Title of Invention

"TRICYCLIC COMPOUNDS HAVING ANTIOXIDANT PROPERTIES"

Abstract

The present invention pertains to tricyclic compounds of general formula as shown in fig. 1 wherein B, n, X, Ar, Y and R1 are as herein described, useful as a potential antidiabetic and antioxidant agent: and/or their pharmaccutically acceptable salts. Further the invention relates to a pharmaceutical composition comprising the tricyclic compounds in combination with pharmaccutically acceptable excipients or carrier.

Full Text

Field of Invention This invention relates to certain new chemical entities and their pharmaceutically acceptable salts, derivatives or solvates useful as potential antidiabetic agents and having antioxidant properties and improved glucose uptake by in vitro skeletal muscle cells. Background of invention Diabetes is associated with a variety of metabolic abnormalities, principle among them being hyperglycaemia. The so called syndrome includes hypertriglyceridemia, reduced HDL, cholesterol and abnormal postprandial lipidemia (Diabetes, 1988, 37, 1597-1607) and atherosclerosis (J. Cardiovasc. Risk 1999, 6(5), 337-346). Type 1 diabetes or insulin dependent diabetes mellitus (IDDM) is a complex, multifactorial disease involving severe destruction of the insulin producing pancreatic (3 cells. Type 2 diabetes or non-insulin dependent diabetes mellitus (NIDDM) typically occurs with older age and obesity (J. Clin. Endocrinol. metab. 1999, 84, 2329-2335). Although glycemic control, insulin treatment and other chemical therapies can control many aspects of diabetes, numerous complications are common and diverse. Diabetic patients have an increased risk of developing various clinical complications that are due to microvascular or macrovascular diseases that includes nephropathy, retinopathy and neuropathy. Insulin resistance is a primary risk factor for type 2 diabetes mellitus. Besides, these patients have elevated serum levels of fatty acids. It appears that control of non esterified fatty acids (NEFA) in the blood could be an important approach to reduce insulin resistance. Studies on the molecular actions of compounds indicate that thiazolidinediones (potent glucose lowering agents) and fibrates (hypolipidaemic agents) exert their action by activating distinct transcriptional factors of the peroxisome proliferator activated receptors (PPAR) family. The former binds predominantly to PPARy and later to PPARa. There have been reports of many newer compounds that show dual PPARy/a activation (JMC, 2001, 44, 2675-2678; JMC, 2003,46, 1306-1317) and these have shown greater potential in treating type 2 diabetes (WOO 157001). It has been shown beyond doubt that diabetic subjects exhibit high lipid peroxides and other forms of oxidative stress. (Bratisl Lek Listy, 2000, 101(10) 541-551). In diabetes, oxidative stress seems to be caused by increased production of reactive oxygen species (ROS), sharp reduction in antioxidant defenses and altered cellular redox status. Consequences of oxidative stress are damage to DNA, lipids, proteins, disruption in cellular homeostasis and accumulation of vascular damages. It has been known that supplementation with an antioxidant is a promising complementary treatment which exerts beneficial effects in diabetes and provides further support for implication of oxidative stress in beta cell dysfunction in diabetes (Diabetes, 1999, 48(12) 2398-2406). Targeting therapy to specific tissues and organs of diabetes by specific antioxidants or combined drug preparations could become a relevant adjuvant pharmacotherapy with improved glycemic control, blood pressure control and management of dyslipidaemia for the treatment or prevention of progression of micro and macro vascular diabetic complications. The molecular mechanism supports that prolonged oxidative stress impairs insulin induced GLUT4 translocation in 3T3-L1 adipocytes (Diabetes, 1998, 47, 1562-1569). Based on the results of King's college in UK, antioxidants such as vitamins C, E and N-acetylcysteine are recommended as supplement in diabetes therapy (Doctor's guide, April 20, 1998) and antioxidants reduces the harmful complications of diabetes (Trends in Endocrinology and metabolism 2001, 12, 179-180). In a previous study, potent ß- and selective a-adrenoceptor blocker, carvedilol (Drugs of Today 1995, 31(Suppl.F) 1-23) which has carbazol moiety, was found to have very potent antioxidant activity. Besides these, there are some antidiabetic drugs, which have antioxidant properties independently to their main role on glycemia control. Sulfonylureas like gliclazide exhibit antioxidant activity. Some thiazolidinediones are able to possess antioxidant properties. As an example, troglitazone has a combined chemical structure of thiazolidinedione and a-tocopherol like structure (chroman ring). In spite of its beneficial antioxidant moiety, troglitazone was removed from European market due to hepatic dysfunction. The Applicant focused their attention on designing antioxidant moieties exhibiting superior euglycemic and hypolipidaemic activities. One of the lead compounds was carbazole containing 3-aryl 2-alkoxy propionic acids which was reported to have good dual activity with respect to PPARy and PPARcc (JMC, 2002, 45, 789-904), (WO 0023425). Summary of the invention: Detailed Description This invention relates to the synthesis of the compounds of general formula as given in Fig. 1 and their intermediates which exhibit antioxidant properties, and (Figure Removed) wherein B is a tricyclic group having structure as in Fig. 2 or Fig. 3; and In represents hydrogen, C1-4-alkyl or aryl selected from (un) substituted 6 membered cyclic ring; and n is 1-3; and A is unsaturated 6-membered ring with or without heteroatom; and R2 is H, C1-4-alkyl, aryl selected from (un) substituted 6 membered cyclic ring, alkylaryl selected from C1-4-alkyl and aryl selected from (un) substituted 6 membered cyclic ring, heterocyclyl selected from (un) substituted 5-6 membered ring either aromatic or nonaromatic having hetero atom like N, S or O, alkylheterocyclyl selected from C1-4-alkyl and heterocyclyl selected from (un) substituted 5-6 membered ring either aromatic or nonaromatic having hetero atom like N, S or O; and X represents nitrogen, oxygen or sulphur; and Ar represents benzene, pyridine, naphathalene, benzopyran or indole; and Y represents -OR3 wherein R3 is C1-4-alkyl or -NHR4 wherein R4 is hydrogen, benzoylalkenyl selected from C2-5-alkenyl and alkylbenzene selected from C1- 4-alkyl. The invention further relates to the synthesis of compounds of general formula as given in Fig 4 wherein R2 is H, C1-4-alkyl, aryl selected from (un) substituted 6 membered cyclic ring, alkylaryl selected from C1-4-alkyl and aryl selected from (un) substituted 6 membered cyclic ring, heterocyclyl selected from (un) substituted 5-6 membered ring either aromatic or nonaromatic having hetero atom like N, S or O, alkylheterocyclyl selected from C1-4-alkyl and heterocyclyl selected from (un) substituted 5-6 / membered ring either aromatic or nonaromatic having hetero atom like N, S or O; starting from hydroxy carbazoles. The O- alkylation was done using weak bases like any of the alkali carbonates (like Li2CO3 , Na2CO3, K2CO3 ) and phase transfer catalysts. The precursors as shown in Fig 4 showed good antioxidant activity. The invention also provides methods for synthesis of compounds of general formula as shown in Fig 10, having B as given in Fig.3, starting from various substituted carbazoles as given in (Figure Removed) Fig. 4 by condensing them with compounds depicted in Fig. 5 using strong bases like metal hydride or metal alkoxides, The solvents can be any aprotic, nonpolar ones like diethyl ether, tetrahydrofuran, and dichloromethane. The compounds of Fig. 10 on hydrogenation gave compounds of general formula as given in Fig. 1; wherein A is unsaturated 6-membered ring with or without heteroatom, R2 is H, C1-4-alkyl, aryl selected from (un) substituted 6 membered cyclic ring; alkylaryl selected from C1-4-alkyl and aryl selected from (un) substituted 6 membered cyclic ring, heterocyclyl selected from (un) substituted 5-6 membered ring either aromatic or nonaromatic having hetero atom like N, S or O, alkylheterocyclyl selected from C1-4-alkyl and heterocyclyl selected from (un) substituted 5-6 membered ring either aromatic or nonaromatic having hetero atom like N, S or O ; (Figure Removed) Another embodiment of this invention relates to the synthesis of compounds with general formula as given in Fig 6 wherein R2 is H, C1-4-alkyl, aryl selected from (un) substituted 6 membered cyclic ring, alkylaryl selected from C1-4-alkyl and aryl selected from (un) substituted 6 membered cyclic ring, heterocyclyl selected from (un) substituted 5-6 membered ring either aromatic or nonaromatic having hetero atom like N, S or O, alkylheterocyclyl selected from C1-4-alkyl and heterocyclyl selected from (un) substituted 5-6 membered ring either aromatic or nonaromatic having hetero atom like N, S or O ; starting from compounds as in Fig 4 and reacting them with 2-bromoethanol. Compounds as in Fig. 6 also depicted antioxidant activity. The invention also relates to compounds as shown in Fig. 6 on reacting with compounds depicted in Fig. 7 also gave compounds of Fig. 10 under itsunobu reaction conditions using DEAD and Ph3P in suitable solvent like tetrahydrofuran, wherein R1 represents hydrogen, C1-4-alkyl or aryl selected from (un) substituted 6 membered cyclic ring; R2 is H, C1-4-alkyl, aryl selected from (un) substituted 6 membered cyclic ring, alkylaryl selected from C1-4-alkyl and aryl selected from (un) substituted 6 membered cyclic ring, heterocyclyl selected from (un) substituted 5-6 membered ring either aromatic or nonaromatic having hetero atom like N, S or O, alkylheterocyclyl selected from C1-4-alkyl and heterocyclyl selected from (un) substituted 5-6 membered ring either aromatic or nonaromatic having hetero atom like N, S or O; Y represents -OR3 wherein R3 is C1-4-alkyl or -NHR4 wherein R4 is hydrogen, benzoylalkenyl selected from C2-5-alkenyl and alkylbenzene selected from C1-4-alkyl. (Figure Removed) In another embodiment of the invention, compounds as in Fig. 8 was reacted with compounds as in Fig. 7 to give compound of Fig. 10, having B as in Fig. 2; under Mitsunobu reaction conditions using diethylazodicarboxylate (DEAD) and triphenylphosphine (Ph3P) in a suitable solvent like tetrahydrofuran. Compounds as in Fig. 8 also depicted antioxidant activity, wherein A is unsaturated 6-membered ring with or without heteroatom. (Figure Removed) In another embodiment of the invention, the compounds as in Fig. 9 is prepared from compounds as in Fig. 4 by reacting it with 4-(2-bromoethoxybenzaldehyde). Further, compounds depicted in Fig. 9 were reacted with ethyl-2-ethoxy-2-diethyl phosphonoacetate to give compounds as in Fig. 10, wherein B is compound having structure as in Fig. 3. Compounds depicted in Fig. 1 was prepared by hydrogenation of compounds depicted in Fig. 10. Structures given in Fig. 9 and Fig. 10 also depicted antioxidant activity. (Figure Removed) In another embodiment all the compounds synthesized thus showed antioxidant properties as seen by lipid peroxidation test. In another embodiment of this invention relates to the preparation of pharmaceutically acceptable salts, intermediates and all the tautomeric forms, stereoisomers, mixture of stereoisomers including a racemic mixture or polymorphs of compounds of general formula Fig. 1 . In another embodiment all the compounds related to Fig. 1, their pharmaceutically acceptable salts showed the capacity of causing increase in glucose uptake in the in vitro skeletal muscle cell line to the extent of pioglitazone or more. Pharmaceutical Composition: In the present invention, compounds of Fig. 1 can be delivered or administered to mammals e.g. a human patient or subject, alone or in form of pharmaceutically acceptable salt or in form of a pharmaceutical composition where the compound is mixed with suitable carriers or excipient(s) in therapeutically effective amount. It may also be possible that compounds of the present invention may be therapeutically administered as the raw chemical, it is also preferable to present the active ingredient as the pharmaceutical formulation. More particularly compounds of Fig. 1 can be Simulated in the preparations in solid, semi-solid, liquid or gaseous forms such as tablets, capsules, pills, powders, ointments, injections and aerosols. The compound can be administered in a local or systemic manner, in depot or sustained release formulations. Tablets and capsules for oral administration may contain conventional excipients such as binding agents (e.g. syrup, acacia, gelatin, sorbitol, tragacanth and mucilage of starch), fillers (e.g. lactose, sugar, cellulose and maize-starch), lubricants (e.g. magnesium stearate, stearic acid, talc and polyethylene glycol), disintegrants (e.g. potato starch) or wetting agents, such as sodium lauryl sulphate.The tablets may be coated according to methods well known in the art. The compounds of Fig. 1 can be dispensed in unit dosage form comprising from Img to 150 mg of active ingredient together with a pharmaceutically acceptable carrier or excipient(s). The amount of composition administered will depend upon the subject being treated, the manner of administration and severity of the affliction. A typical tablet can be prepared as mentioned below: Core Active compound of Fig. l(free or salt form) 10 mg Microcrystalline cellulose 90 mg Colloidal silicon dioxide 2 mg Gum acacia 8 mg Magnesium stearate adequate Coating Coating mixture with plasticiser lOmg If it is desired, pharmaceutical composition of invention may comprise of compounds of Fig. 1 in combination with further pharmacologically active substances such as to treat, prevent, eliminate and alleviate disease related to blood sugar. Pharmacological Methods: 1) In vitro glucose uptake: The final compounds in their suitable salt forms were subjected to glucose uptake assay in the in vitro skeletal muscle cell lines. Methodology: Cell culture: L6E9 rat skeletal muscle cells were proliferated in Dulbeccos Modified Eagle's Medium (DMEM) supplemented with 15% Fetal calf serum (FCS) and antibiotics (Penicillin 100 lU/ml, Streptomycin 100µg/ml) for 2 days. Differentiation was initiated by shifting 70% confluent cells to DMEM supplemented with 2% Horse Serum (HS) for 4 days (fully differentiated) at 37°C in 5% CO2 incubator. Differentiation medium was changed daily. Pioglitazone and respective drug compounds were added during last 24 hrs of differentiation. All the compounds were tested at 50µM concentration. 2-Deoxy - D-glucose-1- 3H uptake: Media in the differentiated cells was changed 1 hr before the start of experiment. The cells were washed twice with the Krebs Ringer Phosphate buffer (KRP): lOmM phosphate (pH 7.2), 136 mM NaCl, 4.7 mM KC1, 1.25mM CaCl2, 1.25mM MgSO4 containing 0.05% BSA. The cells were further incubated twice with KRP buffer at 37° for 30 min. After washing with KRP buffer, DOG (0.2µCi/ml and lµM of unlabelled 2-deoxyglucose) was added and cells were incubated for 10 min. Cells were washed in ice-cold PBS three times and solubilized in 0.1N NaOH. Protein concentration was measured in each sample by BCA method (Smith et al, Anal. Biochem. 1985, 150, 76-85) followed by liquid scintillation counting. Results: To determine the effect of test compounds on basal glucose uptake of normally differentiated skeletal muscle cells in culture, pioglitazone was used as the reference drug. Our test compounds registered between the range of 25-60% increase in glucose uptake as compared to the basal level while pioglitazone showed 35% increase in glucose uptake. This shows that our compounds are close to or better than pioglitazone reference standards as far as glucose uptake is concerned hence indicating that they are capable of reducing hyperglycemic condition. A few representative examples are given below. (Table Removed) 2) Lipid Peroxidation: The evaluation of antioxidant activity of compounds was done by measurement of lipid peroxidation Principle: Lipid peroxidation is a complex process involving the formation and propagation of lipid radicals, the uptake of oxygen, a rearrangement of double bonds in unsaturated lipids and eventual disruption of biological membrane function. The aerobic incubation of rat brain homogenates with agents known to produce reactive oxygen species (ROS) like ferrous chloride and ascorbate. These induce the process of lipid peroxidation, leading to the formation of degradation products of peroxidized lipids including malondialdehyde, which then reacts with thiobarbituric acid to yield a pink color, read spectrophotometrically at absorption maximum wave length of 535 nm and taken as an index of lipid peroxidation. The test compounds depending upon their solubility, were dissolved/diluted in distilled water, DMSO or alcohol to give the final concentration in the ranges of nM to µM for in vitro study. 6-8 concentrations of each compound were tried. Methodology Preparation of rat brain homogenates The male SD rats weighing 280-350g were sacrificed by decapitation and the brains were immediately taken out and cleaned with ice cold 0.9% saline. Whole brain except cerebellum was homogenized with a polytron homogenizer in 10 volumes of ice-cold saline. Then, homogenate volume was adjusted/diluted with ice-cold saline so as to give a final concentration of 10 mg/0.8ml and frozen as aliquots at -20°C, if studied later (with in 2 days). Measurement of lipid peroxidation in rat brain homogenate The rates of membrane lipid peroxidation were measured by the formation of thiobarbituric acid reactive substances (TBARS). The rat brain homogenates (10 mg tissue/0.8ml) were incubated at 37°C for 15 min with different concentrations (at least 6 concentrations) of 10µl of a test compound or vehicle. Lipid peroxidation was initiated by addition of 0.1 ml each of 0.25 mM of FeCl2 and 1 mM ascorbic acid. A final volume of 1 ml reaction mixture was further incubated for 30 min. at 37°C in water bath and then the reaction was stopped by addition of 0.1 ml of 0.2% butylated hydroxytoluene. Thiobarbituric acid (0.67%) (TBA) reagent, 1 ml was then added and the mixture heated for 30 min at 95°C in water bath. The mixture then cooled on ice for 5 min. The TBARS were extracted by adding 2.0 ml of n-butanol and vortexed well for a minute and centrifuged for 5 min at 3000 rpm and the 1 ml aliquot of n-butanol phase was taken for measuring absorbance at 535 nm. Reactions without TBA were taken as blank. The antioxidant activity of test compounds was determined as percent inhibition of TBARS formation from the control absorbance values (i.e. in the absence of the test compound ) which is assumed as 100%. The reference compound used is a well known antioxidant, Trolox. Statistical Analysis: 'Me data were represented as mean ± SEM. A sigmoidal curve was plotted as percent inhibition vs log concentration and IC50 (inhibitory concentration at which occurs 50% inhibition of TBARS formation) value for each compound was found out by nonlinear regression curve fitting using Graph Pad Prism software. Antioxidant activity of some representative compounds are given below. (Table Removed) IC50 (µM) values of different compounds with antioxidant property represents inhibitory concentration at which occurs 50% inhibition of TEARS formation. Each measurement was the average of 2 or 3 experiments performed in duplicates. The results in the table show that all the above compounds can be considered to be antioxidants. But among them, those showing lesser values than the known antioxidant, Trolox , are considered to be very highly antioxidants. EXPERIMENTAL SECTION Examples corresponding to Fig. 4; Example 1 4-Methoxy carbazole 4- hydroxycarbazole (Igm, 5.4 mmol), ethyl acetate (5 ml), K2CO3 (1.128 gm, 1.5 eq.) and phase transfer catalyst tetrabutyl ammonium hydrogen sulphate (TEA, 0.184 gm, 10 mole %)were stirred for 1 hour at room temperature. Methyl iodide (1.16gm, 1.5 eq.) was added to the reaction mixture and stirred at room temperature, for 12 hours. The reaction was monitored by TLC and worked up by washing with distilled water and extracting with ethyl acetate. The organic layer was washed with brine, dried and evaporated to give title compound as white crystals mp 135°C. IR (KBr, cm-1) 3393, 1599, 1452, 1260, 1100 1HNMR δ (CDC3) 4.07 (s, 3H), 6.68(d, J=9Hz, 1H), 7.04(d, J=8.1Hz, 1H), 7.05-7.39 (m, 4H), 8.05(s, 1H), 8.31(d, J=7.8Hz, 1H). MS (El): 197(m/z M+) Example 2 4-Ethoxy carbazole 4-hydroxycarbazole (Igm, 5.4 mmol), ethyl acetate (5 ml), K2CO3 (1.128 gm, 1.5 eq.) and phase transfer catalyst tetrabutyl ammonium hydrogen sulphate (TBA), (0.184 gm, 10 mole %) were stirred for 1 hour at room temperature. Ethyl bromide (0.44 ml, 1.1 eq.) was added to the reaction mixture and re fluxed for 12 hours at 80 °C. The reaction was monitored by TLC and worked up by washing with distilled water and extracting with ethyl acetate. The organic layer was washed with brine, dried and evaporated to give title compound as white solid, mp 150°C. IR (KBr, cm-1) 3395, 1601, 1454, 1262, 1100 1H NMR δ (CDC13) 1.62(m, 3H), 4.25(q, J=6Hz, 2H), 6.66(d, J=8.1IIz,lH), 7.02(d, J=9.3Hz, 1H), 7.20-7.38(m, 4H), 8.03(s, 1H), 8.33(d, J=7.8Hz,lH). MS (El): 211(m/zM+) Example 3 4-Benzyloxycarbazole The title compound, mp 180°C was prepared treating 4-hydroxy carbazole with benzyl bromide by a procedure similar to that described in example 2. I.R. (KBr, cm-1) 3400, 1584, 1439, 1258, 1099 1H NMR δ (CDC13) 5.35(s, 2H), 6.75(d, J=7.8Hz,lH), 7.06(d, J=8.1Hz,lH), 7.25- 7.43(m, 8H), 7.59(d, J=7.2Hz, 1H), 8.06(s, 1H), 8.31(d, J=7.8Hz, 1H). M.S (El): 273 ( m/z M+) Example 4 2-Benzyloxycarbazole The title compound, mp 175°C was prepared treating 2-hydroxy carbazole with benzyl bromide by a procedure similar to that described in example 2. 1H-NMRδ(CDC13) 5.11(s, 2H), 6.91-6.97(m, 2H), 7.14(m, 1H), 7.23(m, 2H), 7.32-7.46(m, 6H), 7.95-8.03(m, 2H). M.S (El): 273 (m/z M+) Examples corresponding to Fig. 9; Example 5 4-(2-(4-methoxycarbazole)-ethoxy)-benzaldehyde To a suspension of sodium hydride (60% mineral oil, l.5eq.) in dry THF was added a solution of 4-methoxycarbazole (Igm, leq.) from example 1 in THF (3 ml) at 25 °C under nitrogen atmosphere. The reaction mixture stirred for one hour and cooled to 0°C and a solution of 4-(2-bromoethoxy) benzaldehyde (l.leq. prepared by known methods) in dry THF was added drop wise. The reaction mixture was stirred overnight at room temp. THF was evaporated and reaction mixture extracted with diethyl ether. The ether layer was then washed with brine and dried and evaporated to give a yellowish oily product. IR(cm-1) 1691,1601,1262,1157,740 1H NMR δ (CDCl3)4.07(s, 3H), 4.39(t, J=6Hz, 2H), 4.71(t, J=6Hz,2H), 6.7(d, J=8.1Hz, 1H), 6.86(d, J=8.7Hz, 2H), 7.1(d, J=8.1Hz, 1H), 7.23-7.28(m,lH), 7.37-7.75(m,3H), 7.74(d, J=8.7Hz, 2H), 8.34(d, J=7.8Hz, 1H), 9.82(s,lH). MS (El): 345 (m/z M+) Example 6 4-(2-(4-ethoxycarbazole)-ethoxy)-benzaldehyde The title compound was prepared from 4-ethoxycarbazole by a procedure similar to that described in example 5. 1HNMRδ (CDC13) 1.59(t, J=6.9Hz, 3H), 4.3(q, J=7.2Hz, 2H), 4.41(t, J=6Hz, 2H), 4.71(t, J=6Hz, 2H), 6.68(d, J=8.1Hz, 1H), 6.88(d, J=9Hz, 1H), 6.98(d, J=9Hz, 2H), 7.07(d, J=8.1Hz, 1H), 7.24-7.44(m, 2H), 7.73(d, J=9Hz, 2H), 8.35(d, J=8.1Hz, 2H), 9.8(s, 1H) MS(CI): 360(m/zM+l) Example 7 4-(2-(4-benzyloxycarbazole)-ethoxy)-benzaldehyde The title compound was prepared from 4-benzyloxycarbazole by a procedure similar to that described in example 5. 1HNMR δ(CDCl3) 4.36(t, J=6Hz, 2H), 4.68(t, J=2 Hz, 2H), 5.35(s, 2H), 6.62(m, IH), 6.77( d, J=9 Hz, 2H), 6.85(d, J=8 Hz, 1H), 6.98(d, J=8.4 Hz, 2H), 7.11(d, J=8 Hz, 1H), 7.28-7.45(m, 5H), 7.56(d, J=7.2 Hz, 2H), 7.9(d, J=8.4 Hz, 1H), 8.34(d, J=7.5 Hz, 1H), 9.79(s, 1H) Example 8 4-(2-(2-benzyloxycarbazole)-ethoxy)-benzaldehyde The title compound was prepared from 2-benzyloxycarbazole by a procedure similar to that described in example 5. 1H NMR δ (CDCl3) 4.42(m, 2H), 4.67(m, 2H), 5.11(s, 2H), 6.65 (m, 1H), 7.03(m, 2H), 7.34 (m,3H), 7.37-7.48(m, 5H), 7.86(d, J=7.2 Hz, 2H), 7.97(m, 3H), 9.83(s, IH) Examples corresponding to Fig. 10; Example 9 Ethyl-2-ethoxy-3- {4- [2-(4-methoxy-carbazole)-ethoxy]-phenyl}-2- propenoate To a suspension of sodium hydride (l.5eq.) in dry THF (5ml) was added ethyl-2-ethoxy-2-diethylphosphonoacetate (l.Seq.). The reaction mixture stirred for half an hour and 4- (2- (4-methoxycarbazole) ethoxy) benzaldehyde (1 eq.) was added drop wise. The reaction mixture was stirred overnight at room temp. THF was evaporated and product extracted with diethyl ether. The organic layer was washed brine, dried and evaporated to give a yellowish oily product. 1H NMR δ (CDC13) 1.12-1.57(m, 6H), 3.94(q, J=6Hz,2H), 4.11(s, 3H), 4.27(q, J=6Hz, 2H), 4.35(t, J=6Hz,2H), 4.7(t, J=6Hz, 2H), 6.71(d, J=7.5Hz, 1H), 6.79(d, J=8.7Hz, 1H), 6.9(s,lH), 7.12(d, J=9Hz, 2H), 7.27(m,lH), 7.37- 7.46(m, 2H), 7.6(d, J=9Hz, 2H), 8.34(d, J=7.5Hz, 2H).MS ( El) : 459(m/z M+) Example 10 Ethyl-2-ethoxy-3-{4-[2-(4-ethoxy-carbazole)-ethoxy]-phenyl}-2- propenoate The title compound was prepared from 4-(2-(4-ethoxycarbazole)-ethoxy)- benzaldehyde by a procedure similar to that described in example 9. 1H NMR δ (CDC13 ) 1.29-1.35(2t, J=6.9Hz, 6H), 1.59(t, J=6.9Hz, 3H), 3.94(m, 1H), 4.08(m, 1H), 4.25-4.37(2q, J=6.6Hz, 4H), 4.41(t, J=6Hz, 2H), 4.65(t, J=6Hz, 2H), 6.68(d, J=8.4Hz, 1H), 6.78(d, J=9Hz, 1H), 6.89(s, 1H), 6.98(d, J=7.5Hz, 2H), 7.07(d, J=8.1Hz, 1H), 7.29-7.43(m, 3H), 7.65(d, J=8.4Hz, 2H), 8.35(d, J=7.2Hz, 1H). Example 11 Ethyl-2-ethoxy-3-{4-[2-(4-benzyloxycarbazole)-ethoxy]-phenyl}-2- propenoate The title compound was prepared from 4-(2-(4-benzyloxycarbazole)-ethoxy)- benzaldehyde by a procedure similar to that described in example 9. 1H-NMRδ (CDC13); 1.28-1.42(t,t, J=6Hz,6 Hz, 6H), 3.93(q, J=6.9Hz, 2H), 4.27(q, J=6.9 Hz, 2H), 4.36(t, J=6Hz, 2H), 4.71(t, J=6Hz, 2H), 5.35(s, 2H), 6.78(m, 4H), 6.92(s, 1H), 7.13(d, J=8.4 Hz, 1H), 7.23(m, 1H), 7.36-7.47(m, 5H), 7.57(d, J=7.5 Hz, 2H), 7.68(d, J=8.7 Hz, 2H), 8.34(d, J=7.2 Hz, 1H) Example 12 Ethyl-2-ethoxy-3-{4-[2-(2-benzyloxycarbazole)-ethoxy]-phenyl}-2- propenoate The title compound was prepared from 4-(2-(2-benzyloxycarbazole)-ethoxy) benzaldehyde by a procedure similar to that described in example 9. 1H-NMR δ(CDC13) 1.12-1.57(m, 6H), 3.63-3.75(m, 1H), 3.9(m, 1H), 4.34(q, J=3.3 Hz, 2H), 4.41(m, 2H), 4.69(m, 2H), 5.11(s, 2H), 6.65 (m, 1H), 6.9 (s, 1H), 6.92-7.0(m, 3H), 7.23(m,2H), 7.28-7.34 (m, 5H), 7.37-7.43(m, 2H), 8.02 (m, 3H) Examples corresponding to Fig. 1; Example 13 Ethyl-2-ethoxy-3-{4-[2-(4-methoxycarbazole)-ethoxy]-phenyl} propionate Ethyl-2-ethoxy-3-{4-[2-(4-methoxy-carbazole) ethoxy] phenyl} 2-propenoate (400mg) was suspended in 10 ml ethyl acetate and hydrogenated over Palladium carbon (10%) catalyst (50mg) at 60 psi for 5 hours. The reaction progress was monitored by TLC and reaction mixture was filtered through celite and the solvent evaporated to give an oily product. 1H NMR δ (CDC13) 1.13(t, J=6.9Hz,3H), 1.34(t, J=6Hz, 3H), 2.9(d, J=6Hz, 2H), 3.3(m,lH), 3.58(m,lH), 3.91(t, J=6Hz,lH), 4.08(s, 3H), 4.16(q, J=6Hz, 2H), 4.30(t, J=6Hz,2H), 4.68(t, J=6Hz, 2H), 6.7l(t, J=9Hz, 2H), 7.10(t, J=6Hz, 2H), 7.27(m, 2H), 7.37-7.45(m, 3H), 8.34(d, J=9Hz, 2H). Example 14 Ethyl-2-ethoxy-3-{4-[2-(4-ethoxycarbazole)-ethoxy]-phenyl} propionate The title compound was prepared from Ethyl-2-ethoxy-3-{4-[2-(4-ethoxy-carbazole) ethoxy] phenyl} 2- propenoate by a procedure similar to that described in example 13. 1H NMR δ (CDC13) 1.31(t, J=7.2Hz, 3H), 1.41(t, J=6.9Hz, 3H), 1.61(t, J=6.6Hz, 3H), 2.90( d, J=6Hz, 2H), 3.27-3.33(m, 1H), 3.51-3.59(m,lH), 3.93(t, J=6.6Hz, 1H), 4.05(q, J=6.9Hz, 2H), 4.14(q, J=6Hz, 2H), 4.30(t, J=6Hz, 2H), 4.67(t, J=6Hz, 2H), 6.73(d, J=8.4Hz, 2H), 6.88(d, J=8.4Hz, 2H),7.9(d, J=7.8Hz, 2H), 7.20(m, 2H), 7.37-7.45(m,2H), 8.35(d, J=7.5Hz, 1H). Example 15 Ethyl-2-ethoxy-3-{4-[2-(4-benzyloxycarbazole)-ethoxy]-phenyl} propionate The title compound was prepared from Ethyl-2-ethoxy-3-{4-[2-(4-benzyloxycarbazole) ethoxy] phenyl} 2- propenoate by a procedure similar to that described in example 13. 1H NMR δ (CDC13) 1.15(t, J=6Hz, 3H), 1.41(t, J=6Hz, 3H), 2.91(d, J=6Hz, 2H), 3.3 (m, 1H), 3.6 (m, 1H), 3.9 (t, 6.9Hz,lH), 4.03(q, J=6Hz, 2H), 4.31(t, J=6Hz, 2H), 4.68(t, J=6Hz, 2H), 5.35(s, 2H), 6.65(d, J=8.4Hz, 1H ), 6.73(d,J=9Hz, 2H), 6.88(d, J=8.4 Hz, 2H), 7.11(d, J=8.4 Hz, 2H), 7.25 (m, 2H), 7.38-7.47(m, 5H), 7.68(d, J=8.7 Hz, 1H), 8.32(d, J=7.2 Hz, 1H) Example 16 Ethyl-2-ethoxy-3-{4-[2-(2-benzyloxycarbazole)-ethoxy]-phenyl} propionate The title compound was prepared from Ethyl-2-ethoxy-3-{4-[2-(2-benzyloxycarbazole) ethoxy] phenyl} 2- propenoate by a procedure similar to that described in example 13. 1H NMRδ (CDC13) 1.12-1.57(m, 6H), 2.91(d, J=6Hz, 2H), 3.33 (m, 1H), 3.68 (m, 1H), 3.94 (t, 6.9Hz,lH), 4.03(q, J=6Hz, 2H), 4.31(t, J=6Hz, 2H), 4.68(t, J=6Hz, 2H),5.11(s, 2H), 6.65 (m, 1H), 7.03(m, 4H), 7.34 (m, 4H), 7.37-7.48(m, 5H), 8.02 (m, 2H) Example 17 Ethyl-2-ethoxy-3-{4-[2-(4-hydroxycarbazole)-ethoxy]-phenyl} propionate METHOD A Ethyl-2-ethoxy-3-{4-[2-(4-benzyloxycarbazole) ethoxy] phenyl} 2-propenoate (400mg) was suspended in 10 ml ethyl acetate and hydrogenated over Palladium carbon (10%) catalyst (50mg) at 60 psi and 50°C for 5 hours. The reaction mixture was filtered through celite and the solvent evaporated to give an oily product. 1H NMR δ (CDC13) 1.12-1.57(m, 6H), 2.89(d, J=6Hz, 2H), 3.4 (m, 1H), 3.6 (m, 1H), 3.9 (t, 6.9Hz, 1H), 4.13(q, J=6Hz, 2H), 4.31(t, J=6Hz, 2H). 4.6(s, 1H), 4.66(t, J=6Hz, 2H), 6.72(d, J=8.7, 1H), 7.01(d, J=8.4 Hz, 2H), 7.08(d, J=8.4 Hz, 2H), 7.25 (m.lH), 7.44(m, 2H), 7.5(m, 2H), 8.32(d, J=7.2 Hz, 1H) METHOD B Ethyl-2-ethoxy-3-{4-[2-(4-benzyloxycarbazole)-ethoxy]-phenyl}-2-propenoate was debenzylated by refluxing in ethanol in the presence of Palladium carbon (10%) and ammonium formate for 10 minutes and reaction was monitored by TLC. The reaction mixture was filtered through celite and the solvent evaporated to give an oily product. The NMR matches exactly to method A. Example 18 Ethyl-2-ethoxy-3-{4-[2-(2-hydroxycarbazole)-ethoxy]-phenyl} propionate METHOD A The title compound was prepare as described in Example 17, Method A using ethyl-2-ethoxy-3-{4-[2-(2-benzyloxycarbazole)-ethoxy]-phenyl}-2-propenoate. 1HNMRδ (CDC13) 1.12-1.57(m, 6H), 2.89(d, J=6Hz, 2H), 3.4 (m, 1H), 3.6 (m, 1H), 3.9 (t, 6.9Hz, 1H), 4.13(q, J=6Hz, 2H), 4.31(t, J=6Hz, 2H), 4.66(t, J=6Hz, 2H), 4.8(s, 1H), 6.72(d, J=8.7, 1H), 7.01(d, J=8.4 Hz, 2H), 7.08(d, J=8.4 Hz, 2H), 7.25 (m,lH), 7.44(m, 2H), 7.5(m, 2H), 8.02(d, J=7.2 Hz, 1H) METHOD B Experiment performed according to method B given in example 17. Example 19 3- (4- (2- (4-Methoxycarbazole)-ethoxy)-phenyl)-2-ethoxy propionic acid Ethyl (3- (4- (2- (4-Methoxycarbazole)-9-yl-ethoxy)-phenyl)-2-ethoxy propionate was dissolved in 10 ml ethanol and 20% NaOH was added(0.2ml,l eq.). The reaction mixture was stirred for 24 hours. Then ethanol was evaporated and distilled water with acetic acid (pH 4) was added to acidify the reaction mixture. The final product was extracted in ethyl acetate and the organic layer evaporated to give an oily product. 1H NMR δ (CDC13) 1.41(t, J=6.9Hz, 3H), 2.9-3.02(m, 2H), 3.39(m, 2H), 3.54(m, 2H), 3.99(m, 1H), 4.08(s, 3H), 4.30(t, J=6Hz, 2H), 4.68(t, J=6Hz, 2H), 6.73(d, J=8.4Hz, 2H), 7.10(t, J=7.5Hz, 2H), 7.25(m, 2H), 7.37-7.48(m,4H), 8.34(d, J=7.8Hz,1H). Example 20 3- (4- (2- (4-Ethoxycarbazole) -9-yl-ethoxy)-phenyl)-2-ethoxy propionic acid The title compound was prepared from Ethyl-2-ethoxy-3-{4-[2-(4- ethoxycarbazole) ethoxy] phenyl} propionate by a procedure similar to that described in example 19. 1H NMR δ (CDC13) 1.41(t, J=6.9Hz, 3H), 1.60(t, J=6.9 Hz, 3H), 2.95-3.05(m, 2H), 3.34(m,lH), 3.65(m, IH), 4.01(m, IH), 4.14(q, J=6Hz, 2H), 4.28(m,4H), 4.67(t, J=6 Hz, 2H), 6.71(m, 2H), 6.88(d, J=8.4 Hz, 2H), 7.09(d, J=8.4 Hz, 2H), 7.26(m, 2H), 7.37-7.45(m, 2H), 8.35(d, J=7.5 Hz, IH). Example 21 3- (4- (2- (4-Benzyloxycarbazole)-9-yl-ethoxy)-phenyl)-2-ethoxy propionic acid The title compound was prepared from Ethyl-2-ethoxy-3-{4-[2-(4- benzyloxycarbazole) ethoxy]-phenyl| propionate by a procedure similar to that described in example 19. 1H NMR δ (CDC13) 1.41(t, J=6Hz, 3H), 2.91(m, 2H), 3.3 (m, IH), 3.6 (m, IH), 3.9 (t, 6.9Hz,lH), 4.31(t, J=6Hz, 2H), 4.68(t, J=6Hz, 2H), 5.35(s, 2H), 6.73(m, IH), 6.88(d, J=8.4 Hz, 2H), 7.11(d, J=8.4 Hz, 2H), 7.25 (m,2H), 7.38- 7.47(m, 5H), 7.57(m, IH), 7.68(d, J=8.7 Hz, 2H), 8.32(d, J=7.2 Hz, IH) Example 22 3- (4- (2- (2-Benzyloxycarbazole)-ethoxy)-phenyl)-2-ethoxy propionic acid The title compound was prepared from Ethyl-2-ethoxy-3-{4-[2-(2- benzyloxycarbazole)-ethoxy]-phenyl}-propionate by a procedure similar to that described in example 19. 1H NMR δ (CDC13) 1.41(t, J=6Hz, 3H), 2.91(m, 2H), 3.3 (m, IH), 3.6 (m, IH), 3.9 (t, 6.9Hz,lH), 4.31(t, J=6Hz, 2H), 4.68(t, J=6Hz, 2H), 5.11(s, 2H), 6.73(m, IH), 6.88(d, J=8.4 Hz, 2H), 7.11(d, J=8.4 Hz, 2H), 7.25 (m,2H), 7.38- 7.47(m, 5H), 7.57(m, IH), 7.68(d, J=8.7 Hz, 2H), 8.32(d, J=7.2 Hz, IH) Example 23 3- (4- (2- (4-hydroxycarbazole)-ethoxy)-phenyl)-2-ethoxy propionic acid The title compound was prepared from Ethyl-2-ethoxy-3-{4-[2-(4- hydroxycarbazole)-ethoxy]-phenyl}-propionate by a procedure similar to that described in example 19. 1H NMR δ (CDC13) 1.12-1.57(m, 3H), 2.89(m, 2H), 3.4 (m, 1H), 3.6 (m, 1H), 3.9 (t, 6.9Hz, 1H), 4.31(t, J=6Hz, 2H), 4.6(s, 1H), 4.66(t, J=6Hz, 2H), 5.72(d, J=8.7, 1H), 7.01(d, J=8.4 Hz, 2H), 7.08(d, J=8.4 Hz, 2H), 7.25 (m,2H), 7.44(m, 1H), 7.5(m, 2H), 8.32(d, J=7.2 Hz, 1H) Example 24 3- (4- (2- (2-hydroxycarbazole)-ethoxy)-phenyl)-2-ethoxy propionic acid The title compound was prepared from Ethyl-2-ethoxy-3-{4-[2-(2- hydroxycarbazole)-ethoxy]-phenyl} propionate by a procedure similar to that described in example 19. 1H NMR δ (CDC13) 1.41(t, J=6Hz, 3H), 2.9l(m, 2H), 3.3 (m, 1H), 3.6 (m, 1H), 3.9 (t, 6.9Hz,lH), 4.31(t, J=6Hz, 2H), 4.56(s, lH),4.68(t, J=6Hz, 2H), 6.73(m, 1H), 6.88(d, J=8.4 Hz, 2H), 7.11(d, J=8.4 Hz, 2H), 7.25 (m,2H), 7.57(m, 1H), 7.68(d, J=8.7 Hz, 2H), 8.32(d, J=7.2 Hz, 1H) Examples corresponding to lysine salt of Fig. 1 ; Example 25 3- (4- (2- (4-Methoxycarbazole)-ethoxy)-phenyl)-2-ethoxy propionic acid, Lysine salt. L-lysine monohydrochloride was converted to free lysine by passing through a cation exchange resin (Dowex) bed and washed with distilled water. The aqueous ammonia solution obtained by washing the resin was evaporated under high vacuum. 3- (4- (2- (4-Methoxycarbazole)-ethoxy) phenyl) 2-ethoxy propionic acid was dissolved in ethanol and free lysine (1 eq.) was added to it and stirred for 2 hours. Then ethanol was evaporated and residue was crystallized by diethyl ether. This was air dried to give 3- (4- (2- (4-Methoxycarbazole)-ethoxy) phenyl) 2-ethoxypropionic acid in lysine salt form. 1H NMR δ (CD3OD) 1.05(t, J=6.9Hz, 3H), 1.27(m, 4H), 1.50(m, 2H), 1.68(m, 2H), 1.87(m, 2H), 2.75(m, 1H), 2.85-2.94(m, 3H), 3.29(m, 1H), 3.57(m, 2H), 3.75(m, 1H), 4.06(s, 3H), 4.34(t, J=6Hz, 2H), 4.70(t, J=6Hz, 2H), 6.75(d, J=7.8Hz,1H),, 6.67(d, J=9Hz, 2H), 7.16(m, 4H), 7.40(m, 2H), 7.53(d, J=8.4Hz, 1H), 8.22(d, J=7.8Hz, 1H). I.R. (KBr, cm-1) 3416, 2928, 1583, 1511, 1459, 1402 M.S (APCI): 579 (m/z M+) Example 26 3- (4- (2- (4-Ethoxycarbazole)-ethoxy)-phenyl)-2-ethoxy propionic acid, Lysine salt. The title compound was prepared from 3- (4- (2- (4-Ethoxycarbazole)-ethoxy)-phenyl)-2-ethoxy propionic acid by a procedure similar to that described in example 25. 1H NMR δ (CD3OD) 1.06(t, J=6.9Hz, 3H), 1.48(m, 2H), 1.56-1.68(m, 5H), 1.82(m, 2H), 2.6(m, 1H), 2.86-2.90(m, 2H), 3.25(m, 1H), 3.50(m, 3H), 3.75(m, 1H), 4.28-4.36(m, 4H), 4.67(t, J=6Hz, 2H), 6.70(t, J=7.8Hz, 3H), 7.09-7.19(m, 4H), 7.32-7.39(m, 2H), 7.53(d, J=8.1Hz, 1H), 8.25(d, J=7.8 Hz, 1H). I.R. (KBr, cm-1) 3909, 2929, 1586, 1505, 1458, 1402, 1336, 1244 M.S (APCI): 593 (m/z M+) Example 27 3- (4- (2- (4-Benzyloxycarbazole) ethoxy)-phenyl)-2-ethoxy propionic acid, Lysine salt. The title compound was prepared from 3- (4- (2- (4-Benzyloxycarbazole) -ethoxy)-phenyl)-2-ethoxy propionic acid by a procedure similar to that described in example 25. 1H NMR δ (CD3OD) 1.01(t, J=6.9Hz, 3H), 1.27(m, 2H), 1.48(m, 2H), 1.69(m, 2H), 1.78(m, 2H), 2.91(m, 2H), 3.3 (m, 1H), 3.49(m, 2H), 3.6(m, 1H), 3.75(m, 1H), 3.9(t, 6.9Hz,lH), 4.38(t, J=6Hz, 2H), 4.68(t, J=6Hz, 2H), 5.35(s, 2H), 6.69(m, 2H), 6.84(d, J=7.8Hz, 1H), 7.10-7.21(m, 4H), 7.39-7.54(m, 5H), 7.57(m, 3H), 8.20 (d, J=7.8 Hz, 1H). I.R. (KBr, cm-1) 3413, 2922, 1637, 1505, 1406, 1244 M.S (APCI): 656 ( m/z M+) Example 28 3- (4- (2- (2-Benzyloxycarbazole)-ethoxy)-phenyl)-2-ethoxy propionic acid, Lysine salt. The title compound was prepared from 3- (4- (2- (2-Benzyloxycarbazole)-ethoxy)-phenyl)-2-ethoxy propionic acid by a procedure similar to that described in example 25. 1H NMRδ (CD3OD) 1.08(t, J=6.9Hz, 3H), 1.27(m, 2H), 1.48(m, 2H), 1.69(m, 2H), 1.78(m, 2H), 2.9l(m, 2H), 3.3 (m, 1H), 3.49(m, 2H), 3.6(m, 1H), 3.75(m, 1H), 3.9(t, 6.9Hz, 1H), 4.31(t, J=6Hz, 2H), 4.68(t, J=6Hz, 2H), 5.11(s, 2H), 6.71(m, 2H), 6.84(d, J=7.8Hz, 1H), 7.10-7.21(m, 4H), 7.39-7.54(m, 5H), 7.57(m, 3H), 8.12 (d, J=7.8 Hz, 1H). I.R. (KBr, cm-1) 3415, 2928, 1632, 1505, 1406, 1344 M.S (APCI): 656 ( m/z M+) Example 29 3- (4- (2- (4-Hydroxycarbazole)-ethoxy)-phenyl)-2-ethoxy propionic acid, Lysine salt. The title compound was prepared from 3- (4- (2- (4-hydroxycarbazole)-ethoxy)-phenyl)-2-ethoxy propionic acid by a procedure similar to that described in example 25. 1H NMR δ (CD3OD) 1.02(t, J=6.9 Hz, 3H), 1.26(m, 2H),1.49(m, 2H), 1.69(m, 2H), 1.84(m, 2H), 2.75(m, 2H), 2.95(m, 2H),3.2 (m, 1H), 3.5(m, 2H), 3.6 (m, 1H), 3.76(m, 1H), 4.02 (t, 6.9Hz, 1H), 4.37(t, J=6Hz, 2H), 4.6(s, 1H), 4.69(t, J=6Hz, 2H), 6.68(t, J=9 Hz, 2H), 7.12(m, 3H), 7.20 (m, 2H), 7.25 (m, 1H), 7.44(m, 1H), 7.6(m, 1H), 8.24(d, J=8.4 Hz, 1H) I.R. (KBr, cm-1) 3416, 2929, 2863, 1586, 1406, 1107 M.S: 567 (m/z M+) Example 30 3- (4- (2- (2-Hydroxycarbazole)-ethoxy)-phenyl)-2-ethoxy propionic acid, Lysine salt. The title compound was prepared from 3-(4-(2-(2-hydroxycarbazole)-ethoxy)-phenyl)-2-ethoxy propionic acid by a procedure similar to that described in example 25. 1H NMR δ (D20) 0.95(t, J=6Hz, 3H), 1.38(m, 2H), 1.63(m, 2H), 1.78(m, 2H), 2.91(m, 4H), 3.18(m, 1H), 3.40(m, 1H), 3.54(m, 2H), 3.76(m, 1H), 3.91(t, 6.9Hz,lH), 4.31(t, J=6Hz, 2H), 4.71(s, 1H), 4.8(t, J=6Hz, 2H), 6.52(m, 2H), 6.95(m, 2H), 7.18 (m, 2H), 7.42(m, 3H), 8.03(m, 2H) (KBr, cm-1) 3420, 2922, 1583, 1402, 1347 M.S : 567 ( m/z M+) Example 31 2-Ethoxy-3-{4-[2-(l-methyl-2-carbolin-9-yl)-ethoxy]-phenyl}-propionic acid, Lysine salt. The title compound was prepared from 2-Ethoxy-3-{4-[2-(l-methyl-2-carbolin-9-yl)-ethoxy]-phenyl}-propionic acid by a procedure similar to that described in example 25. 1H NMR δ (D20) 1.12(t, J=6Hz, 3H), 1.38(m, 2H), 1.63(m, 2H), 1.78(m, 2H), 2.80(s, 3H), 2.91(m, 4H), 3.18(m, 1H), 3.40(m, 1H), 3.54(m, 2H), 3.76(m, 1H), 3.91(t, 6.9Hz,lH), 4.31(t, J=6Hz, 2H), 4.8(t, J=6Hz, 2H), 6.52(m, 2H), 6.95(m, 2H), 7.54 (s, 2H), 7.82(m, 1H), 8.12(m, 1H), 8.36(m, 2H) M.S : 564 ( m/z M+) Example 32 Synthesis of 3-[4-(carbazol-9-yloxy)-phenyl]-2-(l-methyl-3-oxo-3-phenyl-propenylamino) propionic acid, Lysine salt. This title compound was synthesized by following steps: a) Synthesis of 3-(4-Hydroxy-phenyl)-2-methyl-3-oxo-3-phenyl- propenylamino)-propionic acid methyl ester L-tyrosine ester was placed with benzoylacetone and anisole in a two-necked 25 ml round-bottom flask equipped with reflux condenser, Dean Stark apparatus and calcium chloride guard tube and magnetic stirrer. This was made to reflux for 37 h. For work up anisole was evaporated under vacuum and then product was extracted with DCM in separatory funnel, then washed with brine solution and then dried over sodium sulphate. Single spot of the compound was obtained. IR (KBr, cm-1) 3177.8, 1744.1, 1596.1, 1438.5, 1118.2, 745.6 1H NMR CDC13 δ 1.81(s, 3H), 2.99-3.16(m, 4H), 3.72(s, 3H), 5.65(m, 1H), 6.74(d, J= 8.34 Hz, 1H), 7.02(d, J= 6.57Hz, 1H), 7.38(d, J= 6.78Hz, 1H), 7.84(d, J= 7.02Hz, 1H)M.S. (C.I.): 339 (m/Z M+l) b) Synthesis of 3-[4-(Carbazol-9-yloxy)-phenyl]-2-(l-methyl-3-oxo-3-phenyl- propenylamino) propionic acid methyl ester , Tyrosine ester (I mole) joined with benzoylacetone, and carbazole-9-ethyl mesylate (Imole) and potassium carbonate (2 mole) in ethanol and toluene were placed in a 25 ml two round bottomed flask equipped with reflux condenser, calcium chloride guard tube and magnetic stirrer. The reaction mixture was refluxed at 80°C for 10 h. The disappearance of the starting material on TLC indicated the completion of the reaction. For working up the reaction mixture was evaporated on Rotavapor and the compound was extracted with DCM. The organic layer was washed with the distilled water then and then with brine and dried over the sodium sulphate. During this process number of products formed but the desired product was not formed, when confirmed with the help of the mass spectra. IR (cm-1) 2920, 1592, 1458.1,1079.7, 1018.1,750 1H NMR CDC13 δ 1.98(s, 3H), 3.91(m, 4H), 4.11(m, 3H), 4.31(m, 4H), 7.20(m, 5H), 7.42(m, 8H), 8.05(d, J= 7.GHz, 4H) c) 3-[4-(Carbazol-9-yloxy)-phenyl]-2-( 1 -methyl-3-oxo-3-phenyl- propenylamino) propionic acid methyl ester was hydrolysed with aq. NaOH to give its acid. The 3-[4-(Carbazol-9-yloxy)-phenyl]-2-(l-methyl-3-oxo-3-phenyl-propenylamino) propionic acid was dissolved in ethanol and free lysine (1 eq.) was added to it and stirred for 2 hours. Then ethanol was evaporated and residue was crystallized by diethyl ether to give acid in lysine salt form. 1H NMR CDC13 δ1.49(m, 2H), 1.69(m, 2H), 1.87(m, 2H), 1.98(s, 3H), 2.96(m, 2H), 3.32(s, 4H), 3.59(m, 1H), 3.91(m, 4H), 4.31(m, 4H), 7.20(m, 5H), 7.42(m, 8H), 8.05(d, J= 7.6Hz, 4H) Example 33 Synthesis of 3-[5-(2-Carbazol-9-yl-ethoxy)-lH-indol-3-yl]-2-(l-methyl-3-oxo-3-phenyl-propenylamino)-propionic acid methyl ester. a) Synthesis of 3-(5-hydroxy-lH-indol-3-yl)-2-(l-methyl-3oxo-3-phenyl- propenylamino)-propionic acid methyl ester In a two-necked round bottom flask equipped with Dean- Stark apparatus and reflux condenser with calcium chloride guard tube and magnetic stirrer was placed with 100 mg (0.0004 mole) of 5-Hydroxy tryptophan ester and 69.23 mg (0.0004 mole) benzoylacetone and dry anisole. This was made to reflux for 37 h. For work up anisole was evaporated under vacuum and then product was extracted with DCM in separately funnel, then washed with solution and then dried over sodium sulphate. Single spot of the compound was obtained. IR (KBr, cm-1) 3275.7, 1718, 1597.3, 1459.3, 1206.2 M.S. (C.I.): 379 (m/Z M+l) b) In dry reaction condition triphenylphosphine (1.5 mole) was stirred with dry THF at 0°C through septum diethylazodicarboxylate (DEAD) was injected drop wise and solution was stirred for 30 minutes. The red coloration of the complex appeared. Then a solution of 3-(5-hydroxy-lH-indol-3-yl)-2-(l-methyl-3-oxo-3-phenyl-propenylamino)-propionic acid methyl ester and carbazole-9-ethanol in THF was added drop wise to the above reaction mixture. The reaction mixture was stirred overnight from 0°C to room temp. The complete disappearance of the starting material showed the completion of the reaction. For working up the THF was evaporated and reaction mixture extracted with diethyl ether. The ether layer was then washed with distilled water and brine and dried over sodium sulphate. IR (cm-1) 3217.1, 1728.6, 1593.5, 1458.8,1081.1 1H NMR CDC13 δ1.7(s, 5H), 3.36 (s, 1H), 3.91(s, 3H), 4.32(m, 6H), 7.21(m, 5H), 7.40(m, 9H), 8.04(d, J= 7.71Hz, 3H) Example 34 Synthesis of 3-[5-(2-Carbazol-9-yl-ethoxy)-lH-indol-3-yl]-2-(l-methyl-3-oxo-3-phenyl-propenylamino)-propionic acid, Lysine salt. 3-[5-(2-Carbazol-9-yl-ethoxy)-lH-indol-3-yl]-2-(l-methyl-3-oxo-3-phenyl-propenylamino)-propionic acid methyl ester was hydrolysed with aq. NaOH to give its acid. 3-[5-(2-Carbazol-9-yl-ethoxy)-lH-indol-3-yl]-2-(l-methyl-3-oxo-3-phenyl-propenylamino)-propionic acid was dissolved in ethanol and free lysine (1 eq.) was added to it and stirred for 2 hours. Then ethanol was evaporated and residue was crystallized by diethyl ether to give acid in lysine salt form. 1H NMR CDC13 δ 1.50(m, 2H), 1.67(m, 2H), 1.7(s, 5H), 1.86(m, 2H), 2.95(m, 2H), 3.30(s, 4H), 3.36 (s, 1H), 3.60(m, 1H), 4.32(m, 6H), 7.21(m, 5H), 7.40(m, 9H), 8.04(d, J= 7.71Hz, 3H) Example 35 (Synthesis of 3-{4-[2-(9H-Carbazol-4-yloxy)-ethoxy]-phenyl}-2-(l-methyl-3-oxo-3-phenyl-propenylamino)-propionic acid methyl ester. a) Synthesis of 4-(2-Bromo-ethoxy)-9H-carbazole 4- hydroxycarbazole (Igm, 5.4 mmol), acetone (5 ml) and K2CO3 (1.128 gm, 1.5 eq.) were stirred for 1 hour at room temperature. Dibromoethane (1.16gm, 1.1 eq.) was added to the reaction mixture and refluxed for 48 hours. The reaction was monitored by TLC and worked up by washing with distilled water and extracting with ethyl acetate. The organic layer was washed with brine, dried and cone, to give title compound. 1H NMR δ (CDCl3) 3.84 (t, J=6Hz, 2H), 4.55 (t, J=6Hz, 2H), 6.64 (d, J=8.1Hz, 1H), 7.07 (d, J=8.1Hz, 1H), 7.25(m, 2H), 7.36 (d, J=9Hz, 1H), 8.06 (s, 1H), 8.38 (d, J=6.9Hz, 1H) MS (El): 290(m/z M+) b) 3-(4-Hydroxy-phenyl)-2-methyl-3-oxo-3-phenyl-propenylamino)-propionic acid methyl ester (leq.), acetone (5 ml) and K2CO3 (1.5 eq.) were stirred for 1 hour at room temperature. 4-(2-Bromo-ethoxy)-9H-carbazole (l.leq.) was added to the reaction mixture and refluxed for 36 hours. The reaction was monitored by TLC and worked up by washing with distilled water and extracting with ethyl acetate. The organic layer was washed with brine, dried and cone, to give title compound. 1H NMR δ(CDCl3) 1.94 (s, 3H), 3.16 (m, 1H), 3.20 (m, 1H), 3.54 ( t, J=6Hz, 1H), 3.76 (s, 3H), 4.49 (t, J=6Hz, 2H), 4.57 (t, J=6Hz, 2H), 5.6 (s, 1H), 6.74 (d, J= 8.4 Hz, 2H), 6.93 (t, J= 8.4 Hz, 1H), 7.09 (d, J= 8.4 Hz, 2H), 7.20 (m, 5H), 7.33 (d, J= 9 Hz, 2H), 7.87 (m, 3H), 8.01(s, 1H), 8.25 (d, J= 8.4 Hz, 1H) MS (El): 548 (m/z M+) Example 36 Synthesis of 3-{4-[2-(9H-Carbazol-4-yloxy)-ethoxy]-phenyl}-2-( 1-methyl-3-oxo-3-phenyl-propenylamino)-propionic acid, Lysine salt. 3-{4-[2-(9H-Carbazol-4-yloxy)-ethoxy]-phenyl}-2-(l-methyl-3-oxo-3-phenyl-propenyl amino)-propionic acid methyl ester was hydrolysed with aq. NaOH to give its acid. 3-{4-[2-(9H-Carbazol-4-yloxy)-ethoxy]-phenyl}-2-(l-methyl-3-oxo-3-phenyl-propenylamino)-propionic acid was dissolved in ethanol and free lysine (1 eq.) was added to it and stirred for 2 hours. Then ethanol was evaporated and residue was crystallized by diethyl ether to give acid in lysine salt form. 1H NMR CDC13δ 1.48 (m, 2H), 1.68 (m, 2H), 1.86 (m, 2H), 1.94 (s, 3H), 2.97(m, 2H), 3.16 (m, 1H), 3.20-3.30 (m, 5H), 3.54 ( t, J=6Hz, 1H), 3.60 (m, 1H), 4.49 (t, J=6Hz, 2H), 4.57 (t, J=6Hz, 2H), 5.6 (s, 1H), 6.74 (d, J= 8.4 Hz, 2H), 6.93 (t, J= 8.4 Hz, 1H), 7.09 (d, J= 8.4 Hz, 2H), 7.20 (m, 5H), 7.33 (d, J= 9 Hz, 2H), 7.87 (m, 3H), 8.01(s, 1H), 8.25 (d, J= 8.4 Hz, 1H) MS (El): 679 (m/z M+) Example 37 Synthesis of 3-{4-[2-(9H-carbazole-4-yloxy)-ethoxy]-phenyl}-2-ethoxy acrylic acid ethyl ester. a) Synthesis of 4-(2-bromoethoxy) benzaldehyde 4-hydroxybenzaldehyde (leq.), dibromoethane (1.1 eq.) and K2CO3 (0.5 eq.) were refluxed in acetone for 20 hours. The disappearance of starting material indicated the completion of reaction. The product was extracted in ethyl acetate and washed with distilled water. I.R. ( KBr, cm-1) 1685, 1601, 1252, 1160, 1065, 1005 1H NMR CDC13 δ3.67 (t, J= 6Hz, 2H), 4.38 (t, J= 6Hz, 2H), 7.02 (d, J= 9Hz, 2H), 7.85 (d, J= 9Hz, 2H), 9.9 (s, 1H) MS (El): 230 (m/z M+) b) Synthesis of 4-[2-(9H-carbazole-4-yloxy)-ethoxy]-benzaldehyde To a suspension of sodium hydride (60% mineral oil, 1.5eq.) in dry THF was added a solution of 4-hydroxycarbazole (leq.) in THF (3 ml) at 25 °C under nitrogen atmosphere. The reaction mixture stirred for one hour and cooled to 0°C and a solution of 4-(2-bromoethoxy) benzaldehyde (l.leq.) in dry THF was added drop wise. The reaction mixture was stirred overnight at room temp. THF was evaporated and reaction mixture extracted with ethyl acetate. The organic layer treated with brine, dried over sodium sulfate and concentrated. The compound was purified by column chromatography. 1H NMR CDCl3 δ 3.61(t, J= 6 Hz, 2H), 4.27 (t, J= 6 Hz, 2H), 6.57 (d, J= 7.8 Hz, 2H), 6.89 (d, J= 7.8 Hz, 2H), 6.99 (d, J=8.4 Hz, 2H), 7.38 (m, 3H), 8.08 (s, 1H), 8.27(d, J=7.8 Hz, 2H), MS (El): 331(m/z M+) c) To a suspension of sodium hydride (l.5eq.) in dry THF (5ml) was added Ethyl-2-ethoxy-2-diethylphosphonoacetate (l.Seq.). The reaction mixture stirred for half an hour and 4-[2-(9H-carbazole-4-yloxy)-ethoxy]-benzaldehyde (1 eq.) was added drop wise. The reaction mixture was stirred overnight at room temp. THF was evaporated and product extracted with ethyl acetate. The organic layer was washed brine, dried and evaporated to give a yellowish oily product. 1H NMR (CDC13) δ 1.25 (t, J= 6.6 Hz, 3H), 1.38 (t, J= 6.6 Hz, 3H), 3.85 (m, 1H), 3.96 (m, 2H), 4.01(m, 1H), 4.25 (t, J= 6 Hz, 2H), 4.56 (t, J= 6 Hz, 2H), 6.84 (d, J=9 Hz, 2H), 6.96 (s, 1H), 7.08 (d, J=8.4 Hz, 2H), 7.39 (m, 4H), 7.71(d, J=9 Hz, 2H), 8.08 (s, 1H), 8.32 (d, J=8.4 Hz, 1H) MS (El): 445(m/z M+) Example 38 Synthesis of 3-{4-[2-(9H-carbazole-4-yloxy)-ethoxy]-phenyl}-2-ethoxy propionic acid ethyl ester. 3-{4-[2-(9H-carbazole-4-yloxy)-ethoxy]-phenyl}-2-ethoxy acrylic acid ethyl ester was suspended in 10 ml ethyl acetate and hydrogenated over Palladium carbon (10%) catalyst (50mg) at 60 psi and 50°C for 5 hours. The reaction mixture was filtered through celite and the solvent evaporated to give an oily product. 1H NMR (CDC13) δ 1.23 (t, J= 6.6 Hz, 3H), 1.37 (t, J= 6.6 Hz, 3H), 2.9(d, J=6Hz, 2H), 3.85 (m, 1H), 3.95 (m, 2H), 4.01(m, 2H), 4.25 (t, J= 6 Hz, 2H), 4.56 (t, J= 6 Hz, 2H), 6.84 (d, J=9 Hz, 2H), 6.96 (s, 1H), 7.08 (d, J=8.4 Hz, 2H), 7.39 (m, 4H), 7.69(d, J=9 Hz, 2H), 8.06 (s, 1H), 8.30 (d, J=8.4 Hz, 1H) MS (El): 447(m/z M+) Example 39 Synthesis of 3-{4-[2-(9H-carbazole-4-yloxy)-ethoxy]-phenyl}-2-ethoxy propionic acid, Lysine salt. 3-{4-[2-(9H-carbazole-4-yloxy)-ethoxy]-phenyl}-2-ethoxy propionic acid ethyl ester was hydrolysed with aq. NaOH to give its acid. 3-{4-[2-(9H-carbazole-4-yloxy)-ethoxy]-phenyl}-2-ethoxy propionic acid was dissolved in ethanol and free lysine(l eq.) was added to it and stirred for 2 hours. Then ethanol was evaporated and residue was crystallized by diethyl ether to give acid in lysine salt form. 1HNMR CDC13 δ 1.35 (t, J= 6.6 Hz, 3H), 1.48 (m, 2H), 1.65(m, 2H), 1.87(m, 2H), 2.95(m, 4H), 3.32(m, 4H), 3.57(m, IH), 3.85 (m, IH), 4.01(m, 2H), 4.25 (t, J= 6 Hz, 2H), 4.56 (t, J= 6 Hz, 2H), 6.84 (d, J=9 Hz, 2H), 7.08 (d, J=8.4 Hz, 2H), 7.39 (m, 4H), 7.71(d, J=9 Hz, 2H), 8.08 (s, IH), 8.32 (d, J=8.4 Hz, IH) MS (El): 564(m/z M+) We claim 1. A compound 3-{4-[2-(9H-Carbazol-4-yloxy)- ethoxy]-phenyl }-2-(l-methyl-3- oxo-3-phenyl-propenylamino)- propionic acid, Lysine salt represented by formula: (Formula Removed) 2. The compound as claimed in claim 1, having antioxidant property and antidiabetic potential. 3. The compound as claimed in claim 1, capable of causing glucose uptake in the in vitro skeletal muscle cells. 4. The compound as claimed in claim 1, for preparation of a composition in combination with a pharmaceutically acceptable excipient or vehicle, such as herein described.

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