Vorapaxar acts primarily by blocking which structure?

Vorapaxar primarily acts by blocking the tethered ligand, specifically the thrombin receptor (protease-activated receptor-1 or PAR-1) on platelets. This receptor is crucial for platelet activation and aggregation in response to thrombin, a potent pro-aggregatory substance in the coagulation cascade. When thrombin binds to PAR-1, it initiates a cascade of intracellular signaling events that lead to platelet activation and aggregation.

By inhibiting this receptor, vorapaxar effectively disrupts the signaling pathway necessary for platelet activation, thereby reducing the potential for thrombosis. This mechanism is particularly useful in preventing events like myocardial infarction and stroke in patients with a high risk of blood clot formation.

The other options, while related to platelet function and coagulation, do not accurately describe the primary action of vorapaxar. Cyclic AMP is a secondary messenger involved in broader signaling processes and does not represent the direct action of vorapaxar. Platelet aggregation is a consequence of various signaling pathways rather than a structure that can be blocked directly by a drug. Fibrin polymerization is a later step in the coagulation cascade that is not directly affected by vorapaxar's mechanism of action. Thus,