What is the mechanism of action of Clopidogrel?

Clopidogrel is an antiplatelet medication that functions primarily by blocking ADP receptors on platelets. When clopidogrel is administered, it is metabolized in the liver to its active form, which then irreversibly binds to the P2Y12 subtype of ADP receptors on the surface of platelets. This action prevents ADP from binding to these receptors, inhibiting platelet activation and aggregation, which is crucial in preventing thrombus (blood clot) formation.

By blocking the ADP receptors, clopidogrel effectively reduces the ability of platelets to aggregate, which is a key step in the formation of blood clots, especially after vascular injury. This mechanism of action is particularly important in patients who are at risk for thrombotic events, such as those with coronary artery disease or those undergoing certain types of cardiovascular procedures.

In contrast, other choices describe different mechanisms or processes that are not relevant to clopidogrel's action. For instance, inhibiting cyclooxygenase-1 pertains to how Aspirin works, enhancing thromboxane A2 production is related to promoting platelet activation (which clopidogrel opposes), and increasing fibrinogen levels does not accurately depict clopidogrel's action