Ticlopidine, clopidogrel, and prasugrel are thienopyridine prodrugs that inhibit adenosine‐5′‐diphosphate
(ADP)‐mediated platelet aggregation in vivo. These compounds are …

Drugs are discovered by a variety of approaches, which include a systematic evaluation of
synthetic compounds, using extensive structure activity relationships. After a lead compound …

Background: Thienopyridines are metabolized to active metabolites that irreversibly inhibit
the platelet P2Y 12 adenosine diphosphate receptor. The pharmacodynamic response to …

The aim of the current study is to identify the human cytochrome P450 (P450) isoforms
involved in the two oxidative steps in the bioactivation of clopidogrel to its pharmacologically …

BACKGROUND: The aim of this study was to compare rate of onset, magnitude, and consistency
of platelet inhibition after administration of prasugrel or clopidogrel and to relate platelet …

Prasugrel and clopidogrel inhibit platelet aggregation through active metabolite formation.
Prasugrel's active metabolite (R‐138727) is formed primarily by cytochrome P450 (CYP) 3A …

Prasugrel and clopidogrel, thienopyridine prodrugs, are each metabolized to an active
metabolite that inhibits the platelet P2Y 12 ADP receptor. In this open‐label, 4‐period crossover …

Purpose. The aim of this work was a pragmatic, statistically sound and clinically relevant
approach to dose-proportionality analyses that is compatible with common study designs. …

The biotransformation of prasugrel to R-138727 (2-[1-2-cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl]-4-mercapto-3-piperidinylidene]acetic
acid) involves rapid deesterification to R-95913 (…

Prasugrel, a prodrug, is a novel and potent inhibitor of platelet aggregation in vivo. The
metabolism of prasugrel and the elimination and pharmacokinetics of its active metabolite, 2-[1-[2-…