CLOPIDOGREL

Clopidogrel is a thienopyridine that irreversibly inhibits platelet ag gregation by selectively binding to adenylate cyclase-coupled ADP rece ptors on the platelet surface. In animal models, clopidogrel reduced t he formation of bath arterial and venous thrombi. After oral administr ation, clopidogrel is rapidly absorbed and undergoes metabolic activat ion in the liver. The principal circulating metabolite is SR 26334, an inactive carboxylic acid derivative. The active metabolite is not yet known. Findings of a large, well controlled study of clopidogrel vers us aspirin in patients with atherosclerotic vascular disease (CAPRIE s tudy) indicate that clopidogrel has superior efficacy in terms of prev ention of ischaemic stroke, myocardial infarction and vascular death. Clopidogrel-treated patients experienced less frequent gastrointestina l upset, abnormal liver function and gastrointestinal haemorrhage than patients who received aspirin, but more frequent rash and diarrhoea. Neutropenia and thrombocytopenia occurred rarely and at similar rates in both groups.