Clopidogrel (clopidogrel bisulfate)

Clopidogrel bisulfate, a thienopyridine P2Y12 platelet adenosine diphosphate (ADP)-receptor antagonist, is a platelet-aggregation inhibitor.

Clopidogrel bisulfate, a thienopyridine derivative structurally and pharmacologically related to ticlopidine, is a platelet-aggregation inhibitor. Clopidogrel is a prodrug with its platelet-aggregation inhibitory activity dependent on hepatic transformation to an active thiol metabolite.

Biotransformation occurs through a 2-step process where clopidogrel is initially oxidized to a 2-oxo-clopidogrel intermediate metabolite, then subsequently metabolized to the active thiol metabolite. This metabolic pathway has been shown to be mediated by several cytochrome P-450 isoenzymes (e.g., CYP2C19, CYP3A, CYP2B6, CYP1A2). In particular, the CYP2C19 isoenzyme is involved in the formation of both the active metabolite and the 2-oxo-clopidogrel intermediate.

Clopidogrel is an ADP-receptor antagonist; the active metabolite of clopidogrel binds selectively and noncompetitively to a low-affinity, P2Y12 ADP-receptor binding site on the surface of platelets, thereby inhibiting ADP binding to the receptor and subsequent activation of the platelet glycoprotein (GP IIb/IIIa) complex necessary for fibrinogen-platelet binding. Clopidogrel also inhibits ADP-mediated release of platelet dense granule (e.g., ADP, calcium, and serotonin) and alpha granule (e.g., fibrinogen and thrombospondin) contents that augment platelet aggregation. The low-affinity ADP receptor is irreversibly modified by the drug, so platelets exposed to clopidogrel remain affected for the remainder of their lifespan (about 7-10 days).

Unlike aspirin, thienopyridine platelet-aggregation inhibitors such as clopidogrel and ticlopidine do not inactivate platelet cyclooxygenase to prevent synthesis of prostaglandin endoperoxides and thromboxane A.

Clopidogrel is rapidly absorbed after oral administration; at least 50% of an oral dose is absorbed. Peak plasma concentrations of the active metabolite occur approximately 30-60 minutes following an oral dose. When clopidogrel 75 mg is administered daily, inhibition of platelet aggregation is apparent on the first day of therapy, with 40-60% inhibition being achieved at steady state between days 3-7.

Following discontinuance of the drug, platelet aggregation and bleeding time generally return to baseline values within about 5 days.

USES: Clopidogrel is used to prevent heart attacks and strokes in persons with heart disease (recent heart attack), recent stroke, or blood circulation disease (peripheral vascular disease). It is also used with aspirin to treat new/worsening chest pain (new heart attack, unstable angina) and to keep blood vessels open and prevent blood clots after certain procedures (such as cardiac stent). Clopidogrel works by blocking platelets from sticking together and prevents them from forming harmful clots.

It is an antiplatelet drug. It helps keep blood flowing smoothly in your body.

Generic name: clopidogrel bisulfate
Pronunciation: (kloe-PID-oh-grel)

The following indications are listed for Clopidogrel:

• Acute Coronary Syndrome
• Cerebral Thromboembolism Prevention
• Myocardial Reinfarction Prevention
• Peripheral Arterial Thromboembolism Prevention
• Thrombosis Prevention After Percutaneous Coronary Intervention

Also known as: Maintenance Therapy Of Thrombosis Prevention After Pci, Myocardial Reinfarction Prophylaxis, Peripheral Artery Thromboembolism Prophylaxis, Stroke Thromboembolism Prophylaxis, Thrombosis Prophylaxis After Percutaneous Coronary Intervention, Vascular Thrombosis Prevention After Percutaneous Coronary Intervention.

No ICD codes are available for this drug.