159126-30-4

Basic information

• Product Name: Desmethylene Paroxetine Hydrochloride Salt
• Synonyms: Desmethylene Paroxetine Hydrochloride Salt;(3S-trans)-4-[[4-(4-Fluorophenyl)-3-piperidinyl]Methoxy]-1,2-benzenediol Hydrochloride;4-[[(3S,4R)-4-(4-Fluorophenyl)-3-piperidinyl]Methoxy]-1,2-benzenediol Hydrochloride;Paroxetine catechol
• CAS NO: 159126-30-4
• Molecular Formula: C18H21ClFNO3
• Molecular Weight: 353.8156432
• Product Categories: Intermediates & Fine Chemicals;Metabolites & Impurities;Pharmaceuticals;Metabolites & Impurities, Pharmaceuticals, Intermediates & Fine Chemicals
• Mol File: 159126-30-4.mol
• Article Data: 1

Chemical Properties

• Melting Point: 104-107?C
• Boiling Point: 509.6±50.0 °C(Predicted)
• Appearance: /
• Density: 1.233±0.06 g/cm3(Predicted)
• Storage Temp.: -20°C Freezer
• Solubility: DMSO (Slightly), Methanol (Slightly)
• PKA: 9.39±0.10(Predicted)
• CAS DataBase Reference: Desmethylene Paroxetine Hydrochloride Salt(CAS DataBase Reference)
• NIST Chemistry Reference: Desmethylene Paroxetine Hydrochloride Salt(159126-30-4)
• EPA Substance Registry System: Desmethylene Paroxetine Hydrochloride Salt(159126-30-4)

Safety Data

• Hazardous Substances Data: 159126-30-4(Hazardous Substances Data)

Usage

Chemical Properties

Yellow Solid

Uses

A major metabolite of the antidepressant Paroxetine (P205750).

Upstream product

• 61869-08-7 paroxetine 

Relevant articles and documents

Identification of cytochrome P450 isoforms involved in the metabolism of paroxetine and estimation of their importance for human paroxetine metabolism using a population-based simulator

We identify here for the first time the low-affinity cytochrome P450 (P450) isoforms that metabolize paroxetine, using cDNA-expressed human P450s measuring substrate depletion and paroxetine-catechol (product) formation by liquid chromatography-tandem mass spectrometry. CYP1A2, CYP2C19, CYP2D6, CYP3A4, and CYP3A5 were identified as paroxetine-catechol-forming P450 isoforms, and CYP2C19 and CYP2D6 were identified as metabolizing P450 isoforms by substrate depletion. Michaelis-Menten constants Km and Vmax were determined by product formation and substrate depletion. Using selective inhibitory studies and a relative activity factor approach for pooled and single-donor human liver microsomes, we confirmed involvement of the identified P450 isoforms for paroxetine-catechol formation at 1 and 20 μM paroxetine. In addition, we used the population-based simulator Simcyp to estimate the importance of the identified paroxetine-metabolizing P450 isoforms for human metabolism, taking mechanism-based inhibition into account. The amount of active hepatic CYP2D6 and CYP3A4 (not inactivated by mechanism-based inhibition) was also estimated by Simcyp. For extensive and poor metabolizers of CYP2D6, Simcyp-estimated pharmacokinetic profiles were in good agreement with those reported in published in vivo studies. Considering the kinetic parameters, inhibition results, relative activity factor calculations, and Simcyp simulations, CYP2D6 (high affinity) and CYP3A4 (low affinity) are most likely to be the major contributors to paroxetine metabolism in humans. For some individuals CYP1A2 could be of importance for paroxetine metabolism, whereas the importance of CYP2C19 and CYP3A5 is probably limited. Copyright