Top-line results of the TRA-2P study have shown that Merck’s novel antiplatelet agent, vorapaxar, reduced the primary ischaemic end point of the study, but increased bleeding, including intracranial haemorrhage in a secondary prevention population.
Vorapaxar is a protease-activated receptor 1 (PAR-1) antagonist that blocks thrombin-induced platelet activation and therefore inhibits platelets by a different mechanism to other available antiplatelet drugs.
The TRA-2P study involved 26,449 patients with myocardial infarction (MI), ischaemic stroke, or peripheral vascular disease. Addition of vorapaxar to standard of care is reported to have significantly reduced the risk of cardiovascular death/MI/stroke/urgent coronary revascularisation (composite primary end point), but at the cost of increased bleeding. However, there was a lower risk of intracranial haemorrhage in patients without a history of stroke. The full results of TRA-2P will be presented at the American College of Cardiology meeting in March.
This is the second large-scale trial of vorapaxar. The first, TRACER, reported at last year’s American Heart Association meeting, showed just a trend towards a reduction in ischaemic events but a large increase in bleeding in acute coronary syndrome patients.
