119458-27-4

Usage

Uses

Used in Pharmaceutical Industry:
rac N-Desmethyl Mephenytoin-deuterated is used as a labeled metabolite for [application reason] in the pharmaceutical industry. This deuterated analog can be utilized in research and development, as well as in the synthesis of pharmaceutical products.
Used in Research and Development:
rac N-Desmethyl Mephenytoin-deuterated is used as a research tool for studying the metabolism and pharmacokinetics of Mephenytoin. The deuterium labeling allows for easier detection and tracking of the compound in biological systems, providing valuable insights into its behavior and potential applications.
Used in Drug Metabolism Studies:
As a labeled metabolite of Mephenytoin, rac N-Desmethyl Mephenytoin-deuterated is used in drug metabolism studies to understand the metabolic pathways and enzyme interactions involved in the breakdown and elimination of the parent compound. This information can be crucial for optimizing drug dosages and minimizing side effects.
Used in Quality Control and Analysis:
The deuterated nature of rac N-Desmethyl Mephenytoin-deuterated makes it an ideal reference material for quality control and analysis in the pharmaceutical industry. It can be used to ensure the purity and consistency of Mephenytoin products, as well as to develop and validate analytical methods for detecting and quantifying the compound in various matrices.

InChI:InChI=1/C11H12N2O2/c1-2-11(8-6-4-3-5-7-8)9(14)12-10(15)13-11/h3-7H,2H2,1H3,(H2,12,13,14,15)/i3D,4D,5D,6D,7D

Upstream product

• 54419-23-7 1-<(2)H5>phenylpropan-1-one 
• 151-50-8 potassium cyanide 
• 506-87-6 ammonium carbonate 

Relevant academic research and scientific papers

Potent Mechanism-Based Inhibition of Human CYP2B6 by Clopidogrel and Ticlopidine

The thienopyridine derivatives ticlopidine and clopidogrel are inhibitors of ADP-induced platelet aggregation. Pharmacological activity of these prodrugs depends on cytochrome P450 (P450)-dependent oxidation to the active antithrombotic agent. In this study, we investigated the interaction potential of clopidogrel and ticlopidine by using human liver microsomes and recombinantly expressed P450 isoforms. Both clopidogrel and ticlopidine inhibited CYP2B6 with highest potency and CYP2C19 with lower potency, Clopidogrel also inhibited CYP2C9, and ticlopidine also inhibited CYP1A2, with lower potency. Inhibition of CYP2B6 was time- and concentration-dependent, and as shown by dialysis experiments, it was irreversible and dependent on NADPH, suggesting a mechanism-based mode of action. Inactivation was of nonpseudo-first-order type with maximal rates of inactivation (K inact) for clopidogrel and ticlopidine in microsomes (recombinant CYP2B6) of 0.35 (1.5 min-1) and 0.5 min-1 (0.8 min -1), respectively, and half-maximal inactivator concentrations (KI) were 0.5 μM (1.1 μM) for clopidogrel and 0.2 μM (0.8 μM) for ticlopidine. Inhibition was attenuated by the presence of alternative active site ligands but not by nucleophilic trapping agents or reactive oxygen scavengers, further supporting mechanism-based action. A chemical mechanism is discussed based on the known metabolic activation of clopidogrel and on the finding that hemoprotein integrity of recombinant CYP2B6 was not affected by irreversible inhibition. These results suggest the possibility of drug interactions between thienopyridine derivates and drug substrates of CYP2B6 and CYP2C19.