Title of Invention	"ANTICOAGULANT AND ANTIPLATELET AGGREGATION ACTIVITIES OF AQUEOUS EXTRACT OF THE SEEDS OF CORIANDRUM SATIVUM L."
Abstract	Precipitate of aqueous extract of mature seeds of coriander was analysed for their anticoagulant and antiplatelet aggregation activities. The precipitate was adjusted to make 0.25%, 0.5%, 1.0% and 2.0% in 2 ml human blood in 5 ml vials. Two ml blood in empty vials served as control for coagulation and 2 ml in a vial containing 0.5% EDTA (Ethylene Diamine Tetrachlor Acetic Acid) was kept as control for anticoagulant activity. The activity was observed even at 0.25%. This extract when tested with human blood showed complete inhibition of platelet aggregation. The invention of anticoagulant and antiplatelet aggregation activities of coriander may contribute effectively for the prevention and cure of cardiac ischemia, transient ischaemic attacks of brain and many other thrombus-induced diseases. As daily dietary component it may prevent such diseases without any side effect.

Title of Invention

"ANTICOAGULANT AND ANTIPLATELET AGGREGATION ACTIVITIES OF AQUEOUS EXTRACT OF THE SEEDS OF CORIANDRUM SATIVUM L."

Abstract

Precipitate of aqueous extract of mature seeds of coriander was analysed for their anticoagulant and antiplatelet aggregation activities. The precipitate was adjusted to make 0.25%, 0.5%, 1.0% and 2.0% in 2 ml human blood in 5 ml vials. Two ml blood in empty vials served as control for coagulation and 2 ml in a vial containing 0.5% EDTA (Ethylene Diamine Tetrachlor Acetic Acid) was kept as control for anticoagulant activity. The activity was observed even at 0.25%. This extract when tested with human blood showed complete inhibition of platelet aggregation. The invention of anticoagulant and antiplatelet aggregation activities of coriander may contribute effectively for the prevention and cure of cardiac ischemia, transient ischaemic attacks of brain and many other thrombus-induced diseases. As daily dietary component it may prevent such diseases without any side effect.

Full Text	Field of invention A process of preparation of anticoagulant and antiplatelet aggregation agent from the dry seeds of Conundrum sativum. Acute myocardial infarction (AMI) is one of the most common diseases resulting into death. In United States alone, 1.1 million AMls occur each year. The mortality rate with AMI is approximately 30% with more than half of these deaths occurring before the stricken individual reaches the hospital. Although the mortality rate after admission for AMI has declined by about 30% over the last two decades, approximately 1 of every 25 patients who survives initial hospitalization dies in the first year after AMI. Survival is markedly reduced in elderly patients (Over 75), whose mortality rate is 20% at one month and 30% at one year after AMI. The pathogenesis of cardiovascular diseases is responsible for 30% of all deaths in developing and developed countries. Besides, thrombus formation in the arteries of brain can also cause stoke and death. Post operative formation of thrombus in the injured arteries can produce pulmonary embolism or embolism in the coronary arteries and thus produce AMI and death. Generally AMI occurs when coronary blood flow decreases abruptly after thrombotic occlusion of a coronary artery previously narrowed by atherosclerosis; The thrombus develops rapidly at the site of vascular injury. This may be multifactorial, but in most cases, infarction occurs when an atherosclerotic plaque fissures, ruptures or ulcerates and when conditions (Local or systemic) favor thrombogenesis, so that a mural thrombus forms at the site of rupture and leads to coronary artery occlusion. After an initial platelet monolayer forms at the site of the ruptured plaque, various agonists (Collagen, ADP, epinephrine, serotonin) promote platelet activities. After agonist stimulation of platelets, there is production and release of thromboxane A2 (a potent local vasoconstrictor), further platelet activation and potential resistance to thrombolysis. The coagulation cascade is activated on exposure of tissue factor in damaged endothelial cells at the site of the ruptured plaque. Factors VII and X are activated, ultimately leading to the conversion of prothrombin to thrombin, which then converts fibrinogen to fibrin. Fluid phase and clot-bound thrombin participate in an auto amplification reaction that leads to further activation of the coagulation cascade. The culprit coronary artery eventually becomes occluded by a thrombus containing platelet aggregates and fibrin strands. In order to avoid and break this vast chain of mechanisms leading to coronary artery blockade which results into acute myocardial infarction and hence death in quite a high percentage of cases, thrombolytic and antithrombotic agents are required to prevent thrombus formation to stop extension of the thrombus. Thromboiysis The principal goal of thrombolysis is prompt restoration of coronary arterial patency. The thrombolytic agents such as tissue plasminogen activator (tPA), streptokinase, anisoxylated plasminogen streptokinase activator complex (APSAC) and reteplase (rPA), all act by promoting the conversion of plasminogen to plasmin, which subsequently lyses fibrin thrombi. This therapy can reduce the relative risk of in hospital death by up to 50% when administered within the first hour of the onset of symptoms of AMI. Antithrombotic Agents: Thrombosis plays an important role in the pathogenesis of acute Myocardial Infarction and strokes due to vascular insufficiency. The primary goal of treatment with antiplatelet and antithrombin agents is to establish and maintain patency of the infarct- related artery. A secondary goal is to reduce the patient's tendency to thrombosis and thus the likelihood of mural formation or deep venous thrombosis, either of which can result in pulmonary embolisation. The degree to which antiplatelet and antithrombin therapy achieves these goals, partly determines how effectively it reduces the risk of mortality from AMI. At present aspirin is the standard antiplatelet agent tor patients with AMI and for the prevention of stroke and death due to cardiovascular diseases. This is now considered an essential element in the management of patients with suspected AMI and is effective across the entire spectrum of acute coronary syndromes. Buccal absorption of chewed aspirin causes rapid inhibition of cyclooxygenase in platelets followed by a reduction of thromboxane A2 levels. This is followed by regular daily oral administration of the drug, though it has many side effects. Heparin is a mucopolysaccharide which is prepared commercially from a variety of animal tissues. Unfractionated heparin (UFH) is the standard antithrombin agent used in clinical practice, though its precise role in patients treated with thrombolytic agents remains uncertain. Though the available data does not show any convincing benefit of UFH with respect to either coronary arterial patency or mortality rate when added to a regimen of aspirin and a non-fibrin specific thrombolytic agent such as streptokinase, it appears that the immediate administration of intravenous UFH, in addition to a regimen of aspirin and tPA, helps to facilitate thrombolysis and to establish and maintain patency of the infarct-related artery. Also low-molecular weight heparin preparations (LMWHS) are being used with increased frequency as alternative to UFH for anticoagulation in patients with AMI. Though it is regularly used post-operatively or after myocardial infarction to prevent thrombus formation or to stop further extension of thrombus, it has many side effects such as thrombocytopenia, osteoporosis, hyper-sensitivity and transient alopecia. Thus, these are the drugs used in clinical practice as thrombolytic and antithrombotic agents. But all these drugs are prescribed only after the problem of thrombosis starts in coronary arteries. Post problems, aspirin is continued for an extended period as a prophylactic measure but not heparin. Thus, till todate there is no drug available which can be given as a prophylactic measure to the public without causing any side effects. Recently, this antiplatelet aggregation activity has been observed in some fruits and vegetables also which are still not in therapeutic use. Coriandrum sativum is widely cultivated as a spice crop in the tropical and subtropical parts of the world. It is commercially grown for the use of its leaves (Cilantor) in salads. Its mature dry seeds are used as a common spice and is an indispensable ingredient of cooking. This has been traditionally used to treat coughs, chest pains, bladder problems, leprosy, rash fever, diarrhea, headache, mouth and throat disorders, bad breath and many other complications in folk medicine. But its effectiveness for these conditions remains unproved. Recently, it bas been reported to have several pharmacological effects such as antifertility , antihyperglycemic , antihyperlipidemic, antioxidant, antiproliferative , hypotensive carminative, diuretic and anticonvulsant activities as well as reduces the amount of lead deposition. Chemical studies on Coriandrum sativum have shown the presence of constituents such as queretin 3-glucoronide, linalool, camphor, geranyl acetate geranial and coumarius, and many glycosides and glycosides. But till' date its anticoagulant and antiplatelet aggregation activities have not been described. We have invented anticoagulant and antiplatelet aggregation activities in the aqueous extract of seeds of Coriandrum sativum, which has not been reported so far. It is applicable as a dietary component to prevent cardiac ischaemia due to thrombus formation in coronary arteries and many other diseases caused by thrombotic embolism. It can be applied in all those cases where clotting of blood is to be prevented or treated. It can also be used post-operatively to prevent thrombosis and thrombotic embolism. This invention is going to contribute very effectively in the field of medical therapy because for the first time an effective oral drug without any side effect and at the cheapest cost will be available from an edible herb to prevent as well as cure thrombus-induced diseases. Before its application, it has to be processed and developed in the form of a drug in the laboratories of medical firms followed by standardization of dose(s) Since the present drug is prepared from a spice (Coriandrum satum) which is most commonly used in national as well as international kitchens, it can very safely be given as a prophylactic measure even without deciding probability of the disease. It will prevent thrombus formation in the arteries by its antiplatelet aggregation and anticoagulant properties and protect from thrombus caused lethal diseases. Description A process of preparation of anticoagulant and antiplatelet agent from the dry seeds of Coriandrum sativam. The objective of present invention is to provide an antithrombotic drug which can be give by oral route, hence making the application easier and safer. It will reduce rate of death due to diseases caused by arterial thrombosis, which is responsible for 30% of all deaths in developing and developed countries. Process of extraction: Accordingly the present invention provides a process of preparation of anticoagulant and antiplatelet aggregation agent from the dry seeds of Coriandrum sativum, comprising the steps of: A. Crushing ari-dried mature seeds of Coriandrum sativum to powder in an electric grinder. B. Mixing 100 gram of the said powder with 300 ml of distilled water in a conical flask of 500 ml capacity. C. Filtering after 4 days the said powder mixed in water and evaporating the filtrate thus obtained on water bath at 80° C. D. Powdering the solid precipitate thus obtained to get anticoagulant and antiplatelet aggregation agent. Anticoagulant Activity: The solid precipitate was added in vials of 5 ml capacity in the amount adjusted to make 0.25%, 0.5%, 1 % and 2% in 2ml human blood. Empty vials were used as controls for coagulation of blood and vials containing EDT A (Ethylene Diamine Tctrachlor Acetic Acid) to make up 0.5% in 2 ml blood were used as controls for anticoagulant activity. In each vial of different concentrations of dehydrated aqueous extract of seeds of Coriandrum sativum, 2 ml venous blood from human volunteers was added. The blood was also added in empty vials and vials containing EDTA. The extract showed its anticoagulant activity form 0.25% onwards which was the lowest percentage used. It was comparable to the vials containing EDTA as anticoagulant. This experiment was repeated several times and every time, the observation was the same. Antiplatelet aggregation activity: The antiplatelet aggregation activity of seeds of Coriandrum sativum was tested on human blood as follows:- Venous blood was collected from volunteers who had not taken any medication for at least 15 days before donation. Blood was collected in a plastic syringe through sterilized needles. The coagulation of blood was prevented by mixing 9 volumes of blood with one volumes of 3.8% sodium citrate. The sample was centrifuged for 15 minutes at 180 X g and the supernatant platelet rich plasma (PRP) was collected. The PRP (49 urn) was aggregated with epinephrine (10um) in an aggregometer (Chronolog model 600) at 37°c at the stirring speed of 1200 rpm keeping Platelet Poor Plasma (PPP) in the blank cuvette. For experiment with the drug, the PRP (40µm) was preincubated with the drug (l0µm) .at 2%for 5 minutes at 37°C. prior to the addition of the aggregating agent. At this concentration of the sample complete inhibition of platelet aggregation was observed (Fig.I). These experiments have been repeated several times with similar results. Hence, it can be developed pharmaceutically as a medicine for preventing and treating thrombotic diseases in clinical practice, As it is derived form a spice which is most commonly used in national as well as international kitchens, it can be safely given to patients orally to prevent or treat thrombotic diseases, It can also be consumed by general public as prophylactic measure with benefits without being under observation of a physician. We claim 1. A process of preparation of anticoagulant and antiplatelet aggregation agent from the dry seeds of Coriandrum sativum , comprising the steps of: a. Crushing air-dried mature seeds of Conundrum sulivum to powder in an electric grinder. b. Mixing 100 grain of the said powder with 300 ml of distilled water in a conical flask of 500 ml capacity. c. Filtering after 4 days the said powder mixed in water and evaporating the filtrate thus obtained on water bath at 80° C. d. Powdering the solid precipitate thus obtained to get anticoagulant and antiplatelet aggregation agent. 2. A process for the preparation of anticoagulant and antiplatelet aggregation agent from the dry seeds of Conundrum sativum substantially as herein described with the specified figures and drawings.

Full Text

Field of invention
A process of preparation of anticoagulant and antiplatelet aggregation
agent from the dry seeds of Conundrum sativum.
Acute myocardial infarction (AMI) is one of the most common diseases resulting into death. In United States alone, 1.1 million AMls occur each year. The mortality rate with AMI is approximately 30% with more than half of these deaths occurring before the stricken individual reaches the hospital. Although the mortality rate after admission for AMI has declined by about 30% over the last two decades, approximately 1 of every 25 patients who survives initial hospitalization dies in the first year after AMI. Survival is markedly reduced in elderly patients (Over 75), whose mortality rate is 20% at one month and 30% at one year after AMI. The pathogenesis of cardiovascular diseases is responsible for 30% of all deaths in developing and developed countries.
Besides, thrombus formation in the arteries of brain can also cause stoke and death. Post operative formation of thrombus in the injured arteries can produce pulmonary embolism or embolism in the coronary arteries and thus produce AMI and death.
Generally AMI occurs when coronary blood flow decreases abruptly after thrombotic occlusion of a coronary artery previously narrowed by atherosclerosis; The thrombus develops rapidly at the site of vascular injury. This may be multifactorial, but in most cases, infarction occurs when an atherosclerotic plaque fissures, ruptures or ulcerates and when conditions (Local or systemic) favor thrombogenesis, so that a mural thrombus forms at the site of rupture and leads to coronary artery
occlusion. After an initial platelet monolayer forms at the site of the ruptured plaque, various agonists (Collagen, ADP, epinephrine, serotonin) promote platelet activities. After agonist stimulation of platelets, there is production and release of thromboxane A2 (a potent local vasoconstrictor), further platelet activation and potential resistance to thrombolysis.
The coagulation cascade is activated on exposure of tissue factor in damaged endothelial cells at the site of the ruptured plaque. Factors VII and X are activated, ultimately leading to the conversion of prothrombin to thrombin, which then converts fibrinogen to fibrin. Fluid phase and clot-bound thrombin participate in an auto amplification reaction that leads to further activation of the coagulation cascade. The culprit coronary artery eventually becomes occluded by a thrombus containing platelet aggregates and fibrin strands.
In order to avoid and break this vast chain of mechanisms leading to coronary artery blockade which results into acute myocardial infarction and hence death in quite a high percentage of cases, thrombolytic and antithrombotic agents are required to prevent thrombus formation to stop extension of the thrombus.
Thromboiysis
The principal goal of thrombolysis is prompt restoration of coronary arterial patency. The thrombolytic agents such as tissue plasminogen activator (tPA), streptokinase, anisoxylated plasminogen streptokinase activator complex (APSAC) and reteplase (rPA), all act by promoting the conversion of plasminogen to plasmin, which subsequently lyses fibrin thrombi. This
therapy can reduce the relative risk of in hospital death by up to 50% when administered within the first hour of the onset of symptoms of AMI.
Antithrombotic Agents:
Thrombosis plays an important role in the pathogenesis of acute Myocardial Infarction and strokes due to vascular insufficiency. The primary goal of treatment with antiplatelet and antithrombin agents is to establish and maintain patency of the infarct- related artery. A secondary goal is to reduce the patient's tendency to thrombosis and thus the likelihood of mural formation or deep venous thrombosis, either of which can result in pulmonary embolisation. The degree to which antiplatelet and antithrombin therapy achieves these goals, partly determines how effectively it reduces the risk of mortality from AMI.
At present aspirin is the standard antiplatelet agent tor patients with AMI and for the prevention of stroke and death due to cardiovascular diseases. This is now considered an essential element in the management of patients with suspected AMI and is effective across the entire spectrum of acute coronary syndromes. Buccal absorption of chewed aspirin causes rapid inhibition of cyclooxygenase in platelets followed by a reduction of thromboxane A2 levels. This is followed by regular daily oral administration of the drug, though it has many side effects.
Heparin is a mucopolysaccharide which is prepared commercially from a variety of animal tissues. Unfractionated heparin (UFH) is the standard antithrombin agent used in clinical practice, though its precise role in patients treated with thrombolytic agents remains uncertain.
Though the available data does not show any convincing benefit of UFH with respect to either coronary arterial patency or mortality rate when added to a regimen of aspirin and a non-fibrin specific thrombolytic agent such as streptokinase, it appears that the immediate administration of intravenous UFH, in addition to a regimen of aspirin and tPA, helps to facilitate thrombolysis and to establish and maintain patency of the infarct-related artery. Also low-molecular weight heparin preparations (LMWHS) are being used with increased frequency as alternative to UFH for anticoagulation in patients with AMI.
Though it is regularly used post-operatively or after myocardial infarction to prevent thrombus formation or to stop further extension of thrombus, it has many side effects such as thrombocytopenia, osteoporosis, hyper-sensitivity and transient alopecia.
Thus, these are the drugs used in clinical practice as thrombolytic and antithrombotic agents. But all these drugs are prescribed only after the problem of thrombosis starts in coronary arteries. Post problems, aspirin is continued for an extended period as a prophylactic measure but not heparin. Thus, till todate there is no drug available which can be given as a prophylactic measure to the public without causing any side effects.
Recently, this antiplatelet aggregation activity has been observed in some fruits and vegetables also which are still not in therapeutic use.
Coriandrum sativum is widely cultivated as a spice crop in the tropical and subtropical parts of the world. It is commercially grown for the use of its leaves (Cilantor) in salads. Its mature dry seeds are used as a common spice and is an indispensable ingredient of cooking.
This has been traditionally used to treat coughs, chest pains, bladder problems, leprosy, rash fever, diarrhea, headache, mouth and throat disorders, bad breath and many other complications in folk medicine. But its effectiveness for these conditions remains unproved.
Recently, it bas been reported to have several pharmacological effects such as antifertility , antihyperglycemic , antihyperlipidemic, antioxidant, antiproliferative , hypotensive carminative, diuretic and anticonvulsant activities as well as reduces the amount of lead deposition. Chemical studies on Coriandrum sativum have shown the presence of constituents such as queretin 3-glucoronide, linalool, camphor, geranyl acetate geranial and coumarius, and many glycosides and glycosides. But till' date its anticoagulant and antiplatelet aggregation activities have not been described.
We have invented anticoagulant and antiplatelet aggregation activities in the aqueous extract of seeds of Coriandrum sativum, which has not been reported so far. It is applicable as a dietary component to prevent cardiac ischaemia due to thrombus formation in coronary arteries and many other diseases caused by thrombotic embolism. It can be applied in all those cases where clotting of blood is to be prevented or treated. It can also be used post-operatively to prevent thrombosis and thrombotic embolism.
This invention is going to contribute very effectively in the field of medical therapy because for the first time an effective oral drug without any side effect and at the cheapest cost will be available from an edible herb to prevent as well as cure thrombus-induced diseases. Before its application, it has to be processed and developed in the form of a drug in the laboratories of medical firms followed by standardization of dose(s)
Since the present drug is prepared from a spice (Coriandrum satum) which is most
commonly used in national as well as international kitchens, it can very safely be
given as a prophylactic measure even without deciding probability of the disease.
It will prevent thrombus formation in the arteries by its antiplatelet aggregation
and anticoagulant properties and protect from thrombus caused lethal diseases.
Description
A process of preparation of anticoagulant and antiplatelet agent from the dry
seeds of Coriandrum sativam.
The objective of present invention is to provide an antithrombotic drug which can
be give by oral route, hence making the application easier and safer. It will reduce
rate of death due to diseases caused by arterial thrombosis, which is responsible
for 30% of all deaths in developing and developed countries.
Process of extraction:
Accordingly the present invention provides a process of preparation of anticoagulant and antiplatelet aggregation agent from the dry seeds of Coriandrum sativum, comprising the steps of:
A. Crushing ari-dried mature seeds of Coriandrum sativum to powder in an
electric grinder.
B. Mixing 100 gram of the said powder with 300 ml of distilled water in a
conical flask of 500 ml capacity.
C. Filtering after 4 days the said powder mixed in water and evaporating the
filtrate thus obtained on water bath at 80° C.
D. Powdering the solid precipitate thus obtained to get anticoagulant and
antiplatelet aggregation agent.
Anticoagulant Activity:
The solid precipitate was added in vials of 5 ml capacity in the amount adjusted to make 0.25%, 0.5%, 1 % and 2% in 2ml human blood. Empty vials were used as controls for coagulation of blood and vials containing EDT A (Ethylene Diamine Tctrachlor Acetic Acid) to make up 0.5% in 2 ml blood were used as controls for anticoagulant activity.
In each vial of different concentrations of dehydrated aqueous extract of seeds of Coriandrum sativum, 2 ml venous blood from human volunteers was added. The blood was also added in empty vials and vials containing EDTA. The extract showed its anticoagulant activity form 0.25% onwards which was the lowest percentage used. It was comparable to the vials containing EDTA as anticoagulant. This experiment was repeated several times and every time, the observation was the same.
Antiplatelet aggregation activity:
The antiplatelet aggregation activity of seeds of Coriandrum sativum was tested on human blood as follows:-
Venous blood was collected from volunteers who had not taken any medication for at least 15 days before donation. Blood was collected in a plastic syringe through sterilized needles. The coagulation of blood was prevented by mixing 9 volumes of blood with one volumes of 3.8% sodium citrate. The sample was centrifuged for 15 minutes at 180 X g and the supernatant platelet rich plasma (PRP) was collected. The PRP (49 urn) was aggregated with epinephrine (10um) in an aggregometer (Chronolog model 600) at 37°c at the stirring speed of 1200 rpm keeping Platelet Poor Plasma (PPP) in the blank cuvette. For experiment with the drug, the PRP (40µm) was preincubated with the drug (l0µm) .at 2%for 5 minutes at 37°C. prior to the addition of the aggregating agent. At this concentration of the sample complete inhibition of platelet aggregation was observed (Fig.I).
These experiments have been repeated several times with similar results. Hence, it can be developed pharmaceutically as a medicine for preventing and treating thrombotic diseases in clinical practice, As it is derived form a spice which is most commonly used in national as well as international kitchens, it can be safely given to patients orally to prevent or treat thrombotic diseases, It can also be consumed by general public as prophylactic measure with benefits without being under observation of a physician.

We claim
1. A process of preparation of anticoagulant and antiplatelet aggregation agent
from the dry seeds of Coriandrum sativum , comprising the steps of:
a. Crushing air-dried mature seeds of Conundrum sulivum to powder in
an electric grinder.
b. Mixing 100 grain of the said powder with 300 ml of distilled water in a
conical flask of 500 ml capacity.
c. Filtering after 4 days the said powder mixed in water and evaporating
the filtrate thus obtained on water bath at 80° C.
d. Powdering the solid precipitate thus obtained to get anticoagulant and
antiplatelet aggregation agent.
2. A process for the preparation of anticoagulant and antiplatelet aggregation
agent from the dry seeds of Conundrum sativum substantially as herein
described with the specified figures and drawings.

Documents:

1354-del-2003-abstract.pdf

1354-del-2003-claims.pdf

1354-del-2003-correspondence-others.pdf

1354-del-2003-correspondence-po.pdf

1354-del-2003-description (complete).pdf

1354-del-2003-drawings.pdf

1354-del-2003-form-1.pdf

1354-del-2003-form-13.pdf

1354-del-2003-form-19.pdf

1354-del-2003-form-2.pdf

1354-del-2003-form-3.pdf

1354-del-2003-form-5.pdf

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Patent Number

212635

Indian Patent Application Number

1354/DEL/2003

PG Journal Number

50/2007

Publication Date

14-Dec-2007

Grant Date

10-Dec-2007

Date of Filing

04-Nov-2003

Name of Patentee

SINGH UDAI PRATAP

Applicant Address

22 GANESH DHAM COLONY, NEVADA, SUNDERPUR, VARANASI-221005, INDIA.

Inventors:

#	Inventor's Name	Inventor's Address
1	SINGH UDAI PRATAP	22 GANESH DHAM COLONY, NEVADA, SUNDERPUR, VARANASI-221005, INDIA.
2	SINGH MANDAVI	DR. U.P. SINGH 22 GANESH DHAM COLONY, NEVADA, SUNDERPUR, VARANASI-221005, INDIA.

PCT International Classification Number

A61K 35/14

PCT International Application Number

N/A

PCT International Filing date

PCT Conventions:

#	PCT Application Number	Date of Convention	Priority Country
1			NA