916599-27-4

Usage

Uses

Used in Pharmaceutical Industry:
Prasugrel Metabolite M5 is used as an active metabolite for the prevention of arterial thrombotic events. It inhibits platelet aggregation by irreversibly binding to the P2Y12 receptor on platelet surface, thereby reducing the risk of stroke, myocardial infarction, and other cardiovascular complications in patients with atherosclerosis.
Used in Cardiovascular Research:
Prasugrel Metabolite M5 is used as a research tool for studying the mechanism of action of thienopyridine antiplatelet agents and their role in the prevention of arterial thrombotic events. It helps researchers understand the pharmacokinetics, pharmacodynamics, and potential side effects of these drugs, leading to the development of safer and more effective antiplatelet therapies.

Upstream product

• 67-68-5 dimethyl sulfoxide 
• 204204-73-9 R-138727 
• 204204-73-9 R-125687 
• 204204-73-9 R-125688 
• 204204-73-9 R-125689 
• 204204-73-9 R-125690 

Relevant academic research and scientific papers

Hepatic microsomal thiol methyltransferase is involved in stereoselective methylation of pharmacologically active metabolite of prasugrel

Prasugrel, a thienopyridine antiplatelet drug, is converted in animals and humans to the pharmacologically active metabolite R-138727 [(2Z)-{1-[(1RS)-2- cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl]-4-sulfanylpiperidin-3-ylidene} ethanoic acid], which has two chiral centers, occurring as a mixture of four isomers. The RS and RR isomers are more active than the SS and SR isomers (RS > RR > > SR = SS). The pharmacologically active metabolite is further metabolized to an S-methylated metabolite that is the major identified inactive metabolite in humans. In rat, dog, and human liver microsomes supplemented with S-adenosyl methione, the SS and SR isomers of the active metabolite were extensively S-methylated while the RS and RR isomers were not. Addition of 2,3-dichloromethyl benzylamine (50 μM) completely inhibited the S-methylation reaction, indicating that the microsomal and cytosolic thiol methyltransferase but not the cytosolic thiopurine S-methyltransferase is involved in the methylation. The hepatic intrinsic clearance values for methylation of the RS, RR, SS, and SR isomers (ml/min/kg) were 0, 0, 40.4, and 37.6, respectively, in rat liver microsomes, 0, 0, 11.6, and 2.5, respectively, in dog liver microsomes, and 0, 0, 17.3, and 17.7, respectively, in human liver microsomes, indicating that the RS and RR isomers are not methylated in vitro and that the methylation of SS and SR isomers is high with rat > human > dog. This finding in vitro agreed well with the in vivo observation in rats and dogs, where the S-methylated SS and SR isomers were the major metabolites in the plasma whereas negligible amounts of S-methylated RS and RR isomers were detected after intravenous administration of the pharmacologically active metabolites. Copyright