Antiplatelet drugs act on distinct mechanisms of platelet function—adhesion/aggregation (mediated by the glycoprotein IIb/IIIa receptor), and release (mediated by thromboxane A2 and ADP)—and are classified accordingly: cyclooxygenase inhibitors (irreversible, blocking thromboxane A2 synthesis), glycoprotein IIb/IIIa inhibitors (blocking adhesion/aggregation directly), ADP receptor inhibitors (irreversible or reversible, some requiring hepatic activation), and phosphodiesterase inhibitors (increasing cyclic AMP via dual mechanisms to reduce platelet aggregation). This distinction between irreversible versus reversible inhibition, and between the different molecular targets in platelet physiology, is the organizing framework within pharmacology of antithrombotic/antiplatelet therapy.
Antiplatelet drugs act on distinct mechanisms of platelet function—adhesion/aggregation (mediated by the glycoprotein IIb/IIIa receptor), and release (mediated by thromboxane A2 and ADP)—and are clas…