What is the primary mechanism of GP IIb/IIIa inhibitors?

• A. Prevent fibrinogen cross-linking
• B. Inhibit ADP-induced platelet activation
• C. Inhibit thrombin formation
• D. Activate plasminogen

Answer: (A)

GP IIb/IIIa inhibitors block the platelet receptor GP IIb/IIIa, preventing fibrinogen from binding and cross-linking activated platelets. This stops platelet aggregation at its final common pathway, regardless of how the platelets were activated (ADP, thrombin, collagen, etc.). Because of this central action, these drugs blunt aggregation rather than specifically inhibiting ADP signaling, thrombin formation, or plasminogen activation. The effect is most relevant during high-risk ACS and during PCI, where limiting platelet aggregation reduces thrombus formation.