Dual antiplatelet therapy has been the standard therapy in the management of patients with acute coronary syndrome. It involves the use of aspirin along with a thienopyridine, like clopidogrel. However, it has been found that these patients had recurrent ischemic attacks even when on the dual therapy and hence a congener was introduced known as prasugrel which is a third generation thienopyridine. This has recently been approved by United States Food and Drug Administration (FDA). Although structurally similar to clopidogrel, it is found to be more potent, rapidly acting and with better levels of platelet inhibition. Unlike clopidogrel, it promises less inter patient variability in its responsiveness. It is a prodrug which is converted to its active metabolite in liver and only then it can combine with its P2Y12 receptor on the platelet surface to further inhibit the adenosine-diphosphate induced platelet aggregation. But the main limitation of prasugrel has been the increased incidence of bleeding which when compared with clopidogrel was significant. This article focuses on pathophysiology of thrombosis and role of prasugrel along with recent patents in preventing atherothrombotic events including its pharmacological aspects and key clinical trials.