What is the mechanism of action of clopidogrel?

Clopidogrel exerts its therapeutic effects primarily by blocking platelet aggregation through its action on the P2Y12 receptor. This receptor is a subtype of purinergic receptors that plays a critical role in the activation of platelets. When ADP (adenosine diphosphate) binds to the P2Y12 receptor on the platelet surface, it leads to a cascade of intracellular signaling events that enhance platelet activation and recruitment, promoting the formation of a platelet plug during the clotting process.

Clopidogrel is classified as a thienopyridine, and it works as a pro-drug. After metabolic activation, it irreversibly binds to the P2Y12 receptor. This binding inhibits the effects of ADP, thereby preventing the activation of the glycoprotein IIb/IIIa complex, which is essential for platelet aggregation. As a result, clopidogrel is effective in reducing the risk of thrombotic events, such as heart attacks and strokes, in patients at risk.

In summary, clopidogrel's mechanism of action is centered on its ability to inhibit the P2Y12 receptor on platelets, leading to decreased platelet aggregation and a reduced risk of thrombosis.