What is the mechanism of action for P2Y12 inhibitors?

P2Y12 inhibitors function primarily by blocking the P2Y12 receptor on platelets. This mechanism is crucial because the P2Y12 receptor is a key component in the platelet activation process. When adenosine diphosphate (ADP) binds to this receptor, it triggers a cascade of events that leads to increased platelet aggregation and activation, promoting clot formation.

By inhibiting the P2Y12 receptor, these agents prevent ADP from exerting its effect, which in turn reduces platelet activation and aggregation. This action is particularly beneficial in preventing thrombotic events, such as those that can occur in coronary artery disease or after stent placement.

The other options do not describe the action of P2Y12 inhibitors accurately. For instance, reducing blood viscosity is unrelated to the specific mechanism through which these drugs exert their effects on platelets. Similarly, promoting thromboxane production and stimulating fibrinogen binding do not align with the P2Y12 inhibitors' targeted pathway of blocking platelet activation via the P2Y12 receptor. This understanding of the mechanism underscores the role of P2Y12 inhibitors in antithrombotic therapy.