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Vicagrel is a novel oral antiplatelet pro-drug and a thienopyridine derivative designed to inhibit platelet aggregation by antagonizing the P2Y12 ADP receptor on platelets. It is structurally related to clopidogrel but differs in its metabolic activation pathway; vicagrel is hydrolyzed by esterases (including CES2 and AADAC) in the intestine and liver to form 2‑oxo‑clopidogrel, which is then converted into its active metabolite. This mechanism bypasses CYP2C19-dependent activation required for clopidogrel, potentially reducing variability in response due to genetic polymorphisms. Vicagrel demonstrates rapid onset of action, dose-dependent inhibition of ADP-induced platelet aggregation, and greater potency compared with clopidogrel. It has been developed primarily for the prevention of thrombotic events in acute coronary syndromes, peripheral arterial disorders, stroke, and thrombosis[3][4][5][6][7].
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