PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23157194-1 2012 Sulfonamide antimicrobials (sulfamethoxazole) contain an arylamine group, oxidized by CYP2C9 to the hydroxylamine with subsequent auto-oxidation to a highly reactive [-nitroso-] intermediate is a necessary (if not sufficient) cause of drug hypersensitivity. Sulfamethoxazole 28-44 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 86-92 22540071-8 2011 CONCLUSIONS: sulfamethoxazole is catalysed by CYP2C9 and/or myeloperoxidase. Sulfamethoxazole 13-29 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 46-52 22106207-2 2012 The objective of this study was to examine the impact of N-acetyltransferase 2 (NAT2) and CYP2C9 polymorphisms on the pharmacokinetics of SMX in 118 renal transplant recipients. Sulfamethoxazole 138-141 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 90-96 18991696-7 2008 Carbamazepine hypersensitivity is also influenced by gene variants of cytochrome P450 enzymes on the generation of reactive metabolites, while CYP2C9*2 and CYP2C9*3 polymorphisms influence the bioactivation of sulfamethoxazole in prohapten. Sulfamethoxazole 210-226 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 143-149 18765684-1 2008 Sulfamethoxazole is metabolized by microsomal CYP2C9 to a hydroxylamine that is thought to be responsible for the relatively high incidence of hypersensitivity reactions associated with the drug. Sulfamethoxazole 0-16 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 46-52 18991696-7 2008 Carbamazepine hypersensitivity is also influenced by gene variants of cytochrome P450 enzymes on the generation of reactive metabolites, while CYP2C9*2 and CYP2C9*3 polymorphisms influence the bioactivation of sulfamethoxazole in prohapten. Sulfamethoxazole 210-226 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 156-162 12019187-4 2002 With concentrations ranging from 50 to 500 microM, sulfamethoxazole was a selective inhibitor of CYP2C9-mediated tolbutamide hydroxylation in human liver microsomes and recombinant CYP2C9, with apparent IC(50) (K(i)) values of 544 microM (271 microM) and 456 microM, respectively. Sulfamethoxazole 51-67 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 97-103 17442935-7 2007 The enzymes CYP2C9, CYP2C8, and myeloperoxidase catalyzed the conversion of sulfamethoxazole to sulfamethoxazole hydroxylamine. Sulfamethoxazole 76-92 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 12-18 12019187-4 2002 With concentrations ranging from 50 to 500 microM, sulfamethoxazole was a selective inhibitor of CYP2C9-mediated tolbutamide hydroxylation in human liver microsomes and recombinant CYP2C9, with apparent IC(50) (K(i)) values of 544 microM (271 microM) and 456 microM, respectively. Sulfamethoxazole 51-67 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 181-187 12019187-6 2002 Based on estimated total hepatic concentrations (or free plasma concentrations) of the drugs and the scaling model, one would expect in vivo in humans 80% (26%) and 13% (24%) inhibition of the metabolic clearance of CYP2C8 and CYP2C9 substrates by trimethoprim and sulfamethoxazole, respectively. Sulfamethoxazole 265-281 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 227-233 10709776-11 2000 Fluconazole, miconazole and sulfamethoxazole are potent inhibitors of CYP2C9. Sulfamethoxazole 28-44 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 70-76 7628308-8 1995 Recombinant CYP2C9 catalyzed the N-hydroxylation of SMX. Sulfamethoxazole 52-55 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 12-18 7628308-9 1995 SMX-HA formation in human hepatic microsomes was therefore mediated predominantly by CYP2C9. Sulfamethoxazole 0-3 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 85-91 11956677-2 2002 METHODS: Generation of SMX-HA from SMX was measured directly using high-performance liquid chromatography in human liver microsomes or expressed CYP2C9*1, with or without preincubation with reduced nicotinamide adenine dinucleotide phosphate, and the inhibition constant (K(i)) for atovaquone was determined. Sulfamethoxazole 23-26 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 145-151 11956677-8 2002 CONCLUSIONS: Atovaquone is a relatively weak inhibitor of CYP2C9-mediated SMX-HA formation in vitro. Sulfamethoxazole 74-77 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 58-64 10208642-1 1999 Sulphamethoxazole undergoes CYP2C9-mediated bioactivation to a hydroxylamine. Sulfamethoxazole 0-17 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 28-34 10208642-2 1999 In this study, we investigated the effect of the CYP2C9Arg144 to Cys (CYP2C9*2) and CYP2C9Ile359 to Leu (CYP2C9*3) polymorphisms on sulphamethoxazole N-hydroxylation. Sulfamethoxazole 132-149 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 49-55 10208642-5 1999 Microsomes prepared from the cell line expressing the allelic variants CYP2C9-Cys144 and CYP2C9-Leu359 displayed a threefold and 20-fold decrease in intrinsic clearance (Cl(int)) for sulphamethoxazole, respectively, when compared with the wild-type, CYP2C9-Arg144. Sulfamethoxazole 183-200 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 71-77 10208642-5 1999 Microsomes prepared from the cell line expressing the allelic variants CYP2C9-Cys144 and CYP2C9-Leu359 displayed a threefold and 20-fold decrease in intrinsic clearance (Cl(int)) for sulphamethoxazole, respectively, when compared with the wild-type, CYP2C9-Arg144. Sulfamethoxazole 183-200 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 89-95 10208642-5 1999 Microsomes prepared from the cell line expressing the allelic variants CYP2C9-Cys144 and CYP2C9-Leu359 displayed a threefold and 20-fold decrease in intrinsic clearance (Cl(int)) for sulphamethoxazole, respectively, when compared with the wild-type, CYP2C9-Arg144. Sulfamethoxazole 183-200 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 89-95 10208642-11 1999 The CYP2C9*2 and CYP2C9*3 polymorphisms may have some influence on the bioactivation of sulphamethoxazole, particularly in individuals who are homozygous mutants, and this could act as a protective factor against sulphamethoxazole hypersensitivity. Sulfamethoxazole 88-105 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 4-10 10208642-11 1999 The CYP2C9*2 and CYP2C9*3 polymorphisms may have some influence on the bioactivation of sulphamethoxazole, particularly in individuals who are homozygous mutants, and this could act as a protective factor against sulphamethoxazole hypersensitivity. Sulfamethoxazole 88-105 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 17-23 10208642-11 1999 The CYP2C9*2 and CYP2C9*3 polymorphisms may have some influence on the bioactivation of sulphamethoxazole, particularly in individuals who are homozygous mutants, and this could act as a protective factor against sulphamethoxazole hypersensitivity. Sulfamethoxazole 213-230 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 4-10 10208642-11 1999 The CYP2C9*2 and CYP2C9*3 polymorphisms may have some influence on the bioactivation of sulphamethoxazole, particularly in individuals who are homozygous mutants, and this could act as a protective factor against sulphamethoxazole hypersensitivity. Sulfamethoxazole 213-230 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 17-23 34149005-2 2021 SMX is metabolized by N-acetyltransferase (NAT) and cytochrome P450 2C9 (CYP2C9) to nontoxic or toxic intermediates. Sulfamethoxazole 0-3 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 52-71 34149005-2 2021 SMX is metabolized by N-acetyltransferase (NAT) and cytochrome P450 2C9 (CYP2C9) to nontoxic or toxic intermediates. Sulfamethoxazole 0-3 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 73-79