ArticleBritish journal of clinical pharmacology2006
The effects of human CYP2C8 genotype and fluvoxamine on the pharmacokinetics of rosiglitazone in healthy subjects.
Article in British journal of clinical pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 45 citations in OpenAlex.
- Impact of the CYP2C8 *3 polymorphism on the drug-drug interaction between gemfibrozil and pioglitazone.British journal of clinical pharmacology · 2013Trial
- Influence of SLCO1B1 and CYP2C8 gene polymorphisms on rosiglitazone pharmacokinetics in healthy volunteers.Human genomics · 2008Trial
- Stereoselective interaction between the CYP2C8 inhibitor gemfibrozil and racemic ibuprofen.European journal of clinical pharmacology · 2007Trial
- CYP2C8-Mediated Drug-Drug Interactions and the Factors Influencing the Interaction Magnitude.Drug design, development and therapy · 2025Review
- Challenges to assess substrate-dependent allelic effects in CYP450 enzymes and the potential clinical implications.The pharmacogenomics journal · 2019Review
- Assessment of coding region variants in Kuwaiti population: implications for medical genetics and population genomics.Scientific reports · 2018Article
- Rosiglitazone Metabolism in Human Liver Microsomes Using a Substrate Depletion Method.Drugs in R&D · 2017Article
- Effects of Icosapent Ethyl (Eicosapentaenoic Acid Ethyl Ester) on Pharmacokinetic Parameters of Rosiglitazone in Healthy Subjects.Clinical pharmacology in drug development · 2015Article
- Review
- PharmGKB summary: very important pharmacogene information for cytochrome P450, family 2, subfamily C, polypeptide 8.Pharmacogenetics and genomics · 2013Review
- The role of pharmacogenetics in drug disposition and response of oral glucose-lowering drugs.Clinical pharmacokinetics · 2013Review
- Application of in vitro-in vivo extrapolation (IVIVE) and physiologically based pharmacokinetic (PBPK) modelling to investigate the impact of the CYP2C8 polymorphism on rosiglitazone exposure.European journal of clinical pharmacology · 2013Article
- Importance of multi-p450 inhibition in drug-drug interactions: evaluation of incidence, inhibition magnitude, and prediction from in vitro data.Chemical research in toxicology · 2012Review
- Cytochrome P450 2C8 pharmacogenetics: a review of clinical studies.Pharmacogenomics · 2009Article
- CYP2C8 and antimalaria drug efficacy.Pharmacogenomics · 2007Review
- Pharmacokinetic interactions with thiazolidinediones.Clinical pharmacokinetics · 2007Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsTo determine the effect of CYP2C8 genotype and of fluvoxamine on the pharmacokinetics of rosiglitazone.
methodsTwenty-three healthy subjects with the following genotypes were included in a two-phase, open-label, cross-over trial: CYP2C8*3/ *3 (n = 3), CYP2C8*1/ *3 (n = 10) and CYP2C8*1/ *1 (n = 10). In Phase A, the subjects were given 4 mg rosiglitazone as a single oral dose. In Phase B, the subjects were treated with multiple oral doses of 50 mg fluvoxamine maleate for 3 days prior to the single oral administration of 4 mg rosiglitazone. Plasma concentrations of rosiglitazone and relative amounts of N-desmethylrosiglitazone were measured in both phases for 24 h after drug administration.
resultsThe pharmacokinetics of rosiglitazone and N-desmethylrosiglitazone were not significantly different between the CYP2C8 genotypic groups. Fluvoxamine caused a statistically significant (P = 0.0066) increase in the AUC(0-infinity) of rosiglitazone, with a geometric mean ratio of 1.21 [95% confidence interval (CI) 1.06-1.39]. The elimination half-life (t(1/2)) was also significantly higher (P = 0.0203) with a geometric mean ratio of 1.38 [95% CI 1.06-1.79]. The coadministration of fluvoxamine had no influence on the pharmacokinetics of N-desmethylrosiglitazone.
conclusionThe importance of the CYP2C8*3 mutation in the in vivo metabolism of rosiglitazone could not be confirmed. Fluvoxamine increased the AUC(0-infinity) and t(1/2) of rosiglitazone moderately and hence may be a weak inhibitor of CYP2C8.
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