Clopidogrel irreversibly antagonizes the platelet ADP receptor P2T, resulting in 50-70% inhibition of platelet fibrinogen binding, and is associated with reduced gastrointestinal hemorrhage compared to aspirin.
Antiplatelet compounds interfere with the platelet activation cascade at different levels. The antiplatelet effect of the thienopyridine, clopidogrel, results from antagonism of a platelet ADP receptor, P2T, resulting in inhibition of platelet activation. This antagonism is non-competitive, irreversible, and results in a 50-70% inhibition of platelet fibrinogen binding. Additionally, clopidogrel may also antagonize the ADP-induced inhibition of adenylate cyclase, possibly resulting in an elevated platelet cyclic adenosine monophosphate level after stimulation by an appropriate agonist, such as prostacyclin. This spectrum of antiplatelet activities is different from that of aspirin. Further, clopidogrel is associated with a reduction in gastrointestinal hemorrhage, making it a valuable therapeutic alternative to aspirin in oral, long-term prevention of atherothrombotic vascular occlusion.
Karsten Schrör (1998) conducted a review in Atherothrombotic vascular occlusion. Clopidogrel vs. Aspirin was evaluated on Platelet fibrinogen binding inhibition. Clopidogrel irreversibly antagonizes the platelet ADP receptor P2T, resulting in 50-70% inhibition of platelet fibrinogen binding, and is associated with reduced gastrointestinal hemorrhage compared to aspirin.