Clopidogrel is a prodrug requiring hepatic bioactivation. Its mechanism of antiplatelet action once activated is:

• A Reversible competitive antagonism of the ADP receptor P2Y12 on platelets
• B Irreversible inhibition of thromboxane synthase, reducing TXA2-mediated platelet activation
• C Reversible inhibition of glycoprotein IIb/IIIa receptors, preventing fibrinogen binding
• D Irreversible covalent blockade of the P2Y12 (ADP) receptor on platelet membranes ✓

Explanation

Clopidogrel (a thienopyridine) is converted by hepatic CYP2C19 (and CYP3A4) to an active thiol metabolite that irreversibly and covalently binds the P2Y12 ADP receptor on platelets, preventing ADP-mediated platelet activation and aggregation for the platelet's entire 7–10 day lifespan. CYP2C19 poor metabolisers (loss-of-function variants) have reduced conversion and diminished antiplatelet effect — a clinically important pharmacogenomic interaction. Prasugrel and ticagrelor are newer alternatives with more consistent P2Y12 inhibition.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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