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Plavix - clopidogrel bisulfate

By: Ralph Exxor

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Plavix (Clopidogrel) is used to prevent strokes and heart attacks.

Clopidogrel is an oral antiplatelet agent (thienopyridine class) to inhibit blood clots in coronary artery disease, peripheral vascular disease, and cerebrovascular disease. It is marketed by Bristol-Myers Squibb and Sanofi-Aventis under the trade name Plavix, by Sun Pharmaceuticals under the trade name Clopilet, by Ranbaxy Laboratories under the trade name Ceruvin. It works by irreversibly inhibiting a receptor called P2Y12. Adverse effects include hemorrhage.

Clots in the blood cause more than 90% of heart attacks and more than 85% of strokes. And, once you've experienced one clot-related condition, your risk of another never goes away.

PLAVIX is proven to help keep platelets from sticking together and forming clots, which can help protect against a future heart attack or stroke.

Plavix keeps the platelets in your blood from coagulating (clotting) to prevent unwanted blood clots that can occur with certain heart or blood vessel conditions.

Plavix is used to prevent blood clots after a recent heart attack or stroke, and in people with certain disorders of the heart or blood vessels.
Plavix may also be used for other purposes not listed in this medication guide.
Plavix is a pro-drug whose action may be related to adenosine diphosphate (ADP) receptor on platelet cell membranes. The specific subtype of ADP receptor that clopidogrel irreversibly inhibits is P2Y12 and is important in platelet aggregation and the cross-linking of platelets by fibrin.[1] The blockade of this receptor inhibits platelet aggregation by blocking activation of the glycoprotein IIb/IIIa pathway. The IIb/IIIa complex functions as a receptor mainly for fibrinogen and vitronectin but also for fibronectin and von Willebrand factor. Activation of this receptor complex is the "final common pathway" for platelet aggregation, and is important in the cross-linking of platelets by fibrin.

Platelet inhibition can be demonstrated two hours after a single dose of oral clopidogrel, but the onset of action is slow, so that a loading-dose of 300-600 mg is usually administered.

Pharmacokinetics and metabolism

After repeated 75-mg oral doses of clopidogrel (base), plasma concentrations of the parent compound, which has no platelet inhibiting effect, are very low and are generally below the quantification limit (0.000258 mg/L) beyond 2 hours after dosing.

Clopidogrel is a pro-drug activated in the liver by cytochrome P450 enzymes, including CYP2C19. The active metabolite has an elimination half-life of about 8 hours and acts by forming a disulfide bridge with the platelet ADP receptor. Patients with a variant allele of CYP2C19 are 1.5 to 3.5 times more likely to die or have complications than patients with the high-functioning allele.[6][7][8]

Following an oral dose of 14C-labeled clopidogrel in humans, approximately 50% was excreted in the urine and approximately 46% in the feces in the 5 days after dosing.

Effect of Food: Administration of PLAVIX (clopidogrel bisulfate) with meals did not significantly modify the bioa vailability of clopidogrel as assessed by the pharmacokinetics of the main circulating metabolite.

Absorption and Distribution: Clopidogrel is rapidly absorbed after oral administration of repeated doses of 75 mg clopidogrel (base), with peak plasma levels (appx. 3 mg/L) of the main circulating metabolite occurring approximately 1 hour after dosing. The pharmacokinetics of the main circulating metabolite are linear (plasma concentrations increased in proportion to dose) in the dose range of 50 to 150 mg of clopidogrel. Absorption is at least 50% based on urinary excretion of clopidogrel-related metabolites. Clopidogrel and the main circulating metabolite bind reversibly in vitro to human plasma proteins (98% and 94%, respectively). The binding is nonsaturable in vitro up to a concentration of 110 ?g/mL.

Metabolism and Elimination: In vitro and in vivo, clopidogrel undergoes rapid hydrolysis into its carboxylic acid derivative. In plasma and urine, the glucuronide of the carboxylic acid derivative is also observed.

Clopidogrel is an anti-platelet drug, that is, a drug that inhibits the ability of platelets to clump together as part of a blood clot. It is similar to ticlopidine (Ticlid) in chemical structure and in the way it works. Unlike ticlopidine, clopidogrel does not cause serious reductions of white cells in the blood and, therefore, routine blood testing to determine if the white blood cell count is low is not necessary during treatment. The risk of heart attacks and strokes (which usually are caused by blood clots) is increased in patients with a recent history of stroke or heart attack and patients with peripheral vascular disease. (Peripheral vascular disease is the same as atherosclerotic arterial disease or "hardening" of the arteries in which the arteries become narrowed. It frequently occurs in the legs and often causes claudication or pain in the legs upon walking). Clopidogrel is used to reduce the risk of heart attacks and strokes in these patients. Plavix was approved by the FDA in 1997.

Article Source: http://depositarticles.com/

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