PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9157990-6 1997 CYP3A4, CYP2C8, and CYP2C9 protein levels were also increased by exposure of the hepatocytes to cyclophosphamide or ifosfamide (50 microM), which thereby enhanced their own rates of 4-hydroxylation in the cultured hepatocytes. Cyclophosphamide 96-112 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 20-26 9331082-6 1997 On the basis of cytochrome P450 (CYP) isoform-specific chemical inhibitor and cDNA-expressed human P450 isozyme studies, CYP2C9 and CYP3A4/5 seemed to be the major P450 isoforms responsible for HCY formation at low (0.1 mM) and high (0.7 and 5 mM) concentrations of CY, respectively. Cyclophosphamide 33-35 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 121-127 9241661-0 1997 Identification of the polymorphically expressed CYP2C19 and the wild-type CYP2C9-ILE359 allele as low-Km catalysts of cyclophosphamide and ifosfamide activation. Cyclophosphamide 118-134 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 74-80 9241661-4 1997 With cyclophosphamide as substrate, CYP2C19 had the lowest apparent Km, followed by CYP2C9, CYP2C18 and CYP2C8, whereas in the case of ifosfamide, the rank order was: Km CYP2C19 < CYP2C18 < CYP2C9 < CYP2C8. Cyclophosphamide 5-21 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 84-90 9241661-4 1997 With cyclophosphamide as substrate, CYP2C19 had the lowest apparent Km, followed by CYP2C9, CYP2C18 and CYP2C8, whereas in the case of ifosfamide, the rank order was: Km CYP2C19 < CYP2C18 < CYP2C9 < CYP2C8. Cyclophosphamide 5-21 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 196-202 9241661-7 1997 In the case of CYP2C9, a Ile359 to Leu mutation associated with poor metabolism of the hypoglycemic drug tolbutamide decreased catalytic efficiency toward cyclophosphamide by increasing the apparent Km, whereas the same mutation reduced the efficiency of this P450 toward ifosfamide by decreasing the Vmax. Cyclophosphamide 155-171 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 15-21 9241661-8 1997 Substitution of CYP2C9-Gly417 by Asp resulted in a two-fold lower catalytic efficiency for cyclophosphamide metabolism but a three-fold higher efficiency for ifosfamide metabolism. Cyclophosphamide 91-107 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 16-22 9241661-11 1997 Thus (a) wild type CYP2C19 and CYP2C9 are relatively low Km catalysts of cyclophosphamide and ifosfamide activation, and (b) all four human CYP2C enzymes activate these two anticancer prodrugs with varying efficiencies and with striking differences among naturally occurring allelic variants in the case of CYP2C9 and CYP2C18. Cyclophosphamide 73-89 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 31-37 9241661-11 1997 Thus (a) wild type CYP2C19 and CYP2C9 are relatively low Km catalysts of cyclophosphamide and ifosfamide activation, and (b) all four human CYP2C enzymes activate these two anticancer prodrugs with varying efficiencies and with striking differences among naturally occurring allelic variants in the case of CYP2C9 and CYP2C18. Cyclophosphamide 73-89 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 307-313 32390827-12 2020 CYP2C9 *2 or *3 carriers were associated with increased clearance of CPA. Cyclophosphamide 69-72 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 0-6 32390827-18 2020 CYP3A5 and CYP2C9 genotypes, BSA, BMI, and CPA dosage regimen influence PK of CPA. Cyclophosphamide 43-46 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 11-17 32390827-18 2020 CYP3A5 and CYP2C9 genotypes, BSA, BMI, and CPA dosage regimen influence PK of CPA. Cyclophosphamide 78-81 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 11-17 24768782-1 2014 BACKGROUND: Cyclophosphamide (CP), an alkylating chemotherapeutic drug, is catalyzed by the Phase I cytochrome P450 (CYPs) isozymes - CYP3A4, CYP3A5, CYP2B6, CYP2C8, CYP2C9 and CYP2C19. Cyclophosphamide 12-28 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 166-172 28744217-14 2017 Article summary: (1) Children carrying functional alleles in GSTM1 and CYP2C9 are at high risk for developing hemorrhagic cystitis following treatment with busulfan and cyclophosphamide based conditioning regimen. Cyclophosphamide 169-185 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 71-77 26894931-1 2016 AIM: Correlation of outcomes of cyclophosphamide (CP) therapy in antineutrophil cytoplasmic antibody-associated vasculitis with genotype polymorphisms in prodrug activating cytochrome P450 enzyme genes CYP2C9 and CYP2C19. Cyclophosphamide 32-48 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 202-208 26894931-8 2016 CONCLUSION: Patients with variant CYP2C9 are at increased risk for cyclophosphamide-induced leukopenia but may have a better chance to respond to treatment. Cyclophosphamide 67-83 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 34-40 18496131-10 2008 CONCLUSION: This study indicates that the presently evaluated variant alleles in the CYP2B6, CYP2C9, CYP2C19, CYP3A4, CYP3A5, GSTA1, GSTP1, ALDH1A1 and ALDH3A1 genes do not explain the interindividual variability in cyclophosphamide and 4-hydroxycyclophosphamide pharmacokinetics and are, probably, not the cause of the observed variability in toxicity. Cyclophosphamide 216-232 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 93-99 19501186-6 2009 Among these transformants, benzo(a)pyrene-induced or cyclophosphamide-produced micronucleus (MN) frequency was markedly increased in transformants expressing CYP1A2 or CYP2C9, respectively. Cyclophosphamide 53-69 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 168-174 16475710-1 2006 The oxazaphosphorines cyclophosphamide (CP) and ifosfamide (IF) are alkylating agents that require bioactivation via cytochrome (CYP) P450 isoenzymes including CYP2C9 enzymes. Cyclophosphamide 22-38 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 160-166 17580253-2 2007 Fluconazole inhibits cytochrome P450 2C9, which is involved with the activation of CY, and so might provide protection from CY-related toxicities. Cyclophosphamide 83-85 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 21-40 17580253-2 2007 Fluconazole inhibits cytochrome P450 2C9, which is involved with the activation of CY, and so might provide protection from CY-related toxicities. Cyclophosphamide 124-126 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 21-40 17580253-8 2007 These data support the hypothesis that fluconazole, when coadministered with CY, decreases CY-related toxicities by inhibiting cytochrome P450 2C9 metabolism. Cyclophosphamide 77-79 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 127-146 10991840-0 2000 Cytochrome P-450 2C9 sensitizes human prostate tumor cells to cyclophosphamide via a bystander effect. Cyclophosphamide 62-78 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 0-20 12684728-2 2003 The aim of this study was to investigate the contribution of CYP2C9 and CYP2C19 and their polymorphisms to the variability of cyclophosphamide activation. Cyclophosphamide 126-142 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 61-67 12684728-4 2003 The kinetic data obtained in the yeast system revealed that the intrinsic clearance (V(max)/K(m)) of cyclophosphamide by CYP2C9.2 and CYP2C9.3 samples was approximately threefold lower than that by CYP2C9.1. Cyclophosphamide 101-117 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 121-127 12684728-4 2003 The kinetic data obtained in the yeast system revealed that the intrinsic clearance (V(max)/K(m)) of cyclophosphamide by CYP2C9.2 and CYP2C9.3 samples was approximately threefold lower than that by CYP2C9.1. Cyclophosphamide 101-117 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 134-140 12684728-4 2003 The kinetic data obtained in the yeast system revealed that the intrinsic clearance (V(max)/K(m)) of cyclophosphamide by CYP2C9.2 and CYP2C9.3 samples was approximately threefold lower than that by CYP2C9.1. Cyclophosphamide 101-117 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 134-140 10991840-12 2000 H2C9 cells mediated a bystander killing effect for CYP2C9-negative PPC-1 cells, reducing the IC(50) of CPA from about 14 to 3.62+/-0.73 mM in PPC-1 cells when they were cocultured with H2C9 cells. Cyclophosphamide 103-106 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 51-57 16183265-3 2006 The pharmacokinetics of CPA and its active metabolite were related to the genotype of CYP2B6, CYP2C9 and CYP2C19. Cyclophosphamide 24-27 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 94-100 10991840-1 2000 The goal of the present study was to examine the ability of cytochrome P450-2C9 (CYP2C9) to activate cyclophosphamide (CPA) and elicit tumor cell death. Cyclophosphamide 101-117 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 60-79 10991840-1 2000 The goal of the present study was to examine the ability of cytochrome P450-2C9 (CYP2C9) to activate cyclophosphamide (CPA) and elicit tumor cell death. Cyclophosphamide 101-117 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 81-87 10991840-1 2000 The goal of the present study was to examine the ability of cytochrome P450-2C9 (CYP2C9) to activate cyclophosphamide (CPA) and elicit tumor cell death. Cyclophosphamide 119-122 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 60-79 10991840-1 2000 The goal of the present study was to examine the ability of cytochrome P450-2C9 (CYP2C9) to activate cyclophosphamide (CPA) and elicit tumor cell death. Cyclophosphamide 119-122 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 81-87