HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Am J Health-Syst Pharm Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Riley, A. B. Articles by Haber, S. L. PubMed PubMed Citation Articles by Riley, A. B. Articles by Haber, S. L.

AMY B. RILEY, PHARM.D., is Cardiology Pharmacy Practice Resident/ Faculty; MOHAMMAD J. TAFRESHI, PHARM.D., BCPS, is Professor; and Stacy l. Haber, Pharm.D., is Associate Professor, College of Pharmacy—Glendale, Midwestern University, Glendale, AZ.

Address correspondence to Dr. Riley at the College of Pharmacy— Glendale, Midwestern University, 19555 North 59th Avenue, Glendale, AZ 85308 (ariley{at}midwestern.edu).

Purpose. The pharmacology, pharmacokinetics, safety, and adverse effects of prasugrel, a novel antiplatelet agent, are described. Summary. Prasugrel is a third-generation thienopyridine. Like clopidogrel, prasugrel is a prodrug requiring hepatic metabolism to its active form to bind irreversibly to the P2Y12 adenosine diphosphate receptor and inhibits platelet aggregation for the life of the platelet. Prasugrel’s pharmacokinetic profile has not been clearly defined. Several preclinical and early-phase clinical trials of prasugrel have been completed. Five trials have assessed the platelet aggregation of prasugrel alone or compared with placebo or clopidogrel. Certain populations with acute coronary syndrome (ACS) may be at higher risk for major bleeding episodes leading to fatal events when using prasugrel with other antithrombotic agents and antiplatelet agents. Information on drug or food interactions with prasugrel is limited. Since prasugrel is still under investigation, an official recommended dosage regimen has yet to be determined. Clinical trials are still being conducted to determine prasugrel’s exact place in therapy. In early trials, prasugrel has demonstrated a faster onset of action, higher rate of platelet inhibition, and lower rate of response variability compared with clopidogrel. Conclusion. 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. Index terms: Clopidogrel; Drug comparisons; Drug interactions; Drugs; Mechanism of action; Metabolism; Pharmacokinetics; Platelet aggregation inhibitors; Prasugrel; Toxicity

 

Related articles in Am J Health-Syst Pharm:

For better or for worse: The future of antiplatelet therapy

William Alvarez, Jr.
Am J Health-Syst Pharm 2008 65: 1017. [Full Text]