Prasugrel: A novel antiplatelet agent

Abstract

Prasugrel has demonstrated a greater platelet inhibition and a decreased incidence of ischemic events compared with clopidogrel, but with an increased incidence of bleeding events. Future studies with prasugrel should determine its optimal dosage regimen to minimize bleeding risks and evaluate its outcomes in ACS and safety profile in special patient populations.

Oral Antiplatelet Therapy for the Management of Acute Coronary Syndromes: Defining the Role of Prasugrel

“…This orally active agent has been studied extensively in preclinical and phase I, II, and III trials, and it has been recently approved by the FDA for patients with ACS who are undergoing PCI, to reduce the number of cardiovascular events, including stent thrombosis. 6,7,39 Prasugrel is classified as a third-generation thienopyridine derivative because of its similarities to the chemical structure of ticlopidine and clopidogrel. Like clopidogrel, prasugrel is a prodrug that requires hepatic metabolism to be …”

“…21 Other adverse events not related to hemorrhage include dizziness (20%), cellulitis (16%), facial edema (16%), headache (13%), dyspepsia (9%), thrombocytopenia (0.3%), neutropenia (<0.1%), and colonic neoplasms (0.2%). 33,34,39,40 …”

Case files of the medical toxicology fellowship at banner good samaritan medical center in Phoenix, AZ: A non-warfarin anticoagulant overdose

“…Ticagrelor is an ADP antagonist, but rather than belonging to the thienopyridine class, it is a cyclopentyl-triazolo-pyrimidine class drug, which does not require metabolism to be active. It is also a reversible inhibitor of the P2Y12 receptor, unlike the other antagonists [4,11].…”

Critical Review of Prasugrel for Formulary Decision Makers

“…10 Following oral administration, prasugrel is metabolized by esterases in the blood and intestines to an inactive thiolactone. 14 Cytochrome P (CYP) enzymes, principally 3A4 and 2B6, convert the thiolactone to the active metabolite R-138727. 10,[14][15][16] The parent molecule is not active in vitro.…”

“…14 Cytochrome P (CYP) enzymes, principally 3A4 and 2B6, convert the thiolactone to the active metabolite R-138727. 10,[14][15][16] The parent molecule is not active in vitro. 13 Similarly, clopidogrel is converted from the inactive parent compound to the active metabolite via the CYP system in a 2-step process compared with one for prasugrel.…”