PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23307233-0 2013 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. Rosiglitazone 169-182 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 146-152 23307233-1 2013 PURPOSE: To predict the impact of the CYP2C8 3 genotype on rosiglitazone exposure in the absence and presence of trimethoprim. Rosiglitazone 59-72 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 38-44 23307233-3 2013 Specifically, data on the frequency of the different allelic forms of CYP2C8 and their metabolic activity for rosiglitazone were incorporated into a physiologically-based pharmacokinetic (PBPK) model within the Simcyp Simulator (V11.1) to predict differences in the relative exposure of rosiglitazone according to CYP2C8 3 genotype in a virtual population. Rosiglitazone 110-123 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 70-76 23307233-4 2013 RESULTS: Following multiple doses of 8 mg rosiglitazone, the predicted mean AUC(0-24) was 37 % lower in CYP2C8 3 homozygotes compared with wildtype homozygotes (p < 0.001), which was consistent with the 36 % lower value observed in vivo (p < 0.001) Kirchheiner et al. Rosiglitazone 42-55 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 104-110 23307233-6 2013 Predicted median AUC ratios of rosiglitazone in the presence and absence of trimethoprim ranged from 1.35 to 1.66 for ten virtual trials of subjects with the CYP2C8 1/1 genotype, which included the observed value of 1.42. Rosiglitazone 31-44 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 158-164 23426382-1 2013 OBJECTIVE: The aim of this study was to examine the effect of single nucleotide polymorphisms in CYP2C8, LPIN1, PPARGC1A and PPARgamma on rosiglitazone"s (i) trough steady-state plasma concentration (C(ss,min)), (ii) on glycosylated haemoglobin A1c (HbA1c) and (iii) the risk of developing adverse events, mainly oedema, in patients with type 2 diabetes mellitus (T2D). Rosiglitazone 138-151 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 97-103 23426382-6 2013 Carriers of CYP2C8*3 (n=32) (rs10509681 and rs11572080) had a statistically significantly lower mean C(ss,min) than wild types (n=106), and they also had a statistically significantly lower mean absolute difference in HbA1c during rosiglitazone treatment. Rosiglitazone 231-244 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 12-18 23426382-8 2013 CONCLUSION: We showed that CYP2C8*3 was associated with lower plasma levels of rosiglitazone and hence a reduced therapeutic response but also a lower risk of developing oedema during treatment with rosiglitazone. Rosiglitazone 79-92 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 27-33 23426382-8 2013 CONCLUSION: We showed that CYP2C8*3 was associated with lower plasma levels of rosiglitazone and hence a reduced therapeutic response but also a lower risk of developing oedema during treatment with rosiglitazone. Rosiglitazone 199-212 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 27-33 23426382-9 2013 Individualized treatment with rosiglitazone on the basis of the CYP2C8 genotype may therefore be possible. Rosiglitazone 30-43 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 64-70 22242967-0 2012 The effects of febuxostat on the pharmacokinetic parameters of rosiglitazone, a CYP2C8 substrate. Rosiglitazone 63-76 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 80-86 23064958-11 2013 CONCLUSIONS: This DDI study in patients with cancer demonstrated that systemic exposure of rosiglitazone (a CYP2C8 substrate) or OC (ethinyl estradiol/norethindrone) is not altered with concomitant vismodegib. Rosiglitazone 91-104 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 108-114 22242967-1 2012 AIMS: To determine the effect of febuxostat on cytochrome P450 2C8 (CYP2C8) activity using rosiglitazone as a CYP2C8 substrate. Rosiglitazone 91-104 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 47-66 22242967-1 2012 AIMS: To determine the effect of febuxostat on cytochrome P450 2C8 (CYP2C8) activity using rosiglitazone as a CYP2C8 substrate. Rosiglitazone 91-104 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 68-74 22242967-1 2012 AIMS: To determine the effect of febuxostat on cytochrome P450 2C8 (CYP2C8) activity using rosiglitazone as a CYP2C8 substrate. Rosiglitazone 91-104 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 110-116 19477697-1 2009 We present a simple, rapid, and sensitive liquid chromatography (LC)-tandem mass spectrometry (MS/MS) method for the simultaneous quantification of rosiglitazone and its two major metabolites via CYP2C8/9, N-desmethyl and p-hydroxy rosiglitazone, in human plasma. Rosiglitazone 148-161 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 196-202 22680343-1 2012 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: Paclitaxel and rosiglitazone are primarily metabolized by CYP2C8 and their in vitro metabolism by human liver microsomes is correlated. Rosiglitazone 59-72 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 102-108 22680343-6 2012 However, it is acknowledged that there is a need for further studies evaluating the use of rosiglitazone as a CYP2C8 probe and quantifying the relationship, in order to guide dosing of narrow therapeutic index drugs metabolized primarily by CYP2C8, such as paclitaxel. Rosiglitazone 91-104 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 110-116 22680343-6 2012 However, it is acknowledged that there is a need for further studies evaluating the use of rosiglitazone as a CYP2C8 probe and quantifying the relationship, in order to guide dosing of narrow therapeutic index drugs metabolized primarily by CYP2C8, such as paclitaxel. Rosiglitazone 91-104 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 241-247 22680343-10 2012 CONCLUSIONS: The correlation between the exposure of rosiglitazone and paclitaxel likely reflects mutual dependence on the activity of CYP2C8. Rosiglitazone 53-66 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 135-141 22680343-11 2012 Rosiglitazone or similar agents may have value as in vivo probes of CYP2C8 activity. Rosiglitazone 0-13 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 68-74 21726541-3 2011 In this study, the contribution of the redox partners cytochrome P450 reductase (CPR) and cytochrome b5 to the substrate dependent activity of CYP2C8.3 (R139K, K399R) was investigated in human liver microsomes (HLMs) and Escherichia coli expressed recombinant CYP2C8 proteins using amodiaquine, paclitaxel, rosiglitazone and cerivastatin as probe substrates. Rosiglitazone 307-320 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 143-149 21499911-2 2011 In humans, CYP2C8 appears to have a major role in RSG metabolism. Rosiglitazone 50-53 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 11-17 21511944-4 2011 Despite addition of GSH, CBLs of troglitazone and rosiglitazone in human liver microsomes were correlated with CYP3A (or CYP2C8) and CYP2C8 activities, respectively. Rosiglitazone 50-63 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 121-127 21511944-4 2011 Despite addition of GSH, CBLs of troglitazone and rosiglitazone in human liver microsomes were correlated with CYP3A (or CYP2C8) and CYP2C8 activities, respectively. Rosiglitazone 50-63 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 133-139 21245287-0 2011 Discovery of a novel allelic variant of CYP2C8, CYP2C8*11, in Asian populations and its clinical effect on the rosiglitazone disposition in vivo. Rosiglitazone 111-124 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 40-46 21245287-0 2011 Discovery of a novel allelic variant of CYP2C8, CYP2C8*11, in Asian populations and its clinical effect on the rosiglitazone disposition in vivo. Rosiglitazone 111-124 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 48-54 21245287-1 2011 The objectives of this study were to identify the genetic variants of CYP2C8, analyze CYP2C8 single nucleotide polymorphisms (SNPs), and characterize their functional consequences in the CYP2C8 substrate drug rosiglitazone in humans. Rosiglitazone 209-222 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 70-76 21245287-1 2011 The objectives of this study were to identify the genetic variants of CYP2C8, analyze CYP2C8 single nucleotide polymorphisms (SNPs), and characterize their functional consequences in the CYP2C8 substrate drug rosiglitazone in humans. Rosiglitazone 209-222 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 86-92 21245287-1 2011 The objectives of this study were to identify the genetic variants of CYP2C8, analyze CYP2C8 single nucleotide polymorphisms (SNPs), and characterize their functional consequences in the CYP2C8 substrate drug rosiglitazone in humans. Rosiglitazone 209-222 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 86-92 21245287-9 2011 Subjects with CYP2C8*1/*11 exhibited higher plasma concentration-time profiles of rosiglitazone than those of nine control subjects carrying CYP2C8*1/*1. Rosiglitazone 82-95 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 14-20 21245287-10 2011 The area under the concentration-time curve and peak plasma concentration of rosiglitazone in individuals carrying CYP2C8*1/*11 (n = 5) were 54 and 34% higher than the mean values observed in the control subjects carrying CYP2C8*1/*1 (P = 0.015 and P = 0.025, respectively). Rosiglitazone 77-90 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 115-121 21245287-10 2011 The area under the concentration-time curve and peak plasma concentration of rosiglitazone in individuals carrying CYP2C8*1/*11 (n = 5) were 54 and 34% higher than the mean values observed in the control subjects carrying CYP2C8*1/*1 (P = 0.015 and P = 0.025, respectively). Rosiglitazone 77-90 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 222-228 19761371-5 2009 Contrary to in vitro data, clinical data suggest that the CYP2C8*3 allele is associated with increased metabolism of the CYP2C8 substrates, rosiglitazone, pioglitazone and repaglinide. Rosiglitazone 140-153 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 58-64 19761371-5 2009 Contrary to in vitro data, clinical data suggest that the CYP2C8*3 allele is associated with increased metabolism of the CYP2C8 substrates, rosiglitazone, pioglitazone and repaglinide. Rosiglitazone 140-153 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 121-127 16981900-0 2007 Effect of multiple doses of montelukast on the pharmacokinetics of rosiglitazone, a CYP2C8 substrate, in humans. Rosiglitazone 67-80 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 84-90 19129086-0 2008 Influence of SLCO1B1 and CYP2C8 gene polymorphisms on rosiglitazone pharmacokinetics in healthy volunteers. Rosiglitazone 54-67 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 25-31 19129086-9 2008 Subjects with the CYP2C8*1/*3 genotype ( n = 7), however, had significantly lower rosiglitazone area under the plasma concentration-time curve (AUC) and significantly higher rosiglitazone oral clearance, compared with CYP2C8 wild-type homozygotes ( n = 19). Rosiglitazone 82-95 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 18-24 19129086-9 2008 Subjects with the CYP2C8*1/*3 genotype ( n = 7), however, had significantly lower rosiglitazone area under the plasma concentration-time curve (AUC) and significantly higher rosiglitazone oral clearance, compared with CYP2C8 wild-type homozygotes ( n = 19). Rosiglitazone 174-187 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 18-24 19129086-10 2008 Stepwise linear regression analysis revealed that CYP2C8 genotype ( p = 0.006) and weight ( p = 0.022) were significant predictors of rosiglitazone AUC (overall p = 0.002; R 2 = 41.6 per cent). Rosiglitazone 134-147 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 50-56 19129086-11 2008 We concluded that polymorphisms in the CYP2C8 drug-metabolising enzyme gene, but not the SLCO1B1 drug transporter gene, significantly influence rosiglitazone disposition in humans. Rosiglitazone 144-157 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 39-45 18303964-2 2008 It is unknown how genetic polymorphisms affect formation of these diuretic, vasodilatory and anti-inflammatory eicosanoids, and whether the CYP2C8 substrate rosiglitazone inhibits their formation. Rosiglitazone 157-170 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 140-146 16981900-1 2007 AIMS: To investigate the effect of multiple dosing with montelukast, a selective leukotriene-receptor antagonist, on the pharmacokinetics of rosiglitazone, a CYP2C8 substrate, in humans. Rosiglitazone 141-154 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 158-164 17244766-3 2007 Rosiglitazone, a thiazolidenedione, is an insulin sensitizer and mainly metabolized by CYP2C8. Rosiglitazone 0-13 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 87-93 16027405-0 2005 Effect of quercetin on the pharmacokinetics of rosiglitazone, a CYP2C8 substrate, in healthy subjects. Rosiglitazone 47-60 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 64-70 17201456-6 2007 CYP2C8 and CYP3A4 are the main isoenzymes catalysing biotransformation of pioglitazone (as with troglitazone), whereas rosiglitazone is metabolised by CYP2C9 and CYP2C8. Rosiglitazone 119-132 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 162-168 16856883-0 2006 The effects of human CYP2C8 genotype and fluvoxamine on the pharmacokinetics of rosiglitazone in healthy subjects. Rosiglitazone 80-93 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 21-27 16856883-1 2006 AIMS: To determine the effect of CYP2C8 genotype and of fluvoxamine on the pharmacokinetics of rosiglitazone. Rosiglitazone 95-108 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 33-39 16856883-10 2006 CONCLUSION: The importance of the CYP2C8*3 mutation in the in vivo metabolism of rosiglitazone could not be confirmed. Rosiglitazone 81-94 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 34-40 17178266-0 2006 Pharmacokinetics and pharmacodynamics of rosiglitazone in relation to CYP2C8 genotype. Rosiglitazone 41-54 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 70-76 17178266-1 2006 OBJECTIVES: Rosiglitazone is metabolically inactivated predominantly via the cytochrome P450 (CYP) enzyme CYP2C8. Rosiglitazone 12-25 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 106-112 16299161-9 2006 The results described have important implications for the mechanism of the clinical interaction reported between gemfibrozil and CYP2C8 substrates such as cerivastatin, repaglinide, rosiglitazone, and pioglitazone. Rosiglitazone 182-195 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 129-135 15606443-0 2005 The effect of trimethoprim on CYP2C8 mediated rosiglitazone metabolism in human liver microsomes and healthy subjects. Rosiglitazone 46-59 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 30-36 15606443-12 2005 CONCLUSIONS: These results indicate that trimethoprim is a competitive inhibitor of CYP2C8-mediated rosiglitazone metabolism in vitro and that trimethoprim administration increases plasma rosiglitazone concentrations in healthy subjects. Rosiglitazone 100-113 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 84-90 15606443-1 2005 AIMS: Rosiglitazone, a thiazolidinedione antidiabetic medication used in the treatment of Type 2 diabetes mellitus, is predominantly metabolized by the cytochrome P450 (CYP) enzyme CYP2C8. Rosiglitazone 6-19 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 181-187 15606443-3 2005 The purpose of this study was to evaluate the effect of trimethoprim on the CYP2C8 mediated metabolism of rosiglitazone in vivo and in vitro. Rosiglitazone 106-119 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 76-82 15373932-2 2004 Rosiglitazone is a novel thiazolidinedione antidiabetic drug, mainly metabolized by CYP2C8 and to a lesser extent CYP2C9. Rosiglitazone 0-13 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 84-90 16372821-14 2005 CYP2C8 and CYP3A4 are the main enzymes catalysing biotransformation of the thiazolidinediones troglitazone and pioglitazone, whereas rosiglitazone is metabolised by CYP2C9 and CYP2C8. Rosiglitazone 133-146 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 0-6 16372821-14 2005 CYP2C8 and CYP3A4 are the main enzymes catalysing biotransformation of the thiazolidinediones troglitazone and pioglitazone, whereas rosiglitazone is metabolised by CYP2C9 and CYP2C8. Rosiglitazone 133-146 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 176-182 15601807-1 2005 Cytochrome P450 2C8 is involved in the metabolism of drugs such as paclitaxel, repaglinide, rosiglitazone, and cerivastatin, among others. Rosiglitazone 92-105 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 0-19 15373932-9 2004 CONCLUSIONS: This study revealed that ketoconazole affected the disposition of rosiglitazone in humans, probably by the inhibition of CYP2C8 and CYP2C9, leading to increasing rosiglitazone concentrations that could increase the efficacy of rosiglitazone or its adverse events. Rosiglitazone 79-92 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 134-140 15373932-9 2004 CONCLUSIONS: This study revealed that ketoconazole affected the disposition of rosiglitazone in humans, probably by the inhibition of CYP2C8 and CYP2C9, leading to increasing rosiglitazone concentrations that could increase the efficacy of rosiglitazone or its adverse events. Rosiglitazone 175-188 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 134-140 15373932-9 2004 CONCLUSIONS: This study revealed that ketoconazole affected the disposition of rosiglitazone in humans, probably by the inhibition of CYP2C8 and CYP2C9, leading to increasing rosiglitazone concentrations that could increase the efficacy of rosiglitazone or its adverse events. Rosiglitazone 175-188 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 134-140 15371985-0 2004 Effects of trimethoprim and rifampin on the pharmacokinetics of the cytochrome P450 2C8 substrate rosiglitazone. Rosiglitazone 98-111 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 68-87 15371985-16 2004 CONCLUSIONS: Trimethoprim raises and rifampin reduces the plasma concentrations of rosiglitazone by inhibiting and inducing, respectively, the CYP2C8-catalyzed biotransformation of rosiglitazone. Rosiglitazone 83-96 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 143-149 15371985-16 2004 CONCLUSIONS: Trimethoprim raises and rifampin reduces the plasma concentrations of rosiglitazone by inhibiting and inducing, respectively, the CYP2C8-catalyzed biotransformation of rosiglitazone. Rosiglitazone 181-194 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 143-149 15371985-3 2004 OBJECTIVE: Our aims were to investigate possible effects of trimethoprim and rifampin on CYP2C8 activity by use of rosiglitazone, a thiazolidinedione antidiabetic drug metabolized primarily by CYP2C8, as an in vivo probe. Rosiglitazone 115-128 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 89-95 15371985-3 2004 OBJECTIVE: Our aims were to investigate possible effects of trimethoprim and rifampin on CYP2C8 activity by use of rosiglitazone, a thiazolidinedione antidiabetic drug metabolized primarily by CYP2C8, as an in vivo probe. Rosiglitazone 115-128 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 193-199 15063342-2 2004 Rosiglitazone is extensively metabolized by cytochrome P450 2C8 and so may have some utility as an in vivo probe for this enzyme. Rosiglitazone 0-13 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 44-63 15001966-12 2004 CONCLUSION: This study showed that rifampin affected the disposition of rosiglitazone in humans, probably by the induction of cytochrome P450 (CYP) 2C8 and, to a lesser extent, CYP2C9. Rosiglitazone 72-85 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 126-151 10510156-8 1999 Sulphaphenazole caused limited inhibition (<30%) of both pathways in human liver microsomes and microsomes from cells transfected with CYP2C9 cDNA were able to mediate the metabolism of rosiglitazone, in particular the N-demethylation pathway, albeit at a much slower rate than CYP2C8. Rosiglitazone 189-202 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 281-287 10510156-9 1999 Rosiglitazone caused moderate inhibition of paclitaxel 6alpha-hydroxylase activity (CYP2C8; IC50=18 microm ), weak inhibition of tolbutamide hydroxylase activity (CYP2C9; IC50=50 microm ), but caused no marked inhibition of the other cytochrome P450 activities investigated (CYP1A2, 2A6, 2C9, 2C19, 2D6, 2E1, 3A and 4A). Rosiglitazone 0-13 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 84-90 10510156-10 1999 Conclusion CYP2C8 is primarily responsible for the hydroxylation and N-demethylation of rosiglitazone in human liver; with minor contributions from CYP2C9. Rosiglitazone 88-101 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 11-17 28074333-7 2017 The CYP2C8 (69 +- 20%), CYP2C9 (42 +- 10%), CYP3A4 (52 +- 23%), and CEP2E1 (41 +- 13%) inhibitors all significantly inhibited rosiglitazone metabolism. Rosiglitazone 126-139 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 4-10 29174535-6 2017 Using this value, the CVs of AUC/Dose of other major CYP2C8 substrates, rosiglitazone and amodiaquine, were predicted to validate the estimated CV of CLint,h,2C8. Rosiglitazone 72-85 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 53-59 27271184-4 2016 RESULTS: The CYP2C8*3 variant was associated with reduced glycemic response to rosiglitazone (P = 0.01) and less weight gain (P = 0.02). Rosiglitazone 79-92 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 13-19 27271184-8 2016 CONCLUSIONS: These results show that variants in CYP2C8 and SLCO1B1 have a large clinical impact on the therapeutic response to rosiglitazone and highlight the importance of studying transporter and metabolizing genes together in pharmacogenetics. Rosiglitazone 128-141 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 49-55 26581561-4 2016 Amodiaquine, montelukast, quercetin and rosiglitazone, known as substrates or competitive inhibitors of human CYP2C8, were metabolically depleted by recombinant monkey CYP2C8 at relatively high rates. Rosiglitazone 40-53 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 110-116 26581561-4 2016 Amodiaquine, montelukast, quercetin and rosiglitazone, known as substrates or competitive inhibitors of human CYP2C8, were metabolically depleted by recombinant monkey CYP2C8 at relatively high rates. Rosiglitazone 40-53 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 168-174 26467040-9 2016 CYP2C8 promoter activity was increased by ectopic expression of PPARalpha in HepG2 cells, with a further increase after bezafibrate (~18-fold), 4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio acetic acid (~10-fold) treatment, or the antidiabetic drug rosiglitazone, all known PPAR activators. Rosiglitazone 247-260 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 0-6 26721703-3 2016 CYP2C8 substrate drugs include amodiaquine, cerivastatin, dasabuvir, enzalutamide, imatinib, loperamide, montelukast, paclitaxel, pioglitazone, repaglinide, and rosiglitazone, and the number is increasing. Rosiglitazone 161-174 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 0-6