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[india-drug] Re: Drug query on Asmon and Buspiron (2)


  • From: "Sampada Patvardhan" <dicmspc@yahoo.co.in>
  • Date: Mon, 5 Jun 2006 08:53:12 +0100 (BST)

Drug query on Asmon and Buspiron (2)
**********

Following is the information on ASMON which I could get with reference to your query.

Dr. (Mrs.) Sampada Patvardhan (Ph.D.Tech. Pharmacology)
Director, Maharashtra State Pharmacy Council?s Drug Information Centre E.S.I.S. Hospital Compound, L.B.S. Marg, Mulund (W), Mumbai-400 080
Email: Sampada Patvardhan <dicmspc@yahoo.co.in>

ASMON - A MEDICINE FOR ASTHMA

What is ASMON

A group of Scientists at the Indian Institute of Chemical Biology (a unit of CSIR), Kolkata, developed ASMON, a plant based product having plants known to be used by the people over the centuries. The technology has been transferred to M/s HERBO CHEM PVT. LTD., Kolkata. The company received the Drug License for ASMON as a traditional medicine. Bronchial asthma patients of all ages can take this medicine safely. Working on the inhibition of arachidonic acid oxidationby the preparation, it has been proposed as an anti-leukotriene asthma medicine.

Causes of asthma and current drugs
In an asthmatic attack inflammation involves all or part of the main air passage of the lungs. A large and sometimes massive influx of a blood cells (eosinophils) and other inflammatory cells invade the airway wall, which in turn bring about the swelling and mucus secretion in that narrow passage. Biologically active compound leukotrienes are supposed to be the causative agents and prevention of their production by blocking of the oxidation of Arachidonic Acid (AA) by 5-lipoxygenase is thought to be the best treatment. The new class of drugs namely anti-leukotrienes, represent a new direction in the treatment of this disease3,4. Synthetic drugs developed in this direction and introduced in the west are associated with possible side effects, which have restricted their use.

How does ASMON work?
ASMON inhibits oxidation of the arachidonic acid in an ex vivo blood assay system wherein the blood cells were stimulated by calcium ionopher or known stimulator to enhance their oxidative activity. It is known that Guinea pig blood incubated with arachidonic acid, upon stimulation with the stimulator, such as calcium ionophore (A23187) shows 10-fold increase in leukotriene B4 production from the arachidonic acid path way. IICB's experiment with both human and Guineapig blood cells showed ADMON's strong activity in inhibiting Arachidonic acid oxidation2. All the leukotriences including LK B4, formed from the oxidation of arachidonic acid are considered as the principal mediator of asthma, since leukotrienes are the molecules that contribute to the inflammation, swelling (edema), bronchoconstriction (tightening of muscles around the airways) and mucous secretion seen in the airways of patients with asthma. Any substance that inhibits the oxidation of the arachidonic acid
may be considered a potential therapeutic agent for the treatment of bronchial asthma1. ASMON helps to control asthma symptoms including the acute breathing problem arising out of bronchial asthma. ASMON offers asthma patients a new treatment option to enhance the control of their asthma by inhibiting the oxidation of Arachidonic acid. ASMON users have improved airway function with gradual elimination of the currently used medication. When used by patients with mild-to-moderate-to-acute asthma, who were using the inhaled beta-agonists daily, ASMON decreased the number of beta-agonist puffs needed per day gradually. In a few cases the inhaled beta-agonists puffs have been stopped totally. The reduction in the use of these medications was accompanied by improvements in the lung function. Daytime and night-time symptoms have shown dramatic improvements in many patients.

DOSE OF ASMON.
ASMON is recommended for treatment of all cases of bronchial asthmatic problems including acute episodes. This is purely a herbal drug. It is derived from plants known for human use over centuries and is quite safe.
The recommended dosage of ASMON is two to three, 500-mg capsules, or tour to five 300-mg per day or as per the physician" s advice. For liquid preparation the recommended dose is 2 spoon full thrice daily before breakfast and two meals.

References
1. Biochem, Pharmacol,1992 Jan 22, 43, 337-82
2. IICB, Data file: Results of inhibition of Arachidonic acid oxidation by ASMON
3. Lipworth BJ; Leukotriene receptor antagonist Lancet: 1999, 353, 57-62
4. Holgate ST, Sampson AP; Antileukotriene therapy Future direction, Am.J. Respir, Crit. Care Med. 2000, 161, S141-S153.
ASMON

MANUFACTURED BY:

HERBOCHEM REMEDIES INDIA (P) LTD.
REGD. OFFICE & WORKS AT: NARENDRAPUR-743508
SALES OFFICE: 45, PRATAP ADITYA PLACE
CALCUTTA-700 026

Phone: 033-466 6059
033-463 5942
COMPOSITION:
M. paniculata Linn.Syn. M. exotica 90 mg.
H. abelmoschus 50mg
T. ammi 50mg
S. aromaticum 10 mg.
A. vasica Nees 100 mg.
E. hirta 100 mg.
M. koiniegii 100 mg.

Additional Information of Asthma Drug
Inhibition of leukotriene synthesis is one of the major approaches as leukotrienes are accepted as the major mediators of asthma. Th2 cytokines are also involved in the late phase asthmatic reactions, the additional approach is based on the inhibition of these Th2 cytokine (IL-4) synthesis and enhancement of Th1 cytokine (IFN-gamma) production.
The prepared fraction (MK-5) showed inhibition of 5- lipooxygenase mediated arachidonic acid oxidation signifying blockage of leukotriene synthesis and shifting towards Th1 type response from Th2 type. Fraction MK5 blocked leukotriene synthesis and upregulated Th1 type resonse which enhances IFN-gamma production.
In addition, MK5 also augmented IL-2 and TNF-alpha production without having significant effect on Th2 type response (IL-4). On the other hand, fraction J-7-C has only marginal effect on leukotriene synthesis but significantly reduced Th2 response and enhanced Th1 type response. Combinations of MK5 and J07-C inhibited leukotriene synthesis, suppressed Th2 response and enhanced Th1 response and thus blocking the asthma producing symptoms by two-prong effect i.e. by mediating lymphokine pathway (IL-2, IL-R4, IFN-gamma and TNF-alpha) and leukotriene pathway.