PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 8333835-2 1993 We have isolated genomic clones for CYP2C9 and CYP2C18 from the liver of an individual phenotyped in vitro as an extensive metabolizer of S-mephenytoin. Mephenytoin 138-151 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 47-54 8944768-3 1996 CYP 2C9 was the best catalyst for 5-hydroxylation of tienilic acid (K(m) = 5 +/- 1 microM, kcat = 1.7 +/- 0.2 min-1), 30-fold more potent in terms of kcat/K(m) than CYP 2C18 (K(m) = 150 +/- 15 microM, kcat = 1.8 +/- 0.2 min-1) and 300-fold more potent than CYP 2C8 (K(m) = 145 +/- 15 microM, kcat = 0.2 +/- 0.1 min-1). Ticrynafen 53-66 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 165-173 8944768-7 1996 Specific-covalent binding of tienilic acid metabolites to cytochrome P-450 (incubations in the presence of 5 mM glutathione) was markedly higher upon tienilic acid oxidation by CYP 2C9 than by CYP 2C18 and CYP 2C8. Ticrynafen 29-42 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 193-201 8944768-7 1996 Specific-covalent binding of tienilic acid metabolites to cytochrome P-450 (incubations in the presence of 5 mM glutathione) was markedly higher upon tienilic acid oxidation by CYP 2C9 than by CYP 2C18 and CYP 2C8. Glutathione 112-123 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 193-201 8944768-7 1996 Specific-covalent binding of tienilic acid metabolites to cytochrome P-450 (incubations in the presence of 5 mM glutathione) was markedly higher upon tienilic acid oxidation by CYP 2C9 than by CYP 2C18 and CYP 2C8. Ticrynafen 150-163 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 193-201 8894508-7 1996 CYP2C19, CYP2C8, CYP2C18, and CYP2C9 formed a single metabolite with an HPLC retention time identical to that of 5OH-OP. 5oh 113-116 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 17-24 7656504-6 1995 Lansoprazole is extensively metabolised following oral administration into sulphone and 5-hydroxylated metabolites by the cytochrome P450 enzymes CYP3A4 and CYP2C18. Lansoprazole 0-12 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 157-164 7656504-6 1995 Lansoprazole is extensively metabolised following oral administration into sulphone and 5-hydroxylated metabolites by the cytochrome P450 enzymes CYP3A4 and CYP2C18. Sulfones 75-83 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 157-164 8333835-1 1993 There is a genetic polymorphism in humans in the metabolism of S-mephenytoin which has been suggested to be mediated by either CYP2C18 or CYP2C9. Mephenytoin 63-76 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 127-134 8333835-7 1993 The availability of the sequences of the upstream regions and intron-exon junctions of CYP2C9 and CYP2C18 will allow future analysis of these genes in humans which differ in their ability to metabolize S-mephenytoin and other drugs. Sulfur 202-203 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 98-105 1306110-6 1992 Using oligonucleotides derived from the gene sequence, we were able to specifically detect CYP2C18 mRNAs in human liver. Oligonucleotides 6-22 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 91-98 25350082-5 2015 The metabolic pathway of tofogliflozin to M1 was considered to be as follows: first, tofogliflozin was catalyzed to the primary hydroxylated derivative (M4) by CYP2C18, CYP4A11 and CYP4F3B, then M4 was oxidized to M1. 6-((4-ethylphenyl)methyl)-3',4',5',6'-tetrahydro-6'-(hydroxymethyl)spiro(isobenzofuran-1(3H),2'-(2H)pyran)-3',4',5'-triol 25-38 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 160-167 35282004-10 2022 Twenty-one cytochrome P450 (CYP2C9, CYP2C18, and CYP2C19) "metabolism" polymorphisms in locus 10q23.33 were significantly associated with higher beta-carotene concentration. beta Carotene 145-158 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 36-43 35282004-12 2022 Zeaxanthin, lycopene, and beta-carotene serum concentrations might depend on genetic variation in NR1H3, APOB, RDH12 and CYP2C9, CYP2C18, and CYP2C19 genes. Zeaxanthins 0-10 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 129-136 35282004-12 2022 Zeaxanthin, lycopene, and beta-carotene serum concentrations might depend on genetic variation in NR1H3, APOB, RDH12 and CYP2C9, CYP2C18, and CYP2C19 genes. beta Carotene 26-39 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 129-136 33759177-5 2021 Firstly, the CYP2C18/CYP2C19 locus was sequenced from gDNA obtained from 24 patients previously genotyped as CYP2C19*1/*1 showing consistently low serum concentrations of escitalopram (<25 nM/10 mg). Citalopram 171-183 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 13-20 31979355-4 2020 Tofogliflozin is metabolized and inactivated by five different enzymes CYP2C18, CYP3A4, CYP3A5, CYP4A11, and CYP4F3. 6-((4-ethylphenyl)methyl)-3',4',5',6'-tetrahydro-6'-(hydroxymethyl)spiro(isobenzofuran-1(3H),2'-(2H)pyran)-3',4',5'-triol 0-13 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 71-78 29458047-4 2018 Methadone is primarily metabolized in the liver by cytochrome P450 (CYP) enzymes, predominately by CYP2B6, followed by CYP3A4, 2C19, 2D6, and to a lesser extent, CYP2C18, 3A7, 2C8, 2C9, 3A5, and 1A2. Methadone 0-9 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 162-169 1896026-4 1991 cDNA-directed synthesis of CYP2C18 revealed a protein with relative Mr 49,000 on sodium dodecyl sulfate-polyacrylamide gels, which is considerably less than that calculated from the deduced amino acid composition, Mr 55,747. Sodium Dodecyl Sulfate 81-103 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 27-34 1896026-4 1991 cDNA-directed synthesis of CYP2C18 revealed a protein with relative Mr 49,000 on sodium dodecyl sulfate-polyacrylamide gels, which is considerably less than that calculated from the deduced amino acid composition, Mr 55,747. polyacrylamide 104-118 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 27-34 32077582-9 2020 CONCLUSION: This study emphasizes the role of CYP-related genes as major regulators of clopidogrel response, including the poorly-investigated CYP2C8 and CYP2C18. clopidogrel 87-98 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 154-161 30899365-3 2019 In TERT-HNECs treated with Y27632 for 5 days, upregulation of p63, gap junction molecules Cx26, Cx30, Cx43, cytochrome P450 enzymes CYP2C9, CYP2C18, CYP39A1, CYP4B1, CYP2G1P, CYP4Z1, and KLF families KLF10 and KLF11 were observed compared to the control. Y 27632 27-33 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 140-147 28280103-11 2017 Four SNPs-rs2104543, rs12772169, rs1998591 and rs1042194-within CYP2C18 were in high LD, and the genetic polymorphisms had a significant impact on the TEG parameters maximal clot strength (MAThrombin) and ADP-induced platelet-fibrin clot strength (MAADP). Adenosine Diphosphate 205-208 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 64-71 28280103-11 2017 Four SNPs-rs2104543, rs12772169, rs1998591 and rs1042194-within CYP2C18 were in high LD, and the genetic polymorphisms had a significant impact on the TEG parameters maximal clot strength (MAThrombin) and ADP-induced platelet-fibrin clot strength (MAADP). maadp 248-253 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 64-71 27896399-5 2017 Seven isoforms were capable of metabolizing triclosan, with the order of activity being CYP1A2 > CYP2B6 > CYP2C19 > CYP2D6 CYP1B1 > CYP2C18 CYP1A1. Triclosan 44-53 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 146-153 27896399-8 2017 Consistent with the in vitro screening data, triclosan was extensively metabolized in HepG2 cells overexpressing CYP1A2, CYP2B6, CYP2C19, CYP2D6, and CYP2C18, and these cells were much more resistant to triclosan-induced cytotoxicity compared to vector cells, suggesting that CYP-mediated metabolism of triclosan attenuated its cytotoxicity. Triclosan 45-54 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 150-157 25350082-5 2015 The metabolic pathway of tofogliflozin to M1 was considered to be as follows: first, tofogliflozin was catalyzed to the primary hydroxylated derivative (M4) by CYP2C18, CYP4A11 and CYP4F3B, then M4 was oxidized to M1. 6-((4-ethylphenyl)methyl)-3',4',5',6'-tetrahydro-6'-(hydroxymethyl)spiro(isobenzofuran-1(3H),2'-(2H)pyran)-3',4',5'-triol 85-98 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 160-167 23089684-14 2012 However, besides the activity-altering CYP2C9*3 (rs1057910) and CYP2C19*2 (rs4244285) variants, the high derived allele frequencies of novel recently identified acenocoumarol genome-wide associated SNPs at CYP2C9 (rs4086116) and CYP2C18 (rs12772169, rs1998591, rs2104543, rs1042194) loci variants indicated that the CYP2C region may have been influenced by selection. Acenocoumarol 161-174 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 229-236 23743505-10 2013 With a panel of recombinant human cytochrome P450s (CYPs), CYP2C18 and CYP3A4 produced the most noroxycodone, whereas CYP2D6 produced the most oxymorphone. noroxycodone 96-108 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 59-66 23743505-10 2013 With a panel of recombinant human cytochrome P450s (CYPs), CYP2C18 and CYP3A4 produced the most noroxycodone, whereas CYP2D6 produced the most oxymorphone. Oxymorphone 143-154 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 59-66 19578179-11 2009 On chromosome 10, we further identified genetic variation in the cytochrome P450 2C18 (CYP2C18) gene contributing to variance of acenocoumarol dosage. Acenocoumarol 129-142 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 65-85 19958090-7 2009 In addition, our results showed that CYP2C18, PROC and EPHX1 have small but significant associations with warfarin dose. Warfarin 106-114 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 37-44 19038035-1 2008 BACKGROUND: This study was performed to characterize a gene-addition transgenic mouse containing a BAC (bacterial artificial chromosome) clone spanning the human CYP2C18&19 genes (tg-CYP2C18&19). Adenosine Monophosphate 170-173 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 162-169 19706858-9 2009 Thirteen single-nucleotide polymorphisms on chromosome 10q24 within the CYP2C18-CYP2C19-CYP2C9-CYP2C8 cluster were associated with diminished clopidogrel response, with a high degree of statistical significance (P = 1.5 x 10(-13) for rs12777823, additive model). Clopidogrel 142-153 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 72-79 19339376-4 2009 Testosterone treatment of female mice increased CYP2C18 and CYP2C19 expression in kidney, and to a lesser extent in liver, but was without effect in brain or small intestine, where gene expression was not gender-dependent. Testosterone 0-12 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 48-55 19578179-11 2009 On chromosome 10, we further identified genetic variation in the cytochrome P450 2C18 (CYP2C18) gene contributing to variance of acenocoumarol dosage. Acenocoumarol 129-142 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 87-94 19578179-13 2009 Besides age, gender, body mass index and target INR, one polymorphism within each of the VKORC1, CYP2C9, CYP4F2 and CYP2C18 genes could explain 48.8% of acenocoumarol dosage variation. Acenocoumarol 153-166 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 116-123 19038035-5 2008 In female tg-CYP2C18&19, the tissue weights were lower for brain (p < or = 0.001) and spleen (p < or = 0.001) compared to wild-type females. Adenosine Monophosphate 21-24 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 13-20 19038035-6 2008 Male tg-CYP2C18&19 had increased blood glucose levels (p < or = 0.01) while females had decreased blood triglyceride levels (p < or = 0.01). Adenosine Monophosphate 16-19 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 8-15 19038035-6 2008 Male tg-CYP2C18&19 had increased blood glucose levels (p < or = 0.01) while females had decreased blood triglyceride levels (p < or = 0.01). Glucose 43-50 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 8-15 18274956-6 2008 Usnic acid was a relatively weak inhibitor of CYP2D6 and a potent inhibitor of CYP2C19 (the concentration eliciting 50% inhibition (IC(50)) = 9 nM) and CYP2C9 (IC(50) = 94 nM), with less potent inhibition of CYP2C8 (IC(50) = 1.9 microM) and CYP2C18 (IC(50) = 6.3 microM). usnic acid 0-10 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 241-248 18276835-7 2008 A CYP2C18-specific antiserum showed that this enzyme was not expressed in livers or kidneys from heterozygous transgenic mice, but the antiserum had high affinity for recombinant CYP2C18 expressed in COS-7 cells. carbonyl sulfide 200-203 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 2-9 18276835-7 2008 A CYP2C18-specific antiserum showed that this enzyme was not expressed in livers or kidneys from heterozygous transgenic mice, but the antiserum had high affinity for recombinant CYP2C18 expressed in COS-7 cells. carbonyl sulfide 200-203 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 179-186 17084997-3 2006 All of the tested CYPs, except CYP2A6 and CYP2C18, metabolized ethanol into significant amounts of acetaldehyde and displayed K(m) values around 10mM. Ethanol 63-70 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 42-49 17084997-3 2006 All of the tested CYPs, except CYP2A6 and CYP2C18, metabolized ethanol into significant amounts of acetaldehyde and displayed K(m) values around 10mM. Acetaldehyde 99-111 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 42-49 16985168-6 2006 CYP2C18, 2C19, 2C9, 2W1, 3A4, and 4B1 are up-regulated by cellular differentiation; mRNA levels for these CYP genes were inhibited in differentiating keratinocytes exposed to retinoic acid and aryl hydrocarbon receptor (AhR) ligands. Tretinoin 175-188 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 0-7 16978758-7 2006 Since the CYP2C18 content of hepatic microsomes in humans is relatively low, CYP2C9, 2C19, and 3A4 might be the main isoforms of CYP that are responsible for tributyltin and triphenyltin metabolism in the human liver. tributyltin 158-169 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 10-17 16141545-4 2005 The metabolism of clotiazepam was catalyzed by CYP2B6, CYP3A4, CYP2C18, and CYP2C19, and imipramine was metabolized by CYP2D6 most efficiently. clotiazepam 18-29 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 63-70 11853173-2 2002 When determined at 2 mM substrate concentration, nonylphenol (1 mM) most efficiently inhibited aminopyrine N-demethylation by CYP2C9 and CYP2C19, by 61% and 59%, respectively, followed by CYP2D6, CYP1A2, CYP2C18 and CYP2C8 (46-51%), whereas inhibition of the activities by other CYPs was less than 27%. nonylphenol 49-60 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 204-211 12378636-7 2002 The enzyme activity of CYP2C18 catalyzing oxidation of tolbutamide to hydroxytolbutamide in postmitochondrial supernant(S9) fraction of the cell was determined by high performance liquid chromatography(HPLC). Tolbutamide 55-66 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 23-30 12378636-7 2002 The enzyme activity of CYP2C18 catalyzing oxidation of tolbutamide to hydroxytolbutamide in postmitochondrial supernant(S9) fraction of the cell was determined by high performance liquid chromatography(HPLC). hydroxymethyltolbutamide 70-88 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 23-30 15301741-4 2004 The enzyme activity of CYP2C18 to oxidate tolbutamide in postmitochondrial supernate (S9) fraction was determined by HPLC. Tolbutamide 42-53 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 23-30 15301741-12 2004 In contrast, the relative survival of HepG2-CYP2C18 X2 cell was the same as that of HepG2 cell in 0.5 and 1 mmol/L of ifosfamide, but lower than that of HepG2 cell in 2 and 4 mmol/L of ifosfamide. Ifosfamide 118-128 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 44-51 15301741-12 2004 In contrast, the relative survival of HepG2-CYP2C18 X2 cell was the same as that of HepG2 cell in 0.5 and 1 mmol/L of ifosfamide, but lower than that of HepG2 cell in 2 and 4 mmol/L of ifosfamide. Ifosfamide 185-195 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 44-51 15301741-13 2004 CONCLUSION: CYP2C18 X1 could metabolize tolbutamide and ifosfamide efficiently. Tolbutamide 40-51 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 12-19 15301741-13 2004 CONCLUSION: CYP2C18 X1 could metabolize tolbutamide and ifosfamide efficiently. Ifosfamide 56-66 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 12-19 12734935-9 2003 The time-dependent studies showed that PL had the stereoselectivity of S-(-)-isomer in metabolism via CYP2C18 and the stereoselectivity of R-(+)-isomer in metabolism via CYP2C9. Propranolol 39-41 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 102-109 11714868-5 2001 The oligonucleotide-based array made it possible to detect different levels of induction within the CYP2C family, with rifampin causing a 6.5-fold increase in expression of CYP2C8 and a 3.7-fold increase in CYP2C9 while having no effect on the level of CYP2C18 mRNA. Oligonucleotides 4-19 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 253-260 11714868-5 2001 The oligonucleotide-based array made it possible to detect different levels of induction within the CYP2C family, with rifampin causing a 6.5-fold increase in expression of CYP2C8 and a 3.7-fold increase in CYP2C9 while having no effect on the level of CYP2C18 mRNA. Rifampin 119-127 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 253-260 11558570-3 2001 CYP2C18 catalyzed BPA metabolism most efficiently, followed by CYP2C19 and CYP2C9. bisphenol A 18-21 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 0-7 11558570-4 2001 CYP2C9 and CYP2C18 exhibited the highest affinity (Km=3.9 microM) for BPA metabolism. bisphenol A 70-73 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 11-18 10901692-7 2000 In contrast, S-mephenytoin inhibited DDS-NHY by CYP2C9, CYP2C18, and CYP2C19 by 27 +/- 2, 49 +/- 1, and 32 +/- 4%, respectively. Mephenytoin 13-26 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 56-63 10901692-3 2000 The apparent Michaelis-Menten Km values for DDS-NHY by cloned CYP2C8, CYP2C9, CYP2C18, and CYP2C19 were 75 microM, 31 microM, 25 microM, and greater than 1 mM, respectively. Fumigant 93 44-47 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 78-85 10901692-7 2000 In contrast, S-mephenytoin inhibited DDS-NHY by CYP2C9, CYP2C18, and CYP2C19 by 27 +/- 2, 49 +/- 1, and 32 +/- 4%, respectively. Fumigant 93 37-40 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 56-63 10901692-8 2000 Because CYP2C18 and CYP19 are expressed at low concentrations in the human liver, these observations indicate that at clinical DDS concentrations, CYP2C9 is a major and CYP2C8 is a likely minor contributor to DDS-NHY in human liver microsomes. Fumigant 93 127-130 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 8-15 10901692-8 2000 Because CYP2C18 and CYP19 are expressed at low concentrations in the human liver, these observations indicate that at clinical DDS concentrations, CYP2C9 is a major and CYP2C8 is a likely minor contributor to DDS-NHY in human liver microsomes. Fumigant 93 209-212 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 8-15 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 18 Homo sapiens 92-99 10449188-10 1999 Comparison of data obtained with CYP-expressing cells and human hepatocytes suggests that CYP2C8 > CYP2C19 approximately CYP2C18 >> CYP2B6 are the isoforms implicated in the 5-hydroxylation of diclofenac in vivo. Diclofenac 202-212 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 124-131 9766669-5 1998 Strong CPA chemosensitivity was also seen following transduction of CYP2C18-Met, despite a very low level of CYP protein expression (>60-fold lower than that of 2B6). Cyclophosphamide 7-10 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 68-75 9766669-10 1998 CYP2B6 plus P450 reductase and CYP2C18-Met plus P450 reductase thus appear to be excellent gene combinations for use with CPA in P450/prodrug activation-based cancer gene therapy. Cyclophosphamide 122-125 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 31-38 9733665-6 1998 Incubations with purified CYP2C19 and CYP2C18 resulted in formation of mono-OH-M, and also the bis-demethylated metabolite. mono-oh-m 71-80 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 38-45 9733665-12 1998 Although CYP2C18 is an efficient methoxychlor demethylase, its expression in liver is reportedly low or absent, suggesting a negligible role for this enzyme in methoxychlor metabolism. Methoxychlor 33-45 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 9-16 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. Ifosfamide 94-104 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 318-325 10387023-2 1999 Whereas only compounds bearing a negative charge acted as substrates of CYP 2C9 and were hydroxylated at position 5 of their thiophene ring at a significant rate, many neutral 2-aroylthiophenes were 5-hydroxylated by CYP 2C18 with kcat values of >2 min-1. 2-aroylthiophenes 176-193 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 217-225 10387023-3 1999 Among the various compounds that were studied, those bearing an alcohol function were the best CYP 2C18 substrates. Alcohols 64-71 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 95-103 10387023-5 1999 It was regioselectively hydroxylated by CYP 2C18 at position 5 of its thiophene ring with a KM value of 9 +/- 1 microM and a kcat value of 125 +/- 25 min-1, which are the highest described so far for a CYP 2C. Thiophenes 70-79 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 40-48 9733665-4 1998 Incubation of methoxychlor with microsomes from insect cells overexpressing either CYP1A2, CYP2C18, or CYP2C19 yielded mono-OH-M with turnover numbers of 14.9, 15.5, and 39.1 nmol/min/nmol of P450, respectively. Methoxychlor 14-26 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 91-98 9733665-4 1998 Incubation of methoxychlor with microsomes from insect cells overexpressing either CYP1A2, CYP2C18, or CYP2C19 yielded mono-OH-M with turnover numbers of 14.9, 15.5, and 39.1 nmol/min/nmol of P450, respectively. mono-oh-m 119-128 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 91-98 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 18 Homo sapiens 183-190 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. Ifosfamide 135-145 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 92-99 9241661-5 1997 CYP2C18 had the highest in vitro intrinsic clearance/catalytic efficiency (apparent Vmax/Km) in cyclophosphamide and ifosfamide activation, followed by 2C19 > 2C9 approximately 2C8. Cyclophosphamide 96-112 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 0-7 9241661-5 1997 CYP2C18 had the highest in vitro intrinsic clearance/catalytic efficiency (apparent Vmax/Km) in cyclophosphamide and ifosfamide activation, followed by 2C19 > 2C9 approximately 2C8. Ifosfamide 117-127 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 0-7 9241661-6 1997 Examination of a panel of CYP2C allelic variants revealed that CYP2C18-Thr385 had both a higher Vmax and a higher apparent Km toward cyclophosphamide than CYP2C18-Met385 with no difference in catalytic efficiency, whereas with ifosfamide the Thr385 allele exhibited a strikingly lower apparent Km resulting in a six-fold higher catalytic efficiency. Cyclophosphamide 133-149 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 63-70 9241661-6 1997 Examination of a panel of CYP2C allelic variants revealed that CYP2C18-Thr385 had both a higher Vmax and a higher apparent Km toward cyclophosphamide than CYP2C18-Met385 with no difference in catalytic efficiency, whereas with ifosfamide the Thr385 allele exhibited a strikingly lower apparent Km resulting in a six-fold higher catalytic efficiency. Ifosfamide 227-237 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 63-70 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 18 Homo sapiens 318-325