Title of Invention	A POLYHERBAL PREPARATION USEFUL FOR THE PREVENTION OF ATHEROSCLEROSIS AND HYPERLIPIDEMIA
Abstract	This invention relates to a polyherbal preparation useful for the prevention of atherosclerosis and hyperlipidemia comprising a mixtue of 1 to 4 purified commiphora mukul, 0.5 to 4 pure Boswellia serrata, 0.1 to 0.4 purified semecarpus anacardium, 0.4 to 2 purified powder strychnos nux vomica, 0.3 to 2 pure powder of water extract of Termenallia arjuna, 0.5 to 2 shankha Bhusma, adding Rubia Cordifolia or Bacoparmonnieri or Triphala and Trikatu.

Title of Invention

A POLYHERBAL PREPARATION USEFUL FOR THE PREVENTION OF ATHEROSCLEROSIS AND HYPERLIPIDEMIA

Abstract

This invention relates to a polyherbal preparation useful for the prevention of atherosclerosis and hyperlipidemia comprising a mixtue of 1 to 4 purified commiphora mukul, 0.5 to 4 pure Boswellia serrata, 0.1 to 0.4 purified semecarpus anacardium, 0.4 to 2 purified powder strychnos nux vomica, 0.3 to 2 pure powder of water extract of Termenallia arjuna, 0.5 to 2 shankha Bhusma, adding Rubia Cordifolia or Bacoparmonnieri or Triphala and Trikatu.

Full Text	FIELD OF INVENTION This invention relates to a novel polyherbal preparation for the prevention of Atherosclerosis and Hyperlipidemia. BACKGROUND OF INVENTION Atherosclerosis is one of the major problems for young age death. It is an active process of inflammation and cell proliferation. It starts when normal vascular functions go away. Basically, there is blockage in the coronary artery, which leads to the heart attack. This blockage could be due to deposition of lipid, formation of wound or sudden release of lipid from the endotheliat wall due to bursting of plaque. Stow and gradual deposition of fat in the intimal layer of artery is called fatty lesion or plaque. Slowly these fatty lesions get fibrosed and calcium is deposited in it. Initially, it is a reversible process but after fibrosis, it becomes irreversible. In fact, fat deposition in the blood vessel is a natural process with aging, but in some individuals, its rate of formation is significantly high and therefore leads to pathological state of coronary artery disease. There are several reasons for this deposition. However, the basic cause is considered to be the faulty metabolism of lipid in the body. High cholesterol diet or high level of endogenous cholesterol synthesis in die body is the basic cause of artherosclerosis. Of course, there are several precipitating factors for this pathology, such as stress, smoking, diabetes, hypertension, age, male sex, family history leading to elevated homocystein, high serum lipoprotein-a and infection withcytorn egalovirus or chlamydia. More free radical production leading to rapid oxidation of LDL, followed by the excess uptake of oxidised LDL by the macrophages leading to the formation of foam cells is the basic pathology. PRIOR ART As this disease is multi-factorial, there are several approaches to manage artherosclerosis. First and foremost, it is to reduce die lipid load in the body or to increase the HDL content or to reduce the burden of free radicals and oxidized LDL or to remove foam cells and fatty lesions. There are two major steps, (a) Prevention of the formation of fatty plaque; (b) Regression of plaque already formed. At present, there are two main approaches for the management of atherosclerosis (1) Invasive techniques; and (2) Non-invasive techniques. In the non-invasive group of techniques, the most prominent approach is to lower the blood lipid, specially the cholesterol and triglycerides. In this approach, the main pathway is to inhibit the endogenous cholesterol synthesis by blocking the HMG-Co synthase. A drug known is different kind of Statins. In this way, there is reverse cholesterol transport from the tissue to the blood leading to the lowering of the LDL and VLDL. Several medicinal plants products are also available with a hypolipidemic claims, eg. Commiphoraraukul, Terminalia arjuna, Acorus calamus, etc.. In fact, ayurvedic literature discloses such plant names, but not much scientific study has been made with these plants. Yet another approach is to increase the HDL in the blood. Unfortunately, there is no good medicine, which can increase the serum HDL. The exercise is the only way to achieve this goal. Use of cow butter/milk has also shown the property of raising serum HDL upto some extent, but it can not be used as a medicine in the patients of hyp erlip idem ia and arthero sclerosis. Third approach is to prevent die oxidation of LDL hi the blood, because ox LDL is the basic cause of foam celt formation and thereafter its deposition in the arterial wall, forming arthero sclerotic plaque. To achieve this goal, anti-oxidants are being recommended as the diet supplements. Although the use of antioxidants has increased significantly as a diet supplement in the management of artherosclerosis and other coronary artery diseases, but does not fall in the group of therapeutic medicine, because of its non-specific role. Metal chelaters are also used to prevent the formation of free radicals, because iron mediated Fenton's reaction is one the basic cause of hydroxyl radical production. Alter knowing the molecular pathway of atheroma formation, gene therapy is being tried in the management of this disease. It is reported that stable atheroma is not as dangerous as the unstable one. For this unstability, a group of proteases known as MMPs (Matrix Metallo proteinases) are responsible. In fact, they digest the fibrous cap of the plaque and allow the lipid to come out of the plaque and block the arterial blood flow. Attempts are now being made to introduce the genes to inhibit these MMPs. Similarly, the most recent approach of gene therapy is to inhibit a growth factor M-CSF (Macrophage colony stimulating factor), which is responsible for the proliferation of smooth muscle cells and rapid formation of foam cell leading to their deposition. One more approach to manage arthero sclerosis is to regulate the inflammatory cytokines and various enzymes like lipoxygenase and cyclooxygenase, because inflammation is one of the basic factors, responsible for plaque formation. Since arthero sclerosis is a multietio logical factor disease, so doctors recommend a series of medicine to manage this disease and still the disease is not manageable because of uncoordinated approach. However, there is no medicine which can target several ettological factors simultaneously by giving one tablet. The patient is supposed to take several medicines in a day, which gives him a kind of psychological depression. These medicines,w hen given in isolation does not give significant impact on the prevention of atheromalformation, because other factors become more prominent The gene therapy, which is being developed is at the infancy stage and if at ail, it comes to the public use, it will be very expensive and also with several side effects, only the time will tell for its success. There are many claims to prevent the formation of plaque, by reducing the risk factors, by taking more antioxidants or by lowering the cholesterol by the use of several hypolipidemic drugs like Statins, etc.. Once athero ma is detected, the coronary bypass, etc. are the only remedies. In fact, no good drug is available to regress the plaque, already formed. OBJECTS OF THE INVENTION An object of this invention is to propose a novel polyherbal preparation which has the capacity to target several etiological pathways, and finally lead to atherosclerosis. Another object of this invention is to propose a novel polyherbal preparation which is anti-inflammatory, anti-oxidant and increases serum HDL, and more specifically, it inhibits Lox-15, Cox-2 and Ca-deposition in the plaque, increases Collagen in the chronic plaques, increases serum HDL and decreases serum TG. Still another object of this invention is to propose a novel polyherbal preparation which enhances serum HDL and prevents plaque formation even in the presence of high serum lipid. Yet another object of this invention is to propose a novel polyherbal prepara-tion which enhances the collagen tissue in the old plaque indicating towards the stabilisation of the plaque. A further object of this invention is to propose a novel polyherbal preparation which inhibits the Cyclooxygenase-2 and lipoxygenase-15, which are responsible for atherosclerosis. A still further object of this invention is to propose a novel polyherbal preparation which is cost-effective, more effective than its component medicinal plant and does not have any toxic or side effect with high therapeutic safety margin. DESCRIPTION OF INVENTION According to this invention, there is provided a polyherbal preparation useful for the prevention of atherosclerosis and hyperlipidemia comprising a mixture of: purified commiphora mukul 1 to 4, pure Boswellia serrata 0.5 to 4, purified semecarpus anacardium 0.1 to 0.4, purified powder strychnos nux vomica 0.4 to 2, pure powder of water extract Termenallia arjuna 0.3 to 2, shankha Bhusma 0.5 to 2. In accordance with this invention, the constituents are present in the following ratio: Purified Commiphora mukul 1 to 4 Pure Boswellia serrata 0.5 to 4 Purified Semecarpus anacardium 0.1 to 0.4 Purified powder Strychnos nux vomica 0.4 to 2 Pure powder of water extract Termenalia arjuna 0.3 to 2 Shankha Bhusma 0.5 to 2 Further, any one or more of the following constituents are added in the following ratio: Rubia cordifolia 0.05 to 1 Or Bacopa monnieri 0.5 to 3 0.5 to 3 orTriphala 0.5 to 3 and Trikatu 0.5 to 3 Specifically, an advantageous ratio is: Purified Commiphoramukul 3.7 Pure Boswellia serrata 3.0 Purified Semecarpus anacardium 0.1 Purified powder Strychnos nux vomica 1.0 Pure powder-water extract Term en alia arjuna bark 0.7 ShankhaBhusma 1.5 EXAMPLE Composition of atherogenic diet: Atherogenic diet consists of cholesterol rich-rabbit chow, cabbage and gram in the same amount as in control rabbits. Atherogenic diet is made as follows: The chow is powdered and mixed with the following items in a specific ratio as given below and again pellet is made. It is dried in oven and kept in refrigerator. At one time, diet was prepared only for 4 days. Composition of diet: Rabbit chow 57% Milk powder 14% Yeast powder 04% Salt 01% Multivitamin 0.1% Cholesterol 05% Hydrogenated fat 17% Cholic acid 01% Experimental details: Male rabbits were randomly divided into 3 groups, having 12 animals in each. They were kept for 15 days for acclimatization in the laboratory condition. During this period, de-worming was done to each animal and Hostacycline and Vimeral was given in drinking water. The animals were divided into the following groups : Control diet (CD) Atherogenic diet (AD) Atherogenic diet-BHUx 60mg/100g body weight (AD40) Control diet consists of rabbit chow, cabbage and gram 400g/day and water ad libitum. Atherogenic diet was given to the rabbits in the control group, 3 months later, BHUx was given in the experimental group alongwith the atherogenic diet for another 3 months. Therefore, total duration of the experiment was of 6 months. After every one month, lipid profile was carried out in blood and at the end of experiment, animal was sacrificed and heart, liver, kidney, dorsal aorta were saved. These tissues were processed for histological studies. Sections of 5 micron thickness were cut and stained with different stains. In the AD groups (Experimental control) only 2 ml of gum acacia suspension in distilled water (5%) was given in the similar way. Lipip profile was carried out by using Zydus Path line kits (a group and Cadila Healthcare Ltd.) in terms of cholesterol, TG, LDL and HDL. After 3 months, animals were sactificed to collect heart and dorsal aorta (A) Histology: (1) Study with Dorsal Aorta - It was separated from the heart at the point of aortic arch origin and longitudinally cut open. It was stained in Sudan IV stain. After making a tracing of the atherogenic patches, the tissue was fixed and processed for block preparation and section cutting. (2) Study with aortic arch and coronary artery - Whole heart was divided into 2 parts, named H1 and H2. The upper HI part was cut at 6 u thickness and stained with Heraatoxylin and Eosin (H&E). Microscopic study was made in tiie region of aortic arch and coronary artery with reference to intimal thickening. These sections were separately stained with specific stains for the visualisation of collagen tissue and calcium deposition. (3) Study with kidney and liver, - Sections were stained with H&E and with AgNO3 separately to evaluate the degree of fibrosis and necrosis. (B)Biochemical tests - Blood of each animal was selected and plasma/serum was isolated as per need to assay SGOT, SGPT, Alkaline phosphatase and complete lipid profile. (C)In vitor assay - To study the effect of the preparation of the present invention on cyclooxygenase and lipoxygenase, in vitro enzyme assay was carried out by using standard oxygraph technique. The results show that the preparation of the present invention is more sensitive to Cox-2 inhibition than the Cox-1. Similarly, on Lipoxygenase assay, it showed high sensitivity to the 15-Lipoxygenase than the other isoenzymes. Brief description of the accompanying drawings and tables related to result: Fig.l: Bar diagram showing lipid profile with raised HDL. WE CLAIM; 1. A polyherbal preparation useful for the prevention of atherosclerosis and hyperlipidemia comprising a mixtue of 1 to 4 purified commiphora mukul, 0.5 to 4 pure Boswellia serrata, 0.1 to 0.4 purified semecarpus anacardium, 0.4 to 2 purified powder strychnos nux vomica, 0.3 to 2 pure powder of water extract of Termenallia arjuna, 0.5 to 2 shankha Bhusma, adding Rubia Cordifolia Bacoparmonnieri or Triphala and Trikatu. 2. A polyherbal preparation as claimed in claim 1 wherein the following constituents are added in the following ratio: Rubia cordifolia 0.05 to 1 or Bacopa monnieri 0.5 to 3 or Triphala 0.5 to 3 and Trikatu 0.5 to 3 3. A polyherbal preparation as claimed in claim 1 wherein the constituents are present in preferable ratio of Purified Commiphora mukul 3.7 Pure Boswellia serrata 3.0 Purified Semecarpus anacardium 0.1 Purified powder Strychnos nux vomica 1.0 Pure powder-water extract Termenalia arjuna Bark 0.7 Shankha Bhusma 1.5 4. A polyherbal preparation as herein described and illustrated in the Examples.

Full Text

FIELD OF INVENTION
This invention relates to a novel polyherbal preparation for the prevention of Atherosclerosis and Hyperlipidemia.
BACKGROUND OF INVENTION
Atherosclerosis is one of the major problems for young age death. It is an active process of inflammation and cell proliferation. It starts when normal vascular functions go away. Basically, there is blockage in the coronary artery, which leads to the heart attack. This blockage could be due to deposition of lipid, formation of wound or sudden release of lipid from the endotheliat wall due to bursting of plaque. Stow and gradual deposition of fat in the intimal layer of artery is called fatty lesion or plaque. Slowly these fatty lesions get fibrosed and calcium is deposited in it. Initially, it is a reversible process but after fibrosis, it becomes irreversible. In fact, fat deposition in the blood vessel is a natural process with aging, but in some individuals, its rate of formation is significantly high and therefore leads to pathological state of coronary artery disease.
There are several reasons for this deposition. However, the basic cause is considered to be the faulty metabolism of lipid in the body. High cholesterol diet or high level of endogenous cholesterol synthesis in die body is the basic cause of artherosclerosis. Of course, there are several precipitating factors for this pathology, such as stress, smoking, diabetes, hypertension, age, male sex, family history leading to elevated homocystein, high serum lipoprotein-a and infection withcytorn egalovirus or chlamydia. More free radical production leading to rapid oxidation of LDL, followed by the excess uptake of oxidised LDL by the macrophages leading to the formation of foam cells is the basic pathology.
PRIOR ART
As this disease is multi-factorial, there are several approaches to manage artherosclerosis. First and foremost, it is to reduce die lipid load in the body or to increase the HDL content or to reduce the burden of free radicals and oxidized LDL or to remove foam cells and fatty lesions. There are two major steps, (a) Prevention of the formation of fatty plaque; (b) Regression of plaque already formed. At present, there are two main approaches for the management of atherosclerosis (1) Invasive techniques; and (2) Non-invasive techniques. In the non-invasive group of techniques, the most prominent approach is to lower the blood lipid, specially the cholesterol and triglycerides. In this approach, the main pathway is to inhibit the endogenous cholesterol synthesis by blocking the HMG-Co synthase. A drug known is different kind of Statins. In this way, there is reverse cholesterol transport from the tissue to the blood leading to the lowering of the LDL and VLDL. Several medicinal plants products are also available with a hypolipidemic claims, eg. Commiphoraraukul, Terminalia arjuna, Acorus calamus, etc.. In fact, ayurvedic literature discloses such plant names, but not much scientific study has been made with these plants.
Yet another approach is to increase the HDL in the blood. Unfortunately, there is no good medicine, which can increase the serum HDL. The exercise is the only way to achieve this goal. Use of cow butter/milk has also shown the property of raising serum HDL upto some extent, but it can not be used as a medicine in the patients of hyp erlip idem ia and arthero sclerosis. Third approach is to prevent die oxidation of LDL hi the blood, because ox LDL is the basic cause of foam celt formation and thereafter its deposition in the arterial wall, forming arthero sclerotic plaque. To achieve this goal, anti-oxidants are being recommended as the diet supplements. Although the use
of antioxidants has increased significantly as a diet supplement in the management of artherosclerosis and other coronary artery diseases, but does not fall in the group of therapeutic medicine, because of its non-specific role. Metal chelaters are also used to prevent the formation of free radicals, because iron mediated Fenton's reaction is one the basic cause of hydroxyl radical production.
Alter knowing the molecular pathway of atheroma formation, gene therapy is being tried in the management of this disease. It is reported that stable atheroma is not as dangerous as the unstable one. For this unstability, a group of proteases known as MMPs (Matrix Metallo proteinases) are responsible. In fact, they digest the fibrous cap of the plaque and allow the lipid to come out of the plaque and block the arterial blood flow. Attempts are now being made to introduce the genes to inhibit these MMPs. Similarly, the most recent approach of gene therapy is to inhibit a growth factor M-CSF (Macrophage colony stimulating factor), which is responsible for the proliferation of smooth muscle cells and rapid formation of foam cell leading to their deposition.
One more approach to manage arthero sclerosis is to regulate the inflammatory cytokines and various enzymes like lipoxygenase and cyclooxygenase, because inflammation is one of the basic factors, responsible for plaque formation.
Since arthero sclerosis is a multietio logical factor disease, so doctors recommend a series of medicine to manage this disease and still the disease is not manageable because of uncoordinated approach. However, there is no medicine which can target several ettological factors simultaneously by giving one tablet. The patient is supposed to take several medicines in a day, which gives him a kind of psychological depression. These medicines,w hen
given in isolation does not give significant impact on the prevention of atheromalformation, because other factors become more prominent The gene therapy, which is being developed is at the infancy stage and if at ail, it comes to the public use, it will be very expensive and also with several side effects, only the time will tell for its success.
There are many claims to prevent the formation of plaque, by reducing the risk factors, by taking more antioxidants or by lowering the cholesterol by the use of several hypolipidemic drugs like Statins, etc.. Once athero ma is detected, the coronary bypass, etc. are the only remedies. In fact, no good drug is available to regress the plaque, already formed.
OBJECTS OF THE INVENTION
An object of this invention is to propose a novel polyherbal preparation which has the capacity to target several etiological pathways, and finally lead to atherosclerosis.
Another object of this invention is to propose a novel polyherbal preparation which is anti-inflammatory, anti-oxidant and increases serum HDL, and more specifically, it inhibits Lox-15, Cox-2 and Ca-deposition in the plaque, increases Collagen in the chronic plaques, increases serum HDL and decreases serum TG.
Still another object of this invention is to propose a novel polyherbal preparation which enhances serum HDL and prevents plaque formation even in the presence of high serum lipid.
Yet another object of this invention is to propose a novel polyherbal prepara-tion which enhances the collagen tissue in the old plaque indicating towards the stabilisation of the plaque.
A further object of this invention is to propose a novel polyherbal preparation which inhibits the Cyclooxygenase-2 and lipoxygenase-15, which are responsible for atherosclerosis.
A still further object of this invention is to propose a novel polyherbal preparation which is cost-effective, more effective than its component medicinal plant and does not have any toxic or side effect with high therapeutic safety margin.
DESCRIPTION OF INVENTION
According to this invention, there is provided a polyherbal preparation useful for the prevention of atherosclerosis and hyperlipidemia comprising a mixture of:
purified commiphora mukul 1 to 4,
pure Boswellia serrata 0.5 to 4,
purified semecarpus anacardium 0.1 to 0.4,
purified powder strychnos nux vomica 0.4 to 2,
pure powder of water extract Termenallia arjuna 0.3 to 2,
shankha Bhusma 0.5 to 2.
In accordance with this invention, the constituents are present in the following ratio:
Purified Commiphora mukul 1 to 4
Pure Boswellia serrata 0.5 to 4
Purified Semecarpus anacardium 0.1 to 0.4
Purified powder Strychnos nux vomica 0.4 to 2
Pure powder of water extract Termenalia arjuna 0.3 to 2
Shankha Bhusma 0.5 to 2
Further, any one or more of the following constituents are added in the following ratio:
Rubia cordifolia 0.05 to 1
Or Bacopa monnieri 0.5 to 3

0.5 to 3
orTriphala 0.5 to 3
and Trikatu 0.5 to 3
Specifically, an advantageous ratio is:
Purified Commiphoramukul 3.7
Pure Boswellia serrata 3.0
Purified Semecarpus anacardium 0.1
Purified powder Strychnos nux vomica 1.0
Pure powder-water extract Term en alia arjuna
bark 0.7
ShankhaBhusma 1.5
EXAMPLE
Composition of atherogenic diet:
Atherogenic diet consists of cholesterol rich-rabbit chow, cabbage and gram
in the same amount as in control rabbits. Atherogenic diet is made as
follows:
The chow is powdered and mixed with the following items in a specific ratio
as given below and again pellet is made. It is dried in oven and kept in
refrigerator. At one time, diet was prepared only for 4 days.
Composition of diet:
Rabbit chow 57%
Milk powder 14%
Yeast powder 04%
Salt 01%
Multivitamin 0.1%
Cholesterol 05%
Hydrogenated fat 17%
Cholic acid 01%
Experimental details:
Male rabbits were randomly divided into 3 groups, having 12 animals in each. They were kept for 15 days for acclimatization in the laboratory condition. During this period, de-worming was done to each animal and Hostacycline and Vimeral was given in drinking water. The animals were divided into the following groups : Control diet (CD) Atherogenic diet (AD)
Atherogenic diet-BHUx 60mg/100g body weight (AD40) Control diet consists of rabbit chow, cabbage and gram 400g/day and water ad libitum.
Atherogenic diet was given to the rabbits in the control group, 3 months later, BHUx was given in the experimental group alongwith the atherogenic diet for another 3 months. Therefore, total duration of the experiment was of 6 months. After every one month, lipid profile was carried out in blood and at the end of experiment, animal was sacrificed and heart, liver, kidney, dorsal aorta were saved. These tissues were processed for histological studies. Sections of 5 micron thickness were cut and stained with different stains. In the AD groups (Experimental control) only 2 ml of gum acacia suspension in distilled water (5%) was given in the similar way. Lipip profile was carried out by using Zydus Path line kits (a group and Cadila Healthcare Ltd.) in terms of cholesterol, TG, LDL and HDL. After 3 months, animals were sactificed to collect heart and dorsal aorta (A) Histology:
(1) Study with Dorsal Aorta - It was separated from the heart at the point of aortic arch origin and longitudinally cut open. It was stained in Sudan IV
stain. After making a tracing of the atherogenic patches, the tissue was fixed and processed for block preparation and section cutting.
(2) Study with aortic arch and coronary artery - Whole heart was divided
into 2 parts, named H1 and H2. The upper HI part was cut at 6 u thickness
and stained with Heraatoxylin and Eosin (H&E). Microscopic study was
made in tiie region of aortic arch and coronary artery with reference to
intimal thickening. These sections were separately stained with specific
stains for the visualisation of collagen tissue and calcium deposition.
(3) Study with kidney and liver, - Sections were stained with H&E and with
AgNO3 separately to evaluate the degree of fibrosis and necrosis.
(B)Biochemical tests - Blood of each animal was selected and plasma/serum was isolated as per need to assay SGOT, SGPT, Alkaline phosphatase and complete lipid profile.
(C)In vitor assay - To study the effect of the preparation of the present invention on cyclooxygenase and lipoxygenase, in vitro enzyme assay was carried out by using standard oxygraph technique. The results show that the preparation of the present invention is more sensitive to Cox-2 inhibition than the Cox-1. Similarly, on Lipoxygenase assay, it showed high sensitivity to the 15-Lipoxygenase than the other isoenzymes.
Brief description of the accompanying drawings and tables related to result:
Fig.l: Bar diagram showing lipid profile with raised HDL.

WE CLAIM;
1. A polyherbal preparation useful for the prevention of atherosclerosis and hyperlipidemia comprising a mixtue of 1 to 4 purified commiphora mukul, 0.5 to 4 pure Boswellia serrata, 0.1 to 0.4 purified semecarpus anacardium, 0.4 to 2 purified powder strychnos nux vomica, 0.3 to 2 pure powder of water extract of Termenallia arjuna, 0.5 to 2 shankha Bhusma, adding Rubia Cordifolia Bacoparmonnieri or Triphala and Trikatu.
2. A polyherbal preparation as claimed in claim 1 wherein the following constituents are added in the following ratio:
Rubia cordifolia 0.05 to 1
or Bacopa monnieri 0.5 to 3
or Triphala 0.5 to 3
and Trikatu 0.5 to 3
3. A polyherbal preparation as claimed in claim 1 wherein the
constituents are present in preferable ratio of
Purified Commiphora mukul 3.7
Pure Boswellia serrata 3.0
Purified Semecarpus anacardium 0.1
Purified powder Strychnos nux vomica 1.0
Pure powder-water extract Termenalia arjuna
Bark 0.7
Shankha Bhusma 1.5
4. A polyherbal preparation as herein described and illustrated in the Examples.

Documents:

1255-del-2002-Abstract (13-11-2009).pdf

1255-DEL-2002-Abstract-(02-06-2009).pdf

1255-DEL-2002-Abstract-(09-09-2009).pdf

1255-del-2002-abstract.pdf

1255-del-2002-Claims (13-11-2009).pdf

1255-DEL-2002-Claims-(02-06-2009).pdf

1255-DEL-2002-Claims-(09-09-2009).pdf

1255-del-2002-claims.pdf

1255-del-2002-Correspondence-Others (13-11-2009).pdf

1255-DEL-2002-Correspondence-Others-(02-06-2009).pdf

1255-DEL-2002-Correspondence-Others-(09-09-2009).pdf

1255-DEL-2002-Correspondence-Others-(13-08-2009).pdf

1255-del-2002-correspondence-others.pdf

1255-del-2002-correspondence-po.pdf

1255-DEL-2002-Description (Complete)-(02-06-2009).pdf

1255-DEL-2002-Description (Complete)-(09-09-2009).pdf

1255-del-2002-description (complete).pdf

1255-del-2002-drawings.pdf

1255-del-2002-Form-1 (13-11-2009).pdf

1255-DEL-2002-Form-1-(02-06-2009).pdf

1255-DEL-2002-Form-1-(09-09-2009).pdf

1255-del-2002-form-1.pdf

1255-del-2002-form-18.pdf

1255-DEL-2002-Form-2-(02-06-2009).pdf

1255-del-2002-form-2.pdf

1255-DEL-2002-Form-3-(02-06-2009).pdf

1255-del-2002-form-3.pdf

1255-del-2002-GPA (13-11-2009).pdf

1255-DEL-2002-GPA-(09-09-2009).pdf

1255-del-2002-pa.pdf

1255-del-2002-pct-101.pdf

1255-del-2002-pct-102.pdf

1255-del-2002-Petition-137 (13-11-2009).pdf

1255-DEL-2002-Petition-137-(09-09-2009).pdf

1255-DEL-2002-Petition-138-(02-06-2009).pdf

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Patent Number

238258

Indian Patent Application Number

1255/DEL/2002

PG Journal Number

6/2010

Publication Date

05-Feb-2010

Grant Date

27-Jan-2010

Date of Filing

13-Dec-2002

Name of Patentee

DEPARTMENT OF BIOTECHNOLOGY

Applicant Address

BLOCK 2, 7TH FLOOR, CGO COMPLEX, LODI ROAD, NEW DELHI-110003.

Inventors:

#	Inventor's Name	Inventor's Address
1	TRIPATHI YAMINI BHUSHAN	DEPTT OF MEDICINAL CHEMISTRY INSTITUTE OF MEDICAL SCIENCES BANARAS HINDU UNIVERSITY, VARANASI-221 005

PCT International Classification Number

A61K 35/78

PCT International Application Number

N/A

PCT International Filing date

PCT Conventions:

#	PCT Application Number	Date of Convention	Priority Country
1			NA