrido[3,4-bjpyrazine, pyrido[3,2-c]pyridazine, purido(3, 4-b]-pyridine, IH-pyrazole[3,4-d]pyrimidine , pteridine, 2(1H)-cuinolone, 1(2H)-isoquinolone, 1, 4-benzisoxazine , benzothiazole, q u i n o x a 11 n e , quincline-N-oxide, i s c o u in c 11 p. e - I-.' - c x i quinoxaline-N-oxide, quinazoline-N-cxice, p h t h a i a z i n e, cinncline, or having a structure: (Figure Remove) wherein Y is carbon or nitrogen; wherein R: is H, substituted or unsubstituted alkyl, substituted or unsubstituted aryl, halogen, methcxy, methyl amino, methvl thio; In another embodiment of the compound, the compound has the structure: (Figure Remove) wherein m is 1 or 2; wherein ra and re are each independently be H, -OH, -CK20H, -CH:CH:OH, -C(=0)NH2, a heteroatom, or -C (=0) NR,R,' ; wherein R3 is aryi, substituted aryl, or heteroaryi; wherein R:' is alkyl, or XR/', wherein X is 0, or N and R" is substituted alkyl or aryl. In another embodiment of the compound, R:R:N is (D)-2-aminocarbonyl pyrrolidino, (D) -2-hydroxymethyl pyrrolidino, (D) -2-hydrcxynethyl- trar.s-*-. -hydroxy pvrro 3-hydroxymethyl piperadino. In another embodiment of the compound, the compound has the structure : (Figure Remove) ra wherein m is 0, I, 2, or 3; wherein Y is 0, S, or NR, wherein R is ra or Re; wherein ra and re are each independently be H, -OH, -CHzOH, -CK:CH:OH, -C(=0)NH2, a heteroatom, or -C(=0)NR;R/; wherein R, is aryi, substituted aryl, or heteroaryl; wherein R/ is alkyl, or XR:" , wherein X is 0, or N and R" is substituted alkyl or aryl. In another embodiment of the compound, the compound has the structure: (Figure Remove) In another embodiment of the compound, the compound has th« structure : (Figure Remove) (Compound 1601 In another embodiment of the compound, the compound has the structure: (Figure Remove) (Compound 1602) In another embodiment of the compound, the cor structure: (Figure Remove) (Compound 1603! [Compound In another embodiment of the compound, the compound has the structure.: (Figure Remove) In another embodiment of the compound, the ccmpour.d has tr.e structure: HO, (Figure Remove) (Compound 1605) [Compound 1606] In another embodiment of the compound, the compound has the structure: (Figure Remove) In another embodiment cf the compound, the c (Figure Remove) (Compound 1607) In yet another embodiment cf the compound, the compound has the structure: (Figure Remove) In a further embodiment of the compound, the compound has the structure: (Figure Remove) This invention further provides a ccmcound havmc (V) : (Figure Remove) the structure (V! wherein R is H, or methyl. In one embodiment of the compound V, the compound has the structure: (Figure Remove) (Compound 1608) In another embodiment of the compcunc V, the comocunc: nas tne structure: (Figure Remove) This invention also provides a method for treating a disease associated with A2a adenosine receptor in a subject, comprising administering to the subject a therapeutically effective amount of compounds IV, or V. In one embodiment of the method, the compound treats said diseases by stimulating adenylate cyclase. In another embodiment of the method, the subject is a mammal. In another embodiment of the method, the mammal is a human. In another embodiment of the method, said A2a adenosine receptor is associated with Parkinson's disease and diseases associated with locomotcr activity, vasodiiation, platelet inhibition, neutrophil superoxide generation, cognitive disorder, or senile dementia. Diseases associated with adenosine Ai, A2a, A2b and A3 receptors are disclosed in WO 99/06053 and WO-09822465, WO-09705138, WO- G9511681, WO-09733S79, JP-C9291CS9, ? :7/U£9S / 1 6053 ana 'J . 3 . Patent Nc. 5,516,594, the entire content of which are fullv incorporate herein by reference. c c: This invention also provides a water-sciucie procruc compounds IV, or V; wherein said water-soluble crocruc that is metabolized i~ vivc to produce an active drug which selectively inhibit A2a adenosine receptor. In one emoodiment of the prodrug, said prodrug is metabolized in vivo by esterase catalyzed hydrolysis. This invention also provides a pharmaceutical composition comprising the prodrug and a pharmaceutics lly acceptable carrier . This invention also provides a method for inhibiting the activity of an A2a adenosine receptor in a cell, which comprises contacting said cell with compounds IV, or V. In one embodiment of the method, the compound is an antagonist of said A2a adenosine receptor. In another embodiment of the pharmaceutical composition, said pharmaceutical composition is an ophthalmic formulation. In another embodiment of the pharmaceutical composition, said pharmaceutical composition is an periocular, retrobulbar or intraocular injection formulation. In another embodiment of the pharmaceutical composition, said pharmaceutical composition is a systemic formulation. This invention also provides a method for treating a gastrointestinal disorder in an subject, comprising administering to the an effective amount of compounds IV, cr V. In one embodiment of the method, said disorder is diarrhea. In another embodiment of the method, the subject is a human. In another embodiment of the method, the compound is an antagonist of A2a adencsine receptors. This invention further provides a method for treating respiratory disorder in a sub]ect, comprising administering to the subject an effective amount of compounds IV, cr V. In one embodiment of the method, said disorder is asthma, chronic obstructive pulmonary disease, allergic rhinitis, or an upper respiratory disorder. In another embodiment of the method, the subject is a human. In another embodiment of the method, said compound is an antagonist of A2a adenosine receptors. This invention also provides a method for treating damage to the eye of a subject which comprises administering to said sub]ect an effective amount of compounds IV, or V. In one embodiment of the method, said damage comprises retinal or optic nerve head damage. In another embodiment of the method, said damage is acute or chronic. Ir, another embodiment of the method, said damage is the result of glaucoma, edema, ischemia, hypoxia cr trauma. In another embodiment of the method, the subject is a human. In another embodiment of the method, the compound is an antagonist of A2a adenosine receptors. This invention also provide a pharmaceutical composition comprising a therapeuticaily effective amount of compounds IV, cr V and a pharmaceuticaily acceptable carrier. In one embodiment of the pharmaceut .cal composition, said therapeuticaily effective amount is effective to treat Parkinson's disease and diseases associated with locomotor activity, 'vasodilation, platelet inhibition, neutrophil superoxide generation, cognitive disorder, or senile dementia. In another embodiment of the pharmaceutical composition, said pharmaceutical composition is an ophthalmic formulation. In another embodiment of the pharmaceutical composition, said pharmaceutical composition is an periocular, retrobulbar or intraocular injection formulation. In another embodiment of the pharmaceutical composition, said pharmaceutical composition is a systemic formulation. In another embodiment of the pharmaceutical composition, said pharmaceutical composition is a surgical irrigating solution. This invention also provides a combination therapy for Parkinson's disease comprising compounds IV and V, and any of the dcparnir.e enhancers . This invention further provides a combinational therapy fcr cancer comprising compounds IV and V, ana any of the cytctoxic agents. This invention further provides a combinational therapy for glaucoma, comprising compounds IV or V, and a prostagiancir. agonist, a muscrinic agonist, or a b-2 antagonist. This invention also provides a packaged pharmaceutical composition for treating a disease associated with AZa adenosine receptor in a subject, comprising: (a) a container holding a tnerapeutically effective amount of compounds IV, or V; and (b) instructions for using said compound fcr treating said disease in a sub j ect. This invention also provide a method of preparing compound IV, comprising the steps of (Figure Remove) wherein N R, R • is a substituted or ur. substituted 4-5 membered ring; wherein Ar is a substituted or unsubstituted four tc six memberec ring; wherein R; is H, alkyi, substituted -alky!, aryl, arylalkyl, aminc, substituted aryl, wherein said substituted alkyi is -CtRei (R--)XRf, wherein X is 0, S, or NR-, wherein Rf and R-are each independently H or alkyi, wherein R, and R- are each independently alkyi or cycloalkyl, or Re, R- and the nitrogen together form a substituted or unsubstituted ring of between 4 and 7 members. wherein R* is H, alkyi, substituted alkyi, or cycloalkyl; with the proviso that NRiR: is not 3-acetamitio piperadino, 3-hydroxy pyrrolidino, 3-methyloxy carbonylmethyl pyrrolidinc, 3-aminocarbonylmethyl, or pyrrolidino; with the proviso that NR:R: is 3-hydrc.xynethyl piperadino only when Ar is 4-pyridyl. This invention further provides a method of preparing compound V, comprising the steps of (Figure Remove) wherein ?.: is acetomiac ethyl; wherein Ar is 4-pyndyl; wherein R is H, or methyl; wherein R: is N-meihyl-N-oer.iyl aminomethyl. As used herein, "A compound is A-,g selective." means that a compound has a binding constant to adenosine A;a receptor cf at least five time higher then that to adencsine A , a:ci, or A3. The invention, is further illustrated by the following examples which in no way should be construed as being further limiting. The contents of all references, pending patent applications and published patent applications, cited throughout this application, including those referenced in the background section, are hereby incorporated by reference. It should be understood that the models used throughout the examples are accepted models and that the demonstration of efficacy in these models is predictive of efficacy in hurr.ans. This invention will be better understood from the Experimental Details which follow. However, one skilled in the art will readily "appreciate that the specifi-: methods and results discussed are merely illustrative of the invention as described more fully in the claims which follow thereafter. Example 22: Synthesis of Adenosine A2a Antagonists, compounds 1601, 1602, and 1603. (Figure Remove) Compound 26 (10.92g, 50. 7 £ r.T.ci; was cissclvec ir. -Mr ;6~ ~L . 4-Am.idinopyncir.e hydrcchlcride (£.03, 5C.~6 rr.T.cl '> ar.c ZE'J il5.4 g, 101.5 mrr.cl) were aaded sequentially and the reaction was heated to 85°C. After 22 hours, the reaction was cociea tc room temperature and the DM? was removed in vacua. The aarx cil was diluted with 2M HC1 (60 nL) . The reaction was allowed to stand. After 2 hours, the solution was cooled to 10CC and filtered. The solid was washed with cold water and dried to yield 7.4Cg of a yellow solid, compound 27 (69%) . :H-NMR (2COMHz, d,-DMSO) d 6.58 (s, IK), 7.27 (s, 1H), 6.53 (d, 2H, J = 5.6), 9.00 (d, 2H, J = 5.2Hz), 12.35 (brs, 1H). MS (ES): 212 .S (M' + l) - Compound 27 ;7.4 mmol, 29.8 mmol) was diluted with POC1; and heated to 105°C. After 18 hours, the reaction is cooled to room temperature and the POC1-, is removed in vacuc. The thick dark oil is diluted with MeOH (75mL) followed by ether (120mL). The amorphous red solid is filtered and washed with ether to yield 3.82 g of a red solid. The crude solid, compound 28, is approximately 80% pure and used without further purification in the next reaction. :H-NMR (200MKz, dc-DMSO) d 6.58 (s, 1H), 7.27 (s, IK), 8.53 (d, 2H, J = 5.6), 9.00 (d, 2 H, J = 5.2 H 2) , 12.35 (brs, 1H). MS (ES): 212.8 (M'+l). Compound 1601: DMSO (5 mL) and D-prolinol (500mc, 4.94 mmol) were added to compound 28 (500mg, 2.1" mmol) was added. The reaction was heated to 120°C. After 18 hours, The reaction was cooled to room temperature and diluted with EtOAc and K,0. The layers were separated and the aqueous layer was extracted with EtOAc (2x). The combined organic layers were washed with H:0 (2x), brine, dried over MgSO;, filtered and concentrated to yield 200mc of a tan solid. The solid was recrystalii zed from EtOAc to yield 82 rr.c of a tan solid il3%> . -H-N'M?. d,-DMSO) d 2.C5 (m, 4H), 3.43 (m, 1H), 3.7C - 4.00 (m, 2H>, 4 . 5C (brs, IK), 4.92 (brs, 1H), 6.62 (m, IK), 7.22 (M'i-1), mp = 210 - 220;C (decomp.). Compound 1602: Chromatography (silica, 9:1 CKC13/MeOK) yielded 10 me of a tan solid (2%).:H-NMR (d.-DMSO) d 2.0C - 2.50 (m, 4H), 4.05 im, In), 4.21 (m, 1H), 6.71 (c, 1H, J = 3.2 Hz), 7.18 (d, IK, J = 3.2 Hz), 8.37 (d, 2H, J = -. . S Hz), 6.56 (a, 2H, J = 5 .0 Hz). MS (ES): 309.1 (M**l). Compound 1603. Chromatography (silica, 20:1 Hexanes /EtOAc) yielded 135 mg of a tan solid (53%). :H-NMR (d,-DMSO) d 2.00 (m, 4H), 2.43 (brs, IK), 3.74 (brs, 2K), 3.67 (brs, IK), 4.49 (brs, 1H), 4.93 (m, IK), 6.56 (m, 1H), 7.12 (rr., IK), 7.40 (m, 3H) , 8.34 (m, 2K), 11.62 (brs, 1H). MS (ES): 295.1 (M'i-1). Compound 1605. Into a 50mL REF 60mc of 2-(4'-pyridyl)-4- Chloropynmidinopyrrole HC1 salt was dissolved in 2mL anhydrous DMSO. 3-(R)-Hydroy-(D)-prolinol TFA salt (3SOmg) and 500mg sodium bicarbonate were added thereto. The mixture was then flashed with nitrogen gas for 5min and heated to 130r'C. After 2 hours, the reaction was cooled to room temperature and the DMSO was removed in vacuo. The residue was partitioned between EtOAc (15mL) and saturated sodium bicarbonate aqueous solution (15mL). The organic layer was separated and washed with brine (15mL) and dried over Na:SO<. after removal of solvent the crude product was purified by preparative tlc to yield mg :h-nmr cdc1- k ms> Example 23: Synthesis of Adenosine A:. Antagonist, compound 1606. (Figure Remove) w" N Br N BOC Compound 2S Compound 28 (200mg) was treated with DMF (30mL), {, (-dimethylgiycir.e methyl ester (73mg HC1 salt in 2ml water) and SOOmc sodium. Dicarbcr.ate. After 18 hours, the DMF was removed in vacuo. The residue was partitioned between EtOAc (30mL) and saturated sodium bicarbonate aqueous solution (15mL). The organic layer was washed with brine (15mL), dried over sodium sulfate, filtered and concentrated. Chromatography (silica, 10:4 hexanes/EtCAc) yielded 150mg of pure product, compound 29 (69%). '-H-NMR (200MHz, CDC!,), ( 1.4 (s, 6H), 3.5 (s, 3H); 3.9 (S, 2H) ; 6.4 (s, 1H) ; 7.4-7.5 (m, 3H); 6.4 (m, 2H); 9.8 (s, 1H) . Compound 1606: Procedure is the same as Compound 1605 (721) . '• H-NMR (200MHz, CDC1:.), ( 1.3 (s, 6H), 1.7-1.9 (m, 2H); 2.05-2.30 (m, 2H); 3.6-4.1 (m, 11H); 4.80-4.95 (m, 1H); 6.4 (s, 1H); 7.4-7.6 (m, 3K); 8.3-8.4 (d, J = 6.5 Hz, 2H), 10 (s, 1H). MS (ES): 424.0 (M' + l) . The following compounds can be synthesized in the same manner Compound 1600: (51%). MS (ES): 326.0 (K't-1). Compound 1607: :H-NMR ,200MHz, CDC1-.;, 2.SC - 3.50 (it:, 3 H) , 4.60 - 4.60 ;-, 6.2HZ), 7.26 (m, 1H), 6.21 (d, 2H, - 5.6Hz), 11.90 (s, 1H) . MS (ES): 310.1 (M'-l). Compound 1608: (64%). -H-NMR (200MHz, d,-DMSO), ( 1.75 (s, 3n), 2.11 (s, 3H), 2.29 (s, 3H), 3.56 (m, 6H), 7.23 - 7.41 (m, 5H), 6.00 (brs, 1H), 6.23 (d, 2H, J = 6.0Hz), 8.63 (d, 2H, J = 5.4 Hz), 8.82 (brs, 1H), 11.56 (brs, 1H). MS (ES): 444.0 (M'+l). Compound 1604: JH-NMR (200MHz, CD7OD) ( 3.40 (m, 4H), 4.29 (m, 4H), 6.99 (s, 1H), 7.5 - 7.2 (m, 3H), 7.90 (d, 2H), 8.39 (d, 2H), 8.61 (d, 2H). MS (ES): 357.0 (M' +1). TABLE 16. Adenosine A:a Receptor Selective Compounds at least 5 times more selective than other three subtypes. Compound Structure Rela-ive Ki-Ai Kl -A2akelativepelativ€ Ki-A2b IK1-A3 1600? a a es -256 relate tc ccrr.po u n d s s c e c Summary of the Invention The present invention is also oasea or. compounds . r to w i; selectively bind to aaenosine A3 receptor, thereby disease associated with A: aaenosine receptor in a subject by administering to the subject a therapeuticaliy effective amount of such compounds. The disease to be treated are associated with, for example, asthma, hypersensitive ty, rhinitis, hay-fever, serum sickness, allergic vasculitis, atopic dermantitis, dermantitis, psorasis, eczema, idicoathic pulmonary fibrosis, eosinophillic chlorecystitis, chronic airway inflammation, hypereosinophilic syndromes, eosinophilic gastroenteritis, edema, urticaria, eosinophiiic myocardial disease, episodic angioedema with eosinophilia, inflammatory bowel disease, ulcerative colitis, allergic granuiomatosis, carcinomatosis, eosinophilic granuloma, familial histlocytosis, hypertension, mast cell degranulation, tumor, carciac hypoxia, cerebral ischemia, diuresis, renal failure, neurological disorder, mental disorder, cognitive disorder, myccardial ischemia, bronchoconstriction, arthritis, autoimmune disease, Crohn's disease,- Grave's disease, diabetes, multiple sclerosis, anaemia, psoriasis, fertility disorders, lupus erthyematosus, reperfusion injury, brain arteriole diameter, the release of allergic mediators, scleroderma, stroke, global ischemia, central nervous system disorder, cardiovascular disorder, renal disorder, inflammatory disorder, gastrointestinal disorder, eye disorder, allergic disorder, respiratory disorder, or immunological disorder. This invention also features a compounc having the structure: wherein R: is H and R: is cyclopropyl methylamino carbonylethyl, cis-3-hydroxy cyclopentyl, acetamido butyl, methylamino carbonylamino butyl, ethylamino carbonylamino propyl, methylamino carbonylamino propyl, 2-acetyl amino-3-methyl butyl, N,N-diethylamino carbonylamino ethyl, thioacetamidc ethyl, 3-amino acetyloxy cyclcpentyl, 3-hydroxy cyclopentyl, 2-pyrrolyl carbonyl aminoethyl, 2-imidazolidinone ethyl, 1-aminocarbonyl-2-methyl propyl, 1-aminocarbonyl-2-phenyl ethyl, 3-nydroxy azetidino, 2-imidazolyl ethyl, acetamido ethyl, 1-(R)-phenyl-2-hydroxyethyl, N-methylaminocarbonyl pyridyl-2- methyl, or Ri, R: and the nitrogen together are 3-acetamido piperadino, 3-hydroxy pyrrolidino, 3-methyloxy carbonylmethyl pyrrolidino, 3-aminocarbonylmethyl pyrrolidino, or 3-hydroxymethyl piperadino. wherein Po is a substituted or unsubstituted four to six menbered ring, pyrrole, thiophene, furan, thiazole, imidazole, pyrazole, 1,2,4-triazole, pyridine, 2(1H)-pyridone, 4(1H)-pyridone, pyrazine, pyrimidine, pyridazine, isothiazole, isoxazole, oxazole, tetrazole, naphthalene, tetralin, naphthyridine, benzofuran, oenzcthiophene, ir.dole, 2 , 3-dihycrcir.acle , ! ir.doline, benzopyrazole, 1, 3-ber.z cdicxcle , ber.zoxar cie, p u r i r. e , c c u rr, a r i n , c n r c :i c n e , q u i n o 1 i n e , ret ranydrcquinol me , isoqumoline , Der.zirr.idazole, quinazcline, pyrido[2,3-bjpyrazine, pyrico [ 3, 4-b]pyrazine, pyrido [ 3 , 2-c] pyndazine, pundo ; 3 , 4 -c j -pyriaine , 1H-pyrazcie[3,4-d]pyrimidine, ptericine, 2 i1H)-quinolone, 1(2H)-isoquinolone, 1,4-benzisoxazine, benzothiazoie, quinoxaline, quinoline-N-oxide, isoquincline-N-oxide, quinoxaline-N-oxide, quina zoline-N-oxide, ber.zoxazine, phthaiazine, or cinnoline. wherein Rs is H, alkyl, substituted alkyl, or cycloalkyl; wherein Re is H, alkyi, substituted alkyl, aryl, or substituted aryl. This invention also features a method for inhibiting the activity of an A3 adenosine receptor in a cell, which comprises contacting said cell with the above-mentioned compounds. typical practice and is known to those skilled in the art. Typical synthetic schemes for the preparation of deazapurine intermediates of the invention are outlined below in Scheme I. This invention also provides a method of preparing compound IV, comprising the steps of (Figure Remove) wherein R; is H ana R: is cycloprcpyl r~e tr.y lar.ir.c carconylethyl, c-£-3-hydrcxy cycicrer.r vl, aretar.icc butvl, rnethylamno carbcr.ylanino butyl, ethyiamir.c carbor.yla.-ninc propyl, methylaminc carbonylamir.o propyl, 2-acetyl amir.c-3-methyl butyl, N, N-diethyiarr.inc carbor.ylar.inc ethyl, thioacetamido etr.yl, 3-amino acetyloxy cyclopentyl, 3-hydrcxy cyclcpentyl, 2-pyrrolyl carbonyl arr.ir.oethyl, 2-imiaazolidinone ethyl, l-aminocarbcnyl-2-methyl propyl, 1-aminocarbonyi-2-phenyl ethyl, 3-hydrcxy azetidino, 2-imidazolyl ethyl, acetamido ethyl, 1-(R)-phenyl-2-hydrcxyethyl, N-methyiaminocarbonyl pyridyl-2- methyl, or R., R: and the nitrogen together are 3-acetamido piperadino, 3-hydroxy pyrrclidinc, 3-methyloxy carbonyimethyl pyrrolidino, 3-aminocarDonylmethyl pyrrolidino, or 3-hydroxymethyl piperadino. wherein Rj is a substituted or unsubstitutea four to six membered ring; wherein Rs is H, elkyl, substituted aikyl, or cycloalkyl; wherein ^t is H, alkyl, substituted alkyl, aryl, or substituted aryl. This invention also provides a method of preparing compound of V, comprising the steps of (Figure Remove) wherein m is C, 1, or 2; wherein P.: is cyciopropyl methyl, nethvl, methyiarr.inc, cr amir.ome ~r.yl; wherein R: is aryl, substituted aryl, heteroaryi; wherein R; is H, alkyl, substituted alkyl, cr cycloalkyl; wherein Rt is H, alkyl, substituted aikyl, aryl, arylalkyi, amino, substituted aryl, wherein said substituted alkyl is -C(R=) (R:o)NR?Rj, wherein R- and Ric are each H or aikyl, wherein Ri and Rs are each alkyl or cycloalkyl, or R-, Rf and the nitrogen together form a ring system of between 4 and 7 members . This invention further provided a method of preparing compound VI, comprising (Figure Remove) wherei". R: is ur.substituted arvl. wherein Rh is H, alkyi, sucstitut a - k v- , or r vc - oa _ k v_ ; wherein R- H, aikyl, substituted clkyl, aryl, arylalkyl, ammo, substituted aryl, wherein said substituted alkyi is -C(FU) (Ric/NE-Rs, wherein R^ and R; are each H or aikyl, wherein R- and R? are each aikyi cr cycloalkyl, or R-, Rr and the nitrogen together form a ring system of between 4 and "7 members. "his invention also provides a compound having the structure: (Figure Remove) wherein R; is H and R: is cyclopropyl methylamino carbonylethyl, cis-3-hydroxy cyciopentyl, acetamido butyl, methylamino carbonylamino butyl, ethylamino carbonylamino propyl, methylamino carbonylaminc propyl, 2-acetyl amino-3-methyl butyl, N, N-diethylamino carbonylamino ethyl, thioacetamido ethyl, 3-amino acetyloxy cyciopentyl, 3-hydroxy cyciopentyl, 2-pyrrolyl carbonyl aminoethyl, 2-imidazolidinone ethyl, l-aminocarbonyl-2-methyl propyl, 1-aminocarbonyl-2-phenyl ethyl, 3-hydroxy azetidino, 2-imidazolyl ethyl, acetamido ethyl, 1-(R)-phenyl-2-hydroxyethyl, N-methylaminocarbonyl pyridyl-2- methyl, or F.., R. and the nitrogen together are piperadinc, 2-'nydroxy pvrrolidinc, 3 -rnetny icxy carbonylmethyi pyrrol i dine , 3-amincca rbcr.yimethyl pyrrclidino, or 3-'nydroxymethyl piperadinc . wherein P.; is a substituted cr ur.suos ti tuted benzene, pyrrole, thiophene, furan, thiazole, imidazcle, pyrazole, 1,2,4-triazcle, pyridine, 2(IK)-pyridone, 4 i1H;-pyridone, pyrazine, pyrimidine, pyridazir.e, isothiazole, isoxazcle, oxazoie, tetrazole, naphthalene, tetralin, naphthyridine, benzofuran, benzcthiophene, indole, 2,3-dihydrcindole, 1H-indole, ir.doline, benzcpyrazcle , 1, 3-benzodioxcie , benzoxazole, purine, coumarin, enrol-none, quinoline, tet rahyaroquinoline , isoquinol ine , benzirr,idazole , quinazoline, pyrido[2,3-b]pyrazine, pyridc[3,4-b]pyrazine, pyrido[3,2-c]pyridazine, purido[3,4-b]-pyridine, 1H-pyrazole[3,4-d]pyrimidine, pteridine, 2(1H)-quincione, I (2H)-isoquinolone, 1,4-benzisoxazine, benzothiazole, cuinoxaline, quinoline-N-oxide, isoquinoiine-N-oxide, quinoxaline-N-oxide, quinazoline-N-oxide, benzoxazine, phtha-lazine, or cinnoline. wherein Rs is K, alkyl, substituted alkyl, cr cycloalkyl; wherein Rt is H, alkyl, substituted alkyl, aryl, or substituted aryl . In one embodiment: cf the compound, the compound has structure: (Figure Remove) In another embodiment of the compound, R3 is phenyl. In another embodiment of the compound, R: is hydrogen or methyl. In another embodiment of the compound, Re is hydrogen, methyl, phenyl, 3-chlorophenyloxy methyl, or trans-2- phenylamino methyl pyrrolidino methyl. This invention further provides a compound having the structure: (Figure Remove) wherein m is 0, 1, or 2; wherein R: is cyclopropyl methyl, ".ethyl, metr.yiarr.inc, cr aminomethyl ; wherein R: is aryi, substituted aryi, or hetercaryl; wherein R = is H, alkyl, substituted aikyi, or cycioaikyl; wherein Re is H, alkyi, substituted alkyl, aryi, arylalkyl, ammo, substituted aryi, wherein said substituted alkyi is -C(Rt) (R:c)NR:R^, wherein R:- and R:: are each H or aikyl, wherein R- and R- are each alkyl or cycioaikyl, or R-, Re and the nitrogen together form a ring system of between 4 and 7 members. In one embodiment of compound V, m is 0 and R; is phenyl. In another embodiment of compound V, m is 1 and R: is phenyl. In another embodiment of compound V, m is 2 and R: is phenyl. In another embodiment of compound V, R: and Re are methyl. In another embodiment of compound V, Rs and Re are methyl. In another embodiment of compound V, Rs and Re are methyl. In another embodiment of compound V, the compound has the structure: (Figure Remove) (Compound 1316) In another embodiment of compound V, the compound has the structure: (Figure Remove) (Compound 1311 ur.substituted aryl. wherein Re is H, alkyl, substituted alkyl, or cycloaikyl; wherein Re H, alkyl, substituted In one embodiment of compound VI, the con-.pcund has the structure: (Figure Remove) (Compound 1309) In one embodiment of compound 130?, the compound has structure: (Figure Remove) CH3 In another embodiment of compound 1309, the compound has the structure: (Figure Remove) This invention aisc crcvides a ccrrcound havino tne s (Figure Remove) VII wherein R, is 3-hydrcxy cyclopentyi ethyiamino carbonyiamino propyl, N, N-diethylamino ca roor.yiamino ethyl, thioacetamido ethyl, 3-aminc acetylcxy cyclopentyi, 3-hydroxy cyclopentyi, 2-pyrrolyi carbonyl a~inoethyl, 2-imidazolidir.one ethyl, l-aminocarbonyl-2-rnethyl propyl, 1-aminocarbonyl-2-phenyl ethyl, 3-hycroxy azetidino, 2-imidazolyl ethyl, acetamido ethyl, 1-(R)-phenyl-2-hydroxyethyl, cr N-methylaminocarbonyl pyridyl-2- methyl; wherein R2 and R; are independently H, substituted or unsubstituted alkyl, or aryi. In one emooaiment or structure: the compound, the compound has the (Figure Remove) [Comoound 1700 In another embodiment of the compound, structure: HjC . »i t: — ^ 11. •-- ^ _ i . v~* . ; C c ^.,tr V (Figure Remove) (Compound 1701 In another embodiment of the compound, the compound has the structure : 3 (Figure Remove) (Comoound 1702) Ir. another embodiment cf the compound, the ccr.pcunc ha: structure: (Figure Remove) [Compound 1704 In another embodiment of the compound, the compound has the structure: NH (Figure Remove) [Comoound 1705 In another embodiment cf the compound, structure: HO (Figure Remove) (CcmDound 1706; In another embodiment of the compound, the compound has the structure: HCL (Figure Remove) In another enxbcciment of the compound, the corr.pour. structure: HO, (Figure Remove) In another embodiment of the compound, the compound has the structure: (Figure Remove) In anctner er.bcdi.T.ent of t: structure: ,e conoounc, (Figure Remove) i Compound 1707) In another embodiment of the compound, the compound has the structure: (Figure Remove) In another encocirrier.' structure: t n e c c rr.o c u r. o, t p. e c o rr.c c u r. c; (Figure Remove) HN (Compound 1708) In another embodiment of the compound, the compound has the structure: I-UC (Figure Remove) [Compound 1709) it. another embodiment cf the compound, the comoour.c. r.a: structure: (Figure Remove) (Compound 1710; (Compound 1712) In another embodiment cf the compound, the compound has the structure: (Figure Remove) In another embodiment cf the compound, the compound has structure: (Figure Remove) (Compound 1713! In another embodiment of the compounc, the compound has the structure: (Figure Remove) n another embodiment: of the compound, structure: ur.c has (Figure Remove) (Ccmpound 1714) In another embodiment of the compound, the compound has the structure: (Figure Remove) . n a n c t n e r structure: emoociment c: tne cornoour.c, - r~\ c 0 u n; (Figure Remove) ;Compound 1715 In another embodiment of the compound, structure : the compound has the (Figure Remove) In another embodiment of the compound, the compound has the structure: (Figure Remove) invention also provides a corr.ccur.c havinc the str; (Figure Remove) VIII wherein Ri, R: and the nitrogen together are 3-hydroxy pyrrcliaino, 3-methyloxy carbonylmethyi pyrrolidino, 3-aminocarbonyimethyl pyrrolidino, or 3-hydroxymethyl piperadino; wherein R3 and R, are independently H, substituted or unsubstituted alkyl, or aryl. In one embodiment of the compound, the compound has the structure: (Figure Remove) (Compound 1711) In another embo diner,t of the ccmcoup. d, the cc~ccur.o has structure: (Figure Remove) (Compound 1703) In another embodiment of the compound, the compound has the structure: (Figure Remove) In another embodiment of the compound, structure: HO. (Figure Remove) (Compound 1716) In another embodiment of the compound, the compound has the structure: (Figure Remove) In another structure: embodiment of the comocund, the compound r.-s the H,C (Figure Remove) In another embodiment of the compound, the compound has the structure: (Figure Remove) In anctner eznbodiment or the ccir.Dcund, the conoound has the (Figure Remove) [Compound 1717} In another embodiment of the compound, the compound has the structure: NH, (Figure Remove) In another embodiment of the compound, the corr.pcu: structure: (Figure Remove) (Compound 1718; In another embodiment of the compound, the compound has the structure: (Figure Remove) In another embodiment of the compound, structure: tr.e ccr.cour.c nas (Figure Remove) In another embodiment of the compound, the compound has the structure: (Figure Remove) This invention also provides a method for treating a disease associated with A3 'adenosine receptor in a subject, comprising administering to the subject a therapeutically effective amount of any of the compounds IV, V, VI, VI, or VIII. In one embodiment of the method, the subject is a r.armal. In another embodiment cf the methcc, the mammal is a numan. In another embodiment cf the method, said A3 adenosine receptor is associated with a central nervous system disorder, a cardiovascular disorder, asthma, hyper sensitivity, rhinitis, hay fever, serum sickness, allergic vasculitis, atccic dermar.titis, dermantitis, psorasis, eczema, idiopathic pulmonary fibrosis, eosinophillic chlorecystitis, chronic airway inflammation, hypereosinophiilc .syndromes, eosinophilic gastroenteritis, edema, urticaria, eosinophilic myocardial disease, episodic angioedema with eosinophilia, inflammatory bowel disease, uicerative colitis, allergic cranulorr.atosis, carcinomatosis, eosinophilic granuioma, familial histiocytosis, hypertension, mast cell degranulation, zumor, cardiac hypoxia, cerebral ischemia, diuresis, renal failure, neurological disorder, mental disorder, cognitive disorder, myocardial ischemia, bror.choconstriction, arthritis, autoimmune disease, Crohn's disease, Grave's disease, diabetes, multiple sclerosis, anaemia, psoriasis, fertility disorders, lupus erthyematosus, reperfusicr. injury, brain arteriole diameter, the release of allergic mediators, scleroderma, stroke, global ischemia, central nervous system disorder, cardiovascular disorder, renal disorder, inflammatory disorder, gastrointestinal disorder, eye disorder, allergic disorder, respiratory disorder, or immunological disorder. Diseases associated with adenosine Al, A2a, A.2b and A3 receptors are disclosed in WO 99/06053 and WO-09822465, WO-09705138, WO-09511681, WO-09733879, JP-09291089, PCT/US98/16053 and U.S. Patent No. 5,516,894, the entire content of which are fully incorporate herein by reference. This invention also provides a water-soluble prccruc of anv c: the compounds IV, V, VI, VII, or VIII; wherein said water-soluble prodrug that is metabolised in v±vc to an active drug which selectively inhibit A3 adenosine receptor. In one embodiment of the prodrug, said prcdrug is metabolizea 1/7 vivo by esterase catalyzed hydrolysis. This invention also provides a pharmaceutical composition comprising the prodrug and a pharmaceutically acceptable carrier. This invention also provides a method for inhibiting the activity of an A3 adenosine receptor in a cell, which comprises contacting said cell with any of the compounds IV, V, VI, VII, or VIII. In one embodiment of the method, the compound is an antagonist of said A3 adenosine receptor. In another emoodiment of the pharmaceutical composition, said pharmaceutical composition is an ophthalmic formulation. In another embodiment of the pharmaceutical composition, said pharmaceutical composition is an periocular, retrobulbar or intraocular injection formulation. In another embodiment of the pharmaceutical composition, said pharmaceutical composition is a systemic formulation. This invention also provides a method for treating a gastrointestinal disorder in ar. subiect, ccr.cr isir.c administering to the an effective amount cf ar.v cf. the compounds IV, V, VI, VII, or VIII. In one embodiment of the method, said oiscrder is diarrhea. In another embodiment cf the method, the subject is a human. In another embodiment of the method, the compound is an antagonist of A3 adenosine receptors. This invention further provides a method for treating respiratory disorder in a subject, comprising administering to the subject an effective amount of any of the compounds IV, V, VI, VII, or VIII. In one embodiment of the method, said disorder is asthma, chronic obstructive pulmonary disease, allergic rhinitis, or an upper respiratory disorder. In another embodiment cf the method, the subject is a human. In another embodiment of the method, said compound is an antagonist of A3 adenosine receptors. This invention also provides a method for treating carnage to the eye of a subject which comprises administering to said subject an effective amount of any of tne compounds IV, V, VI, VII, or VIII. In one embodiment of the method, said damage comprises retinal cr optic nerve head damage. In another embodiment cf the me mod, said camaae _s acute cr chronic . In another embodiment of the method, said damaae is the result of glaucoma, edema, ischemia, hypoxia or trauma. In another embodiment of the method, the sub]ect is a human. In another embodiment of the methoc, rhe compound is an antagonist cf A3 adenosine receptors. This invention also provide a pharmaceutical composition comprising a therapeutically effective amount cf any of the compounds IV, V, VI, VII, or VIII and a pharmaceutically acceptable carrier. In one embodiment of the pharmaceutical composition, said therapeutically effective amount is effective to treat a respiratory disorder or a gastrointestinal disorder. In another embodiment of the pharmaceutical composition, said gastrointestinal disorder is diarrhea. In another embodiment of the pharmaceutical composition, said respiratory disorder is asthma, allergic rhinitis, cr chronic obstructive pulmonary disease. In another embodiment of the pharmaceutical composition, said pharmaceutical composition is an ophthalmic formulation. In another embodiment cf the pharmaceutical compos 11 icr., saic pharmaceutical ccnposition is ar. periocular, retrcbulbar or intraocular injection formulation. In another embodiment of the pharmaceutical composition, said pnarmaceutica 1 composition is a systemic f crir.ulation . In another embodiment of the pharmaceutical compos it ion, saic pharmaceutical composition is a surgical irrigating solution. This inventio also provides a packaged pharmaceutical composition for treating a disease associated with A3 adencsine receptor in a subject, comprising: (a) a container holding a therapeutically effective amount of any of the compounds IV, V, VI, VII, or VIII; and (b) instructions for using said compound for treating said disease in a subject. Compounds represented by the formula IV, V, VI, VII, and VIII can be synthesized by the Schemes I-IX. As used herein, "A compound is A3 selective." means that a compound has a binding constant to adenosine A3 receptor of at least ten time higher then that to adenosine A;, A2a, or A2b. The invention is further illustrated by the following examples which in no way should be construed as being further limiting. The contents of all references, pending patent applications and published patent applications, cited throughout this application, including those referenced in the background section, are hereby incorporated by reference. It should be understood that the models used throughout the examples are accepted models and that the demonstration of efficacy in these models is predictive of efficacy in nu-ans . A skilled artisan will know that metabolism of tne compounds disclosed herein in a subject produces certain ciclogicaliy active metabclites which can serve as c.rugs. This invention will be better understood from the Experimental Details which follow. However, one skilled in tne art will readily appreciate that the specific methods and results discussed are merely illustrative of the invention as described more fully in the claims which follow thereafter. Example 24: Adenosine A3 Antagonist Experimentals Compound 1700. (Table 17 below): MS (ES): 366.1 (M'-l). Compound 1710 (Table 17 below): MS (ES.: 361.1 (M'-i). Compound 1316 (Table 17 below): MS (ES): 353.2 (M'-l). Compound 1703 (Table 17 below) : MS (ES) : 357.1 (M'-l) . Compound 1719 (Table 17 below): :H-NMR (200MHz, d,-DMSO) ( 1.75 (m, 2H), 3.11 (m, 2H), 3.35 (s, 3H), 3.59 (m, 2H), 5.72 (m, 1H), 5.96 (m, 1H), 6.55 (s, 1H), 7.15 (s, IK), 7.49 (m, 2H), 8.32 (m, 2H) . Compound 1704 (Table 17 below): MS (ES): 367.C (M'~l). Compound 1706 (Table 17 below): !H-NMR (200MHz, CDC13) d 1.22 (m, 2H), 1.60-2.40 (m, 4H), 4.53 (m, 1H), 4.94 (m, 1H), 5.70 (d, 1H, J = 8.2 Hz), 6.35 (d, 1H, J = 2.8 Hz), 6.97 (d, 1H, J = 2.0 Hz), 7.50 (m, 3H), 8.40 (m, 2H), 10.83 (brs, 1H). Compound 1707 (Table 17 below): MS(ES): 347.0 (M'+l). Compound 1708 (Table 17 below): MS ;ES) 399.0 (M'-l . Compound 1709 (Table 17 below): MS (ES! 365.9 (N'-H1 . Compound 1710 (Table 17 below): MS (ES) 434.0 (M'-li- Compound 1711 (Table 17 below): :H-NMR (200MHz, CD,ODi d 3.95 (d, 2H, J = 5.8Hz), 4.23 - 4.31 (m, 2H), 4.53 it, 2K, J = S.BHz), 6.30 (d, IK, J = 3.0Hz), 6.96 (d, 1H, J = 3.GHz), 7.45 - 7.48 (m, 3Hi, 7.83 - 8.42 (m, 2H), 9.70 (brs, 1H). MS (ES;: 281.1 (M'+l). OSIC-148313 -H-NMR (2COMHz, CD,OD) d 3.02 (rr,, 2H), 3.92 (m, 2H), 5.09 (2, 2H), 6.53 (s, 1H), 6.90-7.04 (br s, 1H;, 6.92 m, 2H), 7.02 (m, 1H) , 7.21 (dd, 1H, J = 8.2Hz), 7.40 (m, 3H), 7.50-7.80 (br s, 1H), 8.33 (m, 2K). MS (ES): 445.1 (M*+l). Compound 1713 (Table 17 below) : -H-NMR (2COMHz, CDC1,) d 1.65-1.80(m, 7H), 1 . 88-2 .00 (m, IK), 2.10 - 2.40 (m, 1H), 2.70-3.05 (m, 3H), 3.09-3.14 (m, 2H), 3.16-3.38 (m, 1H), 3.45 (d, 1H, J = 14Hz), 3.53-3.60 (m, 2H), 3.84-3.92 (rr,, 2H), 3.97 (d, 1H, J = 14Hz), 5.55 (t, 1H, J = 5.8Hz), 6.17 (s, 1H), 6.55-6.59 (m, 2H), 6.64-6.71 (m, 1H), 7.11-7.19 (m, 2H), 7.43-7.46 (m, 3H), 8.38-8.42 (m, 2H), MS (ES): 484.0 (M'+l). Compound 1714 (Table 17 below): MS (ES): 471.0 (M'+l). Compound 1715 (Table 17 below): MS (ES): 505.0 (M'-I). Compound 1716 (Table 17 below): 'H-NMR (200MHz, CD,OD) d 1.65 (m, 1H), 2.18 (m, 1H), 2.49 (br d, 2H, J = 6.2Hz), 2.64 (m, IK), 3.38 (m, 1H), 3.69 (s, 3H), 3.72 (m, 1H), 3.93 (m, 1H), 4.10 (m, 1H), 5.06 (2, 2H), 6.58 (s, 1H), 6.92 !ir,, 2H), 7.02 (m, 1H), 7.23 (dd, 1H, J = S.lHz), 7.39 (m, 3H), 8.32 (m, 2H). (Table Remove) Ir. a further embodiment the invention provides a method for treating a disease associated with A: adencsine receptor in a subject, comprising administering to the subject a therapeutically effective amount of compounds 1505, 1506, 1507, In a further embodiment the invention provides the above method, wherein the subject is a mammal. In a further embodiment the invention provides the above method,'wherein the mammal is a human. In a further embodiment the invention provides the above method, wherein said Ai adenosine receptor is associated with cognitive disease, renal failure, cardiac arrhythmias, respiratory epithelia, transmitter release, sedation, vasoconstriction, bradycardia, negative cardiac inotropy and drcmotropy, branchoccnstriction, neutrcpii chemotaxis, reflux condition, or ulcerative condition. In a further embodiment the ir.venticr. rrcvides a water-soluble ;rocrug or ccmDcur. c. _ z >. c , _ t u c , 1512, 1512, 1514, 1516, 15 IT, 1515, 1519, rr 15;:. wnere.n the water-soluble prodrug is metabolized in vivc tr produce an active drug which selectively inhibits A: adenosine receptor. In a further embodiment the invention provides, wherein said prcdrug is metabolized in vivo by esterase catalyzed hydrolysis, In a further embodiment the invention provides a pharmaceutical composition comprising the above prcdrug and a pharmaceuticaliy acceptable carrier. In a further embodiment the invention provides a method for inhibiting the activity of an Ai adenosine receptor in a cell, which comprises contacting the cell with compounds 1505, 15C6, 150", 1508, 1509, 1510, 1511, 1512, 1513, 151 -. , 1516, 1517, 1518, 1519, or 1520. In a further embodiment the invention provides the above method for inhibiting the activity of an Ai adencsine receptor in a cell, wherein the compound is an antagonist of the A: adenosine receptor. In a further embodiment the invention provides the above method for inhibiting the activity of an Ai adenosine receptor in a cell, wherein the cell is human cell. In a further embodiment the invention provides the above method for inhibiting the activity of an Ai adenosine receptor in a human cell, wherein the compound is an antagonist of Ai adenosine receotors. I r. a runner err.cc-inent tr.e ir.Yer.~icr. crevices a method icr treating a disease associated with A: adenosine recectcr ir. a subject, wherein said disease is asthr.a, chronic obstructive pulmonary disease, allergic rhinitis, or an upper respiratory disorder. In c. furtner err.bcdiir.ent the ir.ventior: treating a disease associated with Ai adencsine receptor in a subject, wherein said disease is asthma, chronic obstructive pulmonary disease, allergic rhinitis, or an upper respiratory disorder and wherein the subject is a human. In a further embodiment the invention crcvides a method for treating the above disease, wherein said compound is an antagonist of Ai adenosine receptors. In a further embodiment the invention provides a combination therapy for asthma, comprising the compound 15C5, 1506, 1507, 1508, 1509, 1510, 1511, 1512, 1513, 1514, 1516, 1517, 1518, 1519, or 1520, and a steroid, P2 agonist, glucocorticoid, lucotriene antagonist, or anticolinergic agonist. In a further embodiment the invention proviaes a pharmaceutical composition comprising a therapeutically effective amount of the compound 1505, 1506, 1507, 1508, 1509, 1510, 1511, 1512, 1513, 1514, 1516, 1517, 1518, 1519, or 1520, and a pharmaceutically acceptable carrier. In a further embodiment the invention provides a method for treating a respiratory disorder with the compound 1505, 1506, 1507, 1508, 1509, 1510, 1511, 1512, 1513, 1514, 1516, 1517, 1518, 1519, or 1520, wherein said respiratory disorder is asthma, allergic rhinitis, or chronic obstructive pulmonary disease. t -^ 5; f u *" t *"' e *" ^ r~ C1 o d i m e n t t n *" • ~ v •- ~.11 ~ p c *~ o v i 3 -^c en*"" a c ~' * •-• pharmaceutical compos it icr. ( s ) , wherein said pharmaceutical composition is an periocular, recrccuibar cr intraocular injection formulation. In a further embodiment the invention provides the above cr.armaceut ical composition Is) , wherein said pnarmaceutical composition is a systemic formulation. In a further embodiment the invention provides the above pharmaceutical composition(s), wherein said pharmaceutical composition is a surgical irrigating solution. In a further embodiment the invention provides a packaged pharmaceutical composition for treating a disease associated with Ai adenosine receptor in a subject, comprising: a container holding a therapeutically effective amount of the compounds 1505, 1506, 150"?, 1508, 15C9, 1510, 1511, 1512, 1513, 1514, 1516, 1517, 1518, 1519, or 1520; and instructions for using said compound for treating said disease in a subject. In a further embodiment the invention provides a pharmaceutically acceptable salt of the compound 1505, 1506, 1507, 1508, 1509, 1510, 1511, 1512, 1513, 1514, 1516, 1517, 1518, 1519, or 1520. In a further embodiment the invention provides the above pharmaceutically acceptable salt, wherein the pharmaceutically acceptable salt of the compound 1505, 1511, 1515, 1518, or 1519 contains a cation selected from the group consisting of sodium, (Figure Remove) Calcium ar.c. ammonium. " *~ v e t a fc u K " h ~ r emoocirTient the ^ ^ v s n ~ i c r. c *" o v ^ ^ ^ s a rn c c n c g z c "** treating a disease associated with A; sdencsine receptor in 5 subject, wherein the Ai adenosine receptor is associated with congestive heart failure. Exemplification Example 21: Synthesis of 1- [ 6- i 4 -Hydrcxy-4 -phenyl -piperidin- i -y 1 - m e t .n y i ; - 2 - p h e n y 1 - ~ K - p y r r o 1 o [ 2 , 2 - d ] pyrir. idin-4-yl] -cvr roll dir.e-2 -carboxylic acid amide Compound 1505 was synthesized in a manner similar to that of Example 1~ using synthesis scheme IX with L-prolineamide and 4-cnenvi -ciDericin-4 -ol to ootain: (Figure Remove) 1505 "-H-NMR (df.-DMSO) c 1.53 (s, 1H), 1.60 ;s, 1H), 1.84-2.30 (m, 6K), 2.66 (m, 2H!, 3.6C (s, 2H), 3.85 (m, 1H), 4.02 (m, 1H), 4.66 (d, 1H, J = 6.8Hz), 4.73 (s, 1H) , 6.44 (s, IK), 6.94 (s, 1H), 7.12 - 7.50 (m, 10H), 8.35 (m, 2H), 11.6 !brs, 1H); MS (ES) : 305.1 {M'-i; ; me = 234-235°C. Example 22 : [ I , 2 ~ d j p v r i m i c i n - 4 - v 1 ; (1) - o r o i i r. £ m i ci e ', 1 5 \,' c Compound 1506 was synthesized using synthesis s. l-srolinearnide tc cbtain: NH (Figure Remove) :H-NMR (DMSO-c'c.) d 2.05 (m, 4H), 3.55 ti, 1H^, 4.05 (m, IH), 4.70 (d, IHY J=8.0Hz), 6.58 (brs, IK), 6.95 (brs, IH), 7.15 (d, IH, J=2.4Hz;, ".40 (m, 3H), 7.50 (brs, IH), 8.40 ;m, 2K), 11.6 ifcrs, IH) ; MS (ES): 306.3 (M' + I). rnp= 236-236'-'C. Example 23: Synthesis of [ N- ( 2-pher.y 1 -6-methoxymethyl-7H-pyrrclo [ 2 , 2-a']pyrimidin-4-yl) - (L) -proiin amide (1507) Compound 1507 was synthesized using precursor compound 23 of svnthesis scheme IX to cbtain: (Figure Remove) Brorr.ioe 23 ;4.23c, IGrLTiol,- is dissolved ir. anr.vdrous ~etr.ar.rl for '- n • Tp.e solid is removed by filtration a no washec witr. I-C:\ !2x.20mLi . The filtrate is concentrated ir. vac'jc. Tne residue is redissclveo in DCM iSOmL;. The resulted sc_uticn is tnen wasneo with saturated N a H C 0 - solution and brine, dried over ".-". g S C , filtered and concentrated to aive 2 . 71 c ' 4, ? ? 't i off white solid. :h-s:-;r (cd:i;.) d 1.75 (s, 9n;, -.51 •, = , 3H , 2H), 6.70 !s, 1H), 7.47 (i^, 3H), 8.52 in, 2H). (Figure Remove) (l5mL), L-prolineamide combined and heated to cticn is cooled to room ; . The resulted slurry ned organic layers are and brine, dried over 2.48g brown solid. Pure flash column as white HF/hexane. M.p. = 213-; .52 (m, 1H) , 3.26 (s, (s, 2H) , 5.08 (d, 1H, , 7.08 (brs, 1H), 7.42 MS (ES) : 352.2 (M' + l) . Aryl chloride 4 (2.448g, 6.55mmol), DMSC (4.Cg, 35.0nmol) and NaHCC, ;2.9g) are 12C-C under nitrogen. After 4h, the rea temperature and diluted with water (60ml is extracted with DCM (lOx). The combi washed with saturated NaHCO. solution MgSO., filtered and concentrated to give product (I.86g, 81%) is obtained after solid. White crystals are gotten from T 215°c! ^-NMR (CDC1J d 2.15 (m, 3K), 2 3H) , 3.92 (m, 1H), 4.10 (m, 1H), 4.42 J=8.2Hz), 5.49 (brs, 1H), 6.48 (s, 1H) (m, 3H), 8.38 (m, 2H), 9.78 (brs, 1H); (Table Remove) HiTuTid • were cc~cir.ee a"e nested to t C • 7 _:r. der ar~rr. for approximately 3.5h. Tne mixture was then pcurec, ir.tr water !' 1 0 U rr 1 ; a r. d e x t r a c t ^ d wp 11 h t h **" e e 0 C1 ~1 o ~ ~~ ~ * c *" c c * " " C ~. c ~*~ ~ •£ ccntined orcar.ic layers were thcrcugr.l \' wasnec v-;itr. water, orine, cried ever MqSO;, filtered anc concentrated tc give a yellow solid which was purified by trituratinc w_th ethanci. to give 1.55g of a pale yellow solid (1} . The ^ict.-.er liqucr was purified by flash cnror.atcgrapny (1C? EtOAc in he.xane) tc give an additional 454mg (60%). -H-NMR (CDC1.) c 1.7T ,5, 9H), T.25 !s, 1H; , T.45 (m, 3H), 6.52 (m, 2H) 10.39 is, !;-:•; m.p.= 15cc'C (Figure Remove) Aldehyde 7 ioGOng, l.Tmmol) was dissolved in dry THF (20ml) and coded to 0;'C under argon. To this was aaded a 0°C solution of (t e r t - b u t o x y c a r b c n y 1 rr.e t h y 1 e n e ) -1 r i p h e n y 1 p h o s p h c r a n e (694 mg , l.Srruncl'1 in 1 Orr.l of dry THF dropwise through a cannula. After 3h the mixture was concentrated and purified oy triturating with etnanol to give 565mg (73%) of a white solid (8) . :HNMR (CDC1,) d 1.56 (s, 9K), 1 . ~> 9 (s, 9H), 6.46 (d, IH), 6.95 (s, 1H.>, 7.46 (n-., 3H) , 8.09 (d, IH), 6.56 t., 2H). (Figure Remove) A solution c~ compound 8 (565ma 1.2mmcl; in 5rrii Tr. : was ai luted m^ with EtOA c. Alter adding cQCmc ci catalyst 51 wt ?c, 50* H-0) and purging with argon, the mixture was hydrogens tec under atrr.cspher ic pressure. After 8h the mixture was filtered, concentrated and purified with flash chrornatograpr.y :10-o EtOAc in hexane; tc isolate 20Cmg (35%) cf 9 as a clear oil that crystallised upcn standing. -HNMR (CDC1 ! c 1.42 ;s, 9H!, 1.75 s, 9H;, 2.6= it, 2H), 2.32 (t, 2H!, 6 . -: 1 ;s, 1H! ~ . 4 5 !m, 3H), (Figure Remove) Aryl chicriae 9 (20Cmg, C.44mmci), DMSO (10ml) and L-prclmamide (440mg, 4.4nmol) were combined and heated to 85°C under argon. After 14 hours the mixture is cooled tc room temperature and partitioned between water and ethyl acetate. The layers were separated and the aqueous layer washed with EtOAc (3x) . The combined organic layers were thcrcugnly washed with water (3 x) , brine, aried over M g S C (Figure Remove) :er 10 ' -. i..'m c;, m-TiO'l) in 5ml oioxane was h'/oro- '.'leo cv ; •;centrated in vacuc and recrystalitec in ItCH: EtC ;ain 1509 as a white solid (20mg, 61%-. MS i ES,: 3SO i Example 26: Synthesis cf [ N- { 2-phenyi-f -air.mccarccnyl metncxynetnyl-7H-pyrroio [2 , 3-d] pyriT.idir.-4 -yi ; - •. 1 ' -prolinamide (1510) Compound 1510 was obtained using precursor compound 23 of synthesis scheme IX to obtain: (Figure Remove) Bromide 23 ;i.27g, 3mrnol) and molecular sieve ;5g, are stirred in anhydrous methyl glycolate (5.8g, 6jTjnoi) and DCM ( A OmL) . The solution is treated with AgCTf under N: and allowed to stir for 3h. The solid is removed by filtration and washed with DCM (2x2 Oml) . Tne filtrate is concentrated : r. The residue is . t r. water, saturated N a H C C - s c 1 u 11 j 3 C -, iilt~red anc concentrated tc ;lld '12-. '-H-NMF fCCCl;! a 1.75 i s , i . , c . 7 ? ; s , in', 7.47 .. n-,, 3 H : , E. (Figure Remove) Aryl cnlcriae 12 (177mg, 0.4Inmol), DMSO (10~L:, L-proiinamide (456rr.c, 4rrjr,cl) anc NaHCO, (SOOma! are combined and heated to 12C unaer r.itrccer.. :er 4h, the reaction is cooled to room temperature and diluted with water (cOml) . The resulted slurry The combined rgani laers is extracted with DCM (5x30n-li. are washed with saturated NaHCC-. solution anc brine, dried over MqSC., filtered and concentrated to cive brcwn solid. Pure product (154mc, 92%) is obtained after flash column as white soli a (13). -H-NMR (CDC1,) d 2.15 irr, '•'-], 2.52 •. m, IH), 3.55 (s, 3H), 4.58 (s, 2H), 5.06 (s, IH, }, 5.65 :'brs, IH), 6.46 (s, ih; , 7 .ce tors, ih;, 7.42 IH) ; MS (ES) : 410.1 (M' + l ) . : m, ^ ri - , C . 55 (brs, Vs' Nh- 0—' H NH3/HOCH3 rt, 4h 1510 C C N n - (Figure Remove) Methyl ester 13 (124rr,g, C.Bnrr.cl) is dissolved ir. HCCH- i,15r,L'i . .-jTJTtonia is bubbled through the solution for 0.5r.. The reaction mixture is then stirred fcr another 3h at rt. After removal of solvent lllmg of a white solid (1510, 92%) is cctained. :H-NMR •;rDCl;.; a 1.62 !rr\, 3H), 2.20 (m, 1H), 2.SC (n, 1H), 3.1C (m, " '—' i 4 ^ ~ ' m ^ H ^ "i Q ^ ' m 9 M ^ i- 7 ^ ; - " '—' '• f ^ r ( '^ r c; " H ) ~ . . / f T.--' ,illj -.I*// *^ . -*1 W \i['/ i- . I ; / W . _' — '•-/ J..-'/ ^.^'^ ^»--i.O/ *ll// ~.ll (brs, 1H), 7.37 (m, 3H;, 6.28 (m, 2H), 11.46 :brs, 1H); KS , ZS) : 394 . 8 (M' + l ; . Example 27: Synthesis of [ 4 - ( 2-Ca rbarr.oylpyrrcl idin- I -yl 1 -2 -pnenyl-7.L:"-pyrroloi2, 3-d]pyrirr.idine-c-carbcxylic acid] (1511) Compound 1511 was synthesized using synthesis scheme VII to obtain: :recursor oomocund 15 of Cl N 15 NaH. then PhSO2CI — "• •"'-.- - » DMF 0-»20°C, 4h _ r. 1 - -•-, or r_micine 15 2.00c, Atr 5 nin , benzenes u i for. vl or. _oride added, rie cooling bath s rem . , tne h a c e t; 10. T: t 83% be c: e i u e n o e c into a mixture or ice a n o sat -~^»-^,'-"-»—'"•'"' i t~ £i ^ c r"~"i ' ~ '•"' 1 Q ~ •• *• .3 • • o **! ,—.»-* ;:'"•"' •-*-. —• *. Cr w — t-*' — *. a L ™ *-t O^'^.j.v-* —O j._— -"—trj^i ^ —, .. C-.-w _»^. one i3 ) and rr.ethancl (2 ;, yielding 2.2"c of a oeige riis solid (16) contains approx. 10mol-:; "•!-;" (based on y'leid; ana can be used in tne next step; a pure sample tained by chromatography or. silica gel using acetone = i-j - 1 U! -. . _ n _ , -H-NMR (CDC1,): d c.'O _i C _ p H5; IR (solid): n = 3146 cm"-, 1565, 1539, 1506, , 1356, 13~0, 1 1 £ 6 , 1176, 1154, 1111, 1015, 919, 6, , 616, 607; MS (ES): 372/370 (MH'); :nc = 226-227 °C.(Figure Remove) To a solution of the A/'-sulfonyl compound 16 (337mg, 0.911rrjnol) in ary THF (34mL), cooled by dry ice/acetone, is added LDA'THF (l.OmL, 1. 5M solution in cyclohexane, 1.5n.-.ol) . After 45min, oarcon dioxide is cubbled into the solution for 5mm, then the cooling bath is removed. When the solution has reached ambient temp., the solvents are evaporated, yie_ding 398mg of the salt 17, containing 0.3 equiv. of ( iPr) :NCO: Li , as yellow solid. The (Figure Remove) solution of the lithium salt 17 (50mg) and L-prolinar.icie 22r.c, l.C'rnmoi) in DMSO ( 1 . 5mL) is heated under nitroaen to 5 >n . 4% a; acetic acid lOrnL: is adaed to the oled solution, and the mixture is extracted with EtOAc '10mL; . The combined organic layers are washed with 4% aq . etic acia (iOmLj, water (10ml! and brine ilOrr.L; and are driea ver MgS04 . Filtration and concentration gives 4 Orng of 18 as yellowish solid, which is used without purification in the ext step. -H-NME (CD, CD!: d = 1.95-2.26 (n, 4H;, 3.85-3.95 (m, H>, 3. 95-4. I"7 (m, IHi, 4.72 (bis, 1H), 7.14 (s, In), 7.35-7.45 m, 3 H ; , ".45-7.70 (rr., 3 H ; , 6.33-6.5C :-, 4H). (Figure Remove) 1 U t 1 O *~ ~ L S O O " U "T1 P V C """ C X ~ Q "~ ' "~1 ^ "•"• *" n a "". 0 ' ' 3 rf1 "~ ~* P" *"~ " i c a d c e c c c c c u ~ ~ c n c ~ ~ i ~ o v *~ *" c ~'rr;ic.i*~e 18 . 6 rr. i x 5' "05" c f t h a nn 9 " h s n o 1 is GVcDcrst.s3, wirr. EiC'Ac (5 lOrr.L,, the ccmbinec crcar.ir layers are washec v;iir. brine and dried ever KcSO, . yields 24r'C ci s. pale yellow solid, which is triturated with tc luene/EtC-.-.c/MeO.H tc yield 15.6mg iSSVj cf the acici 1511 as slightiy yeilowisn sclid. :H-KMR (CD^CD;: d = 2.C5-2.2G tn, is, 1H; , 7.25-7.42 (m, 3 H) , 6.36-6.45 (rr,, 2H); IR (solid): n = 23, 2877, 1662, 1614, 1567, 1521, 1454, 1374, 2, 1190, 974, ~54, 70C; M3 (ES>: 252 (X'-l); m.D. = 220 °C iceconp.;. Example 28: Synthesis cf 1- ( 6-iTethyl-2-phenyl-~.::'-pyr rolo [ 2 , 3-d] pyr irr.idine-4-yl) - ( S )-pyr roiidine-2 -carboxylic acid amide V 1 -/ J. i Ccmpound 1512 was synthesitec by the fcllowing steps: (Figure Remove) Aryl chloride 20 (3c, 1C.7 toio!;, DMSO (50ml) and (S)-prclinamide were combined and heated to 65°C unaer argon. After stirrina overnicnt (14hrs), the mixture was cooled to room iemoerature were tncro'jgn_y was nee witr. water .j :•: j'_ „ ~._ o y *-*'*" McSC f ' ^ ~ •" ^ c c and oono^^^^a^eo ~ "• ~ i" --sz_id. Tne soiio was recrysta_liiec twice ;rcr~ Cj ^ r~, ' C ~" c _ ^ _ - _ ^ c ^ l : ^ / -^ r -i o i - •„• M V Z Pt r^' C " ^ - . ^ j v- 4 H . , 2.2 {s, 2H), 2 . B (rr., 1H), 4 . C :m., 1H; , 4.6 £ - ; c " H 1 ~ ? ; r-i "3 H \ ~ ~ . c • '_' i C J -.. ^ u._- '^/ ~ » I r .*- i.-I, -;.-,, .^ \^, -../, '^-.^ (s, 1H); MS (ES): 222 !M"+1) -."-_. ^ i rr,, - r. ' c . _ ; s , Example 29: Synthesis cf 1 - [ 6- i 2 -Hycro.xv-e tnox\'~e ~. r.vl ' -2-pher.yl-'7H-pyrrolo[2,3-djpyrirnidin-4-yIj-pyrrclidine-2-carb cxvlic acic amidei1513) 1513 Compound 1513 was synthesized in a manner similar to that of Example 1~ using synthesis scheme IX with L-prclineamide and etr.ane-l,2-diol to obtain: A scluticr. cf the lithium salt 17 (C.12mmol! in dry DM|F (4mL) is stirred with methyl iodide (O.lmL, l.Smmol) at 20 °t under argon for 3h. DMF is evaporated, and aeneous ammonium chloride solution is added (15ml) . The mixture is extracted witjh EtOAc (3'15mL), the combined organic layers are washed with water (2'10mL) and brine (lOmL) and are dried over MgSO, . Filltration and concentration gives 2 Ing (38%) of the methyl ester: 22. Cl 1. DMSO. 80 °C. 5h, then 20 °C, 13.5h 2. NaOH. MeOH. 20 min A soluticr. cf the methyl ester 22 \2-..z~\o, C . C; • ~~.z li' ana -;-tra.TS-amir.Gcyciohexar.cl (66mc, G.5"rjr.c_' ir. DMSC 1!. rrr.L 15 heated under r. itroaen to 60 °C for 5:., tner. the r.ejatir.c is stopped, and stirring at 20 °C is continued for 12 . : ~ . -i :- ac. acetic acid (10ml) is added tc the codec scluticn,! and tr.e mixture is extracted with EtOAc (2'10mLi. Tr.e comcineqi organic layers are washed with 4% aq. acetic acid (10ml;, water- iiOir.L1 2N NaOH (lOmL), water (lOmL), and brine (IGmL! and alre dried over MgSO;. To a solution of the crude material obtained after filtration and concentration (1H NMP indicates about 501 removal of the benzenesulfonyl group) in THF !2mL) isj added a solution of NaOH -in MeOH {0. 5mL of 5t-: solution, 2.5;mmol) at ambient temperature. After 20min, water and sat. NaHCO, solution (Srr.l each) are added, and the mixture is extracted with EtCAc' (4'15rr.L). The combined organic layers ane washed with 2N NaOH (lOmL), water (lOmL), and brine (lOmL)^ and are dried over MgSO<. chromatography of the crude materialiobtained after filtration and concentration on silica gel eiuting with hexanes yields .6 a white solid mp. : d="1" . i ir n="3352" cm ms> Example 34: Synthesis cf N - ( I'-CarC'c^cvi -rvrrolicin- 1 -vl • -2-phenyl-~H-pyrrcic•2,3-d] pyrir.idin-c-'.-l.Tezhcxvl methyl ester (1518) Compound 1518 was synthesized- in a ir.ar.ner sir.ilar tr exancle using precursor compound 12 to cbtair.: (Figure Remove) 1518 MS (ES) : 410 Example 35: Synthesis of [ 4-(2-Carbarr.oyl-pyrrciidin-l-yl) -2-phenyl-7H-pyrrclo[2, 3-d]pyrimidir.-6-ylrr.ethoxy] -acetic acid (1519) . Compound 1519 was synthesized in a rr.ar.r.er simile 1518 wherein the methyl esier arcup- was r.var elite a C a 5 - 1519 Exaanple •• " : Synthesis of 4- ( 4 -Hydroxy-cyclohexylamino) -2-phenyl-7H- rrolo [2, 3-d ] pynmidine-6-carbcxyi ic acid: amide (1520) NH-, MeOH 20 °C.10d HN N ...QH NH2 O H 1520 ume C v. Gaseous ammor.ia is conaer.sea ir.tc a s Activity of Compounds Adenosine 1 (A:) receptor subtype saturation and competition radio ligand binding were carried out fcr compounds 1505, 1506, 1507, 1508, 1509, 1510, 1511, 1512, 1513, 1514, 1516, 1517, 1518, 1519, and 1520 as described herein and inter alia, on pages 152-153 of this specification. Ail of the: above-referenced compounds equaled or surpassed the A, receptor binding affinity of reference compounds 1318 or 1319 as described herein and, inter alia, in Table 13, on page 171 of the specification. The water solubilities of the above compounds listed in Table 18 are expected to be better than reference compounds 1318 or 1315 cue co tr.eir cleg? values, which were calculated u$inc: tr.e ccT.puter program C2 Cher.Draw, ChemDraw 'Jltra ver. c.C *lfrf as provided by Ca.mbriageScf t Ccrpcra ~ icr., _OC Ca-rridge Far-: Drive, Cambridge, MA 0214C. The compounds specific to the A- receptor listed in Table 18 had lower clog? values, between about 1.5 to about 2.4, as compared to reference compounds 1318 or 1319 with a clog? value about 3.5. It was not predicted that the more polar A- receptor compounds listed in Table 18 having lower clog? values than the reference compounds 1318 or 1319 would still retain the:pctency and A: receptor binding selectivity as compared to those reference comcounds. (Table Remove) Faces 2SS-293 relate t; recestor This invention orovides a compound havinc the structure (Figure Remove) 1609 This invention also provides a compound having the strMcture NH, (Figure Remove) 1610 In a further embodiment the invention provides a method for treat-ing a disease associated with A2a adenosine receptjor in a subject, comprising administering to the subject a therapeutically effective amount of. compounds 1609 or icic. The invention also provides the above method, wnerein the subject is a mammal. The invention further provides the above method, wherein the mammal is a human. I ; The invention also provides the method for treating a disease associated with A2a adenosine receptor in a sub]ect, wherein the A:a adenosine receptor is associated with iocomotor activity, vasodilation, platelet inhibition, neutrophil superoxide generation, cognitive disorder, senile dementia, or Parkinson's disease. The invention provides the above method, wherein the cbmpound treats the diseases by stimulating adenylate cyciase. The invention also provides a water-soluble prodrug of the compound 1609 or 1610, wherein the water-soluble prodrug is metabolized in vivo to an active drug to selectively inhibit an A2a adenosine receptor. The invention also provides a water-soluble prodrug of the compound 1609 or 1610, wherein the prodrug is metabolized in vivo by esterase catalyzed hydrolysis. The invention also provides a pharmaceutical composition comprising the water-soluble prodrug cf the compound 1609 or 1610, and a pharmaceutically acceptable carrier. The invention also provides a method :cr activity of ar. A-. ader.csine receptor in a cell, contactinc the cell with compound 1605 ~r 161C The invention also provides a method for inhibiting the activity of ar. A;i adenosine receptor in a cell, which comprises contacting the cell with compound 160? or 161C, wherein the compound is an antagonist of said A;a adenosine receptor. The invention also provides the above method, wherein the cell is a human cell. The invention also provides the above method, wherein the cell is a human cell and the compound is an antagonist: of A:a adenosine receptors. The invention also provides a pharmaceutical composition comprising a therapeutically effective amount of the compound 1609 or 1610 and a pharmaceutically acceptable carrier. The invention also provides the above pharmaceutical composition, wherein the therapeuticaliy effective amount is effective to treat Parkinson's disease and diseases associated with Iqcomotor activity, vasodilation, platelet inhibition, neutrophil superoxide generation, cognitive disorder, or senile dementia. The invention also provides the above pharmaceutical composition, wherein the pharmaceutical composition is an ophthalmic formulation. The invention also provides the above pharmaceutical composition, wherein the pharmaceutical ccmpcsir ion is ar. periocuiar, retrcbulbar or intraocular injection formulation. The invention also provides the above pharmaceutical composition, wherein the pharmaceutical composition is a 'systemic formulation. The invention also provides the above pharmaceutical composition, wherein the pharmaceutical composition is a surgical irrigating solution. The invention also provides a combination therapy for Parkinson's disease, comprising the compounds 16CS or 1610, and any of the dopamine enhancers. The invention also provides a combination therapy for cancer, comprising the compound 1609 or 1610, and any of the cytotoxic agents. The invention also provides a combination therapy for glaucoma, comprising the compound 1609 or 1610, and a prcstaglandin agonist, a muscrinic agonist, or a P-2 antagonist. The invention also provides a packaged pharmaceutical composition for treating a disease associated with A:a adenosine receptor in a subject, comprising: (a) a container holding a therapeutically effective amount of the compound 1609 or 1610; and (b) instructions for using the co-pound for cr disease in a subiect. eating sai; Exenplif ication Example 41: pyrrole[2,2-d]pyri amide (1609;. thesis of l-;6-?heny rr.i d i n - 4 - v 11 -cvrrciidine- I - c a r b c >: v 11 c a; Compound 1609 was synthesized by reacting L-prolinanutie with the appropriate cnicride intermediate described in synthesis scheme II on oace 62 to obtain: (Figure Remove) 1609 ;H-NMR (df-DMSO) d 1.95-2.15 (m, 4H), 4.00 (brs, 1H), 4.15 (brs, 1H), 4.72 (brs, 1H), 6.90 (brs, 1H), 7.19 !brs, 1H), 7.30 (t, IK, J = 7.CH2), 7.44 (t, 2H, J = ~.OHz), 7.59 (s, 1H), 7.92 (brs, 2H), 8.26 (d,2H, J = 6.2Hz), 5.65 (d, 2H, J = 6.2Hz); MS (ES) : 384.9 (M'-l); Mpt = 280-316°C (decomp.). Example 42: Synthesis cf 1- [ 6- ; 2 -Met: yl- "r-cyrroio [ 2 , 3-c'j pynmici n- 4 -yl; -acic amide (1610). Compound 1610 was synthesized by react the appropriate chloride intermediate scheme II en page 82 to obtain: _ - p r c 11.-. a m i a e w 11 r. rribed in svnthesis (Figure Remove) 1610 ;H-NMR(d.:-DMSO) d 2.07(m,4H), 3.55is,3H!, 4 . 02 (m, 1H1 , 4.17(rn,lH), 4.75(m,lH), 6.89(m,lH), ~.OC(s,lrii, 7.23:(s,lH), .35 (t, IK, J=8.2Hz) , 7.53(s,2H), 7.60(s,iH), 5 . 28 (d, 2H, J«5 . 8Hz ) , . 67 (d, 2H, J=5.8Hz) , 12 . 37 ( s , 1H ) ; MS (ES): 415.0 (M' + l). Activity of Compounds Adencsirie 2a (A,4) receptor subtype competition radio^ ligand binding were carried out for compounds 1609 and 1610 as described herein and incer alia, on page 153 of this specification. Compounds 1609 and 1610 were found have A:a receptor binding affinity and selectivity. Pages 294-300 relate to additional cc^rounds specific to .: receptor This invention also provides a compound having the structure (Figure Remove) 1720 In a further embodiment the invention provides a method for inhibiting the activity of an A3 adenosine receptor in a cell, which comprises contacting the cell with the compound 1720. In a further embodiment the invention provides a method for inhibiting the activity of an A3 adenosine receptor in a cell, wherein the compound is an antagonist of the A3 adenosine receptor. In a further embodiment the invention provides the above; method for inhibiting the activity of an A3 adenosine receptor in a cell, wherein the ceil is human cell. In a further embodiment the invention provides the abovemethod for inhibiting the activity of an A3 adenosine receptor in a cell, wherein the cell is a human cell and wherein the compound is an antagonist of aj adenosine receptors. comrises In a further embodiment the invention crevices a me the: treating damage to the eye of a subject whirr, administering to the subject a composition comprising a therapeutically effective amount of the compound 1~20. In a further embodiment the invention provides the above method, wherein the damage comprises retinal or optic nerve head damage. In a further embodiment the invention provides a therapy for glaucoma, comprising administering to a subject a therapeutically effective amount of the compound 1720. In a further embodiment the invention provides a therapy for glaucoma comprising one or more adenosine receptor antagonists, preferably comprising an adenosine receptor A3 antagonist (preferably an N-6 substituted 7-deazapurine, most preferably [ 2 - (3H-Imidazol-4-yl) -ethyl] - (2-phenyl-7h'-pyrrolo[2, 3 -dj pynmidin-4-yl)-amine ) . In an alternative embodiment the invention provides a combination therapy for glaucoma comprising an adenosine receptor A3 antagonist (preferably an N-6 substituted 7-deazapurine, most preferably [2-(3H-Im_dazol-4-yi)-ethyl]-(2-phenyl-7H-pyrrolo[2,3-d]pyrimidin-4-yl)-amine)) and one or more other compounds selected from the group consisting of beta adrenoceptor antagonists (i.e. beta adrenergic antagonists or c-biockers) ie.c. timclcl naleate, betaxolcl, caiteclcl, levobunoicl, metipranolcl, L-65232S !the acetate este;r cf I_-£52698), beta I adrenoceptcr antagonists', e.lpha-Z acreriocectcr agonists (e.g. aplaclonidine, brinonidine, AGK-155~ ?'S, AGN-190S3" (an analog of Bay-a-67S1) 1 , carbonic arthydrase inhibitors (brinzoiarr.ide, dcrzolamide, MK-9Z" (an inhibitor of the human carbonic ar.hydrase II isoer.zyrnei , inhibitors of carbonic anhydrase IV isoenzymei , cnciinercic agonists ,e.g. muscarinic chclinergic agonists, carbachcl, pilocarpine HC1, piiocarpine nitrate, piiocarpine, pilocarpine prodrugs (e.g. DD-22A)}, prostagiandins and prostagiandin receptor agonists (e.g. latanoprost, unoprostone isopropyl, PGF2 alpha agonists, prostanoid-selective FP receptor agonists, PG agonistsisuch as the hypctensive prostamides) , angiotensin converting; enzyme (ACE) inhibitors (e.g. Spirapril, spirapriiat), AMPA receptor antagonists, 5-HT agonists (e.g. a selective 5-KT 1A receptor agonist such as MKC-242 (5-3-[((2S)-1,A-benzodioxan-2-ylmethyl)amino]prcpoxy-1,3-benxodioxole HC1), angiogenesis inhibitors (e.g. the steroid anecortave), NMDA antagonists (e.g. KU-211, memantine, the cannabinoid NMDA-receptor;agonist dexanabinol, prodrugs and analogs of dexanabinol> NR2E-selective antagonists (e.g. eliprodii (SL-82.0715) ):/ renin inhibitors (e.g. CGP-38560, SR-43645), cannabinoid feceptor agonists (e.g. tetrahyarocannabincl (7HC! and TKC analogs, selective CB2 cannabinoid receptor agonists (e.g. L-76{3242, L-759787), compounds such as anandamide that bind to both brain-specific CB1 receptors and peripheral CE2 receptors), angiotensin receptor antagonists (e.g., angiotensin II receptor antagonists (e.g. CS-088), selective angiotensin II AT-I receptor antagonists, sucr. as hydrochiorotr.iatide (HCTZ1,, scmatcstatin agonists •-• = • t-,r nor.-peptide somatcstatin agonist NNC-Ic-?1JO; , glurcccrticcid antagonists, mast cell degrar.ulsti.or. ir.r.ib_ tcrs e.g. nedocror.il :• , alpna-adrenergic receptcr blcr-'.ers .e.g. dapipraioie, alpha-2 adrencceptor antagonists, alpha I adrenoceptcr antagonists (e.g. ounazosir.) ) , aipha-2 adrenoceptor antagonists, thromboxane A2 nineties, protein kinase inhibitors (e.g. H7), prostagiandin F derivatives (e.g. S-1033), prostaglandin-2 alpha antagonists (e.g. PhXA-34), doparriine Dl and 5-H72 agonists (f enoidopam) , nitric-oxide-releasing agents (e.g. NCX-904 or NCX-905, nitric-oxide-releasing derivatives of timolol), 5-HT 2 antagonists (e.g. sarpogrelate) , NMDA antagonists (e.g. proarugs and analogs of dexanabinci) , alpha I adrenoceptor antagonists (e.g. bur.azosin), cyclocxygenase inhibitors (e.g. diclofenac, or the non-steroidai compound nepafenac), incsine, dopamane D2 receptor and alpha 2 adrenoceptor agonists (e.g. talipexole), dcpamine Dl receptor antagonist and D2 receptor agonists (e.g. SDZ-GLC-756) , vasopressin receptor antagonists (e.g. vasopressin V2 receptor antagonists (e.g. SR-121463)), endothelin antagonists (e.g. TBC-25'76), 1- i 3-hydroxy-2-phosphonylmethoxypropyl;cytosine (HPMPC) and related analogs and prodrucs, thyroid hormone receptor ligands (e.g. KB-130015)/ muscarinic Ml agonists, NMDA-receptor antagonists (e.g. the cannabinoid NMDA-receptor antagonist dexanabinol), PG agonists such as the hypotensive lipics, prostamides, sodium channel blockers, NMDA antagonists, mixed-action ion channel blockers, beta adrenoceptor antagonist and ?GF2 alpha.agonist ccrubinaticr.s (e.g. latanoprost and timolcl; , c'_ activators (e.g. atrial r.atriuretic oeptide peptide mimetics, inhibitors of AN"? neutral r.i trovasodilators (e.c. nitrcalycerin, r.itroprusside', , endothelin receptor modulatcrs e.g. £7-1 ;: r.on-peptide mimetics , saraf ctoxir.-Scc ; , ethacrynic acid, ether phenoxyacetic acic analogs (e.g. indacrinone, titrynafen!, actin disrupters (e.g. iatrunculin), calcium channel biockers (e.g. verapamil, nifedipine, brovincar.ine, nivaldipine) and neurcprotective agents. A combination therapy for glaucoma, comprising the compound of 1702, and one or more compounds selected from the group consisting of beta adrenoceptor antagonists, alpha-2 adrenoceptor agonists, carbonic anhycrase inhibitors, chclinergic agonists and prostaglandin receptor agonisits. In a further embodiment the invention provides a pharmaceutical composition comprising a therapeuticaliy effective anjount of the compound 1720 and a pharmaceutically acceptable carrier. In a further embodiment the invention provides a packaged pharmaceutical composition for treating a disease associated with A3 adenosine receptor in a subject, comprising: a container holding a therapeuticaliy effective amount of the compound 1720; and instructions for using said compound for treating said disease in a subject. In a furtr.er embodiment the invention prcvides a method cf making a composition which comprises the compound 172C, the method comprising admixing the compound 1TC2 with a suitable carrier. '. In a further embodiment the inventicr. rrovioes a pharmaceutically acceptable salt of compound 1720, wherein the pharmaceutically acceptable salt contains an anion selected from the group consisting of maleic, fumaric, tartaric, acetate, phosphate and mesylate. Exemplification Example 43: Synthesis of [2-(3£-Imidazcl-4-ylj-ethyl]-(2- pher.yl-"/#-pyrrolo [ 2 , 3-dj pyrimidin-4-yl) -amine :'1"2C) Compound 1720 was synthesized using precursor compound 1 of synthesis scheme VII to obtain: (Figure Remove) Aryl chloride 1 (400mg, l.SOrtunol), DMSO ilOml ar.c histarr.ine (1.67g, 15.Ommol) are combined and heated to lZOrC unaer nitrogen. After 6.5h, the reaction is cooled tc room temperature and partitioned between EtCAc and water. The layers are separated and the aqueous layer is extracted with EtOAc (3x). The combined organic layers are washed with brine (2x), dried over MgSC4, filtered and concentrated tc yield 494mg of a brown solid. The solid is washec with cold MeOH and recrystallized from MeOH to yield 197mc (43%) of an off white solid (1720). !K-NMR (CD,OD) d 3.05 (t, 2K, J = 7.OH:}/ 3.94 (t, 2H, J = 7.0HZ), 6.50 id, 1H, J = 3.5Hz), 6.88 (brs, 1H), 7.04 (d, 1H, J = 3.5H2), 7.42 (m, 3H), 7.57 (s, IK), 8.34 (m, 2H); MS (ES): 305.1 (M'+l); Mpt = 234-235^C. Activity of Compounds Adenosine 3 (A3) receptor competition radio ligand binding was carried out for compound 1720 as described herein and inter alia, on pages 153-154 of this specification. Compound 1720 was found to have an A- receptor binding affinity greater than 10 times that of reference compound 1308 as descnoed herein and, inter alia, in Table 13, on page 169 of the specification. Incorporation by Reference All parents, published patent applications an; disclosed herein are hereby expressly -ir.ccr reference Equivalents Those skilled in the art will recognize, or be able tc ascertain, using no more than routine experimentation, nar.y equivalents to specific embodiments cf the invention descriced specifically herein. Such equivalents are intended- to be encompassed in the scope of the following claims. This invention further provides compounds having the formula: (Figure Remove) XI wnerein R:NR2 together form a ring having the structure (Figure Remove) sR5 is H, or substituted or unsubstituted alkyl or alkylaryl. We Claim; 1. A N-6 substituted 7-deazapurine compound having the structure: (Structure Removed) wherein when R3 is phenyl, RiNR2 together form a ring having the structure (Structure Removed) or Rx is H and R2 is (Structure Removed) or R! is H and R2 is: (Structure Removed) R5 is H, or substituted or unsubstituted alkyl or alkylaryl, when R3 is (Structure Removed) RiNR2 together form a ring having the structure: (Structure Removed) R5 is phenyl or (Structure Removed) and a pharmaceutically acceptable salt thereof. 2. The compound as claimed in claim 1, having the structure: (Structure Removed) 3. The compound as claimed in claim 1, structure: having the (Structure Removed) 4. The compound as claimed in claim 1, having the structure: (Structure Removed) 5.The compound as claimed in claim 1, having the structure: (Structure Removed) 6. The compound as claimed in claim 1, having the structure: (Structure Removed) 7. The compound as claimed in claim 1, having the structure: (Structure Removed) 8.The compound as claimed in claim 1, having the structure: (Structure Removed) 9.The compound as claimed in claim 1, having the structure: (Structure Removed) 10. The compound as claimed in claim 1, having the structure: (Structure Removed) 11. The compound as claimed in claim 1, structure: having the (Structure Removed) 12. The compound as claimed in claim 1, structure: having the (Structure Removed) 13. The compound as claimed in claim 1, having the structure: (Structure Removed) 14. The compound as claimed in claim 1, having the structure: (Structure Removed) 15. The compound as claimed in claim 1, having the structure: (Structure Removed) 16. The compound as claimed in claim 1, having the structure: (Structure Removed) 17. The compound as claimed in claim 1, having the structure: (Structure Removed) and pharmaceutically acceptable salt thereof. 18. The compound as claimed in claim 1, wherein the pharmaceutically acceptable salt of the compound of claims 6, 8, 12, 15, or 16 contains a cation selected from the group consisting of sodium, calcium and ammonium. 19. The compound as claimed in claim 1 having the structure: (Structure Removed) 20. The compound as claimed in claim 1 having the structure: (Structure Removed) 21. The compound as claimed in claim 1 having the structure: (Structure Removed) 22. The compound as claimed in claim 1, wherein the pharmaceutically acceptable salt contains an anion selected from the group consisting of maleic, fumaric, tartaric, acetate, phosphate and mesylate. 23.A N-6 substituted 7-deazapurine substantially as herein described with reference to the foregoing examples.

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