What is the mechanism of action for vorapaxar?

Vorapaxar is an antiplatelet agent that specifically acts as an antagonist of the protease-activated receptor-1 (PAR-1). This receptor is activated by thrombin, leading to platelet activation and aggregation. By blocking the tethered ligand mechanism associated with PAR-1, vorapaxar effectively inhibits thrombin-induced platelet activation.

This inhibition is crucial for reducing the risk of thrombotic cardiovascular events as it prevents platelets from aggregating inappropriately. Understanding the specific interaction of vorapaxar with the thrombin pathway is essential for utilizing this drug in clinical settings for patients at risk of cardiovascular disease.

The other response options do not accurately represent vorapaxar's primary mechanism of action. For instance, inhibitors of phosphodiesterase type 3 (PDE3) and GP IIb/IIIa activators are linked to different classes of antiplatelet therapies that work via distinct pathways. Similarly, increasing fibrinogen levels does not align with vorapaxar's role, as the drug's focus is on platelet activity rather than manipulating fibrinogen levels.