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Omeprazole (OME) is a CYP2C19 phenotyping probe, marketed as a racemic (S)/(R) mixture or as an S-enantiomer. Both CYP2C19 and CYP3A4 enzymes mediate (R)-OME hydroxylation to (R)-5-hydroxyomeprazole, while (S)-OME is exclusively hydroxylated via CYP2C19. This study investigates OME and its 5-hydroxymetabolite enantiomers' pharmacokinetics using data from two studies involving healthy volunteers. In Study A, volunteers received OME alone in Session 1, OME combined with voriconazole and fluvoxamine in Session 2 and finally OME with rifampicin in Session 3. In Study B, volunteers received OME alone in Session 1, OME combined with voriconazole in Session 2 and finally OME with fluvoxamine in Session 3. Despite low metabolic ratio values of (S)-OME, detectable modulation of CYP2C19 activity suggests both (R)- and (S)-OME isomers could effectively assess CYP2C19 activity. Further research is needed for precise cut-offs in different phenotype groups.
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http://dx.doi.org/10.1111/bcpt.14095 | DOI Listing |
Clin Pharmacol Ther
September 2025
Molecular Brain Science Department, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Tanenbaum Centre for Pharmacogenetics, Toronto, Ontario, Canada.
Pharmacogenomics enables the personalization of drug therapy by linking genetic variations to differences in drug metabolism, efficacy, and risk of adverse reactions. Genetic polymorphisms within cytochrome P450 (CYP) genes significantly affect enzyme activity, influencing drug plasma levels, responses, and safety. Central to this process is accurate genotype-to-phenotype translation, especially for the CYP enzyme family, which metabolizes 70-80% of clinically used drugs.
View Article and Find Full Text PDFPharmaceuticals (Basel)
August 2025
Division of Clinical Pharmacology and Toxicology, The Hospital for Sick Children, Toronto, ON M5G 1X8, Canada.
Medication discontinuation attributable to adverse drug reactions (ADRs) and/or inefficacy remains a concern of psychotropic medications among children and adolescents. Pharmacogenetic (PGx) testing has been proposed to individualize treatment, although its utility remains uncertain. We retrospectively evaluated whether PGx testing of two key metabolism genes (i.
View Article and Find Full Text PDFDrug Metab Rev
September 2025
Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.
Alzheimer's disease (AD) is a complex neurodegenerative disorder that poses significant therapeutic challenges. Currently available treatments offer symptomatic relief but often yield suboptimal outcomes due to inter-individual variability in drug metabolism. Cytochrome P450 (CYP450) enzymes, particularly those exhibiting genetic polymorphisms, play a central role in the hepatic metabolism of many AD medications.
View Article and Find Full Text PDFArch Toxicol
August 2025
Institute for Occupational, Social and Environmental Medicine, Medical Faculty, RWTH Aachen University, Pauwelsstrasse 30, 52074, Aachen, Germany.
Polychlorinated biphenyls (PCBs) are widespread environmental contaminants that interfere with xenobiotic metabolism, primarily by modulating cytochrome P450 (CYP) enzymes. However, their pharmacokinetic consequences in exposed individuals remain poorly defined. Here, we investigated the impact of PCB exposure on CYP enzyme activity using a combined clinical pharmacokinetic and in vitro mechanistic approach.
View Article and Find Full Text PDFJ Clin Pharmacol
August 2025
Pumas-AI, Inc., Baltimore, MD, USA.
Mavacamten, a cardiac myosin inhibitor, is primarily metabolized by the cytochrome P450 (CYP) enzymes CYP2C19 and CYP3A4, and coadministration with strong CYP3A4 or CYP2C19 inhibitors was contraindicated in patients with obstructive hypertrophic cardiomyopathy (HCM) in the US Prescribing Information. This study assessed the safety and efficacy of modifying mavacamten posology to accommodate coadministration with strong CYP3A4 and strong/moderate CYP2C19 inhibitors. Simulations of 5000 virtual patients with obstructive HCM with an equal distribution of CYP2C19 metabolizer phenotypes were performed using population pharmacokinetic and exposure-response modeling approaches.
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