PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
23279643-0	2013	The VKORC1 and CYP2C9 genotypes are associated with over-anticoagulation during initiation of warfarin therapy in children.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
23348161-0	2013	The relationship between CYP2C9 gene polymorphisms and upper gastrointestinal bleeding in patients who used warfarin.	Warfarin	108-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
23348161-3	2013	CYP2C9 is a hepatic microsomal enzyme and has a primary role in metabolism of warfarin and genetic variations of CYP2C9 may cause a serious effect on the response to warfarin in patients.	Warfarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
23348161-3	2013	CYP2C9 is a hepatic microsomal enzyme and has a primary role in metabolism of warfarin and genetic variations of CYP2C9 may cause a serious effect on the response to warfarin in patients.	Warfarin	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
23348161-3	2013	CYP2C9 is a hepatic microsomal enzyme and has a primary role in metabolism of warfarin and genetic variations of CYP2C9 may cause a serious effect on the response to warfarin in patients.	Warfarin	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
23348161-4	2013	The aim of this study was to determine the efficiency of CYP2C9 gene polymorphisms on drug metabolism in patients who had upper gastrointestinal system bleeding while using warfarin.	Warfarin	173-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
23348161-11	2013	CONCLUSION: CYP2C9*2 and CYP2C9*3 polymorphisms were related to the increase of excessive anticoagulation and bleeding risk in the patients who used warfarin.	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
23348161-11	2013	CONCLUSION: CYP2C9*2 and CYP2C9*3 polymorphisms were related to the increase of excessive anticoagulation and bleeding risk in the patients who used warfarin.	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
23452606-2	2013	Although numerous candidate gene studies in epilepsy PGX have been published, to date only two validated associations exist: the association of the *2 and *3 alleles of CYP2C9 with phenytoin metabolism and the association of HLA-B*1502 with serious hypersensitivity reactions to carbamazepine.	Phenytoin	181-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
23241944-3	2013	RESULTS: The rate of generation of human-predominant drug metabolites for S-mephenytoin and diclofenac in the chimeric mice was correlated with the CYP2C19 (n=9 donors, P=0.0005) or CYP2C9 (n=7 donors, P=0.0394) genotype, respectively, of the transplanted human hepatocytes.	Mephenytoin	74-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	182-188
23241944-3	2013	RESULTS: The rate of generation of human-predominant drug metabolites for S-mephenytoin and diclofenac in the chimeric mice was correlated with the CYP2C19 (n=9 donors, P=0.0005) or CYP2C9 (n=7 donors, P=0.0394) genotype, respectively, of the transplanted human hepatocytes.	Diclofenac	92-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	182-188
23469684-0	2013	Simvastatin pharmacokinetics in healthy Chinese subjects and its relations with CYP2C9, CYP3A5, ABCB1, ABCG2 and SLCO1B1 polymorphisms.	Simvastatin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
23159229-0	2013	The influence of VKORC1 and CYP2C9 gene sequence variants on the stability of maintenance phase warfarin treatment.	Warfarin	96-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
23159229-1	2013	INTRODUCTION: A substantial part of the inter-individual variation in vitamin K-antagonist dose can be explained by certain sequence variants in the genes CYP2C9 (NG_008385.1:g.8633C>T or *1/*2, NG_008385.1:g.47639A>C or *1/*3) and VKORC1 (NG_011564.1:g.6399C>T).	Vitamin K	70-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
23159229-7	2013	CONCLUSIONS: We observed modest effects of common gene sequence variants in CYP2C9 and VKORC1 on stability of maintenance phase warfarin therapy.	Warfarin	128-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
23640947-6	2013	Among genes associated with metabolism of the most commonly applied anaesthetics such as propofol and sevoflurane, the following ones can be mentioned: CYP2E1, CYP2B6, CYP2C9, GSTP1, UGT1A9, SULT1A1 and NQO1.	Propofol	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
23640947-6	2013	Among genes associated with metabolism of the most commonly applied anaesthetics such as propofol and sevoflurane, the following ones can be mentioned: CYP2E1, CYP2B6, CYP2C9, GSTP1, UGT1A9, SULT1A1 and NQO1.	Sevoflurane	102-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
23118328-3	2013	The aim of this study is to evaluate the possible association between sex, polymorphisms in the CYP2C8 and CYP2C9 genes, and the pharmacokinetics of losartan, valsartan, candesartan, and telmisartan.	Telmisartan	187-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
23302640-6	2013	In a metabolic inhibition study using human liver microsomes, cytochrome P450 (CYP) 2C9-mediated hydroxylation of S-warfarin was almost unaffected by MTZ at the corresponding concentrations.	Warfarin	114-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-87
23774101-0	2013	The bleeding risk during warfarin therapy is associated with the number of variant alleles of CYP2C9 and VKORC1 genes.	Warfarin	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
23774101-4	2013	AIM: It was the aim of this study to assess the impact of the total variant allele count of CYP2C9 and VKORC1 genes on bleeding related to warfarin treatment.	Warfarin	139-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
22917719-0	2013	A multiplex assay to detect variations in the CYP2C9, VKORC1, CYP4F2 and APOE genes involved in acenocoumarol metabolism.	Acenocoumarol	96-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
22917719-3	2013	DESIGN AND METHODS: We developed a PCR multiplex SNaPshot reaction that targets 6 SNPs (single nucleotide polymorphisms) in CYP2C9, CYP4F2, VKORC1 and APOE genes, which are associated with acenocoumarol dose requirements.	Acenocoumarol	189-202	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
23118328-3	2013	The aim of this study is to evaluate the possible association between sex, polymorphisms in the CYP2C8 and CYP2C9 genes, and the pharmacokinetics of losartan, valsartan, candesartan, and telmisartan.	Losartan	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
22892446-1	2013	The aim of this study was to reveal the contribution of CYP4F2, CYP2C9, and VKORC1 genetic polymorphisms on the pharmacokinetics and pharmacodynamics of warfarin in Japanese pediatric patients.	Warfarin	153-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
22892446-6	2013	In patients with the CYP2C9 *3 allele, the unbound oral clearance values (normalized to body surface area) for S-warfarin were found to be significantly lower than in patients with the wild-type allele.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
23118328-3	2013	The aim of this study is to evaluate the possible association between sex, polymorphisms in the CYP2C8 and CYP2C9 genes, and the pharmacokinetics of losartan, valsartan, candesartan, and telmisartan.	Valsartan	159-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
23118328-7	2013	CYP2C9 variants were associated only with losartan pharmacokinetics: the half-life of losartan was higher in CYP2C9*3 allele carriers (3.1 +- 0.4 hours) than in volunteers with the wild-type genotype (2.3 +- 0.1 hours) (P <= 0.05).	Losartan	42-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
23229783-2	2013	Recently, we reported that culture of human hepatocellular carcinoma FLC-4 cells on micro-space cell culture plates could increase the functional expression of drug-metabolizing enzymes including CYP3A4 and CYP2C9, which are involved in 1"-hydroxylation and 6-hydroxylation of BBR, respectively.	Benzbromarone	277-280	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	207-213
23118328-7	2013	CYP2C9 variants were associated only with losartan pharmacokinetics: the half-life of losartan was higher in CYP2C9*3 allele carriers (3.1 +- 0.4 hours) than in volunteers with the wild-type genotype (2.3 +- 0.1 hours) (P <= 0.05).	Losartan	42-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
23118328-7	2013	CYP2C9 variants were associated only with losartan pharmacokinetics: the half-life of losartan was higher in CYP2C9*3 allele carriers (3.1 +- 0.4 hours) than in volunteers with the wild-type genotype (2.3 +- 0.1 hours) (P <= 0.05).	Losartan	86-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
23118328-7	2013	CYP2C9 variants were associated only with losartan pharmacokinetics: the half-life of losartan was higher in CYP2C9*3 allele carriers (3.1 +- 0.4 hours) than in volunteers with the wild-type genotype (2.3 +- 0.1 hours) (P <= 0.05).	Losartan	86-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
23257392-1	2013	The cytochrome P450 (P450, CYP) 2A6 inhibitor chalepensin was found to inhibit human CYP1A1, CYP1A2, CYP2A13, CYP2C9, CYP2D6, CYP2E1, and CYP3A4 to different extents.	3-(alpha,alpha-dimethylallyl)psoralen	46-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
23385314-3	2013	Efavirenz was a moderate inhibitor of CYP2C9 (K(i) = 19.46 microM) and CYP2C19 (K(i) = 21.31 microM); and a weak inhibitor of CYP3A (K(i) = 40.33 microM).	efavirenz	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
23118328-9	2013	These results suggest that genotypes for CYP2C9 and CYP2C8 are relevant to the pharmacokinetics of losartan and valsartan, respectively, but not the pharmacokinetics of candesartan or telmisartan.	Losartan	99-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
23118328-9	2013	These results suggest that genotypes for CYP2C9 and CYP2C8 are relevant to the pharmacokinetics of losartan and valsartan, respectively, but not the pharmacokinetics of candesartan or telmisartan.	Valsartan	112-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
23481074-0	2013	Cytochrome P450 (CYP2C9*2,*3) & vitamin-K epoxide reductase complex (VKORC1 -1639G<A) gene polymorphisms & their effect on acenocoumarol dose in patients with mechanical heart valve replacement.	Acenocoumarol	134-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
23545593-0	2013	A case-report of unpredictable and massive voriconazole intoxication in a patient with extensive CYP2C19 and CYP2C9 polymorphisms.	Voriconazole	43-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
23545593-1	2013	This case-report describes a massive voriconazole (VRZ) intoxication in a patient with a poor metabolizer profile, highlighted by low plasma main metabolite concentrations (N-oxide voriconazole), despite an extensive genetic profile for CYP2C19 and CYP2C9.	Voriconazole	37-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	249-255
23545593-1	2013	This case-report describes a massive voriconazole (VRZ) intoxication in a patient with a poor metabolizer profile, highlighted by low plasma main metabolite concentrations (N-oxide voriconazole), despite an extensive genetic profile for CYP2C19 and CYP2C9.	Voriconazole	51-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	249-255
23481074-1	2013	BACKGROUND & OBJECTIVES: Studies have demonstrated the effect of CYP2C9 (cytochrome P450) and VKORC1 (vitamin K epoxide reductase complex) gene polymorphisms on the dose of acenocoumarol.	Adenosine Monophosphate	12-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
23481074-1	2013	BACKGROUND & OBJECTIVES: Studies have demonstrated the effect of CYP2C9 (cytochrome P450) and VKORC1 (vitamin K epoxide reductase complex) gene polymorphisms on the dose of acenocoumarol.	Acenocoumarol	177-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
23481074-3	2013	The aim of this study was to determine the occurrence of CYP2C9*2,*3 and VKORC 1 -1639G>A gene polymorphisms and to study their effects on the dose of acenocoumarol required to maintain a target International Normalized Ratio (INR) in patients with mechanical heart valve replacement.	Acenocoumarol	154-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
23481074-12	2013	INTERPRETATION & CONCLUSIONS: The study findings point towards the role of CYP2C9 and VKORC1 gene polymorphisms in determining the inter-individual dose variability of acenocoumarol in the Indian patients with mechanical heart valve replacement.	Acenocoumarol	172-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
24324494-3	2013	The gene variants in CYP2C9, ABCC8/KCNJ11, and TCF7L2 were associated with the effect of sulfonylureas.	Sulfonylurea Compounds	89-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
24324494-4	2013	CYP2C9 encodes sulfonylurea metabolizing cytochrome P450 isoenzyme 2C9, ABCC8 and KCNJ11 genes encode proteins constituting ATP-sensitive K(+) channel which is a therapeutic target for sulfonylureas, and TCF7L2 is a gene with the strongest association with type 2 diabetes.	Sulfonylurea Compounds	15-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24324494-4	2013	CYP2C9 encodes sulfonylurea metabolizing cytochrome P450 isoenzyme 2C9, ABCC8 and KCNJ11 genes encode proteins constituting ATP-sensitive K(+) channel which is a therapeutic target for sulfonylureas, and TCF7L2 is a gene with the strongest association with type 2 diabetes.	Sulfonylurea Compounds	185-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
23958198-3	2013	Based on in vitro evidence cranberry juice is an inhibitor of CYP enzymes and at higher amounts as potent as ketoconazole (CYP3A) and fluconazole (CYP2C9).	Fluconazole	134-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
23400742-1	2013	The nonnucleoside reverse transcriptase inhibitor etravirine, approved for use in treatment-experienced, HIV-1-infected patients, is a substrate and inducer of cytochrome P450 (CYP) 3A4 and a substrate and inhibitor of CYP2C9/CYP2C19.	etravirine	50-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	219-225
23563037-0	2013	Variability in CYP2C9 allele frequency: a pilot study of its predicted impact on warfarin response among healthy South and North Indians.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
24800477-0	2013	[Relationship between warfarin dosing and activity of CYP2C9 assessed by the content of losartan and its metabolite E-3174 in the urine of patients with mechanical prosthetic heart valves].	Warfarin	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
24800477-0	2013	[Relationship between warfarin dosing and activity of CYP2C9 assessed by the content of losartan and its metabolite E-3174 in the urine of patients with mechanical prosthetic heart valves].	Losartan	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
24800477-0	2013	[Relationship between warfarin dosing and activity of CYP2C9 assessed by the content of losartan and its metabolite E-3174 in the urine of patients with mechanical prosthetic heart valves].	losartan carboxylic acid	116-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
24800477-1	2013	We evaluated effect of activity of cytochrome P450 CYP2C9 on maintenance doses of warfarin in 33 patients with implanted artificial heart valves.	Warfarin	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
24858991-1	2013	BACKGROUND AND OBJECTIVE: VKORC1, CYP2C9, and CYP4F2 are known to be responsible for the metabolism of warfarin.	Warfarin	103-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
23111422-1	2013	OBJECTIVES: Etravirine (ETV) is metabolized by cytochrome P450 (CYP) 3A, 2C9, and 2C19.	etravirine	12-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-76
23111422-1	2013	OBJECTIVES: Etravirine (ETV) is metabolized by cytochrome P450 (CYP) 3A, 2C9, and 2C19.	etravirine	24-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-76
23343733-2	2013	Used concomitantly with coumarin derivatives, it may enhance their anticoagulant effects by inhibiting the CYP2C9 isoenzyme; an interaction which has been well described for oral and vaginal administrations of miconazole.	coumarin	24-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
23343733-2	2013	Used concomitantly with coumarin derivatives, it may enhance their anticoagulant effects by inhibiting the CYP2C9 isoenzyme; an interaction which has been well described for oral and vaginal administrations of miconazole.	Miconazole	210-220	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
24399734-0	2013	Effect of CYP2C9 and VKORC1 genetic variations on warfarin dose requirements in Indian patients.	Warfarin	50-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
24399734-2	2013	The management of warfarin therapy is challenging because it shows large inter and intra individual variability in patient response due to factors like age, gender, diet, concurrent drug interactions and variations in CYP2C9 and VKORC1 genes.	Warfarin	18-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
24399734-3	2013	Studies implicate that polymorphisms in VKORC1 and CYP2C9 genes are associated with reduced doses of warfarin.	Warfarin	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
24399734-4	2013	The aim of our current study was to characterize the effects of VKORC1 and CYP2C9 gene variations that contribute to variability in warfarin dosing in Indian patients.	Warfarin	132-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
23563037-8	2013	The variation in the frequency of combined CYP2C9/ VKORC1 genotypes revealed plausible difference in warfarin response among SI and NI.	Warfarin	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
23196355-7	2013	In conclusion, we developed a prediction algorithm using clinical data and three polymorphisms in  VKORC1, CYP2C9*  and  CYP4F2  genes that provided a steady acenocoumarol dose for about 50% of patients in the Validation Cohort.	Acenocoumarol	158-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
22917556-6	2012	Formation of 12-hydroxyellipticine is generated mainly by CYP2C19, followed by CYP2C9>3A4>2D6>2E1 and >2A6.	12-hydroxyellipticine	13-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
23237631-6	2012	The aim of this study is to evaluate the effectiveness and efficiency of an acenocoumarol dosing algorithm developed by our group which includes demographic, clinical and pharmacogenetic variables (VKORC1, CYP2C9, CYP4F2 and ApoE) in patients with venous thromboembolism (VTE).	Acenocoumarol	76-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	206-212
23089473-7	2012	Hypoxia induced SP cell proliferation, and microarray analysis showed that the expression of CYP2C9 was significantly increased in hypoxic than normoxic SP cells.	sp	16-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
23342320-0	2012	CYP2C9 Mutation Affecting the Individual Variability of Warfarin Dose Requirement.	Warfarin	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
23342320-5	2012	There are two identified genes that are responsible for the main proportion of the genetic effect: CYP2C9, which codes for the enzyme cytochrome P450 2C9 that metabolizes S-warfarin, and VKORC1, which codes for warfarin"s target, vitamin K epoxide reductase.	Warfarin	173-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
23342320-5	2012	There are two identified genes that are responsible for the main proportion of the genetic effect: CYP2C9, which codes for the enzyme cytochrome P450 2C9 that metabolizes S-warfarin, and VKORC1, which codes for warfarin"s target, vitamin K epoxide reductase.	Warfarin	173-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-153
23342320-5	2012	There are two identified genes that are responsible for the main proportion of the genetic effect: CYP2C9, which codes for the enzyme cytochrome P450 2C9 that metabolizes S-warfarin, and VKORC1, which codes for warfarin"s target, vitamin K epoxide reductase.	Warfarin	211-219	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
23342320-5	2012	There are two identified genes that are responsible for the main proportion of the genetic effect: CYP2C9, which codes for the enzyme cytochrome P450 2C9 that metabolizes S-warfarin, and VKORC1, which codes for warfarin"s target, vitamin K epoxide reductase.	Warfarin	211-219	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-153
23342320-6	2012	We report a case of intolerance to warfarin dosing, due to impaired drug metabolism in a patient with CYP2C9(*)1/(*)3 and VKORC 1173TT.	Warfarin	35-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
23089473-9	2012	These results indicate that STAT3 is critical for CSC survival and hypoxia-inducible CYP2C9 expression is responsible the doxorubicin resistance of CSCs under hypoxic conditions.	Doxorubicin	122-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
23132553-7	2012	Our results show that the CYP4F2 p.V433M polymorphism is associated with interindividual variability in response to coumarin drugs, but with a low effect size that is confirmed to be lower than those contributed by VKORC1 and CYP2C9 polymorphisms.	coumarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	226-232
23018470-1	2012	BACKGROUND AND OBJECTIVE: Genetic polymorphisms of cytochrome P450 (CYP) 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) and patient demographic characteristics are responsible for inter-individual differences in warfarin maintenance dosage requirements.	Warfarin	237-245	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-76
23781667-3	2012	The variability of Warfarin dosage is largely genetically determined, and it can be partly explained by the C1173T and G-1639A polymorphisms of vitamin K epoxide reductase complex subunit 1 (VKORC1) which is its target and *2 and *3 allele of Cytochrome P-450 (CYP) 2C9 [CYP2C9] enzyme which metabolizes to its inactive form.	Warfarin	19-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	243-269
23018470-1	2012	BACKGROUND AND OBJECTIVE: Genetic polymorphisms of cytochrome P450 (CYP) 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) and patient demographic characteristics are responsible for inter-individual differences in warfarin maintenance dosage requirements.	Warfarin	237-245	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
23153186-2	2012	AREAS COVERED: This review focuses on the effect of CYP2C enzymes on metabolism of sulphonylureas (SUs), meglitinides, and thiazolidinediones (TZDs) discussing their impact on pharmacokinetics, drug interactions and toxicological profiles.	Sulfonylurea Compounds	83-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-57
23153186-2	2012	AREAS COVERED: This review focuses on the effect of CYP2C enzymes on metabolism of sulphonylureas (SUs), meglitinides, and thiazolidinediones (TZDs) discussing their impact on pharmacokinetics, drug interactions and toxicological profiles.	Sulfonylurea Compounds	99-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-57
23153186-2	2012	AREAS COVERED: This review focuses on the effect of CYP2C enzymes on metabolism of sulphonylureas (SUs), meglitinides, and thiazolidinediones (TZDs) discussing their impact on pharmacokinetics, drug interactions and toxicological profiles.	meglitinide	105-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-57
23153186-2	2012	AREAS COVERED: This review focuses on the effect of CYP2C enzymes on metabolism of sulphonylureas (SUs), meglitinides, and thiazolidinediones (TZDs) discussing their impact on pharmacokinetics, drug interactions and toxicological profiles.	Thiazolidinediones	123-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-57
23153186-2	2012	AREAS COVERED: This review focuses on the effect of CYP2C enzymes on metabolism of sulphonylureas (SUs), meglitinides, and thiazolidinediones (TZDs) discussing their impact on pharmacokinetics, drug interactions and toxicological profiles.	Thiazolidinediones	143-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-57
23153186-4	2012	EXPERT OPINION: Genetic polymorphisms of CYP2C9 enzymes (*2/*2, *2/*3, *3/*3) influence the glycaemic response to SUs and impair their substrate metabolism.	Sulfonylurea Compounds	114-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
23153186-6	2012	Functional polymorphisms of CYP2C8- and CYP2C9 drug metabolizing genes affect markedly pharmacokinetics of meglitinides.	meglitinide	107-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
23781667-0	2012	Prevalence of VKORC1 and CYP2C9 gene polymorphisms in Indian population and its effect on warfarin response.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
23781667-3	2012	The variability of Warfarin dosage is largely genetically determined, and it can be partly explained by the C1173T and G-1639A polymorphisms of vitamin K epoxide reductase complex subunit 1 (VKORC1) which is its target and *2 and *3 allele of Cytochrome P-450 (CYP) 2C9 [CYP2C9] enzyme which metabolizes to its inactive form.	Warfarin	19-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	271-277
23781667-14	2012	CONCLUSION: In the present study the effect of CYP2C9*2, *3, and VKORC1 (C1173T and G-1639A) genotypes on warfarin dose was observed.	Warfarin	106-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
22205719-2	2012	Bosentan, an endothelin (ET) receptor-type ET(A) and ET(B) antagonist, is metabolized to active metabolites by and an inducer of cytochrome P450 (CYP)2C9 and CYP3A.	Bosentan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-153
23104259-10	2012	CYP2C9*3 may be the main genetic factor in hemorrhagic complications in Chinese patients under warfarin anticoagulation.	Warfarin	95-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
23089684-9	2012	Our data set included CYP2C9*3 (rs1057910) and CYP2C19*2 (rs4244285) enzyme activity-altering variants associated in a recent genome-wide study with acenocoumarol-induced and warfarin-induced anticoagulation or to the antiplatelet effect of clopidogrel, respectively.	Acenocoumarol	149-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
23015069-8	2012	In conclusion, PG refinement algorithm integrating early INR response and three genotypes (CYP2C9*3, VKORC1-1639A/G, CYP4F2 rs2108622) improves the accuracy of warfarin dose prediction in Chinese patients mainly under low-intensity anticoagulation.	Warfarin	160-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
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 9	Homo sapiens	206-212
22259022-9	2012	In order to investigate whether the polymorphism of CYP2C9 and CYP2C19 enzymes could be related to the metabolism of mitotane, RT-PCR analysis was performed.	Mitotane	117-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
26605619-5	2012	The hydrogen abstraction from camphor, and hydrogen abstraction and C-O addition of cyclohexene and propene by P450cam have been modeled, along with the addition of benzene to Compound I in CYP2C9, at the B3LYP-D2/CHARMM27 level of theory.	Hydrogen	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
26605619-5	2012	The hydrogen abstraction from camphor, and hydrogen abstraction and C-O addition of cyclohexene and propene by P450cam have been modeled, along with the addition of benzene to Compound I in CYP2C9, at the B3LYP-D2/CHARMM27 level of theory.	Camphor	30-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
26605619-5	2012	The hydrogen abstraction from camphor, and hydrogen abstraction and C-O addition of cyclohexene and propene by P450cam have been modeled, along with the addition of benzene to Compound I in CYP2C9, at the B3LYP-D2/CHARMM27 level of theory.	Hydrogen	43-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
26605619-5	2012	The hydrogen abstraction from camphor, and hydrogen abstraction and C-O addition of cyclohexene and propene by P450cam have been modeled, along with the addition of benzene to Compound I in CYP2C9, at the B3LYP-D2/CHARMM27 level of theory.	cyclohexene	84-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
26605619-5	2012	The hydrogen abstraction from camphor, and hydrogen abstraction and C-O addition of cyclohexene and propene by P450cam have been modeled, along with the addition of benzene to Compound I in CYP2C9, at the B3LYP-D2/CHARMM27 level of theory.	propylene	100-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
26605619-5	2012	The hydrogen abstraction from camphor, and hydrogen abstraction and C-O addition of cyclohexene and propene by P450cam have been modeled, along with the addition of benzene to Compound I in CYP2C9, at the B3LYP-D2/CHARMM27 level of theory.	Benzene	165-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
22941809-0	2012	CYP2C9*3(1075A>C), MDR1 G2677T/A and MDR1 C3435T are determinants of inter-subject variability in fluvastatin pharmacokinetics in healthy Chinese volunteers.	Fluvastatin	101-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
22941809-1	2012	To evaluate the impact of single-nucleotide polymorphisms (SNPs) in CYP2C9, MDR1, SLCO1B1 and ABCG2 on the pharmacokinetics of fluvastatin in Chinese participants.A pharmacokinetic study of fluvastatin (single dose 40 mg) was conducted in 12 healthy Chinese volunteers.	single-nucleotide	26-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
22941809-1	2012	To evaluate the impact of single-nucleotide polymorphisms (SNPs) in CYP2C9, MDR1, SLCO1B1 and ABCG2 on the pharmacokinetics of fluvastatin in Chinese participants.A pharmacokinetic study of fluvastatin (single dose 40 mg) was conducted in 12 healthy Chinese volunteers.	Fluvastatin	127-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
22941809-4	2012	The SNPs were determined by TaqMan (MGB) genotyping assay.Effect of CYP2C9*3 (c.1075A>C) on area under the plasma concentration-time curve (AUC) of fluvastatin was statistically significant.	Fluvastatin	151-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
23287317-3	2012	Polymorphic alleles CYP2C9 FNx01 2 and CYP2C9 FNx01 3 occur in the Indian population and this may serve as the basis for using genotyping as a tool to predict phenytoin toxicity.	Phenytoin	159-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
22791347-3	2012	The present study reviews the literature on genetic contributions to fluoxetine response in children and adults, and concludes that the different polymorphisms of CYP2D6 and CYP2C9 may influence the blood concentrations of fluoxetine.	Fluoxetine	69-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	174-180
22791347-3	2012	The present study reviews the literature on genetic contributions to fluoxetine response in children and adults, and concludes that the different polymorphisms of CYP2D6 and CYP2C9 may influence the blood concentrations of fluoxetine.	Fluoxetine	223-233	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	174-180
23287317-0	2012	Association of CYP2C9 polymorphisms with phenytoin toxicity in Indian patients.	Phenytoin	41-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
22933344-10	2012	The formation of 5,6-dihydroxy BBR from 6-hydroxy BBR was catalysed by recombinant CYP2C9 and CYP1A2.	5,6-dihydroxy bbr	17-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
22933344-10	2012	The formation of 5,6-dihydroxy BBR from 6-hydroxy BBR was catalysed by recombinant CYP2C9 and CYP1A2.	6-hydroxybenzbromarone	40-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
22933344-13	2012	These results suggest that (i) the formation of 1"-hydroxy BBR and 6-hydroxy BBR is mainly catalysed by CYP3A4 and CYP2C9, respectively, and (ii) the formation of 5,6-dihydroxy BBR is catalysed by CYP2C9 and CYP1A2 in human liver microsomes.	1'-hydroxybenzbromarone	48-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
22933344-13	2012	These results suggest that (i) the formation of 1"-hydroxy BBR and 6-hydroxy BBR is mainly catalysed by CYP3A4 and CYP2C9, respectively, and (ii) the formation of 5,6-dihydroxy BBR is catalysed by CYP2C9 and CYP1A2 in human liver microsomes.	1'-hydroxybenzbromarone	48-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
22933344-13	2012	These results suggest that (i) the formation of 1"-hydroxy BBR and 6-hydroxy BBR is mainly catalysed by CYP3A4 and CYP2C9, respectively, and (ii) the formation of 5,6-dihydroxy BBR is catalysed by CYP2C9 and CYP1A2 in human liver microsomes.	6-hydroxybenzbromarone	67-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
22933344-13	2012	These results suggest that (i) the formation of 1"-hydroxy BBR and 6-hydroxy BBR is mainly catalysed by CYP3A4 and CYP2C9, respectively, and (ii) the formation of 5,6-dihydroxy BBR is catalysed by CYP2C9 and CYP1A2 in human liver microsomes.	6-hydroxybenzbromarone	67-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
22933344-13	2012	These results suggest that (i) the formation of 1"-hydroxy BBR and 6-hydroxy BBR is mainly catalysed by CYP3A4 and CYP2C9, respectively, and (ii) the formation of 5,6-dihydroxy BBR is catalysed by CYP2C9 and CYP1A2 in human liver microsomes.	5,6-dihydroxy bbr	163-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
22933344-13	2012	These results suggest that (i) the formation of 1"-hydroxy BBR and 6-hydroxy BBR is mainly catalysed by CYP3A4 and CYP2C9, respectively, and (ii) the formation of 5,6-dihydroxy BBR is catalysed by CYP2C9 and CYP1A2 in human liver microsomes.	5,6-dihydroxy bbr	163-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
22896727-1	2012	(S)-Warfarin 7-hydroxylation and midazolam 1"-hydroxylation are among the preferred probe substrate reactions for CYP2C9 and CYP3A4/5, respectively.	Warfarin	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
22896727-1	2012	(S)-Warfarin 7-hydroxylation and midazolam 1"-hydroxylation are among the preferred probe substrate reactions for CYP2C9 and CYP3A4/5, respectively.	Midazolam	33-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
22859722-3	2012	Raloxifene, a drug known to undergo CYP3A-mediated reactive metabolite formation and time-dependent inhibition in vitro, was used to explore the potential for bioactivation and enzyme inactivation of additional P450 enzymes (CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A5).	Raloxifene Hydrochloride	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	241-247
23287317-3	2012	Polymorphic alleles CYP2C9 FNx01 2 and CYP2C9 FNx01 3 occur in the Indian population and this may serve as the basis for using genotyping as a tool to predict phenytoin toxicity.	Phenytoin	159-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
23287317-4	2012	AIMS: To evaluate the association between the presence of polymorphic alleles CYP2C9 FNx01 2 and FNx013 and phenytoin toxicity in Indian patients with epilepsy.	Phenytoin	108-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
23287317-16	2012	We found a significant association between polymorphic alleles CYP2C9 FNx01 2 and FNx013 and toxic phenytoin levels.	Phenytoin	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
22853867-4	2012	RESULTS: The AUC and t1/2 of glibenclamide following the microdosing tended to be higher and longer, respectively, in CYP2C9*1/*3 than CYP2C9*1/*1 subjects.	Glyburide	29-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
23148630-0	2012	Influence of the CYP2C9*3 allele on the pharmacological interaction between warfarin and simvastatin.	Warfarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
23148630-0	2012	Influence of the CYP2C9*3 allele on the pharmacological interaction between warfarin and simvastatin.	Simvastatin	89-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
23148630-2	2012	A clinically significant interaction between warfarin and simvastatin is unique to carriers of the CYP2C9*3 allele.	Warfarin	45-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
23041981-0	2012	Effect of genetic variants, especially CYP2C9 and VKORC1, on the pharmacology of warfarin.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
23041981-1	2012	The genes encoding the cytochrome P450 2C9 enzyme (CYP2C9) and vitamin K-epoxide reductase complex unit 1 (VKORC1) are major determinants of anticoagulant response to warfarin.	Warfarin	167-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-42
23041981-1	2012	The genes encoding the cytochrome P450 2C9 enzyme (CYP2C9) and vitamin K-epoxide reductase complex unit 1 (VKORC1) are major determinants of anticoagulant response to warfarin.	Warfarin	167-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
22571484-4	2012	In addition, it has been proposed that the residues involved in substrate recognition sites (SRS) 1, SRS 3, and/or SRS 4 are important for the metabolizing capacity and/or the substrate binding of CYP2C9 and CYP2C19.	srs	93-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
22533669-4	2012	SYBR Green-based real-time polymerase chain reaction (PCR) assay was used for studying VKORC1 (C1173T) and CYP2C9*3 polymorphisms.	sybr green	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
22533669-8	2012	VKORC1 TT and CYP2C9*2\*2 were associated with a significantly lower warfarin dose.	Warfarin	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
22533669-9	2012	VKORC1 and CYP2C9 accounted for 31.7% and 15.6% of warfarin dose variability, respectively, and together with clinical factors explained 61.3% of total variability.	Warfarin	51-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
23148630-2	2012	A clinically significant interaction between warfarin and simvastatin is unique to carriers of the CYP2C9*3 allele.	Simvastatin	58-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
23113310-0	2012	CYP2C9 and VKORC1 gene polymorphism is inessential for bleeding development under conditions of oral application of anticoagulant acenocoumarol in Russian patients at high risk of thromboembolic complications.	Acenocoumarol	130-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
22752007-4	2012	In addition, we revealed that sesamin caused a mechanism-based inhibition (MBI) of CYP2C9, the P450 enzyme responsible for sesamin monocatecholization.	sesamin	30-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
22752007-4	2012	In addition, we revealed that sesamin caused a mechanism-based inhibition (MBI) of CYP2C9, the P450 enzyme responsible for sesamin monocatecholization.	sesamin	123-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
22752007-7	2012	The P450 enzymes responsible for S- and R-monocatechol formation were CYP2C9 and CYP1A2, respectively.	Sulfur	33-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
22752007-7	2012	The P450 enzymes responsible for S- and R-monocatechol formation were CYP2C9 and CYP1A2, respectively.	r-monocatechol	40-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
22853867-1	2012	OBJECTIVES: To test whether the multiple phenotype and genotype relationships established using therapeutic dose, can be reproduced following oral microdosing using substrates of CYP2C9 (warfarin and glibenclamide), CYP2C19 (lansoprazole), CYP2D6 (dextromethorphan), and OATPs (glibenclamide).	Warfarin	187-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	179-185
22853867-4	2012	RESULTS: The AUC and t1/2 of glibenclamide following the microdosing tended to be higher and longer, respectively, in CYP2C9*1/*3 than CYP2C9*1/*1 subjects.	Glyburide	29-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-141
22886551-7	2012	These indicate a long-range haplotype containing the CYP2C9*13 and CYP2C19*2 mutation, which means most CYP2C9*13 carriers will carry the CYP2C19*2 allele and the six SNPs of the CYP2C9*1B haplotype group, and may have more reduced intrinsic clearance of drugs such as phenytoin, tolbutamide and chlorpropamide that are metabolized by both CYP2C9 and CYP2C19.	Chlorpropamide	296-310	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
22486182-9	2012	A final multivariate regression model that included the target International Normalized Ratio, VKORC1 and CYP2C9 genotypes explained 36 2% of the overall interindividual variability in acenocoumarol dose requirement.	Acenocoumarol	185-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
22486182-11	2012	VKORC1 and CYP2C9 variants significantly affected acenocoumarol dose, in-line with results in other populations.	Acenocoumarol	50-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
22486182-12	2012	For the Moroccan population, the SNPs that have the largest effect on acecoumarol dose are CYP2C9 rs1799853, CYP2C9 rs1057910 and VKORC1 rs9923231.	acecoumarol	70-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
22486182-12	2012	For the Moroccan population, the SNPs that have the largest effect on acecoumarol dose are CYP2C9 rs1799853, CYP2C9 rs1057910 and VKORC1 rs9923231.	acecoumarol	70-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
22943175-9	2012	The inhibitory action of glycyrrhetinic acid was observed in CYP2C9 for 4-hydroxylation of diclofenac, CYP2C19 for 4"-hydroxylation of (S)-mephenytoin and CYP3A4 for 1"-hydroxylation of midazolam with half maximal inhibitory concentration (IC50) values of 4.3-fold, 3.8-fold and 9.6-fold higher than specific inhibitors in HLM, respectively.	Glycyrrhetinic Acid	25-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
22943175-9	2012	The inhibitory action of glycyrrhetinic acid was observed in CYP2C9 for 4-hydroxylation of diclofenac, CYP2C19 for 4"-hydroxylation of (S)-mephenytoin and CYP3A4 for 1"-hydroxylation of midazolam with half maximal inhibitory concentration (IC50) values of 4.3-fold, 3.8-fold and 9.6-fold higher than specific inhibitors in HLM, respectively.	Diclofenac	91-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
22943175-9	2012	The inhibitory action of glycyrrhetinic acid was observed in CYP2C9 for 4-hydroxylation of diclofenac, CYP2C19 for 4"-hydroxylation of (S)-mephenytoin and CYP3A4 for 1"-hydroxylation of midazolam with half maximal inhibitory concentration (IC50) values of 4.3-fold, 3.8-fold and 9.6-fold higher than specific inhibitors in HLM, respectively.	Mephenytoin	135-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
23047421-2	2012	Genotypes for two single nucleotide polymorphisms (SNPs) in the cytochrome P 450 2C9 gene, affecting warfarin metabolism, and one SNP in vitamin K reductase complex 1 gene, affecting warfarin sensitivity, account for approximately 30% of therapeutic warfarin dosing variability in whites and Asians.	Warfarin	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-84
23047421-2	2012	Genotypes for two single nucleotide polymorphisms (SNPs) in the cytochrome P 450 2C9 gene, affecting warfarin metabolism, and one SNP in vitamin K reductase complex 1 gene, affecting warfarin sensitivity, account for approximately 30% of therapeutic warfarin dosing variability in whites and Asians.	Warfarin	183-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-84
23047421-2	2012	Genotypes for two single nucleotide polymorphisms (SNPs) in the cytochrome P 450 2C9 gene, affecting warfarin metabolism, and one SNP in vitamin K reductase complex 1 gene, affecting warfarin sensitivity, account for approximately 30% of therapeutic warfarin dosing variability in whites and Asians.	Warfarin	183-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-84
22947619-6	2012	The surrounding SAM, a polyethylene glycol silane, displayed very little affinity toward the P450 isozyme CYP2C9, as demonstrated by x-ray photoelectron spectroscopy and surface plasmon resonance.	poly(ethylene glycol)silane	23-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
22886551-7	2012	These indicate a long-range haplotype containing the CYP2C9*13 and CYP2C19*2 mutation, which means most CYP2C9*13 carriers will carry the CYP2C19*2 allele and the six SNPs of the CYP2C9*1B haplotype group, and may have more reduced intrinsic clearance of drugs such as phenytoin, tolbutamide and chlorpropamide that are metabolized by both CYP2C9 and CYP2C19.	Phenytoin	269-278	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
22886551-7	2012	These indicate a long-range haplotype containing the CYP2C9*13 and CYP2C19*2 mutation, which means most CYP2C9*13 carriers will carry the CYP2C19*2 allele and the six SNPs of the CYP2C9*1B haplotype group, and may have more reduced intrinsic clearance of drugs such as phenytoin, tolbutamide and chlorpropamide that are metabolized by both CYP2C9 and CYP2C19.	Phenytoin	269-278	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
22886551-7	2012	These indicate a long-range haplotype containing the CYP2C9*13 and CYP2C19*2 mutation, which means most CYP2C9*13 carriers will carry the CYP2C19*2 allele and the six SNPs of the CYP2C9*1B haplotype group, and may have more reduced intrinsic clearance of drugs such as phenytoin, tolbutamide and chlorpropamide that are metabolized by both CYP2C9 and CYP2C19.	Phenytoin	269-278	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
22886551-7	2012	These indicate a long-range haplotype containing the CYP2C9*13 and CYP2C19*2 mutation, which means most CYP2C9*13 carriers will carry the CYP2C19*2 allele and the six SNPs of the CYP2C9*1B haplotype group, and may have more reduced intrinsic clearance of drugs such as phenytoin, tolbutamide and chlorpropamide that are metabolized by both CYP2C9 and CYP2C19.	Phenytoin	269-278	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
22886551-7	2012	These indicate a long-range haplotype containing the CYP2C9*13 and CYP2C19*2 mutation, which means most CYP2C9*13 carriers will carry the CYP2C19*2 allele and the six SNPs of the CYP2C9*1B haplotype group, and may have more reduced intrinsic clearance of drugs such as phenytoin, tolbutamide and chlorpropamide that are metabolized by both CYP2C9 and CYP2C19.	Tolbutamide	280-291	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
22886551-7	2012	These indicate a long-range haplotype containing the CYP2C9*13 and CYP2C19*2 mutation, which means most CYP2C9*13 carriers will carry the CYP2C19*2 allele and the six SNPs of the CYP2C9*1B haplotype group, and may have more reduced intrinsic clearance of drugs such as phenytoin, tolbutamide and chlorpropamide that are metabolized by both CYP2C9 and CYP2C19.	Tolbutamide	280-291	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
22886551-7	2012	These indicate a long-range haplotype containing the CYP2C9*13 and CYP2C19*2 mutation, which means most CYP2C9*13 carriers will carry the CYP2C19*2 allele and the six SNPs of the CYP2C9*1B haplotype group, and may have more reduced intrinsic clearance of drugs such as phenytoin, tolbutamide and chlorpropamide that are metabolized by both CYP2C9 and CYP2C19.	Tolbutamide	280-291	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
22886551-7	2012	These indicate a long-range haplotype containing the CYP2C9*13 and CYP2C19*2 mutation, which means most CYP2C9*13 carriers will carry the CYP2C19*2 allele and the six SNPs of the CYP2C9*1B haplotype group, and may have more reduced intrinsic clearance of drugs such as phenytoin, tolbutamide and chlorpropamide that are metabolized by both CYP2C9 and CYP2C19.	Tolbutamide	280-291	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
22854539-2	2012	We studied the functional polymorphisms of CYP2C9, CYP4F2 and VKORC1 genes to evaluate their impact on the warfarin maintenance dose in an admixed Omani patient cohort with Caucasian, African and Asian ancestries.	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
22854539-4	2012	Univariate analysis revealed that age, gender, weight, atrial fibrillation, deep vein thrombosis/pulmonary embolism and variant genotypes of CYP2C9 and VKORC1 loci were significantly associated with warfarin dose in the studied patient population.	Warfarin	199-207	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
22943175-12	2012	The results suggest that glycyrrhetinic acid has the potential to interact with a wide range of xenobiotics or endogenous chemicals that are CYP2C9, CYP2C19 and CYP3A4 substrates.	Glycyrrhetinic Acid	25-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
23156991-5	2012	The results revealed that a combination of glimepiride with piperine led to the enhancement of the bioavailability of glimepiride by inhibiting the CYP2C9 enzyme, which suggested that piperine might be beneficial as an adjuvant to glimepiride in a proper dose, in diabetic patients.	glimepiride	43-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
23156991-5	2012	The results revealed that a combination of glimepiride with piperine led to the enhancement of the bioavailability of glimepiride by inhibiting the CYP2C9 enzyme, which suggested that piperine might be beneficial as an adjuvant to glimepiride in a proper dose, in diabetic patients.	piperine	60-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
23156991-5	2012	The results revealed that a combination of glimepiride with piperine led to the enhancement of the bioavailability of glimepiride by inhibiting the CYP2C9 enzyme, which suggested that piperine might be beneficial as an adjuvant to glimepiride in a proper dose, in diabetic patients.	glimepiride	118-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
23156991-5	2012	The results revealed that a combination of glimepiride with piperine led to the enhancement of the bioavailability of glimepiride by inhibiting the CYP2C9 enzyme, which suggested that piperine might be beneficial as an adjuvant to glimepiride in a proper dose, in diabetic patients.	piperine	184-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
23156991-5	2012	The results revealed that a combination of glimepiride with piperine led to the enhancement of the bioavailability of glimepiride by inhibiting the CYP2C9 enzyme, which suggested that piperine might be beneficial as an adjuvant to glimepiride in a proper dose, in diabetic patients.	glimepiride	118-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
22886551-7	2012	These indicate a long-range haplotype containing the CYP2C9*13 and CYP2C19*2 mutation, which means most CYP2C9*13 carriers will carry the CYP2C19*2 allele and the six SNPs of the CYP2C9*1B haplotype group, and may have more reduced intrinsic clearance of drugs such as phenytoin, tolbutamide and chlorpropamide that are metabolized by both CYP2C9 and CYP2C19.	Chlorpropamide	296-310	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
22886551-7	2012	These indicate a long-range haplotype containing the CYP2C9*13 and CYP2C19*2 mutation, which means most CYP2C9*13 carriers will carry the CYP2C19*2 allele and the six SNPs of the CYP2C9*1B haplotype group, and may have more reduced intrinsic clearance of drugs such as phenytoin, tolbutamide and chlorpropamide that are metabolized by both CYP2C9 and CYP2C19.	Chlorpropamide	296-310	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
22886551-7	2012	These indicate a long-range haplotype containing the CYP2C9*13 and CYP2C19*2 mutation, which means most CYP2C9*13 carriers will carry the CYP2C19*2 allele and the six SNPs of the CYP2C9*1B haplotype group, and may have more reduced intrinsic clearance of drugs such as phenytoin, tolbutamide and chlorpropamide that are metabolized by both CYP2C9 and CYP2C19.	Chlorpropamide	296-310	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
22735459-0	2012	Effects of CYP2C9*1/*3 and *1/*13 on the pharmacokinetics of losartan and its active metabolite E-3174.	Losartan	61-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
22696420-7	2012	A direct comparison of SR-9186 and ketoconazole under typical assay conditions used in reaction phenotyping studies demonstrated that SR-9186 had selectivity over CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A5 greater than or equal to that of ketoconazole.	1-(4-imidazopyridinyl-7-phenyl)-3-(4'-cyanobiphenyl)urea	134-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
23331088-10	2012	Intriguingly, CYP2C19 may contributeto S-warfarin metabolism in patients, especially when CYP2C9 activity is compromised due to drug interactions orgenetic polymorphisms.	Warfarin	41-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
22735459-6	2012	However, AUC0-  of losartan was greater in CYP2C9*1/*3 subjects than in CYP2C9*1/*1, but these results were not significant (p < 0.05, but statistical power < 0.8).	Losartan	19-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
22735459-6	2012	However, AUC0-  of losartan was greater in CYP2C9*1/*3 subjects than in CYP2C9*1/*1, but these results were not significant (p < 0.05, but statistical power < 0.8).	Losartan	19-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
22735459-9	2012	CONCLUSION: These results suggest that CYP2C9*1/*3 and CYP2C9*1/*13 are similarly associated with decreased formation of E-3174 from losartan, but the clinical effects of losartan may not be reduced by CYP2C9*1/*3 and CYP2C9*1/*13.	losartan carboxylic acid	121-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
22735459-9	2012	CONCLUSION: These results suggest that CYP2C9*1/*3 and CYP2C9*1/*13 are similarly associated with decreased formation of E-3174 from losartan, but the clinical effects of losartan may not be reduced by CYP2C9*1/*3 and CYP2C9*1/*13.	losartan carboxylic acid	121-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
22735459-9	2012	CONCLUSION: These results suggest that CYP2C9*1/*3 and CYP2C9*1/*13 are similarly associated with decreased formation of E-3174 from losartan, but the clinical effects of losartan may not be reduced by CYP2C9*1/*3 and CYP2C9*1/*13.	losartan carboxylic acid	121-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
22735459-9	2012	CONCLUSION: These results suggest that CYP2C9*1/*3 and CYP2C9*1/*13 are similarly associated with decreased formation of E-3174 from losartan, but the clinical effects of losartan may not be reduced by CYP2C9*1/*3 and CYP2C9*1/*13.	losartan carboxylic acid	121-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
22735459-5	2012	The CYP2C9*1/*3 subjects showed lower oral clearance (p < 0.001) of losartan and higher Cmax (p < 0.01) and longer half-life (p < 0.01) of E-3174 than the CYP2C9*1/*1 subjects.	Losartan	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
22735459-1	2012	OBJECTIVE: The effects of CYP2C9*1/*3 and *1/*13 genotypes were evaluated on the pharmacokinetics of losartan and its active metabolite, E-3174, in Korean subjects.	Losartan	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
22735459-9	2012	CONCLUSION: These results suggest that CYP2C9*1/*3 and CYP2C9*1/*13 are similarly associated with decreased formation of E-3174 from losartan, but the clinical effects of losartan may not be reduced by CYP2C9*1/*3 and CYP2C9*1/*13.	Losartan	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
22735459-9	2012	CONCLUSION: These results suggest that CYP2C9*1/*3 and CYP2C9*1/*13 are similarly associated with decreased formation of E-3174 from losartan, but the clinical effects of losartan may not be reduced by CYP2C9*1/*3 and CYP2C9*1/*13.	Losartan	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
22735459-4	2012	RESULTS: The CYP2C9*1/*13 subjects showed lower oral clearance (p < 0.001) and greater AUC0-  (p < 0.01) of losartan and higher Cmax (p < 0.01) and longer half-life (p < 0.001) of E-3174 than the CYP2C9*1/*1 subjects, but AUC0-  of E-3174 was not different.	Losartan	114-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
22735459-9	2012	CONCLUSION: These results suggest that CYP2C9*1/*3 and CYP2C9*1/*13 are similarly associated with decreased formation of E-3174 from losartan, but the clinical effects of losartan may not be reduced by CYP2C9*1/*3 and CYP2C9*1/*13.	Losartan	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
22735459-9	2012	CONCLUSION: These results suggest that CYP2C9*1/*3 and CYP2C9*1/*13 are similarly associated with decreased formation of E-3174 from losartan, but the clinical effects of losartan may not be reduced by CYP2C9*1/*3 and CYP2C9*1/*13.	Losartan	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
23167228-0	2012	The combined effects of clinical factors and CYP2C9 and VKORC1 gene polymorphisms on initiating warfarin treatment in patients after cardiac valve surgery.	Warfarin	96-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
23167228-2	2012	The study aim was to analyze the influence of certain clinical factors and CYP2C9 and VKORC1 gene polymorphisms on the efficacy of initiation of warfarin treatment in patients after cardiac valve surgery.	Warfarin	145-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
22847201-0	2012	Lipid-lowering effect of fluvastatin in relation to cytochrome P450 2C9 variant alleles frequently distributed in the Czech population.	Fluvastatin	25-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-71
22966884-3	2012	Results of a bivariate analysis demonstrated that among tested polymorphisms, carriers of the variant CYP2C9*3 tended to require significantly lower maintenance PHT dosages than wild-type carriers (p < 0.0001); on the other hand, carriers of the variants CYP2C9*3 or CYP2C19*3 revealed significantly higher CDRs than wild-type carriers (p < 0.004).	Phenytoin	161-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
22966884-3	2012	Results of a bivariate analysis demonstrated that among tested polymorphisms, carriers of the variant CYP2C9*3 tended to require significantly lower maintenance PHT dosages than wild-type carriers (p < 0.0001); on the other hand, carriers of the variants CYP2C9*3 or CYP2C19*3 revealed significantly higher CDRs than wild-type carriers (p < 0.004).	Phenytoin	161-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	258-264
22966884-3	2012	Results of a bivariate analysis demonstrated that among tested polymorphisms, carriers of the variant CYP2C9*3 tended to require significantly lower maintenance PHT dosages than wild-type carriers (p < 0.0001); on the other hand, carriers of the variants CYP2C9*3 or CYP2C19*3 revealed significantly higher CDRs than wild-type carriers (p < 0.004).	cdrs	310-314	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
22966889-1	2012	Genotyping patients for CYP2C9 and VKORC1 polymorphisms can improve the accuracy of dosing during the initiation of anticoagulation with vitamin K antagonists (coumarin derivatives).	Vitamin K	137-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
22966889-1	2012	Genotyping patients for CYP2C9 and VKORC1 polymorphisms can improve the accuracy of dosing during the initiation of anticoagulation with vitamin K antagonists (coumarin derivatives).	coumarin	160-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
22538270-4	2012	The aim of the present study was to investigate the effect of gemfibrozil (CYP2C9 inhibitor) and its 1-O-beta-glucuronide (CYP2C8 inhibitor) on BRV disposition both in vivo (healthy participants) and in vitro (human liver microsomes and hepatocytes).	Gemfibrozil	62-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
22538270-11	2012	Overall, in vitro and in vivo data suggest that CYP2C8 and CYP2C9 are not involved in BRV hydroxylation, whereas hydroxylation of BRV-AC to BRV-OHAC is likely to be mediated by CYP2C9.	brv-ac	130-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	177-183
22538270-11	2012	Overall, in vitro and in vivo data suggest that CYP2C8 and CYP2C9 are not involved in BRV hydroxylation, whereas hydroxylation of BRV-AC to BRV-OHAC is likely to be mediated by CYP2C9.	brv-ohac	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	177-183
22743353-0	2012	Electrochemically driven drug metabolism via cytochrome P450 2C9 isozyme microsomes with cytochrome P450 reductase and indium tin oxide nanoparticle composites.	indium tin oxide	119-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-64
22673786-5	2012	Ibuprofen"s clearance varies with CYP2C9*3 genotype.	Ibuprofen	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
22847201-1	2012	BACKGROUND: CYP2C9*3 allele has been reported to correlate with increased plasma concentration of fluvastatin active form in healthy volunteers.	Fluvastatin	98-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
22847201-2	2012	We analyzed the correlation between the CYP2C9 genotype and cholesterol-lowering effect of fluvastatin in human hypercholesterolemic patients.	Cholesterol	60-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
22847201-2	2012	We analyzed the correlation between the CYP2C9 genotype and cholesterol-lowering effect of fluvastatin in human hypercholesterolemic patients.	Fluvastatin	91-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
22847201-4	2012	CYP2C9 genotype was determined by PCR-RFLP assay in 87 patients on concomitant fluvastatin therapy, in 48 patients on monotherapy, and in a control group of 254 healthy volunteers of Czech nationality.	Fluvastatin	79-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
22847201-9	2012	The CYP2C9*1/*3 genotype was associated with a decrease in LDL-C levels (by 40.0% for CYP2C9*1/*3, but only by 22.4% for CYP2C9*1/*1), and with the reduction of TC (by 28.6% in CYP2C9*1/*3 versus 20.2% in CYP2C9*1/*1).	Technetium	161-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
22847201-9	2012	The CYP2C9*1/*3 genotype was associated with a decrease in LDL-C levels (by 40.0% for CYP2C9*1/*3, but only by 22.4% for CYP2C9*1/*1), and with the reduction of TC (by 28.6% in CYP2C9*1/*3 versus 20.2% in CYP2C9*1/*1).	Technetium	161-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
22847201-9	2012	The CYP2C9*1/*3 genotype was associated with a decrease in LDL-C levels (by 40.0% for CYP2C9*1/*3, but only by 22.4% for CYP2C9*1/*1), and with the reduction of TC (by 28.6% in CYP2C9*1/*3 versus 20.2% in CYP2C9*1/*1).	Technetium	161-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
22847201-9	2012	The CYP2C9*1/*3 genotype was associated with a decrease in LDL-C levels (by 40.0% for CYP2C9*1/*3, but only by 22.4% for CYP2C9*1/*1), and with the reduction of TC (by 28.6% in CYP2C9*1/*3 versus 20.2% in CYP2C9*1/*1).	Technetium	161-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
22847201-9	2012	The CYP2C9*1/*3 genotype was associated with a decrease in LDL-C levels (by 40.0% for CYP2C9*1/*3, but only by 22.4% for CYP2C9*1/*1), and with the reduction of TC (by 28.6% in CYP2C9*1/*3 versus 20.2% in CYP2C9*1/*1).	Technetium	161-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
22847201-10	2012	CONCLUSIONS: In hypercholesterolemic patients, LDL-C serum concentration was decreased more significantly in fluvastatin-treated subjects bearing the CYP2C9*1/*3 genotype compared to CYP2C9*1/*1 genotype.	Fluvastatin	109-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
22847201-10	2012	CONCLUSIONS: In hypercholesterolemic patients, LDL-C serum concentration was decreased more significantly in fluvastatin-treated subjects bearing the CYP2C9*1/*3 genotype compared to CYP2C9*1/*1 genotype.	Fluvastatin	109-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	183-189
22547083-5	2012	METHODS: We assayed the activities of CYP2C9.1, CYP2C9.2, and CYP2C9.3 to metabolize diclofenac, flurbiprofen, and tolbutamide using a wild type or one of four POR variants (Q153R, A287P, R457H, and A503V).	Diclofenac	85-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
22674970-2	2012	Polymorphisms in the cytochrome P450 (CYP) 2C9 and vitamin K epoxide reductase genes change warfarin pharmacokinetics and pharmacodynamics, respectively.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-46
21358752-1	2012	To optimize the warfarin dose, a population-specific pharmacogenomic algorithm was developed using multiple linear regression model with vitamin K intake and cytochrome P450 IIC polypeptide9 (CYP2C9(*)2 and (*)3), vitamin K epoxide reductase complex 1 (VKORC1(*)3, (*)4, D36Y and -1639 G>A) polymorphism profile of subjects who attained therapeutic international normalized ratio as predictors.	Warfarin	16-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	192-198
22547083-5	2012	METHODS: We assayed the activities of CYP2C9.1, CYP2C9.2, and CYP2C9.3 to metabolize diclofenac, flurbiprofen, and tolbutamide using a wild type or one of four POR variants (Q153R, A287P, R457H, and A503V).	Diclofenac	85-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
22547083-5	2012	METHODS: We assayed the activities of CYP2C9.1, CYP2C9.2, and CYP2C9.3 to metabolize diclofenac, flurbiprofen, and tolbutamide using a wild type or one of four POR variants (Q153R, A287P, R457H, and A503V).	Diclofenac	85-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
22547083-5	2012	METHODS: We assayed the activities of CYP2C9.1, CYP2C9.2, and CYP2C9.3 to metabolize diclofenac, flurbiprofen, and tolbutamide using a wild type or one of four POR variants (Q153R, A287P, R457H, and A503V).	Flurbiprofen	97-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
21383771-4	2012	We confirmed the roles of three well-established loci (CYP2C9, VKORC1 and CYP4F2) in explaining warfarin dosage variation in the three Asian populations.	Warfarin	96-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
22547083-5	2012	METHODS: We assayed the activities of CYP2C9.1, CYP2C9.2, and CYP2C9.3 to metabolize diclofenac, flurbiprofen, and tolbutamide using a wild type or one of four POR variants (Q153R, A287P, R457H, and A503V).	Flurbiprofen	97-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
22547083-5	2012	METHODS: We assayed the activities of CYP2C9.1, CYP2C9.2, and CYP2C9.3 to metabolize diclofenac, flurbiprofen, and tolbutamide using a wild type or one of four POR variants (Q153R, A287P, R457H, and A503V).	Flurbiprofen	97-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
22547083-5	2012	METHODS: We assayed the activities of CYP2C9.1, CYP2C9.2, and CYP2C9.3 to metabolize diclofenac, flurbiprofen, and tolbutamide using a wild type or one of four POR variants (Q153R, A287P, R457H, and A503V).	Tolbutamide	115-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
22547083-5	2012	METHODS: We assayed the activities of CYP2C9.1, CYP2C9.2, and CYP2C9.3 to metabolize diclofenac, flurbiprofen, and tolbutamide using a wild type or one of four POR variants (Q153R, A287P, R457H, and A503V).	Tolbutamide	115-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
22547083-5	2012	METHODS: We assayed the activities of CYP2C9.1, CYP2C9.2, and CYP2C9.3 to metabolize diclofenac, flurbiprofen, and tolbutamide using a wild type or one of four POR variants (Q153R, A287P, R457H, and A503V).	Tolbutamide	115-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
22571356-2	2012	The effects of genetic polymorphisms at the vitamin K epoxide reductase [VKORC1] and cytochrome P450 2C9 [CYP2C9] loci have been increasingly acknowledged as contributory factors of enhanced warfarin sensitivity.	Warfarin	191-199	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-104
22233204-8	2012	METHODS: In vitro experiments were conducted to assess the inhibition and induction potential of tofacitinib for major drug metabolizing enzymes (CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 and CYP3A4).	tofacitinib	97-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-176
22360448-2	2012	CYP2C11 and CYP2C6 are considered as counterparts of human CYP2C9, which metabolizes many drugs including S-warfarin, diclofenac or ibuprofen.	Warfarin	106-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
22360448-2	2012	CYP2C11 and CYP2C6 are considered as counterparts of human CYP2C9, which metabolizes many drugs including S-warfarin, diclofenac or ibuprofen.	Diclofenac	118-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
22360448-2	2012	CYP2C11 and CYP2C6 are considered as counterparts of human CYP2C9, which metabolizes many drugs including S-warfarin, diclofenac or ibuprofen.	Ibuprofen	132-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
22360448-7	2012	Therefore, it should be taken into consideration that drugs metabolized by CYP2C9 in human could interact with rosuvastatin, as it has been already suggested for warfarin (rosuvastatin has increased its anticoagulant effect in human), and for telmisartan, sildenafil and glimepiride.	Rosuvastatin Calcium	111-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
22360448-7	2012	Therefore, it should be taken into consideration that drugs metabolized by CYP2C9 in human could interact with rosuvastatin, as it has been already suggested for warfarin (rosuvastatin has increased its anticoagulant effect in human), and for telmisartan, sildenafil and glimepiride.	Warfarin	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
22360448-7	2012	Therefore, it should be taken into consideration that drugs metabolized by CYP2C9 in human could interact with rosuvastatin, as it has been already suggested for warfarin (rosuvastatin has increased its anticoagulant effect in human), and for telmisartan, sildenafil and glimepiride.	Rosuvastatin Calcium	172-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
22360448-7	2012	Therefore, it should be taken into consideration that drugs metabolized by CYP2C9 in human could interact with rosuvastatin, as it has been already suggested for warfarin (rosuvastatin has increased its anticoagulant effect in human), and for telmisartan, sildenafil and glimepiride.	Telmisartan	243-254	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
22360448-7	2012	Therefore, it should be taken into consideration that drugs metabolized by CYP2C9 in human could interact with rosuvastatin, as it has been already suggested for warfarin (rosuvastatin has increased its anticoagulant effect in human), and for telmisartan, sildenafil and glimepiride.	Sildenafil Citrate	256-266	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
22360448-7	2012	Therefore, it should be taken into consideration that drugs metabolized by CYP2C9 in human could interact with rosuvastatin, as it has been already suggested for warfarin (rosuvastatin has increased its anticoagulant effect in human), and for telmisartan, sildenafil and glimepiride.	glimepiride	271-282	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
22571356-2	2012	The effects of genetic polymorphisms at the vitamin K epoxide reductase [VKORC1] and cytochrome P450 2C9 [CYP2C9] loci have been increasingly acknowledged as contributory factors of enhanced warfarin sensitivity.	Warfarin	191-199	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
22496396-5	2012	CYP2C9 and CYP2C19 were the primary enzymes responsible for formation of the N-hydroxylated metabolite.	Nitrogen	77-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
23087510-0	2012	Effect of anti-tuberculosis therapy on polymorphic drug metabolizing enzyme CYP2C9 using phenytoin as a probe drug.	Phenytoin	89-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
22531045-6	2012	In human liver microsomes, carnosic acid did not exhibit significant time-dependent inhibition for any of the cytochrome P450 enzymes investigated, although it did inhibit CYP2C9- and CYP3A4-catalyzed reactions with K(i) values of 9.2 and 4.3 muM, respectively.	salvin	27-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
22294058-0	2012	Search for the molecular basis of ultra-rapid CYP2C9-catalysed metabolism: relationship between SNP IVS8-109A>T and the losartan metabolism phenotype in Swedes.	Losartan	123-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
22288731-0	2012	Allele and genotype frequencies of CYP2C9 within an Iranian population (Mazandaran).	mazandaran	72-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
23087510-7	2012	Phenotyping for CYP2C9 enzyme was done by measuring the ratio of phenytoin and its metabolite p-HPPH (para hydroxy phenyl hydantoin) by reverse phase HPLC (high performance liquid chromatography) method before and after one month of ATT.	Phenytoin	65-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
23087510-7	2012	Phenotyping for CYP2C9 enzyme was done by measuring the ratio of phenytoin and its metabolite p-HPPH (para hydroxy phenyl hydantoin) by reverse phase HPLC (high performance liquid chromatography) method before and after one month of ATT.	p-hpph	94-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
23087510-7	2012	Phenotyping for CYP2C9 enzyme was done by measuring the ratio of phenytoin and its metabolite p-HPPH (para hydroxy phenyl hydantoin) by reverse phase HPLC (high performance liquid chromatography) method before and after one month of ATT.	para hydroxy phenyl hydantoin	102-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
23087510-8	2012	RESULTS: In the CYP2C9*1*1 genotype, the mean plasma concentrations of phenytoin before and after one month of ATT were 5.2 +- 0.3 mug/ml and 3.5 +- 0.4 mug/ml respectively, a reduction by 33% showing significant induction (P < 0.001).	Phenytoin	71-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
22528326-5	2012	We also confirmed CYP2C9 *3 variant was related to lower warfarin dose (2.01 +- 0.23 mg/d) requirement compared to wild type (3.21 +- 0.11 mg/d) (P = 0.001).	Warfarin	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
22528326-7	2012	The multiple linear regression model including VKORC1-1639G>A, CYP2C9, CYP4F2 and clinical factors (body surface area (BSA) and age) could explain 42 % of the variance in the warfarin maintenance dose.	Warfarin	178-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
21911247-1	2012	INTRODUCTION: The optimal dose of the oral anticoagulant warfarin varies with polymorphisms of the vitamin K epoxide reductase complex subunit 1 (VKORC1) and cytochrome P450 2C9 (CYP2C9) genes.	Warfarin	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-177
21911247-1	2012	INTRODUCTION: The optimal dose of the oral anticoagulant warfarin varies with polymorphisms of the vitamin K epoxide reductase complex subunit 1 (VKORC1) and cytochrome P450 2C9 (CYP2C9) genes.	Warfarin	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	179-185
22192158-2	2012	It is well known that gene polymorphisms of CytochromeP450 (CYP) 2C9 gene and the vitamin K epoxide reductase complex 1 (VKORC1) were significantly associated with warfarin dose.	Warfarin	164-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-68
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.	Sulfonamides	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
22692316-6	2012	RESULTS: CYP1A2, CYP2C9, CYP2C19 and CYP3A4 in HLM were involved in bakuchiol metabolism, among which CYP2C19 showed  the highest metabolic rate.	bakuchiol	68-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
22692316-7	2012	Co-incubation with ABT (2.5 mmol/L) could inhibit more than 90% of the enzyme activities for CYP1A2, CYP2C9, CYP2C19 and  CYP3A4.	1-aminobenzotriazole	19-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
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
22594566-1	2012	OBJECTIVE: Phenotyping cytochrome P450 (CYP) 2C9 activity with S-warfarin requires extensive blood sampling to characterize area under the concentration-time curve (AUC).	Warfarin	63-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-48
22594566-2	2012	This retrospective data analysis was conducted to determine if truncated S-warfarin AUCs can be used to measure CYP2C9 activity.	Warfarin	75-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
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.	aniline	57-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
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.	Hydroxylamine	100-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
22561479-0	2012	The cytochrome P-450 2C9/2C19 but not the ABCB1 genetic polymorphism may be associated with the liver cytochrome 3A4 induction by phenytoin.	Phenytoin	130-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-24
21811894-0	2012	Acenocoumarol sensitivity and pharmacokinetic characterization of CYP2C9 *5/*8,*8/*11,*9/*11 and VKORC1*2 in black African healthy Beninese subjects.	Acenocoumarol	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
21811894-1	2012	This study aimed at investigating the contribution of CYP2C9 and VKORC1 genetic polymorphisms to inter-individual variability of acenocoumarol pharmacokinetics and pharmacodynamics in Black Africans from Benin.	Acenocoumarol	129-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
21811894-8	2012	At 8 h post dose, the (S)-acenocoumarol concentrations in the CYP2C9*5/*8 and CYP2C9*9/*11 genotypes were about 1.9 and 5.1 fold higher compared with the CYP2C9*1/*1 genotype and 2.2- and 6.0-fold higher compared with the CYP2C9*1/*9 group, respectively.	Acenocoumarol	22-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
21811894-8	2012	At 8 h post dose, the (S)-acenocoumarol concentrations in the CYP2C9*5/*8 and CYP2C9*9/*11 genotypes were about 1.9 and 5.1 fold higher compared with the CYP2C9*1/*1 genotype and 2.2- and 6.0-fold higher compared with the CYP2C9*1/*9 group, respectively.	Acenocoumarol	22-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
21811894-8	2012	At 8 h post dose, the (S)-acenocoumarol concentrations in the CYP2C9*5/*8 and CYP2C9*9/*11 genotypes were about 1.9 and 5.1 fold higher compared with the CYP2C9*1/*1 genotype and 2.2- and 6.0-fold higher compared with the CYP2C9*1/*9 group, respectively.	Acenocoumarol	22-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
21811894-8	2012	At 8 h post dose, the (S)-acenocoumarol concentrations in the CYP2C9*5/*8 and CYP2C9*9/*11 genotypes were about 1.9 and 5.1 fold higher compared with the CYP2C9*1/*1 genotype and 2.2- and 6.0-fold higher compared with the CYP2C9*1/*9 group, respectively.	Acenocoumarol	22-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
21811894-11	2012	Significant association between plasma (S)-acenocoumarol concentration and CYP2C9 genotypes suggested the use of (S)-acenocoumarol for the phenotyping purpose.	Acenocoumarol	39-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
21811894-11	2012	Significant association between plasma (S)-acenocoumarol concentration and CYP2C9 genotypes suggested the use of (S)-acenocoumarol for the phenotyping purpose.	Acenocoumarol	113-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
22450566-3	2012	The objective of the present work was to evaluate the impact of vanillin and ethyl vanillin on the activities of CYP2C9, CYP2E1, CYP3A4, CYP2B6 and CYP1A2 in human liver microsomes (HLM) in vitro, and impact on the activities of CYP1A2, CYP2C, CYP3A and CYP2E1 in rat liver microsomes (RLM) in vivo.	vanillin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
22450566-3	2012	The objective of the present work was to evaluate the impact of vanillin and ethyl vanillin on the activities of CYP2C9, CYP2E1, CYP3A4, CYP2B6 and CYP1A2 in human liver microsomes (HLM) in vitro, and impact on the activities of CYP1A2, CYP2C, CYP3A and CYP2E1 in rat liver microsomes (RLM) in vivo.	vanillin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-118
22450566-3	2012	The objective of the present work was to evaluate the impact of vanillin and ethyl vanillin on the activities of CYP2C9, CYP2E1, CYP3A4, CYP2B6 and CYP1A2 in human liver microsomes (HLM) in vitro, and impact on the activities of CYP1A2, CYP2C, CYP3A and CYP2E1 in rat liver microsomes (RLM) in vivo.	ethyl vanillin	77-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
22450566-3	2012	The objective of the present work was to evaluate the impact of vanillin and ethyl vanillin on the activities of CYP2C9, CYP2E1, CYP3A4, CYP2B6 and CYP1A2 in human liver microsomes (HLM) in vitro, and impact on the activities of CYP1A2, CYP2C, CYP3A and CYP2E1 in rat liver microsomes (RLM) in vivo.	ethyl vanillin	77-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-118
22328583-9	2012	Danazol inhibited CYP2C9, CYP2C8, and CYP2D6 with IC(50) values of 1.44, 1.95, and 2.74 muM, respectively.	Danazol	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
22076061-1	2012	Molecular docking and molecular dynamics (MD) simulations are used to investigate the interactions of curcumin analogues (CAs) with human cytochrome P450 2 C9 (CYP2C9 or 2 C9) and the conformations of their binding sites.	Curcumin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-158
22076061-1	2012	Molecular docking and molecular dynamics (MD) simulations are used to investigate the interactions of curcumin analogues (CAs) with human cytochrome P450 2 C9 (CYP2C9 or 2 C9) and the conformations of their binding sites.	Curcumin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
22076061-3	2012	Results demonstrate that the most CAs studied lie 4~15 A above the heme of CYP2C9.	cas	34-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
22076061-3	2012	Results demonstrate that the most CAs studied lie 4~15 A above the heme of CYP2C9.	Heme	67-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
22076061-4	2012	The presence of CAs makes some residues in bound CYP2C9s become more flexible.	cas	16-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
22311023-1	2012	Metabolic transformations of two substrates for human cytochrome P450 (CYP450) 2C9, tolbutamide and diclofenac, were investigated in hepatic microsomes from Atlantic salmon (Salmo salar L.).	Tolbutamide	84-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-82
22311023-1	2012	Metabolic transformations of two substrates for human cytochrome P450 (CYP450) 2C9, tolbutamide and diclofenac, were investigated in hepatic microsomes from Atlantic salmon (Salmo salar L.).	Diclofenac	100-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-82
22311023-4	2012	Addition of sulfaphenazole, an inhibitor for mammalian CYP2C9, in a range from 1 to 200 muM decreased formation of TBOH in a concentration-dependent manner, but not to 50%.	Sulfaphenazole	12-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
22311023-4	2012	Addition of sulfaphenazole, an inhibitor for mammalian CYP2C9, in a range from 1 to 200 muM decreased formation of TBOH in a concentration-dependent manner, but not to 50%.	tboh	115-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
22534826-0	2012	A new algorithm to predict warfarin dose from polymorphisms of CYP4F2 , CYP2C9 and VKORC1 and clinical variables: derivation in Han Chinese patients with non valvular atrial fibrillation.	Warfarin	27-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
22534826-2	2012	The objective of this study was to develop a new algorithm by polymorphisms of CYP2C9, VKORC1 and CYP4F2 to predict the daily stable dose of warfarin in Chinese patients with NVAF.	Warfarin	141-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
22549502-7	2012	RESULTS: From multiple linear regression models, vitamin K epoxide reductase complex subunit 1, CYP2C9, CYP4F2, and age were found to have significant effects on warfarin stable dose.	Warfarin	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
22436668-0	2012	Simultaneous determination of fluoxetine and norfluoxetine enantiomers using isotope discrimination mass spectroscopy solution method and its application in the CYP2C9-mediated stereoselective interactions.	Fluoxetine	30-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
22436668-0	2012	Simultaneous determination of fluoxetine and norfluoxetine enantiomers using isotope discrimination mass spectroscopy solution method and its application in the CYP2C9-mediated stereoselective interactions.	norfluoxetine	45-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
22436668-1	2012	In this study, we developed an LC-MS/MS method based on an isotope discrimination mass spectroscopy solution (IDMSS) technology to simultaneously quantify enantiomers of fluoxetine (FLX) and norfluoxetine (NFLX) in a CYP2C9 incubation mixture.	Fluoxetine	170-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	217-223
22436668-1	2012	In this study, we developed an LC-MS/MS method based on an isotope discrimination mass spectroscopy solution (IDMSS) technology to simultaneously quantify enantiomers of fluoxetine (FLX) and norfluoxetine (NFLX) in a CYP2C9 incubation mixture.	norfluoxetine	191-204	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	217-223
22436668-8	2012	No significant kinetic isotope effect was found in the metabolism of S-FLX-d5 catalyzed by CYP2C9*1 and CYP2C9*2.	s-flx-d5	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
22436668-9	2012	The half-maximal inhibitory concentration values between R-FLX and S-FLX catalyzed by CYP2C9*1 and CYP2C9*2 were determined in this study.	r-flx	57-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
22436668-9	2012	The half-maximal inhibitory concentration values between R-FLX and S-FLX catalyzed by CYP2C9*1 and CYP2C9*2 were determined in this study.	r-flx	57-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
22436668-9	2012	The half-maximal inhibitory concentration values between R-FLX and S-FLX catalyzed by CYP2C9*1 and CYP2C9*2 were determined in this study.	Fluoxetine	67-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
22436668-9	2012	The half-maximal inhibitory concentration values between R-FLX and S-FLX catalyzed by CYP2C9*1 and CYP2C9*2 were determined in this study.	Fluoxetine	67-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
22436668-10	2012	The inhibitory effects of R- to S-FLX were stronger than those of S- to R-FLX in both CYP2C9*1 and CYP2C9*2.	r- to s-flx	26-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
22436668-10	2012	The inhibitory effects of R- to S-FLX were stronger than those of S- to R-FLX in both CYP2C9*1 and CYP2C9*2.	r- to s-flx	26-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
22436668-10	2012	The inhibitory effects of R- to S-FLX were stronger than those of S- to R-FLX in both CYP2C9*1 and CYP2C9*2.	Sulfur	32-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
22436668-10	2012	The inhibitory effects of R- to S-FLX were stronger than those of S- to R-FLX in both CYP2C9*1 and CYP2C9*2.	Sulfur	32-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
22436668-10	2012	The inhibitory effects of R- to S-FLX were stronger than those of S- to R-FLX in both CYP2C9*1 and CYP2C9*2.	r-flx	72-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
22436668-10	2012	The inhibitory effects of R- to S-FLX were stronger than those of S- to R-FLX in both CYP2C9*1 and CYP2C9*2.	r-flx	72-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
22943641-2	2012	METHODS: CYP2C9*3 (1075A/C, rs1057910) and VKORC1 (-1639A/G, rs9923231) genotyping was detected in 100 patients receiving Warfarin therapy by the newly developed HRM method and traditional genotyping methods including PCR-restriction fragment length polymorphism (PCR-RFLP), TaqMan probe and DNA sequencing.	Warfarin	122-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
22331994-1	2012	Long-chain unsaturated fatty acids inhibit several cytochrome P450 and UDP-glucuronosyltransferase (UGT) enzymes involved in drug metabolism, including CYP2C8, CYP2C9, UGT1A9, UGT2B4, and UGT2B7.	long-chain unsaturated fatty acids	0-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
22071881-0	2012	Factor VII R353Q genetic polymorphism is associated with altered warfarin sensitivity among CYP2C9 *1/*1 carriers.	Warfarin	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
22071881-13	2012	The prospective use of this polymorphism, along with CYP2C9 and VKORC1, may enhance the accuracy of warfarin loading.	Warfarin	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
22483397-2	2012	CYP isoform specific substrates and their metabolites of CYP1A2 (caffeine), CYP2C9 (losartan), CYP2C19 (omeprazole), CYP2D6 (dextromethorphan) and CYP3A (midazolam) were all simultaneously analyzed using LC-MS/MS after administration of a mixture of five drugs (i.e., a "cocktail approach") to healthy volunteers.	Losartan	84-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
22108774-1	2012	PURPOSE: Zafirlukast is a substrate of cytochrome P450 2C9 (CYP2C9) and cytochrome P450 3A4 (CYP3A4) in vitro, but the role of these enzymes in its metabolism in vivo is unknown.	zafirlukast	9-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-58
22108774-1	2012	PURPOSE: Zafirlukast is a substrate of cytochrome P450 2C9 (CYP2C9) and cytochrome P450 3A4 (CYP3A4) in vitro, but the role of these enzymes in its metabolism in vivo is unknown.	zafirlukast	9-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
22108774-7	2012	CONCLUSIONS: Fluconazole, but not itraconazole, increases zafirlukast plasma concentrations, strongly suggesting that CYP2C9 but not CYP3A4 participates in zafirlukast metabolism in humans.	Fluconazole	13-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
22108774-7	2012	CONCLUSIONS: Fluconazole, but not itraconazole, increases zafirlukast plasma concentrations, strongly suggesting that CYP2C9 but not CYP3A4 participates in zafirlukast metabolism in humans.	zafirlukast	156-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
22409277-0	2012	An evaluation of gene-gene interaction between the CYP2C9 and VKORC1 genotypes affecting the anticoagulant effect of phenprocoumon and acenocoumarol.	Phenprocoumon	117-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
22409277-0	2012	An evaluation of gene-gene interaction between the CYP2C9 and VKORC1 genotypes affecting the anticoagulant effect of phenprocoumon and acenocoumarol.	Acenocoumarol	135-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
22409277-2	2012	OBJECTIVES: We aimed to provide a definite answer regarding the question whether there exists a gene-gene interaction between the CYP2C9 and VKORC1 genotypes affecting the anticoagulant effect of phenprocoumon and acenocoumarol.	Phenprocoumon	196-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
22409277-2	2012	OBJECTIVES: We aimed to provide a definite answer regarding the question whether there exists a gene-gene interaction between the CYP2C9 and VKORC1 genotypes affecting the anticoagulant effect of phenprocoumon and acenocoumarol.	Acenocoumarol	214-227	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
21814747-8	2012	Norendoxifen inhibited placental aromatase with an IC(50) of 90 nM, while it inhibited human liver CYP2C9 and CYP3A with IC(50) values of 990 and 908 nM, respectively.	N,N-didesmethyl-4-hydroxytamoxifen	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
22594507-0	2012	A clinically significant interaction between warfarin and simvastatin is unique to carriers of the CYP2C9*3 allele.	Warfarin	45-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
22594507-0	2012	A clinically significant interaction between warfarin and simvastatin is unique to carriers of the CYP2C9*3 allele.	Simvastatin	58-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
22594507-2	2012	PATIENTS & METHODS: The influence of the CYP2C9*2 and CYP2C9*3 polymorphisms on the interaction between simvastatin and warfarin was analyzed in data from 1132 patients.	Simvastatin	108-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
22594507-2	2012	PATIENTS & METHODS: The influence of the CYP2C9*2 and CYP2C9*3 polymorphisms on the interaction between simvastatin and warfarin was analyzed in data from 1132 patients.	Simvastatin	108-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
22594507-3	2012	RESULTS: Simvastatin use reduced warfarin dose requirements by 29% in carriers of the CYP2C9*3 allele, compared with 5% in noncarriers.	Simvastatin	9-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
22594507-3	2012	RESULTS: Simvastatin use reduced warfarin dose requirements by 29% in carriers of the CYP2C9*3 allele, compared with 5% in noncarriers.	Warfarin	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
22594507-4	2012	A regression model showed a significant influence of CYP2C9*3 on the drug-drug interaction, predicting a warfarin dose reduction of 25% in CYP2C9*3 heterozygotes and 43% in CYP2C9*3 homozygotes.	Warfarin	105-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
22594507-4	2012	A regression model showed a significant influence of CYP2C9*3 on the drug-drug interaction, predicting a warfarin dose reduction of 25% in CYP2C9*3 heterozygotes and 43% in CYP2C9*3 homozygotes.	Warfarin	105-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	139-145
22594507-4	2012	A regression model showed a significant influence of CYP2C9*3 on the drug-drug interaction, predicting a warfarin dose reduction of 25% in CYP2C9*3 heterozygotes and 43% in CYP2C9*3 homozygotes.	Warfarin	105-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	139-145
22594507-5	2012	CONCLUSION: Our data indicate that the CYP2C9*3 polymorphism predisposes for a pharmacologic interaction between warfarin and simvastatin.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
22594507-5	2012	CONCLUSION: Our data indicate that the CYP2C9*3 polymorphism predisposes for a pharmacologic interaction between warfarin and simvastatin.	Simvastatin	126-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
22266406-3	2012	RESULTS: We confirm the association between high-frequency SNPs, VKORC1 c.-1639G>A and CYP2C9 *2/*3 and warfarin sensitivity, and contribute additional evidence that the VKORC1 p.Asp36Tyr variant is recurrent and independently associated with warfarin resistance in our population.	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
22378156-0	2012	Decreased warfarin clearance associated with the CYP2C9 R150H (*8) polymorphism.	Warfarin	10-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
22378156-1	2012	The cytochrome P450 (CYP) 2C9 R150H (*8) allele occurs commonly in African Americans and is associated with lower warfarin dose requirements.	Warfarin	114-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-29
22378156-2	2012	We conducted a pharmacokinetic study to examine whether the CYP2C9*8 allele impacts warfarin clearance in African-American patients.	Warfarin	84-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
22378156-4	2012	We observed a 30% reduction in the unbound oral clearance of S-warfarin and a 25% lower R- to S-warfarin plasma concentration ratio in patients with the CYP2C9*8 allele (n = 12) as compared to CYP2C9*1 homozygotes (n = 26).	Warfarin	63-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
22378156-4	2012	We observed a 30% reduction in the unbound oral clearance of S-warfarin and a 25% lower R- to S-warfarin plasma concentration ratio in patients with the CYP2C9*8 allele (n = 12) as compared to CYP2C9*1 homozygotes (n = 26).	Warfarin	96-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
22378156-6	2012	These data show that the R150H variant protein expressed by the CYP2C9*8 allele is associated with lower S-warfarin clearance.	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
22378156-7	2012	This finding provides clinical and experimental evidence to explain the lower warfarin dose requirements in patients with the CYP2C9*8 allele.	Warfarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
22205778-4	2012	To this end, the selective CYP2C9 mechanism-based inactivator tienilic acid was used to reduce irreversibly the total CYP2C9 activity in human liver microsomes.	Ticrynafen	62-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
22205778-4	2012	To this end, the selective CYP2C9 mechanism-based inactivator tienilic acid was used to reduce irreversibly the total CYP2C9 activity in human liver microsomes.	Ticrynafen	62-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
22205778-5	2012	Tienilic acid concentrations were effectively titrated to produce microsomal preparations with 43 and 73% less activity, mimicking the CYP2C9*1/*3 and CYP2C9*3/*3 genotypes, respectively.	Ticrynafen	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-141
22205778-5	2012	Tienilic acid concentrations were effectively titrated to produce microsomal preparations with 43 and 73% less activity, mimicking the CYP2C9*1/*3 and CYP2C9*3/*3 genotypes, respectively.	Ticrynafen	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	151-157
22205778-7	2012	In lieu of using rare human liver microsomes from CYP2C9*1/*3 and CYP2C9*3/*3 individuals, a tienilic acid-created knockdown in human liver microsomes may be an appropriate in vitro model to determine CYP2C9-mediated metabolism of a given substrate, to determine whether other drug-metabolizing enzymes may compensate for reduced CYP2C9 activity, and to predict the extent of genotype-dependent drug-drug interactions.	Ticrynafen	93-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
22205778-7	2012	In lieu of using rare human liver microsomes from CYP2C9*1/*3 and CYP2C9*3/*3 individuals, a tienilic acid-created knockdown in human liver microsomes may be an appropriate in vitro model to determine CYP2C9-mediated metabolism of a given substrate, to determine whether other drug-metabolizing enzymes may compensate for reduced CYP2C9 activity, and to predict the extent of genotype-dependent drug-drug interactions.	Ticrynafen	93-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
22205778-7	2012	In lieu of using rare human liver microsomes from CYP2C9*1/*3 and CYP2C9*3/*3 individuals, a tienilic acid-created knockdown in human liver microsomes may be an appropriate in vitro model to determine CYP2C9-mediated metabolism of a given substrate, to determine whether other drug-metabolizing enzymes may compensate for reduced CYP2C9 activity, and to predict the extent of genotype-dependent drug-drug interactions.	Ticrynafen	93-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
22329513-0	2012	Differential oxidation of two thiophene-containing regioisomers to reactive metabolites by cytochrome P450 2C9.	Thiophenes	30-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-110
22317799-4	2012	Ideally, such an assay would use a single PCR reaction and, without further processing, a single microchip electrophoresis (ME) run to determine the 3 single-nucleotide polymorphisms (SNPs) affecting warfarin sensitivity [i.e., CYP2C9 (cytochrome P450, family 2, subfamily C, polypeptide 9) *2, CYP2C9 *3, and the VKORC1 (vitamin K epoxide reductase complex 1) A/B haplotype].	Warfarin	200-208	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	228-234
22317799-4	2012	Ideally, such an assay would use a single PCR reaction and, without further processing, a single microchip electrophoresis (ME) run to determine the 3 single-nucleotide polymorphisms (SNPs) affecting warfarin sensitivity [i.e., CYP2C9 (cytochrome P450, family 2, subfamily C, polypeptide 9) *2, CYP2C9 *3, and the VKORC1 (vitamin K epoxide reductase complex 1) A/B haplotype].	Warfarin	200-208	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	295-301
22266406-3	2012	RESULTS: We confirm the association between high-frequency SNPs, VKORC1 c.-1639G>A and CYP2C9 *2/*3 and warfarin sensitivity, and contribute additional evidence that the VKORC1 p.Asp36Tyr variant is recurrent and independently associated with warfarin resistance in our population.	Warfarin	246-254	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
22266406-5	2012	CONCLUSION: Warfarin sensitivity was predicted by known VKORC1 and CYP2C9 SNPs.	Warfarin	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
22269145-6	2012	Two monohydroxylated metabolites of lower abundance were formed by CYP3A4, and interestingly, although CYP2C9 showed no activity toward the parent compound, this enzyme appeared to act in concert with CYP3A4 to form two minor dihydroxylated products of ETR.	etravirine	253-256	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
22589111-0	2012	Rapid testing of clopidogrel resistance by genotyping of CYP2C19 and CYP2C9 polymorphisms using denaturing on-chip capillary electrophoresis.	Clopidogrel	17-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
22269145-10	2012	Taken together, these data suggest that ETR and ETR metabolites are substrates of CYP2C19, CYP3A4, CYP2C9, UGT1A3, and UGT1A8 and that ETR is a PXR-dependent modulator of CYP3A4 mRNA levels.	etravirine	40-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
22269145-10	2012	Taken together, these data suggest that ETR and ETR metabolites are substrates of CYP2C19, CYP3A4, CYP2C9, UGT1A3, and UGT1A8 and that ETR is a PXR-dependent modulator of CYP3A4 mRNA levels.	etravirine	48-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
22269145-10	2012	Taken together, these data suggest that ETR and ETR metabolites are substrates of CYP2C19, CYP3A4, CYP2C9, UGT1A3, and UGT1A8 and that ETR is a PXR-dependent modulator of CYP3A4 mRNA levels.	etravirine	48-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
22589111-4	2012	Genotyping of CYP2C19 and CYP2C9 polymorphisms allows to identify slow metabolizers showing resistance to clopidogrel therapy.	Clopidogrel	106-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
22334041-10	2012	In single-SNP adjusted analysis, nine SNPs in the XPC, CYP2C9, PAX4, MTRR, and GAN genes were associated with cyclosporine nephrotoxicity.	Cyclosporine	110-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
22270321-0	2012	Population pharmacokinetic modelling of S-warfarin to evaluate the design of drug-drug interaction studies for CYP2C9.	Sulfur	40-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
22270321-1	2012	This study is to assess pharmacokinetic (PK) sampling time schedules and trial size requirements of drug-drug interaction (DDI) studies for CYP2C9, based on S-warfarin population PK models.	Warfarin	159-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
21507031-0	2012	Clinical relevance of VKORC1 (G-1639A and C1173T) and CYP2C9*3 among patients on warfarin.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
21507031-1	2012	WHAT IS KNOWN AND OBJECTIVES: Testing for cytochrome P450-2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) variant alleles is recommended by the FDA for dosing of warfarin.	Warfarin	186-194	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-61
21507031-1	2012	WHAT IS KNOWN AND OBJECTIVES: Testing for cytochrome P450-2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) variant alleles is recommended by the FDA for dosing of warfarin.	Warfarin	186-194	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
21507031-3	2012	We therefore studied the impact of genetic polymorphisms of CYP2C9 and VKORC1 on warfarin dose requirement in Malaysia.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
21507031-8	2012	RESULTS AND DISCUSSION: A model which included age and variants of CYP2C9 and VKORC1 account for about 37% of the variability in warfarin dose required to achieve INR of 2-4.	Warfarin	129-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
22252093-0	2012	Long-term anticoagulant effects of the CYP2C9 and VKORC1 genotypes in acenocoumarol users.	Acenocoumarol	70-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
22252093-1	2012	BACKGROUND: The required acenocoumarol dose and the risk of underanticoagulation and overanticoagulation are associated with the CYP2C9 and VKORC1 genotypes.	Acenocoumarol	25-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
22252093-5	2012	RESULTS: Patients with polymorphisms in CYP2C9 and VKORC1 had a higher risk of overanticoagulation (up to 74%) and a lower risk of underanticoagulation (down to 45%) in the first month of treatment with acenocoumarol, but this effect diminished after 1-6 months.	Acenocoumarol	203-216	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
22459452-3	2012	Hence there are chances of drug-drug interaction because modulations of isoenzymes involved in metabolism of phenytoin and aceclofenac are CYP2C9/10 and CYP2C19.	Phenytoin	109-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	139-145
22459452-3	2012	Hence there are chances of drug-drug interaction because modulations of isoenzymes involved in metabolism of phenytoin and aceclofenac are CYP2C9/10 and CYP2C19.	aceclofenac	123-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	139-145
22321050-1	2012	We recently designed the CIME cocktail consisting of 10 drugs to assess the activity of the major human CYPs (CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6 and CYP3A), a phase II enzyme (UGT1A1/6/9), two drug transporters (P-gp and OATP1B1) and a component of the renal function ( Videau et al.	cime	25-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
22364953-8	2012	An overrepresentation was seen for poly-aromatic hydrocarbons (group of procarcinogens) among CYP2C9 active and mutagenic compounds compared to CYP2C9 inactive and mutagenic compounds.	poly-aromatic hydrocarbons	35-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
21881887-6	2012	INR levels and S-warfarin concentrations were associated with CYP2C9 and VKORC1 genotypes.	Warfarin	17-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
21883387-0	2012	Impact of genetic factors (VKORC1, CYP2C9, CYP4F2 and EPHX1) on the anticoagulation response to fluindione.	fluindione	96-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
21883387-1	2012	AIM: Genetic variants of the enzyme that metabolizes warfarin, cytochrome P-450 2C9 (CYP2C9) and of a key pharmacologic target of vitamin K antagonists, vitamin K epoxide reductase (VKORC1), contribute to differences in patients" responses to coumarin derivatives.	Vitamin K	130-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-83
21883387-1	2012	AIM: Genetic variants of the enzyme that metabolizes warfarin, cytochrome P-450 2C9 (CYP2C9) and of a key pharmacologic target of vitamin K antagonists, vitamin K epoxide reductase (VKORC1), contribute to differences in patients" responses to coumarin derivatives.	Vitamin K	130-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
21883387-1	2012	AIM: Genetic variants of the enzyme that metabolizes warfarin, cytochrome P-450 2C9 (CYP2C9) and of a key pharmacologic target of vitamin K antagonists, vitamin K epoxide reductase (VKORC1), contribute to differences in patients" responses to coumarin derivatives.	coumarin	243-251	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-83
21883387-1	2012	AIM: Genetic variants of the enzyme that metabolizes warfarin, cytochrome P-450 2C9 (CYP2C9) and of a key pharmacologic target of vitamin K antagonists, vitamin K epoxide reductase (VKORC1), contribute to differences in patients" responses to coumarin derivatives.	coumarin	243-251	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
21820929-6	2012	RESULTS: CYP3A4 was responsible for the metabolism of lovastatin, simvastatin and atorvastatin; fluvastatin depends on CYP2C9; P-glycoprotein is responsible for decreased atorvastatin, pravastatin, simvastatin and lovastatin concentrations.	Fluvastatin	96-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
22198820-5	2012	RESULTS: Single-nucleotide polymorphism association analysis showed that VKORC1, CYP2C9 and CYP4F2 variations were highly associated with the warfarin maintenance dose.	Warfarin	142-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
21935704-5	2012	METHODS: In a cross-sectional study, we interviewed 244 patients in the maintenance phase of warfarin therapy and detected polymorphisms in the VKORC1 and CYP2C9 genes.	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
22198820-7	2012	The final pharmacogenetic equation explained 43.65% of interindividual variation of warfarin maintenance dose with age, body surface area, VKORC1 g.3588G>A, CYP2C9*3, CYP4F2 c.1297G>A, amiodarone, fluconazole, and diltiazem accounting for 1.97, 2.74, 24.12, 3.94, 1.64, 5.92, 2.47, and 0.84% of variation.	Warfarin	84-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
22198820-8	2012	CONCLUSION: The present study indicated that VKORC1, CYP4F2, and CYP2C9 genotypes and interacting drugs had a significant impact on the warfarin maintenance dose in Chinese patients with heart valve replacement and demonstrated that integrating interacting drugs can largely improve the predictability of the dose algorithm.	Warfarin	136-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
22022918-6	2012	This reaction was inhibited significantly by ketoconazole, a CYP3A inhibitor, and azamulin, a mechanism-based inhibitor of CYP3A, while no substantial effect was observed using selective inhibitors for eight other P450s (CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, and CYP2E1).	Ketoconazole	45-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	253-259
22186153-5	2012	Human CYP2C9(*)1, CYP2C19 and rat CYP2C6 were the major CYP isoforms producing 5-OH MEHP and 5-Oxo MEHP metabolites; however, only human CYP2C9(*)1 and 2C9(*)2 produced 5-carboxy MEPP from MEHP.	5-oh mehp	79-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
22186153-5	2012	Human CYP2C9(*)1, CYP2C19 and rat CYP2C6 were the major CYP isoforms producing 5-OH MEHP and 5-Oxo MEHP metabolites; however, only human CYP2C9(*)1 and 2C9(*)2 produced 5-carboxy MEPP from MEHP.	5-oxo mehp	93-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
22186153-5	2012	Human CYP2C9(*)1, CYP2C19 and rat CYP2C6 were the major CYP isoforms producing 5-OH MEHP and 5-Oxo MEHP metabolites; however, only human CYP2C9(*)1 and 2C9(*)2 produced 5-carboxy MEPP from MEHP.	5-carboxy mepp	169-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
22186153-5	2012	Human CYP2C9(*)1, CYP2C19 and rat CYP2C6 were the major CYP isoforms producing 5-OH MEHP and 5-Oxo MEHP metabolites; however, only human CYP2C9(*)1 and 2C9(*)2 produced 5-carboxy MEPP from MEHP.	mono-(2-ethylhexyl)phthalate	84-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
22186153-7	2012	Percent total normalized rates (%TNR) by CYP2C9(*)1 in human liver microsomes (HLM) were 94%, 98% and 100%, respectively, for 5-OH MEHP, 5-Oxo MEHP, 5-carboxy MEPP, and 76% for PA production by CYP3A4.	5-oh mehp	126-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
22186153-7	2012	Percent total normalized rates (%TNR) by CYP2C9(*)1 in human liver microsomes (HLM) were 94%, 98% and 100%, respectively, for 5-OH MEHP, 5-Oxo MEHP, 5-carboxy MEPP, and 76% for PA production by CYP3A4.	5-carboxy mepp	149-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
22379999-2	2012	Warfarin is a typical example of where pharmacogenetics could help the individual patient by modeling the dose, based on clinical factors and genetic variation in CYP2C9 and VKORC1.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-169
22022918-6	2012	This reaction was inhibited significantly by ketoconazole, a CYP3A inhibitor, and azamulin, a mechanism-based inhibitor of CYP3A, while no substantial effect was observed using selective inhibitors for eight other P450s (CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, and CYP2E1).	azamulin	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	253-259
22117526-5	2012	Comparing two assessment results for CYP2D6 and CYP2C9 inhibitors, the FDA assessment suggested potential DDI risks for sulphinpyrazone and amitriptyline, while the EMEA assessment indicated no potential risk for these drugs.	Sulfinpyrazone	120-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
22226725-2	2012	The only human CYP known to produce relevant amounts of 3-OH-Ibu is CYP2C9 and as genetic polymorphisms of CYP2C9 influence the metabolization of numerous drugs, the availability of reference standards for CYP2C9-specific metabolites is of considerable interest.	3-oh-ibu	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
22226725-2	2012	The only human CYP known to produce relevant amounts of 3-OH-Ibu is CYP2C9 and as genetic polymorphisms of CYP2C9 influence the metabolization of numerous drugs, the availability of reference standards for CYP2C9-specific metabolites is of considerable interest.	3-oh-ibu	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
22226725-2	2012	The only human CYP known to produce relevant amounts of 3-OH-Ibu is CYP2C9 and as genetic polymorphisms of CYP2C9 influence the metabolization of numerous drugs, the availability of reference standards for CYP2C9-specific metabolites is of considerable interest.	3-oh-ibu	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
22226725-4	2012	The recombinant fission yeast strain CAD68 coexpressing human CYP2C9 and CPR was used for the whole-cell biotransformation of Ibu to 3-OH-Ibu in 1L batch-scale for 75h.	Ibuprofen	126-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
22226725-4	2012	The recombinant fission yeast strain CAD68 coexpressing human CYP2C9 and CPR was used for the whole-cell biotransformation of Ibu to 3-OH-Ibu in 1L batch-scale for 75h.	3-oh-ibu	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
22274142-0	2012	Prediction of warfarin dose reductions in Puerto Rican patients, based on combinatorial CYP2C9 and VKORC1 genotypes.	Warfarin	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
22274142-1	2012	BACKGROUND: The influence of CYP2C9 and VKORC1 polymorphisms on warfarin dose has been investigated in white, Asian, and African American populations but not in Puerto Rican Hispanic patients.	Warfarin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
22274142-10	2012	Among patients with a given CYP2C9 genotype, warfarin dose requirements declined from GG to AA haplotypes; whereas, within each VKORC1 haplotype, the dose decreased as the number of CYP2C9 variants increased.	Warfarin	45-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
21838784-1	2012	AIM: According to product information, montelukast is extensively metabolized by CYP3A4 and CYP2C9.	montelukast	39-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
21842338-0	2012	CYP2C9 3 and 13 alleles significantly affect the pharmacokinetics of irbesartan in healthy Korean subjects.	Irbesartan	69-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21842338-1	2012	PURPOSE: To evaluate the effects of two major polymorphisms of CYP2C9, CYP2C9 3 and CYP2C9 13, on the pharmacokinetics of irbesartan in healthy Korean volunteers.	Irbesartan	122-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
21842338-1	2012	PURPOSE: To evaluate the effects of two major polymorphisms of CYP2C9, CYP2C9 3 and CYP2C9 13, on the pharmacokinetics of irbesartan in healthy Korean volunteers.	Irbesartan	122-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
21842338-1	2012	PURPOSE: To evaluate the effects of two major polymorphisms of CYP2C9, CYP2C9 3 and CYP2C9 13, on the pharmacokinetics of irbesartan in healthy Korean volunteers.	Irbesartan	122-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
21842338-8	2012	CONCLUSIONS: CYP2C9 genetic polymorphisms markedly affected the pharmacokinetics of irbesartan in this study sample.	Irbesartan	84-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
21842338-9	2012	The CYP2C9 3 and CYP2C9 13 alleles appear to be associated with the decreased metabolism of irbesartan.	Irbesartan	92-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
21842338-9	2012	The CYP2C9 3 and CYP2C9 13 alleles appear to be associated with the decreased metabolism of irbesartan.	Irbesartan	92-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
21870106-7	2012	In addition, losartan/E-3174 ratio doubled (P < 0.01) after BBR administration, indicating a decrease in CYP2C9 activity.	Losartan	13-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
21870106-7	2012	In addition, losartan/E-3174 ratio doubled (P < 0.01) after BBR administration, indicating a decrease in CYP2C9 activity.	losartan carboxylic acid	22-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
21208246-0	2012	Frequency of CYP2C9 variant alleles, including CYP2C9*13 in a Korean population and effect on glimepiride pharmacokinetics.	glimepiride	94-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
21208246-11	2012	Our data on the one subject with this genotype suggest that CYP2C9*3/*3 momozygotes have lower clearance of glimepiride and are exposed to higher levels of the drug than wild-type homozygotes.	glimepiride	108-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
22188360-6	2012	CONCLUSION: These data indicate that copy number variants in the principal genes involved in warfarin dose variability (CYP2C9, VKORC1), including genes with lesser effect (CYP4F2, GGCX), and those that may be more relevant among certain racial groups (CALU), are rare in multiethnic populations, including African-Americans.	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
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
22452429-0	2012	Warfarin pharmacogenetics: polymorphisms of the CYP2C9, CYP4F2, and VKORC1 loci in a genetically admixed Omani population.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
22248286-7	2012	CONCLUSION: We developed a pharmacogenetic dose algorithm for warfarin treatment that uses genotypes from two genes (VKORC1 and CYP2C9) and clinical variables to predict therapeutic maintenance doses in Chinese patients with venous thromboembolism.	Warfarin	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
22117526-5	2012	Comparing two assessment results for CYP2D6 and CYP2C9 inhibitors, the FDA assessment suggested potential DDI risks for sulphinpyrazone and amitriptyline, while the EMEA assessment indicated no potential risk for these drugs.	Amitriptyline	140-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
22149257-0	2012	A pharmacokinetic-pharmacodynamic model for predicting the impact of CYP2C9 and VKORC1 polymorphisms on fluindione and acenocoumarol during induction therapy.	fluindione	104-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
22130800-4	2012	The results showed that height, target international normalized ratio and VKORC1 and CYP2C9 genotypes were the main determinants of warfarin dose requirement, accounting for 48.1%, 4.4%, 18.2%, and 2.0% of variability, respectively, and explaining 69.7% of the variability.	Warfarin	132-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
21692828-10	2012	RESULTS: Bodyweight, age, sex and CYP2C9 genotype significantly influenced S-warfarin clearance.	Warfarin	77-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
22149257-12	2012	CONCLUSION: During initiation of therapy, CYP2C9 and VKORC1 genetic polymorphisms are important predictors of fluindione and acenocoumarol pharmacokinetic-pharmacodynamic responses.	fluindione	110-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
22010099-0	2012	VKORC1 and CYP2C9 genotype and patient characteristics explain a large proportion of the variability in warfarin dose requirement among children.	Warfarin	104-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
22010099-4	2012	Multiple regression analysis of the data showed that, although CYP4F2 made no contribution to the dose model, 72.4% of the variability in warfarin dose requirement is attributed to by patient height, genetic polymorphisms in VKORC1 and CYP2C9, and indication for warfarin.	Warfarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	236-242
22293514-3	2012	Etravirine, a second-generation non-nucleoside reverse transcriptase inhibitor has been shown to induce CYP3A4, while inhibiting CYP2C9 and CYP2C19.	etravirine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
22149257-12	2012	CONCLUSION: During initiation of therapy, CYP2C9 and VKORC1 genetic polymorphisms are important predictors of fluindione and acenocoumarol pharmacokinetic-pharmacodynamic responses.	Acenocoumarol	125-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
22149257-0	2012	A pharmacokinetic-pharmacodynamic model for predicting the impact of CYP2C9 and VKORC1 polymorphisms on fluindione and acenocoumarol during induction therapy.	Acenocoumarol	119-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
22447115-4	2012	When cells were treated with a typical CYP3A substrate (triazolam), CYP2C9 substrate (diclofenac) or UGT1A1 substrate (SN-38), large amounts of their metabolites were detected in the medium of cells cultured on micro-space cell culture plates.	Diclofenac	86-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
21890570-9	2012	It is hypothesized that warfarin and dapsone compete for binding on the CYP2C9 and CYP3A4 isoenzymes and therefore serum concentration of warfarin was elevated.	Warfarin	24-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
21890570-9	2012	It is hypothesized that warfarin and dapsone compete for binding on the CYP2C9 and CYP3A4 isoenzymes and therefore serum concentration of warfarin was elevated.	Dapsone	37-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
21890570-9	2012	It is hypothesized that warfarin and dapsone compete for binding on the CYP2C9 and CYP3A4 isoenzymes and therefore serum concentration of warfarin was elevated.	Warfarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
22447115-5	2012	The formation of metabolites from triazolam, diclofenac and SN-38 was strongly inhibited by co-treatment with a CYP3A inhibitor (ketoconazole), CYP2C9 inhibitor (sulfaphenazole) and UGT1A1 inhibitor (ketoconazole), respectively.	Triazolam	34-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
22447115-5	2012	The formation of metabolites from triazolam, diclofenac and SN-38 was strongly inhibited by co-treatment with a CYP3A inhibitor (ketoconazole), CYP2C9 inhibitor (sulfaphenazole) and UGT1A1 inhibitor (ketoconazole), respectively.	Diclofenac	45-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
22447115-5	2012	The formation of metabolites from triazolam, diclofenac and SN-38 was strongly inhibited by co-treatment with a CYP3A inhibitor (ketoconazole), CYP2C9 inhibitor (sulfaphenazole) and UGT1A1 inhibitor (ketoconazole), respectively.	Irinotecan	60-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
23093260-0	2012	Development of a HPLC method for the determination of losartan urinary metabolic ratio to be used for the determination of CYP2C9 hydroxylation phenotypes.	Losartan	54-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
22447115-5	2012	The formation of metabolites from triazolam, diclofenac and SN-38 was strongly inhibited by co-treatment with a CYP3A inhibitor (ketoconazole), CYP2C9 inhibitor (sulfaphenazole) and UGT1A1 inhibitor (ketoconazole), respectively.	Sulfaphenazole	162-176	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
23093260-1	2012	BACKGROUND: Losartan is metabolized to losartan carboxylic acid (E-3174) by the polymorphic cytochrome CYP2C9.	Losartan	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
23093260-1	2012	BACKGROUND: Losartan is metabolized to losartan carboxylic acid (E-3174) by the polymorphic cytochrome CYP2C9.	losartan carboxylic acid	39-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
22375877-2	2012	In this study, we examined the inhibitory potentials of capsaicin and dihydrocapsaicin against CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4/5 activities in human liver microsomes.	Capsaicin	56-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
23093260-1	2012	BACKGROUND: Losartan is metabolized to losartan carboxylic acid (E-3174) by the polymorphic cytochrome CYP2C9.	losartan carboxylic acid	65-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
23093260-6	2012	Analyses with the present HPLC method show significant differences (p<0.05) in losartan MRs between the four CYP2C9 genotype groups in 13 Spanish healthy volunteers.	Losartan	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
23093260-8	2012	Therefore, it appears to be useful for CYP2C9 phenotyping using losartan as a drug test in populations, such as Hispanics with different allele combinations.	Losartan	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
23099353-0	2012	Effects of UGT1A6, UGT2B7, and CYP2C9 genotypes on plasma concentrations of valproic acid in Chinese children with epilepsy.	Valproic Acid	76-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
22375877-2	2012	In this study, we examined the inhibitory potentials of capsaicin and dihydrocapsaicin against CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4/5 activities in human liver microsomes.	dihydrocapsaicin	70-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
22166891-2	2012	These phytocannabinoids concentration-dependently inhibited S-warfarin 7-hydroxylase and diclofenac 4"-hydroxylase activities of human liver microsomes (HLMs) and recombinant CYP2C9 (rCYP2C9).	phytocannabinoids	6-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	175-181
22166891-8	2012	These results indicated that the three major phytocannabinoids but not PAHs contained in marijuana smoke potently inhibited CYP2C9 activity and that these cannabinoids can be characterized as direct inhibitors for CYP2C9.	phytocannabinoids	45-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
22166891-8	2012	These results indicated that the three major phytocannabinoids but not PAHs contained in marijuana smoke potently inhibited CYP2C9 activity and that these cannabinoids can be characterized as direct inhibitors for CYP2C9.	phytocannabinoids	45-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	214-220
22166891-8	2012	These results indicated that the three major phytocannabinoids but not PAHs contained in marijuana smoke potently inhibited CYP2C9 activity and that these cannabinoids can be characterized as direct inhibitors for CYP2C9.	Cannabinoids	50-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
22166891-8	2012	These results indicated that the three major phytocannabinoids but not PAHs contained in marijuana smoke potently inhibited CYP2C9 activity and that these cannabinoids can be characterized as direct inhibitors for CYP2C9.	Cannabinoids	50-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	214-220
22098100-8	2012	A mechanism-based inhibition of human CYP2C9 by sesamin was recently discovered, suggesting that it is important to evaluate the interaction between sesamin and drugs that are mainly metabolised by CYP2C9.	sesamin	48-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
22098100-8	2012	A mechanism-based inhibition of human CYP2C9 by sesamin was recently discovered, suggesting that it is important to evaluate the interaction between sesamin and drugs that are mainly metabolised by CYP2C9.	sesamin	48-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	198-204
22098100-8	2012	A mechanism-based inhibition of human CYP2C9 by sesamin was recently discovered, suggesting that it is important to evaluate the interaction between sesamin and drugs that are mainly metabolised by CYP2C9.	sesamin	149-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
22098100-8	2012	A mechanism-based inhibition of human CYP2C9 by sesamin was recently discovered, suggesting that it is important to evaluate the interaction between sesamin and drugs that are mainly metabolised by CYP2C9.	sesamin	149-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	198-204
22927772-1	2012	BACKGROUND: The polymorphisms of VKORC1 and CYP2C9 play increasingly important roles in the inter-individual variability in warfarin dose.	Warfarin	124-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
22927772-10	2012	CONCLUSION: Based on CYP2C9 and VKORC1 genotypes, the pharmacogenetic-based warfarin-dosing algorithm may shorten the time elapse from initiation of warfarin therapy until warfarin maintenance dose.	Warfarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
22927772-10	2012	CONCLUSION: Based on CYP2C9 and VKORC1 genotypes, the pharmacogenetic-based warfarin-dosing algorithm may shorten the time elapse from initiation of warfarin therapy until warfarin maintenance dose.	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
22927772-10	2012	CONCLUSION: Based on CYP2C9 and VKORC1 genotypes, the pharmacogenetic-based warfarin-dosing algorithm may shorten the time elapse from initiation of warfarin therapy until warfarin maintenance dose.	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
22952875-0	2012	Influence of CYP2C9 and VKORC1 on patient response to warfarin: a systematic review and meta-analysis.	Warfarin	54-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
23353843-2	2012	This cytochrome P450 is considered to be a counterpart of human CYP2C9, which metabolizes many drugs, including diclofenac, ibuprofen or warfarin.	Diclofenac	112-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
23353843-2	2012	This cytochrome P450 is considered to be a counterpart of human CYP2C9, which metabolizes many drugs, including diclofenac, ibuprofen or warfarin.	Ibuprofen	124-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
23353843-2	2012	This cytochrome P450 is considered to be a counterpart of human CYP2C9, which metabolizes many drugs, including diclofenac, ibuprofen or warfarin.	Warfarin	137-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
23353843-9	2012	CONCLUSION: The results presented open the possibility that in humans, rosuvastatin may affect the metabolism of many drugs by influencing expression and activity of CYP2C6 (counterpart of human CYP2C9).	Rosuvastatin Calcium	71-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
22393834-1	2012	BACKGROUND: VKORC1, CYP2C9 and CYP4F2 are three critical genes associated with inter-individual variation of warfarin dose.	Warfarin	109-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
22952875-3	2012	Two genes, CYP2C9 and VKORC1, have been associated with this variability, leading to genotype-guided dosing tables in warfarin labeling.	Warfarin	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
21726410-0	2011	Effects of the CYP2C9*1/*13 genotype on the pharmacokinetics of lornoxicam.	lornoxicam	64-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
22116191-1	2012	A significant proportion of warfarin dose variability is explained by variation in the genotypes of the cytochrome P450 CYP2C9 and the vitamin K epoxide reductase complex, VKORC1, enzymes that influence warfarin metabolism and sensitivity, respectively.	Warfarin	28-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
22116191-1	2012	A significant proportion of warfarin dose variability is explained by variation in the genotypes of the cytochrome P450 CYP2C9 and the vitamin K epoxide reductase complex, VKORC1, enzymes that influence warfarin metabolism and sensitivity, respectively.	Warfarin	203-211	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
22178823-6	2011	CONCLUSION: It is of important clinical significance in individualized warfarin therapy to systematically study distribution  of mutation frequencies at 12 polymorphisms loci in 4 genes including  CYP2C9, CYP3A4 , VKORC1 and GGCX related  to warfarin pharmacodynamics and pharmacokinetics in the Chinese Han population receiving valve replacement.	Warfarin	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
22178823-6	2011	CONCLUSION: It is of important clinical significance in individualized warfarin therapy to systematically study distribution  of mutation frequencies at 12 polymorphisms loci in 4 genes including  CYP2C9, CYP3A4 , VKORC1 and GGCX related  to warfarin pharmacodynamics and pharmacokinetics in the Chinese Han population receiving valve replacement.	Warfarin	242-250	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
21726410-1	2011	Lornoxicam is extensively metabolized by CYP2C9, and a CYP2C9*13 is one of the principal variant alleles in East Asian populations.	lornoxicam	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
21726410-1	2011	Lornoxicam is extensively metabolized by CYP2C9, and a CYP2C9*13 is one of the principal variant alleles in East Asian populations.	lornoxicam	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
21726410-2	2011	The aim of this study was to evaluate the effects of CYP2C9*1/*13 on the pharmacokinetic parameters of lornoxicam in healthy individuals.	lornoxicam	103-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
21726410-5	2011	In individuals with CYP2C9*1/*13, lornoxicam had a higher C(max) (p < 0.001), a longer half-life (p < 0.001), a lower oral clearance (p < 0.001) and a higher area under the plasma concentration-time curve from zero to infinity (AUC(inf) ) than in CYP2C9*1/*1 individuals (p < 0.001).	lornoxicam	34-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
21726410-5	2011	In individuals with CYP2C9*1/*13, lornoxicam had a higher C(max) (p < 0.001), a longer half-life (p < 0.001), a lower oral clearance (p < 0.001) and a higher area under the plasma concentration-time curve from zero to infinity (AUC(inf) ) than in CYP2C9*1/*1 individuals (p < 0.001).	lornoxicam	34-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	256-262
21726410-6	2011	The C(max) and AUC(inf) of 5"-hydroxylornoxicam were lower in CYP2C9*1/*13 individuals than in CYP2C9*1/*1 individuals, but the half-life of 5"-hydroxylornoxicam did not differ between the two groups.	5'-hydroxylornoxicam	27-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
21726410-6	2011	The C(max) and AUC(inf) of 5"-hydroxylornoxicam were lower in CYP2C9*1/*13 individuals than in CYP2C9*1/*1 individuals, but the half-life of 5"-hydroxylornoxicam did not differ between the two groups.	5'-hydroxylornoxicam	27-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
21726410-7	2011	The half-life, oral clearance and AUC(inf) of lornoxicam were similar in individuals with CYP2C9*1/*13 and those with CYP2C9*1/*3.	lornoxicam	46-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
21726410-9	2011	A CYP2C9*1/*13 genotype markedly reduced the conversion of lornoxicam to 5"-hydroxylornoxicam, to a similar extent as that observed with the CYP2C9*1/*3 genotype.	lornoxicam	59-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	2-8
21726410-9	2011	A CYP2C9*1/*13 genotype markedly reduced the conversion of lornoxicam to 5"-hydroxylornoxicam, to a similar extent as that observed with the CYP2C9*1/*3 genotype.	lornoxicam	59-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
21726410-9	2011	A CYP2C9*1/*13 genotype markedly reduced the conversion of lornoxicam to 5"-hydroxylornoxicam, to a similar extent as that observed with the CYP2C9*1/*3 genotype.	5'-hydroxylornoxicam	73-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	2-8
21726410-9	2011	A CYP2C9*1/*13 genotype markedly reduced the conversion of lornoxicam to 5"-hydroxylornoxicam, to a similar extent as that observed with the CYP2C9*1/*3 genotype.	5'-hydroxylornoxicam	73-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
21691805-8	2011	However, only in the gliclazide group a significant association between CYP2C9 genotype and hypoglycaemic attacks was observed (P = 0.035).	Gliclazide	21-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
21930825-3	2011	Statistically significant induction of CYP1A2 (2.1-, 2.9-, and 2.2-fold), CYP2B6 (1.8-, 2.4-, and 4-fold), and CYP2C9 (1.3-, 1.8-, and 2.6-fold) was observed after NFV, RTV, or RIF treatment, respectively (as expected, CYP2D6 was not induced).	Nelfinavir	164-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
21930825-3	2011	Statistically significant induction of CYP1A2 (2.1-, 2.9-, and 2.2-fold), CYP2B6 (1.8-, 2.4-, and 4-fold), and CYP2C9 (1.3-, 1.8-, and 2.6-fold) was observed after NFV, RTV, or RIF treatment, respectively (as expected, CYP2D6 was not induced).	Ritonavir	169-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
21930825-3	2011	Statistically significant induction of CYP1A2 (2.1-, 2.9-, and 2.2-fold), CYP2B6 (1.8-, 2.4-, and 4-fold), and CYP2C9 (1.3-, 1.8-, and 2.6-fold) was observed after NFV, RTV, or RIF treatment, respectively (as expected, CYP2D6 was not induced).	Rifampin	177-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
21691805-10	2011	CONCLUSIONS: CYP2C9 polymorphisms leading to decreased enzyme activity show a modest impact on the risk of mild hypoglycaemia attacks during oral antidiabetic treatment, with a significant association in patients treated with gliclazide.	Gliclazide	226-236	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
21713461-5	2011	Wogonin was a potent, competitive inhibitor of CYP1A2 (K (i) = 0.24 muM), and a weak inhibitor of CYP2C19 (IC(50) = 101.10 muM), but was not able to inhibit CYP2C9, CYP2D6, CYP2E1 and CYP3A4 (IC(50) > 200 muM).	wogonin	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
22116286-0	2011	Inhibition of CYP3A4 and CYP2C9 by podophyllotoxin: implication for clinical drug-drug interactions.	Podophyllotoxin	35-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
22116286-3	2011	Inhibition of CYP3A4, CYP2C9, CYP2C8, CYP2D6, CYP2E1 and CYP2A6 by PPT was investigated in the human liver microsomal system.	Podophyllotoxin	67-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
22116286-5	2011	The results showed that PPT strongly exhibited inhibitory effects on CYP3A4 and CYP2C9 in a concentration-dependent manner.	Podophyllotoxin	24-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
22116286-7	2011	Inhibition kinetic analysis showed that PPT exhibited competitive inhibition towards CYP3A4 and CYP2C9 with Ki of 1.6 and 2.0 meu M, respectively.	Podophyllotoxin	40-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
22116286-9	2011	Our experimental data indicate that potential drug-drug interaction (DDI) might exist when PPT is co-administered with the substrates which mainly undergo CYP3A4- or CYP2C9-mediated metabolism.	Podophyllotoxin	91-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	166-172
21939641-3	2011	In this brief review, we discussed the impact of CYP2C polymorphisms on the metabolic fate of small-molecule antidiabetics including sulfonylureas, meglitinides, thiazolidinediones, gliptins, and gliflozins, with the key drug-protein molecular interactions highlighted.	Sulfonylurea Compounds	133-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-54
22148003-9	2011	In conclusion, fluvastatin should be used with caution in patients with liver cirrhosis, especially with other medications metabolized with CYP2C9.	Fluvastatin	15-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
22338910-0	2011	An instructive case suggesting warfarin resistance which is independent on the regulation of the CYP2C9 and VKORC1 genotype.	Warfarin	31-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
22161100-5	2011	RESULTS: Of the 5 genes, VKORC1, CYP2C9 and GGCX were associated with warfarin stable dose.	Warfarin	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
22161100-6	2011	The multiple linear regression analysis indicated that  VKORC1, CYP2C9 and GGCX genes, age and weight,  had significant influence on inter-individual variation in warfarin stable dose, which contributed 30.2%, 22.8%, 1.5%, 4.7% and 6.7% respectively.	Warfarin	163-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
21782804-0	2011	Low dose requirement for warfarin treatment in a patient with CYP2C9*3/*13 genotype.	Warfarin	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
21782804-2	2011	Here we describe a patient who was intolerant of warfarin treatment because of impaired drug metabolism related to the CYP2C9*3/*13 genotype and high warfarin sensitivity associated with the VKORC1 1173TT genotype.	Warfarin	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
21782804-6	2011	CONCLUSIONS: To the best of our knowledge, this is the first report of a patient with CYP2C9*3/*13 and VKORC1 1173TT genotypes who had slower than normal warfarin metabolism, resulting in the need to administer an extremely low dose of warfarin in order to achieve the target INR value.	Warfarin	154-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
21782804-6	2011	CONCLUSIONS: To the best of our knowledge, this is the first report of a patient with CYP2C9*3/*13 and VKORC1 1173TT genotypes who had slower than normal warfarin metabolism, resulting in the need to administer an extremely low dose of warfarin in order to achieve the target INR value.	Warfarin	236-244	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
21143257-1	2011	WHAT IS KNOWN AND OBJECTIVE: Miconazole is a strong inhibitor of CYP2C9, one of the main enzymes involved in the metabolism of warfarin.	Miconazole	29-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
21143257-1	2011	WHAT IS KNOWN AND OBJECTIVE: Miconazole is a strong inhibitor of CYP2C9, one of the main enzymes involved in the metabolism of warfarin.	Warfarin	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
22122181-4	2011	The genes encoding for cytochrome P450 (CYP) 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) are the major genetic determinants of warfarin pharmacokinetics and pharmacodynamics, respectively.	Warfarin	155-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-48
22122181-4	2011	The genes encoding for cytochrome P450 (CYP) 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) are the major genetic determinants of warfarin pharmacokinetics and pharmacodynamics, respectively.	Warfarin	155-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
22122181-6	2011	The CYP2C9 gene has also been associated with bleeding risk with warfarin.	Warfarin	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
21939641-3	2011	In this brief review, we discussed the impact of CYP2C polymorphisms on the metabolic fate of small-molecule antidiabetics including sulfonylureas, meglitinides, thiazolidinediones, gliptins, and gliflozins, with the key drug-protein molecular interactions highlighted.	meglitinide	148-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-54
21939641-3	2011	In this brief review, we discussed the impact of CYP2C polymorphisms on the metabolic fate of small-molecule antidiabetics including sulfonylureas, meglitinides, thiazolidinediones, gliptins, and gliflozins, with the key drug-protein molecular interactions highlighted.	Thiazolidinediones	162-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-54
22023129-7	2011	For all 3 species, inhibitors of CYP3A4, CYP2A6, CYP2C19, CYP2B6, and CYP2C9 diminished N-demethylation of ketamine.	Ketamine	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
21964418-4	2011	Although all of the oxidation reactions tested were more or less inhibited by PFOS, diclofenac 4"-hydroxylation mediated mainly by CYP2C9 was most strongly inhibited (K(i) value of 40 nM), followed by paclitaxel 6alpha-hydroxylation mediated mainly by CYP2C8 (K(i) value of 4 muM).	diclofenac 4"	84-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
21964418-8	2011	These results suggest that the metabolism of medicines which are substrates for CYP2C9 may be altered by PFOS in human bodies, and that PFOS is a mechanism-based inhibitor of CYP2A6.	perfluorooctane sulfonic acid	105-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
21964418-8	2011	These results suggest that the metabolism of medicines which are substrates for CYP2C9 may be altered by PFOS in human bodies, and that PFOS is a mechanism-based inhibitor of CYP2A6.	perfluorooctane sulfonic acid	136-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
22023129-7	2011	For all 3 species, inhibitors of CYP3A4, CYP2A6, CYP2C19, CYP2B6, and CYP2C9 diminished N-demethylation of ketamine.	Nitrogen	88-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
22023129-8	2011	Anti-CYP3A4, anti-CYP2C9, and anti-CYP2B6 antibodies also inhibited ketamine N-demethylation.	Ketamine	68-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
22023129-11	2011	Although the human CYP2C9 inhibitor blocked ketamine N-demethylation completely in the canine ortholog CYP2C21, a strong inhibition was also obtained by the chemical inhibitors of CYP2C19 and CYP2B6.	Ketamine	44-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
22023129-13	2011	CONCLUSIONS AND CLINICAL RELEVANCE: Human-specific inhibitors of CYP2A6, CYP2C19, CYP3A4, CYP2B6, and CYP2C9 diminished ketamine N-demethylation in dogs and horses.	ketamine n	120-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
21953762-5	2011	Naringenin was able to inhibit CYP19, CYP2C9, and CYP2C19 with IC50 values below 5 muM.	naringenin	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
22152281-3	2011	Unlike other statins, the cyclopropyl group on the pitavastatin molecule appears to divert the drug away from metabolism by cytochrome P450 (CYP) 3 A4 and allows only a small degree of clinically insignificant metabolism by CYP2C9.	pitavastatin	51-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	224-230
21968795-1	2011	This short communication is aimed to investigate whether the widely used hypolipidemic drug fenofibrate affects CYP2C11 and CYP2C6 in rats, both counterparts of human CYP2C9, known to metabolise many drugs including S-warfarin and largely used non-steroidal antiinflammatory drugs such as ibuprofen, diclofenac and others.	Fenofibrate	92-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
21968795-1	2011	This short communication is aimed to investigate whether the widely used hypolipidemic drug fenofibrate affects CYP2C11 and CYP2C6 in rats, both counterparts of human CYP2C9, known to metabolise many drugs including S-warfarin and largely used non-steroidal antiinflammatory drugs such as ibuprofen, diclofenac and others.	Sulfur	216-217	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
21968795-5	2011	The results indicate that the combination of fenofibrate with drugs metabolised by CYP2C9 in humans should be taken with caution as it may lead, for example, to the potentiation of warfarin effects.	Warfarin	181-189	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
21953762-7	2011	Whereas (S)-naringenin was 2-fold more potent as an inhibitor of CYP19 and CYP2C19 than (R)-naringenin, (R)-naringenin was 2-fold more potent for CYP2C9 and CYP3A.	(R)-naringenin	104-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
21590310-2	2011	We designed a study to determine the associations between the polymorphisms and haplotype structures of CYP2C9 and VKORC1 and warfarin dose response in Sudanese patients, one of the most genetically diverse populations in Africa.	Warfarin	126-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
21590310-4	2011	RESULTS: Patients with the CYP2C9*2,*5,*6, or *11 variant required a daily warfarin dose that was 21% lower than those with CYP2C9*1/*1 (4.7 vs 5.8 mg/day, P < 0.001).	Warfarin	75-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
21590310-7	2011	CONCLUSION: Our data revealed that VKORC1 and CYP2C9 polymorphisms are important factors that influence warfarin dose response in Sudanese patients.	Warfarin	104-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
21651319-1	2011	BACKGROUND: Polymorphisms in the genes encoding the cytochrome P450 2C9 enzyme (CYP2C9) and the vitamin K epoxide reductase (VKORC1) are known to contribute to variability in sensitivity to coumarins.	Coumarins	190-199	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-71
22012312-1	2011	A significant proportion of the interindividual variability in warfarin dose requirements can be explained on the basis of CYP2C9 and VKORC1 genotypes.	Warfarin	63-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
21605066-0	2011	Comparison of metabolic soft spot predictions of CYP3A4, CYP2C9 and CYP2D6 substrates using MetaSite and StarDrop.	stardrop	105-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
21651319-1	2011	BACKGROUND: Polymorphisms in the genes encoding the cytochrome P450 2C9 enzyme (CYP2C9) and the vitamin K epoxide reductase (VKORC1) are known to contribute to variability in sensitivity to coumarins.	Coumarins	190-199	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
21651319-2	2011	Patients with certain common genetic variants of CYP2C9 (*2 & *3) or a VKORC1 polymorphism (-1639A Allele) require a lower dose of coumarin and are also at higher risk for over-anticoagulation and serious bleeding.	coumarin	135-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
21550074-10	2011	With specific inhibitors of CYP3A, CYP2B6, CYP2D6, CYP2C9, and CYP2C19, active metabolite production was decreased by 38% +- 15% with 4-(4-chlorobenzyl)pyridine (CYP2B6 inhibitor) and by 45 +- 16% with ketoconazole (CYP3A inhibitor).	4-(4-Chlorobenzyl)pyridine	134-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
22011696-5	2011	DISCUSSION: The drug interaction between warfarin and S-1 presumably leads to elevated PT-INR because the 5-fluorouracil (5-FU), which is metabolite of FT in S-1, inhibits the metabolic processing of S-warfarin by cytochrome P450 (CYP) 2C9.	Warfarin	41-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	214-239
22011696-5	2011	DISCUSSION: The drug interaction between warfarin and S-1 presumably leads to elevated PT-INR because the 5-fluorouracil (5-FU), which is metabolite of FT in S-1, inhibits the metabolic processing of S-warfarin by cytochrome P450 (CYP) 2C9.	Fluorouracil	106-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	214-239
22011696-5	2011	DISCUSSION: The drug interaction between warfarin and S-1 presumably leads to elevated PT-INR because the 5-fluorouracil (5-FU), which is metabolite of FT in S-1, inhibits the metabolic processing of S-warfarin by cytochrome P450 (CYP) 2C9.	Fluorouracil	122-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	214-239
21550074-10	2011	With specific inhibitors of CYP3A, CYP2B6, CYP2D6, CYP2C9, and CYP2C19, active metabolite production was decreased by 38% +- 15% with 4-(4-chlorobenzyl)pyridine (CYP2B6 inhibitor) and by 45 +- 16% with ketoconazole (CYP3A inhibitor).	Ketoconazole	202-214	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
22120087-5	2011	The results dis-played that three variants of the warfarin metabolism-related genetic polymorphism (CYP2C9*2, CYP2C9*3, and VKORC1(-1693)) could be simultaneously detected using three different sequencing primers in a single-tube (one test), and 96 tests could be carried out each time.	Warfarin	50-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
21713378-3	2011	In this study, we evaluated allele frequencies and effects of CYP2C9 and VKORC1 on warfarin response during initial anticoagulation therapy in Korean patients.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
21713378-10	2011	Patients with the CYP2C9*3 allele received a lower warfarin dose (P = 0.018) and tended to show more rapid PT-INR increase than CYP2C9*1/*1 genotype.	Warfarin	51-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
21713378-12	2011	The CYP2C9*3 and VKORC1-1639G alleles influenced warfarin response during the first month of anticoagulation therapy.	Warfarin	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
21713378-13	2011	Considering these results, CYP2C9 and VKORC1 genotyping can be an useful tool to estimate initial warfarin dose and frequency of PT-INR monitoring during the first month of anticoagulation therapy.	Warfarin	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
22120087-5	2011	The results dis-played that three variants of the warfarin metabolism-related genetic polymorphism (CYP2C9*2, CYP2C9*3, and VKORC1(-1693)) could be simultaneously detected using three different sequencing primers in a single-tube (one test), and 96 tests could be carried out each time.	Warfarin	50-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
21841812-0	2011	Frequency of CYP2C9 alleles in Koreans and their effects on losartan pharmacokinetics.	Losartan	60-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
21745145-5	2011	Of the CYPs evaluated, NGF1568 was found to inhibit only CYP2C9, by an uncompetitive mechanism and with a K(i) value of 349 muM.	NGF 1568	23-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
21771587-2	2011	Herein, we report a case study in which the plasma concentration of the CYP2C9 substrate (S)-warfarin, and not the CYP3A4 substrate (R)-warfarin, increased with itraconazole coadministration.	(S)-Warfarin	89-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
21771587-2	2011	Herein, we report a case study in which the plasma concentration of the CYP2C9 substrate (S)-warfarin, and not the CYP3A4 substrate (R)-warfarin, increased with itraconazole coadministration.	Itraconazole	161-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
21744854-0	2011	Membrane position of ibuprofen agrees with suggested access path entrance to cytochrome P450 2C9 active site.	Ibuprofen	21-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-96
21744854-4	2011	We constructed an atomistic model of complete CYP2C9 in a dioleoylphosphatidylcholine membrane and evolved it by molecular dynamics simulations in explicit water on a 100+ ns time-scale.	1,2-oleoylphosphatidylcholine	58-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
21744854-7	2011	The positions of openings of the substrate access and product egress channels correspond to free energy minima of CYP2C9 substrate ibuprofen and its metabolite in the membrane, respectively.	Ibuprofen	131-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
21757329-0	2011	Polysaccharide peptides from Coriolus versicolor competitively inhibit tolbutamide 4-hydroxylation in specific human CYP2C9 isoform and pooled human liver microsomes.	Polysaccharides	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
21757329-0	2011	Polysaccharide peptides from Coriolus versicolor competitively inhibit tolbutamide 4-hydroxylation in specific human CYP2C9 isoform and pooled human liver microsomes.	Tolbutamide	71-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
21841812-5	2011	The enzymatic activity of each CYP2C9 genotype was evaluated using losartan as the substrate.	Losartan	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
21841812-8	2011	In the pharmacokinetics studies, the AUC(0- ) of losartan in CYP2C9*3/*3 subjects was 1.42-fold larger than that in CYP2C9*1/*1 subjects, and the AUC(0- ) of E-3174, a more active metabolite of losartan, in CYP2C9*3/*3 subjects was only 12% of that in CYP2C9*1/*1 subjects.	Losartan	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
21841812-8	2011	In the pharmacokinetics studies, the AUC(0- ) of losartan in CYP2C9*3/*3 subjects was 1.42-fold larger than that in CYP2C9*1/*1 subjects, and the AUC(0- ) of E-3174, a more active metabolite of losartan, in CYP2C9*3/*3 subjects was only 12% of that in CYP2C9*1/*1 subjects.	Losartan	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
21841812-8	2011	In the pharmacokinetics studies, the AUC(0- ) of losartan in CYP2C9*3/*3 subjects was 1.42-fold larger than that in CYP2C9*1/*1 subjects, and the AUC(0- ) of E-3174, a more active metabolite of losartan, in CYP2C9*3/*3 subjects was only 12% of that in CYP2C9*1/*1 subjects.	Losartan	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
21900891-2	2011	Common genetic variants in the cytochrome P450-2C9 (CYP2C9) and vitamin K-epoxide reductase complex (VKORC1) enzymes, in addition to known nongenetic factors, account for ~50% of warfarin dose variability.	Warfarin	179-187	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-50
21841812-8	2011	In the pharmacokinetics studies, the AUC(0- ) of losartan in CYP2C9*3/*3 subjects was 1.42-fold larger than that in CYP2C9*1/*1 subjects, and the AUC(0- ) of E-3174, a more active metabolite of losartan, in CYP2C9*3/*3 subjects was only 12% of that in CYP2C9*1/*1 subjects.	Losartan	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
21841812-10	2011	CYP2C9*3/*3 subjects metabolized much less losartan into E-3174 than CYP2C9*1/*1 subjects.	Losartan	43-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21841812-10	2011	CYP2C9*3/*3 subjects metabolized much less losartan into E-3174 than CYP2C9*1/*1 subjects.	losartan carboxylic acid	57-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21966608-0	2011	Polymorphisms of Aspirin-Metabolizing Enzymes CYP2C9, NAT2 and UGT1A6 in Aspirin-Intolerant Urticaria.	Aspirin	17-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
21966608-0	2011	Polymorphisms of Aspirin-Metabolizing Enzymes CYP2C9, NAT2 and UGT1A6 in Aspirin-Intolerant Urticaria.	Aspirin	73-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	0-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-106
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	0-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	23-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-106
21966608-1	2011	Acetyl salicylic acid (ASA) is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6), cytochrome P4502C9 (CYP2C9), and N-acetyl transferase 2 (NAT2).	Aspirin	23-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
21981797-1	2011	BACKGROUND: The pharmacokinetics and pharmacodynamics of warfarin are affected by polymorphisms in the genes coding for cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1).	Warfarin	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-139
21981797-1	2011	BACKGROUND: The pharmacokinetics and pharmacodynamics of warfarin are affected by polymorphisms in the genes coding for cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1).	Warfarin	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
21981797-5	2011	RESULTS: A multivariate regression model including the variables of age, VKORC1 and CYP2C9 genotype, body surface area, and statin status produced the best model for estimating the warfarin dose (R(2) = 0.62).	Warfarin	181-189	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
21900891-2	2011	Common genetic variants in the cytochrome P450-2C9 (CYP2C9) and vitamin K-epoxide reductase complex (VKORC1) enzymes, in addition to known nongenetic factors, account for ~50% of warfarin dose variability.	Warfarin	179-187	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
21900891-3	2011	The purpose of this article is to assist in the interpretation and use of CYP2C9 and VKORC1 genotype data for estimating therapeutic warfarin dose to achieve an INR of 2-3, should genotype results be available to the clinician.	Warfarin	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
21148049-9	2011	The concentrations of R- and S-warfarin in plasma were significantly correlated with CYP2C9 genotypes.	r- and s-warfarin	22-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
24250426-2	2011	Diclofenac liver cytotoxicity was associated with reactive oxygen species (ROS) formation and lipid peroxidation which were inhibited by antioxidants and ROS scavengers, ferric chelator, inhibitors of reduced CYP2E1 and CYP2C9, mitochondrial permeability transition (MPT) pore sealing agents and endocytosis inhibitors.	Diclofenac	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	220-226
24250426-8	2011	We finally concluded that diclofenac hepatotoxicity is a result of metabolic activation by CYP2E1 and CYP2C9 and ROS formation, leading to a mitochondrial/lysosomal toxic cross-talk in the liver hepatocytes.	Diclofenac	26-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
21148049-10	2011	For acenocoumarol, time to reach target INR was more prolonged in patients carrying any CYP2C9 variant allele but failed to reach statistical significance because of low numbers of patients.	Acenocoumarol	4-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
21148049-13	2011	The authors showed that both CYP2C9 and VKORC1 polymorphisms are common in Lebanon and influence warfarin and acenocoumarol dose requirements, with the CYP2C9*2 polymorphism having less effect on acenocoumarol, the most commonly used oral anticoagulant in Lebanon.	Warfarin	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
21148049-13	2011	The authors showed that both CYP2C9 and VKORC1 polymorphisms are common in Lebanon and influence warfarin and acenocoumarol dose requirements, with the CYP2C9*2 polymorphism having less effect on acenocoumarol, the most commonly used oral anticoagulant in Lebanon.	Acenocoumarol	110-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
22321278-0	2011	[Impact of CYP2C9 and VKORC1 polymorphism on warfarin response during initiation of therapy].	Warfarin	45-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
21638223-0	2011	Extreme sensitivity to acenocoumarol therapy in patient with both VKORC.-1639 A/A and CYP2C9*1/*3 genotypes.	Acenocoumarol	23-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
21638223-8	2011	The genotyping results performed after introducing of VKA showed the patient was homozygous for vitamin K epoxide reductase (VKORC1) c.-1639 G>A, and heterozygous for cytochrome P450 2C9 (CYP2C9)*3 which pointed to extreme sensitivity to acenocoumarol.	Acenocoumarol	241-254	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-189
21726172-8	2011	Although clinical doses of toremifene produce steady state exposures to toremifene and NDMT that may be sufficient to cause pharmacokinetic drug-drug interactions with other drugs metabolised by CYP2B6, CYP2C8, CYP3A4, CYP2C9 and CYP2C19, these data indicate that toremifene is unlikely to play a role in clinical drug-drug interactions with substrate drugs of CYP1A2 and CYP2D6.	Toremifene	27-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	219-225
22321278-1	2011	OBJECTIVE: To investigate potential contributions of genetic variants of cytochrome P-450 2C9 (CYP2C9) and vitamin K expoxide reductase (VKORC1) to the anticoagulation response during the initiation of warfarin therapy in the Han Chinese population.	Warfarin	202-210	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-93
22321278-1	2011	OBJECTIVE: To investigate potential contributions of genetic variants of cytochrome P-450 2C9 (CYP2C9) and vitamin K expoxide reductase (VKORC1) to the anticoagulation response during the initiation of warfarin therapy in the Han Chinese population.	Warfarin	202-210	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
22321278-10	2011	CONCLUSION: Detecting genetic polymorphism of CYP2C9 and VKORC1 could guide clinical use of warfarin to reduce the risk of adverse reactions including bleeding in patients receiving chronic anticoagulation therapy.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
21320153-1	2011	AIMS: To investigate the influence of polymorphisms in CYP2C9, VKORC1, CYP4F2 and F2 genes on warfarin dose-response and develop a model including genetic and non-genetic factors for warfarin dose prediction needed for each patient.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
21725053-1	2011	Single-nucleotide polymorphisms in genes that affect warfarin metabolism (cytochrome P450 2C9 gene, CYP2C9) and response (vitamin K epoxide reductase complex 1 gene, VKORC1) have an important influence on warfarin therapy, particularly during initiation; however, there is a lack of consensus regarding the optimal pharmacogenetics-based initiation strategy.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-93
21725053-1	2011	Single-nucleotide polymorphisms in genes that affect warfarin metabolism (cytochrome P450 2C9 gene, CYP2C9) and response (vitamin K epoxide reductase complex 1 gene, VKORC1) have an important influence on warfarin therapy, particularly during initiation; however, there is a lack of consensus regarding the optimal pharmacogenetics-based initiation strategy.	Warfarin	205-213	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-93
21725053-1	2011	Single-nucleotide polymorphisms in genes that affect warfarin metabolism (cytochrome P450 2C9 gene, CYP2C9) and response (vitamin K epoxide reductase complex 1 gene, VKORC1) have an important influence on warfarin therapy, particularly during initiation; however, there is a lack of consensus regarding the optimal pharmacogenetics-based initiation strategy.	Warfarin	205-213	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
21622626-1	2011	Our previous study revealed that CYP2C9 played a central role in sesamin monocatecholization.	sesamin	65-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
21622626-14	2011	On the basis of these results, we concluded that CYP2C9, UGT2B7, and COMT played essential roles in the metabolism of sesamin in the human liver.	sesamin	118-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
21338443-0	2011	A candidate gene study of antiepileptic drug tolerability and efficacy identifies an association of CYP2C9 variants with phenytoin toxicity.	Phenytoin	121-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
21338443-8	2011	RESULTS:   We identified significant associations of CYP2C9 variant alleles with presence of phenytoin (PHT) adverse drug reactions (ADRs) and of GSTM1 copy number variation with the presence of carbamazepine ADRs.	Phenytoin	93-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
21338443-8	2011	RESULTS:   We identified significant associations of CYP2C9 variant alleles with presence of phenytoin (PHT) adverse drug reactions (ADRs) and of GSTM1 copy number variation with the presence of carbamazepine ADRs.	Phenytoin	104-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
21826053-2	2011	The inhibitory potential of corydaline on the activities of seven major human cytochrome P450 and four UDP-glucuronosyltransferase enzymes in human liver microsomes was investigated using LC-tandem MS. Corydaline was found to inhibit CYP2C19-catalyzed S-mephenytoin-4"-hydroxylatoin and CYP2C9-catalyzed diclofenac 4-hydroxylation, with K(i) values of 1.7 and 7.0 mM, respectively.	corydaline	28-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	287-293
22040439-0	2011	Extremely low warfarin dose in patients with genotypes of CYP2C9*3/*3 and VKORC1-1639A/A.	Warfarin	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
22040439-1	2011	BACKGROUND: Patients with the genotypes of both CYP2C9*3/*3 and VKORC1-1639 A/A are expected to require the lowest dose of warfarin, and to have a greatly increased risk of bleeding.	Warfarin	123-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
22040439-13	2011	CONCLUSIONS: Two Chinese with the rare genotypes of both CYP2C9*3/*3 and VKORC1-1639 A/A were found to require the extremely low dose of warfarin.	Warfarin	137-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
22040439-14	2011	The pharmacogenetic algorithm incorporating the variances of VKORC1 and CYP2C9 genotypes, as well as the non-genetic factors could predict their stable dose of warfarin with high accuracy.	Warfarin	160-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
21906462-4	2011	TAM is known to be metabolised to its active metabolites N-desmethyl TAM and 4-hydroxytamoxifen by a number of CYP450 enzymes, including CYP2D6, CYP3A4, CYP2C9, CYP2C19 and CYP2B6.	Tamoxifen	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
21906462-4	2011	TAM is known to be metabolised to its active metabolites N-desmethyl TAM and 4-hydroxytamoxifen by a number of CYP450 enzymes, including CYP2D6, CYP3A4, CYP2C9, CYP2C19 and CYP2B6.	hydroxytamoxifen	77-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
21985811-11	2011	INTERPRETATION & CONCLUSIONS: Our results demonstrated significant involvement of CYP2C9 genetic variants in the modulation of epilepsy pharmacotherapy confirming the important role of CYP2C9 mutants preventing epilepsy patients from developing drug resistance.	Adenosine Monophosphate	16-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
21386709-6	2011	Solid evidence supports the importance of gene variants in CYP2C9 and VKORC1 for warfarin dosing and in CYP2C19 for clopidogrel response in adult patients.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
21476064-0	2011	Population pharmacokinetic analysis of glimepiride with CYP2C9 genetic polymorphism in healthy Korean subjects.	glimepiride	39-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
21476064-1	2011	PURPOSE: The purpose of this study was to develop a population pharmacokinetic (PPK) model of glimepiride and to investigate the influence of genetic polymorphisms in CYP2C9 on the PPK of glimepiride in healthy Korean subjects.	glimepiride	188-199	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
21476064-6	2011	The CYP2C9 genotypes as covariate significantly (P < 0.001) influenced the apparent oral clearance (CL/F) of glimepiride.	glimepiride	112-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
21476064-7	2011	The estimated CL/F of glimepiride was higher (1.60-fold) in CYP2C9*1/*1 subjects than in CYP2C9*1/*3 subjects.	glimepiride	22-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
21476064-7	2011	The estimated CL/F of glimepiride was higher (1.60-fold) in CYP2C9*1/*1 subjects than in CYP2C9*1/*3 subjects.	glimepiride	22-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
21476064-8	2011	CONCLUSIONS: This study indicates that genetic polymorphisms of CYP2C9 influence the substantial interindividual variability in the disposition of glimepiride, and these polymorphisms may affect the clinical response to glimepiride therapy.	glimepiride	147-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
21476064-8	2011	CONCLUSIONS: This study indicates that genetic polymorphisms of CYP2C9 influence the substantial interindividual variability in the disposition of glimepiride, and these polymorphisms may affect the clinical response to glimepiride therapy.	glimepiride	220-231	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
21516380-0	2011	Clinical pharmacokinetics of ketoprofen enantiomers in wild type of Cyp 2c8 and Cyp 2c9 patients with rheumatoid arthritis.	Ketoprofen	29-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-87
21826053-2	2011	The inhibitory potential of corydaline on the activities of seven major human cytochrome P450 and four UDP-glucuronosyltransferase enzymes in human liver microsomes was investigated using LC-tandem MS. Corydaline was found to inhibit CYP2C19-catalyzed S-mephenytoin-4"-hydroxylatoin and CYP2C9-catalyzed diclofenac 4-hydroxylation, with K(i) values of 1.7 and 7.0 mM, respectively.	corydaline	202-212	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	287-293
21826053-5	2011	These in vitro results suggest that corydaline should be evaluated for potential pharmacokinetic drug interactions in vivo due to potent inhibition of CYP2C19 and CYP2C9.	corydaline	36-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-169
21332946-0	2011	Effect of atorvastatin on CYP2C9 metabolic activity as measured by the formation rate of losartan metabolite in hypercholesterolaemic patients.	Atorvastatin	10-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
21332946-0	2011	Effect of atorvastatin on CYP2C9 metabolic activity as measured by the formation rate of losartan metabolite in hypercholesterolaemic patients.	Losartan	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
21332946-4	2011	The aim of this study was to determine the effect of atorvastatin on the activity of CYP2C9 in a group of Turkish hypercholesterolaemic patients.	Atorvastatin	53-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
21332946-5	2011	We prospectively investigated the atorvastatin effect on CYP2C9 activity in a sample of Turkish hypercholesterolaemia patients (11 women, 7 men) who commenced atorvastatin (10 mg/day).	Atorvastatin	34-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
21332946-6	2011	Losartan was used as a probe drug to determine CYP2C9 metabolic activity.	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
21636598-1	2011	AIMS: Polymorphisms in CYP2C9 and VKORC1 influence patients" phenprocoumon (PHE) and acenocoumarol (ACE) dose requirements.	Phenprocoumon	61-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
21636598-1	2011	AIMS: Polymorphisms in CYP2C9 and VKORC1 influence patients" phenprocoumon (PHE) and acenocoumarol (ACE) dose requirements.	Phenprocoumon	76-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
21636598-1	2011	AIMS: Polymorphisms in CYP2C9 and VKORC1 influence patients" phenprocoumon (PHE) and acenocoumarol (ACE) dose requirements.	Acenocoumarol	85-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
21636598-1	2011	AIMS: Polymorphisms in CYP2C9 and VKORC1 influence patients" phenprocoumon (PHE) and acenocoumarol (ACE) dose requirements.	Acenocoumarol	100-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
21636598-4	2011	Single nucleotide polymorphisms relevant to coumarin derivative dosing on the CYP2C9 and VKORC1 genes were determined.	coumarin	44-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
21336994-0	2011	Influence of CYP2C9 gene polymorphisms on response to glibenclamide in type 2 diabetes mellitus patients.	Glyburide	54-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
21636598-8	2011	CYP2C9 and VKORC1 genotype, weight, height, sex, age, and amiodarone use contributed to the maintenance dose of PHE and ACE.	Phenprocoumon	112-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21336994-1	2011	PURPOSE: The antidiabetic drug glibenclamide is metabolized by the enzyme cytochrome P450 2C9 (CYP2C9) encoded by the polymorphic gene CYP2C9.	Glyburide	31-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-93
21636598-8	2011	CYP2C9 and VKORC1 genotype, weight, height, sex, age, and amiodarone use contributed to the maintenance dose of PHE and ACE.	Acenocoumarol	120-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21336994-1	2011	PURPOSE: The antidiabetic drug glibenclamide is metabolized by the enzyme cytochrome P450 2C9 (CYP2C9) encoded by the polymorphic gene CYP2C9.	Glyburide	31-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
22075505-4	2011	The pharmacokinetic sensitivity of warfarin was significantly higher in the CYP2C9 *1/*3 genotypes than in the CYP2C9 *1/*1 genotypes [ratio of S-warfarin concentration/dose, 0.53 vs. 0.21; p=0.01].	Warfarin	35-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
21336994-1	2011	PURPOSE: The antidiabetic drug glibenclamide is metabolized by the enzyme cytochrome P450 2C9 (CYP2C9) encoded by the polymorphic gene CYP2C9.	Glyburide	31-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-141
21336994-2	2011	Previous studies involving healthy volunteers have shown a significant influence of variant CYP2C9 genotypes on glibenclamide metabolism.	Glyburide	112-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
21336994-3	2011	The aim of this study was to investigate the influence of genetic polymorphisms of CYP2C9 on the response to glibenclamide and on glibenclamide plasma levels in type 2 diabetes mellitus patients.	Glyburide	109-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
21336994-9	2011	There was a significant association (p < 0.001) between genotype status of CYP2C9 and the control of diabetes in patients receiving treatment with glibenclamide.	Glyburide	150-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
21336994-11	2011	CONCLUSION: The type 2 diabetes mellitus patients participating in this study with variant genotypes of CYP2C9 were found to respond better to treatment with glibenclamide than those with the normal genotype.	Glyburide	158-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
21120554-5	2011	Interestingly, at the binding sites of all PPI-CYP2C9 complexes except for Lan/CYP2C9, there are hydrogen-bonding networks made of PPIs, water molecules, and some residues of 2C9.	Hydrogen	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
21120554-5	2011	Interestingly, at the binding sites of all PPI-CYP2C9 complexes except for Lan/CYP2C9, there are hydrogen-bonding networks made of PPIs, water molecules, and some residues of 2C9.	Hydrogen	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
21120554-5	2011	Interestingly, at the binding sites of all PPI-CYP2C9 complexes except for Lan/CYP2C9, there are hydrogen-bonding networks made of PPIs, water molecules, and some residues of 2C9.	Water	137-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
21120554-5	2011	Interestingly, at the binding sites of all PPI-CYP2C9 complexes except for Lan/CYP2C9, there are hydrogen-bonding networks made of PPIs, water molecules, and some residues of 2C9.	Water	137-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
21704641-7	2011	Seven of 14 recombinant human CYP enzymes examined (CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) were capable of metabolizing CBD.	Cannabidiol	142-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
22075505-4	2011	The pharmacokinetic sensitivity of warfarin was significantly higher in the CYP2C9 *1/*3 genotypes than in the CYP2C9 *1/*1 genotypes [ratio of S-warfarin concentration/dose, 0.53 vs. 0.21; p=0.01].	Warfarin	35-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
22075505-7	2011	The increase of over-anticoagulation risk and warfarin sensitivity is related to the CYP2C9*3 allele and old age with the VKORC1 1173 T allele in Korean patients with thromboembolic disease.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
21672908-8	2011	Associations between known variants in VKORC1 and CYP2C9 and warfarin stable weekly dose were performed with linear regression adjusted for age, gender, and body mass index.	Warfarin	61-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
21666702-8	2011	Ticlopidine inhibited CYP2C9 and 3A4 with IC50 values of 26.0 and 32.3 mumol/L, respectively.	Ticlopidine	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
21666702-10	2011	CONCLUSION: The significant increase in the AUC of losartan (9 mg/kg) by ticlopidine (10 mg/kg) could be attributed to the inhibition of CYP2C9- and 3A4-mediated losartan metabolism in small intestine and/or in liver.	Losartan	51-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
21666702-10	2011	CONCLUSION: The significant increase in the AUC of losartan (9 mg/kg) by ticlopidine (10 mg/kg) could be attributed to the inhibition of CYP2C9- and 3A4-mediated losartan metabolism in small intestine and/or in liver.	Ticlopidine	73-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
21666702-10	2011	CONCLUSION: The significant increase in the AUC of losartan (9 mg/kg) by ticlopidine (10 mg/kg) could be attributed to the inhibition of CYP2C9- and 3A4-mediated losartan metabolism in small intestine and/or in liver.	Losartan	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
21460231-7	2011	In addition, PPOH and MS-PPOH displayed time- and NADPH-dependent inhibition of CYP2C9 and other epoxygenases.	propenylphosphonic acid	13-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
21460231-7	2011	In addition, PPOH and MS-PPOH displayed time- and NADPH-dependent inhibition of CYP2C9 and other epoxygenases.	propenylphosphonic acid	25-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
21460231-7	2011	In addition, PPOH and MS-PPOH displayed time- and NADPH-dependent inhibition of CYP2C9 and other epoxygenases.	NADP	50-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
21476972-7	2011	It has been demonstrated that CYP2J2 generates cardioprotective EETs, whereas another isozyme in the heart, CYP2C, generates EETs as well as detrimental ROS.	Reactive Oxygen Species	153-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-113
21672908-5	2011	The authors then conducted an association analysis between an automatically extracted stable weekly dose of warfarin and four genetic variants of VKORC1 and CYP2C9 genes.	Warfarin	108-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
21672908-10	2011	Using the automatically extracted weekly doses of warfarin, the authors successfully replicated the previous known associations between warfarin stable dose and genetic variants in VKORC1 and CYP2C9.	Warfarin	50-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	192-198
21672908-10	2011	Using the automatically extracted weekly doses of warfarin, the authors successfully replicated the previous known associations between warfarin stable dose and genetic variants in VKORC1 and CYP2C9.	Warfarin	136-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	192-198
21635147-0	2011	Novel CYP2C9 and VKORC1 gene variants associated with warfarin dosage variability in the South African black population.	Warfarin	54-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
21493749-4	2011	We hypothesize that this may occur because of the sex steroid-dependent activation of estrogen receptor alpha (ERalpha) with further transactivation of the CYP2C9 gene.	Steroids	54-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
21365364-2	2011	In vitro probe-based high performance liquid chromatography assays were developed to determine CYP2C9-dependent tolbutamide methylhydroxylation, CYP2D6-dependent dextromethorphan O-demethylation and CYP3A4-dependent testosterone 6beta-hydroxylation activities in the presence and absence of AP extracts and andrographolide.	Tolbutamide	112-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
21635147-9	2011	CONCLUSION: We demonstrate that CYP2C9*8 and two novel CYP2C9 SNPs (g.16179 and g.46028) are associated with a decrease in warfarin dosage, beta-blockers are independently associated with a decrease in warfarin dosage and two known VKORC1 variants (rs7200749 and rs7294) are associated with an increase in warfarin dosage.	Warfarin	123-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
21635147-9	2011	CONCLUSION: We demonstrate that CYP2C9*8 and two novel CYP2C9 SNPs (g.16179 and g.46028) are associated with a decrease in warfarin dosage, beta-blockers are independently associated with a decrease in warfarin dosage and two known VKORC1 variants (rs7200749 and rs7294) are associated with an increase in warfarin dosage.	Warfarin	123-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
21635147-9	2011	CONCLUSION: We demonstrate that CYP2C9*8 and two novel CYP2C9 SNPs (g.16179 and g.46028) are associated with a decrease in warfarin dosage, beta-blockers are independently associated with a decrease in warfarin dosage and two known VKORC1 variants (rs7200749 and rs7294) are associated with an increase in warfarin dosage.	Warfarin	202-210	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
21635147-9	2011	CONCLUSION: We demonstrate that CYP2C9*8 and two novel CYP2C9 SNPs (g.16179 and g.46028) are associated with a decrease in warfarin dosage, beta-blockers are independently associated with a decrease in warfarin dosage and two known VKORC1 variants (rs7200749 and rs7294) are associated with an increase in warfarin dosage.	Warfarin	202-210	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
21635147-9	2011	CONCLUSION: We demonstrate that CYP2C9*8 and two novel CYP2C9 SNPs (g.16179 and g.46028) are associated with a decrease in warfarin dosage, beta-blockers are independently associated with a decrease in warfarin dosage and two known VKORC1 variants (rs7200749 and rs7294) are associated with an increase in warfarin dosage.	Warfarin	202-210	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
21635147-9	2011	CONCLUSION: We demonstrate that CYP2C9*8 and two novel CYP2C9 SNPs (g.16179 and g.46028) are associated with a decrease in warfarin dosage, beta-blockers are independently associated with a decrease in warfarin dosage and two known VKORC1 variants (rs7200749 and rs7294) are associated with an increase in warfarin dosage.	Warfarin	202-210	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
21635147-10	2011	The CYP2C9 and VKORC1 variants and a small subset of environmental factors used in the study explain approximately 45% of warfarin dosage variability in the South African black population.	Warfarin	122-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
21639946-1	2011	BACKGROUND: CYP2C9 and VKORC1 are two major genetic factors associated with inter-individual variability in warfarin dose.	Warfarin	108-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
21447389-4	2011	This was done by using human substrates of CYP3A4 (verapamil and testosterone), CYP2C9 (diclofenac) and CYP2D6 (dextromethorphan).	Diclofenac	88-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
21639946-4	2011	METHODS: Direct sequencing method was used to identify SNPs in CYP2C9, VKORC1, CYP4F2, EPHX1, PROC and GGCX genes in warfarin-treated patients.	Warfarin	117-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
21639946-6	2011	RESULTS: From the 40 SNPs analyzed, CYP2C9 rs17847036 and VKORC1 rs9923231 showed significant association with warfarin sensitivity.	Warfarin	111-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
21639946-9	2011	CYP2C9 and VKORC1 genetic variants as well as non-genetic factors such as age, body weight and body height account for 15.4% of variance in warfarin dose among our study population.	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21110192-0	2011	Contribution of VKORC1 and CYP2C9 polymorphisms in the interethnic variability of warfarin dose in Malaysian populations.	Warfarin	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
21574568-4	2011	We used structure-activity data from the PubChem database to develop a topomer CoMFA model that guided the design of novel sulfonamides with high selectivity for HIF-1 over CYP2C9 inhibition.	Sulfonamides	123-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	173-179
21356265-0	2011	Reduced catalytic activity of human CYP2C9 natural alleles for gliclazide: molecular dynamics simulation and docking studies.	Gliclazide	63-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
21356265-1	2011	Amongst sulfonylureas, gliclazide is one of the mostly prescribed drugs to diabetic patients and is metabolized extensively by P450 CYP2C9.	Sulfonylurea Compounds	8-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
21356265-1	2011	Amongst sulfonylureas, gliclazide is one of the mostly prescribed drugs to diabetic patients and is metabolized extensively by P450 CYP2C9.	Gliclazide	23-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
21356265-2	2011	Among 24-CYP2C9 alleles, the *2/*2 and *3/*3 genotypes showed significantly lower gliclazide clearances with reductions of 25 and 57%, respectively.	Gliclazide	82-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
21356265-4	2011	In the present study, we used molecular dynamics simulation and autodocking studies to provide models for gliclazide-bound complexes of CYP2C9*2, *3 and *2/*3 mutants, which give insight into CYP2C9-gliclazide interactions and explain the reduced enzymatic activity seen in these variants.	Gliclazide	106-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
21356265-4	2011	In the present study, we used molecular dynamics simulation and autodocking studies to provide models for gliclazide-bound complexes of CYP2C9*2, *3 and *2/*3 mutants, which give insight into CYP2C9-gliclazide interactions and explain the reduced enzymatic activity seen in these variants.	Gliclazide	106-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	192-198
21356265-4	2011	In the present study, we used molecular dynamics simulation and autodocking studies to provide models for gliclazide-bound complexes of CYP2C9*2, *3 and *2/*3 mutants, which give insight into CYP2C9-gliclazide interactions and explain the reduced enzymatic activity seen in these variants.	Gliclazide	199-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
21356265-4	2011	In the present study, we used molecular dynamics simulation and autodocking studies to provide models for gliclazide-bound complexes of CYP2C9*2, *3 and *2/*3 mutants, which give insight into CYP2C9-gliclazide interactions and explain the reduced enzymatic activity seen in these variants.	Gliclazide	199-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	192-198
21318593-2	2011	This study sought to systematically investigate the effects of genetic polymorphisms of VKORC1, STX4A, CYP2C9, CYP3A4, and GGCX and interacting drugs on the initial responses to warfarin in Chinese patients with heart valve replacement (HVR).	Warfarin	178-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
21318593-8	2011	CONCLUSIONS: Not only VKORC1 and CYP2C9 genotypes, but also interacting drugs, had a significant impact on the variability of the initial response to warfarin.	Warfarin	150-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
21451434-0	2011	Characterization of a novel CYP2C9 gene mutation and structural bioinformatic protein analysis in a warfarin hypersensitive patient.	Warfarin	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
21349323-2	2011	The median inhibitory concentrations (IC50) of asiaticoside and madecassoside were determined for CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1 and CYP3A4.	asiaticoside	47-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
21349323-2	2011	The median inhibitory concentrations (IC50) of asiaticoside and madecassoside were determined for CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1 and CYP3A4.	madecassoside	64-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
21815482-4	2011	Recent studies have shown that genetic variations in a subunit of VKOR complex, VKORC1, and in cytochrome P 450 (CYP) 2C9 genes are strong determinants of individuals" warfarin sensitivity.	Warfarin	168-176	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-121
21815482-5	2011	Algorithms have been proposed to predict warfarin doses, and about 55% of the variance in warfarin dose could be attributed to variations in the VKORC1 and CYP2C9 genes together with age, sex, body-surface area, and presence or absence of heart valve replacement.	Warfarin	41-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
21815482-5	2011	Algorithms have been proposed to predict warfarin doses, and about 55% of the variance in warfarin dose could be attributed to variations in the VKORC1 and CYP2C9 genes together with age, sex, body-surface area, and presence or absence of heart valve replacement.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
21815482-6	2011	Contributions of polymorphisms in VKORC1 and CYP2C9 to inter-individual differences of warfarin dose, however, are different among races.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
21451434-4	2011	We genotyped common polymorphisms in VKORC1, CYP2C9, and CYP4F2 genes, known to be involved in warfarin dosing.	Warfarin	95-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
21480951-1	2011	AIM: To investigate the impact of genetic polymorphisms in CYP2D6, CYP3A5, CYP2C9 and CYP2C19 on the pharmacokinetics of tamoxifen and its metabolites in Asian breast cancer patients.	Tamoxifen	121-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
21497079-3	2011	The MWCNT structuring improves the sensitivity from 5.1 to 20.5 nA/mM mm(2) in case of CYP2B4-mediated Benzphetamine detection, from 0.26 to 0.63 nA/muM mm(2) in case of CYP3A4-mediated Cyclophosphamide detection, and from 0.11 to 0.25 nA/muM mm(2) in case of CYP2C9-mediated Naproxen detection.	Benzphetamine	103-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	260-266
21289076-1	2011	According to published in vitro studies, cytochrome P450 3A4 catalyzes montelukast 21-hydroxylation (M5 formation), whereas CYP2C9 catalyzes 36-hydroxylation (M6), the primary step in the main metabolic pathway of montelukast.	montelukast	214-225	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
21289076-6	2011	The CYP2C8 inhibitors gemfibrozil 1-O-beta glucuronide and trimethoprim inhibited the depletion of 0.02 muM montelukast and formation of M6 from 0.05 muM montelukast more potently than did the CYP2C9 inhibitor sulfaphenazole.	Trimethoprim	59-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	193-199
21213107-2	2011	As the genetically polymorphic cytochrome P450 (CYP), enzyme CYP2C9 is mainly responsible for the hepatic metabolism of sulfonylureas (SUs), we hypothesized that the slow-metabolizer genotypes *2/*2, *2/*3, and *3/*3 might be overrepresented in type 2 diabetic patients with SH.	Sulfonylurea Compounds	120-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
21321060-0	2011	CYP2C9-mediated metabolic activation of losartan detected by a highly sensitive cell-based screening assay.	Losartan	40-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21321060-6	2011	Metabolic activation of losartan by CYP2C9 has never been reported, although the metabolic activations of benzbromarone and tienilic acid have been reported.	Losartan	24-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
21321060-8	2011	Two CYP2C9-specific semicarbazide adducts of losartan (S1 and S2) were detected.	carbamylhydrazine	20-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
21321060-8	2011	Two CYP2C9-specific semicarbazide adducts of losartan (S1 and S2) were detected.	Losartan	45-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
21321060-10	2011	In conclusion, a highly sensitive cell-based assay to evaluate CYP2C9-mediated metabolic activation was established, and we found for the first time that CYP2C9 is involved in the metabolic activation of losartan.	Losartan	204-212	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
21321060-10	2011	In conclusion, a highly sensitive cell-based assay to evaluate CYP2C9-mediated metabolic activation was established, and we found for the first time that CYP2C9 is involved in the metabolic activation of losartan.	Losartan	204-212	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
21220010-5	2011	The IC(50) concerning the CYP 2C9-mediated 4-hydroxylation of diclofenac has been calculated to be 0.04 mM (PS80), 0.30 mM (TPGS), 0.07 mM (sucrose laurate), 0.03 mM (CrEL), and 0.03 mM (Cr RH 40).	Diclofenac	62-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-33
21220010-5	2011	The IC(50) concerning the CYP 2C9-mediated 4-hydroxylation of diclofenac has been calculated to be 0.04 mM (PS80), 0.30 mM (TPGS), 0.07 mM (sucrose laurate), 0.03 mM (CrEL), and 0.03 mM (Cr RH 40).	sucrose monolaurate	140-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-33
21213107-2	2011	As the genetically polymorphic cytochrome P450 (CYP), enzyme CYP2C9 is mainly responsible for the hepatic metabolism of sulfonylureas (SUs), we hypothesized that the slow-metabolizer genotypes *2/*2, *2/*3, and *3/*3 might be overrepresented in type 2 diabetic patients with SH.	Sulfonylurea Compounds	135-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
21213107-9	2011	However, in the control group, patients with CYP2C9 genotypes, predicting slower metabolism of SU drugs, were treated with significantly lower doses (p = 0.027) than were extensive metabolizers, whereas in the patient group with severe hypoglycemia, the dose was the same for all genotype groups.	Sulfonylurea Compounds	95-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
21220010-1	2011	The purpose of the study was to investigate the impact of commonly used non-ionic surfactants on cytochrome P450 (CYP) 3A4-mediated metabolism of testosterone and the CYP2C9-mediated metabolism of diclofenac.	Diclofenac	197-207	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
21543033-1	2011	OBJECTIVE: To investigate the effect of the estimated highest therapeutic dose of linagliptin (5 mg) on the pharmacokinetics and pharmacodynamics of warfarin, a CYP2C9 substrate.	Linagliptin	82-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
21543033-1	2011	OBJECTIVE: To investigate the effect of the estimated highest therapeutic dose of linagliptin (5 mg) on the pharmacokinetics and pharmacodynamics of warfarin, a CYP2C9 substrate.	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
21277363-4	2011	Fluvoxamine maleate, gemfibrozil, amiodarone hydrochloride, omeprazole, quinidine, diethyldithiocarbamic acid and ketoconazole were successfully applied as test inhibitors for CYP1A2, CYP2C8, CYP2C9, CYP2C19*1, CYP2D6*1, CYP2E1 and CYP3A4/5 in HLMs, respectively.	Fluvoxamine	0-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	192-198
21292004-6	2011	NCOA6 enhances the synergistic activation of CYP2C9 and CYP3A4 promoter activity by PXR and HNF4alpha in the presence of rifampicin.	Rifampin	121-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
21294626-4	2011	CYP2C8, CYP2C9, CYP2C19, and CYP3A4 were identified as the major enzymes responsible for the formation of the two O-desmethyl magnolins (M1 and M2), on the basis of a combination of correlation analysis and experiments, including immunoinhibition of magnolin in human liver microsomes and metabolism of magnolin by human cDNA-expressed CYP enzymes.	magnolin	126-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
21294626-4	2011	CYP2C8, CYP2C9, CYP2C19, and CYP3A4 were identified as the major enzymes responsible for the formation of the two O-desmethyl magnolins (M1 and M2), on the basis of a combination of correlation analysis and experiments, including immunoinhibition of magnolin in human liver microsomes and metabolism of magnolin by human cDNA-expressed CYP enzymes.	magnolin	250-258	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
21277363-4	2011	Fluvoxamine maleate, gemfibrozil, amiodarone hydrochloride, omeprazole, quinidine, diethyldithiocarbamic acid and ketoconazole were successfully applied as test inhibitors for CYP1A2, CYP2C8, CYP2C9, CYP2C19*1, CYP2D6*1, CYP2E1 and CYP3A4/5 in HLMs, respectively.	Ketoconazole	114-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	192-198
20927605-7	2011	In addition, the preparative of synthesis of 2.8 g of 4"-hydroxydiclofenac was achieved by whole-cell biotransformation of diclofenac using a CPR-CYP2C9 coexpressing fission yeast strain.	4'-hydroxydiclofenac	54-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
20927605-7	2011	In addition, the preparative of synthesis of 2.8 g of 4"-hydroxydiclofenac was achieved by whole-cell biotransformation of diclofenac using a CPR-CYP2C9 coexpressing fission yeast strain.	Diclofenac	64-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
21395648-6	2011	The oral clearance of meloxicam was significantly lower in the CYP2C9*1/*13 group (37.9% of wild type) than in the CYP2C9*1/*1 group.	Meloxicam	22-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
21395648-7	2011	The t(1/2) of meloxicam was 1.84-fold longer in the CYP2C9*1/*13 group than in the CYP2C9*1/*1 group.	Meloxicam	14-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
21395648-0	2011	Effects of CYP2C9*1/*13 on the pharmacokinetics and pharmacodynamics of meloxicam.	Meloxicam	72-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
21395648-7	2011	The t(1/2) of meloxicam was 1.84-fold longer in the CYP2C9*1/*13 group than in the CYP2C9*1/*1 group.	Meloxicam	14-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
21395648-1	2011	AIMS: To determine the effects of the CYP2C9*1/*13 genotype on the pharmacokinetics and pharmacodynamics of meloxicam in Korean subjects.	Meloxicam	108-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
21395648-9	2011	CONCLUSIONS: The CYP2C9*1/*13 genotype is associated with decreased metabolism and increased pharmacodynamic effects of meloxicam.	Meloxicam	120-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
21395648-2	2011	METHODS: Meloxicam (15 mg) was orally administered to 21 healthy Korean volunteers with either the CYP2C9*1/*1 or the CYP2C9*1/*13 genotype.	Meloxicam	9-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
21395648-2	2011	METHODS: Meloxicam (15 mg) was orally administered to 21 healthy Korean volunteers with either the CYP2C9*1/*1 or the CYP2C9*1/*13 genotype.	Meloxicam	9-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
21177984-5	2011	Ticagrelor moderately inhibited CYP2C9 activity in human liver microsomes with an IC(50) of 10.5 muM, while exhibiting little or no inhibition of CYP1A2, CYP2B6, CYP2C8, CYP2C19, CYP2D6, and CYP2E1.	Ticagrelor	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
21395648-5	2011	RESULTS: The AUC(0, ) and C(max) of meloxicam were 2.43- and 1.46-fold higher in the CYP2C9*1/*13 group than in the CYP2C9*1/*1 group, respectively.	Meloxicam	36-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
21395648-5	2011	RESULTS: The AUC(0, ) and C(max) of meloxicam were 2.43- and 1.46-fold higher in the CYP2C9*1/*13 group than in the CYP2C9*1/*1 group, respectively.	Meloxicam	36-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
21395648-6	2011	The oral clearance of meloxicam was significantly lower in the CYP2C9*1/*13 group (37.9% of wild type) than in the CYP2C9*1/*1 group.	Meloxicam	22-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
21768671-0	2011	Association and treatment response to capecitabine-based chemoradiotherapy with CYP2C9 polymorphism in head and neck cancer.	Capecitabine	38-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
21537551-0	2011	CYP2C9 polymorphism in patients with epilepsy: genotypic frequency analyzes and phenytoin adverse reactions correlation.	Phenytoin	80-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21537551-12	2011	The role of CYP2C9 polymorphism influence on phenytoin adverse reaction remains to be determined since some literature evidence and our data found negative results.	Phenytoin	45-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
21270790-0	2011	The missing association: sequencing-based discovery of novel SNPs in VKORC1 and CYP2C9 that affect warfarin dose in African Americans.	Warfarin	99-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
20458343-4	2011	The CYP2C9*2 frequency was expected to be lower in the indigenous MT than in the two other groups, and lower in MM than in SP as in our earlier study.	sp	123-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
20458343-8	2011	The frequencies of CYP2C9*2 were 0.01, 0.07, 0.08, and 0.16 for MT, MM, MA, and SP subjects, respectively.	sp	80-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
20458343-9	2011	In agreement with our hypothesis, CYP2C9*2 was significantly lower in the Mexican populations than in the SP (P<0.05), and among Mexicans in the MT than in the MM and MA groups (P<0.05), which presented similar frequencies.	sp	106-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
20458343-10	2011	Moreover, the frequency of CYP2C9*3 was found to be lower (P<0.05) in MM (0.015) and MT (0.015) than in MA (0.06) and SP (0.08).	sp	121-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
21483991-8	2011	The group that required low dose warfarin (n=25) showed significantly higher CYP2C9 polymorphism, required 40% less warfarin and had a higher rate of bleeding (5% versus 1.8%).	Warfarin	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
21483991-10	2011	Patients with the CYP2C9 polymorphism required 40% less warfarin and had more serious bleeds.	Warfarin	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
21270790-5	2011	Through ethnicity-specific warfarin dose model building in 330 African Americans, we identified two novel genetic associations with higher warfarin dose, namely, VKORC1-8191 (rs61162043, P = 0.0041) and 18786 in CYP2C9 (rs7089580, P = 0.035).	Warfarin	139-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
21326313-6	2011	The SNPs of VKORC1, CYP2C9, CYP4F2 and GGCX showed significant correlation with warfarin dose.	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
21326313-10	2011	This study shows that age, gender, BSA, INR and VKORC1, CYP2C9 and CYP4F2 polymorphism affect warfarin dose requirements in Koreans.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
21294704-7	2011	It has also shown mild activation effect on CYP 269 and CYP 2C9 enzymes, indicating the usefulness of thiosemicarbazones as anticonvulsants.	Thiosemicarbazones	102-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-63
21270790-1	2011	It is well recognized that the genetic variants VKORC1-1639, CYP2C9*2, and CYP2C9*3 contribute to warfarin dose response.	Warfarin	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
21270790-1	2011	It is well recognized that the genetic variants VKORC1-1639, CYP2C9*2, and CYP2C9*3 contribute to warfarin dose response.	Warfarin	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
21270790-5	2011	Through ethnicity-specific warfarin dose model building in 330 African Americans, we identified two novel genetic associations with higher warfarin dose, namely, VKORC1-8191 (rs61162043, P = 0.0041) and 18786 in CYP2C9 (rs7089580, P = 0.035).	Warfarin	27-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
21185752-8	2011	The combination of the VKORC1-1639G>A and CYP2C9 genotypes and clinical factors explained 56% of the inter-patient variability in warfarin dose.	Warfarin	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
21336516-7	2011	The most selective inhibitors available are furafylline (in co-incubation and pre-incubation conditions) for CYP1A2, 2-phenyl-2-(1-piperidinyl)propane (PPP) for CYP2B6, montelukast for CYP2C8, sulfaphenazole for CYP2C9, (-)-N-3-benzyl-phenobarbital for CYP2C19 and quinidine for CYP2D6.	2-phenyl-2-(1-piperidinyl)propane	152-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
21553654-4	2011	In vitro inhibitory effects of DES on CYP isoforms were investigated, and the results showed that DES could competitively inhibit CYP3A4, CYP2C8, CYP2C9 and CYP2E1.	Diethylstilbestrol	31-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
21553654-4	2011	In vitro inhibitory effects of DES on CYP isoforms were investigated, and the results showed that DES could competitively inhibit CYP3A4, CYP2C8, CYP2C9 and CYP2E1.	Diethylstilbestrol	98-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
21553654-6	2011	Based on peak serum DES level after drip influsion of 500 mg of fosfestrol (DES diphosphate) in patients, [I]/Ki was calculated to be 4.3, 6.2, 3.7 and 2.3 for CYP3A4, CYP2C9, CYP2E1 and CYP2C8, which suggested that DES was likely to induce in vivo DDI through inhibition of these four major CYP isoforms.	fosfestrol	64-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
21553655-1	2011	Polymorphisms in cytochrome P450 (CYP) 2C9 and the vitamin K oxide reductase complex subunit 1 (VKORC1) greatly affect the maintenance dose of warfarin.	Warfarin	143-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-42
21194699-3	2011	Acetaminophen (CYP1A2), dextrorphan (CYP2D6), hydroxy-chlorzoxazone (CYP2E1) and hydroxy-mephenytoin (CYP2C19) can be derivatized because of the presence of a phenolic OH, whereas hydroxy-midazolam (CYP3A4) and hydroxy-tolbutamide (CYP2C9) remain unchanged.	hydroxy-chlorzoxazone	46-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	232-238
21194699-3	2011	Acetaminophen (CYP1A2), dextrorphan (CYP2D6), hydroxy-chlorzoxazone (CYP2E1) and hydroxy-mephenytoin (CYP2C19) can be derivatized because of the presence of a phenolic OH, whereas hydroxy-midazolam (CYP3A4) and hydroxy-tolbutamide (CYP2C9) remain unchanged.	hydroxy-mephenytoin	81-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	232-238
21194699-3	2011	Acetaminophen (CYP1A2), dextrorphan (CYP2D6), hydroxy-chlorzoxazone (CYP2E1) and hydroxy-mephenytoin (CYP2C19) can be derivatized because of the presence of a phenolic OH, whereas hydroxy-midazolam (CYP3A4) and hydroxy-tolbutamide (CYP2C9) remain unchanged.	hydroxy-midazolam	180-197	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	232-238
21194699-3	2011	Acetaminophen (CYP1A2), dextrorphan (CYP2D6), hydroxy-chlorzoxazone (CYP2E1) and hydroxy-mephenytoin (CYP2C19) can be derivatized because of the presence of a phenolic OH, whereas hydroxy-midazolam (CYP3A4) and hydroxy-tolbutamide (CYP2C9) remain unchanged.	hydroxymethyltolbutamide	211-230	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	232-238
21194699-3	2011	Acetaminophen (CYP1A2), dextrorphan (CYP2D6), hydroxy-chlorzoxazone (CYP2E1) and hydroxy-mephenytoin (CYP2C19) can be derivatized because of the presence of a phenolic OH, whereas hydroxy-midazolam (CYP3A4) and hydroxy-tolbutamide (CYP2C9) remain unchanged.	Acetaminophen	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	232-238
21223634-8	2011	However, one subject"s data was suggestive of being poor metabolizer of flurbiprofen which supports the presence of CYP2C9 polymorphism contributing to inter-individual differences in flurbiprofen disposition.	Flurbiprofen	72-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
20931329-2	2011	Like montelukast, zafirlukast is a substrate of CYP2C9 and CYP3A4 and a potent inhibitor of CYP2C8 in vitro.	montelukast	5-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
20931329-2	2011	Like montelukast, zafirlukast is a substrate of CYP2C9 and CYP3A4 and a potent inhibitor of CYP2C8 in vitro.	zafirlukast	18-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
21223634-8	2011	However, one subject"s data was suggestive of being poor metabolizer of flurbiprofen which supports the presence of CYP2C9 polymorphism contributing to inter-individual differences in flurbiprofen disposition.	Flurbiprofen	184-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
20641061-5	2011	Among seven major CYP isoforms tested, corynoline showed strong inhibitory effects on the activities of CYP3A4 and CYP2C9, with an IC(50) of 3.3 +- 0.9 microm and 31.5 +- 0.5 microm, respectively.	corynoline	39-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
21469766-1	2011	BACKGROUND: Variant alleles of vitamin K epoxide reductase complex subunit 1 gene (VKORC1), the target molecule of vitamin K antagonists, and of cytochrome P450 (CYP) 2C9, an enzyme involved in coumarin metabolism, affect the anticoagulant response of coumarins, which have a narrow therapeutic window.	coumarin	194-202	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-170
21469766-1	2011	BACKGROUND: Variant alleles of vitamin K epoxide reductase complex subunit 1 gene (VKORC1), the target molecule of vitamin K antagonists, and of cytochrome P450 (CYP) 2C9, an enzyme involved in coumarin metabolism, affect the anticoagulant response of coumarins, which have a narrow therapeutic window.	Coumarins	252-261	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-170
20641061-6	2011	Kinetic analysis showed that inhibition of CYP3A4 by corynoline was best fit to a noncompetitive manner with K(i) of 3.2 microm, while inhibition of CYP2C9 by corynoline was best fit to a competitive manner with K(i) of 6.3 microm.	corynoline	159-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
21167292-7	2011	Selective inhibition of CYP2C9 decreased tumor cell proliferation (KYSE30, PT1590 and OE19) in vitro, which was abolished by 11,12-epoxyeicosatrienoic acid (11,12-EET).	pt1590	75-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
21167292-7	2011	Selective inhibition of CYP2C9 decreased tumor cell proliferation (KYSE30, PT1590 and OE19) in vitro, which was abolished by 11,12-epoxyeicosatrienoic acid (11,12-EET).	11,12-epoxy-5,8,14-eicosatrienoic acid	125-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
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
21167292-7	2011	Selective inhibition of CYP2C9 decreased tumor cell proliferation (KYSE30, PT1590 and OE19) in vitro, which was abolished by 11,12-epoxyeicosatrienoic acid (11,12-EET).	11,12-epoxy-5,8,14-eicosatrienoic acid	157-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
21691466-4	2011	We sought in a pilot study to identify if testing for common CYP2C9 and VKORC1 single nucleotide polymorphisms (SNPs) in patients who were likely to begin warfarin treatment was feasible in an ED setting.	Warfarin	155-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
21157402-2	2011	(S)-Warfarin has more potent anticoagulant activity than (R)-warfarin and is metabolized mainly to (S)-7-hydroxywarfarin by CYP2C9.	Warfarin	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
21157402-2	2011	(S)-Warfarin has more potent anticoagulant activity than (R)-warfarin and is metabolized mainly to (S)-7-hydroxywarfarin by CYP2C9.	7-hydroxywarfarin	99-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
21532165-4	2011	Recombinant human CYP2C9 exhibited appreciable catalytic activity with respect to 6-HNA formation from 6-MNA.	6-Mna	103-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
21532165-6	2011	Sulfaphenazole (a selective inhibitor of CYP2C9) inhibited the formation of 6-HNA in pooled human microsomes by 89%, but failed to inhibit this reaction in rat liver microsomes.	Sulfaphenazole	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
21142266-3	2011	In vivo, etravirine is a substrate for, and weak inducer of, the hepatic cytochrome P450 (CYP) isoenzyme 3A4 and a substrate and weak inhibitor of CYP2C9 and CYP2C19.	etravirine	9-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
21184622-2	2011	Nilotinib has shown competitive inhibition of cytochrome P450 enzyme (CYP) 2C9 in vitro, but its effect on CYP2C9 activity in humans is unknown.	nilotinib	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-78
21184622-2	2011	Nilotinib has shown competitive inhibition of cytochrome P450 enzyme (CYP) 2C9 in vitro, but its effect on CYP2C9 activity in humans is unknown.	nilotinib	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
21184622-3	2011	This study evaluated the effects of nilotinib on the pharmacokinetics and pharmacodynamics of warfarin, a sensitive CYP2C9 substrate, in healthy subjects.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
21084763-1	2011	The aim of this study was to investigate the effect of the dipeptidyl peptidase-4 inhibitor linagliptin on the pharmacokinetics of glyburide (a CYP2C9 and CYP3A4 substrate) and vice versa.	Linagliptin	92-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
21182487-1	2011	CYP2C9 metabolizes more than 100 clinically used drugs including phenytoin, S-warfarin, tolbutamide, glipizide, diclofenac, and losartan with varying contributions.	Phenytoin	65-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21182487-1	2011	CYP2C9 metabolizes more than 100 clinically used drugs including phenytoin, S-warfarin, tolbutamide, glipizide, diclofenac, and losartan with varying contributions.	Warfarin	76-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21182487-1	2011	CYP2C9 metabolizes more than 100 clinically used drugs including phenytoin, S-warfarin, tolbutamide, glipizide, diclofenac, and losartan with varying contributions.	Tolbutamide	88-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21182487-1	2011	CYP2C9 metabolizes more than 100 clinically used drugs including phenytoin, S-warfarin, tolbutamide, glipizide, diclofenac, and losartan with varying contributions.	Glipizide	101-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21182487-1	2011	CYP2C9 metabolizes more than 100 clinically used drugs including phenytoin, S-warfarin, tolbutamide, glipizide, diclofenac, and losartan with varying contributions.	Diclofenac	112-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21182487-1	2011	CYP2C9 metabolizes more than 100 clinically used drugs including phenytoin, S-warfarin, tolbutamide, glipizide, diclofenac, and losartan with varying contributions.	Losartan	128-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21182487-10	2011	Polymorphisms in CYP2C9 have the potential to affect the clearance and clinical response of CYP2C9 substrate drugs with low therapeutic indices such as warfarin, phenytoin, and certain antidiabetic drugs.	Warfarin	152-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
21182487-10	2011	Polymorphisms in CYP2C9 have the potential to affect the clearance and clinical response of CYP2C9 substrate drugs with low therapeutic indices such as warfarin, phenytoin, and certain antidiabetic drugs.	Warfarin	152-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
21182487-10	2011	Polymorphisms in CYP2C9 have the potential to affect the clearance and clinical response of CYP2C9 substrate drugs with low therapeutic indices such as warfarin, phenytoin, and certain antidiabetic drugs.	Phenytoin	162-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
21182487-10	2011	Polymorphisms in CYP2C9 have the potential to affect the clearance and clinical response of CYP2C9 substrate drugs with low therapeutic indices such as warfarin, phenytoin, and certain antidiabetic drugs.	Phenytoin	162-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
21557672-5	2011	In light of the present evidence, patients treated with PHT could benefit from CYP2C9 and CYP2C19 genotyping/phenotyping.	Phenytoin	56-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
21084763-1	2011	The aim of this study was to investigate the effect of the dipeptidyl peptidase-4 inhibitor linagliptin on the pharmacokinetics of glyburide (a CYP2C9 and CYP3A4 substrate) and vice versa.	Glyburide	131-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
21084764-5	2011	In patients harboring VKORC1 diplotypes associated with low warfarin requirements, a linear regression model which included age, weight, CYP2C9 and CYP4F2 variants accounted for 38% of the variability in warfarin dose.	Warfarin	204-212	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
21176721-6	2011	The multiple linear regression model for warfarin dose indicated significant contributions from the VKORC1 (1173C > T) genotype (r2 = 0.355; p < 0.001), and age, body weight, and CYP2C9 and VKORC1 genotype together (r2 = 0.513; p < 0.001).	Warfarin	41-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	185-191
21127708-5	2011	Our results indicate that pharmacogenetic testing for VKORC1*2, CYP2C9*2 and CYP2C9*3 is more informative regarding warfarin dose requirements than testing for VKORC1*3, VKORC1*4, and CYP4F2 (1347 C > T) polymorphisms.	Warfarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
21321468-0	2011	Clinical significance of combined CYP2C9 and VKORC1 genotypes in Japanese patients requiring warfarin.	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
21321468-9	2011	Thus, CYP2C9 and VKORC1 haplotype analysis allows prediction of warfarin maintenance dosage.	Warfarin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
20852447-0	2011	Role of CYP2C9 genetic variants for salt sensitivity and the regulation of the renin-angiotensin-aldosterone system in normotensive men.	Salts	36-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
20852447-1	2011	OBJECTIVE: Cytochrome P450 (CYP) 2C9 gene polymorphisms have been implicated in regulation of the renin-angiotensin-aldosterone system (RAAS) and salt sensitivity in hypertensive patients.	Salts	146-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-36
20852447-6	2011	CYP2C9*3 carriers showed a significantly lower PRA compared with CYP2C9*1/*1 individuals in the overall study cohort (high salt: 0.39 +- 0.05 vs. 0.62 +- 0.04 ng/ml per h, P = 0.009; low salt: 2.19 +- 0.27 vs. 2.87 +- 0.13 ng/ml per h, P = 0.013).	Salts	123-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20852447-6	2011	CYP2C9*3 carriers showed a significantly lower PRA compared with CYP2C9*1/*1 individuals in the overall study cohort (high salt: 0.39 +- 0.05 vs. 0.62 +- 0.04 ng/ml per h, P = 0.009; low salt: 2.19 +- 0.27 vs. 2.87 +- 0.13 ng/ml per h, P = 0.013).	Salts	187-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20852447-7	2011	Salt-sensitive CYP2C9*3 carriers exhibited the lowest PRA values and significantly lower 24 h sodium excretion rates during high-salt intake (P = 0.005 vs. CYP2C9*1/*1).	Salts	0-4	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
20852447-7	2011	Salt-sensitive CYP2C9*3 carriers exhibited the lowest PRA values and significantly lower 24 h sodium excretion rates during high-salt intake (P = 0.005 vs. CYP2C9*1/*1).	Salts	0-4	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
20852447-7	2011	Salt-sensitive CYP2C9*3 carriers exhibited the lowest PRA values and significantly lower 24 h sodium excretion rates during high-salt intake (P = 0.005 vs. CYP2C9*1/*1).	Sodium	94-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
20852447-7	2011	Salt-sensitive CYP2C9*3 carriers exhibited the lowest PRA values and significantly lower 24 h sodium excretion rates during high-salt intake (P = 0.005 vs. CYP2C9*1/*1).	Salts	129-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
20852447-8	2011	Lower plasma aldosterone concentrations were only observed in salt-resistant CYP2C9*3 carriers under low salt (P = 0.039).	Salts	62-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
20852447-8	2011	Lower plasma aldosterone concentrations were only observed in salt-resistant CYP2C9*3 carriers under low salt (P = 0.039).	Salts	105-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
20852447-11	2011	Further studies are needed to analyze the long-term effects of CYP2C9*3 for salt sensitivity and hypertensive diseases.	Salts	76-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
21160360-0	2011	CYP2C9 variants and blood pressure response to salt: when salt sensitivity meets pharmacogenomics.	Salts	58-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21127708-5	2011	Our results indicate that pharmacogenetic testing for VKORC1*2, CYP2C9*2 and CYP2C9*3 is more informative regarding warfarin dose requirements than testing for VKORC1*3, VKORC1*4, and CYP4F2 (1347 C > T) polymorphisms.	Warfarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
20585834-9	2011	CYP2C9 and VKORC1 genotype, age, weight and vitamin K intake were identified by stepwise regression modelling to produce the best model for estimating warfarin dose (R (2) = 68%, P < 0.001).	Warfarin	151-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21681008-1	2011	UNLABELLED: A clinical effect of warfarin depends on highly polymorphic drug-metabolizing (CYP2C9) and drug-target (VKORC1) enzymes.	Warfarin	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
20585834-1	2011	CYP2C9 and VKORC1 genotypes could be used to predict warfarin requirement.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
21681008-2	2011	The objective of this study was to investigate the impact of CYP2C9*2, CYP2C9*3, and VKORC1 (G-1639A) polymorphisms on the variability of warfarin dosage requirements in Lithuanian patients after heart valve replacement.	Warfarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
21681008-2	2011	The objective of this study was to investigate the impact of CYP2C9*2, CYP2C9*3, and VKORC1 (G-1639A) polymorphisms on the variability of warfarin dosage requirements in Lithuanian patients after heart valve replacement.	Warfarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
21681008-8	2011	WT CYP2C9*1/*1 genotype was associated with a higher daily warfarin dosage (5.84 mg [SD, 2.84]) as compared to other CYP2C9 genotypes.	Warfarin	59-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	3-9
21681008-10	2011	Patients having CYP2C9*1/*1 or 1/*2 in combination with VKORC1 (G/G) or (G/A) genotypes required the highest daily warfarin dosage in comparison to other combinations of genotypes.	Warfarin	115-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
21681008-12	2011	Analysis of combined CYP2C9 and VKORC1 gene variants allows the prediction of warfarin dosage.	Warfarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
23226058-5	2011	This is the case with warfarin, with lower doses often necessary in carriers of a variant CYP2C9*2 or *3 allele to avoid supratherapeutic anticoagulation.	Warfarin	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
21063236-1	2011	BACKGROUND: Genome-wide association studies (GWAS) on warfarin and acenocoumarol showed that interindividual dosage variation is mainly associated with single nucleotide polymorphisms (SNPs) in VKORC1 and to a lesser extent in CYP2C9 and CYP4F2.	Warfarin	54-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	227-233
21063236-1	2011	BACKGROUND: Genome-wide association studies (GWAS) on warfarin and acenocoumarol showed that interindividual dosage variation is mainly associated with single nucleotide polymorphisms (SNPs) in VKORC1 and to a lesser extent in CYP2C9 and CYP4F2.	Acenocoumarol	67-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	227-233
21063236-6	2011	RESULTS: Within our study population (N=244), VKORC1, CYP2C9, CYP4F2 genotypes together explained 46% of phenprocoumon maintenance dosage variation.	Phenprocoumon	105-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
21174619-0	2011	VKORC1, CYP2C9 and CYP4F2 genetic-based algorithm for warfarin dosing: an Italian retrospective study.	Warfarin	54-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
21142408-2	2011	Both clopidogrel and the oral hypoglycemic drug class sulfonylureas are metabolized by the iso-enzyme CYP2C9.	Clopidogrel	5-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
21462897-6	2011	At concentration up to 50 micromol x L(-1), GA inhibited CYP2C19, CYP2C9 and CYP3A4 enzyme activities with the inhibitory potencies up to 50%.	Glycyrrhetinic Acid	44-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
21142408-2	2011	Both clopidogrel and the oral hypoglycemic drug class sulfonylureas are metabolized by the iso-enzyme CYP2C9.	Sulfonylurea Compounds	54-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
22114699-5	2011	Regression analysis demonstrated that CYP2C9 genotype, kidney function, and gender were independent determinants of S-warfarin clearance.	Warfarin	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
21786578-1	2011	AIM: To investigate frequency of carriage of genetic polymorphisms CYP2C9 and VKORC1 in patients with venous thromboembolic complications (VTEC) in Moscow population given warfarin treatment and effects of this carriage on stability of anticoagulation and frequency of hemorrhagic complications (HC) in warfarin treatment.	Warfarin	172-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
21786578-1	2011	AIM: To investigate frequency of carriage of genetic polymorphisms CYP2C9 and VKORC1 in patients with venous thromboembolic complications (VTEC) in Moscow population given warfarin treatment and effects of this carriage on stability of anticoagulation and frequency of hemorrhagic complications (HC) in warfarin treatment.	Warfarin	303-311	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
21786578-10	2011	A mean warfarin dose, supporting an adequaite INR, was asspciated with both genotype CYP2C9 and VKORC1.	Warfarin	7-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
21786578-11	2011	Warfarin doses were highest in carriers of wile genotypes CYP2C9 and VKORC1 (6,9 and 8,8 mg/day), the lowest--in patients with genotypes CYP2C9*1/*3 and VKORC1 (4,5 and 4,0 mg/day).	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
21786578-11	2011	Warfarin doses were highest in carriers of wile genotypes CYP2C9 and VKORC1 (6,9 and 8,8 mg/day), the lowest--in patients with genotypes CYP2C9*1/*3 and VKORC1 (4,5 and 4,0 mg/day).	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
21786578-15	2011	The results of multifactorial regression analysis also indicated that carriage of genotype CYP2C9*1/*3, a female gender and the range of INR in warfarin treatment > or = 2,66 are independent predictors of HC in VTEC patients on warfarin treatment.	Warfarin	144-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
21786578-15	2011	The results of multifactorial regression analysis also indicated that carriage of genotype CYP2C9*1/*3, a female gender and the range of INR in warfarin treatment > or = 2,66 are independent predictors of HC in VTEC patients on warfarin treatment.	Warfarin	231-239	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
21786578-16	2011	CONCLUSION: Carriage of gene CYP2C9 and VKORC1 polymorphisms affects suppoting dose of warfarin and rate of hemorrhage in patients with VTEC in Moscow population.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
21786578-17	2011	Frequency of HC is the highest in carriers of genotypes CYP2C9*1/*3 and AA VKORC1, they need minimal supporting dose of warfarin.	Warfarin	120-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
21786578-18	2011	Carriage of genotype CYP2C9*1/*3 in line with a female gender and instability of INR is an independent predictor of HC in VTEC patients in Moscow population on warfarin treatment.	Warfarin	160-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
21532277-6	2011	These findings indicate that polymorphism of CYP2C9 and CYP2C19 plays an important role in phenytoin metabolism in children.	Phenytoin	91-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
21532277-7	2011	With a total processing time for this assay of less than 3 hours, prediction of the optimal phenytoin dosage based on the CYP2C9 and CYP2C19 genotypes will be possible before commencement of therapy, resulting in the prevention of phenytoin overdoses in pediatric patients with epilepsy.	Phenytoin	92-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
21532277-7	2011	With a total processing time for this assay of less than 3 hours, prediction of the optimal phenytoin dosage based on the CYP2C9 and CYP2C19 genotypes will be possible before commencement of therapy, resulting in the prevention of phenytoin overdoses in pediatric patients with epilepsy.	Phenytoin	231-240	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
20609441-5	2010	Norketamine was formed by CYP3A4, CYP2C19, CYP2B6, CYP2A6, CYP2D6 and CYP2C9, whereas CYP2B6 and CYP2A6 were identified to be the only enzymes which enable the hydroxylation of norketamine.	norketamine	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
23120787-2	2011	The development of undesirable pharmacological phenomena at reception of average therapeutic doses of valproic acid has been caused by the primary (idiopathic) and secondary (valproate-induced) infringement of a folic cycle against a combination of CYP2C9*3 gene polymorphism and a mutation in the MTHFR gene.	Valproic Acid	102-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	249-255
23120787-2	2011	The development of undesirable pharmacological phenomena at reception of average therapeutic doses of valproic acid has been caused by the primary (idiopathic) and secondary (valproate-induced) infringement of a folic cycle against a combination of CYP2C9*3 gene polymorphism and a mutation in the MTHFR gene.	Valproic Acid	175-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	249-255
19715737-1	2010	Human cytochrome P450 2C9 (CYP2C9) accounts for ~20% of hepatic total CYP content and metabolizes ~15% clinical drugs such as phenytoin, S-warfarin, tolbutamide, losartan, and many nonsteroidal anti-inflammatory agents (NSAIDs).	Phenytoin	126-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-25
19715737-1	2010	Human cytochrome P450 2C9 (CYP2C9) accounts for ~20% of hepatic total CYP content and metabolizes ~15% clinical drugs such as phenytoin, S-warfarin, tolbutamide, losartan, and many nonsteroidal anti-inflammatory agents (NSAIDs).	Phenytoin	126-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
19715737-1	2010	Human cytochrome P450 2C9 (CYP2C9) accounts for ~20% of hepatic total CYP content and metabolizes ~15% clinical drugs such as phenytoin, S-warfarin, tolbutamide, losartan, and many nonsteroidal anti-inflammatory agents (NSAIDs).	Warfarin	137-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-25
19715737-1	2010	Human cytochrome P450 2C9 (CYP2C9) accounts for ~20% of hepatic total CYP content and metabolizes ~15% clinical drugs such as phenytoin, S-warfarin, tolbutamide, losartan, and many nonsteroidal anti-inflammatory agents (NSAIDs).	Warfarin	137-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
19715737-1	2010	Human cytochrome P450 2C9 (CYP2C9) accounts for ~20% of hepatic total CYP content and metabolizes ~15% clinical drugs such as phenytoin, S-warfarin, tolbutamide, losartan, and many nonsteroidal anti-inflammatory agents (NSAIDs).	Tolbutamide	149-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-25
19715737-1	2010	Human cytochrome P450 2C9 (CYP2C9) accounts for ~20% of hepatic total CYP content and metabolizes ~15% clinical drugs such as phenytoin, S-warfarin, tolbutamide, losartan, and many nonsteroidal anti-inflammatory agents (NSAIDs).	Tolbutamide	149-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
19715737-1	2010	Human cytochrome P450 2C9 (CYP2C9) accounts for ~20% of hepatic total CYP content and metabolizes ~15% clinical drugs such as phenytoin, S-warfarin, tolbutamide, losartan, and many nonsteroidal anti-inflammatory agents (NSAIDs).	Losartan	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-25
19715737-1	2010	Human cytochrome P450 2C9 (CYP2C9) accounts for ~20% of hepatic total CYP content and metabolizes ~15% clinical drugs such as phenytoin, S-warfarin, tolbutamide, losartan, and many nonsteroidal anti-inflammatory agents (NSAIDs).	Losartan	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
20736323-6	2010	The inhibitory potency of DBZ toward CYP3A4 was greater than that toward other P450 isoforms, including CYP1A2, CYP2C8, CYP2C9, CYP2C19, and CYP2D6.	dibenzazepine	26-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
21193152-7	2010	Pitavastatin is only slightly metabolised by cytochrome P450 (CYP) 2C9 and not at all by CYP3A4.	pitavastatin	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-70
20851877-4	2010	Based on the kinetic data and average contents of the P450 isoforms in the human liver, the putative contribution of P450s for sesamin metabolism was large in the order of CYP2C9, 1A2, 2C19, and 2D6.	sesamin	127-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
20833655-8	2010	Our study also implied that common SNPs other than those in the CYP2C9, VKORC1 and CYP4F2 genes that show strong effect on the therapeutic warfarin dose might not exist.	Warfarin	139-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
20851877-5	2010	A good correlation was observed between sesamin catecholization activity and CYP2C9-specific activity in in vitro studies using 10 individual human liver microsomes, strongly suggesting that CYP2C9 is the most important P450 isoform for sesamin catecholization in human liver.	sesamin	40-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
20851877-5	2010	A good correlation was observed between sesamin catecholization activity and CYP2C9-specific activity in in vitro studies using 10 individual human liver microsomes, strongly suggesting that CYP2C9 is the most important P450 isoform for sesamin catecholization in human liver.	sesamin	40-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
20851877-5	2010	A good correlation was observed between sesamin catecholization activity and CYP2C9-specific activity in in vitro studies using 10 individual human liver microsomes, strongly suggesting that CYP2C9 is the most important P450 isoform for sesamin catecholization in human liver.	sesamin	237-244	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
20851877-5	2010	A good correlation was observed between sesamin catecholization activity and CYP2C9-specific activity in in vitro studies using 10 individual human liver microsomes, strongly suggesting that CYP2C9 is the most important P450 isoform for sesamin catecholization in human liver.	sesamin	237-244	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
20851877-7	2010	We also examined the inhibitory effect of sesamin for P450 isoform-specific activities and found a mechanism-based inhibition of CYP2C9 by sesamin.	sesamin	42-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
20851877-7	2010	We also examined the inhibitory effect of sesamin for P450 isoform-specific activities and found a mechanism-based inhibition of CYP2C9 by sesamin.	sesamin	139-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
20851877-9	2010	Our findings strongly suggest that further studies are needed to reveal the interaction between sesamin and therapeutic drugs mainly metabolized by CYP2C9.	sesamin	96-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
21261182-10	2010	We conclude that the rapid rise in INR observed upon the initiation of warfarin therapy and the final effective warfarin dose of 1.5 mg/day, are attributable in some part to the presence of two minor alleles in CYP2C9, which together significantly reduce warfarin metabolism.	Warfarin	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	211-217
20578979-0	2010	Inhibitory effects of phthalimide derivatives on the activity of the hepatic cytochrome P450 monooxygenases CYP2C9 and CYP2C19.	phthalimide	22-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
20578979-5	2010	In addition similar patterns of phthalimide inhibition for CYP2C9 and CYP2C19 were found, whereas the unrelated isoforms CYP2D6 and CYP3A4 were not specifically affected.	phthalimide	32-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
20578979-7	2010	Analyses of structure-function relationships revealed that the substituent at the nitrogen atom in the isoindole ring is of crucial impact for the activity of CYP2C9/19.	Nitrogen	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
20578979-7	2010	Analyses of structure-function relationships revealed that the substituent at the nitrogen atom in the isoindole ring is of crucial impact for the activity of CYP2C9/19.	Isoindoles	103-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
20735727-10	2010	Consistently, R-warfarin significantly induced CYP3A4 and CYP2C9 mRNAs in cultures of primary human hepatocytes or in LS174T intestinal cells.	Warfarin	14-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
20735727-12	2010	In addition, we showed that racemic 10- and 4"-hydroxywarfarins are also highly potent PXR ligands and inducers of CYP3A4 and CYP2C9 mRNA in human hepatocytes.	10- and 4"-hydroxywarfarins	36-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
20735727-13	2010	CONCLUSION: We showed that R-warfarin can significantly up-regulate major drug-metabolizing enzymes CYP3A4 and CYP2C9 in the liver and thus may cause drug-drug interactions (DDI) with co-administered drugs.	Warfarin	27-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
21261182-10	2010	We conclude that the rapid rise in INR observed upon the initiation of warfarin therapy and the final effective warfarin dose of 1.5 mg/day, are attributable in some part to the presence of two minor alleles in CYP2C9, which together significantly reduce warfarin metabolism.	Warfarin	112-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	211-217
21261182-10	2010	We conclude that the rapid rise in INR observed upon the initiation of warfarin therapy and the final effective warfarin dose of 1.5 mg/day, are attributable in some part to the presence of two minor alleles in CYP2C9, which together significantly reduce warfarin metabolism.	Warfarin	112-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	211-217
21068649-1	2010	The objective of this study was to study the effect of CYP2C9 genetic polymorphism and undernourishment on free phenytoin concentrations in epileptic patients.	Phenytoin	112-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
21068649-9	2010	The percentage increase in free phenytoin concentration by undernourishment, CYP2C9 allelic variants, and undernourishment cum CYP2C9 allelic variants were 127%, 290%, and 472%, respectively, compared with well-nourished patients with the wild-type CYP2C9 genotype (G1) group.	Phenytoin	32-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
21068649-10	2010	The contribution of undernourishment and genetic factors (CYP2C9 allelic variant) for developing phenytoin toxicity was calculated to have an odds ratio of 37.3 (P < 0.0001).	Phenytoin	97-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
21068649-11	2010	Undernourishment and variant CYP2C9 alleles elevate free phenytoin concentrations individually and in combination show additive effects.	Phenytoin	57-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
20809476-7	2010	Fluvastatin and nifedipine increased the systemic exposure of nateglinide in rabbits, probably due to their inhibitory action on the metabolism of nateglinide by CYP2C5 (human CYP2C9).	Fluvastatin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
21428138-7	2010	We analyzed the prevalence of the different CYP2C9 and VKORC1 genotypes in this population and found that the warfarin doses required to maintain patients at their desired anticoagulation target were significantly different among carriers of the different genotypes.	Warfarin	110-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
20809476-7	2010	Fluvastatin and nifedipine increased the systemic exposure of nateglinide in rabbits, probably due to their inhibitory action on the metabolism of nateglinide by CYP2C5 (human CYP2C9).	Nifedipine	16-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
20809476-7	2010	Fluvastatin and nifedipine increased the systemic exposure of nateglinide in rabbits, probably due to their inhibitory action on the metabolism of nateglinide by CYP2C5 (human CYP2C9).	Nateglinide	62-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
20809476-7	2010	Fluvastatin and nifedipine increased the systemic exposure of nateglinide in rabbits, probably due to their inhibitory action on the metabolism of nateglinide by CYP2C5 (human CYP2C9).	Nateglinide	147-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
21121772-0	2010	Effect of CYP2C9 polymorphisms on prescribed dose and time-to-stable dose of sulfonylureas in primary care patients with Type 2 diabetes mellitus.	Sulfonylurea Compounds	77-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
20955109-5	2010	WHAT THE READER WILL GAIN: Following oral administration, idebenone is rapidly metabolized via oxidative shortening by a number CYP isoenzymes (CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4) to yield QS10, QS8, QS6 and QS4.	idebenone	58-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	152-158
21121772-1	2010	AIMS: Sulfonylureas are mainly metabolized by the enzyme CYP2C9.	Sulfonylurea Compounds	6-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
21121772-2	2010	Two allelic variants, CYP2C9*2 and CYP2C9*3, result in decreased metabolic capacity and have been associated with elevated sulfonylurea serum levels.	Sulfonylurea Compounds	123-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
21031626-3	2010	The inhibition of seven CYP isoforms (CYP3A4, CYP1A2, CYP2A6, CYP2D6, CYP2C9, CYP2C8 and CYP2E1) by tiliroside was investigated using in vitro human liver microsomal incubation assays.	tiliroside	100-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
21121772-2	2010	Two allelic variants, CYP2C9*2 and CYP2C9*3, result in decreased metabolic capacity and have been associated with elevated sulfonylurea serum levels.	Sulfonylurea Compounds	123-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
21121772-4	2010	In this study, the effect of CYP2C9*2 and CYP2C9*3 alleles on prescribed dose and time-to-stable dose of sulfonylureas was investigated.	Sulfonylurea Compounds	105-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
21031626-4	2010	The results showed that tiliroside strongly inhibited the activity of CYP3A4 (IC(50) = 9.0 +- 1.7 mum), CYP2C8 (IC(50) = 12.1 +- 0.9 mum) and CYP2C9 (IC(50) = 10.2 +- 0.9 mum) with other CYP isoforms negligibly influenced.	tiliroside	24-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
21121772-4	2010	In this study, the effect of CYP2C9*2 and CYP2C9*3 alleles on prescribed dose and time-to-stable dose of sulfonylureas was investigated.	Sulfonylurea Compounds	105-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
21031626-8	2010	Therefore, attention should be given to the probable drug-drug interaction between tiliroside-containing herbs and substrates of CYP3A4, CYP2C9 and CYP2C8.	tiliroside	83-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
21121772-8	2010	However, a trend towards a lower stable glimepiride dose for carriers of the CYP2C9*3 allele was observed.	glimepiride	40-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
21044367-9	2010	We find that our method can increase the power of the GWAS to identify both VKORC1 and CYP2C9 as warfarin pharmacogenes, where the original analysis had only identified VKORC1.	Warfarin	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
20937004-3	2010	CYP3A4 and CYP3A5 appeared to be the primary enzymes mediating the formation of pharmacologically active ketone metabolite (M1), whereas CYP3A4, CYP3A5, and CYP2C9 appeared to be the enzymes responsible for the formation of the hydroxylated metabolite (M2).	Ketones	105-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
20979644-10	2010	Dig 1, non cytotoxic and not inducing caspases by itself, is able to prevent Roundup-induced cell death in a time-dependant manner with an important efficiency of up to 89%, within 48 h. In addition, we evidenced that it prevents Caspases 3/7 activation and CYP3A4 enhancement, and not GST reduction, but in turn it slightly inhibited CYP2C9 when added before Roundup.	dig 1	0-5	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	335-341
20848598-0	2010	Study of atypical kinetic behaviour of cytochrome P450 2C9 isoform with diclofenac at low substrate concentrations by sweeping-MEKC combination.	Diclofenac	72-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-58
20934550-5	2010	Inhibition of CYP2C9 by amiodarone and its major metabolite potentiates the anticoagulant effects of warfarin, increasing the risk of serious bleeding.	Amiodarone	24-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
20934550-5	2010	Inhibition of CYP2C9 by amiodarone and its major metabolite potentiates the anticoagulant effects of warfarin, increasing the risk of serious bleeding.	Warfarin	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
20848598-1	2010	In view of the fact that several studies have shown that diclofenac hydroxylation by cytochrome P450 2C9 deviated from Michaelis-Menten kinetics at low substrate concentrations, sweeping combined with MEKC was applied for the kinetic study of this pharmacologically important reaction.	Diclofenac	57-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-104
20884456-0	2010	Impact of CYP2C9 genetic polymorphism on warfarin dose requirements in Pakistani population.	Warfarin	41-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
20698928-0	2010	Potential CYP2C9-mediated drug-drug interactions in hospitalized type 2 diabetes mellitus patients treated with the sulphonylureas glibenclamide, glimepiride or glipizide.	Glyburide	131-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
20698928-0	2010	Potential CYP2C9-mediated drug-drug interactions in hospitalized type 2 diabetes mellitus patients treated with the sulphonylureas glibenclamide, glimepiride or glipizide.	glimepiride	146-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
20698928-0	2010	Potential CYP2C9-mediated drug-drug interactions in hospitalized type 2 diabetes mellitus patients treated with the sulphonylureas glibenclamide, glimepiride or glipizide.	Glipizide	161-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
20698928-2	2010	Based on laboratory findings, we determined the clinical significance of potential CYP2C9-mediated drug-drug interactions in hospitalized patients receiving glibenclamide, glimepiride or glipizide, all of which are metabolized by CYP2C9, together with a CYP2C9 inhibitor.	Glyburide	157-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
20698928-2	2010	Based on laboratory findings, we determined the clinical significance of potential CYP2C9-mediated drug-drug interactions in hospitalized patients receiving glibenclamide, glimepiride or glipizide, all of which are metabolized by CYP2C9, together with a CYP2C9 inhibitor.	Glyburide	157-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	230-236
20698928-2	2010	Based on laboratory findings, we determined the clinical significance of potential CYP2C9-mediated drug-drug interactions in hospitalized patients receiving glibenclamide, glimepiride or glipizide, all of which are metabolized by CYP2C9, together with a CYP2C9 inhibitor.	Glyburide	157-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	230-236
20698928-2	2010	Based on laboratory findings, we determined the clinical significance of potential CYP2C9-mediated drug-drug interactions in hospitalized patients receiving glibenclamide, glimepiride or glipizide, all of which are metabolized by CYP2C9, together with a CYP2C9 inhibitor.	glimepiride	172-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
20698928-2	2010	Based on laboratory findings, we determined the clinical significance of potential CYP2C9-mediated drug-drug interactions in hospitalized patients receiving glibenclamide, glimepiride or glipizide, all of which are metabolized by CYP2C9, together with a CYP2C9 inhibitor.	glimepiride	172-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	230-236
20698928-2	2010	Based on laboratory findings, we determined the clinical significance of potential CYP2C9-mediated drug-drug interactions in hospitalized patients receiving glibenclamide, glimepiride or glipizide, all of which are metabolized by CYP2C9, together with a CYP2C9 inhibitor.	glimepiride	172-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	230-236
20698928-2	2010	Based on laboratory findings, we determined the clinical significance of potential CYP2C9-mediated drug-drug interactions in hospitalized patients receiving glibenclamide, glimepiride or glipizide, all of which are metabolized by CYP2C9, together with a CYP2C9 inhibitor.	Glipizide	187-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
20698928-2	2010	Based on laboratory findings, we determined the clinical significance of potential CYP2C9-mediated drug-drug interactions in hospitalized patients receiving glibenclamide, glimepiride or glipizide, all of which are metabolized by CYP2C9, together with a CYP2C9 inhibitor.	Glipizide	187-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	230-236
20698928-2	2010	Based on laboratory findings, we determined the clinical significance of potential CYP2C9-mediated drug-drug interactions in hospitalized patients receiving glibenclamide, glimepiride or glipizide, all of which are metabolized by CYP2C9, together with a CYP2C9 inhibitor.	Glipizide	187-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	230-236
20698928-5	2010	RESULTS: Almost 20% of patients were exposed to a potential drug-drug interaction with a CYP2C9 inhibitor during sulphonylurea treatment.	Sulfonylurea Compounds	113-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
20698928-10	2010	CONCLUSIONS: Concomitant use of a CYP2C9 inhibitor results in exaggerated pharmacodynamic effects of sulphonylureas and increases the risk of hypoglycaemia in T2DM patients receiving glibenclamide, glimepiride or glipizide.	Sulfonylurea Compounds	101-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
20698928-10	2010	CONCLUSIONS: Concomitant use of a CYP2C9 inhibitor results in exaggerated pharmacodynamic effects of sulphonylureas and increases the risk of hypoglycaemia in T2DM patients receiving glibenclamide, glimepiride or glipizide.	Glyburide	183-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
20698928-10	2010	CONCLUSIONS: Concomitant use of a CYP2C9 inhibitor results in exaggerated pharmacodynamic effects of sulphonylureas and increases the risk of hypoglycaemia in T2DM patients receiving glibenclamide, glimepiride or glipizide.	glimepiride	198-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
20698928-10	2010	CONCLUSIONS: Concomitant use of a CYP2C9 inhibitor results in exaggerated pharmacodynamic effects of sulphonylureas and increases the risk of hypoglycaemia in T2DM patients receiving glibenclamide, glimepiride or glipizide.	Glipizide	213-222	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
20602621-0	2010	Influence of CYP2C9 polymorphism on metabolism of valproate and its hepatotoxin metabolite in Iranian patients.	Valproic Acid	50-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
20602621-3	2010	The formation of 4-ene-VPA is catalyzed by cytochrome P450 2C9 (CYP2C9).	2-propyl-4-pentenoic acid	17-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-62
20602621-3	2010	The formation of 4-ene-VPA is catalyzed by cytochrome P450 2C9 (CYP2C9).	2-propyl-4-pentenoic acid	17-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
20884456-2	2010	The objective of our study was to estimate the frequency of genetic and allelic variants of CYP2C9 in Punjabi population of Pakistan and their effects on warfarin dose requirement.	Warfarin	154-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
20884456-10	2010	Individuals with CYP2C9*3/3* need lowest (8.75+-1.76 mg/week) daily warfarin dose.	Warfarin	68-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
20884456-12	2010	Presence of CYP2C9*2 or *3 variants is an independent predictor of low warfarin dose requirement in our patients.	Warfarin	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
20642349-1	2010	Voriconazole (VRC), a triazole agent is extensively metabolized by CYP2C19, CYP2C9, and to a lesser extent, by CYP3A4.	Voriconazole	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
20602621-4	2010	CYP2C9 allele mutation is closely related to the attenuation of the enzymatic activity and 4-ene-VPA production.	4-ene	91-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20602621-4	2010	CYP2C9 allele mutation is closely related to the attenuation of the enzymatic activity and 4-ene-VPA production.	Valproic Acid	97-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20602621-5	2010	In the present work, VPA, 2-ene-VPA, and 4-ene-VPA in serum of patients receiving VPA were determined and the correlation between CYP2C9 polymorphism and 4-ene-VPA concentration was examined.	2-propyl-4-pentenoic acid	154-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
20602621-15	2010	In conclusion, the role of CYP2C9*2 and CYP2C9*3 in attenuation of 4-ene-VPA formation cannot be confirmed.	4-ene	67-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
20602621-15	2010	In conclusion, the role of CYP2C9*2 and CYP2C9*3 in attenuation of 4-ene-VPA formation cannot be confirmed.	4-ene	67-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
20839301-9	2010	Disappearance of the hydrogen bond between K helix and beta4 loop was observed in CYP2C9*5.	Hydrogen	21-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
20642349-1	2010	Voriconazole (VRC), a triazole agent is extensively metabolized by CYP2C19, CYP2C9, and to a lesser extent, by CYP3A4.	Voriconazole	14-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
20877236-4	2010	Eupatilin and jaceosidin potently inhibited CYP1A2-catalyzed phenacetin O-deethylation with 50% inhibitory concentration (IC(50)) values of 9.4 microM and 5.3 microM, respectively, and CYP2C9-catalyzed diclofenac 4-hydroxylation with IC(50) values of 4.1 microM and 10.2 microM, respectively.	eupatilin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	185-191
20877236-4	2010	Eupatilin and jaceosidin potently inhibited CYP1A2-catalyzed phenacetin O-deethylation with 50% inhibitory concentration (IC(50)) values of 9.4 microM and 5.3 microM, respectively, and CYP2C9-catalyzed diclofenac 4-hydroxylation with IC(50) values of 4.1 microM and 10.2 microM, respectively.	jaceosidin	14-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	185-191
20877236-4	2010	Eupatilin and jaceosidin potently inhibited CYP1A2-catalyzed phenacetin O-deethylation with 50% inhibitory concentration (IC(50)) values of 9.4 microM and 5.3 microM, respectively, and CYP2C9-catalyzed diclofenac 4-hydroxylation with IC(50) values of 4.1 microM and 10.2 microM, respectively.	Phenacetin	61-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	185-191
20877236-6	2010	Kinetic analysis of human liver microsomes showed that eupatilin is a competitive inhibitor of CYP1A2 with a K(i) value of 2.3 microM and a mixed-type inhibitor of CYP2C9 with a K(i) value of 1.6 microM.	eupatilin	55-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	164-170
20877236-7	2010	Jaceosidin was shown to be a competitive inhibitor of CYP1A2 with a K(i) value of 3.8 microM and a mixed-type inhibitor of CYP2C9 with K(i) value of 6.4 microM in human liver microsomes.	jaceosidin	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
20877236-8	2010	These in vitro results suggest that eupatilin and jaceosidin should be further examined for potential pharmacokinetic drug interactions in vivo due to inhibition of CYP1A2 and CYP2C9.	eupatilin	36-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
20877236-8	2010	These in vitro results suggest that eupatilin and jaceosidin should be further examined for potential pharmacokinetic drug interactions in vivo due to inhibition of CYP1A2 and CYP2C9.	jaceosidin	50-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
20638257-3	2010	Dihydrotanshinone was a competitive inhibitor of human CYP1A2 (K(i)=0.53 microM) and CYP2C9 (K(i)=1.92 microM), a noncompetitive inhibitor of CYP3A4 (K(i)=2.11 microM) but an uncompetitive CYP2E1 inhibitor.	DIHYDROTANSHINONE	0-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
20877452-0	2010	Testing of VKORC1 and CYP2C9 alleles to guide warfarin dosing.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
20877452-4	2010	Testing for variants of the vitamin K epoxide reductase complex 1 (VKORC1) and cytochrome P450 2C9 (CYP2C9) genes has been proposed for use in guiding the initial dose of warfarin, thus achieving optimal dosing more quickly and with lower risk of bleeding.	Warfarin	171-179	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-98
20877452-4	2010	Testing for variants of the vitamin K epoxide reductase complex 1 (VKORC1) and cytochrome P450 2C9 (CYP2C9) genes has been proposed for use in guiding the initial dose of warfarin, thus achieving optimal dosing more quickly and with lower risk of bleeding.	Warfarin	171-179	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
20488169-2	2010	Besides, allele frequencies for clinically relevant genetic markers in warfarin response (i.e., CYP2C9 and VKORC1) have not yet been fully characterized in this population.	Warfarin	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
20716240-1	2010	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: Variants in the CYP2C9 (i.e. *2 and *3) and VKORC1 (i.e. 1173C/T or -1639G/A) genes have been shown to influence warfarin dose requirements.	Warfarin	155-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
20716240-3	2010	WHAT THIS STUDY ADDS: In African Americans, the VKORC1 rs17886199 variant was statistically significantly associated with log-transformed warfarin maintenance dose, independent of the influence of VKORC1 1173C>T and CYP2C9*2 and *3.	Warfarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	219-225
20668444-4	2010	Whereas glucosamine had no significant effect on CYP activity, noscapine caused marked inhibition of CYP2C9 (4.9-fold increase in urinary losartan/E3174 ratio) and CYP2C19 (3.6-fold increase in the plasma omeprazole/5-hydroxyomeprazole ratio).	Noscapine	63-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
20668444-4	2010	Whereas glucosamine had no significant effect on CYP activity, noscapine caused marked inhibition of CYP2C9 (4.9-fold increase in urinary losartan/E3174 ratio) and CYP2C19 (3.6-fold increase in the plasma omeprazole/5-hydroxyomeprazole ratio).	Losartan	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
20668444-4	2010	Whereas glucosamine had no significant effect on CYP activity, noscapine caused marked inhibition of CYP2C9 (4.9-fold increase in urinary losartan/E3174 ratio) and CYP2C19 (3.6-fold increase in the plasma omeprazole/5-hydroxyomeprazole ratio).	losartan carboxylic acid	147-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
20668444-5	2010	Noscapine-dependent inhibition of CYP2C9 may explain the interaction with warfarin.	Noscapine	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
20668444-5	2010	Noscapine-dependent inhibition of CYP2C9 may explain the interaction with warfarin.	Warfarin	74-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
20420818-0	2010	Standard warfarin dose in a patient with the CYP2C9*3/*3 genotype leads to hematuria.	Warfarin	9-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
20420818-1	2010	BACKGROUND: Patients with certain CYP2C9 genetic variants have increased sensitivity to warfarin and are at increased risk of over-coagulation with standard warfarin dose.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
20420818-1	2010	BACKGROUND: Patients with certain CYP2C9 genetic variants have increased sensitivity to warfarin and are at increased risk of over-coagulation with standard warfarin dose.	Warfarin	157-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
20420818-2	2010	We report over-anticoagulation and hematuria manifest as a slow increase in the international normalized ratio (INR) due to warfarin treatment in a patient with the CYP2C9*3/*3 allele.	Warfarin	124-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	165-171
20420818-8	2010	INR response to warfarin in this CYP2C9*3/*3 patient was slow.	Warfarin	16-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
20420818-11	2010	In this case, increased risk of bleeding could have been identified by prospective genotyping of CYP2C9 and VKORC1 prior to initiating warfarin therapy.	Warfarin	135-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
20716633-8	2010	Resveratrol intervention was found to inhibit the phenotypic indices of CYP3A4, CYP2D6, and CYP2C9 and to induce the phenotypic index of 1A2.	Resveratrol	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
20555338-1	2010	The aim of the study is to improve our understanding of the worldwide allele frequency distribution of four genetic polymorphisms known to influence warfarin dosing (VKORC1 rs9923231, CYP2C9 rs1799853, CYP2C9 rs1057910 and CYP4F2 rs2108622).	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	184-190
20555338-1	2010	The aim of the study is to improve our understanding of the worldwide allele frequency distribution of four genetic polymorphisms known to influence warfarin dosing (VKORC1 rs9923231, CYP2C9 rs1799853, CYP2C9 rs1057910 and CYP4F2 rs2108622).	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	202-208
20569971-0	2010	Algorithms using clinical and genetic data (CYP2C9, VKORC1) are relevant to predict warfarin dose in patients with different INR targets.	Warfarin	84-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
27713373-3	2010	The defective alleles of cytochrome P450 (CYP) 2C9 and/or CYP2C19 could affect not only the pharmacokinetics, but also the pharmacodynamics of phenytoin therapy.	Phenytoin	143-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-50
20615525-2	2010	Genetic variability in the VKORC1 and CYP2C9 genes is associated with increased warfarin sensitivity.	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
20615525-4	2010	VKORC1 and CYP2C9 variability associated with altered warfarin response is less well characterized in African and mixed-raced populations such as Brazilians.	Warfarin	54-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
20615525-5	2010	To determine genetic variability associated with altered warfarin response among Brazilian patients, sixty-two adult patients with extreme resistance or sensitivity to warfarin were genotyped for variants in CYP2C9 and VKORC1.	Warfarin	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	208-214
20615525-7	2010	Additionally, 52.9% of warfarin sensitive patients had at least one CYP2C9*2 or CYP2C9*3 decreased metabolism allele, 63.6% of Caucasians and 54% of African-descent patients.	Warfarin	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
20615525-7	2010	Additionally, 52.9% of warfarin sensitive patients had at least one CYP2C9*2 or CYP2C9*3 decreased metabolism allele, 63.6% of Caucasians and 54% of African-descent patients.	Warfarin	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
20615525-9	2010	Brazilian patients requiring low doses of warfarin have a high frequency of VKORC1 and CYP2C9 variants associated with warfarin sensitivity.	Warfarin	42-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
20615525-9	2010	Brazilian patients requiring low doses of warfarin have a high frequency of VKORC1 and CYP2C9 variants associated with warfarin sensitivity.	Warfarin	119-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
20808793-0	2010	Are cytochrome P450 CYP2C8 and CYP2C9 polymorphisms associated with ibuprofen response in very preterm infants?	Ibuprofen	68-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
20808793-7	2010	Comparing infants with wild type or variant CYP2C8 and CYP2C9 genotypes, response rate to ibuprofen was significantly higher in wild type than in mutated carriers in univariate analysis (73% versus 52%, p = 0.04).	Ibuprofen	90-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
20808793-8	2010	Comparing responders (ductus closure; n = 75) and non-responders (surgical ligation; n = 36), the only two factors significantly associated with the response to ibuprofen using multivariate analysis were higher gestational age and non Caucasian ethnicity but not CYP2C polymorphism.	Ibuprofen	161-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	263-268
27713373-5	2010	The defective alleles of CYP2C9 and/or CYP2C19 were also found to have clinically significant effects on the inter-individual variabilities in the population pharmacokinetics of phenobarbital, valproic acid and zonisamide.	Phenobarbital	178-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
27713373-5	2010	The defective alleles of CYP2C9 and/or CYP2C19 were also found to have clinically significant effects on the inter-individual variabilities in the population pharmacokinetics of phenobarbital, valproic acid and zonisamide.	Valproic Acid	193-206	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
27713373-5	2010	The defective alleles of CYP2C9 and/or CYP2C19 were also found to have clinically significant effects on the inter-individual variabilities in the population pharmacokinetics of phenobarbital, valproic acid and zonisamide.	Zonisamide	211-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
20653669-1	2010	The considerable variability in the warfarin dose-response relationship between individuals, is explained mainly by genetic variation in its major metabolic (CYP2C9) and target (VKORC1) enzymes.	Warfarin	36-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
20653676-5	2010	* This study developed a multiple regression model including CYP2C9, VKORC1 3673G>A, CYP4F2 genotypes and age, weight, combination use of amiodarone which could explain 56.1% of the individual variability in warfarin dose CYP4F2 could explain 4% of the variance in warfarin dose.	Warfarin	268-276	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
20653674-0	2010	A haplotype of CYP2C9 associated with warfarin sensitivity in mechanical heart valve replacement patients.	Warfarin	38-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
20653674-1	2010	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * CYP2C9 single nucleotide polymorphisms (SNPs) are important in safe and effective oral anticoagulation with warfarin use.	Warfarin	151-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
20653674-2	2010	* Although CYP2C9*2 and *3 are important genetic factors for the warfarin dose, one of the CYP2C9 SNPs, IVS-65G>C, has been suggested to be associated with warfarin sensitivity.	Warfarin	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
20653674-2	2010	* Although CYP2C9*2 and *3 are important genetic factors for the warfarin dose, one of the CYP2C9 SNPs, IVS-65G>C, has been suggested to be associated with warfarin sensitivity.	Warfarin	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
20653674-2	2010	* Although CYP2C9*2 and *3 are important genetic factors for the warfarin dose, one of the CYP2C9 SNPs, IVS-65G>C, has been suggested to be associated with warfarin sensitivity.	Warfarin	159-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
20405111-0	2010	Fluconazole-induced intoxication with phenytoin in a patient with ultra-high activity of CYP2C9.	Fluconazole	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
20653674-2	2010	* Although CYP2C9*2 and *3 are important genetic factors for the warfarin dose, one of the CYP2C9 SNPs, IVS-65G>C, has been suggested to be associated with warfarin sensitivity.	Warfarin	159-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
20653674-4	2010	WHAT THIS PAPER ADDS * New information on CYP2C9 SNPs and their occurrences in common haplotype structures in healthy unrelated Koreans and in individuals who require low warfarin dose after mechanical heart valve replacements (MHVRs) were studied.	Warfarin	171-179	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
20653674-8	2010	Additional direct DNA sequencing of the CYP2C9 gene was conducted in 36 of the 267 MHVR patients who required low maintenance warfarin doses without carrying CYP2C9*3 and VKORC1 1173T mutations.	Warfarin	126-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
20653674-9	2010	The effects of CYP2C9 genetics on warfarin maintenance dose were assessed in 267 MHVR patients.	Warfarin	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
20653674-11	2010	One of the CYP2C9 haplotypes exhibited an association with warfarin low dose requirement.	Warfarin	59-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
20653676-1	2010	WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT * Genetic polymorphisms of VKORC1 and CYP2C9 are known to influence warfarin dosage.	Warfarin	109-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
20653676-5	2010	* This study developed a multiple regression model including CYP2C9, VKORC1 3673G>A, CYP4F2 genotypes and age, weight, combination use of amiodarone which could explain 56.1% of the individual variability in warfarin dose CYP4F2 could explain 4% of the variance in warfarin dose.	Amiodarone	141-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
20653676-5	2010	* This study developed a multiple regression model including CYP2C9, VKORC1 3673G>A, CYP4F2 genotypes and age, weight, combination use of amiodarone which could explain 56.1% of the individual variability in warfarin dose CYP4F2 could explain 4% of the variance in warfarin dose.	Warfarin	211-219	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
20501911-3	2010	The kinetics of metabolite formation from phenacetin, tolbutamide, and alprazolam and midazolam, selected as substrates probes for CYP1A2, CYP2C9, and CYP3A4, respectively, were characterized in this in vitro system.	Phenacetin	42-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	139-145
20501911-3	2010	The kinetics of metabolite formation from phenacetin, tolbutamide, and alprazolam and midazolam, selected as substrates probes for CYP1A2, CYP2C9, and CYP3A4, respectively, were characterized in this in vitro system.	Alprazolam	71-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	139-145
20501911-3	2010	The kinetics of metabolite formation from phenacetin, tolbutamide, and alprazolam and midazolam, selected as substrates probes for CYP1A2, CYP2C9, and CYP3A4, respectively, were characterized in this in vitro system.	Midazolam	86-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	139-145
20405111-0	2010	Fluconazole-induced intoxication with phenytoin in a patient with ultra-high activity of CYP2C9.	Phenytoin	38-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
20405111-1	2010	PURPOSE: The cytochrome P450 enzyme CYP2C9 metabolizes several important drugs, such as warfarin and oral antidiabetic drugs.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
20405111-5	2010	When fluconazole, a potent inhibitor of CYP2C9, was added to the treatment regimen, the patient developed ataxia, tremor, fatigue, slurred speech and somnolence, indicating phenytoin intoxication.	Fluconazole	5-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
20405111-5	2010	When fluconazole, a potent inhibitor of CYP2C9, was added to the treatment regimen, the patient developed ataxia, tremor, fatigue, slurred speech and somnolence, indicating phenytoin intoxication.	Phenytoin	173-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
20405111-6	2010	On suspicion of ultra-high activity of CYP2C9, a phenotyping test for CYP2C9 with losartan was performed.	Losartan	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
20405111-8	2010	CONCLUSIONS: Our finding of an ultrarapid metabolism of losartan and phenytoin may apply to other CYP2C9 substrates, where inhibition of CYP2C9 may cause severe adverse drug reactions.	Losartan	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
20405111-8	2010	CONCLUSIONS: Our finding of an ultrarapid metabolism of losartan and phenytoin may apply to other CYP2C9 substrates, where inhibition of CYP2C9 may cause severe adverse drug reactions.	Losartan	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
20405111-8	2010	CONCLUSIONS: Our finding of an ultrarapid metabolism of losartan and phenytoin may apply to other CYP2C9 substrates, where inhibition of CYP2C9 may cause severe adverse drug reactions.	Phenytoin	69-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
20405111-8	2010	CONCLUSIONS: Our finding of an ultrarapid metabolism of losartan and phenytoin may apply to other CYP2C9 substrates, where inhibition of CYP2C9 may cause severe adverse drug reactions.	Phenytoin	69-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
20509749-3	2010	In liver microsomes from PB-treated pigs, these transcriptional activations were accompanied by an increase of various marker activities of human CYP2B6, CYP3As, CYP2C9, CYP2C19.	Phenobarbital	25-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
20135639-7	2010	In incubations with human liver microsomes and selective inhibitors, CYP2E1 was found to be principally responsible for producing the dominant, hydroxylation product, whereas CYP2C9 was the principal source of the epoxides and CYP1A2 was responsible for the dealkylation product.	Epoxy Compounds	214-222	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	175-181
20509749-4	2010	Among the extrahepatic tissues, a significant induction by PB was observed only in kidney for the marker activities of CYP2C9.	Phenobarbital	59-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
20400659-6	2010	The current study compares the application of such d-optimal designs with that of a conventional approach in assessing the competitive inhibitory potency of fluconazole and sertraline toward CYP2C9 and 2D6, respectively.	Fluconazole	157-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
20677151-0	2010	[Association of polymorphisms of cytochrome P450 2C9 exon 4 and -65G>C with warfarin sensitivity].	Warfarin	79-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-52
20677151-1	2010	OBJECTIVE: To investigate the association of the polymorphisms of cytochrome P450 2C9 (CYP2C9) exon 4 608T/G, 561A/C, 537A/C and 527A/C, and -65G/C with warfarin sensitivity.	Warfarin	153-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-85
20677151-1	2010	OBJECTIVE: To investigate the association of the polymorphisms of cytochrome P450 2C9 (CYP2C9) exon 4 608T/G, 561A/C, 537A/C and 527A/C, and -65G/C with warfarin sensitivity.	Warfarin	153-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
20677151-10	2010	Warfarin daily dosage in CYP2C9 exon 4 -65C carriers was 3.106+/-0.619 mg/d, while it was (2.555+/-0.708) mg/d in individuals with wild-type -65G (P=0.020).	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
20677151-11	2010	Receiver operating characteristic (ROC) analysis showed that warfarin daily dosage of more than 2.5 mg/d can be used to predict the CYP2C9 exon 4 -65GC genotype (AUC: 0.770, P=0.005, 95%CI:0.626-0.915).	Warfarin	61-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
20677151-15	2010	The warfarin maintenance dosage in CYP2C9 exon 4 -65CG carriers was significantly higher than those with wild-type -65GG.	Warfarin	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
20733952-1	2010	Genetic testing for common variants in the CYP2C9 and VKORC1 genes may provide useful clinical information to guide dosing patients receiving oral warfarin.	Warfarin	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
20733952-2	2010	Specifically, the CYP2C9*2, CYP2C9*3 and either the VKORC1-1639 G>A or VKORC1 1173C>T polymorphisms can be used to help predict an approximate warfarin maintenance dose needed for a particular patient.	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
20733952-2	2010	Specifically, the CYP2C9*2, CYP2C9*3 and either the VKORC1-1639 G>A or VKORC1 1173C>T polymorphisms can be used to help predict an approximate warfarin maintenance dose needed for a particular patient.	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
20210733-0	2010	Distribution of CYP2C9 and VKORC1 risk alleles for warfarin sensitivity and resistance in the Israeli population.	Warfarin	51-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
20210733-1	2010	PURPOSE: This study was designed to delineate the relative frequency of CYP2C9 and VKORC1 polymorphisms known to affect warfarin response in the highly heterogeneous Israeli population.	Warfarin	120-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
20210733-4	2010	RESULTS: Arab Moslems had a higher frequency of warfarin "sensitive" CYP2C9*2, CYP2C9*3 and VKROC1 -1639G>A alleles (0.21, 0.07 and 0.58, respectively) than both Jews (0.13, 0.11 and 0.57, respectively) and Druze (0.12, 0.06 and 0.53, respectively).	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
20210733-8	2010	The results presented demonstrate that allelic variants in CYP2C9 and VKORC1 are very common in Israel with approximately 95% of Jews, approximately 84% of Druze and approximately 91% of Arab Moslems manifesting at least one known warfarin "sensitive" or "resistant" allele.	Warfarin	231-239	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
20226775-0	2010	Comparison of assay systems for warfarin-related CYP2C9 and VKORC1 genotyping.	Warfarin	32-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
20400659-6	2010	The current study compares the application of such d-optimal designs with that of a conventional approach in assessing the competitive inhibitory potency of fluconazole and sertraline toward CYP2C9 and 2D6, respectively.	Sertraline	173-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
20390258-0	2010	Influence of CYP2C9 and CYP2C19 genetic polymorphisms on phenytoin-induced neurological toxicity in Indian epileptic patients.	Phenytoin	57-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
20390258-9	2010	CONCLUSION: Our results show that CYP2C9 genetic polymorphisms (particularly the *3 allele) were associated with high risk of epileptic patients developing PHT-induced neurological toxicity.	Phenytoin	156-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
23964176-2	2010	METHOD: CYP2C9-mediated 4"-hydroxylation of tolbutamide (TB) to 4"-hydroxytolbutamide (4-OH-TB) was utilized to assess the metabolic activity of CYP2C9.	Tolbutamide	57-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
20162308-11	2010	Down regulation of CYP2C9 and CYP2C19 synthesis by 5FU therapies may explain the adverse effect of 5FU on the clinical disposition of warfarin and phenytoin.	Fluorouracil	51-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
20162308-11	2010	Down regulation of CYP2C9 and CYP2C19 synthesis by 5FU therapies may explain the adverse effect of 5FU on the clinical disposition of warfarin and phenytoin.	Warfarin	134-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
20162308-11	2010	Down regulation of CYP2C9 and CYP2C19 synthesis by 5FU therapies may explain the adverse effect of 5FU on the clinical disposition of warfarin and phenytoin.	Phenytoin	147-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
20133511-2	2010	Treprostinil is metabolized primarily by cytochrome P450 (CYP) 2C8 with minor contribution from CYP2C9.	treprostinil	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
20133511-3	2010	It is expected that oral treprostinil will be administered with bosentan, approved for the treatment of PAH and known to induce CYP2C9 and 3A4.	treprostinil	25-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
20133511-3	2010	It is expected that oral treprostinil will be administered with bosentan, approved for the treatment of PAH and known to induce CYP2C9 and 3A4.	Bosentan	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
20865058-2	2010	The mechanism could involve inhibition of the hepatic CYP2C9-mediated metabolic clearance of warfarin by components in cranberry.	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
20865058-4	2010	METHODS: The inhibitory effects of five types of cranberry juices were compared with those of water on CYP2C9 activity (S-warfarin 7-hydroxylation) in human liver microsomes (HLM).	Water	94-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
20865058-4	2010	METHODS: The inhibitory effects of five types of cranberry juices were compared with those of water on CYP2C9 activity (S-warfarin 7-hydroxylation) in human liver microsomes (HLM).	Warfarin	122-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
23964176-2	2010	METHOD: CYP2C9-mediated 4"-hydroxylation of tolbutamide (TB) to 4"-hydroxytolbutamide (4-OH-TB) was utilized to assess the metabolic activity of CYP2C9.	Tolbutamide	44-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
23964176-2	2010	METHOD: CYP2C9-mediated 4"-hydroxylation of tolbutamide (TB) to 4"-hydroxytolbutamide (4-OH-TB) was utilized to assess the metabolic activity of CYP2C9.	Tolbutamide	44-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
23964176-2	2010	METHOD: CYP2C9-mediated 4"-hydroxylation of tolbutamide (TB) to 4"-hydroxytolbutamide (4-OH-TB) was utilized to assess the metabolic activity of CYP2C9.	Tolbutamide	57-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
23964176-2	2010	METHOD: CYP2C9-mediated 4"-hydroxylation of tolbutamide (TB) to 4"-hydroxytolbutamide (4-OH-TB) was utilized to assess the metabolic activity of CYP2C9.	4'-hydroxytolbutamide	64-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
23964176-2	2010	METHOD: CYP2C9-mediated 4"-hydroxylation of tolbutamide (TB) to 4"-hydroxytolbutamide (4-OH-TB) was utilized to assess the metabolic activity of CYP2C9.	4'-hydroxytolbutamide	64-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
23964176-2	2010	METHOD: CYP2C9-mediated 4"-hydroxylation of tolbutamide (TB) to 4"-hydroxytolbutamide (4-OH-TB) was utilized to assess the metabolic activity of CYP2C9.	4-oh-tb	87-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
23964176-2	2010	METHOD: CYP2C9-mediated 4"-hydroxylation of tolbutamide (TB) to 4"-hydroxytolbutamide (4-OH-TB) was utilized to assess the metabolic activity of CYP2C9.	4-oh-tb	87-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
23964176-8	2010	CONCLUSION: The results of this study have shown that alcoholic extracts of curcuma and aniseed were capable of inhibiting and activating; respectively, the CYP2C9-mediated 4-OH-TB formation in human liver microsomes, suggesting that these herbs have the potential to interact with CYP2C9 drug substrates.	4-oh-tb	173-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
23964176-8	2010	CONCLUSION: The results of this study have shown that alcoholic extracts of curcuma and aniseed were capable of inhibiting and activating; respectively, the CYP2C9-mediated 4-OH-TB formation in human liver microsomes, suggesting that these herbs have the potential to interact with CYP2C9 drug substrates.	4-oh-tb	173-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	282-288
20393654-1	2010	HyBeacon probes have been used to characterise SNPs in the CYP2C9 and VKORC1 genes associated with variations in the efficiency of warfarin metabolism.	Warfarin	131-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
20381283-2	2010	BACKGROUND: Genotypic variations in CYP2C9 and VKORC1 have been shown to predict warfarin dosing, but no large-scale studies have prospectively evaluated the clinical effectiveness of genotyping in naturalistic settings across the U.S. METHODS: This national, prospective, comparative effectiveness study compared the 6-month incidence of hospitalization in patients receiving warfarin genotyping (n = 896) versus a matched historical control group (n = 2,688).	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
20436375-2	2010	CYP2C enzymes catalyze the metabolism of arachidonic acid to EETs.	Arachidonic Acid	41-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-5
20442691-0	2010	Extending and evaluating a warfarin dosing algorithm that includes CYP4F2 and pooled rare variants of CYP2C9.	Warfarin	27-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
20442691-10	2010	CONCLUSION: CYP4F2 and pooled rare variants of CYP2C9 significantly improve the ability to estimate warfarin dose.	Warfarin	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
20585445-0	2010	A novel, single algorithm approach to predict acenocoumarol dose based on CYP2C9 and VKORC1 allele variants.	Acenocoumarol	46-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
20585445-1	2010	The identification of CYP2C9 and VKORC1 genes has strongly stimulated the research on pharmacogenetics of coumarins in the last decade.	Coumarins	106-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
20376629-2	2010	Polymorphisms in the vitamin K epoxide reductase complex subunit 1 (VKORC1) and the liver enzyme cytochrome P450 2C9 (CYP2C9) effectively account for the variability in warfarin and acenocoumarol response but are less well-defined pharmacogenetic predictors in phenprocoumon therapy.	Warfarin	169-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-116
20410877-0	2010	A pharmacometric model describing the relationship between warfarin dose and INR response with respect to variations in CYP2C9, VKORC1, and age.	Warfarin	59-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
20445534-0	2010	CYP2C9*3 Loss-of-Function Allele Is Associated With Acute Upper Gastrointestinal Bleeding Related to the Use of NSAIDs Other Than Aspirin.	Aspirin	130-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20445534-1	2010	Nonsteroidal anti-inflammatory drugs (NSAIDs), other than aspirin, are to some extent metabolized by cytochrome P450 2C9 (CYP2C9).	Aspirin	58-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-120
20445534-1	2010	Nonsteroidal anti-inflammatory drugs (NSAIDs), other than aspirin, are to some extent metabolized by cytochrome P450 2C9 (CYP2C9).	Aspirin	58-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
20445534-5	2010	In the aspirin group, 12 patients (9.2%) had the CYP2C9 359Leu allele as compared with 19 (33.3%) in the non-ASP group (odds ratio (OR) = 5.0; 95% confidence interval 2.2-11.1, P < 0.0001).	Aspirin	7-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
20445534-6	2010	In a multivariate analysis, CYP2C9 359Leu remained associated with the non-ASP group (OR = 7.2 (2.6-20.3), P = 0.0002) even though 40% of these patients were under treatment with antiulcer drugs at the time of admission.	Aspartic Acid	75-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
20215413-4	2010	CYP2C9-mediated metabolism of S-naproxen and S-flurbiprofen was inhibited up to 80% by coincubation with CYP3A4, although K(m) values were unchanged.	Naproxen	30-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20215413-4	2010	CYP2C9-mediated metabolism of S-naproxen and S-flurbiprofen was inhibited up to 80% by coincubation with CYP3A4, although K(m) values were unchanged.	Flurbiprofen	45-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20637959-15	2010	Multiple linear regression analysis found that sex (P = 0.045), height (P = 0.024), age (P = 0.081), and VKORC1 (P = 0.004) and CYP2C9 (P = 0.011) polymorphism had significant influence on the maintenance dose of warfarin.	Warfarin	213-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
20637959-18	2010	CONCLUSION: Among the demographic and genetic factors evaluated in these Iranian patients, sex, height, age, CYP2C9, and VKORC1 had significant effects on warfarin maintenance dose requirements.	Warfarin	155-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
20376629-2	2010	Polymorphisms in the vitamin K epoxide reductase complex subunit 1 (VKORC1) and the liver enzyme cytochrome P450 2C9 (CYP2C9) effectively account for the variability in warfarin and acenocoumarol response but are less well-defined pharmacogenetic predictors in phenprocoumon therapy.	Warfarin	169-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
20376629-2	2010	Polymorphisms in the vitamin K epoxide reductase complex subunit 1 (VKORC1) and the liver enzyme cytochrome P450 2C9 (CYP2C9) effectively account for the variability in warfarin and acenocoumarol response but are less well-defined pharmacogenetic predictors in phenprocoumon therapy.	Acenocoumarol	182-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-116
20376629-2	2010	Polymorphisms in the vitamin K epoxide reductase complex subunit 1 (VKORC1) and the liver enzyme cytochrome P450 2C9 (CYP2C9) effectively account for the variability in warfarin and acenocoumarol response but are less well-defined pharmacogenetic predictors in phenprocoumon therapy.	Acenocoumarol	182-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
20831536-0	2010	Influence of CYP2C9 and CYP2C19 genetic polymorphisms on pharmacokinetics and pharmacodynamics of gliclazide in healthy Chinese Han volunteers.	Gliclazide	98-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
20831536-1	2010	BACKGROUND AND OBJECTIVE: CYP2C9 is the major contributor to gliclazide metabolic clearance in vitro, while the pharmacokinetics of gliclazide modified release are affected mainly by CYP2C19 genetic polymorphisms in vivo.	Gliclazide	61-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
20831536-2	2010	This study aims to investigate the influence of CYP2C9 and CYP2C19 genetic polymorphisms on the pharmacokinetics and pharmacodynamics of gliclazide in healthy Chinese Han volunteers.	Gliclazide	137-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
20429590-0	2010	Hydroxywarfarin metabolites potently inhibit CYP2C9 metabolism of S-warfarin.	hydroxywarfarin	0-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
20386359-2	2010	The relationship between warfarin sensitivity and CYP2C9 and VKORC1 variants is strong, and is the basis for several proposed dosing algorithms.	Warfarin	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
20386359-11	2010	In addition, the results of this study confirm those of others demonstrating clear relationship of genotype for CYP2C9 and VKORC1 with warfarin dose requirements; as the number of variants in these genes increases, the dose requirement decreases.	Warfarin	135-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
20421126-0	2010	A regression model to predict warfarin dose from clinical variables and polymorphisms in CYP2C9, CYP4F2, and VKORC1: Derivation in a sample with predominantly a history of venous thromboembolism.	Warfarin	30-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
20429590-0	2010	Hydroxywarfarin metabolites potently inhibit CYP2C9 metabolism of S-warfarin.	Warfarin	66-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
20429590-5	2010	We hypothesized that hydroxywarfarins inhibit the hydroxylation of warfarin by CYP2C9, thereby limiting enzymatic capacity toward S-warfarin.	hydroxywarfarins	21-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
20429590-5	2010	We hypothesized that hydroxywarfarins inhibit the hydroxylation of warfarin by CYP2C9, thereby limiting enzymatic capacity toward S-warfarin.	Warfarin	28-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
20429590-5	2010	We hypothesized that hydroxywarfarins inhibit the hydroxylation of warfarin by CYP2C9, thereby limiting enzymatic capacity toward S-warfarin.	Warfarin	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
20429590-6	2010	To test this hypothesis, we investigated the ability of all five racemic hydroxywarfarins to block CYP2C9 activity toward S-warfarin using recombinant enzyme and human liver microsomes.	hydroxywarfarins	73-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
20429590-6	2010	To test this hypothesis, we investigated the ability of all five racemic hydroxywarfarins to block CYP2C9 activity toward S-warfarin using recombinant enzyme and human liver microsomes.	Sulfur	122-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
20429590-6	2010	To test this hypothesis, we investigated the ability of all five racemic hydroxywarfarins to block CYP2C9 activity toward S-warfarin using recombinant enzyme and human liver microsomes.	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
20429590-7	2010	We initially screened for the inhibition of CYP2C9 by hydroxywarfarins using a P450-Glo assay to determine IC(50) values for each hydroxywarfarin.	hydroxywarfarins	54-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
20429590-7	2010	We initially screened for the inhibition of CYP2C9 by hydroxywarfarins using a P450-Glo assay to determine IC(50) values for each hydroxywarfarin.	hydroxywarfarin	54-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
20429590-8	2010	Compared to the substrate, CYP2C9 bound its hydroxywarfarin products with less affinity but retained high affinity for 10- and 4"-hydroxywarfarins, products from CYP3A4 reactions.	hydroxywarfarin	44-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
20429590-8	2010	Compared to the substrate, CYP2C9 bound its hydroxywarfarin products with less affinity but retained high affinity for 10- and 4"-hydroxywarfarins, products from CYP3A4 reactions.	10- and 4"-hydroxywarfarins	119-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
20429590-9	2010	S-Warfarin steady-state inhibition studies with recombinant CYP2C9 and pooled human liver microsomes confirmed that hydroxywarfarin products from CYP reactions possess the capacity to competitively inhibit CYP2C9 with biologically relevant inhibition constants.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
20429590-9	2010	S-Warfarin steady-state inhibition studies with recombinant CYP2C9 and pooled human liver microsomes confirmed that hydroxywarfarin products from CYP reactions possess the capacity to competitively inhibit CYP2C9 with biologically relevant inhibition constants.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	206-212
20429590-9	2010	S-Warfarin steady-state inhibition studies with recombinant CYP2C9 and pooled human liver microsomes confirmed that hydroxywarfarin products from CYP reactions possess the capacity to competitively inhibit CYP2C9 with biologically relevant inhibition constants.	hydroxywarfarin	116-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
20429590-9	2010	S-Warfarin steady-state inhibition studies with recombinant CYP2C9 and pooled human liver microsomes confirmed that hydroxywarfarin products from CYP reactions possess the capacity to competitively inhibit CYP2C9 with biologically relevant inhibition constants.	hydroxywarfarin	116-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	206-212
20429590-10	2010	Inhibition of CYP2C9 by 7-hydroxywarfarin may be significant given its abundance in human plasma, despite its weak affinity for the enzyme.	7-hydroxywarfarin	24-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
20429590-11	2010	10-Hydroxywarfarin, which has been reported as the second most abundant plasma metabolite, was the most potent inhibitor of CYP2C9, displaying approximately 3-fold higher affinity than S-warfarin.	10-hydroxywarfarin	0-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
20429590-11	2010	10-Hydroxywarfarin, which has been reported as the second most abundant plasma metabolite, was the most potent inhibitor of CYP2C9, displaying approximately 3-fold higher affinity than S-warfarin.	Warfarin	10-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
20429590-12	2010	These results indicate that hydroxywarfarin metabolites produced by CYP2C9 and other CYPs may limit metabolic capacity toward S-warfarin through competitive inhibition.	hydroxywarfarin	28-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
20429590-12	2010	These results indicate that hydroxywarfarin metabolites produced by CYP2C9 and other CYPs may limit metabolic capacity toward S-warfarin through competitive inhibition.	Warfarin	35-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
20375999-1	2010	Well-characterized genes that affect warfarin metabolism (cytochrome P450 (CYP) 2C9) and sensitivity (vitamin K epoxide reductase complex 1 (VKORC1)) explain one-third of the variability in therapeutic dose before the international normalized ratio (INR) is measured.	Warfarin	37-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-83
20437462-5	2010	The present study systematically investigated the contributions of various human CYP isoforms (CYP3A4, CYP3A5, CYP2C8, CYP2C9 and CYP2C19) to in vitro metabolism of GLB.	Glyburide	165-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
20203262-1	2010	Warfarin-dosing algorithms incorporating CYP2C9 and VKORC1 -1639G>A improve dose prediction compared with algorithms based solely on clinical and demographic factors.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
20089352-0	2010	The influence of cytochrome oxidase CYP2A6, CYP2B6, and CYP2C9 polymorphisms on the plasma concentrations of valproic acid in epileptic patients.	Valproic Acid	109-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
20375999-3	2010	After adjusting for INR, CYP2C9 and VKORC1 genotypes remained significant predictors (P < 0.001) of warfarin dose.	Warfarin	103-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
20609060-1	2010	OBJECTIVES: Nateglinide is metabolized by CYP2C9 and CYP3A4, therefore drug-drug interactions through cytochrome P450 (CYP) inhibition may occur.	Nateglinide	12-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
20354686-0	2010	Increased frequency of CYP2C9 variant alleles and homozygous VKORC1*2B carriers in warfarin-treated patients with excessive INR response.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
20354686-1	2010	BACKGROUND: Several studies have linked mutations in the genes encoding cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex 1 (VKORC1) to a reduced warfarin dose requirement and an increased risk of bleeding with warfarin treatment, but the implementation of genotyping as routine practice is still controversial.	Warfarin	165-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-91
20354686-1	2010	BACKGROUND: Several studies have linked mutations in the genes encoding cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex 1 (VKORC1) to a reduced warfarin dose requirement and an increased risk of bleeding with warfarin treatment, but the implementation of genotyping as routine practice is still controversial.	Warfarin	165-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
20354686-1	2010	BACKGROUND: Several studies have linked mutations in the genes encoding cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex 1 (VKORC1) to a reduced warfarin dose requirement and an increased risk of bleeding with warfarin treatment, but the implementation of genotyping as routine practice is still controversial.	Warfarin	230-238	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-91
20354686-1	2010	BACKGROUND: Several studies have linked mutations in the genes encoding cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex 1 (VKORC1) to a reduced warfarin dose requirement and an increased risk of bleeding with warfarin treatment, but the implementation of genotyping as routine practice is still controversial.	Warfarin	230-238	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
20354686-2	2010	The objective of this study was to investigate whether the frequencies of CYP2C9 variant alleles (*2 and *3), and VKORC1 haplotypes (*2A/B) were increased in a population of warfarin-treated patients with an excessive INR response.	Warfarin	174-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
20354686-10	2010	CONCLUSION: The presence of CYP2C9 variant alleles and the homozygous VKORC1*2B genotype was associated with elevated INR values in warfarin-treated patients.	Warfarin	132-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
20609060-4	2010	KEY FINDINGS: The results showed that nateglinide inhibited CYP2C9 and CYP2C19 with an IC50(app) (apparent value of the 50% inhibitory concentration) of 125 micromol/l and 946 micromol/l, respectively, while M1 did not inhibit any of the CYP isoforms.	Nateglinide	38-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
20609060-5	2010	The inhibition constant (K(i)) value of the inhibitory effect of nateglinide on CYP2C9 and the 1 + I(in,max,u)/K(i) value were estimated (where I(in,max,u)= the maximum unbound concentration of nateglinide).	Nateglinide	65-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
18998206-5	2010	Polymorphic sites in three genes, cytochrome P450 (CYP) 2C9, vitamin K 2,3 epoxide reductase complex 1 (VKORC1), and CYP4F2, have been shown to affect stable warfarin dose.	Warfarin	158-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-59
20609060-7	2010	The influence of pre-incubation on the inhibition by nateglinide of CYP3A4, CYP2C9 and CYP2C19 was examined.	Nateglinide	53-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
20609060-3	2010	METHODS: We used typical substrates (7-ethoxyresorufin for CYP1A1/2, tolbutamide for CYP2C9, S-mephenytoin for CYP2C19, bufuralol for CYP2D6, chlorzoxazone for CYP2E1 and midazolam for CYP3A4) in the evaluation of the inhibitory effects, and examined the possibility of mechanism-based inhibition (MBI) by evaluating the influence of pre-incubation in the inhibition.	Tolbutamide	69-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
20149073-12	2010	CONCLUSION: Two clinical data, age and BSA, and three SNPs in the VKORC1, CYP2C9 and CYP4F2 genes strongly predict outlier patients treated with acenocoumarol.	Acenocoumarol	145-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
20086032-3	2010	In the present study, we used primary cultures of human hepatocytes to investigate the role of HNF4alpha in the pregnane X receptor (PXR)/rifampicin-mediated up-regulation of CYP2C8, CYP2C9, and CYP2C19 gene expression.	Rifampin	138-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	183-189
29776219-1	2010	AIMS: Patient demographics and variant alleles in the CYP2C9 and VKORC1 genes account for 50% of the population variability in warfarin maintenance doses.	Warfarin	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
20072124-2	2010	In a cohort of 226 African-American patients, weekly warfarin dose requirements were lower in those with the CYP2C9*8 allele (34 (30-47) mg; P = 0.023) and the CYP2C9 *2, *3, *5, *6, or *11 allele (33(28-40 mg); P < 0.001) as compared with those with the CYP2C9*1/*1 genotype (43 (35-56) mg).	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
20072124-2	2010	In a cohort of 226 African-American patients, weekly warfarin dose requirements were lower in those with the CYP2C9*8 allele (34 (30-47) mg; P = 0.023) and the CYP2C9 *2, *3, *5, *6, or *11 allele (33(28-40 mg); P < 0.001) as compared with those with the CYP2C9*1/*1 genotype (43 (35-56) mg).	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
20072124-2	2010	In a cohort of 226 African-American patients, weekly warfarin dose requirements were lower in those with the CYP2C9*8 allele (34 (30-47) mg; P = 0.023) and the CYP2C9 *2, *3, *5, *6, or *11 allele (33(28-40 mg); P < 0.001) as compared with those with the CYP2C9*1/*1 genotype (43 (35-56) mg).	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
20072124-3	2010	The combination of CYP2C9 alleles, VKORC1 -1639G>A genotype, and clinical variables explained 36% of the interpatient variability in warfarin dose requirements.	Warfarin	136-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
20072124-6	2010	The inclusion of additional CYP2C9 variants may improve the predictive ability of warfarin dosing algorithms for African Americans.	Warfarin	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
20086032-7	2010	Mutational studies showed that the HNF4alpha sites are needed for up-regulation of the CYP2C8 and CYP2C9 promoters by rifampicin.	Rifampin	118-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
20086032-8	2010	Furthermore, silencing of HNF4alpha abolished transactivation of the CYP2C8 and CYP2C9 promoters by rifampicin.	Rifampin	100-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
20586862-5	2010	Carrying the CYP2C9 variants is reported a significantly increased risk of non-aspirin NSAID-related GI bleeding.	Aspirin	79-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
19960413-0	2010	Inhibitory effects of deoxypodophyllotoxin from Anthriscus sylvestris on human CYP2C9 and CYP3A4.	deoxypodophyllotoxin	22-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
19960413-3	2010	When a mixture of specific CYP substrates was incubated with DPT in HLM, CYP2C9-catalyzed diclofenac 4-hydroxylation and CYP3A4-catalyzed midazolam 1-hydroxylation were strongly inhibited by DPT, with IC (50) values of 6.3 and 9.2 microM, respectively.	deoxypodophyllotoxin	61-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
19960413-3	2010	When a mixture of specific CYP substrates was incubated with DPT in HLM, CYP2C9-catalyzed diclofenac 4-hydroxylation and CYP3A4-catalyzed midazolam 1-hydroxylation were strongly inhibited by DPT, with IC (50) values of 6.3 and 9.2 microM, respectively.	Diclofenac	90-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
19960413-3	2010	When a mixture of specific CYP substrates was incubated with DPT in HLM, CYP2C9-catalyzed diclofenac 4-hydroxylation and CYP3A4-catalyzed midazolam 1-hydroxylation were strongly inhibited by DPT, with IC (50) values of 6.3 and 9.2 microM, respectively.	deoxypodophyllotoxin	191-194	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
19960413-5	2010	From these results, DPT was characterized to be a competitive inhibitor of CYP2C9 and CYP3A4, with K(i) values of 3.5 and 10.8 microM in HLM and 24.9 and 3.5 microM in baculovirus-insect cell-expressed human CYPs, respectively.	deoxypodophyllotoxin	20-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
20200517-1	2010	Warfarin demonstrates a wide interindividual variability in response that is mediated partly by variants in cytochrome P450 2C9 (CYP2C9) and vitamin K 2,3-epoxide reductase complex subunit 1 (VKORC1).	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-127
20200517-1	2010	Warfarin demonstrates a wide interindividual variability in response that is mediated partly by variants in cytochrome P450 2C9 (CYP2C9) and vitamin K 2,3-epoxide reductase complex subunit 1 (VKORC1).	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
19562511-1	2010	Acenocoumarol is mainly catabolized by CYP2C9 isoform of cytochrome P450 (CYP) liver complex and exerts its anticoagulant effect through the inhibition of Vitamin K Epoxide Reductase (VKOR).	Acenocoumarol	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
19562511-2	2010	The most important genetic polymorphisms which lead to an impaired enzymatic activity and therefore predispose to acenocoumarol sensitivity, are considered to be CYP2C9*2 (Arg144Cys), CYP2C9*3 (Ile359Leu) and VKORC1-1639G>A, respectively.	Acenocoumarol	114-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
19562511-2	2010	The most important genetic polymorphisms which lead to an impaired enzymatic activity and therefore predispose to acenocoumarol sensitivity, are considered to be CYP2C9*2 (Arg144Cys), CYP2C9*3 (Ile359Leu) and VKORC1-1639G>A, respectively.	Acenocoumarol	114-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	184-190
19562511-2	2010	The most important genetic polymorphisms which lead to an impaired enzymatic activity and therefore predispose to acenocoumarol sensitivity, are considered to be CYP2C9*2 (Arg144Cys), CYP2C9*3 (Ile359Leu) and VKORC1-1639G>A, respectively.	ile359leu	194-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
19562511-2	2010	The most important genetic polymorphisms which lead to an impaired enzymatic activity and therefore predispose to acenocoumarol sensitivity, are considered to be CYP2C9*2 (Arg144Cys), CYP2C9*3 (Ile359Leu) and VKORC1-1639G>A, respectively.	ile359leu	194-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	184-190
19347265-1	2010	Seven fungal cultures were studied for the metabolism of diclofenac in order to elucidate the nature of enzymes involved in biotransformation, as diclofenac is a specific substrate to cytochrome P450 (CYP) 2C9 isozyme in mammals.	Diclofenac	57-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	184-209
20350128-3	2010	Several retrospective and a few small prospective clinical studies have shown that polymorphisms in CYP2C9 and VKORC1 genes together account for 35-50% of the variability in warfarin initiation and maintenance dose requirements.	Warfarin	174-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
19942260-2	2010	It has been suggested that anticoagulation effect of warfarin is significantly associated with the polymorphism of certain genes, including Cytochrome P450 complex subunit 2C9 (CYP2C9), Vitamin K Epoxide Reductase Complex Subunit 1 (VKORC1), Gamma-Glutamyl Carboxylase (GGCX) and Apolipoprotein E (APOE) etc.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-175
19942260-2	2010	It has been suggested that anticoagulation effect of warfarin is significantly associated with the polymorphism of certain genes, including Cytochrome P450 complex subunit 2C9 (CYP2C9), Vitamin K Epoxide Reductase Complex Subunit 1 (VKORC1), Gamma-Glutamyl Carboxylase (GGCX) and Apolipoprotein E (APOE) etc.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	177-183
19347265-3	2010	The study included clopidogrel, a selective inhibitor of CYP2C9 isozyme, to inhibit the metabolism of diclofenac.	Clopidogrel	19-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
19347265-3	2010	The study included clopidogrel, a selective inhibitor of CYP2C9 isozyme, to inhibit the metabolism of diclofenac.	Diclofenac	102-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
19995889-1	2010	CYP2C9 is an important drug-metabolizing enzyme that metabolizes, e.g., warfarin, antidiabetics, and antiphlogistics.	Warfarin	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20178046-5	2010	Fluvastatin, which is metabolized by CYP2C9, is less prone to pharmacokinetic interactions, while pravastatin, rosuvastatin and pitavastatin are not susceptible to any CYP inhibition.	Fluvastatin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
20339978-4	2010	The mean warfarin daily dose requirement was higher in CYP2C9 homozygous wild-type patients, compared to those with the variant *3 allele (P < 0.05), similar to those with the variant *2 allele (P > 0.05) and highest in patients with the VKORC1 -1639 GG genotype compared to those with the GA genotype and the AA genotype (P < 0.01).	Warfarin	9-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
20020283-7	2010	A multiple regression model including age, sex, last INR, VKORC1, and CYP2C9 genotypes explained ~50% of the variability in AC/PC dose requirements.	Acenocoumarol	124-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
20020283-7	2010	A multiple regression model including age, sex, last INR, VKORC1, and CYP2C9 genotypes explained ~50% of the variability in AC/PC dose requirements.	Phenprocoumon	127-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
20222813-4	2010	In this article, we review a study examining the association of genetic variation in the cytochrome P450 2C9 enzyme with glycemic response to sulfonylureas in a large cohort of patients with Type 2 diabetes from the Genetics of Diabetes Audit and Research Tayside Study (Go-DARTS).	Sulfonylurea Compounds	142-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-108
20339978-7	2010	VKORC1 genotype and CYP2C9 polymorphism affect daily dose requirements and time to therapeutic INR in Turkish patients receiving warfarin for anticoagulation.	Warfarin	129-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
20402581-2	2010	Variations in two genes, VKORC1 and CYP2C9, have been associated with variation in warfarin metabolism among individuals.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
20093140-4	2010	CYP epoxygenases such as CYP1A2, CYP2C, and CYP2J2 metabolize arachidonic acid to epoxyeicosatrienoic acids (EETs) which generally possess vasodilating, anti-inflammatory, anti-apoptotic, anti-thrombotic, natriuretic, and cardioprotective effects.	Arachidonic Acid	62-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-38
19934397-0	2010	Two flavonolignans from milk thistle (Silybum marianum) inhibit CYP2C9-mediated warfarin metabolism at clinically achievable concentrations.	Flavonolignans	4-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
19934397-0	2010	Two flavonolignans from milk thistle (Silybum marianum) inhibit CYP2C9-mediated warfarin metabolism at clinically achievable concentrations.	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
20402581-5	2010	The prevalence of CYP2C9 and VKORC1 polymorphisms vary among different ethnic groups, and can account for over 30% of variance in warfarin dose.	Warfarin	130-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
20233183-10	2010	CONCLUSIONS: TDI of CYP3A4 and CYP2C9 by noscapine potentially explains clinical noscapine-warfarin interaction.	Warfarin	91-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
20169036-4	2010	Etravirine is a substrate of CYP3A4, CYP2C9, CYP2C19, and uridine diphosphate glucuronyltransferase, and induces CYP3A4, weakly inhibits CYP2C9 and moderately inhibits CYP2C19.	etravirine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
20169036-4	2010	Etravirine is a substrate of CYP3A4, CYP2C9, CYP2C19, and uridine diphosphate glucuronyltransferase, and induces CYP3A4, weakly inhibits CYP2C9 and moderately inhibits CYP2C19.	etravirine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
20233183-0	2010	Time-dependent inhibition (TDI) of CYP3A4 and CYP2C9 by noscapine potentially explains clinical noscapine-warfarin interaction.	Noscapine	56-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
20093140-4	2010	CYP epoxygenases such as CYP1A2, CYP2C, and CYP2J2 metabolize arachidonic acid to epoxyeicosatrienoic acids (EETs) which generally possess vasodilating, anti-inflammatory, anti-apoptotic, anti-thrombotic, natriuretic, and cardioprotective effects.	epoxyeicosatrienoic acids	82-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-38
20093140-4	2010	CYP epoxygenases such as CYP1A2, CYP2C, and CYP2J2 metabolize arachidonic acid to epoxyeicosatrienoic acids (EETs) which generally possess vasodilating, anti-inflammatory, anti-apoptotic, anti-thrombotic, natriuretic, and cardioprotective effects.	eets	109-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-38
19717402-1	2010	AIMS: A CYP2C9-dependent endothelium-derived hyperpolarizing factor (EDHF) controls blood flow in many microvascular beds of various species by targeting vascular smooth muscle potassium channels.	1-hexadecyl-2-acetyl-glycero-3-phosphocholine	61-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
19717402-1	2010	AIMS: A CYP2C9-dependent endothelium-derived hyperpolarizing factor (EDHF) controls blood flow in many microvascular beds of various species by targeting vascular smooth muscle potassium channels.	edhf	69-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
19717402-6	2010	Local superfusion of the CYP2C9 inhibitor sulfaphenazole, at doses known to block EDHF-dependent dilations, significantly augmented PVWI, as did inhibition of NO synthase.	Sulfaphenazole	42-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
19717402-6	2010	Local superfusion of the CYP2C9 inhibitor sulfaphenazole, at doses known to block EDHF-dependent dilations, significantly augmented PVWI, as did inhibition of NO synthase.	edhf	82-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
19717402-9	2010	The prothrombotic effects of CYP2C9 inhibition in vivo were reversed by exogenous superfusion with 11,12-epoxyeicosatrienoic acids.	11,12-epoxy-5,8,14-eicosatrienoic acid	99-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
19717402-12	2010	CONCLUSION: The arteriolar endothelium in vivo continuously releases a CYP2C9-derived EDHF.	edhf	86-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
19925783-0	2010	AFM study of the interaction of cytochrome P450 2C9 with phospholipid bilayers.	Phospholipids	57-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-51
19925783-2	2010	In this study, atomic force microscopy was applied to characterise the association of CYP2C9 to dimyristoylphosphatidylcholine (DMPC) supported phospholipid bilayers.	Dimyristoylphosphatidylcholine	96-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
19925783-2	2010	In this study, atomic force microscopy was applied to characterise the association of CYP2C9 to dimyristoylphosphatidylcholine (DMPC) supported phospholipid bilayers.	Dimyristoylphosphatidylcholine	128-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
19925783-2	2010	In this study, atomic force microscopy was applied to characterise the association of CYP2C9 to dimyristoylphosphatidylcholine (DMPC) supported phospholipid bilayers.	Phospholipids	144-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
19925783-3	2010	CYP2C9 was found to exclusively localise in the gel domains of partially melted DMPC bilayers.	Dimyristoylphosphatidylcholine	80-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19925783-4	2010	Despite lacking the N-terminus transmembrane spanning domain, the CYP2C9 protein appeared to partially embed into the membrane bilayer, as evidenced by an increase in melting temperature of surrounding phospholipids.	Phospholipids	202-215	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
19925783-5	2010	Reversible binding of CYP2C9 via an engineered His tag to a phospholipid bilayer was facilitated using nickel-chelating lipids, presenting potential applications for biosensor technologies.	Histidine	47-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
19925783-5	2010	Reversible binding of CYP2C9 via an engineered His tag to a phospholipid bilayer was facilitated using nickel-chelating lipids, presenting potential applications for biosensor technologies.	Phospholipids	60-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
19925783-5	2010	Reversible binding of CYP2C9 via an engineered His tag to a phospholipid bilayer was facilitated using nickel-chelating lipids, presenting potential applications for biosensor technologies.	Nickel	103-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
20233183-0	2010	Time-dependent inhibition (TDI) of CYP3A4 and CYP2C9 by noscapine potentially explains clinical noscapine-warfarin interaction.	Noscapine	96-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
20233183-0	2010	Time-dependent inhibition (TDI) of CYP3A4 and CYP2C9 by noscapine potentially explains clinical noscapine-warfarin interaction.	Warfarin	106-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
20233183-6	2010	Kinetic analysis showed that inhibition of CYP2C9 by noscapine was best fit to a noncompetitive type with K(i) value of 8.8 microm, while inhibition of CYP3A4 by noscapine was best fit to a competitive manner with K(i) value of 5.2 microm.	Noscapine	53-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
20233183-7	2010	Noscapine also exhibited TDI to CYP3A4 and CYP2C9.	Noscapine	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
20233183-10	2010	CONCLUSIONS: TDI of CYP3A4 and CYP2C9 by noscapine potentially explains clinical noscapine-warfarin interaction.	Noscapine	41-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
20233183-10	2010	CONCLUSIONS: TDI of CYP3A4 and CYP2C9 by noscapine potentially explains clinical noscapine-warfarin interaction.	Noscapine	81-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
19855097-0	2010	CYP2C9*1B promoter polymorphisms, in linkage with CYP2C19*2, affect phenytoin autoinduction of clearance and maintenance dose.	Phenytoin	68-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19567378-0	2010	Pharmacogenetic impact of VKORC1 and CYP2C9 allelic variants on warfarin dose requirements in a hispanic population isolate.	Warfarin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
19567378-9	2010	A stepwise multivariate linear regression analysis showed that 38.2% of the warfarin dose response variance was accounted for by a model involving age (20.9%), VKORC1-1639G/A (11.3%), and CYP2C9*1, *2, and *3 variants (7.1%).	Warfarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	188-194
20022989-7	2010	The role of cytochrome P450 epoxygenase (CYP 2C9)-derived endothelium-derived hyperpolarizing factor (EDHF) was assessed by repeating acetylcholine under intraarterial sulfaphenazole.	endothelium-derived hyperpolarizing factor	58-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-48
20022989-7	2010	The role of cytochrome P450 epoxygenase (CYP 2C9)-derived endothelium-derived hyperpolarizing factor (EDHF) was assessed by repeating acetylcholine under intraarterial sulfaphenazole.	edhf	102-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-48
20022989-7	2010	The role of cytochrome P450 epoxygenase (CYP 2C9)-derived endothelium-derived hyperpolarizing factor (EDHF) was assessed by repeating acetylcholine under intraarterial sulfaphenazole.	Acetylcholine	134-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-48
20022989-7	2010	The role of cytochrome P450 epoxygenase (CYP 2C9)-derived endothelium-derived hyperpolarizing factor (EDHF) was assessed by repeating acetylcholine under intraarterial sulfaphenazole.	Sulfaphenazole	168-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-48
20022989-15	2010	A compensatory CYP 2C9-derived EDHF pathway is activated to sustain endothelium-dependent vasodilation.	edhf	31-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-22
19941044-10	2010	The presence of a single *2 or *3 CYP2C9 allele reduced mean [SE (standard error)] S-warfarin clearance by 35% from 0.276 (0.04) to 0.180 (0.11) l/h.	Warfarin	85-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
19941044-13	2010	Steady state simulations showed that whilst CYP2C9 polymorphisms affect the PK of warfarin, VKORC1 haplotypes may be better predictors of warfarin response.	Warfarin	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
20121287-10	2010	CONCLUSION: Genotyping of four SNPs for VKORC1 and CYP2C9 polymorphisms is useful in predicting a high probability of the occurrence of DAH in patients receiving oral anticoagulants.	dah	136-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
20206792-2	2010	OBJECTIVE: The aim of this study was to determine whether folic acid supplementation increases the dosage requirement of the CYP2C9 substrate warfarin, and the formation clearance of the CYP2C9-mediated product, (S)-7-hydroxywarfarin.	Folic Acid	58-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
20206792-2	2010	OBJECTIVE: The aim of this study was to determine whether folic acid supplementation increases the dosage requirement of the CYP2C9 substrate warfarin, and the formation clearance of the CYP2C9-mediated product, (S)-7-hydroxywarfarin.	7-hydroxywarfarin	212-233	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	187-193
19847408-0	2010	The effects of CYP2C9 and CYP2C19 genetic polymorphisms on the pharmacokinetics and pharmacodynamics of glipizide in Chinese subjects.	Glipizide	104-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
19847408-1	2010	OBJECTIVE: To study the effects of CYP2C9 and CYP2C19 genetic polymorphisms on the pharmacokinetics and pharmacodynamics of glipizide.	Glipizide	124-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
19847408-8	2010	CONCLUSIONS: These results suggest that CYP2C9 polymorphism significantly influences the pharmacokinetics and pharmacodynamics of glipizide, which needs to be considered in clinical practice.	Glipizide	130-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
19891972-1	2010	The cytochrome P450 (CYP) epoxygenase enzymes CYP2J and CYP2C catalyze the epoxidation of arachidonic acid to epoxyeicosatrienoic acids (EETs), which are rapidly hydrolyzed to dihydroxyeicosatrienoic acids (DHETs) by soluble epoxide hydrolase (sEH).	Arachidonic Acid	90-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-61
19891972-1	2010	The cytochrome P450 (CYP) epoxygenase enzymes CYP2J and CYP2C catalyze the epoxidation of arachidonic acid to epoxyeicosatrienoic acids (EETs), which are rapidly hydrolyzed to dihydroxyeicosatrienoic acids (DHETs) by soluble epoxide hydrolase (sEH).	epoxyeicosatrienoic acids	110-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-61
19891972-1	2010	The cytochrome P450 (CYP) epoxygenase enzymes CYP2J and CYP2C catalyze the epoxidation of arachidonic acid to epoxyeicosatrienoic acids (EETs), which are rapidly hydrolyzed to dihydroxyeicosatrienoic acids (DHETs) by soluble epoxide hydrolase (sEH).	eets	137-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-61
19891972-1	2010	The cytochrome P450 (CYP) epoxygenase enzymes CYP2J and CYP2C catalyze the epoxidation of arachidonic acid to epoxyeicosatrienoic acids (EETs), which are rapidly hydrolyzed to dihydroxyeicosatrienoic acids (DHETs) by soluble epoxide hydrolase (sEH).	dihydroxyeicosatrienoic acids	176-205	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-61
19891972-1	2010	The cytochrome P450 (CYP) epoxygenase enzymes CYP2J and CYP2C catalyze the epoxidation of arachidonic acid to epoxyeicosatrienoic acids (EETs), which are rapidly hydrolyzed to dihydroxyeicosatrienoic acids (DHETs) by soluble epoxide hydrolase (sEH).	dhets	207-212	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-61
20121287-2	2010	OBJECTIVE: We hypothesized that in patients treated with coumarins, alveolar hemorrhage is associated with vitamin K epoxide reductase (VKORC1) and cytochrome P450 (CYP) 2C9 (CYP2C9) variant alleles.	Coumarins	57-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-173
20121287-2	2010	OBJECTIVE: We hypothesized that in patients treated with coumarins, alveolar hemorrhage is associated with vitamin K epoxide reductase (VKORC1) and cytochrome P450 (CYP) 2C9 (CYP2C9) variant alleles.	Coumarins	57-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	175-181
19855097-1	2010	The commonly prescribed antiepileptic drug phenytoin has a narrow therapeutic range and wide interindividual variability in clearance explained in part by CYP2C9 and CYP2C19 coding variants.	Phenytoin	43-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
19855097-2	2010	After finding a paradoxically low urinary phenytoin metabolite (S)/(R) ratio in subjects receiving phenytoin maintenance therapy with a CYP2C9*1/*1 and CYP2C19*1/*2 genotype, we hypothesized that CYP2C9 regulatory polymorphisms (rPMs), G-3089A and -2663delTG, in linkage disequilibrium with CYP2C19*2 were responsible.	Phenytoin	42-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
19855097-2	2010	After finding a paradoxically low urinary phenytoin metabolite (S)/(R) ratio in subjects receiving phenytoin maintenance therapy with a CYP2C9*1/*1 and CYP2C19*1/*2 genotype, we hypothesized that CYP2C9 regulatory polymorphisms (rPMs), G-3089A and -2663delTG, in linkage disequilibrium with CYP2C19*2 were responsible.	Phenytoin	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
19855097-4	2010	We hypothesized the rPMs affected CYP2C9 induction by phenytoin, a pregnane X receptor (PXR), and constitutive androstane receptor (CAR) activator.	rpms	20-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
19855097-5	2010	Transfection studies showed that CYP2C9 reporters with wild-type versus variant alleles had similar basal activity but significantly greater phenytoin induction by cotransfected PXR, CAR, and Nrf2 and less Yin Yang 1 transcription factor repression.	Phenytoin	141-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
19855097-6	2010	Phenytoin induction of CYP2C9 was greater in human hepatocytes with the CYP2C9 wild type versus variant haplotype.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
19855097-6	2010	Phenytoin induction of CYP2C9 was greater in human hepatocytes with the CYP2C9 wild type versus variant haplotype.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
19855097-7	2010	Therefore, CYP2C9 rPMs affect phenytoin-dependent induction of CYP2C9 and phenytoin metabolism in humans, with an effect size comparable with that for CYP2C9*2 and 2C9*3.	rpms	18-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
19855097-7	2010	Therefore, CYP2C9 rPMs affect phenytoin-dependent induction of CYP2C9 and phenytoin metabolism in humans, with an effect size comparable with that for CYP2C9*2 and 2C9*3.	rpms	18-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
19855097-7	2010	Therefore, CYP2C9 rPMs affect phenytoin-dependent induction of CYP2C9 and phenytoin metabolism in humans, with an effect size comparable with that for CYP2C9*2 and 2C9*3.	rpms	18-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
19855097-7	2010	Therefore, CYP2C9 rPMs affect phenytoin-dependent induction of CYP2C9 and phenytoin metabolism in humans, with an effect size comparable with that for CYP2C9*2 and 2C9*3.	Phenytoin	30-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
19855097-7	2010	Therefore, CYP2C9 rPMs affect phenytoin-dependent induction of CYP2C9 and phenytoin metabolism in humans, with an effect size comparable with that for CYP2C9*2 and 2C9*3.	Phenytoin	30-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
19855097-7	2010	Therefore, CYP2C9 rPMs affect phenytoin-dependent induction of CYP2C9 and phenytoin metabolism in humans, with an effect size comparable with that for CYP2C9*2 and 2C9*3.	Phenytoin	30-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
19855097-7	2010	Therefore, CYP2C9 rPMs affect phenytoin-dependent induction of CYP2C9 and phenytoin metabolism in humans, with an effect size comparable with that for CYP2C9*2 and 2C9*3.	Phenytoin	74-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
19686083-5	2010	Although the polymorphisms in CYP2C9 and VKORC1 explain a significant proportion of the interindividual variability in warfarin dose requirement, currently available evidence based on a few small studies relating to the use of pharmacogenetics-guided dosing in the initiation of warfarin therapy has not shown improved outcomes in either safety or efficacy of therapy.	Warfarin	279-287	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
21215088-4	2010	One hundred and one patients with stable anticoagulation with warfarin under a target international normalized ratio (INR) of 2.0 to 3.0 were enrolled for studying the relationship between the CYP2C9 and VKORC1 gene polymorphism and the warfarin maintaining dosage.	Warfarin	237-245	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	193-199
19686083-3	2010	Single nucleotide polymorphisms in the cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKOR) genes have been shown to have a significant effect on warfarin dose requirement.	Warfarin	161-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-58
19903527-2	2010	Additionally, the influence of optimized GRDDS on the bioavailability of Losartan and the formation extent of active metabolite E3174 by CYP2C9 polymorphism was investigated.	losartan carboxylic acid	128-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
19903527-9	2010	The lower bioavailability of Losartan in the CYP2C9*1/*1 subjects than CYP2C9*1/*3 subjects was found and could be due to the variety of enzymatic activity.	Losartan	29-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
19903527-9	2010	The lower bioavailability of Losartan in the CYP2C9*1/*1 subjects than CYP2C9*1/*3 subjects was found and could be due to the variety of enzymatic activity.	Losartan	29-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
19686083-3	2010	Single nucleotide polymorphisms in the cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKOR) genes have been shown to have a significant effect on warfarin dose requirement.	Warfarin	161-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
19686083-5	2010	Although the polymorphisms in CYP2C9 and VKORC1 explain a significant proportion of the interindividual variability in warfarin dose requirement, currently available evidence based on a few small studies relating to the use of pharmacogenetics-guided dosing in the initiation of warfarin therapy has not shown improved outcomes in either safety or efficacy of therapy.	Warfarin	119-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
20834094-3	2010	Etravirine is a weak inducer of cytochrome P450 (CYP)3A and a weak inhibitor of CYP2C9/CYP2C19 and P-glycoprotein, and although etravirine is metabolized by the CYP enzyme system, the extent of clinically relevant interactions with other antiretrovirals is limited.	etravirine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
19794411-4	2010	In addition to age, genetic variants of VKORC1, CYP2C9, CYP4F2, and EPHX1 were found to be significant predictor variables for the maintenance dose of warfarin, explaining 26.6% of dose variability.	Warfarin	151-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
20671989-5	2010	The exact mechanism of this interaction is unknown but may be related to downregulation of cytochrome P450 2C9 by capecitabine or its metabolites.	Capecitabine	114-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-110
19794411-0	2010	Genetic factors (VKORC1, CYP2C9, EPHX1, and CYP4F2) are predictor variables for warfarin response in very elderly, frail inpatients.	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
19794412-0	2010	Loss-of-function CYP2C9 variants improve therapeutic response to sulfonylureas in type 2 diabetes: a Go-DARTS study.	Sulfonylurea Compounds	65-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
19794412-1	2010	Sulfonylureas are metabolized mainly by the cytochrome p450 2C9 (CYP2C9) enzyme.	Sulfonylurea Compounds	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-63
19794412-1	2010	Sulfonylureas are metabolized mainly by the cytochrome p450 2C9 (CYP2C9) enzyme.	Sulfonylurea Compounds	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
19794412-7	2010	In conclusion, CYP2C9 loss-of-function alleles are associated with greater response to sulfonylureas and decreased failure of therapy consistent with the pharmacokinetic role of CYP2C9.	Sulfonylurea Compounds	87-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
20205664-1	2010	The identification of the genes encoding CYP2C9, the principal metabolizing enzyme of the coumarins, and VKORC1, the molecular target for coumarins, has strongly stimulated the research on pharmacogenetics of vitamin K antagonists, also designated as coumarins.	Coumarins	90-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
20171411-1	2010	BACKGROUND: Bosentan is an endothelin-receptor antagonist that reportedly induces both cytochrome P450 (CYP) 3A4 and CYP2C9 enzymes, which are also involved in warfarin metabolism.	Bosentan	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
20171411-1	2010	BACKGROUND: Bosentan is an endothelin-receptor antagonist that reportedly induces both cytochrome P450 (CYP) 3A4 and CYP2C9 enzymes, which are also involved in warfarin metabolism.	Warfarin	160-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
20171411-7	2010	CONCLUSIONS: Bosentan has CYP3A4- and CYP2C9-inducing properties and is therefore likely to cause decreased concentrations of warfarin.	Bosentan	13-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
20877134-0	2010	Flavonoids diosmetin and hesperetin are potent inhibitors of cytochrome P450 2C9-mediated drug metabolism in vitro.	Flavonoids	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-80
20877134-0	2010	Flavonoids diosmetin and hesperetin are potent inhibitors of cytochrome P450 2C9-mediated drug metabolism in vitro.	diosmetin	11-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-80
20877134-0	2010	Flavonoids diosmetin and hesperetin are potent inhibitors of cytochrome P450 2C9-mediated drug metabolism in vitro.	hesperetin	25-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-80
20877134-1	2010	The aim of this study was to examine in vitro, by means of kinetic analysis and molecular docking simulations, the effects of the flavone diosmetin and its flavanone analog hesperetin on CYP (cytochrome P450) 2C9-mediated drug metabolism.	flavone	130-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	192-212
20877134-1	2010	The aim of this study was to examine in vitro, by means of kinetic analysis and molecular docking simulations, the effects of the flavone diosmetin and its flavanone analog hesperetin on CYP (cytochrome P450) 2C9-mediated drug metabolism.	diosmetin	138-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	192-212
20877134-1	2010	The aim of this study was to examine in vitro, by means of kinetic analysis and molecular docking simulations, the effects of the flavone diosmetin and its flavanone analog hesperetin on CYP (cytochrome P450) 2C9-mediated drug metabolism.	flavanone	156-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	192-212
20877134-2	2010	To this purpose, the conversion of diclofenac to 4"-hydroxydiclofenac by human liver microsomes was used as a model assay for assessing the CYP2C9 inhibitory activity of these two flavonoids.	4'-hydroxydiclofenac	49-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
20877134-2	2010	To this purpose, the conversion of diclofenac to 4"-hydroxydiclofenac by human liver microsomes was used as a model assay for assessing the CYP2C9 inhibitory activity of these two flavonoids.	Flavonoids	180-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
20877134-6	2010	The results of molecular docking simulations were consistent with those of kinetic analysis, since they showed that the putative binding sites of both diosmetin and hesperetin coincided with the CYP2C9 substrate binding site.	diosmetin	151-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
20877134-6	2010	The results of molecular docking simulations were consistent with those of kinetic analysis, since they showed that the putative binding sites of both diosmetin and hesperetin coincided with the CYP2C9 substrate binding site.	hesperetin	165-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
20877134-7	2010	The demonstration that diosmetin and hesperetin inhibit CYP2C9-mediated diclofenac metabolism at low micromolar concentrations is of potential clinical relevance because CYP2C9 is responsible for the biotransformation of various therapeutically important drugs that have narrow therapeutic indexes.	diosmetin	23-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
20877134-7	2010	The demonstration that diosmetin and hesperetin inhibit CYP2C9-mediated diclofenac metabolism at low micromolar concentrations is of potential clinical relevance because CYP2C9 is responsible for the biotransformation of various therapeutically important drugs that have narrow therapeutic indexes.	diosmetin	23-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-176
20877134-7	2010	The demonstration that diosmetin and hesperetin inhibit CYP2C9-mediated diclofenac metabolism at low micromolar concentrations is of potential clinical relevance because CYP2C9 is responsible for the biotransformation of various therapeutically important drugs that have narrow therapeutic indexes.	hesperetin	37-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
20877134-7	2010	The demonstration that diosmetin and hesperetin inhibit CYP2C9-mediated diclofenac metabolism at low micromolar concentrations is of potential clinical relevance because CYP2C9 is responsible for the biotransformation of various therapeutically important drugs that have narrow therapeutic indexes.	hesperetin	37-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-176
20877134-7	2010	The demonstration that diosmetin and hesperetin inhibit CYP2C9-mediated diclofenac metabolism at low micromolar concentrations is of potential clinical relevance because CYP2C9 is responsible for the biotransformation of various therapeutically important drugs that have narrow therapeutic indexes.	Diclofenac	72-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-176
20930419-0	2010	Pharmacokinetic and pharmacodynamic variation associated with VKORC1 and CYP2C9 polymorphisms in Thai patients taking warfarin.	Warfarin	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
20930419-1	2010	We investigated the influence of genetic polymorphisms of CYP2C9 and VKORC1 genotypes on the pharmacokinetics and pharmacodynamics of warfarin and established an equation for predicting the maintenance dose of warfarin in the Thai population using genetic and non-genetic factors.	Warfarin	134-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
20930419-1	2010	We investigated the influence of genetic polymorphisms of CYP2C9 and VKORC1 genotypes on the pharmacokinetics and pharmacodynamics of warfarin and established an equation for predicting the maintenance dose of warfarin in the Thai population using genetic and non-genetic factors.	Warfarin	210-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
20930419-4	2010	CYP2C9 polymorphisms affect warfarin metabolism as shown by a significant difference in warfarin clearance, whereas VKORC1 genotypes cause a significant difference in warfarin sensitivity index (INR:Cp).	Warfarin	28-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20930419-4	2010	CYP2C9 polymorphisms affect warfarin metabolism as shown by a significant difference in warfarin clearance, whereas VKORC1 genotypes cause a significant difference in warfarin sensitivity index (INR:Cp).	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20930419-4	2010	CYP2C9 polymorphisms affect warfarin metabolism as shown by a significant difference in warfarin clearance, whereas VKORC1 genotypes cause a significant difference in warfarin sensitivity index (INR:Cp).	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20930419-5	2010	The mean weekly warfarin dose was significantly different among different VKORC1 and CYP2C9 genotypes.	Warfarin	16-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
20930419-6	2010	Patients with the VKORC1 BB haplotype and CYP2C9*1/*1 required about twice the warfarin dose compared to those with the VKORC1 AA haplotype and CYP2C9*1/*1.	Warfarin	79-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
20930419-7	2010	Using stepwise multiple linear regression, clinical factors (age and weight) and genetic factors (CYP2C9 and VKORC1) could explain about 53.8% of the variance of the warfarin maintenance dose.	Warfarin	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
20930419-8	2010	CYP2C9 and VKORC1 genotypes played an important role in the inter-individual variation in warfarin maintenance dose in a Thai population.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20877134-7	2010	The demonstration that diosmetin and hesperetin inhibit CYP2C9-mediated diclofenac metabolism at low micromolar concentrations is of potential clinical relevance because CYP2C9 is responsible for the biotransformation of various therapeutically important drugs that have narrow therapeutic indexes.	Diclofenac	72-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
20962433-1	2010	Benzbromarone is a uricosuric drug and has been shown to be metabolized predominantly by cytochrome P450(CYP)2C9 in vitro findings.	Benzbromarone	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-112
20962433-2	2010	This study aims to investigate the influence of the CYP2C9 genotype on plasma levels of benzbromarone and 6-hydroxybenzbromarone, as well as uric acid lowering effects.	Benzbromarone	88-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
20962433-2	2010	This study aims to investigate the influence of the CYP2C9 genotype on plasma levels of benzbromarone and 6-hydroxybenzbromarone, as well as uric acid lowering effects.	6-hydroxybenzbromarone	106-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
20962433-4	2010	The oral clearance of benzbromarone in the CYP2C9*1/*1 genotype and CYP2C9*1/*3 genotype was 58.8+-25.2 L/hr/kg (mean+-SD) and 51.3+-7.9 L/hr/kg, respectively, whereas 8.58 L/hr/kg in the CYP2C9*3/*3 genotype.	Benzbromarone	22-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
20962433-5	2010	The metabolic ratio (6-hydroxybenzbromarone/benzbromarone) in urine was 38.6+-10.7 in the CYP2C9*1/*1 genotype, 35.4+-12.4 in the CYP2C9*1/*3 genotype and 12.9 in the CYP2C9*3/*3 genotype.	6-hydroxybenzbromarone	21-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
20962433-7	2010	These results suggest a critical role for CYP2C9 in the metabolism of benzbromarone in humans and a possible risk of toxicity in the CYP2C9*3 homozygote by lowering clearance of the drug.	Benzbromarone	70-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
20962433-8	2010	Further studies are required to assess the clinical impact of CYP2C9 on the metabolism of benzbromarone.	Benzbromarone	90-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
20205664-1	2010	The identification of the genes encoding CYP2C9, the principal metabolizing enzyme of the coumarins, and VKORC1, the molecular target for coumarins, has strongly stimulated the research on pharmacogenetics of vitamin K antagonists, also designated as coumarins.	Coumarins	138-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
20205664-1	2010	The identification of the genes encoding CYP2C9, the principal metabolizing enzyme of the coumarins, and VKORC1, the molecular target for coumarins, has strongly stimulated the research on pharmacogenetics of vitamin K antagonists, also designated as coumarins.	Vitamin K	209-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
20205664-1	2010	The identification of the genes encoding CYP2C9, the principal metabolizing enzyme of the coumarins, and VKORC1, the molecular target for coumarins, has strongly stimulated the research on pharmacogenetics of vitamin K antagonists, also designated as coumarins.	Coumarins	138-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
20205664-2	2010	From 1999 to 2004 a number of observational studies firmly established associations between being carrier of the CYP2C9*2 and especially the CYP2C9*3 allele and reduced coumarin dose requirements and increased risks of overanticoagulation and even major bleeding compared to CYP2C9 wild type patients.	coumarin	169-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
20205664-2	2010	From 1999 to 2004 a number of observational studies firmly established associations between being carrier of the CYP2C9*2 and especially the CYP2C9*3 allele and reduced coumarin dose requirements and increased risks of overanticoagulation and even major bleeding compared to CYP2C9 wild type patients.	coumarin	169-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
20205664-2	2010	From 1999 to 2004 a number of observational studies firmly established associations between being carrier of the CYP2C9*2 and especially the CYP2C9*3 allele and reduced coumarin dose requirements and increased risks of overanticoagulation and even major bleeding compared to CYP2C9 wild type patients.	coumarin	169-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
22134997-3	2010	Polymorphisms of two genes encoding enzymes involved in vitamin K and/or VKA metabolism such as vitamin K epoxide reductase complex subunit 1 (VKORC1) and cytochrome P450 2C9 isoform (CYP2C9) play a key role in this variance.	Vitamin K	56-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-174
21152245-9	2010	Strong correlations between allelic variation in the tamoxifen pathway at CYP1A1-CYP3A4, CYP3A4-CYP2C9, and CYP2C9-SULT1A2, in addition to CYP2D6 and its adjacent genes, were seen in the placebo-arm but not the tamoxifen-arm.	Tamoxifen	53-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
19883715-3	2010	In this study, we systematically evaluated the inhibitory effects of 60 polyphenols and related compounds on human cytochrome P450 (CYP) 3A4 and CYP2C9 activity by in vitro assay to investigate whether some polyphenols induce drug interactions.	Polyphenols	72-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
19883715-5	2010	Three coumarins and 12 flavonoids significantly suppressed CYP3A4 or CYP2C9 activities.	Coumarins	6-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
19883715-5	2010	Three coumarins and 12 flavonoids significantly suppressed CYP3A4 or CYP2C9 activities.	Flavonoids	23-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
19883715-6	2010	Lineweaver-Burk plot analysis indicated that apigenin and its dimer amentoflavone and imperatorin displayed a mixed type of inhibition on CYP3A4 or CYP2C9.	amentoflavone	68-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
19883715-7	2010	Among the inhibitors, amentoflavone was the most potent inhibitor of CYP3A4 and CYP2C9 activities with IC(50) values of 0.07 and 0.03 microM, respectively.	amentoflavone	22-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
19883715-8	2010	The K(i) value of amentoflavone was significantly lower than that of the CYP2C9 inhibition positive control sulfaphenazole.	amentoflavone	18-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
19883715-8	2010	The K(i) value of amentoflavone was significantly lower than that of the CYP2C9 inhibition positive control sulfaphenazole.	Sulfaphenazole	108-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
20393255-2	2010	Voriconazole, a CYP2C9 inhibitor, has many potential drug interactions.	Voriconazole	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
19874474-0	2010	Ability of VKORC1 and CYP2C9 to predict therapeutic warfarin dose during the initial weeks of therapy.	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
19874474-1	2010	BACKGROUND: CYP2C9 and VKORC1 genotypes predict therapeutic warfarin dose at initiation of therapy; however, the predictive ability of genetic information after a week or longer is unknown.	Warfarin	60-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
22134997-3	2010	Polymorphisms of two genes encoding enzymes involved in vitamin K and/or VKA metabolism such as vitamin K epoxide reductase complex subunit 1 (VKORC1) and cytochrome P450 2C9 isoform (CYP2C9) play a key role in this variance.	Vitamin K	56-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	184-190
20014877-1	2010	BACKGROUND: In 2007, the US FDA added information about pharmacogenomics to the warfarin label based on the influence of the CYP2C9 and VKORC1 genes on anticoagulation-related outcomes.	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
20617424-3	2010	Significant findings have been documented showing the effect of certain genetic variations (e.g., in CYP2C9 and VKORC1) on the dose response to warfarin.	Warfarin	144-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
19934793-0	2010	Besides CYP2C19*2, the variant allele CYP2C9*3 is associated with higher on-clopidogrel platelet reactivity in patients on dual antiplatelet therapy undergoing elective coronary stent implantation.	Clopidogrel	76-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
20017677-1	2010	AIMS: VKORC1 and CYP2C9 are important genetic factors affecting warfarin dose requirement.	Warfarin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
19934793-10	2010	CONCLUSION: Besides CYP2C19*2, the variant allele CYP2C9*3 plays an important role in the response to clopidogrel in patients on dual antiplatelet therapy undergoing coronary stenting.	Clopidogrel	102-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
19614891-0	2009	The role of human CYP2C8 and CYP2C9 variants in pioglitazone metabolism in vitro.	Pioglitazone	48-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
19952982-2	2010	The goal of this study was to assess the effect of maternal genotype of functional polymorphisms in two genes involved in phenytoin metabolism, CYP2C9 (R144C, I395L) and EPHX1 (Y113H, H139R), on the presence of major craniofacial abnormalities (CFAs) in the child.	Phenytoin	122-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
20597268-15	2010	The determination of CYP2C9 and VCORC1 genotypes in patients with APS before warfarin use allows excessive hypocoagulation and related hemorrhages to be avoided.	Warfarin	77-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
19614891-6	2009	Mean intrinsic clearance of pioglitazone to the metabolite M-IV was highest for CYP2C8 and CYP1A2 with 58 pmol M-IV/min/nmol CYP P450/microM pioglitazone each, 53 for CYP2D6*1, 40 for CYP2C19*1, and 34 for CYP2C9*2, respectively.	Pioglitazone	28-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	206-212
19614891-3	2009	Pioglitazone (2-400 microM) was incubated with isolated cytochrome P450 enzymes or human liver microsomes, some of them carrying either the CYP2C8*3/*3 genotype (and also the CYP2C9*2/*2 genotype) or the CYP2C8*1/*1 genotype (five samples each).	Pioglitazone	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	175-181
20116625-3	2009	ETR acts as an inducer of CYP3A4 and inhibitor of CYP2C9 and CYP2C19.	etravirine	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
19756559-0	2009	Effects of CYP2C19 and CYP2C9 genotypes on pharmacokinetic variability of valproic acid in Chinese epileptic patients: nonlinear mixed-effect modeling.	Valproic Acid	74-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
19756559-1	2009	PURPOSE: To evaluate the effects of CYP2C19 and CYP2C9 genotypes on the pharmacokinetic variability of valproic acid (VPA) in epileptic patients using a population pharmacokinetic (PPK) approach.	Valproic Acid	103-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
19958586-1	2009	OBJECTIVES: It has been reported that hepatic cytochrome P450 (CYP)2C9 and CYP3A4 are responsible for the metabolism of sildenafil and formation of its metabolite, N-desmethylsildenafil, in humans.	Sildenafil Citrate	120-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-70
20167002-5	2009	As an example, we present modelling and simulation approaches of the CYP2C9 gene expression in human hepatocytes treated with well-known CYP2C9 inducers: the steroid hormone precursor dehydroepiandrosterone (DHEA) and the synthetic glucocorticoid dexamethasone (DXM).	Dexamethasone	262-265	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
20167002-6	2009	The results of the analysis suggest that in addition to the potent function of GR and the further involvement of PXR and CAR activated by DXM or DHEA, an additional factor might play a role in CYP2C9 regulation by DHEA.	Dehydroepiandrosterone	214-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	193-199
20167002-7	2009	The novel potential candidate for DHEA action in CYP2C9 induction is likely to be the estrogen receptor.	Dehydroepiandrosterone	34-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
20167002-8	2009	Additionally, the balance of DHEA sulphation-desulphation processes should also be considered in any description of DHEA-induced CYP2C9 profiles.	Dehydroepiandrosterone	116-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
20167000-9	2009	Currently, there are three X-ray structures of the human CYP2C9 in Protein Database (PDB): one ligand-free protein (1OG2), and two in complex with S-warfarin (1OG5) or flurbiprofen (1R9O).	Sulfur	147-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
20167000-9	2009	Currently, there are three X-ray structures of the human CYP2C9 in Protein Database (PDB): one ligand-free protein (1OG2), and two in complex with S-warfarin (1OG5) or flurbiprofen (1R9O).	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
20167000-9	2009	Currently, there are three X-ray structures of the human CYP2C9 in Protein Database (PDB): one ligand-free protein (1OG2), and two in complex with S-warfarin (1OG5) or flurbiprofen (1R9O).	Flurbiprofen	168-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
20167000-13	2009	In the structures of CYP2C9 without ligand bound or with bound S-warfarin, residues 101-106 in the B-C loop form helix B".	Warfarin	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
20167000-17	2009	CYP2C9 is activated by dapsone and its analogues and R-lansoprazole in a stereo-specific and substrate-dependent manner, probably through binding to the active site and inducing positive cooperativity.	Dapsone	23-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20167000-17	2009	CYP2C9 is activated by dapsone and its analogues and R-lansoprazole in a stereo-specific and substrate-dependent manner, probably through binding to the active site and inducing positive cooperativity.	Dexlansoprazole	53-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20167001-5	2009	CYP2C9 also plays a role in the metabolism of several endogenous compounds such as steroids, melatonin, retinoids and arachidonic acid.	Steroids	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20167001-5	2009	CYP2C9 also plays a role in the metabolism of several endogenous compounds such as steroids, melatonin, retinoids and arachidonic acid.	Melatonin	93-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20167001-5	2009	CYP2C9 also plays a role in the metabolism of several endogenous compounds such as steroids, melatonin, retinoids and arachidonic acid.	Retinoids	104-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20167001-5	2009	CYP2C9 also plays a role in the metabolism of several endogenous compounds such as steroids, melatonin, retinoids and arachidonic acid.	Arachidonic Acid	118-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20167001-6	2009	Typical substrates of CYP2C9 such as celecoxib, ibuprofen, flurbiprofen, and diclofenac are relatively small, lipophilic and contain acidic groupings with pK(a) values in the range 3.8-8.1 which will be ionized at physiological pH.	Celecoxib	37-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
20167001-6	2009	Typical substrates of CYP2C9 such as celecoxib, ibuprofen, flurbiprofen, and diclofenac are relatively small, lipophilic and contain acidic groupings with pK(a) values in the range 3.8-8.1 which will be ionized at physiological pH.	Ibuprofen	48-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
20167001-6	2009	Typical substrates of CYP2C9 such as celecoxib, ibuprofen, flurbiprofen, and diclofenac are relatively small, lipophilic and contain acidic groupings with pK(a) values in the range 3.8-8.1 which will be ionized at physiological pH.	Flurbiprofen	59-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
20167001-6	2009	Typical substrates of CYP2C9 such as celecoxib, ibuprofen, flurbiprofen, and diclofenac are relatively small, lipophilic and contain acidic groupings with pK(a) values in the range 3.8-8.1 which will be ionized at physiological pH.	Diclofenac	77-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
20167001-7	2009	The carboxylate groups of tienilic acid and diclofenac have been shown to be responsible for substrate preference and orientation in the active site of CYP2C9.	carboxylate	4-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	152-158
20167001-7	2009	The carboxylate groups of tienilic acid and diclofenac have been shown to be responsible for substrate preference and orientation in the active site of CYP2C9.	Ticrynafen	26-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	152-158
20167001-7	2009	The carboxylate groups of tienilic acid and diclofenac have been shown to be responsible for substrate preference and orientation in the active site of CYP2C9.	Diclofenac	44-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	152-158
20167001-12	2009	Pharmacophore models have revealed that hydrogen bonding, ion-pair interactions, and probably hydrophobic interactions play a major role in determining the substrate specificity and inhibitor selectivity of CYP2C9.	Hydrogen	40-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	207-213
20167002-5	2009	As an example, we present modelling and simulation approaches of the CYP2C9 gene expression in human hepatocytes treated with well-known CYP2C9 inducers: the steroid hormone precursor dehydroepiandrosterone (DHEA) and the synthetic glucocorticoid dexamethasone (DXM).	Steroids	158-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
20167002-5	2009	As an example, we present modelling and simulation approaches of the CYP2C9 gene expression in human hepatocytes treated with well-known CYP2C9 inducers: the steroid hormone precursor dehydroepiandrosterone (DHEA) and the synthetic glucocorticoid dexamethasone (DXM).	Steroids	158-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
20167002-5	2009	As an example, we present modelling and simulation approaches of the CYP2C9 gene expression in human hepatocytes treated with well-known CYP2C9 inducers: the steroid hormone precursor dehydroepiandrosterone (DHEA) and the synthetic glucocorticoid dexamethasone (DXM).	Dehydroepiandrosterone	184-206	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
20167002-5	2009	As an example, we present modelling and simulation approaches of the CYP2C9 gene expression in human hepatocytes treated with well-known CYP2C9 inducers: the steroid hormone precursor dehydroepiandrosterone (DHEA) and the synthetic glucocorticoid dexamethasone (DXM).	Dehydroepiandrosterone	184-206	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
20167002-5	2009	As an example, we present modelling and simulation approaches of the CYP2C9 gene expression in human hepatocytes treated with well-known CYP2C9 inducers: the steroid hormone precursor dehydroepiandrosterone (DHEA) and the synthetic glucocorticoid dexamethasone (DXM).	Dehydroepiandrosterone	208-212	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
20167002-5	2009	As an example, we present modelling and simulation approaches of the CYP2C9 gene expression in human hepatocytes treated with well-known CYP2C9 inducers: the steroid hormone precursor dehydroepiandrosterone (DHEA) and the synthetic glucocorticoid dexamethasone (DXM).	Dehydroepiandrosterone	208-212	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
20167002-5	2009	As an example, we present modelling and simulation approaches of the CYP2C9 gene expression in human hepatocytes treated with well-known CYP2C9 inducers: the steroid hormone precursor dehydroepiandrosterone (DHEA) and the synthetic glucocorticoid dexamethasone (DXM).	Dexamethasone	247-260	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
20167002-5	2009	As an example, we present modelling and simulation approaches of the CYP2C9 gene expression in human hepatocytes treated with well-known CYP2C9 inducers: the steroid hormone precursor dehydroepiandrosterone (DHEA) and the synthetic glucocorticoid dexamethasone (DXM).	Dexamethasone	247-260	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
20167002-5	2009	As an example, we present modelling and simulation approaches of the CYP2C9 gene expression in human hepatocytes treated with well-known CYP2C9 inducers: the steroid hormone precursor dehydroepiandrosterone (DHEA) and the synthetic glucocorticoid dexamethasone (DXM).	Dexamethasone	262-265	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
20043560-3	2009	Vitamin K epoxide reductase (VKORC1) and cytochrome P450 2C9 (CYP2C9) enzyme conjointly determine the warfarin maintenance dose.	Warfarin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-60
20043560-3	2009	Vitamin K epoxide reductase (VKORC1) and cytochrome P450 2C9 (CYP2C9) enzyme conjointly determine the warfarin maintenance dose.	Warfarin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
19958586-1	2009	OBJECTIVES: It has been reported that hepatic cytochrome P450 (CYP)2C9 and CYP3A4 are responsible for the metabolism of sildenafil and formation of its metabolite, N-desmethylsildenafil, in humans.	Sildenafil Citrate	164-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-70
19955245-4	2009	For the 189 Mayo Clinic patients initiating warfarin therapy to achieve a target international normalized ratio (INR) in the range of 2.0 to 3.5, we analyzed the CYP2C9 (cytochrome P450 2C9) and VKORC1 (vitamin K epoxide reductase complex, subunit 1) genetic loci to study the relationship among the initial warfarin dose, steady-state dose, time to achieve steady-state dose, variations in INR, and allelic variance.	Warfarin	44-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
19955245-4	2009	For the 189 Mayo Clinic patients initiating warfarin therapy to achieve a target international normalized ratio (INR) in the range of 2.0 to 3.5, we analyzed the CYP2C9 (cytochrome P450 2C9) and VKORC1 (vitamin K epoxide reductase complex, subunit 1) genetic loci to study the relationship among the initial warfarin dose, steady-state dose, time to achieve steady-state dose, variations in INR, and allelic variance.	Warfarin	44-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-189
19955245-9	2009	Polymorphisms in CYP2C9 and VKORC1 have a considerable effect on warfarin dose in white people.	Warfarin	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
19958090-2	2009	Polymorphisms in CYP2C9 and VKORC1 have been shown to be associated with warfarin dose requirements.	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
19955245-10	2009	A correlation between steady-state warfarin dose and allelic variants of CYP2C9 and VKORC1 has been demonstrated by many previous reports and is reconfirmed in this report.	Warfarin	35-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
19881396-1	2009	OBJECTIVE: Variants of two genes, CYP2C9 and VKORC1, explain approximately one third of variability in warfarin maintenance dose requirements.	Warfarin	103-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
19881396-10	2009	CONCLUSION: Our initial results imply that pharmacogenomic-guided warfarin dosing may be more useful in settings with less intensive patient follow-up, and when adjustments are made for slower therapeutic response in patients with a CYP2C9 variant.	Warfarin	66-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	233-239
22478935-11	2009	Drug-drug interactions with other substrates of CYP2C9, CYP2C19, and CYP3A4 can also alter voriconazole concentrations.	Voriconazole	91-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
19843839-8	2009	Although the exact mechanism of the interaction is unknown, one theory is that tamoxifen inhibits CYP2C9, which metabolizes the S-isomer of warfarin.	Tamoxifen	79-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
19843839-8	2009	Although the exact mechanism of the interaction is unknown, one theory is that tamoxifen inhibits CYP2C9, which metabolizes the S-isomer of warfarin.	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
19663817-1	2009	Fluvastatin has been considered to be metabolised to 5-hydroxy fluvastatin (M-2), 6-hydroxy fluvastatin (M-3) and N-desisopropyl fluvastatin (M-5) in human liver microsomes by primarily CYP2C9.	Fluvastatin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	186-192
20214591-4	2009	Among the enzymes involved in aspirin biodisposition a major role is played by the enzymes UDP-glucuronosyltransferase UGT1A6, cytochrome P450 CYP2C9 and the xenobiotic/medium chain fatty acid:CoA ligase ACSM2, although other UGTs and ACSMs enzymes may significantly contribute to aspirin metabolism.	Aspirin	30-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
20214591-4	2009	Among the enzymes involved in aspirin biodisposition a major role is played by the enzymes UDP-glucuronosyltransferase UGT1A6, cytochrome P450 CYP2C9 and the xenobiotic/medium chain fatty acid:CoA ligase ACSM2, although other UGTs and ACSMs enzymes may significantly contribute to aspirin metabolism.	Aspirin	281-288	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
20214591-7	2009	Major polymorphisms related to aspirin biodisposition are rs2070959, rs1105879 and rs6759892 for the UGT1A6 gene, rs1133607 for the ACSM2 gene, and rs1799853, rs1057910, rs28371686, rs9332131 and rs28371685 for the CYP2C9 gene.	Aspirin	31-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	215-221
19651758-8	2009	In contrast, activity of CYP2A6 (p = 0.001) and CYP2C9 (diclofenac, p = 0.0001; tolbutamide, p = 0.004) was significantly increased with NAFLD progression.	Tolbutamide	80-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
19582440-3	2009	PCR-based methods were performed to analyze genetic polymorphisms in the genes pharmacokinetically and pharmacodynamically related to warfarin reactions, including cytochrome P450 (CYP) 2C9, vitamin K epoxide reductase complex subunit 1 (VKORC1), gamma-glutamyl carboxylase (GGCX) and factor VII (FVII).	Warfarin	134-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	164-189
19582440-4	2009	RESULTS: The presence of CYP2C9*3 and VKORC1-1639G>A had a significant impact on the mean maintenance dose of warfarin (CYP2C9*1/*1 2.74 +/- 1.24 mg/day vs. *1/*3 and *3/*3 1.56 +/- 0.85 mg/day, P = 0.009; VKORC1-1639AA 2.42 +/- 0.95 mg/day vs. GA 3.71 +/- 1.43 mg/day vs. GG 7.25 +/- 0.35 mg/day, P < 0.001).	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
19582440-4	2009	RESULTS: The presence of CYP2C9*3 and VKORC1-1639G>A had a significant impact on the mean maintenance dose of warfarin (CYP2C9*1/*1 2.74 +/- 1.24 mg/day vs. *1/*3 and *3/*3 1.56 +/- 0.85 mg/day, P = 0.009; VKORC1-1639AA 2.42 +/- 0.95 mg/day vs. GA 3.71 +/- 1.43 mg/day vs. GG 7.25 +/- 0.35 mg/day, P < 0.001).	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
19582440-5	2009	In the multiple linear regression model, the combination of age, body surface area, and genotypes of CYP2C9*3 and VKORC1-1639G>A explained 54.8% of the variance in warfarin dose requirements.	Warfarin	167-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
19582440-6	2009	CONCLUSIONS: The influences of CYP2C9*3 and VKORC1-1639G>A on the maintenance dose of warfarin were well-defined in Japanese patients, while polymorphisms of GGCX and FVII did not affect it.	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
19651758-8	2009	In contrast, activity of CYP2A6 (p = 0.001) and CYP2C9 (diclofenac, p = 0.0001; tolbutamide, p = 0.004) was significantly increased with NAFLD progression.	Diclofenac	56-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
19891554-0	2009	Presence of CYP2C9*3 allele increases risk for hypoglycemia in Type 2 diabetic patients treated with sulfonylureas.	Sulfonylurea Compounds	101-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
19891554-2	2009	Impaired metabolism of sulfonylureas due to gene polymorphisms in the metabolic enzyme CYP2C9 might lead to hypoglycemia.	Sulfonylurea Compounds	23-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
19891554-3	2009	In the present study we explored the association of the CYP2C9 variant alleles CYP2C9*2 and CYP2C9*3 with the incidence of hypoglycemic events in diabetic patients receiving the sulfonylureas glimepiride and gliclazide.	Sulfonylurea Compounds	178-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
19891554-3	2009	In the present study we explored the association of the CYP2C9 variant alleles CYP2C9*2 and CYP2C9*3 with the incidence of hypoglycemic events in diabetic patients receiving the sulfonylureas glimepiride and gliclazide.	Sulfonylurea Compounds	178-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
19891554-3	2009	In the present study we explored the association of the CYP2C9 variant alleles CYP2C9*2 and CYP2C9*3 with the incidence of hypoglycemic events in diabetic patients receiving the sulfonylureas glimepiride and gliclazide.	Sulfonylurea Compounds	178-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
19891554-3	2009	In the present study we explored the association of the CYP2C9 variant alleles CYP2C9*2 and CYP2C9*3 with the incidence of hypoglycemic events in diabetic patients receiving the sulfonylureas glimepiride and gliclazide.	glimepiride	192-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
19891554-3	2009	In the present study we explored the association of the CYP2C9 variant alleles CYP2C9*2 and CYP2C9*3 with the incidence of hypoglycemic events in diabetic patients receiving the sulfonylureas glimepiride and gliclazide.	glimepiride	192-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
19891554-3	2009	In the present study we explored the association of the CYP2C9 variant alleles CYP2C9*2 and CYP2C9*3 with the incidence of hypoglycemic events in diabetic patients receiving the sulfonylureas glimepiride and gliclazide.	glimepiride	192-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
19891554-3	2009	In the present study we explored the association of the CYP2C9 variant alleles CYP2C9*2 and CYP2C9*3 with the incidence of hypoglycemic events in diabetic patients receiving the sulfonylureas glimepiride and gliclazide.	Gliclazide	208-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
19891554-9	2009	In a model adjusted for age, BMI, mean daily dose of sulfonylurea, duration of T2DM and renal function, CYP2C9*1/*3 genotype increased the hypoglycemia risk in response to sulfonylurea (odds ratio: 1.687; p = 0.011).	Sulfonylurea Compounds	53-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
19891554-9	2009	In a model adjusted for age, BMI, mean daily dose of sulfonylurea, duration of T2DM and renal function, CYP2C9*1/*3 genotype increased the hypoglycemia risk in response to sulfonylurea (odds ratio: 1.687; p = 0.011).	Sulfonylurea Compounds	172-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
19891554-11	2009	DISCUSSION & CONCLUSION: The presence of CYP2C9*3 appears to be protective for development of T2DM.	Adenosine Monophosphate	12-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
19891554-12	2009	Furthermore, in T2DM patients, CYP2C9*3 increases the risk of hypoglycemia when they are treated with sulfonylureas, possibly due to impaired metabolism of these drugs.	Sulfonylurea Compounds	102-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
19891554-13	2009	CYP2C9 genotyping might thus be a useful tool for predicting adverse effects caused by sulfonylureas and help clinicians in safer prescribing of oral hypoglycemic agents.	Sulfonylurea Compounds	87-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19484231-0	2009	Severely diminished response to vitamin K-treatment for self-inflicted warfarin intoxication in a patient genotyped as CYP2C9*3*3.	Vitamin K	32-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
19484231-0	2009	Severely diminished response to vitamin K-treatment for self-inflicted warfarin intoxication in a patient genotyped as CYP2C9*3*3.	Warfarin	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
19593208-6	2009	A suggestive finding of less pronounced ambulatory BP response to losartan in CYP2C9*1*3 patients with low-normal kidney function was made.	Losartan	66-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
19593208-0	2009	CYP2C9 genotype modifies activity of the renin-angiotensin-aldosterone system in hypertensive men.	Aldosterone	59-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
20073138-1	2009	Polymorphisms in the cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) genes significantly alter the effective warfarin dose.	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-40
20073138-1	2009	Polymorphisms in the cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) genes significantly alter the effective warfarin dose.	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
20073138-8	2009	Combinatorial genotyping of CYP2C9 and VKORC1 can allow for individualized dosing of warfarin among patients with gene polymorphisms, potentially reducing the risk of stroke or bleeding.	Warfarin	85-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
19578179-12	2009	Thus we confirmed earlier findings that acenocoumarol dosage mainly depends on polymorphisms in the VKORC1 and CYP2C9 genes.	Acenocoumarol	40-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
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 9	Homo sapiens	97-103
19593208-1	2009	BACKGROUND: Two variants of the CYP2C9 gene, CYP2C9*2 and CYP2C9*3, have been indicated to have impaired enzyme function, and thus suspected to reduce the formation of the active metabolite of losartan.	Losartan	193-201	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
19593208-1	2009	BACKGROUND: Two variants of the CYP2C9 gene, CYP2C9*2 and CYP2C9*3, have been indicated to have impaired enzyme function, and thus suspected to reduce the formation of the active metabolite of losartan.	Losartan	193-201	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
19593208-1	2009	BACKGROUND: Two variants of the CYP2C9 gene, CYP2C9*2 and CYP2C9*3, have been indicated to have impaired enzyme function, and thus suspected to reduce the formation of the active metabolite of losartan.	Losartan	193-201	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
19593208-7	2009	At baseline of the GENRES Study, CYP2C9*1*3 patients had significantly lower plasma renin activity and aldosterone levels than CYP2C9*1*1 patients (both P values 0.004).	Aldosterone	103-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
19593208-8	2009	In a replication study in patients with treatment-resistant hypertension, men with CYP2C9*3 allele also had lower plasma renin activity (P = 0.03) and aldosterone levels (P = 0.18).	Aldosterone	151-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
19593208-10	2009	CONCLUSION: The CYP2C9*3 allele was associated with lower activity of the renin-angiotensin-aldosterone system in hypertensive men, which may reflect a more efficient sodium reabsorption capacity.	Aldosterone	92-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
19593208-10	2009	CONCLUSION: The CYP2C9*3 allele was associated with lower activity of the renin-angiotensin-aldosterone system in hypertensive men, which may reflect a more efficient sodium reabsorption capacity.	Sodium	167-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
19541829-6	2009	For diclofenac 4"-hydroxylation, the intrinsic clearance was decreased markedly (by >80%) in CYP2C9.13, CYP2C9.30, and CYP2C9.33 and variably (63-76%) in CYP2C9.3, CYP2C9.26, and CYP2C9.28 due to increased K(m) and/or decreased V(max) values.	Diclofenac	4-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
19752777-1	2009	BACKGROUND: In this prospective cohort study, we have undertaken a comprehensive evaluation of clinical parameters along with variation in 29 genes (including CYP2C9 and VKORC1) to identify factors determining interindividual variability in warfarin response.	Warfarin	241-249	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
19604036-0	2009	Effects of the CYP2C9*13 allele on the pharmacokinetics of losartan in healthy male subjects.	Losartan	59-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
19604036-1	2009	The aim of the study was to determine the pharmacokinetics of losartan in relation to the CYP2C9*13 allele.	Losartan	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
19604036-7	2009	Compared with the subjects in the CYP2C9*1/*1 group, individuals carrying the CYP2C9*1/*13 genotype showed significantly a longer t(1/2) of losartan and E3174 and markedly increased the area under the curve (AUC) of losartan.	Losartan	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
19604036-7	2009	Compared with the subjects in the CYP2C9*1/*1 group, individuals carrying the CYP2C9*1/*13 genotype showed significantly a longer t(1/2) of losartan and E3174 and markedly increased the area under the curve (AUC) of losartan.	Losartan	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
19604036-7	2009	Compared with the subjects in the CYP2C9*1/*1 group, individuals carrying the CYP2C9*1/*13 genotype showed significantly a longer t(1/2) of losartan and E3174 and markedly increased the area under the curve (AUC) of losartan.	Losartan	216-224	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
19604036-7	2009	Compared with the subjects in the CYP2C9*1/*1 group, individuals carrying the CYP2C9*1/*13 genotype showed significantly a longer t(1/2) of losartan and E3174 and markedly increased the area under the curve (AUC) of losartan.	Losartan	216-224	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
19604036-9	2009	The ratio of AUC(E3174)/AUC(losartan) after losartan administration in the CYP2C9*1/*13 and CYP2C9*1/*3 groups was also statistically different from that in the CYP2C9*1/*1 group.	Losartan	28-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
19604036-10	2009	The data indicate that the presence of the CYP2C9*13 allele results in poor metabolism of losartan after a single oral dose.	Losartan	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
20031873-1	2009	BACKGROUND: CYP2C9 and VKORC1 genotyping has been advocated as a means of improving the accuracy of warfarin dosing.	Warfarin	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
19541829-8	2009	For glimepiride hydroxylation, the K(m) of CYP2C9.13 was increased 7-fold, and the V(max) values of all variants significantly decreased, resulting in reductions in the intrinsic clearance by >80% in CYP2C9.3, CYP2C9.13, CYP2C9.26, and CYP2C9.33 and by 56 to 75% in CYP2C9.28 and CYP2C9.30.	glimepiride	4-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	203-209
19541829-8	2009	For glimepiride hydroxylation, the K(m) of CYP2C9.13 was increased 7-fold, and the V(max) values of all variants significantly decreased, resulting in reductions in the intrinsic clearance by >80% in CYP2C9.3, CYP2C9.13, CYP2C9.26, and CYP2C9.33 and by 56 to 75% in CYP2C9.28 and CYP2C9.30.	glimepiride	4-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	203-209
19652664-1	2009	Cytochrome P450 2C9 (CYP2C9) enzymes metabolize warfarin and arachidonic acid.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
19652664-1	2009	Cytochrome P450 2C9 (CYP2C9) enzymes metabolize warfarin and arachidonic acid.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
19652664-1	2009	Cytochrome P450 2C9 (CYP2C9) enzymes metabolize warfarin and arachidonic acid.	Arachidonic Acid	61-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
19652664-1	2009	Cytochrome P450 2C9 (CYP2C9) enzymes metabolize warfarin and arachidonic acid.	Arachidonic Acid	61-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
19925388-1	2009	Human cytochrome P450 2C9 (CYP2C9) accounts for approximately 20% of total hepatic CYP content and metabolizes approximately 15% clinically used drugs including S-warfarin, tolbutamide, phenytoin, losartan, diclofenac, and celecoxib.	Warfarin	161-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-25
19925388-1	2009	Human cytochrome P450 2C9 (CYP2C9) accounts for approximately 20% of total hepatic CYP content and metabolizes approximately 15% clinically used drugs including S-warfarin, tolbutamide, phenytoin, losartan, diclofenac, and celecoxib.	Warfarin	161-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
19925388-1	2009	Human cytochrome P450 2C9 (CYP2C9) accounts for approximately 20% of total hepatic CYP content and metabolizes approximately 15% clinically used drugs including S-warfarin, tolbutamide, phenytoin, losartan, diclofenac, and celecoxib.	Tolbutamide	173-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-25
19925388-1	2009	Human cytochrome P450 2C9 (CYP2C9) accounts for approximately 20% of total hepatic CYP content and metabolizes approximately 15% clinically used drugs including S-warfarin, tolbutamide, phenytoin, losartan, diclofenac, and celecoxib.	Tolbutamide	173-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
19925388-1	2009	Human cytochrome P450 2C9 (CYP2C9) accounts for approximately 20% of total hepatic CYP content and metabolizes approximately 15% clinically used drugs including S-warfarin, tolbutamide, phenytoin, losartan, diclofenac, and celecoxib.	Phenytoin	186-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-25
19925388-1	2009	Human cytochrome P450 2C9 (CYP2C9) accounts for approximately 20% of total hepatic CYP content and metabolizes approximately 15% clinically used drugs including S-warfarin, tolbutamide, phenytoin, losartan, diclofenac, and celecoxib.	Phenytoin	186-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
19925388-1	2009	Human cytochrome P450 2C9 (CYP2C9) accounts for approximately 20% of total hepatic CYP content and metabolizes approximately 15% clinically used drugs including S-warfarin, tolbutamide, phenytoin, losartan, diclofenac, and celecoxib.	Losartan	197-205	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-25
19925388-1	2009	Human cytochrome P450 2C9 (CYP2C9) accounts for approximately 20% of total hepatic CYP content and metabolizes approximately 15% clinically used drugs including S-warfarin, tolbutamide, phenytoin, losartan, diclofenac, and celecoxib.	Losartan	197-205	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
19925388-1	2009	Human cytochrome P450 2C9 (CYP2C9) accounts for approximately 20% of total hepatic CYP content and metabolizes approximately 15% clinically used drugs including S-warfarin, tolbutamide, phenytoin, losartan, diclofenac, and celecoxib.	Diclofenac	207-217	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-25
19925388-1	2009	Human cytochrome P450 2C9 (CYP2C9) accounts for approximately 20% of total hepatic CYP content and metabolizes approximately 15% clinically used drugs including S-warfarin, tolbutamide, phenytoin, losartan, diclofenac, and celecoxib.	Diclofenac	207-217	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
19925388-1	2009	Human cytochrome P450 2C9 (CYP2C9) accounts for approximately 20% of total hepatic CYP content and metabolizes approximately 15% clinically used drugs including S-warfarin, tolbutamide, phenytoin, losartan, diclofenac, and celecoxib.	Celecoxib	223-232	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-25
19925388-1	2009	Human cytochrome P450 2C9 (CYP2C9) accounts for approximately 20% of total hepatic CYP content and metabolizes approximately 15% clinically used drugs including S-warfarin, tolbutamide, phenytoin, losartan, diclofenac, and celecoxib.	Celecoxib	223-232	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
19925388-8	2009	Numerous clinical studies have shown that the CYP2C9 polymorphism should be considered in warfarin therapy and practical algorithms how to consider it in therapy are available.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
19925388-11	2009	Polymorphisms in CYP2C9 have the potential to affect the toxicity of CYP2C9 drugs with somewhat lower therapeutic indices such as warfarin, phenytoin, and certain antidiabetic drugs.	Warfarin	130-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
19541829-6	2009	For diclofenac 4"-hydroxylation, the intrinsic clearance was decreased markedly (by >80%) in CYP2C9.13, CYP2C9.30, and CYP2C9.33 and variably (63-76%) in CYP2C9.3, CYP2C9.26, and CYP2C9.28 due to increased K(m) and/or decreased V(max) values.	Diclofenac	4-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
19541829-6	2009	For diclofenac 4"-hydroxylation, the intrinsic clearance was decreased markedly (by >80%) in CYP2C9.13, CYP2C9.30, and CYP2C9.33 and variably (63-76%) in CYP2C9.3, CYP2C9.26, and CYP2C9.28 due to increased K(m) and/or decreased V(max) values.	Diclofenac	4-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
19541829-6	2009	For diclofenac 4"-hydroxylation, the intrinsic clearance was decreased markedly (by >80%) in CYP2C9.13, CYP2C9.30, and CYP2C9.33 and variably (63-76%) in CYP2C9.3, CYP2C9.26, and CYP2C9.28 due to increased K(m) and/or decreased V(max) values.	Diclofenac	4-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
19925388-11	2009	Polymorphisms in CYP2C9 have the potential to affect the toxicity of CYP2C9 drugs with somewhat lower therapeutic indices such as warfarin, phenytoin, and certain antidiabetic drugs.	Warfarin	130-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
19541829-6	2009	For diclofenac 4"-hydroxylation, the intrinsic clearance was decreased markedly (by >80%) in CYP2C9.13, CYP2C9.30, and CYP2C9.33 and variably (63-76%) in CYP2C9.3, CYP2C9.26, and CYP2C9.28 due to increased K(m) and/or decreased V(max) values.	Diclofenac	4-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
19925388-11	2009	Polymorphisms in CYP2C9 have the potential to affect the toxicity of CYP2C9 drugs with somewhat lower therapeutic indices such as warfarin, phenytoin, and certain antidiabetic drugs.	Phenytoin	140-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
19925388-11	2009	Polymorphisms in CYP2C9 have the potential to affect the toxicity of CYP2C9 drugs with somewhat lower therapeutic indices such as warfarin, phenytoin, and certain antidiabetic drugs.	Phenytoin	140-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
19541829-6	2009	For diclofenac 4"-hydroxylation, the intrinsic clearance was decreased markedly (by >80%) in CYP2C9.13, CYP2C9.30, and CYP2C9.33 and variably (63-76%) in CYP2C9.3, CYP2C9.26, and CYP2C9.28 due to increased K(m) and/or decreased V(max) values.	Diclofenac	4-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
19541829-7	2009	For losartan oxidation, CYP2C9.13 and CYP2C9.28 showed 2.5- and 1.8-fold higher K(m) values, respectively, and all variants except for CYP2C9.34 showed >77% lower V(max) and intrinsic clearance values.	Losartan	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
19541829-7	2009	For losartan oxidation, CYP2C9.13 and CYP2C9.28 showed 2.5- and 1.8-fold higher K(m) values, respectively, and all variants except for CYP2C9.34 showed >77% lower V(max) and intrinsic clearance values.	Losartan	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
19541829-7	2009	For losartan oxidation, CYP2C9.13 and CYP2C9.28 showed 2.5- and 1.8-fold higher K(m) values, respectively, and all variants except for CYP2C9.34 showed >77% lower V(max) and intrinsic clearance values.	Losartan	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
19541829-8	2009	For glimepiride hydroxylation, the K(m) of CYP2C9.13 was increased 7-fold, and the V(max) values of all variants significantly decreased, resulting in reductions in the intrinsic clearance by >80% in CYP2C9.3, CYP2C9.13, CYP2C9.26, and CYP2C9.33 and by 56 to 75% in CYP2C9.28 and CYP2C9.30.	glimepiride	4-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
19541829-8	2009	For glimepiride hydroxylation, the K(m) of CYP2C9.13 was increased 7-fold, and the V(max) values of all variants significantly decreased, resulting in reductions in the intrinsic clearance by >80% in CYP2C9.3, CYP2C9.13, CYP2C9.26, and CYP2C9.33 and by 56 to 75% in CYP2C9.28 and CYP2C9.30.	glimepiride	4-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	203-209
19541829-8	2009	For glimepiride hydroxylation, the K(m) of CYP2C9.13 was increased 7-fold, and the V(max) values of all variants significantly decreased, resulting in reductions in the intrinsic clearance by >80% in CYP2C9.3, CYP2C9.13, CYP2C9.26, and CYP2C9.33 and by 56 to 75% in CYP2C9.28 and CYP2C9.30.	glimepiride	4-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	203-209
19541829-8	2009	For glimepiride hydroxylation, the K(m) of CYP2C9.13 was increased 7-fold, and the V(max) values of all variants significantly decreased, resulting in reductions in the intrinsic clearance by >80% in CYP2C9.3, CYP2C9.13, CYP2C9.26, and CYP2C9.33 and by 56 to 75% in CYP2C9.28 and CYP2C9.30.	glimepiride	4-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	203-209
19541829-8	2009	For glimepiride hydroxylation, the K(m) of CYP2C9.13 was increased 7-fold, and the V(max) values of all variants significantly decreased, resulting in reductions in the intrinsic clearance by >80% in CYP2C9.3, CYP2C9.13, CYP2C9.26, and CYP2C9.33 and by 56 to 75% in CYP2C9.28 and CYP2C9.30.	glimepiride	4-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	203-209
19669737-0	2009	CYP2C9 genotype and pharmacodynamic responses to losartan in patients with primary and secondary kidney diseases.	Losartan	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19669737-4	2009	AIM: The study aims were to determine whether CYP2C9 variant alleles (*2 and *3) altered urinary protein excretion, glomerular filtration rate, and blood pressure in Caucasian patients prescribed losartan.	Losartan	196-204	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
19669737-8	2009	CONCLUSION: These preliminary results suggest a possible influence of CYP2C9 genotype on proteinuria and blood pressure in Caucasian CKD patients treated with losartan.	Losartan	159-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
19998810-6	2009	The genetic variants c.430CC and c.1075AA of the CYP2C9 gene were identified, predisposing to rapid warfarin metabolism, as well as the c.-1639GG variant of the VKORC1 gene, associated with low sensitivity to the drug.	Warfarin	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
19698014-11	2009	Prasugrel does not appear to interact to any clinically relevant extent with other drugs, including those also metabolized by the hepatic cytochrome P450 isoenzymes CYP3A4, CYP2C9, CYP2C19, and CYP2B6, which are responsible for prasugrel metabolism.	Prasugrel Hydrochloride	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	173-179
19761365-4	2009	MATERIALS & METHODS: Seven polymorphic variations in four genes that encode enzymes from phase I (CYP2C9, CYP3A4 and CYP3A5) or phase III (ABCB1) of drug metabolism were analyzed in population samples from Cabinda (n = 107), Mozambique (n = 109) and Sao Tome e Principe (n = 126).	Adenosine Monophosphate	11-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
19761366-0	2009	Effects of genetic variation at the CYP2C19/CYP2C9 locus on pharmacokinetics of chlorcycloguanil in adult Gambians.	cycloguanil	80-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
19761366-2	2009	MATERIALS & METHODS: Polymorphisms in CYP2C19 and CYP2C9 in 43 adult Gambians treated with chlorproguanil/dapsone for uncomplicated malaria were assessed.	Dapsone	110-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
19761366-7	2009	CONCLUSION: CYP2C19*17 determines antimalarial biguanide metabolic profile at the CYP2C19/CYP2C9 locus.	Biguanides	47-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
19694738-1	2009	AIM: To investigate a potential interaction between cranberry juice and diclofenac, a substrate of CYP2C9.	Diclofenac	72-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
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 9	Homo sapiens	88-94
19899329-0	2009	CYP2C9 gene analysis of some Iranian hypersensitive patients to warfarin.	Warfarin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19899329-1	2009	For the first time in this study, the pharmacogenetic effects of CYP2C9 polymorphism on warfarin sensitivity in some Iranian patients who are on warfarin treatment were shown.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
19899329-1	2009	For the first time in this study, the pharmacogenetic effects of CYP2C9 polymorphism on warfarin sensitivity in some Iranian patients who are on warfarin treatment were shown.	Warfarin	145-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
19702548-1	2009	The present study demonstrated that in addition to CYP3A4 and CYP2D6, the metabolism of loratadine is also catalyzed by CYP1A1, CYP2C19, and to a lesser extent by CYP1A2, CYP2B6, CYP2C8, CYP2C9 and CYP3A5.	Loratadine	88-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	187-193
19448135-6	2009	CYP2D6 coincubation inhibited CYP2C9-mediated (S)-flurbiprofen metabolism in a protein concentration-dependent manner.	Flurbiprofen	46-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
19448135-8	2009	Spectral binding studies revealed a 20-fold increase in the K(S) of CYP2C9 toward (S)-flurbiprofen in the presence of CYP2D6.	Flurbiprofen	82-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
19454483-1	2009	17alpha-Ethinyl estradiol (EE) was systematically evaluated as a reversible and time-dependent inhibitor of 11 human drug-metabolizing cytochromes P450 (P450s) (CYP1A1, CYP1A2, CYP1B1, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2J2, CYP3A4, and CYP3A5) in vitro.	Ethinyl Estradiol	0-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	201-207
19453939-1	2009	BACKGROUND: Polymorphisms in the VKORC1 and CYP2C9 genes influence warfarin requirements.	Warfarin	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
19297219-0	2009	Influence of CYP2C9 and VKORC1 on warfarin response during initiation of therapy.	Warfarin	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
18629445-9	2009	Mean phenprocoumon dosage per week to achieve therapeutic anticoagulation was lower (higher) in patients with than without the VKORC1 polymorphism -1639G > A (3730G > A) or the CYP2C9 polymorphisms.	Phenprocoumon	5-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	183-189
19663669-1	2009	AIMS: Although the frequencies of pharmacogenetic variants differ among racial groups, most pharmacogenetic algorithms for genotype-guided warfarin dosing only include two CYP2C9 alleles (*2 and *3) and a single VKORC1 allele (g.-1639G>A or g.1173C>T) commonly found among Caucasians.	Warfarin	139-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
19663669-2	2009	Therefore, this study sought to identify other CYP2C9 and VKORC1 alleles important in warfarin dose variability and to determine their frequencies in different racial and ethnic groups.	Warfarin	86-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
19663669-3	2009	MATERIALS & METHODS: The CYP2C9 and VKORC1 genes were sequenced in selected sensitive (< 21 mg/week) and resistant (> 49 mg/week) individuals with discrepant therapeutic and algorithm-predicted warfarin doses based on prior CYP2C9 and VKORC1 genotyping.	Warfarin	204-212	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
19663669-5	2009	RESULTS: Sequencing identified an African-American male with a lower than predicted therapeutic warfarin dose (14.4 mg/week), previously genotyped as CYP2C9*1/*1, who was homozygous for CYP2C9*8 (c.449G>A; p.R150H).	Warfarin	96-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
19663669-5	2009	RESULTS: Sequencing identified an African-American male with a lower than predicted therapeutic warfarin dose (14.4 mg/week), previously genotyped as CYP2C9*1/*1, who was homozygous for CYP2C9*8 (c.449G>A; p.R150H).	Warfarin	96-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	186-192
19663669-10	2009	Thus, in this racial group, the incorporation of CYP2C9*8 into genotyping panels may improve dose prediction of CYP2C9-metabolized drugs, including warfarin.	Warfarin	148-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
19663669-10	2009	Thus, in this racial group, the incorporation of CYP2C9*8 into genotyping panels may improve dose prediction of CYP2C9-metabolized drugs, including warfarin.	Warfarin	148-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
20140106-3	2009	Achieving safe and effective doses of warfarin therapy is both an urgent and important concern for many clinicians.Recent research has focused on single-nucleotide polymorphisms (SNPs) of genes that encode two proteins: the cytochrome P450 2C9 enzyme and VKORC1 (vitamin K epoxide reductase complex).	Warfarin	38-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	224-243
20140106-4	2009	Studies suggest that CYP 2C9 influences warfarin metabolism, whereas VKORC1 plays a role in the pharmacodynamic response in expression of the enzymatic target of warfarin.	Warfarin	40-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-28
20140106-5	2009	Patients who carry CYP 2C9*2 and CYP 2C9*3 alleles tend to require lower warfarin maintenance doses because of their slowed metabolism compared with patients who carry the "wild-type" allele.	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-26
20140106-5	2009	Patients who carry CYP 2C9*2 and CYP 2C9*3 alleles tend to require lower warfarin maintenance doses because of their slowed metabolism compared with patients who carry the "wild-type" allele.	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-40
19297219-1	2009	BACKGROUND: Although multiple reports have documented the influence of CYP2C9 and VKORC1 variants on warfarin dose, risk of over-anticoagulation and hemorrhage, their influence on anticoagulation maintenance and individual proportion of time spent in target INR range (PPTR) is limited.	Warfarin	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
19297219-3	2009	Herein we present the influence of CYP2C9 and VKORC1 C1173T on warfarin response during the first 30 days of therapy.	Warfarin	63-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
19291087-10	2009	We conclude that a NO- and PGI(2)-independent vasodilator mechanism, potentially attributable to EDHF, contributes substantialy to the ACh-induced vasodilatation in human skin microcirculation and that it is probably not a CYP 2C9-derived metabolite.	Acetylcholine	135-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	223-230
19501215-1	2009	BACKGROUND: Etravirine, a non-nucleoside reverse transcriptase inhibitor (NNRTI) active against NNRTI-resistant HIV, is an inducer of CYP3A4 and an inhibitor of CYP2C9/19.	etravirine	12-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
19369937-3	2009	In 130 volunteers, CYP2C9 activity was measured in vivo using tolbutamide as a probe drug.	Tolbutamide	62-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
19464879-0	2009	R(+)XK469 inhibits hydroxylation of S-warfarin by CYP2C9.	Sulfur	36-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
19369937-9	2009	But the difference in activity levels between the CYP2C9*1/*1 and *3/*3 genotypes before the administration of rifampin was sixfold.	Rifampin	111-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
19799531-5	2009	S-warfarin, predominantly responsible for the anticoagulation effect, is metabolized mostly by the CYP2C9 enzyme.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
19339377-11	2009	Taken together, glucuronidation of cannabinoids depends on upstream processing including enzymes such as CYP2C9 and CYP3A4.	Cannabinoids	35-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
19464879-0	2009	R(+)XK469 inhibits hydroxylation of S-warfarin by CYP2C9.	Warfarin	38-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
19464879-1	2009	INTRODUCTION: XK469 is a novel topoisomerase II inhibitor structurally akin to several propionic acid derivatives, such as ibuprofen and diclofenac, which are metabolised by CYP2C9.	propionic acid	87-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	174-180
19464879-1	2009	INTRODUCTION: XK469 is a novel topoisomerase II inhibitor structurally akin to several propionic acid derivatives, such as ibuprofen and diclofenac, which are metabolised by CYP2C9.	Ibuprofen	123-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	174-180
19464879-1	2009	INTRODUCTION: XK469 is a novel topoisomerase II inhibitor structurally akin to several propionic acid derivatives, such as ibuprofen and diclofenac, which are metabolised by CYP2C9.	Diclofenac	137-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	174-180
19464879-3	2009	The aim of the study is to investigate whether R(+)XK469 interacts with S-warfarin by inhibition of CYP2C9.	Warfarin	72-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
19464879-8	2009	This suggests that coadministration of R(+)XK469 and warfarin results in a clinically significant pharmacokinetic interaction due to CYP2C9 inhibition by R(+)XK469.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
19589229-9	2009	CONCLUSIONS: Fluorophenylpiperazine, methoxyphenylpiperazine, chlorophenylpiperazine, methylbenzylpiperazine and methylenedioxybenzylpiperazine had significant inhibitory effects on CYP2D6, CYP1A2, CYP3A4, CYP2C19 and CYP2C9 isoenzymes but each piperazine had a different inhibitory profile.	diethyl 4-methylbenzylphosphonate	86-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
19525490-8	2009	Fluorogenic assays with CYP3A4, CYP2C9, and CYP2D6 on the alginate microarrays exhibited Z" factors ranging from 0.75 to 0.85, sensitive detection of inhibitory compounds, and reactivity comparable to that in solution, thereby demonstrating the reliability and accuracy of the microarray platform.	Alginates	58-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
19589229-9	2009	CONCLUSIONS: Fluorophenylpiperazine, methoxyphenylpiperazine, chlorophenylpiperazine, methylbenzylpiperazine and methylenedioxybenzylpiperazine had significant inhibitory effects on CYP2D6, CYP1A2, CYP3A4, CYP2C19 and CYP2C9 isoenzymes but each piperazine had a different inhibitory profile.	fluorophenylpiperazine	13-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
19589229-9	2009	CONCLUSIONS: Fluorophenylpiperazine, methoxyphenylpiperazine, chlorophenylpiperazine, methylbenzylpiperazine and methylenedioxybenzylpiperazine had significant inhibitory effects on CYP2D6, CYP1A2, CYP3A4, CYP2C19 and CYP2C9 isoenzymes but each piperazine had a different inhibitory profile.	methoxyphenylpiperazine	37-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
19589229-9	2009	CONCLUSIONS: Fluorophenylpiperazine, methoxyphenylpiperazine, chlorophenylpiperazine, methylbenzylpiperazine and methylenedioxybenzylpiperazine had significant inhibitory effects on CYP2D6, CYP1A2, CYP3A4, CYP2C19 and CYP2C9 isoenzymes but each piperazine had a different inhibitory profile.	Piperazine	25-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
19589229-9	2009	CONCLUSIONS: Fluorophenylpiperazine, methoxyphenylpiperazine, chlorophenylpiperazine, methylbenzylpiperazine and methylenedioxybenzylpiperazine had significant inhibitory effects on CYP2D6, CYP1A2, CYP3A4, CYP2C19 and CYP2C9 isoenzymes but each piperazine had a different inhibitory profile.	chlorophenylpiperazine	62-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
19458107-1	2009	BACKGROUND: osartan is metabolized by CYP2C9 and CYP3A4 to an active metabolite, E-3174, which has greater antihypertensive activity than the parent compound.	osartan	12-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
19496669-6	2009	RESULTS: A concentration-dependent decrease in luminescence signal was detected for ibuprofen and diclofenac in the assay for CYP 2C9 in human and equine liver microsomes but not in the assay for CYP 3A4 and methadone or xylazine in any of the species.	Ibuprofen	84-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-133
19496669-6	2009	RESULTS: A concentration-dependent decrease in luminescence signal was detected for ibuprofen and diclofenac in the assay for CYP 2C9 in human and equine liver microsomes but not in the assay for CYP 3A4 and methadone or xylazine in any of the species.	Diclofenac	98-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-133
19479657-2	2009	The cytochrome P450 (CYP)2C9 and vitamin K epoxide reductase complex 1 (VKORC1) genes have recently been determined to be associated with warfarin dose requirements, with reduced doses of this drug being required in patients with the variant CYP2C9*2, CYP2C9*3, or VKORC1 -1639A allele.	Warfarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-28
19378397-4	2009	With cisplatin and oxaliplatin, a minor inhibition of CYP2C9 enzyme (75% of control at 400 miromol/l of these complexes) was seen; cisplatin also inhibited slightly the CYP2B6 activity (85% of control).	Cisplatin	5-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
19378397-4	2009	With cisplatin and oxaliplatin, a minor inhibition of CYP2C9 enzyme (75% of control at 400 miromol/l of these complexes) was seen; cisplatin also inhibited slightly the CYP2B6 activity (85% of control).	Oxaliplatin	19-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
19378397-4	2009	With cisplatin and oxaliplatin, a minor inhibition of CYP2C9 enzyme (75% of control at 400 miromol/l of these complexes) was seen; cisplatin also inhibited slightly the CYP2B6 activity (85% of control).	miromol	91-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
19378397-9	2009	Interestingly, clinically non-significant inhibition was found with the CYP2C9 and CYP2C8 indicating low probability of interactions with, for example, warfarin.	Warfarin	152-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
19251823-5	2009	Olomoucine II significantly inhibited the enzymatic activities of CYP1A2, CYP2C9, and (to a lesser degree) CYP3A4.	olomoucine II	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
19251823-6	2009	The results indicate that use of olomoucine II as a drug could affect the activities of CYP3A4, CYP1A2, and CYP2C9 in vivo.	olomoucine II	33-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
19221727-4	2009	RESULTS: The area under the plasma concentration-time curve (AUC) of losartan increased significantly following a 14-day silymarin treatment in subjects with the CYP2C9*1/*1 genotype, but not in those with the CYP2C9*1/*3 genotype.	Losartan	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
19221727-4	2009	RESULTS: The area under the plasma concentration-time curve (AUC) of losartan increased significantly following a 14-day silymarin treatment in subjects with the CYP2C9*1/*1 genotype, but not in those with the CYP2C9*1/*3 genotype.	Losartan	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	210-216
19221727-4	2009	RESULTS: The area under the plasma concentration-time curve (AUC) of losartan increased significantly following a 14-day silymarin treatment in subjects with the CYP2C9*1/*1 genotype, but not in those with the CYP2C9*1/*3 genotype.	Silymarin	121-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
19221727-5	2009	The AUC of E-3174 decreased significantly with a silymarin pretreatment in both CYP2C9*1/*1 and the CYP2C9*1/*3 subjects.	losartan carboxylic acid	11-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
19221727-5	2009	The AUC of E-3174 decreased significantly with a silymarin pretreatment in both CYP2C9*1/*1 and the CYP2C9*1/*3 subjects.	losartan carboxylic acid	11-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
19221727-5	2009	The AUC of E-3174 decreased significantly with a silymarin pretreatment in both CYP2C9*1/*1 and the CYP2C9*1/*3 subjects.	Silymarin	49-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
19221727-5	2009	The AUC of E-3174 decreased significantly with a silymarin pretreatment in both CYP2C9*1/*1 and the CYP2C9*1/*3 subjects.	Silymarin	49-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
19221727-6	2009	The metabolic ratio of losartan (ratio of AUC(0-infinity) of E-3174 to AUC(0-infinity) of losartan) decreased significantly after a 14-day treatment with silymarin in individuals with the CYP2C9*1/*1 genotype (p < 0.05), but not in those with the CYP2C9*1/*3 genotype (p = 0.065).	Losartan	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	188-194
19221727-6	2009	The metabolic ratio of losartan (ratio of AUC(0-infinity) of E-3174 to AUC(0-infinity) of losartan) decreased significantly after a 14-day treatment with silymarin in individuals with the CYP2C9*1/*1 genotype (p < 0.05), but not in those with the CYP2C9*1/*3 genotype (p = 0.065).	Losartan	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	250-256
19221727-6	2009	The metabolic ratio of losartan (ratio of AUC(0-infinity) of E-3174 to AUC(0-infinity) of losartan) decreased significantly after a 14-day treatment with silymarin in individuals with the CYP2C9*1/*1 genotype (p < 0.05), but not in those with the CYP2C9*1/*3 genotype (p = 0.065).	Silymarin	154-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	188-194
19221727-6	2009	The metabolic ratio of losartan (ratio of AUC(0-infinity) of E-3174 to AUC(0-infinity) of losartan) decreased significantly after a 14-day treatment with silymarin in individuals with the CYP2C9*1/*1 genotype (p < 0.05), but not in those with the CYP2C9*1/*3 genotype (p = 0.065).	Silymarin	154-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	250-256
19221727-7	2009	CONCLUSION: Silymarin inhibits the metabolism of losartan to E-3174, with the magnitude of the interaction differing in individuals with different CYP2C9 genotypes.	Silymarin	12-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
19479657-2	2009	The cytochrome P450 (CYP)2C9 and vitamin K epoxide reductase complex 1 (VKORC1) genes have recently been determined to be associated with warfarin dose requirements, with reduced doses of this drug being required in patients with the variant CYP2C9*2, CYP2C9*3, or VKORC1 -1639A allele.	Warfarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	242-248
19479657-2	2009	The cytochrome P450 (CYP)2C9 and vitamin K epoxide reductase complex 1 (VKORC1) genes have recently been determined to be associated with warfarin dose requirements, with reduced doses of this drug being required in patients with the variant CYP2C9*2, CYP2C9*3, or VKORC1 -1639A allele.	Warfarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	252-258
19479657-4	2009	Racial differences in the association between genotype and a patient"s response to warfarin treatment may be caused by racial differences in the frequencies of the variant CYP2C9*2, CYP2C9*3, and VKORC1 -1639A alleles or by the influence of non-genetic factors.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
19233181-0	2009	Cytochrome P450 2C9 variants influence response to celecoxib for prevention of colorectal adenoma.	Celecoxib	51-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
19479657-4	2009	Racial differences in the association between genotype and a patient"s response to warfarin treatment may be caused by racial differences in the frequencies of the variant CYP2C9*2, CYP2C9*3, and VKORC1 -1639A alleles or by the influence of non-genetic factors.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	182-188
19233181-1	2009	BACKGROUND & AIMS: Variants in the cytochrome P450 2C9 (CYP2C9) gene are associated with impaired metabolism of celecoxib.	Adenosine Monophosphate	12-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-58
19258521-2	2009	Although it is well established that CYP2C9 is the major cytochrome P450 enzyme controlling metabolic elimination of phenytoin through its oxidative conversion to (S)-5-(4-hydroxyphenyl)-5-phenylhydantoin (p-HPPH), nothing is known about the amino acid binding determinants within the CYP2C9 active site that promote metabolism and maintain the tight stereocontrol of hydroxy metabolite formation.	p-hpph	206-212	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
19233181-1	2009	BACKGROUND & AIMS: Variants in the cytochrome P450 2C9 (CYP2C9) gene are associated with impaired metabolism of celecoxib.	Adenosine Monophosphate	12-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
19233181-1	2009	BACKGROUND & AIMS: Variants in the cytochrome P450 2C9 (CYP2C9) gene are associated with impaired metabolism of celecoxib.	Celecoxib	116-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-58
19233181-1	2009	BACKGROUND & AIMS: Variants in the cytochrome P450 2C9 (CYP2C9) gene are associated with impaired metabolism of celecoxib.	Celecoxib	116-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
19233181-10	2009	CONCLUSIONS: The greater efficacy of high-dose celecoxib, compared with the low-dose, in preventing colorectal adenoma appears confined to individuals with slow metabolizer (CYP2C9*3) genotypes.	Celecoxib	47-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	174-180
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	aceclofenac	169-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	aceclofenac	169-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	Celecoxib	182-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	Celecoxib	182-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	Diclofenac	193-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	Diclofenac	193-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	Ibuprofen	205-214	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	Ibuprofen	205-214	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	Indomethacin	216-229	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	Indomethacin	216-229	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	lornoxicam	231-241	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	lornoxicam	231-241	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	Meloxicam	243-252	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	Meloxicam	243-252	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	Naproxen	254-262	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	Naproxen	254-262	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	Piroxicam	264-273	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	Piroxicam	264-273	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	tenoxicam	275-284	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	tenoxicam	275-284	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	valdecoxib	289-299	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
19422321-1	2009	Polymorphisms in CYP2C8 and CYP2C9 are common in all the human populations and many CYP2C8 and CYP2C9 gene variations cause decreased enzyme activity towards the NSAIDs aceclofenac, celecoxib, diclofenac, ibuprofen, indomethazine, lornoxicam, meloxicam, naproxen, piroxicam, tenoxicam and valdecoxib.	valdecoxib	289-299	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
19258521-0	2009	CYP2C9 amino acid residues influencing phenytoin turnover and metabolite regio- and stereochemistry.	Phenytoin	39-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19258521-2	2009	Although it is well established that CYP2C9 is the major cytochrome P450 enzyme controlling metabolic elimination of phenytoin through its oxidative conversion to (S)-5-(4-hydroxyphenyl)-5-phenylhydantoin (p-HPPH), nothing is known about the amino acid binding determinants within the CYP2C9 active site that promote metabolism and maintain the tight stereocontrol of hydroxy metabolite formation.	Phenytoin	117-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
19258521-2	2009	Although it is well established that CYP2C9 is the major cytochrome P450 enzyme controlling metabolic elimination of phenytoin through its oxidative conversion to (S)-5-(4-hydroxyphenyl)-5-phenylhydantoin (p-HPPH), nothing is known about the amino acid binding determinants within the CYP2C9 active site that promote metabolism and maintain the tight stereocontrol of hydroxy metabolite formation.	Phenytoin	117-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	285-291
19258521-2	2009	Although it is well established that CYP2C9 is the major cytochrome P450 enzyme controlling metabolic elimination of phenytoin through its oxidative conversion to (S)-5-(4-hydroxyphenyl)-5-phenylhydantoin (p-HPPH), nothing is known about the amino acid binding determinants within the CYP2C9 active site that promote metabolism and maintain the tight stereocontrol of hydroxy metabolite formation.	hydroxyphenytoin	163-204	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
19258521-2	2009	Although it is well established that CYP2C9 is the major cytochrome P450 enzyme controlling metabolic elimination of phenytoin through its oxidative conversion to (S)-5-(4-hydroxyphenyl)-5-phenylhydantoin (p-HPPH), nothing is known about the amino acid binding determinants within the CYP2C9 active site that promote metabolism and maintain the tight stereocontrol of hydroxy metabolite formation.	p-hpph	206-212	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	285-291
19258521-5	2009	This pattern of effects differs substantially from that found previously for (S)-warfarin and (S)-flurbiprofen metabolism, suggesting that these three ligands bind within discrete locations in the CYP2C9 active site.	Warfarin	77-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
19258521-5	2009	This pattern of effects differs substantially from that found previously for (S)-warfarin and (S)-flurbiprofen metabolism, suggesting that these three ligands bind within discrete locations in the CYP2C9 active site.	Flurbiprofen	94-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
19662888-2	2009	The application of pharmacogenetics in testing individual polymorphisms of two genes CYP 2C9 (pharmacokinetics of warfarin) and VKORC1 (sensitivity on warfarin) is promising tactics leading to a safe anticoagulation.	Warfarin	114-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-92
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.	Benzo(a)pyrene	27-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
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
19480553-0	2009	Pharmacokinetic studies of enantiomers of ibuprofen and its chiral metabolites in humans with different variants of genes coding CYP2C8 and CYP2C9 isoenzymes.	Ibuprofen	42-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
19480553-5	2009	Impaired metabolism of ibuprofen enantiomers was associated with the presence of CYP2C8*3, CYP2C9*2 and CYP2C9*3 alleles.	Ibuprofen	23-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
19480553-5	2009	Impaired metabolism of ibuprofen enantiomers was associated with the presence of CYP2C8*3, CYP2C9*2 and CYP2C9*3 alleles.	Ibuprofen	23-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
19297519-1	2009	Genetic polymorphisms in VKORC1 and CYP2C9, genes controlling vitamin K(1) (VK1) epoxide reduction and (S)-warfarin metabolism, respectively, are major contributors to interindividual variability in warfarin dose.	Vitamin K	62-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
19297519-1	2009	Genetic polymorphisms in VKORC1 and CYP2C9, genes controlling vitamin K(1) (VK1) epoxide reduction and (S)-warfarin metabolism, respectively, are major contributors to interindividual variability in warfarin dose.	Epoxy Compounds	81-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
19297519-1	2009	Genetic polymorphisms in VKORC1 and CYP2C9, genes controlling vitamin K(1) (VK1) epoxide reduction and (S)-warfarin metabolism, respectively, are major contributors to interindividual variability in warfarin dose.	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
19297519-1	2009	Genetic polymorphisms in VKORC1 and CYP2C9, genes controlling vitamin K(1) (VK1) epoxide reduction and (S)-warfarin metabolism, respectively, are major contributors to interindividual variability in warfarin dose.	Warfarin	199-207	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
19662888-2	2009	The application of pharmacogenetics in testing individual polymorphisms of two genes CYP 2C9 (pharmacokinetics of warfarin) and VKORC1 (sensitivity on warfarin) is promising tactics leading to a safe anticoagulation.	Warfarin	151-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-92
19255811-1	2009	BACKGROUND: Genetic variants of the warfarin sensitivity gene CYP2C9 have been associated with increased bleeding risk during warfarin initiation.	Warfarin	36-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
19245785-6	2009	CYP2C92 catalyzed diclofenac metabolism was 20-fold slower than the human counterpart, CYP2C9.	Diclofenac	18-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19245785-7	2009	CYP2C92 demonstrated comparable tolbutamide and (S)-warfarin hydroxylase activity compared to CYP2C9, upon addition of b(5) to the reactions.	Tolbutamide	32-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19196847-3	2009	Relative activity factors were measured by determining the intrinsic clearance (CL(int)) of probe substrates (bufuralol-CYP2D6, diclofenac-CYP2C9, midazolam-CYP3A4, and phenacetin-CYP1A2) in recombinant P450s and 16 HLM donors.	Diclofenac	128-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	139-145
19255811-9	2009	RESULTS: In the base case, testing and treating patients with CYP2C9*2 and/or CYP2C9*3 with aspirin rather than warfarin was best (8.97 QALYs).	Aspirin	92-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
19255811-1	2009	BACKGROUND: Genetic variants of the warfarin sensitivity gene CYP2C9 have been associated with increased bleeding risk during warfarin initiation.	Warfarin	126-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
19255811-9	2009	RESULTS: In the base case, testing and treating patients with CYP2C9*2 and/or CYP2C9*3 with aspirin rather than warfarin was best (8.97 QALYs).	Aspirin	92-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
19495518-0	2009	CYP2C9 polymorphism: prevalence in healthy and warfarin-treated Malay and Chinese in Malaysia.	Warfarin	47-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19442216-3	2009	In order to understand the metabolic mechanism of various drugs, two crystal structures of CYP2C9 have been studied, and their structural differences and structure-activity relationships with the drugs of Fluoxetine, Ibuprofen, Naproxen, Suprofen, and Mefenamic acid were investigated.	Fluoxetine	205-215	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
19442216-3	2009	In order to understand the metabolic mechanism of various drugs, two crystal structures of CYP2C9 have been studied, and their structural differences and structure-activity relationships with the drugs of Fluoxetine, Ibuprofen, Naproxen, Suprofen, and Mefenamic acid were investigated.	Ibuprofen	217-226	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
19442216-3	2009	In order to understand the metabolic mechanism of various drugs, two crystal structures of CYP2C9 have been studied, and their structural differences and structure-activity relationships with the drugs of Fluoxetine, Ibuprofen, Naproxen, Suprofen, and Mefenamic acid were investigated.	Naproxen	228-236	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
19442216-3	2009	In order to understand the metabolic mechanism of various drugs, two crystal structures of CYP2C9 have been studied, and their structural differences and structure-activity relationships with the drugs of Fluoxetine, Ibuprofen, Naproxen, Suprofen, and Mefenamic acid were investigated.	Suprofen	238-246	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
19442216-3	2009	In order to understand the metabolic mechanism of various drugs, two crystal structures of CYP2C9 have been studied, and their structural differences and structure-activity relationships with the drugs of Fluoxetine, Ibuprofen, Naproxen, Suprofen, and Mefenamic acid were investigated.	Mefenamic Acid	252-266	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
19324988-1	2009	Responses to warfarin (Coumadin) anticoagulation therapy are affected by genetic variability in both the CYP2C9 and VKORC1 genes.	Warfarin	13-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
19324988-1	2009	Responses to warfarin (Coumadin) anticoagulation therapy are affected by genetic variability in both the CYP2C9 and VKORC1 genes.	Warfarin	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
19324988-3	2009	We compared four platforms for determining the relevant single nucleotide polymorphisms (SNPs) in both CYP2C9 and VKORC1 that are associated with warfarin sensitivity (Third Wave Invader Plus, ParagonDx/Cepheid Smart Cycler, Idaho Technology LightCycler, and AutoGenomics Infiniti).	Warfarin	146-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
19495518-2	2009	CYP2C9 has been reported to be the enzyme responsible for the metabolism of many drugs, including warfarin and other drugs with a narrow therapeutic index.	Warfarin	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19495518-4	2009	We aimed to evaluate the prevalence of the types and frequencies of common CYP2C9 alleles (*1, *2, *3 and *4) among the healthy unrelated individuals and diseased patients prescribed with warfarin.	Warfarin	188-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
19495518-12	2009	Among the warfarin-treated group, only CYP2C9*1 and *3 were detected.	Warfarin	10-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
19495518-14	2009	CONCLUSION: Based on the above-observed genotypes, the prevalence of CYP2C9*2 and *3 was low in healthy and warfarin-treated Malays and Chinese in Malaysia.	Warfarin	108-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
19225451-1	2009	The objective of this study was to investigate the influence of genotypes associated with reduced activity of vitamin K epoxide reductase complex subunit 1 (VKORC1) and cytochrome P450 2C9 (CYP2C9) on anticoagulation with acenocoumarol during the first 6 weeks of treatment.	Acenocoumarol	222-235	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-188
19022234-6	2009	By co-treatment with specific inhibitors for cytochrome P450 (CYP) 2C and CYP3A - the major phase I enzymes involved in liver xenobiotic metabolism - we could confirm the prominent role of CYP3A in the bioactivation of troglitazone as well as the role of CYP3A and CYP2C in the activation of diclofenac.	Troglitazone	219-231	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-69
19022234-6	2009	By co-treatment with specific inhibitors for cytochrome P450 (CYP) 2C and CYP3A - the major phase I enzymes involved in liver xenobiotic metabolism - we could confirm the prominent role of CYP3A in the bioactivation of troglitazone as well as the role of CYP3A and CYP2C in the activation of diclofenac.	Diclofenac	292-302	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-69
19233910-0	2009	A multiplex assay for detecting genetic variations in CYP2C9, VKORC1, and GGCX involved in warfarin metabolism.	Warfarin	91-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
19233910-2	2009	Genetic variations in the cytochrome P450, family 2, subfamily C, polypeptide 9 (CYP2C9), vitamin K epoxide reductase complex, subunit 1 (VKORC1), and gamma-glutamyl carboxylase (GGCX) genes have been shown to contribute to impaired metabolism of warfarin.	Warfarin	247-255	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-79
19074728-0	2009	Relative contribution of CYP2C9 and VKORC1 genotypes and early INR response to the prediction of warfarin sensitivity during initiation of therapy.	Warfarin	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
19074728-1	2009	Genetic variants in CYP2C9 and VKORC1 strongly affect steady-state warfarin dose.	Warfarin	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
19074728-4	2009	In 214 patients starting warfarin with INR-guided dose adjustments, we determined whether CYP2C9 and VKORC1 genotypes were associated with early measures of warfarin sensitivity (time to INR >/= lower limit of therapeutic range; time to INR > 4; and first stable warfarin dose) after adjusting for early (days 4-6) and week 1 (days 7-9) INR values.	Warfarin	157-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
19074728-4	2009	In 214 patients starting warfarin with INR-guided dose adjustments, we determined whether CYP2C9 and VKORC1 genotypes were associated with early measures of warfarin sensitivity (time to INR >/= lower limit of therapeutic range; time to INR > 4; and first stable warfarin dose) after adjusting for early (days 4-6) and week 1 (days 7-9) INR values.	Warfarin	157-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
19074728-9	2009	Thus, much of the information provided by CYP2C9 and VKORC1 genotypes during warfarin initiation is captured by the early INR response.	Warfarin	77-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
18950609-12	2009	Results with the isoform-selective inhibitors suggest that the isoforms inhibited by ketoconazole (mainly CYP3A4) and diethyldithiocarbamate (mainly CYP2A6, and CYP2E1), but not the isoforms inhibited by furafylline (mainly CYP1A2), sulfaphenazole (mainly CYP2C9) and quinidine (mainly CYP2D6) are involved in the metabolic activation of AFB1.	Ketoconazole	85-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	256-262
18950609-12	2009	Results with the isoform-selective inhibitors suggest that the isoforms inhibited by ketoconazole (mainly CYP3A4) and diethyldithiocarbamate (mainly CYP2A6, and CYP2E1), but not the isoforms inhibited by furafylline (mainly CYP1A2), sulfaphenazole (mainly CYP2C9) and quinidine (mainly CYP2D6) are involved in the metabolic activation of AFB1.	Ditiocarb	118-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	256-262
19181737-0	2009	Rapid single-nucleotide polymorphism detection of cytochrome P450 (CYP2C9) and vitamin K epoxide reductase (VKORC1) genes for the warfarin dose adjustment by the SMart-amplification process version 2.	Warfarin	130-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
19181737-1	2009	BACKGROUND: Polymorphisms of the CYP2C9 (cytochrome P450, family 2, subfamily C, polypeptide 9) gene (CYP2C9*2, CYP2C9*3) and the VKORC1 (vitamin K epoxide reductase complex, subunit 1) gene (-1639G>A) greatly impact the maintenance dose for the drug warfarin.	Warfarin	254-262	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
19181737-1	2009	BACKGROUND: Polymorphisms of the CYP2C9 (cytochrome P450, family 2, subfamily C, polypeptide 9) gene (CYP2C9*2, CYP2C9*3) and the VKORC1 (vitamin K epoxide reductase complex, subunit 1) gene (-1639G>A) greatly impact the maintenance dose for the drug warfarin.	Warfarin	254-262	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-94
19181737-1	2009	BACKGROUND: Polymorphisms of the CYP2C9 (cytochrome P450, family 2, subfamily C, polypeptide 9) gene (CYP2C9*2, CYP2C9*3) and the VKORC1 (vitamin K epoxide reductase complex, subunit 1) gene (-1639G>A) greatly impact the maintenance dose for the drug warfarin.	Warfarin	254-262	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
19181737-1	2009	BACKGROUND: Polymorphisms of the CYP2C9 (cytochrome P450, family 2, subfamily C, polypeptide 9) gene (CYP2C9*2, CYP2C9*3) and the VKORC1 (vitamin K epoxide reductase complex, subunit 1) gene (-1639G>A) greatly impact the maintenance dose for the drug warfarin.	Warfarin	254-262	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
19225451-1	2009	The objective of this study was to investigate the influence of genotypes associated with reduced activity of vitamin K epoxide reductase complex subunit 1 (VKORC1) and cytochrome P450 2C9 (CYP2C9) on anticoagulation with acenocoumarol during the first 6 weeks of treatment.	Acenocoumarol	222-235	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
19225451-6	2009	Our conclusion was that an initial standard dosing regimen with acenocoumarol increases the risk of severe overanticoagulation in patients with variant alleles of the VKORC1 and CYP2C9 genes.	Acenocoumarol	64-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	178-184
19031075-0	2009	Influence of CYP2C9 genotype on warfarin dose requirements--a systematic review and meta-analysis.	Warfarin	32-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
19031075-1	2009	PURPOSE: To quantify the influence of common cytochrome P450 2C9 (CYP2C9) polymorphisms on warfarin dose requirements.	Warfarin	91-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-64
19031075-1	2009	PURPOSE: To quantify the influence of common cytochrome P450 2C9 (CYP2C9) polymorphisms on warfarin dose requirements.	Warfarin	91-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
19031075-2	2009	METHODS: A systematic review and a meta-analysis, calculating the warfarin dose reduction associated with the five most common variant CYP2C9 genotypes.	Warfarin	66-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-141
19031075-6	2009	CONCLUSIONS: Previous studies have rarely been powered to determine the quantitative influence of specific CYP2C9 genotypes on warfarin dose requirements.	Warfarin	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
19442086-6	2009	CYP2B6, CYP3A4 and CYP2C9 play a relevant role in the metabolism of ketamine.	Ketamine	68-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
19171677-2	2009	To address whether the need for redox transfer proteins and the NADPH cofactor protein could be obviated, CYP2C9 was bonded to a gold electrode through an 11-mercaptoundecanoic acid and octanethiol self-assembled monolayer (SAM) through which a current could be applied.	11-mercaptoundecanoic acid	155-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
19171677-2	2009	To address whether the need for redox transfer proteins and the NADPH cofactor protein could be obviated, CYP2C9 was bonded to a gold electrode through an 11-mercaptoundecanoic acid and octanethiol self-assembled monolayer (SAM) through which a current could be applied.	n-octanethiol	186-197	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
19171677-3	2009	Cyclic voltammetry demonstrated direct electrochemistry of the CYP2C9 enzyme bonded to the electrode and fast electron transfer between the heme iron and the gold electrode.	Heme	140-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
19171677-3	2009	Cyclic voltammetry demonstrated direct electrochemistry of the CYP2C9 enzyme bonded to the electrode and fast electron transfer between the heme iron and the gold electrode.	Iron	145-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
19171677-4	2009	To determine whether this system could metabolize warfarin analogous to microsomal or expressed enzyme systems containing CYP2C9, warfarin was incubated with the CYP2C9-SAM-gold electrode and a controlled potential was applied.	Warfarin	130-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
19171677-5	2009	The expected 7-hydroxywarfarin metabolite was observed, analogous to expressed CYP2C9 systems, wherein this is the predominant metabolite.	7-hydroxywarfarin	13-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
19171677-7	2009	In summary, the CYP2C9-SAM-gold electrode system was able to carry out the metabolism of warfarin only after application of an electrical potential, but in the absence of either CPR or NADPH.	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
19083245-0	2009	A potentially deleterious new CYP2C9 polymorphism identified in an African American patient with major hemorrhage on warfarin therapy.	Warfarin	117-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
19005461-0	2009	Interindividual variation in the pharmacokinetics of Delta9-tetrahydrocannabinol as related to genetic polymorphisms in CYP2C9.	Dronabinol	53-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
19005461-1	2009	The impact of the CYP2C9 polymorphism on the pharmacokinetics of orally administered 9-tetrahydrocannabinol (THC) was studied in 43 healthy volunteers.	Dronabinol	85-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
19005461-3	2009	However, the median area under the curve of THC was threefold higher and that of 11-nor-9-carboxy-9-tetrahydrocannabinol was 70% lower in CYP2C9*3/*3 homozygotes than in CYP2C9*1/*1 homozygotes.	Dronabinol	44-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
19005461-3	2009	However, the median area under the curve of THC was threefold higher and that of 11-nor-9-carboxy-9-tetrahydrocannabinol was 70% lower in CYP2C9*3/*3 homozygotes than in CYP2C9*1/*1 homozygotes.	11-nor-9-carboxy-9-tetrahydrocannabinol	81-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
19005461-3	2009	However, the median area under the curve of THC was threefold higher and that of 11-nor-9-carboxy-9-tetrahydrocannabinol was 70% lower in CYP2C9*3/*3 homozygotes than in CYP2C9*1/*1 homozygotes.	11-nor-9-carboxy-9-tetrahydrocannabinol	81-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-176
19005461-4	2009	CYP2C9*3 carriers also showed a trend toward increased sedation following administration of THC.	Dronabinol	92-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19005461-5	2009	Therefore, the CYP2C9*3 variant may influence both the therapeutic and adverse effects of THC.	Dronabinol	90-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
19601875-3	2009	Glutathione and cyanide did not inhibit the enzymes at concentrations up to 10 mM; however methoxylamine did show inhibition, with IC(50) values of 0.53 mM for CYP1A2, 4.12 mM for CYP2C9, 2.04 mM for CYP2C19, 9.72 mM for CYP2D6, and 1.26 and >10 mM for CYP3A4/5 (for testosterone and midazolam, respectively, as substrates).	methoxyamine	91-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	180-186
19289643-3	2009	We aimed to assess the effect of sulfaphenazole, a specific CYP 2C9 inhibitor, on tPA release in normotensive subjects and patients with essential hypertension.	Sulfaphenazole	33-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-67
19289643-11	2009	CONCLUSIONS: Sulfaphenazole inhibits bradykinin-induced tPA release, which suggests a modulatory role of CYP 2C9-derived endothelium-derived hyperpolarizing factors in tPA release in humans.	Sulfaphenazole	13-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-112
19252308-0	2009	Effect of ethanol on S-warfarin and diclofenac metabolism by recombinant human CYP2C9.1.	Ethanol	10-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
19252308-0	2009	Effect of ethanol on S-warfarin and diclofenac metabolism by recombinant human CYP2C9.1.	Warfarin	21-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
19252308-0	2009	Effect of ethanol on S-warfarin and diclofenac metabolism by recombinant human CYP2C9.1.	Diclofenac	36-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
19252308-1	2009	The effect of ethanol on the metabolism of S-warfarin and diclofenac by recombinant cytochrome P450 2C9.1 microsomes (CYP2C9.1) was studied.	Ethanol	14-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-103
19252308-1	2009	The effect of ethanol on the metabolism of S-warfarin and diclofenac by recombinant cytochrome P450 2C9.1 microsomes (CYP2C9.1) was studied.	Warfarin	43-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-103
19252308-1	2009	The effect of ethanol on the metabolism of S-warfarin and diclofenac by recombinant cytochrome P450 2C9.1 microsomes (CYP2C9.1) was studied.	Warfarin	43-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
19252308-1	2009	The effect of ethanol on the metabolism of S-warfarin and diclofenac by recombinant cytochrome P450 2C9.1 microsomes (CYP2C9.1) was studied.	Diclofenac	58-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-103
19252308-1	2009	The effect of ethanol on the metabolism of S-warfarin and diclofenac by recombinant cytochrome P450 2C9.1 microsomes (CYP2C9.1) was studied.	Diclofenac	58-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
19252308-5	2009	Ethanol at a concentration of 3.0 vol% (510 mM) increased the K(m) value of diclofenac metabolism without changes in the V(max), which indicates that diclofenac 4"-hydroxylation by CYP2C9.1 was competitively inhibited by ethanol.	Ethanol	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
19252308-5	2009	Ethanol at a concentration of 3.0 vol% (510 mM) increased the K(m) value of diclofenac metabolism without changes in the V(max), which indicates that diclofenac 4"-hydroxylation by CYP2C9.1 was competitively inhibited by ethanol.	Diclofenac	76-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
19252308-5	2009	Ethanol at a concentration of 3.0 vol% (510 mM) increased the K(m) value of diclofenac metabolism without changes in the V(max), which indicates that diclofenac 4"-hydroxylation by CYP2C9.1 was competitively inhibited by ethanol.	Diclofenac	150-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
19252308-5	2009	Ethanol at a concentration of 3.0 vol% (510 mM) increased the K(m) value of diclofenac metabolism without changes in the V(max), which indicates that diclofenac 4"-hydroxylation by CYP2C9.1 was competitively inhibited by ethanol.	Ethanol	221-228	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
19252308-6	2009	S-Warfarin metabolism by CYP2C9.1 was more sensitive to ethanol than diclofenac metabolism.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
19252308-6	2009	S-Warfarin metabolism by CYP2C9.1 was more sensitive to ethanol than diclofenac metabolism.	Ethanol	56-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
19252308-7	2009	These results suggest that ethanol inhibits the metabolism by CYP2C9.1 in a substrate-dependent manner.	Ethanol	27-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
19074529-0	2009	Mechanism of CYP2C9 inhibition by flavones and flavonols.	Flavones	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
19074529-0	2009	Mechanism of CYP2C9 inhibition by flavones and flavonols.	Flavonols	47-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
19074529-2	2009	With the exception of flavone, all flavonoids were shown to inhibit CYP2C9-mediated diclofenac 4"-hydroxylation in the CYP2C9 RECO system, with K(i) value <or= 2.2 microM.	Flavonoids	35-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
19074529-2	2009	With the exception of flavone, all flavonoids were shown to inhibit CYP2C9-mediated diclofenac 4"-hydroxylation in the CYP2C9 RECO system, with K(i) value <or= 2.2 microM.	Flavonoids	35-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
19074529-2	2009	With the exception of flavone, all flavonoids were shown to inhibit CYP2C9-mediated diclofenac 4"-hydroxylation in the CYP2C9 RECO system, with K(i) value <or= 2.2 microM.	Diclofenac	84-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
19074529-2	2009	With the exception of flavone, all flavonoids were shown to inhibit CYP2C9-mediated diclofenac 4"-hydroxylation in the CYP2C9 RECO system, with K(i) value <or= 2.2 microM.	Diclofenac	84-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
19074529-3	2009	In terms of the mechanism of inhibition, 6-hydroxyflavone was found to be a noncompetitive inhibitor of CYP2C9, whereas the other flavonoids were competitive inhibitors.	6-hydroxyflavone	41-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
19074529-4	2009	Computer docking simulation and constructed mutants substituted at residue 100 of CYP2C9.1 indicate that the noncompetitive binding site of 6-hydroxyflavone lies beside Phe100, similar to the reported allosteric binding site of warfarin.	6-hydroxyflavone	140-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
19074529-4	2009	Computer docking simulation and constructed mutants substituted at residue 100 of CYP2C9.1 indicate that the noncompetitive binding site of 6-hydroxyflavone lies beside Phe100, similar to the reported allosteric binding site of warfarin.	Warfarin	228-236	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
19074529-5	2009	The other flavonoids exert competitive inhibition through interaction with the substrate binding site of CYP2C9 accessed by flurbiprofen.	Flavonoids	10-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
19074529-5	2009	The other flavonoids exert competitive inhibition through interaction with the substrate binding site of CYP2C9 accessed by flurbiprofen.	Flurbiprofen	124-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
19074529-6	2009	These results suggest flavonoids can participate in interactions with drugs that act as substrates for CYP2C9 and provide a possible molecular basis for understanding cooperativity in human P450-mediated drug-drug interactions.	Flavonoids	22-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
19442086-8	2009	Propofol is metabolized mainly by glucuronidation by uridine diphosphate-glucuronosyltransferases (UGTs) and by hydroxylation by CYP2B6 and CYP2C enzymes.	Propofol	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-145
19022226-6	2009	At 10 microM PCEEA, CBP reduced metabolite formation by 61%, while inhibition of CYP3A4 by ketoconazole and inhibition of CYP2C9 by sulfaphenazole showed no inhibitory effect.	Sulfaphenazole	132-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
19300499-0	2009	A genome-wide association study confirms VKORC1, CYP2C9, and CYP4F2 as principal genetic determinants of warfarin dose.	Warfarin	105-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
19300499-5	2009	We initially tested each of 325,997 GWAS SNPs for association with warfarin dose by univariate regression and found the strongest statistical signals (p<10(-78)) at SNPs clustering near VKORC1 and the second lowest p-values (p<10(-31)) emanating from CYP2C9.	Warfarin	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	257-263
19277427-0	2009	Pharmacogenetics of acenocoumarol: CYP2C9 *2 and VKORC1 c.-1639G>A, 497C>G, 1173C>T, and 3730G>A variants influence drug dose in anticoagulated patients.	Acenocoumarol	20-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
19337788-0	2009	Frequency of CYP3A4, CYP3A5, CYP2C9, and CYP2C19 variant alleles in patients receiving clopidogrel that experience repeat acute coronary syndrome.	Clopidogrel	87-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
19337788-2	2009	This research evaluated the frequency of variant alleles in the genes coding for CYP3A4, CYP3A5, CYP2C9, and CYP2C19 enzymes in patients on clopidogrel therapy and experiencing repeat acute coronary syndrome (ACS) compared to a control group with a matching ethnic composition.	Clopidogrel	140-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
19177029-0	2009	Validation of VKORC1 and CYP2C9 genotypes on interindividual warfarin maintenance dose: a prospective study in Chinese patients.	Warfarin	61-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
19029318-5	2009	In pilot experiments, voriconazole showed inhibition of CYP2B6, CYP2C9, CYP2C19, and CYP3A (half-maximal [50%] inhibitory concentrations, <6 microM); its effect on CYP1A2, CYP2A6, CYP2C8, and CYP2D6 was marginal (<25% inhibition at 100 microM voriconazole).	Voriconazole	22-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
19029318-6	2009	Further detailed experiments with HLMs showed that voriconazole is a potent competitive inhibitor of CYP2B6 (K(i) < 0.5), CYP2C9 (K(i) = 2.79 microM), and CYP2C19 (K(i) = 5.1 microM).	Voriconazole	51-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
19029318-8	2009	Prediction of the in vivo interaction of voriconazole from these in vitro data suggests that voriconazole would substantially increase the exposure of drugs metabolized by CYP2B6, CYP2C9, CYP2C19, and CYP3A.	Voriconazole	41-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	180-186
19029318-8	2009	Prediction of the in vivo interaction of voriconazole from these in vitro data suggests that voriconazole would substantially increase the exposure of drugs metabolized by CYP2B6, CYP2C9, CYP2C19, and CYP3A.	Voriconazole	93-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	180-186
19280158-0	2009	Effect of CYP2C9*3 allele on the pharmacokinetics of naproxen in Korean subjects.	Naproxen	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
19095442-3	2009	These studies culminated in the identification of anthranilimides 16 and 22 which displayed potent in vitro inhibition of GPa in addition to reduced inhibition of CYP2C9 and excellent pharmacokinetic properties.	anthranilimides	50-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-169
19280158-1	2009	The genetically polymorphic CYP2C9 metabolizes many non-steroidal anti-inflammatory agents, including naproxen.	Naproxen	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
19280158-2	2009	This study examined the effects of a CYP2C9 genetic polymorphism on the pharmacokinetics of naproxen in Korean subjects.	Naproxen	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
19280158-6	2009	The mean plasma concentration-time profiles of naproxen in the CYP2C9*1/*3 and CYP2C9*1/*1 individuals were similar.	Naproxen	47-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
19196837-8	2009	The mechanism of interaction between antiretroviral agents and warfarin appears to be mediated through alteration in CYP2C9 metabolism.	Warfarin	63-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
18971317-9	2009	Rosuvastatin was found to increase human constitutive androstane receptor (hCAR)-mediated transcription of CYP3A4, CYP2C9, and CYP2B6 genes, predicting the consequent potential for drug interactions with several coadministered drugs.	Rosuvastatin Calcium	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
18971317-10	2009	Activation of hCAR and hPXR by atorvastatin and the subsequent induction of not only CYP2B6 and CYP3A4 but also of CYP2C9 present an additional target by which atorvastatin, a widely used cholesterol-lowering drug, can modify the kinetics of numerous drugs.	Atorvastatin	160-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
18971317-10	2009	Activation of hCAR and hPXR by atorvastatin and the subsequent induction of not only CYP2B6 and CYP3A4 but also of CYP2C9 present an additional target by which atorvastatin, a widely used cholesterol-lowering drug, can modify the kinetics of numerous drugs.	Cholesterol	188-199	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
19077919-3	2009	RESULTS: In the early phase of warfarin therapy, the combined genotypes of CYP2C9 and VKORC1 caused statistically significant difference in warfarin dose from day 7 of warfarin dosing and the subsequent time course of dose increase showed significant difference among the three different genotypes (P<0.001).	Warfarin	31-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
19033450-1	2009	In vitro data on the metabolism of the antifungal voriconazole suggest that its pharmacokinetics might be influenced by the activity of CYP2C19, CYP2C9, and CYP3A.	Voriconazole	50-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
19077919-1	2009	OBJECTIVES: The effect of CYP2C9 and vitamin K epoxide reductase complex subunit 1 (VKORC1) genotypes was evaluated for the early-phase and steady-state warfarin dosing in Korean patients with mechanical heart valve replacement.	Warfarin	153-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
18541345-0	2009	The metabolism of CYP2C9 and CYP2C19 for gliclazide by homology modeling and docking study.	Gliclazide	41-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
18541345-5	2009	Then, with the refined model of CYP2C19 and the crystal structure of CYP2C9, the metabolisms of them for gliclazide in two different metabolic pathways were studied and the results show that both enzymes have more favorable interaction energies and stronger affinity with gliclazide in methylhydroxylation pathway than in 6beta-hydroxylation pathway.	Gliclazide	105-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
18541345-5	2009	Then, with the refined model of CYP2C19 and the crystal structure of CYP2C9, the metabolisms of them for gliclazide in two different metabolic pathways were studied and the results show that both enzymes have more favorable interaction energies and stronger affinity with gliclazide in methylhydroxylation pathway than in 6beta-hydroxylation pathway.	Gliclazide	272-282	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
18541345-6	2009	It is exciting that substrate inhibition phenomenon can be found in metabolisms of CYP2C9 and CYP2C19 for gliclazide in two metabolic pathways.	Gliclazide	106-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
18541345-7	2009	Gliclazide can change the conformation of the active sites and decrease obviously the affinities between gliclazide in the active site and enzymes when it is docked in the second active sites in CYP2C9 and CYP2C19.	Gliclazide	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
18541345-7	2009	Gliclazide can change the conformation of the active sites and decrease obviously the affinities between gliclazide in the active site and enzymes when it is docked in the second active sites in CYP2C9 and CYP2C19.	Gliclazide	105-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
19179293-5	2009	A substantial number of studies demonstrate that common variants of two genes, VKORC1 and CYP2C9, along with other nongenetic factors, correlate significantly with warfarin dosing.	Warfarin	164-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
19179293-6	2009	The genotypes of VKORC1 and CYP2C9 alone account for nearly 3 times more of the variability ( approximately 30%) in warfarin dosing than do age, weight, gender, and other clinical factors combined ( approximately 12%).	Warfarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
19077919-3	2009	RESULTS: In the early phase of warfarin therapy, the combined genotypes of CYP2C9 and VKORC1 caused statistically significant difference in warfarin dose from day 7 of warfarin dosing and the subsequent time course of dose increase showed significant difference among the three different genotypes (P<0.001).	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
19077919-3	2009	RESULTS: In the early phase of warfarin therapy, the combined genotypes of CYP2C9 and VKORC1 caused statistically significant difference in warfarin dose from day 7 of warfarin dosing and the subsequent time course of dose increase showed significant difference among the three different genotypes (P<0.001).	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
19077919-6	2009	The observed warfarin maintenance dose was best explained by a model including covariates of age, weight, concurrent congestive heart failure/cardiomyopathy, INR-increasing drugs, aspirin, dietary supplements, and CYP2C9 and VKORC1 genotypes (R=0.56).	Warfarin	13-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	214-220
19077919-7	2009	CONCLUSION: The heterozygous CYP2C9 and VKORC1 genotypes influence warfarin dosing in an early phase as well as steady state of warfarin therapy in Korean patients with mechanical heart valve replacement.	Warfarin	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
19077919-7	2009	CONCLUSION: The heterozygous CYP2C9 and VKORC1 genotypes influence warfarin dosing in an early phase as well as steady state of warfarin therapy in Korean patients with mechanical heart valve replacement.	Warfarin	128-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
19139476-4	2009	Cytochrome P-450 isoenzyme 2C9 (CYP2C9) metabolizes S-warfarin into two inactive metabolites.	Warfarin	52-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-30
18574025-1	2009	Genetic variants of cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1) are known to influence warfarin dose, but the effect of other genes has not been fully elucidated.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-39
18574025-1	2009	Genetic variants of cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1) are known to influence warfarin dose, but the effect of other genes has not been fully elucidated.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
18574025-3	2009	CYP2C9*2 and *3 explained 12% (P = 6.63 x 10(-34)) of the variation in warfarin dose, while a single VKORC1 SNP explained 30% (P = 9.82 x 10(-100)).	Warfarin	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
18574025-7	2009	A multiple regression model using the predictors CYP2C9, VKORC1, age, sex, and druginteractions explained 59% of the variance in warfarin dose, and 53% in an independent sample of 181 Swedish individuals.	Warfarin	129-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
18574025-8	2009	In conclusion, CYP2C9 and VKORC1 significantly influenced warfarin dose and predicted individuals predisposed to unstable anticoagulation.	Warfarin	58-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
19348697-3	2009	Genotype for CYP2C9, which encodes the main cytochrome P450 enzyme that metabolizes warfarin, and VKORC1, the gene encoding the warfarin target vitamin K epoxide reductase, together account for approximately 30% of the variability in dose requirement.	Warfarin	84-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
19348697-7	2009	A recently published whole genome association study confirms that the main genes important in warfarin response are CYP2C9 and VKORC1.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
19139476-4	2009	Cytochrome P-450 isoenzyme 2C9 (CYP2C9) metabolizes S-warfarin into two inactive metabolites.	Warfarin	52-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
19139476-5	2009	Genetic variations to the gene encoding CYP2C9 (CYP2C9 ) are known to affect warfarin clearance.	Warfarin	77-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
19139476-5	2009	Genetic variations to the gene encoding CYP2C9 (CYP2C9 ) are known to affect warfarin clearance.	Warfarin	77-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
19117406-0	2009	SYBR Green-based real-time PCR assay for detection of VKORC1 and CYP2C9 polymorphisms that modulate warfarin dose requirement.	sybr green	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
26110197-6	2009	CYP2C9 is the principal cytochrome P450 enzyme that modulates the anticoagulant activity of warfarin.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
26110197-7	2009	From results of clinical studies, genetic variation in the CYP2C9 and/or VKORC1 genes can, in concert with clinical factors, predict how each individual responds to warfarin.	Warfarin	165-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
26110197-11	2009	Pharmacogenomic testing of CYP2C9 or VKORC1 alleles to predict a patient"s response to warfarin occurs ideally prior to initiation of the drug.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
19067473-4	2009	Based on in vitro studies, dexlansoprazole has the potential to inhibit activity of these isoenzymes and also may induce human hepatic CYP1A and CYP2C9 activity.	Dexlansoprazole	27-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
19117406-0	2009	SYBR Green-based real-time PCR assay for detection of VKORC1 and CYP2C9 polymorphisms that modulate warfarin dose requirement.	Warfarin	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
19117406-1	2009	BACKGROUND: Polymorphisms in VKORC1 (vitamin K epoxide reductase complex subunit 1) and CYP2C9 (cytochrome P450 2C9) genes are considered the major genetic factors modulating warfarin dose requirement.	Warfarin	175-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
19397481-5	2009	Growing evidence indicates that up to 60% of the individual pharmacological response to coumarins might be due to genetic variables and affected by polymorphisms in the genes encoding two enzymes, namely, vitamin K epoxide reductase (VKOR) and cytochrome P450 CYP2C9.	Coumarins	88-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	260-266
19117406-1	2009	BACKGROUND: Polymorphisms in VKORC1 (vitamin K epoxide reductase complex subunit 1) and CYP2C9 (cytochrome P450 2C9) genes are considered the major genetic factors modulating warfarin dose requirement.	Warfarin	175-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-115
19117406-3	2009	METHODS: In this study, we developed and validated a melting temperature (T(m))-shift genotyping assay for detection of VKORC1 C1173T and CYP2C9 A1075C polymorphisms by using SYBR Green-based multiplex allele-specific PCR and consequent melting curve analysis.	sybr green	175-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
19071883-9	2009	In addition to the clinical pharmacokinetic analysis, the ability of mipomersen sodium to inhibit the major CYP isoform enzymes (namely CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4) was evaluated in cryo-preserved human hepatocytes in vitro.	Sodium	80-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
19725591-6	2009	Etravirine is metabolized by cytochrome P450 (CYP) 3A, 2C9 and 2C19; the metabolites are subsequently glucuronidated by uridine diphosphate glucuronosyltransferase.	etravirine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-58
19725591-8	2009	Etravirine has the potential for interactions by inducing CYP3A and inhibiting CYP2C9 and 2C19; it is a mild inhibitor of P-glycoprotein but not a substrate.	etravirine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
18948380-10	2009	Human P450 isoforms that showed activity toward multiple pyrethroids were CYP2C8, CYP2C9, CYP2C19, and CYP3A4.	Pyrethrins	57-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
22461099-8	2009	However, only variations in VKORC1 and CYP2C9 have consistently been associated with drug response (coumarins) and have clinical implications.	Coumarins	100-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
19515014-2	2009	CYP2C9 metabolizes more than 100 therapeutic drugs, including tolbutamide, glyburide, diclofenac, celecoxib, torasemide, phenytoin losartan, and S-warfarin).	Tolbutamide	62-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-2	2009	CYP2C9 metabolizes more than 100 therapeutic drugs, including tolbutamide, glyburide, diclofenac, celecoxib, torasemide, phenytoin losartan, and S-warfarin).	Glyburide	75-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-2	2009	CYP2C9 metabolizes more than 100 therapeutic drugs, including tolbutamide, glyburide, diclofenac, celecoxib, torasemide, phenytoin losartan, and S-warfarin).	Diclofenac	86-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-2	2009	CYP2C9 metabolizes more than 100 therapeutic drugs, including tolbutamide, glyburide, diclofenac, celecoxib, torasemide, phenytoin losartan, and S-warfarin).	Celecoxib	98-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-2	2009	CYP2C9 metabolizes more than 100 therapeutic drugs, including tolbutamide, glyburide, diclofenac, celecoxib, torasemide, phenytoin losartan, and S-warfarin).	Torsemide	109-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-2	2009	CYP2C9 metabolizes more than 100 therapeutic drugs, including tolbutamide, glyburide, diclofenac, celecoxib, torasemide, phenytoin losartan, and S-warfarin).	phenytoin losartan	121-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-2	2009	CYP2C9 metabolizes more than 100 therapeutic drugs, including tolbutamide, glyburide, diclofenac, celecoxib, torasemide, phenytoin losartan, and S-warfarin).	Warfarin	145-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-4	2009	CYP2C9 also plays a role in the metabolism of several endogenous compounds such as steroids, melatonin, retinoids and arachidonic acid.	Steroids	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-4	2009	CYP2C9 also plays a role in the metabolism of several endogenous compounds such as steroids, melatonin, retinoids and arachidonic acid.	Melatonin	93-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-4	2009	CYP2C9 also plays a role in the metabolism of several endogenous compounds such as steroids, melatonin, retinoids and arachidonic acid.	Retinoids	104-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-4	2009	CYP2C9 also plays a role in the metabolism of several endogenous compounds such as steroids, melatonin, retinoids and arachidonic acid.	Arachidonic Acid	118-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-9	2009	CYP2C9 is activated by dapsone and its analogues and R-lansoprazole in a stereo-specific and substrate-dependent manner, probably through binding to the active site and inducing positive cooperativity.	Dapsone	23-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-9	2009	CYP2C9 is activated by dapsone and its analogues and R-lansoprazole in a stereo-specific and substrate-dependent manner, probably through binding to the active site and inducing positive cooperativity.	Dexlansoprazole	53-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-10	2009	CYP2C9 is subject to induction by rifampin, phenobarbital, and dexamethasone, indicating the involvement of pregnane X receptor, constitutive androstane receptor and glucocorticoid receptor in the regulation of CYP2C9.	Rifampin	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-10	2009	CYP2C9 is subject to induction by rifampin, phenobarbital, and dexamethasone, indicating the involvement of pregnane X receptor, constitutive androstane receptor and glucocorticoid receptor in the regulation of CYP2C9.	Rifampin	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	211-217
19515014-10	2009	CYP2C9 is subject to induction by rifampin, phenobarbital, and dexamethasone, indicating the involvement of pregnane X receptor, constitutive androstane receptor and glucocorticoid receptor in the regulation of CYP2C9.	Phenobarbital	44-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-10	2009	CYP2C9 is subject to induction by rifampin, phenobarbital, and dexamethasone, indicating the involvement of pregnane X receptor, constitutive androstane receptor and glucocorticoid receptor in the regulation of CYP2C9.	Phenobarbital	44-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	211-217
19515014-10	2009	CYP2C9 is subject to induction by rifampin, phenobarbital, and dexamethasone, indicating the involvement of pregnane X receptor, constitutive androstane receptor and glucocorticoid receptor in the regulation of CYP2C9.	Dexamethasone	63-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-10	2009	CYP2C9 is subject to induction by rifampin, phenobarbital, and dexamethasone, indicating the involvement of pregnane X receptor, constitutive androstane receptor and glucocorticoid receptor in the regulation of CYP2C9.	Dexamethasone	63-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	211-217
19515014-12	2009	Tienilic acid, suprofen and silybin are mechanism-based inhibitors of CYP2C9.	Ticrynafen	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
19515014-12	2009	Tienilic acid, suprofen and silybin are mechanism-based inhibitors of CYP2C9.	Suprofen	15-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
19515014-12	2009	Tienilic acid, suprofen and silybin are mechanism-based inhibitors of CYP2C9.	Silybin	28-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
19354002-0	2009	Rosuvastatin-induced rhabdomyolysis probably via CYP2C9 saturation.	Rosuvastatin Calcium	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
19354002-8	2009	Our patient was taking rosuvastatin, warfarin and telmisartan, which are metabolised by CYP2C9; we therefore hypothesised that the rosuvastatin-induced rhabdomyolysis was probably by CYP2C9 enzyme saturation.	Rosuvastatin Calcium	23-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
19354002-8	2009	Our patient was taking rosuvastatin, warfarin and telmisartan, which are metabolised by CYP2C9; we therefore hypothesised that the rosuvastatin-induced rhabdomyolysis was probably by CYP2C9 enzyme saturation.	Rosuvastatin Calcium	23-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	183-189
19354002-8	2009	Our patient was taking rosuvastatin, warfarin and telmisartan, which are metabolised by CYP2C9; we therefore hypothesised that the rosuvastatin-induced rhabdomyolysis was probably by CYP2C9 enzyme saturation.	Warfarin	37-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
19354002-8	2009	Our patient was taking rosuvastatin, warfarin and telmisartan, which are metabolised by CYP2C9; we therefore hypothesised that the rosuvastatin-induced rhabdomyolysis was probably by CYP2C9 enzyme saturation.	Warfarin	37-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	183-189
19354002-8	2009	Our patient was taking rosuvastatin, warfarin and telmisartan, which are metabolised by CYP2C9; we therefore hypothesised that the rosuvastatin-induced rhabdomyolysis was probably by CYP2C9 enzyme saturation.	Telmisartan	50-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
19354002-8	2009	Our patient was taking rosuvastatin, warfarin and telmisartan, which are metabolised by CYP2C9; we therefore hypothesised that the rosuvastatin-induced rhabdomyolysis was probably by CYP2C9 enzyme saturation.	Telmisartan	50-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	183-189
19354002-8	2009	Our patient was taking rosuvastatin, warfarin and telmisartan, which are metabolised by CYP2C9; we therefore hypothesised that the rosuvastatin-induced rhabdomyolysis was probably by CYP2C9 enzyme saturation.	Rosuvastatin Calcium	131-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
19354002-8	2009	Our patient was taking rosuvastatin, warfarin and telmisartan, which are metabolised by CYP2C9; we therefore hypothesised that the rosuvastatin-induced rhabdomyolysis was probably by CYP2C9 enzyme saturation.	Rosuvastatin Calcium	131-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	183-189
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	Aspirin	45-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
19067731-8	2009	Heterogeneity in the way patients respond to aspirin and clopidogrel may in part reflect variation in cyclooxygenase (COX)-1, COX-2, glycoprotein (GP) Ib alpha, GP Ia/IIa, GP IIb/IIIa, UGT1A6*2, P2Y(1), P2Y(12), CYP2C9, CYP3A4 and CYP3A5 genotypes.	Clopidogrel	57-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
19745563-8	2009	The percent variability explained by VKORC1 diplotype status was 59.1% while the CYP2C9 genotype status accounted for 6.9% variability in warfarin dose requirements.	Warfarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
20408500-2	2009	Inhibition of CYP1A2, CYP2E1, CYP2C19, CYP2C9, CYP2D6, and CYP3A4 by CGS was assessed using recombinant human enzymes incubated with CGS (up to 3 mM expressed as free base).	cysteinylglycine	69-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
20408500-3	2009	Induction of CYP1A2, CYP2B6, CYP2C9, CYP2C19 and CYP3A4 by CGS (0.01, 0.3 and 3 mM) was evaluated in cryopreserved human hepatocytes, by determining CYP mRNA expression using quantitative RT-PCR.	cysteinylglycine	59-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
19053752-0	2008	Cytochrome P450 2C9 type II binding studies on quinoline-4-carboxamide analogues.	quinoline-4-carboxamide	47-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
18838506-0	2009	Mechanism-based inactivation of cytochrome P450 2C9 by tienilic acid and (+/-)-suprofen: a comparison of kinetics and probe substrate selection.	Ticrynafen	55-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-51
18838506-0	2009	Mechanism-based inactivation of cytochrome P450 2C9 by tienilic acid and (+/-)-suprofen: a comparison of kinetics and probe substrate selection.	Suprofen	73-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-51
23226035-7	2009	For example, it has been found that patients with CYP2C9 and VKORC1 gene variations have a different response to warfarin.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
18754597-0	2008	QM/MM modeling of benzene hydroxylation in human cytochrome P450 2C9.	Benzene	18-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-68
18754597-1	2008	The mechanism of benzene hydroxylation was investigated in the realistic enzyme environment of the human CYP 2C9 by using quantum mechanical/molecular mechanical (QM/MM) calculations of the whole reaction profile using the B3LYP method to describe the QM region.	Benzene	17-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-112
19430171-2	2009	In this study, we investigated whether these mice show similar metabolic profile to humans by examining the hydroxylation of S-warfarin reported to be mainly metabolized to S-7-hydroxywarfarin (7-OH-warfarin), catalyzed by CYP2C9, in humans.	Warfarin	125-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	223-229
19430171-2	2009	In this study, we investigated whether these mice show similar metabolic profile to humans by examining the hydroxylation of S-warfarin reported to be mainly metabolized to S-7-hydroxywarfarin (7-OH-warfarin), catalyzed by CYP2C9, in humans.	7-hydroxywarfarin	173-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	223-229
19430171-2	2009	In this study, we investigated whether these mice show similar metabolic profile to humans by examining the hydroxylation of S-warfarin reported to be mainly metabolized to S-7-hydroxywarfarin (7-OH-warfarin), catalyzed by CYP2C9, in humans.	7-oh-warfarin	194-207	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	223-229
19202563-3	2009	Clotrimazole, rifampin, ritonavir, phenytoin, and phenobarbital induced CYP2C9 consistent with previous findings for CYP3A4.	Clotrimazole	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
19202563-3	2009	Clotrimazole, rifampin, ritonavir, phenytoin, and phenobarbital induced CYP2C9 consistent with previous findings for CYP3A4.	Rifampin	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
19202563-3	2009	Clotrimazole, rifampin, ritonavir, phenytoin, and phenobarbital induced CYP2C9 consistent with previous findings for CYP3A4.	Ritonavir	24-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
19202563-3	2009	Clotrimazole, rifampin, ritonavir, phenytoin, and phenobarbital induced CYP2C9 consistent with previous findings for CYP3A4.	Phenytoin	35-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
19202563-3	2009	Clotrimazole, rifampin, ritonavir, phenytoin, and phenobarbital induced CYP2C9 consistent with previous findings for CYP3A4.	Phenobarbital	50-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
19202563-6	2009	In 17 donors, rifampin increased mean basal CYP2C9 activity from 59 +/- 43 to 143 +/- 68 pmol/mg protein/min; fold induction ranged from 1.4- to 6.4-fold.	Rifampin	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
18992346-0	2009	Pharmacogenetic relevance of the CYP2C9*3 allele in a tenoxicam bioequivalence study performed on Spaniards.	tenoxicam	54-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
18992346-1	2009	We performed a study to quantify CYP2C9 and CYP2C8 alleles influence on the variability observed in tenoxicam pharmacokinetic (PK) and implication in a bioequivalence study design performed on Spaniards.	tenoxicam	100-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
18992346-5	2009	CYP2C9*3 allele is associated to a longer elimination time of tenoxicam.	tenoxicam	62-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19219744-4	2009	This method was used to determine the bioactivation of acetaminophen at two concentrations: 50 microM therapeutic and 1 mM toxic by using nine human recombinant CYP enzymes: CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4; and with different microsomes from experimental animals.	Acetaminophen	55-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	206-212
19017829-1	2008	OBJECTIVE: To report a case in which the anticoagulation effect of warfarin appeared to be potentiated by torsemide, possibly due to an interference of metabolism through competition for the CYP2C9 isoenzyme and protein-binding displacement of warfarin.	Warfarin	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
19026171-0	2008	Determination of the inhibitory potential of 6 fluoroquinolones on CYP1A2 and CYP2C9 in human liver microsomes.	6 fluoroquinolones	45-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
19026171-2	2008	METHODS: Probe substrates, phenacetin (CYP1A2), and tolbutamide (CYP2C9) were incubated with human liver microsomes and the metabolites were analyzed by liquid chromatography/mass spectrometry using electrospray ionization in positive or negative mode.	Tolbutamide	52-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
19026171-4	2008	The inhibitory potential of fluoroquinolones on CYP1A2 and CYP2C9 was investigated.	Fluoroquinolones	28-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
19026171-6	2008	Ciprofloxacin showed weak inhibition on both the activity of CYP1A2 (IC50 135 micromol/L) and CYP2C9 (IC50 180 micromol/L), whereas levofloxacin inhibited only CYP2C9 (IC50 210 micromol/L).	Ciprofloxacin	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
19017829-1	2008	OBJECTIVE: To report a case in which the anticoagulation effect of warfarin appeared to be potentiated by torsemide, possibly due to an interference of metabolism through competition for the CYP2C9 isoenzyme and protein-binding displacement of warfarin.	Torsemide	106-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
19026171-8	2008	CONCLUSION: Caderofloxacin, antofloxacin, moxifloxacin, and gatifloxacin are negligible inhibitors to CYP1A2 and CYP2C9.	cadrofloxacin	12-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
19017829-5	2008	DISCUSSION: Both torsemide and warfarin are highly protein-bound to albumin and are major substrates for the CYP2C9 isoenzyme.	Torsemide	17-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
19017829-5	2008	DISCUSSION: Both torsemide and warfarin are highly protein-bound to albumin and are major substrates for the CYP2C9 isoenzyme.	Warfarin	31-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
19026171-8	2008	CONCLUSION: Caderofloxacin, antofloxacin, moxifloxacin, and gatifloxacin are negligible inhibitors to CYP1A2 and CYP2C9.	antofloxacin	28-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
19026171-8	2008	CONCLUSION: Caderofloxacin, antofloxacin, moxifloxacin, and gatifloxacin are negligible inhibitors to CYP1A2 and CYP2C9.	Moxifloxacin	42-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
19017829-8	2008	Therefore, it is possible that the addition of torsemide may potentiate the anticoagulant effect of warfarin by (1) competition for metabolism through CYP2C9, with a decrease in the clearance of warfarin, and (2) protein-binding displacement of warfarin from albumin, transiently potentiating anticoagulant activity.	Torsemide	47-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	151-157
19026171-8	2008	CONCLUSION: Caderofloxacin, antofloxacin, moxifloxacin, and gatifloxacin are negligible inhibitors to CYP1A2 and CYP2C9.	Gatifloxacin	60-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
19017829-8	2008	Therefore, it is possible that the addition of torsemide may potentiate the anticoagulant effect of warfarin by (1) competition for metabolism through CYP2C9, with a decrease in the clearance of warfarin, and (2) protein-binding displacement of warfarin from albumin, transiently potentiating anticoagulant activity.	Warfarin	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	151-157
18787056-4	2008	In the presence of HLMs, sulfaphenazole (CYP2C9 inhibitor), and anti-CYP2C9 monoclonal antibodies (mAbs) inhibited (73-100%) the 2- and 3-hydroxylation of both IBU enantiomers (1 and 20 microM).	Sulfaphenazole	25-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
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.	Hydroxylamine	58-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
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
18799803-3	2008	SKF525A and its metabolite and primary amine analog all inhibited CYP2B6-, CYP2C9-, CYP2C19-, CYP2D6-, and CYP3A-selective reactions to varying degrees but had little effect on CYP1A2, CYP2A6, and CYP2E1 reactions.	Proadifen	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
18784266-0	2008	CYP2C9-catalyzed metabolism of S-warfarin to 7-hydroxywarfarin in vivo and in vitro in chimeric mice with humanized liver.	Warfarin	31-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
18784266-0	2008	CYP2C9-catalyzed metabolism of S-warfarin to 7-hydroxywarfarin in vivo and in vitro in chimeric mice with humanized liver.	7-hydroxywarfarin	45-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
18799803-3	2008	SKF525A and its metabolite and primary amine analog all inhibited CYP2B6-, CYP2C9-, CYP2C19-, CYP2D6-, and CYP3A-selective reactions to varying degrees but had little effect on CYP1A2, CYP2A6, and CYP2E1 reactions.	Amines	39-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
18787056-4	2008	In the presence of HLMs, sulfaphenazole (CYP2C9 inhibitor), and anti-CYP2C9 monoclonal antibodies (mAbs) inhibited (73-100%) the 2- and 3-hydroxylation of both IBU enantiomers (1 and 20 microM).	Ibuprofen	160-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
18787056-4	2008	In the presence of HLMs, sulfaphenazole (CYP2C9 inhibitor), and anti-CYP2C9 monoclonal antibodies (mAbs) inhibited (73-100%) the 2- and 3-hydroxylation of both IBU enantiomers (1 and 20 microM).	Ibuprofen	160-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
18784266-2	2008	In this study, we investigated whether these mice have a capacity for drug metabolism similar to that of humans by examining hydroxylation of S-warfarin, which is predominantly metabolized to S-7-hydroxywarfarin, catalyzed by CYP2C9, in humans but not mice.	Warfarin	142-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	226-232
18784266-2	2008	In this study, we investigated whether these mice have a capacity for drug metabolism similar to that of humans by examining hydroxylation of S-warfarin, which is predominantly metabolized to S-7-hydroxywarfarin, catalyzed by CYP2C9, in humans but not mice.	7-hydroxywarfarin	192-211	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	226-232
18787056-7	2008	When (S)-(+)-IBU and (R)-(-)-IBU (1 microM) were incubated with a panel of recombinant human P450s, only CYP2C9 formed appreciable amounts of the hydroxy metabolites.	Ibuprofen	5-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
18787056-7	2008	When (S)-(+)-IBU and (R)-(-)-IBU (1 microM) were incubated with a panel of recombinant human P450s, only CYP2C9 formed appreciable amounts of the hydroxy metabolites.	Ibuprofen	21-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
18787056-11	2008	On the other hand, CYP2C9 inhibition and genotype are expected to have an impact on the PK of (S)-(+)-IBU.	Ibuprofen	94-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
25855835-20	2008	CONCLUSIONS: Certain CYP2C9 and VKORC1 variants are associated with lower warfarin maintenance doses, and CYP2C9 variants are associated with increased bleeding rates among patients who use warfarin.	Warfarin	74-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
25855835-6	2008	RESULTS: The 99 included articles reported 103 studies: 29 tested the association of CYP2C9 and the response to warfarin; 19 tested the association of VKORC1 and the response to warfarin; 44 tested the association of Apo E and the response to statins; and 11 tested the association of MTHFR with the response to antifolate chemotherapy.CYP2C9 AND VKORC1 GENE POLYMORPHISMS AND RESPONSE TO WARFARIN THERAPY: Of the 29 studies of CYP2C9 gene polymorphisms, 26 evaluated their association with responses to maintenance does of warfarin.	Warfarin	112-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
19132230-7	2008	The impact of the CYP2C9 and VKORC1 genotype is most significant during the initial period of coumarin anticoagulant therapy.	coumarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
19132230-9	2008	The CYP2C9 polymorphism is associated with delayed stabilisation for coumarin anticoagulants.	coumarin	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
18922023-0	2008	Functional analysis of phenylalanine residues in the active site of cytochrome P450 2C9.	Phenylalanine	23-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-87
18922023-1	2008	The two published crystal structures of cytochrome P450 2C9, complexed with ( S)-warfarin or flurbiprofen, implicate a cluster of three active site phenylalanine residues (F100, F114, F476) in ligand binding.	Warfarin	76-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-59
18922023-1	2008	The two published crystal structures of cytochrome P450 2C9, complexed with ( S)-warfarin or flurbiprofen, implicate a cluster of three active site phenylalanine residues (F100, F114, F476) in ligand binding.	Flurbiprofen	93-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-59
18922023-1	2008	The two published crystal structures of cytochrome P450 2C9, complexed with ( S)-warfarin or flurbiprofen, implicate a cluster of three active site phenylalanine residues (F100, F114, F476) in ligand binding.	Phenylalanine	148-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-59
18922023-3	2008	To elucidate the importance of CYP2C9"s active site phenylalanines on substrate binding, orientation, and catalytic turnover, a series of leucine and tryptophan mutants were constructed and their interactions with ( S)-warfarin and ( S)-flurbiprofen examined.	Phenylalanine	52-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
18922023-3	2008	To elucidate the importance of CYP2C9"s active site phenylalanines on substrate binding, orientation, and catalytic turnover, a series of leucine and tryptophan mutants were constructed and their interactions with ( S)-warfarin and ( S)-flurbiprofen examined.	Leucine	138-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
18922023-3	2008	To elucidate the importance of CYP2C9"s active site phenylalanines on substrate binding, orientation, and catalytic turnover, a series of leucine and tryptophan mutants were constructed and their interactions with ( S)-warfarin and ( S)-flurbiprofen examined.	Tryptophan	150-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
18922023-3	2008	To elucidate the importance of CYP2C9"s active site phenylalanines on substrate binding, orientation, and catalytic turnover, a series of leucine and tryptophan mutants were constructed and their interactions with ( S)-warfarin and ( S)-flurbiprofen examined.	Warfarin	214-227	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
18922023-3	2008	To elucidate the importance of CYP2C9"s active site phenylalanines on substrate binding, orientation, and catalytic turnover, a series of leucine and tryptophan mutants were constructed and their interactions with ( S)-warfarin and ( S)-flurbiprofen examined.	Flurbiprofen	232-249	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
25855835-8	2008	Carriers of the CYP2C9 gene variant alleles *2 or *3 had lower mean maintenance warfarin dose requirements than did non-carriers.	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
25855835-9	2008	Few studies investigated the relationship between genetic variations in CYP2C9 or VKORC1 and warfarin dose requirements in the induction phase.	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
25855835-10	2008	CYP2C9 variants were associated with an increased rate of bleeding complications during the induction phase of warfarin therapy, but the studies did not report whether affected patients had normal or supratherapeutic INR ranges.	Warfarin	111-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25855835-20	2008	CONCLUSIONS: Certain CYP2C9 and VKORC1 variants are associated with lower warfarin maintenance doses, and CYP2C9 variants are associated with increased bleeding rates among patients who use warfarin.	Warfarin	190-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
19018719-0	2008	VKORC1 and CYP2C9 allelic variants influence acenocoumarol dose requirements in Greek patients.	Acenocoumarol	45-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
18787075-5	2008	Moreover, VEGF-stimulated endothelial cell sprouting in a modified spheroid assay was reduced by CYP2C antisense oligonucleotides.	Oligonucleotides	113-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-102
19069171-4	2008	Recently genetic factors such as the CYP2C9 and VKORC1 genes have been demonstrated to be determinants of warfarin response.	Warfarin	106-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
19069171-5	2008	CYP2C9 is the enzyme primarily responsible for the metabolic clearance of the S-enantiomer of warfarin.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19069171-8	2008	On the basis of these observations, the Food and Drug Administration (FDA) approved a labeling change for warfarin that includes the genetic information of VKORC1 and CYP2C9 as factors influencing interindividual variability in warfarin dosing.	Warfarin	106-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
19069171-8	2008	On the basis of these observations, the Food and Drug Administration (FDA) approved a labeling change for warfarin that includes the genetic information of VKORC1 and CYP2C9 as factors influencing interindividual variability in warfarin dosing.	Warfarin	228-236	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
19108785-11	2008	Nilotinib is a competitive inhibitor of cytochrome P450 (CYP) 3A4, CYP2C8, CYP2C9, and CYP2D6.	nilotinib	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
19211991-0	2008	Limited applicability of 7-methoxy-4-trifluoromethylcoumarin as a CYP2C9-selective substrate.	7-methoxy-4-trifluoromethylcoumarin	25-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
19211991-2	2008	7-Methoxy-4-trifluoromethylcoumarin (MFC) has been reported as a CYP2C9-selective substrate.	7-methoxy-4-trifluoromethylcoumarin	0-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
19211991-2	2008	7-Methoxy-4-trifluoromethylcoumarin (MFC) has been reported as a CYP2C9-selective substrate.	7-methoxy-4-trifluoromethylcoumarin	37-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
17961958-3	2008	To our knowledge, this is the first description of phenytoin intoxication due to CYP2C9 inhibition by clozapine.	Phenytoin	51-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
17961958-3	2008	To our knowledge, this is the first description of phenytoin intoxication due to CYP2C9 inhibition by clozapine.	Clozapine	102-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
19018719-8	2008	In a multivariable regression model, CYP2C9, VKORC1 genotypes and age explained 55% of acenocoumarol dosing variability.	Acenocoumarol	87-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
19018719-9	2008	CONCLUSION: VKORC1-1639G>A, CYP2C9*2 and CYP2C9*3 polymorphisms were found to predispose to acenocoumarol sensitivity in Greeks.	Acenocoumarol	95-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
19018719-9	2008	CONCLUSION: VKORC1-1639G>A, CYP2C9*2 and CYP2C9*3 polymorphisms were found to predispose to acenocoumarol sensitivity in Greeks.	Acenocoumarol	95-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
18548238-2	2008	We have demonstrated the relevance of CYP2C9 genotypes for diclofenac 4"-hydroxylation in healthy volunteers, so that the present study was aimed at analyzing the role of both CYP2C8 and CYP2C9 genotypes on diclofenac metabolism, as well as determining the CYP2C8 allele frequencies and their relationship with CYP2C9 variants.	diclofenac 4"	59-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
18680736-7	2008	The associations of SNPs rs9934438 and rs9923231 of VKORC1, the 3 (rs1057910) and C(-65) (rs9332127) alleles of CYP2C9, and SNP rs4653436 of EPHXI with the dose of warfarin were significant.	Warfarin	164-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
18680736-8	2008	CONCLUSION: A multiple regression model based on the genetic polymorphisms of VKORC1, CYP2C9, EPHX1 and the non-genetic factors of age and body weight can explain 40.2% of the variance in warfarin dose in Han Chinese patients.	Warfarin	188-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
18758764-3	2008	Carriers of cytochrome P450 2C9 (CYP2C9)-deficient alleles have a reduced clearance of warfarin and are exposed to dramatic overdoses in the first weeks of treatment.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-31
18758764-3	2008	Carriers of cytochrome P450 2C9 (CYP2C9)-deficient alleles have a reduced clearance of warfarin and are exposed to dramatic overdoses in the first weeks of treatment.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
18758764-6	2008	Several warfarin dosing algorithms have been constructed, adapted on CYP2C9 and VKORC1 genotypes and clinical factors, to predict the best dose for each patient.	Warfarin	8-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
18669935-3	2008	We hypothesized that inhibition of CYP 2C9 signaling with sulfaphenazole would improve EDD in older, but not young, healthy sedentary adults.	Sulfaphenazole	58-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-42
18606741-4	2008	We expressed and purified the R108E and R108E/D293N mutants and compared their ability with that of native CYP2C9 to interact with (S)-warfarin, diclofenac, pyrene, propranolol, and ibuprofen amine.	Warfarin	131-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
18606741-4	2008	We expressed and purified the R108E and R108E/D293N mutants and compared their ability with that of native CYP2C9 to interact with (S)-warfarin, diclofenac, pyrene, propranolol, and ibuprofen amine.	Diclofenac	145-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
18606741-4	2008	We expressed and purified the R108E and R108E/D293N mutants and compared their ability with that of native CYP2C9 to interact with (S)-warfarin, diclofenac, pyrene, propranolol, and ibuprofen amine.	pyrene	157-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
18606741-4	2008	We expressed and purified the R108E and R108E/D293N mutants and compared their ability with that of native CYP2C9 to interact with (S)-warfarin, diclofenac, pyrene, propranolol, and ibuprofen amine.	Propranolol	165-176	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
18679669-2	2008	In vitro, nebicapone has showed an inhibitory effect upon CYP2C9, which is responsible for the metabolism of S-warfarin.	nebicapone	10-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
18679669-2	2008	In vitro, nebicapone has showed an inhibitory effect upon CYP2C9, which is responsible for the metabolism of S-warfarin.	Warfarin	109-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
18548238-2	2008	We have demonstrated the relevance of CYP2C9 genotypes for diclofenac 4"-hydroxylation in healthy volunteers, so that the present study was aimed at analyzing the role of both CYP2C8 and CYP2C9 genotypes on diclofenac metabolism, as well as determining the CYP2C8 allele frequencies and their relationship with CYP2C9 variants.	Diclofenac	59-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
18975556-7	2008	Moreover, testing for CYP2C9*3 and VKORC1 6484 C>T was shown to be useful for the safe administration of warfarin.	Warfarin	108-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
18855533-6	2008	RESULTS: VKORC1 explained 18% (30% with CYP2C9) variability in warfarin dose among European-Americans and 5% (8% with CYP2C9) among African-Americans.	Warfarin	63-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
18855533-10	2008	CONCLUSIONS: Our findings support the use of CYP2C9, VKORC1 polymorphisms (rs9934438 or rs9923231) and clinical covariates to predict warfarin dose in both African- and European-Americans.	Warfarin	134-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
18855533-11	2008	A uniform set of common polymorphisms in CYP2C9 and VKORC1, and limited clinical covariates can be used to improve warfarin dose prediction for a racially diverse population.	Warfarin	115-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
18584988-3	2008	The 384-well assay used human liver microsomes in conjunction with a cocktail of probe substrates metabolized by the five major CYPs (tacrine for CYP1A2, diclofenac for CYP2C9, (S)-mephenytoin for CYP2C19, dextromethorphan for CYP2D6 and midazolam for CYP3A4).	Diclofenac	154-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
18682545-12	2008	CONCLUSIONS: There is growing evidence that variant alleles for CYP2C9 and VKORC1 genotypes account for a proportion of the variability seen in warfarin dosing.	Warfarin	144-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
18585438-3	2008	CYP2C9 and CYP2C19 possessed high enantioselectivity favoring the formation of S-Mono-OH-M; CYP2C3 showed no enantioselectivity, whereas CYP2C5 slightly favored the formation of R-Mono-OH-M.	1,1,1-trichloro-2-(4-hydroxyphenyl)-2-(4-methoxyphenyl)ethane	79-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
18585438-3	2008	CYP2C9 and CYP2C19 possessed high enantioselectivity favoring the formation of S-Mono-OH-M; CYP2C3 showed no enantioselectivity, whereas CYP2C5 slightly favored the formation of R-Mono-OH-M.	r-mono-oh-m	178-189	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
18542936-0	2008	VKORC1 and CYP2C9 polymorphisms are associated with warfarin dose requirements in Turkish patients.	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
18542936-1	2008	OBJECTIVES: The objective of this study was to determine the quantitative influence of vitamin K epoxide reductase complex subunit 1 (VKORC1) and cytochrome P450 2C9 (CYP 2C9) polymorphisms on warfarin dose requirements in Turkish patients.	Warfarin	193-201	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-165
18542936-6	2008	Patients who carried VKORC1 and CYP2C9 variants needed a 40% lower mean weekly warfarin dose compared to wild types.	Warfarin	79-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
18542936-8	2008	CONCLUSION: Polymorphisms in VKORC1 and CYP2C9 genes were important determinants of warfarin dose requirements in Turkish patients.	Warfarin	84-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
18752379-2	2008	We review the evidence of the influence of the two key genes of interest, the cytochrome P450 2C9 gene, CYP2C9, and the vitamin K epoxide reductase complex 1 gene, VKORC1, on warfarin response and discuss the implications of current knowledge for clinical practice.	Warfarin	175-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-97
18752379-2	2008	We review the evidence of the influence of the two key genes of interest, the cytochrome P450 2C9 gene, CYP2C9, and the vitamin K epoxide reductase complex 1 gene, VKORC1, on warfarin response and discuss the implications of current knowledge for clinical practice.	Warfarin	175-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
18752379-3	2008	The influence of CYP2C9 and VKORC1 genotypes on warfarin dose requirements has been consistently demonstrated in diverse racial and ethnic patient groups in observational studies and randomized clinical trials.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
18480186-3	2008	The curcuminoid extract inhibited SULT > CYP2C19 > CYP2B6 > UGT > CYP2C9 > CYP3A activities with IC(50) values ranging from 0.99 +/- 0.04 to 25.3 +/- 1.3 microM, whereas CYP2D6, CYP1A2, and CYP2E1 activities were less affected (IC(50) values > 60 microM).	curcuminoid	4-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
18535201-1	2008	Warfarin dosing is correlated with polymorphisms in vitamin K epoxide reductase complex 1 (VKORC1) and the cytochrome P450 2C9 (CYP2C9) genes.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-126
18535201-1	2008	Warfarin dosing is correlated with polymorphisms in vitamin K epoxide reductase complex 1 (VKORC1) and the cytochrome P450 2C9 (CYP2C9) genes.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
18763667-7	2008	The combination of physiologic factors (30%), CYP2C9 variations (20%) and VKORC1 variants (25%) accounts for approximately 75% of warfarin dose variability.	Warfarin	130-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
19032008-5	2008	Following completion of the Human Genome Project, several genetic variants of CYP2C9 and VKORC1 have been identified that account for a greater proportion of the variability in patient response to warfarin than is explained by nongenetic factors.	Warfarin	197-205	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
18781859-3	2008	For example, persons of African descent have lower allele frequencies of the CYP2C9*2 and *3 and VKORC1 1173T allele, which have been associated with lower warfarin dose requirements in Caucasians.	Warfarin	156-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
18816302-0	2008	Disposition of a CYP2C9 phenotyping agent, losartan, is not influenced by the common 3435C > T variation of the drug transporter gene ABCB1 (MDR1).	Losartan	43-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
18816302-1	2008	Losartan is oxidized to E3174 by cytochrome P450 2C9 (CYP2C9); it has been suggested as a useful probe drug for CYP2C9 activity.	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-52
18816302-1	2008	Losartan is oxidized to E3174 by cytochrome P450 2C9 (CYP2C9); it has been suggested as a useful probe drug for CYP2C9 activity.	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
18816302-1	2008	Losartan is oxidized to E3174 by cytochrome P450 2C9 (CYP2C9); it has been suggested as a useful probe drug for CYP2C9 activity.	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
18816302-1	2008	Losartan is oxidized to E3174 by cytochrome P450 2C9 (CYP2C9); it has been suggested as a useful probe drug for CYP2C9 activity.	losartan carboxylic acid	24-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-52
18816302-1	2008	Losartan is oxidized to E3174 by cytochrome P450 2C9 (CYP2C9); it has been suggested as a useful probe drug for CYP2C9 activity.	losartan carboxylic acid	24-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
18816302-1	2008	Losartan is oxidized to E3174 by cytochrome P450 2C9 (CYP2C9); it has been suggested as a useful probe drug for CYP2C9 activity.	losartan carboxylic acid	24-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
18474675-2	2008	Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A).	Clopidogrel	41-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	301-307
18474675-2	2008	Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A).	Ticlopidine	54-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	301-307
18474675-2	2008	Mechanism-based CYP2B6 inhibitors (i.e., clopidogrel, ticlopidine, and triethylenethiophoramide) significantly inhibited the formation of M1 from sibutramine and M2 from M1, respectively; in contrast, no effect was observed when using potent inhibitors of eight P450 isozymes (CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A).	triethylenethiophoramide	71-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	301-307
18480186-8	2008	All three curcuminoids had similar effects on CYP3A, UGT, and SULT activity, but demethoxycurcumin (IC(50) = 8.8 +/- 1.2 microM) was more active against CYP2C9 than either curcumin or bisdemethoxycurcumin (IC(50) > 50 microM).	demethoxycurcumin	81-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
18480186-10	2008	administered curcuminoid/piperine combination is most likely to inhibit CYP3A, CYP2C9, UGT, and SULT metabolism within the intestinal mucosa.	curcuminoid	13-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
18480186-10	2008	administered curcuminoid/piperine combination is most likely to inhibit CYP3A, CYP2C9, UGT, and SULT metabolism within the intestinal mucosa.	piperine	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
18971529-0	2008	Genetic variations of CYP2C9 in 724 Japanese individuals and their impact on the antihypertensive effects of losartan.	Losartan	109-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
18662109-7	2008	Etravirine is an inducer of CYP3A4 and a weak inhibitor of CYP2C9, CYP2C19 and P-glycoprotein.	etravirine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
18971529-1	2008	CYP2C9, a drug-metabolizing enzyme, converts the angiotensin II receptor blocker losartan to its active form, which is responsible for its antihypertensive effect.	Losartan	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
18971529-5	2008	After 3 months of losartan treatment, systolic blood pressure was not lowered in two patients with CYP2C9* 1/*30, suggesting that they exhibited impaired in vivo CYP2C9 activity.	Losartan	18-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
18971529-6	2008	CYP2C9*30 might be associated with a diminished response to the antihypertensive effects of losartan.	Losartan	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
18485885-0	2008	Substrate proton to heme distances in CYP2C9 allelic variants and alterations by the heterotropic activator, dapsone.	Heme	20-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
18485885-4	2008	Co-incubation with dapsone resulted in reduced substrate proton to heme-iron distances for all enzymes, providing at least a partial mechanism for the activation of CYP2C9 variants by dapsone.	Dapsone	19-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	165-171
18485885-4	2008	Co-incubation with dapsone resulted in reduced substrate proton to heme-iron distances for all enzymes, providing at least a partial mechanism for the activation of CYP2C9 variants by dapsone.	Heme	67-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	165-171
18628990-3	2008	Herein, we first evaluated the inhibitory effects of fifteen ginsenosides and sapogenins on human CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4 enzymes by using commercially available fluorescent probes.	Ginsenosides	61-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
18485885-4	2008	Co-incubation with dapsone resulted in reduced substrate proton to heme-iron distances for all enzymes, providing at least a partial mechanism for the activation of CYP2C9 variants by dapsone.	Iron	72-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	165-171
18485885-4	2008	Co-incubation with dapsone resulted in reduced substrate proton to heme-iron distances for all enzymes, providing at least a partial mechanism for the activation of CYP2C9 variants by dapsone.	Dapsone	184-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	165-171
18485885-5	2008	In summary, neither altered binding affinity nor substrate orientation appear to be major factors in the reduced catalytic activity noted in the CYP2C9 variants, but dapsone co-incubation caused similar changes in substrate proton to heme-iron distances suggesting at least partial common mechanisms in the activation of the CYP2C9 forms.	Dapsone	166-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	325-331
18776969-3	2008	Genetic polymorphism of the VKORC1 and CYP2C9 genes, as well as clinical factors such as age, gender, body mass index and interacting drugs explain less than 55% of variability in warfarin dose requirements.	Warfarin	180-188	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
18628990-3	2008	Herein, we first evaluated the inhibitory effects of fifteen ginsenosides and sapogenins on human CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4 enzymes by using commercially available fluorescent probes.	Sapogenins	78-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
18503607-3	2008	Glyburide, a sulphonylurea, is an insulin sensitizer and mainly metabolized by CYP2C9.	Glyburide	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
18503607-3	2008	Glyburide, a sulphonylurea, is an insulin sensitizer and mainly metabolized by CYP2C9.	Sulfonylurea Compounds	13-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
18378563-2	2008	Previous in vitro work has demonstrated that genotype-dependent inhibition of CYP2C9 mediated flurbiprofen metabolism, suggesting the possibility of genotype-dependent inhibition interactions in vivo.	Flurbiprofen	94-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
18381488-4	2008	Fluconazole is also a moderate inhibitor of CYP2C9 and CYP2C19.	Fluconazole	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
18385292-8	2008	The P450 probe substrates indicate a decrease in CYP1A2, CYP2B6, CYP2C9, and CYP3A4 activities in HepaRG cells 1 day after removal of DMSO from the medium.	Dimethyl Sulfoxide	134-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
18690342-1	2008	The objective of this study was to assess the relative influence of VKORC1 and CYP2C9 genetic variants on several clinical outcomes related to warfarin treatment.	Warfarin	143-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
18690342-7	2008	CYP2C9 alone, VKORC1 alone, and a combination of genetic and clinical factors explained 12%, 27%, and 50%, respectively, of the variation in warfarin maintenance dose.	Warfarin	141-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
18183038-0	2008	Prospective study of warfarin dosage requirements based on CYP2C9 and VKORC1 genotypes.	Warfarin	21-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
18183038-1	2008	Polymorphisms in CYP2C9 and VKORC1 have been shown to be associated with warfarin dose requirements and could be used to predict warfarin dose.	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
18183038-1	2008	Polymorphisms in CYP2C9 and VKORC1 have been shown to be associated with warfarin dose requirements and could be used to predict warfarin dose.	Warfarin	129-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
18183038-2	2008	We conducted a prospective study in which warfarin dose was prescribed based on CYP2C9 and VKORC1 polymorphisms in 108 Han-Chinese patients without prior warfarin treatments.	Warfarin	42-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
18694831-0	2008	Influence of CYP2C8 and CYP2C9 polymorphisms on pharmacokinetic and pharmacodynamic parameters of racemic and enantiomeric forms of ibuprofen in healthy volunteers.	Ibuprofen	132-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
18576910-7	2008	Warfarin has two enantiomers, R-and S-warfarin, which are substrates primarily of cytochrome P450 (CYP) 3A4 (R-warfarin), CYP1A2 (R-warfarin), and CYP2C9 (S-warfarin).	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
18576910-7	2008	Warfarin has two enantiomers, R-and S-warfarin, which are substrates primarily of cytochrome P450 (CYP) 3A4 (R-warfarin), CYP1A2 (R-warfarin), and CYP2C9 (S-warfarin).	Ranolazine	30-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
18793590-10	2008	CONCLUSIONS: CYP2C9 activity as measured by apparent oral clearance and urinary metabolic ratio following oral tolbutamide appear similar in people with and without cancer.	Tolbutamide	111-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
18576910-7	2008	Warfarin has two enantiomers, R-and S-warfarin, which are substrates primarily of cytochrome P450 (CYP) 3A4 (R-warfarin), CYP1A2 (R-warfarin), and CYP2C9 (S-warfarin).	Sulfur	36-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
18576910-7	2008	Warfarin has two enantiomers, R-and S-warfarin, which are substrates primarily of cytochrome P450 (CYP) 3A4 (R-warfarin), CYP1A2 (R-warfarin), and CYP2C9 (S-warfarin).	Warfarin	38-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
18694831-7	2008	CYP2C9*3 allele had a decreased racemic ibuprofen metabolism, leading to a 30% augmentation of AUC(0-infinity) and a 30% reduction of clearance compared to CYP2C9*1 (p < 0.05).	Ibuprofen	40-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
18694831-7	2008	CYP2C9*3 allele had a decreased racemic ibuprofen metabolism, leading to a 30% augmentation of AUC(0-infinity) and a 30% reduction of clearance compared to CYP2C9*1 (p < 0.05).	Ibuprofen	40-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
18694831-9	2008	CYP2C9*3 had a 45% reduction of clearance, as well as a 87% and 47% augmentation of AUC(0-infinity) and t(1/2) with respect to CYP2C9*1 of S-ibuprofen and a 30% reduction of clearance of R-ibuprofen.	Ibuprofen	139-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
18694831-9	2008	CYP2C9*3 had a 45% reduction of clearance, as well as a 87% and 47% augmentation of AUC(0-infinity) and t(1/2) with respect to CYP2C9*1 of S-ibuprofen and a 30% reduction of clearance of R-ibuprofen.	Ibuprofen	139-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-133
18694831-9	2008	CYP2C9*3 had a 45% reduction of clearance, as well as a 87% and 47% augmentation of AUC(0-infinity) and t(1/2) with respect to CYP2C9*1 of S-ibuprofen and a 30% reduction of clearance of R-ibuprofen.	Ibuprofen	187-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
18694831-9	2008	CYP2C9*3 had a 45% reduction of clearance, as well as a 87% and 47% augmentation of AUC(0-infinity) and t(1/2) with respect to CYP2C9*1 of S-ibuprofen and a 30% reduction of clearance of R-ibuprofen.	Ibuprofen	187-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-133
18694831-12	2008	CONCLUSIONS: This study suggest an impaired metabolism of racemic, S-ibuprofen and R-ibuprofen in CYP2C9*3; an increased R-ibuprofen metabolism in CYP2C8*3; and fewer adverse events in CYP2C8*3 volunteers; that correlates with a decreased expression of iNOS.	Ibuprofen	67-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
18694831-12	2008	CONCLUSIONS: This study suggest an impaired metabolism of racemic, S-ibuprofen and R-ibuprofen in CYP2C9*3; an increased R-ibuprofen metabolism in CYP2C8*3; and fewer adverse events in CYP2C8*3 volunteers; that correlates with a decreased expression of iNOS.	Ibuprofen	83-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
18362161-4	2008	In vitro studies have shown that CYP2C19, CYP3A4, and to a lesser extent CYP2C9 contribute to the oxidative metabolism of voriconazole.	Voriconazole	122-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
18559094-0	2008	Warfarin dose and INR related to genotypes of CYP2C9 and VKORC1 in patients with myocardial infarction.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
18559094-2	2008	Individual dosage requirement has recently partly been explained by genetic variation of the warfarin metabolizing enzyme CYP2C9 and the Vitamin K-activating enzyme VKORC1.	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
18559094-4	2008	AIMS: The primary aim of the present study was to investigate the relation between genotypes of CYP2C9 and VKORC1 and warfarin maintenance dose in myocardial infarction.	Warfarin	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
18559094-10	2008	Warfarin dosage requirement was significantly associated with CYP2C9 and VKORC1 genotypes, treatment group and age.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
18559094-12	2008	CONCLUSION: CYP2C9 and VKORC1 genotype frequencies in myocardial infarction patients appear similar to other patient groups and have similar impact on warfarin maintenance dose.	Warfarin	151-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
18576910-9	2008	The increased warfarin doses required in these two patients may have been caused by induction of CYP3A4 by nevirapine, CYP2C9 by nelfinavir, or CYP2C9 by lopinavir-ritonavir.	Warfarin	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
18576910-9	2008	The increased warfarin doses required in these two patients may have been caused by induction of CYP3A4 by nevirapine, CYP2C9 by nelfinavir, or CYP2C9 by lopinavir-ritonavir.	Warfarin	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
18576910-9	2008	The increased warfarin doses required in these two patients may have been caused by induction of CYP3A4 by nevirapine, CYP2C9 by nelfinavir, or CYP2C9 by lopinavir-ritonavir.	Nelfinavir	129-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
18576910-9	2008	The increased warfarin doses required in these two patients may have been caused by induction of CYP3A4 by nevirapine, CYP2C9 by nelfinavir, or CYP2C9 by lopinavir-ritonavir.	Lopinavir	154-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
18576910-9	2008	The increased warfarin doses required in these two patients may have been caused by induction of CYP3A4 by nevirapine, CYP2C9 by nelfinavir, or CYP2C9 by lopinavir-ritonavir.	Ritonavir	164-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
17851564-3	2008	We hypothesized that capecitabine inhibits the synthesis of CYP2C9, which metabolizes indisulam.	Capecitabine	21-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
17851564-3	2008	We hypothesized that capecitabine inhibits the synthesis of CYP2C9, which metabolizes indisulam.	N-(3-chloro-7-indolyl)-1,4-benzenedisulphonamide	86-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
18043684-0	2008	The polymorphisms Asn130Asp and Val174Ala in OATP1B1 and the CYP2C9 allele *3 independently affect torsemide pharmacokinetics and pharmacodynamics.	Torsemide	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
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
18756910-0	2008	Association of CYP2C9 gene polymorphism with bleeding as a complication of warfarin therapy.	Warfarin	75-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
18756910-1	2008	The aim of this study was to determine the association of bleeding as a complication of warfarin therapy with polymorphism of CYP2C9 gene (alleles 1, 2 and 3).	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
18756910-2	2008	The CYP2C9 is the main enzyme for warfarin metabolism.	Warfarin	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
18756910-11	2008	Polymorphism of CYP2C9 could determine dose of warfarin therapy and thus it could be related to the risk of bleeding complications.	Warfarin	47-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
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.	hydroxycyclophosphamide	239-262	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
18496133-2	2008	CYP2J2, CYP2C8, and CYP2C9 are known to be a source of epoxyeicosatrienoic acids in cardiac tissues.	epoxyeicosatrienoic acids	55-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
29783498-0	2008	High carrier prevalence of combinatorial CYP2C9 and VKORC1 genotypes affecting warfarin dosing.	Warfarin	79-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
18234403-3	2008	In particularly, molecular analysis of two genes, encoding for the enzyme responsible for the warfarin (S)-isoform catabolism (CYP2C9) and for the target enzyme vitamin K epoxide reductase complex 1 (VKORC1), strongly suggested that their genetic variations greatly affect the individual response to oral anticoagulants.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-133
18294321-3	2008	CYP2C9 and VKORC1 polymorphisms have been shown to affect warfarin dose requirement.	Warfarin	58-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
18305126-3	2008	Tadalafil is mainly metabolized by cytochrome P450 (CYP) 3A4, and as bosentan induces CYP2C9 and CYP3A4, a pharmacokinetic interaction is possible between these agents.	Bosentan	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
18356043-2	2008	Screening with well-established chemical inhibitors showed that the formation of norethindrone was potently inhibited by CYP3A4 inhibitor ketoconazole (IC(50)=0.02 microM) and with CYP2C9 inhibitor sulphaphenazole (IC(50)=2.13 microM); the further biotransformation of norethindrone was strongly inhibited by ketoconazole (IC(50)=0.09 microM).	Norethindrone	81-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
18356043-2	2008	Screening with well-established chemical inhibitors showed that the formation of norethindrone was potently inhibited by CYP3A4 inhibitor ketoconazole (IC(50)=0.02 microM) and with CYP2C9 inhibitor sulphaphenazole (IC(50)=2.13 microM); the further biotransformation of norethindrone was strongly inhibited by ketoconazole (IC(50)=0.09 microM).	Sulfaphenazole	198-213	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
18356043-4	2008	Lynestrenol bioactivation was mainly catalysed by recombinant human CYP2C9, CYP2C19 and CYP3A4; rCYP3A4 was responsible for the hydroxylation of norethindrone.	Lynestrenol	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
18356043-4	2008	Lynestrenol bioactivation was mainly catalysed by recombinant human CYP2C9, CYP2C19 and CYP3A4; rCYP3A4 was responsible for the hydroxylation of norethindrone.	Norethindrone	145-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
18356043-5	2008	A significant correlation was observed between norethindrone formation and tolbutamide hydroxylation, a CYP2C9-selective activity (r=0.63; p=0.01).	Norethindrone	47-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
18356043-5	2008	A significant correlation was observed between norethindrone formation and tolbutamide hydroxylation, a CYP2C9-selective activity (r=0.63; p=0.01).	Tolbutamide	75-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
18570163-0	2008	Role of pharmacodiagnostic of CYP2C9 variants in the optimization of warfarin therapy in Malaysia: a 6-month follow-up study.	Warfarin	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
18570163-2	2008	A retrospective study was conducted to explore the importance of CYP2C9 genotyping for the initiation and maintenance therapy of warfarin in clinical practice.	Warfarin	129-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
18030307-0	2008	Combination of phenotype assessments and CYP2C9-VKORC1 polymorphisms in the determination of warfarin dose requirements in heavily medicated patients.	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
18030307-8	2008	Thus, combination of a phenotypic measure to CYP2C9-VKORC1 genotypes represents a useful strategy to predict warfarin doses in patients receiving multiple drugs (11+/-4 drugs/day).	Warfarin	109-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
18256202-0	2008	The "albumin effect" and in vitro-in vivo extrapolation: sequestration of long-chain unsaturated fatty acids enhances phenytoin hydroxylation by human liver microsomal and recombinant cytochrome P450 2C9.	long-chain unsaturated fatty acids	74-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	184-203
18256202-0	2008	The "albumin effect" and in vitro-in vivo extrapolation: sequestration of long-chain unsaturated fatty acids enhances phenytoin hydroxylation by human liver microsomal and recombinant cytochrome P450 2C9.	Phenytoin	118-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	184-203
18256202-2	2008	BSA and essentially fatty acid-free human serum albumin (HSA-FAF) reduced the K(m) values for PHY hydroxylation (based on unbound substrate concentration) by human liver microsomes (HLMs) and recombinant CYP2C9 by approximately 75%, with only a minor effect on V(max).	Fatty Acids	20-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	204-210
18256202-5	2008	A mixture of arachidonic, linoleic and oleic acids, at a concentration corresponding to 1/20 of the content of HLMs, doubled the K(m) for PHY hydroxylation by CYP2C9, without affecting V(max).	arachidonic	13-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
18256202-5	2008	A mixture of arachidonic, linoleic and oleic acids, at a concentration corresponding to 1/20 of the content of HLMs, doubled the K(m) for PHY hydroxylation by CYP2C9, without affecting V(max).	Linoleic Acid	26-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
18256202-5	2008	A mixture of arachidonic, linoleic and oleic acids, at a concentration corresponding to 1/20 of the content of HLMs, doubled the K(m) for PHY hydroxylation by CYP2C9, without affecting V(max).	Oleic Acids	39-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
18256202-7	2008	K(i) values for arachidonic acid inhibition of human liver microsomal- and CYP2C9-catalyzed PHY hydroxylation were 3.8 and 1.6 microM, respectively.	Arachidonic Acid	16-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
18356043-9	2008	Both lynestrenol and norethindrone were weak inhibitors of CYP2C9 (IC(50) of 32 microM and 46 microM for tolbutamide hydroxylation, respectively).	Lynestrenol	5-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
18356043-9	2008	Both lynestrenol and norethindrone were weak inhibitors of CYP2C9 (IC(50) of 32 microM and 46 microM for tolbutamide hydroxylation, respectively).	Norethindrone	21-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
18356043-9	2008	Both lynestrenol and norethindrone were weak inhibitors of CYP2C9 (IC(50) of 32 microM and 46 microM for tolbutamide hydroxylation, respectively).	Tolbutamide	105-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
18356043-10	2008	In conclusion, CYP2C9, CYP2C19 and CYP3A4 are the primary cytochromes in the bioactivation of lynestrenol in vitro, while CYP3A4 catalyses the further metabolism of norethindrone.	Lynestrenol	94-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
18356043-10	2008	In conclusion, CYP2C9, CYP2C19 and CYP3A4 are the primary cytochromes in the bioactivation of lynestrenol in vitro, while CYP3A4 catalyses the further metabolism of norethindrone.	Norethindrone	165-178	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
18466099-0	2008	Influence of CYP2C9 and VKORC1 on warfarin dose, anticoagulation attainment and maintenance among European-Americans and African-Americans.	Warfarin	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
18466099-4	2008	RESULTS & CONCLUSION: CYP2C9 and VKORC1 accounted for up to 30% of the variability in warfarin dose among European-Americans and 10% among African-Americans.	Adenosine Monophosphate	9-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
18466099-4	2008	RESULTS & CONCLUSION: CYP2C9 and VKORC1 accounted for up to 30% of the variability in warfarin dose among European-Americans and 10% among African-Americans.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
29783498-1	2008	BACKGROUND: Polymorphisms in the cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) genes significantly alter the effective warfarin dose.	Warfarin	161-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-52
29783498-1	2008	BACKGROUND: Polymorphisms in the cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) genes significantly alter the effective warfarin dose.	Warfarin	161-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
29783498-2	2008	The CYP2C9*2 (430C>T), CYP2C9*3 (1075A>C) and VKORC1 -1639 G>A polymorphisms affect warfarin dose through altered metabolism (CYP2C9) and sensitivity (VKORC1).	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
29783498-2	2008	The CYP2C9*2 (430C>T), CYP2C9*3 (1075A>C) and VKORC1 -1639 G>A polymorphisms affect warfarin dose through altered metabolism (CYP2C9) and sensitivity (VKORC1).	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
29783498-2	2008	The CYP2C9*2 (430C>T), CYP2C9*3 (1075A>C) and VKORC1 -1639 G>A polymorphisms affect warfarin dose through altered metabolism (CYP2C9) and sensitivity (VKORC1).	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
29783498-9	2008	Combinatorial genotyping of CYP2C9 and VKORC1 can allow for individualized dosing of warfarin amongst patients with gene polymorphisms potentially reducing the risk of accentuated responses and bleeding.	Warfarin	85-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
18204476-0	2008	Effects of St John"s wort and CYP2C9 genotype on the pharmacokinetics and pharmacodynamics of gliclazide.	Gliclazide	94-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
18634396-8	2008	A common mutation in the gene coding for the cytochrome P450 (CYP2C9), with one or more combinations of its polymorphisms, is responsible for the reduced warfarin requirements or for the resistance to warfarin.	Warfarin	154-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
18634396-8	2008	A common mutation in the gene coding for the cytochrome P450 (CYP2C9), with one or more combinations of its polymorphisms, is responsible for the reduced warfarin requirements or for the resistance to warfarin.	Warfarin	201-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
18322281-1	2008	BACKGROUND: Genetic variants of the enzyme that metabolizes warfarin, cytochrome P-450 2C9 (CYP2C9), and of a key pharmacologic target of warfarin, vitamin K epoxide reductase (VKORC1), contribute to differences in patients" responses to various warfarin doses, but the role of these variants during initial anticoagulation is not clear.	Warfarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-90
17868191-2	2008	Carriers of CYP2C9 mutant alleles exhibit a diminished CYP2C9 metabolic capacity leading to decreased endothelium-derived hyperpolarizing factors (EDHF) synthesis and an increased risk for atherosclerosis.	hyperpolarizing factors	122-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
17868191-2	2008	Carriers of CYP2C9 mutant alleles exhibit a diminished CYP2C9 metabolic capacity leading to decreased endothelium-derived hyperpolarizing factors (EDHF) synthesis and an increased risk for atherosclerosis.	hyperpolarizing factors	122-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
17868191-2	2008	Carriers of CYP2C9 mutant alleles exhibit a diminished CYP2C9 metabolic capacity leading to decreased endothelium-derived hyperpolarizing factors (EDHF) synthesis and an increased risk for atherosclerosis.	edhf	147-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
17868191-2	2008	Carriers of CYP2C9 mutant alleles exhibit a diminished CYP2C9 metabolic capacity leading to decreased endothelium-derived hyperpolarizing factors (EDHF) synthesis and an increased risk for atherosclerosis.	edhf	147-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
18702389-0	2008	Acenocoumarol and phenytoin toxicity in the presence of CYP2C9 mutation.	Acenocoumarol	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
18702389-0	2008	Acenocoumarol and phenytoin toxicity in the presence of CYP2C9 mutation.	Phenytoin	18-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
18315785-1	2008	BACKGROUND AND OBJECTIVE: CYP2C9 is a polymorphic enzyme that has been reported to metabolize several clinically useful drugs such as warfarin, phenytoin and non-steroidal anti-inflammatory drugs.	Warfarin	134-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
18315785-1	2008	BACKGROUND AND OBJECTIVE: CYP2C9 is a polymorphic enzyme that has been reported to metabolize several clinically useful drugs such as warfarin, phenytoin and non-steroidal anti-inflammatory drugs.	Phenytoin	144-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
18367977-9	2008	Of all the AEDs, only phenytoin undergoes significant metabolism by cytochrome P450 isozymes with significant genetic polymorphisms (CYP2C9, CYP2C19).	Phenytoin	22-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
18311908-4	2008	In this study, the structural characteristics of nitrogen-containing compounds, which bind to the iron atom in two CYP isoforms (CYP2C9 and CYP3A4), were investigated.	Nitrogen	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
18311908-4	2008	In this study, the structural characteristics of nitrogen-containing compounds, which bind to the iron atom in two CYP isoforms (CYP2C9 and CYP3A4), were investigated.	Iron	98-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
18206980-5	2008	Among the several CYPs tested, CYP2C9/2C19 and 1A2 were the most efficient in EPA and DHA epoxidations.	Eicosapentaenoic Acid	78-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
18206980-5	2008	Among the several CYPs tested, CYP2C9/2C19 and 1A2 were the most efficient in EPA and DHA epoxidations.	Docosahexaenoic Acids	86-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
18206980-6	2008	It ensued that 10muM of these two omega3 fatty acids decreased by more than 80% and 60%, respectively, the formation by CYP2C9 of AA-epoxidised derivatives.	Fatty Acids, Omega-3	34-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
18322281-7	2008	CONCLUSIONS: Initial variability in the INR response to warfarin was more strongly associated with genetic variability in the pharmacologic target of warfarin, VKORC1, than with CYP2C9.	Warfarin	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	178-184
18322281-1	2008	BACKGROUND: Genetic variants of the enzyme that metabolizes warfarin, cytochrome P-450 2C9 (CYP2C9), and of a key pharmacologic target of warfarin, vitamin K epoxide reductase (VKORC1), contribute to differences in patients" responses to various warfarin doses, but the role of these variants during initial anticoagulation is not clear.	Warfarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
18322281-1	2008	BACKGROUND: Genetic variants of the enzyme that metabolizes warfarin, cytochrome P-450 2C9 (CYP2C9), and of a key pharmacologic target of warfarin, vitamin K epoxide reductase (VKORC1), contribute to differences in patients" responses to various warfarin doses, but the role of these variants during initial anticoagulation is not clear.	Warfarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-90
18322281-1	2008	BACKGROUND: Genetic variants of the enzyme that metabolizes warfarin, cytochrome P-450 2C9 (CYP2C9), and of a key pharmacologic target of warfarin, vitamin K epoxide reductase (VKORC1), contribute to differences in patients" responses to various warfarin doses, but the role of these variants during initial anticoagulation is not clear.	Warfarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
18322281-6	2008	Both the CYP2C9 genotype and VKORC1 haplotype had a significant influence on the required warfarin dose after the first 2 weeks of therapy.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
17226852-0	2008	Oral anticoagulation with warfarin is significantly influenced by steroids and CYP2C9 polymorphisms in children with cancer.	Warfarin	26-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
17851566-0	2008	CYP2C9 genotype-guided warfarin prescribing enhances the efficacy and safety of anticoagulation: a prospective randomized controlled study.	Warfarin	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
17851566-1	2008	Warfarin anticoagulation effect is characterized by marked variability, some of which has been attributed to CYP2C9 polymorphisms.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
17851566-2	2008	This study prospectively examines whether a priori knowledge of CYP2C9 genotype may improve warfarin therapy.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
17851566-7	2008	In conclusion, CYP2C9 genotype-guided warfarin therapy is more efficient and safer than the "average-dose" protocol.	Warfarin	38-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
17999057-8	2008	All are eliminated by hepatic metabolism involving mainly CYP2C9 (celecoxib, lumiracoxib) and CYP3A4 (etoricoxib).	Celecoxib	66-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
17999057-8	2008	All are eliminated by hepatic metabolism involving mainly CYP2C9 (celecoxib, lumiracoxib) and CYP3A4 (etoricoxib).	lumiracoxib	77-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
17226852-5	2008	Thus, awareness of CYP2C9 genotype and steroid-induced responsiveness to warfarin may be important when administrating oral anticoagulation in children.	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
29783347-6	2008	Pharmacogenetic studies have determined that variants in the CYP2C9 and VKORC1 genes help to predict the therapeutic warfarin dose.	Warfarin	117-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
18303964-1	2008	UNLABELLED: The cytochrome P450 enzymes CYP2C8, CYP2C9 and CYP2J2 generate 8,9-, 11,12-, and 14,15-epoxyeicosatrienic acid (EET) from arachidonic acid, and these EETs are then hydrolyzed to dihydroxyeicosatrienoic acids (DHET) before excretion into the urine.	8,9-, 11,12-, and 14,15-epoxyeicosatrienic acid	75-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
18303964-1	2008	UNLABELLED: The cytochrome P450 enzymes CYP2C8, CYP2C9 and CYP2J2 generate 8,9-, 11,12-, and 14,15-epoxyeicosatrienic acid (EET) from arachidonic acid, and these EETs are then hydrolyzed to dihydroxyeicosatrienoic acids (DHET) before excretion into the urine.	EET	124-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
18303964-1	2008	UNLABELLED: The cytochrome P450 enzymes CYP2C8, CYP2C9 and CYP2J2 generate 8,9-, 11,12-, and 14,15-epoxyeicosatrienic acid (EET) from arachidonic acid, and these EETs are then hydrolyzed to dihydroxyeicosatrienoic acids (DHET) before excretion into the urine.	Arachidonic Acid	134-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
18303964-1	2008	UNLABELLED: The cytochrome P450 enzymes CYP2C8, CYP2C9 and CYP2J2 generate 8,9-, 11,12-, and 14,15-epoxyeicosatrienic acid (EET) from arachidonic acid, and these EETs are then hydrolyzed to dihydroxyeicosatrienoic acids (DHET) before excretion into the urine.	dihydroxyeicosatrienoic acids	190-219	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
18252229-0	2008	Warfarin pharmacogenetics: CYP2C9 and VKORC1 genotypes predict different sensitivity and resistance frequencies in the Ashkenazi and Sephardi Jewish populations.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
18303964-1	2008	UNLABELLED: The cytochrome P450 enzymes CYP2C8, CYP2C9 and CYP2J2 generate 8,9-, 11,12-, and 14,15-epoxyeicosatrienic acid (EET) from arachidonic acid, and these EETs are then hydrolyzed to dihydroxyeicosatrienoic acids (DHET) before excretion into the urine.	dhet	221-225	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
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 9	Homo sapiens	152-158
18443385-3	2008	Hence, there are chances of drug-drug interaction because modulations of isoenzymes involved in metabolism CYP2C9/10 and CYP2C19 which partially inhibited by etoricoxib.	Etoricoxib	158-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
18237107-2	2008	The molecular alignment program ROCS was used with the query molecule flurbiprofen as a basis for predicting the correct active site orientation of the CYP2C9 database molecules.	Flurbiprofen	70-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	152-158
18237107-4	2008	Transposition of the first 39 correctly aligned molecules into the CYP2C9 active site yielded an average site of metabolism to iron heme distance of 5.21 A, in good agreement with previous experimental observations.	iron heme	127-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
18445991-0	2008	The effect of bucolome, a CYP2C9 inhibitor, on the pharmacokinetics of losartan.	Losartan	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
17597710-1	2008	Sulfonylurea hypoglycemics are mainly metabolized by the cytochrome P450 2C9 (CYP2C9) enzyme.	Sulfonylurea Compounds	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-76
17597710-1	2008	Sulfonylurea hypoglycemics are mainly metabolized by the cytochrome P450 2C9 (CYP2C9) enzyme.	Sulfonylurea Compounds	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
17597710-4	2008	Associations between CYP2C9 polymorphisms, prescribed doses of sulfonylurea, and change in glucose levels after the start of sulfonylurea therapy were assessed in all patients with incident diabetes mellitus starting on sulfonylurea therapy in the Rotterdam Study, a population-based cohort study of 7,983 elderly people.	Glucose	91-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
17597710-5	2008	In CYP2C9*3 allele carriers using tolbutamide, the prescribed dose was lower compared to patients with the wild-type CYP2C9 genotype.	Tolbutamide	34-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	3-9
17597710-5	2008	In CYP2C9*3 allele carriers using tolbutamide, the prescribed dose was lower compared to patients with the wild-type CYP2C9 genotype.	Tolbutamide	34-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
17597710-7	2008	In CYP2C9*3 allele carriers, the mean decrease in fasting serum glucose levels after the start of tolbutamide therapy was larger than in patients with the wild-type genotype, although not statistically significant.	Glucose	64-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	3-9
17597710-7	2008	In CYP2C9*3 allele carriers, the mean decrease in fasting serum glucose levels after the start of tolbutamide therapy was larger than in patients with the wild-type genotype, although not statistically significant.	Tolbutamide	98-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	3-9
17597710-8	2008	Patients with diabetes mellitus who are carriers of a CYP2C9*3 allele require lower doses of tolbutamide to regulate their serum glucose levels compared to patients with the wild-type genotype.	Tolbutamide	93-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
17597710-8	2008	Patients with diabetes mellitus who are carriers of a CYP2C9*3 allele require lower doses of tolbutamide to regulate their serum glucose levels compared to patients with the wild-type genotype.	Glucose	129-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
18281922-0	2008	Pharmacogenetic testing of CYP2C9 and VKORC1 alleles for warfarin.	Warfarin	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
18281922-8	2008	Variants of two genes, CYP2C9 and VKORC1, account for 30-50% of the variability in dosing of warfarin; thus, many believe that testing of these genes will aid in warfarin dosing recommendations.	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
18281922-8	2008	Variants of two genes, CYP2C9 and VKORC1, account for 30-50% of the variability in dosing of warfarin; thus, many believe that testing of these genes will aid in warfarin dosing recommendations.	Warfarin	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
18281922-10	2008	In an effort to address this situation, a multidisciplinary expert group was organized in November 2006 to evaluate the role of CYP2C9 and VKORC1 testing in altering warfarin-related therapeutic goals and reduction of adverse drug events.	Warfarin	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
18281922-16	2008	Although the routine use of warfarin genotyping is not endorsed by this work group at this time, in certain situations, CYP2C9 and VKORC1 testing may be useful, and warranted, in determining the cause of unusual therapeutic responses to warfarin therapy.	Warfarin	237-245	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
18370846-0	2008	Dosing algorithm for warfarin using CYP2C9 and VKORC1 genotyping from a multi-ethnic population: comparison with other equations.	Warfarin	21-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
18370846-1	2008	OBJECTIVES: Polymorphism in the genes for cytochrome (CYP)2C9 and the vitamin K epoxide reductase complex subunit 1 (VKORC1) affect the pharmacokinetics and pharmacodynamics of warfarin.	Warfarin	177-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-61
18370846-3	2008	METHODS: We determined the allele and haplotype frequencies of genes for CYP2C9 and VKORC1 on 167 Caucasian, African-American, Asian and Hispanic patients on warfarin.	Warfarin	158-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
19099951-0	2008	[Association between CYP2C9 and VKORC1 genetic polymorphism and warfarin dose requirements].	Warfarin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
19099951-8	2008	The multiple linear regression model for warfarin dose indicated age, weight and VKORC1 genotype could explain the inter-individual variation in dose requirement of 9.3%, 7.4%, 51.9% patients, respectively; age, weight, CYP2C9 and VKORC1 genotype together could explain the inter-individual variation in dose requirement of 64.1% patients.	Warfarin	41-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	220-226
19099951-9	2008	CONCLUSION: This study showed that age, weight and VKORC1 and CYP2C9 polymorphism had significant influences on warfarin dose requirements and should be considered on dosing regimens modification to improve the safety of warfarin therapy.	Warfarin	112-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
19099951-9	2008	CONCLUSION: This study showed that age, weight and VKORC1 and CYP2C9 polymorphism had significant influences on warfarin dose requirements and should be considered on dosing regimens modification to improve the safety of warfarin therapy.	Warfarin	221-229	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
17975109-7	2008	EET production by human recombinant CYP 2C9 and 2J2, 2 major epoxygenase isozymes expressed in human coronary arterioles, was directly inhibited in a concentration-dependent fashion by H2O2 in vitro, as observed by high-performance liquid chromatography (HPLC); however, EETs were not directly sensitive to oxidative modification.	Hydrogen Peroxide	185-189	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-43
17895500-0	2008	Variant CYP2C9 alleles and warfarin concentrations in patients receiving low-dose versus average-dose warfarin therapy.	Warfarin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
17895500-7	2008	A warfarin requirement of <2.5 mg/day and an elevated warfarin S/R concentration ratio were each associated with a higher frequency of variant CYP2C9 alleles.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
17895500-7	2008	A warfarin requirement of <2.5 mg/day and an elevated warfarin S/R concentration ratio were each associated with a higher frequency of variant CYP2C9 alleles.	Warfarin	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
18698879-8	2008	Compared with homozygous carriers of CYP2C9*1, patients homozygous for CYP2C9*3 were estimated to need 3.3-fold lower mean doses of warfarin to achieve the same international normalized ratio, with *2 carriers and heterozygous patients in between.	Warfarin	132-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
18698879-8	2008	Compared with homozygous carriers of CYP2C9*1, patients homozygous for CYP2C9*3 were estimated to need 3.3-fold lower mean doses of warfarin to achieve the same international normalized ratio, with *2 carriers and heterozygous patients in between.	Warfarin	132-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
18788834-13	2008	Any greater than expected increases in bleeding secondary to anticoagulation may potentially offset any benefit gained from cardioembolic stroke reduction, although this has not been fully resolved.Finally, there are racial/ethnic differences in the prevalence of certain polymorphisms in genes that influence warfarin pharmacokinetics and pharmacodynamics (e.g. cytochrome P450 2C9 and vitamin K epoxide reductase).	Warfarin	310-318	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	363-382
19026034-4	2008	Systemic triazoles are inhibitors of cytochrome P450 (CYP) isozymes, such as CYP3A4, CYP2C9 and CYP2C19, to varying degrees.	Triazoles	9-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
18636784-8	2008	The half-life of benzbromarone is generally short (about 3 hours); however, a uricosuric metabolite, 6-hydroxybenzbromarone, has a much longer half-life (up to 30 hours) and is the major species responsible for the uricosuric activity of benzbromarone, although its metabolism by cytochrome P450 (CYP) 2C9 in the liver may vary between patients as a result of polymorphisms in this enzyme.	6-hydroxybenzbromarone	101-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	280-305
17687273-6	2008	The most likely mechanism for the interaction between terbinafine and venlafaxine is the inhibition of CYP2D6-mediated O-demethylation of venlafaxine, whereas the minor effects of voriconazole are probably due to the inhibition of CYP3A4-, CYP2C9-, or CYP2C19-mediated metabolism of venlafaxine.	Terbinafine	54-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	240-246
17687273-6	2008	The most likely mechanism for the interaction between terbinafine and venlafaxine is the inhibition of CYP2D6-mediated O-demethylation of venlafaxine, whereas the minor effects of voriconazole are probably due to the inhibition of CYP3A4-, CYP2C9-, or CYP2C19-mediated metabolism of venlafaxine.	Venlafaxine Hydrochloride	70-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	240-246
17906972-2	2008	SNPs in the cytochrome P450 complex (CYP2C9) affect warfarin metabolism: patients who have the CYP2C9*2 and/or CYP2C9*3 variants metabolize warfarin slowly and are more likely to have an elevated International Normalized Ratio INR or to hemorrhage during warfarin initiation than patients without these variants.	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
17906972-2	2008	SNPs in the cytochrome P450 complex (CYP2C9) affect warfarin metabolism: patients who have the CYP2C9*2 and/or CYP2C9*3 variants metabolize warfarin slowly and are more likely to have an elevated International Normalized Ratio INR or to hemorrhage during warfarin initiation than patients without these variants.	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
17906972-2	2008	SNPs in the cytochrome P450 complex (CYP2C9) affect warfarin metabolism: patients who have the CYP2C9*2 and/or CYP2C9*3 variants metabolize warfarin slowly and are more likely to have an elevated International Normalized Ratio INR or to hemorrhage during warfarin initiation than patients without these variants.	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
17906972-2	2008	SNPs in the cytochrome P450 complex (CYP2C9) affect warfarin metabolism: patients who have the CYP2C9*2 and/or CYP2C9*3 variants metabolize warfarin slowly and are more likely to have an elevated International Normalized Ratio INR or to hemorrhage during warfarin initiation than patients without these variants.	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
17906972-2	2008	SNPs in the cytochrome P450 complex (CYP2C9) affect warfarin metabolism: patients who have the CYP2C9*2 and/or CYP2C9*3 variants metabolize warfarin slowly and are more likely to have an elevated International Normalized Ratio INR or to hemorrhage during warfarin initiation than patients without these variants.	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
17906972-2	2008	SNPs in the cytochrome P450 complex (CYP2C9) affect warfarin metabolism: patients who have the CYP2C9*2 and/or CYP2C9*3 variants metabolize warfarin slowly and are more likely to have an elevated International Normalized Ratio INR or to hemorrhage during warfarin initiation than patients without these variants.	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
17906972-2	2008	SNPs in the cytochrome P450 complex (CYP2C9) affect warfarin metabolism: patients who have the CYP2C9*2 and/or CYP2C9*3 variants metabolize warfarin slowly and are more likely to have an elevated International Normalized Ratio INR or to hemorrhage during warfarin initiation than patients without these variants.	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
17906972-2	2008	SNPs in the cytochrome P450 complex (CYP2C9) affect warfarin metabolism: patients who have the CYP2C9*2 and/or CYP2C9*3 variants metabolize warfarin slowly and are more likely to have an elevated International Normalized Ratio INR or to hemorrhage during warfarin initiation than patients without these variants.	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
17906972-2	2008	SNPs in the cytochrome P450 complex (CYP2C9) affect warfarin metabolism: patients who have the CYP2C9*2 and/or CYP2C9*3 variants metabolize warfarin slowly and are more likely to have an elevated International Normalized Ratio INR or to hemorrhage during warfarin initiation than patients without these variants.	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
18399713-12	2008	CONCLUSION: This study shows that the CYP2C9*3 and SLCO1B1 c.521TC genotype and female gender are significant and independent predictors of the pharmacokinetics of torasemide.	Torsemide	164-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
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.	Carbamazepine	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
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.	Carbamazepine	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
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
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
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.	prohapten	230-239	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
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.	prohapten	230-239	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
18445991-1	2008	Losartan, a selective angiotensin receptor antagonist, is mainly metabolized by CYP2C9 to an active carboxylic acid, E3174, which is pharmacologically more potent inhibitor than the parent compound.	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
18445991-1	2008	Losartan, a selective angiotensin receptor antagonist, is mainly metabolized by CYP2C9 to an active carboxylic acid, E3174, which is pharmacologically more potent inhibitor than the parent compound.	Carboxylic Acids	100-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
18445991-1	2008	Losartan, a selective angiotensin receptor antagonist, is mainly metabolized by CYP2C9 to an active carboxylic acid, E3174, which is pharmacologically more potent inhibitor than the parent compound.	losartan carboxylic acid	117-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
18445991-2	2008	We evaluated the effect of bucolome, a CYP2C9 inhibitor, on the pharmacokinetics of losartan and E3174, which were measured by high performance liquid chromatography in human volunteers and rats.	bucolome	27-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
18636784-8	2008	The half-life of benzbromarone is generally short (about 3 hours); however, a uricosuric metabolite, 6-hydroxybenzbromarone, has a much longer half-life (up to 30 hours) and is the major species responsible for the uricosuric activity of benzbromarone, although its metabolism by cytochrome P450 (CYP) 2C9 in the liver may vary between patients as a result of polymorphisms in this enzyme.	Benzbromarone	110-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	280-305
18636784-15	2008	If all the reported cases are assumed to be due to benzbromarone, the estimated risk of hepatotoxicity in Europe was approximately 1 in 17 000 patients but may be higher in Japan.Benzbromarone is also an inhibitor of CYP2C9 and so may be involved in drug interactions with drugs dependent on this enzyme for clearance, such as warfarin.	Benzbromarone	51-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	217-223
18636784-15	2008	If all the reported cases are assumed to be due to benzbromarone, the estimated risk of hepatotoxicity in Europe was approximately 1 in 17 000 patients but may be higher in Japan.Benzbromarone is also an inhibitor of CYP2C9 and so may be involved in drug interactions with drugs dependent on this enzyme for clearance, such as warfarin.	Benzbromarone	179-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	217-223
18636784-15	2008	If all the reported cases are assumed to be due to benzbromarone, the estimated risk of hepatotoxicity in Europe was approximately 1 in 17 000 patients but may be higher in Japan.Benzbromarone is also an inhibitor of CYP2C9 and so may be involved in drug interactions with drugs dependent on this enzyme for clearance, such as warfarin.	Warfarin	327-335	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	217-223
19074093-1	2008	Polymorphisms in CYP2C9, a critical cytochrome P-450 enzyme in the metabolism of warfarin, alters its clearance and affects dosing.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
18429757-0	2008	[Cytochrome P4502C9(CYP2C9) gene polymorphism and safety of therapy with warfarin].	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
17955230-1	2008	OBJECTIVE: To evaluate the impact of the two most common CYP2C9 variant alleles (*2 and *3) on the maintenance dose of warfarin and on the quality of anticoagulation control in Brazilians.	Warfarin	119-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
17955230-9	2008	Patients with CYP2C9*3, but not CYP2C9*2, required significantly (one-sided P = 0.001, Mann-Whitney U-test) lower warfarin maintenance doses (3.1 +/- 1.8 mg) than CYP2C9*1*1 patients (5.3 +/- 2.1 mg).	Warfarin	114-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
17955230-10	2008	CONCLUSION: Patients with either CYP2C9*2 or CYP2C9*3 show higher risk of over-anticoagulation compared to CYP2C9*1*1 subjects and could benefit from a reduction in the initial warfarin standard dose (e.g., to 2.5 mg/day).	Warfarin	177-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
17955230-10	2008	CONCLUSION: Patients with either CYP2C9*2 or CYP2C9*3 show higher risk of over-anticoagulation compared to CYP2C9*1*1 subjects and could benefit from a reduction in the initial warfarin standard dose (e.g., to 2.5 mg/day).	Warfarin	177-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
17955230-10	2008	CONCLUSION: Patients with either CYP2C9*2 or CYP2C9*3 show higher risk of over-anticoagulation compared to CYP2C9*1*1 subjects and could benefit from a reduction in the initial warfarin standard dose (e.g., to 2.5 mg/day).	Warfarin	177-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
18025525-7	2008	The decrease in voriconazole exposure during coadministration is probably mainly due to the induction of CYP2C19 and CYP2C9 by efavirenz.	Voriconazole	16-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
18429757-1	2008	Aim of the study was to investigate frequency and influence of alleles CYP2C9*2 and CYP2C9*3 on pharmacokinetics, pharmacodynamics and dosing regimen of warfarin and on development of hemorrhagic complications.	Warfarin	153-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
18836275-1	2008	OBJECTIVE: The aim of the present study was to investigate the role of CYP2C9 gene polymorphisms after heart valve replacement in a group of patients on warfarin therapy.	Warfarin	153-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
18836275-5	2008	RESULTS: The patients with CYP2C9*1/*3 and CYP2C9*2/*3 genotypes were taking 28.21 and 24.47 mg, respectively, as mean weekly warfarin dose, whereas patients with CYP2C9*1/*1 genotype were taking 33.90 mg.	Warfarin	126-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
18429757-1	2008	Aim of the study was to investigate frequency and influence of alleles CYP2C9*2 and CYP2C9*3 on pharmacokinetics, pharmacodynamics and dosing regimen of warfarin and on development of hemorrhagic complications.	Warfarin	153-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
18836275-5	2008	RESULTS: The patients with CYP2C9*1/*3 and CYP2C9*2/*3 genotypes were taking 28.21 and 24.47 mg, respectively, as mean weekly warfarin dose, whereas patients with CYP2C9*1/*1 genotype were taking 33.90 mg.	Warfarin	126-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
18836275-6	2008	CONCLUSION: The data show that patients with CYP2C9*1/*3 and CYP2C9*2/*3 genotypes needed a lower maintenance dose of warfarin than patients with CYP2C9*1/*1 wild-type genotype.	Warfarin	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
18836275-6	2008	CONCLUSION: The data show that patients with CYP2C9*1/*3 and CYP2C9*2/*3 genotypes needed a lower maintenance dose of warfarin than patients with CYP2C9*1/*1 wild-type genotype.	Warfarin	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
18429757-6	2008	Average maintenance doses of warfarin for patients with allele variants CYP 2C9 *2 and 2C9 *3 were 3.6 and 3.1 mg/day, respectively, what was significantly lower than in wild type homozygotes (6.1 mg/day).	Warfarin	29-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-79
18836275-6	2008	CONCLUSION: The data show that patients with CYP2C9*1/*3 and CYP2C9*2/*3 genotypes needed a lower maintenance dose of warfarin than patients with CYP2C9*1/*1 wild-type genotype.	Warfarin	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
17899045-1	2007	OBJECTIVE: The objective of this study was to assess the contribution of the VKORC1 and CYP2C9 genotypes and age, body size, and weight of the patients to the warfarin dose requirement in a Chinese population.	Warfarin	159-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
18374198-5	2008	SNPs of cytochrome P450 2C9 (CYP2C9) gene have been shown to decrease the catabolism of warfarin.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-27
18374198-5	2008	SNPs of cytochrome P450 2C9 (CYP2C9) gene have been shown to decrease the catabolism of warfarin.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
18374198-6	2008	The combined analysis of VKORC1, CYP2C9 SNPs, and age may account for more than 50% of the individual variability in the warfarin maintenance dosage.	Warfarin	121-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
18159128-1	2007	Nateglinide is an antidiabetic agent metabolized by CYP2C9 and CYP3A4; hence inhibitors of these CYP isozymes may interact with nateglinide.	Nateglinide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
18159128-1	2007	Nateglinide is an antidiabetic agent metabolized by CYP2C9 and CYP3A4; hence inhibitors of these CYP isozymes may interact with nateglinide.	Nateglinide	128-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
17951033-4	2007	However, in microsomes prepared from native human hepatocytes, only relatively specific competitors (inhibitors and/or substrates) of CYP1A2, CYP2C8, CYP2C9 and CYP3A4 reduced notably the degradation cyamemazine.	cyamemazine	200-211	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
17951033-5	2007	The main routes of cyamemazine biotransformation are N-mono-demethylation (CYP1A2, CYP3A4 and CYP2C8) and mono-oxidation (either S-oxidized or hydroxylated derivatives which could not be discriminated because characterized by the same mass value) by CYP1A2 and CYP2C9.	cyamemazine	19-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	261-267
17872452-3	2007	METHODS AND RESULTS: In native CYP2C-expressing endothelial cells, bradykinin elicited a Ca(2+) influx that was potentiated by the soluble epoxide hydrolase inhibitor, 1-adamantyl-3-cyclohexylurea (ACU), and attenuated by CYP inhibition.	CHEMBL242255	168-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-36
17872452-4	2007	Similar effects were observed in cultured endothelial cells overexpressing CYP2C9, but not in CYP2C9-deficient cells, and were prevented by the EET antagonist 14,15-epoxyeicosa-5(Z)-enoic acid as well as by the cAMP antagonist, Rp-cAMPS.	EET	144-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
17872452-4	2007	Similar effects were observed in cultured endothelial cells overexpressing CYP2C9, but not in CYP2C9-deficient cells, and were prevented by the EET antagonist 14,15-epoxyeicosa-5(Z)-enoic acid as well as by the cAMP antagonist, Rp-cAMPS.	14,15-episulfide eicosatrienoic acid	159-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
17872452-4	2007	Similar effects were observed in cultured endothelial cells overexpressing CYP2C9, but not in CYP2C9-deficient cells, and were prevented by the EET antagonist 14,15-epoxyeicosa-5(Z)-enoic acid as well as by the cAMP antagonist, Rp-cAMPS.	Cyclic AMP	211-215	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
18020424-5	2007	CYP2C9 was the major recombinant enzyme capable of catalyzing the formation of 6-OH BBR, although CYP2C19 also showed a lower degree of activity.	6-oh bbr	79-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
18020424-9	2007	Isoform profiling with recombinant human P450s suggested that CYP2C9 is primarily responsible for the formation of this reactive quinone intermediate.	quinone	129-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
17899045-7	2007	The multiple linear regression model for warfarin dose indicated significant contributions from age (r (2) = 0.084; P < 0.001), weight (r (2) = 0.063; P < 0.001), VKORC1 genotype (r (2) = 0.494; P < 0.001), and age, weight, and CYP2C9 and VKORC1 genotype together (r (2) = 0.628; P < 0.001).	Warfarin	41-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	237-243
17899045-8	2007	CONCLUSION: This study shows that age, weight and the VKORC1 and CYP2C9 polymorphism affect warfarin dose requirements in our sample of Chinese patients receiving long-term therapy and showing stable control of anticoagulation.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
17899045-9	2007	It is anticipated that the use of dosing regimens modified by taking into account the contribution of age, weight, and the CYP2C9 and VKORC1 genotypes has the potential to improve the safety of warfarin therapy.	Warfarin	194-202	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
18034666-1	2007	The nonsteroidal anti-inflammatory drug diclofenac is extensively metabolized by cytochrome P450 (CYP) enzymes, mainly by CYP2C9.	Diclofenac	40-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
17904094-9	2007	Turnover rates for luciferin ME and H metabolism by CYP2C9 and mutants were at least one order of magnitude higher in experiments with membranes compared to whole cells, consistent with impaired product egress from cells.	D-luciferin	19-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
18034666-11	2007	The inhibition of CYP2C9, and to some extent that of CYP3A4 and CYP2C19 enzymes during the first-pass metabolism of diclofenac seems to be involved in the interaction.	Diclofenac	116-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
18021343-0	2007	Pharmacogenetics of acenocoumarol: CYP2C9, CYP2C19, CYP1A2, CYP3A4, CYP3A5 and ABCB1 gene polymorphisms and dose requirements.	Acenocoumarol	20-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
17900275-0	2007	Common polymorphisms of CYP2C19 and CYP2C9 affect the pharmacokinetic and pharmacodynamic response to clopidogrel but not prasugrel.	Clopidogrel	102-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
17900275-8	2007	CONCLUSIONS: The common loss of function polymorphisms of CYP2C19 and CYP2C9 are associated with decreased exposure to the active metabolite of clopidogrel but not prasugrel.	Clopidogrel	144-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
17900275-8	2007	CONCLUSIONS: The common loss of function polymorphisms of CYP2C19 and CYP2C9 are associated with decreased exposure to the active metabolite of clopidogrel but not prasugrel.	Prasugrel Hydrochloride	164-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
17904094-11	2007	Finally screening with a panel of CYP2C ligands using CYP2C9 or active mutants revealed different patterns of inhibition and heteroactivation of metabolism of luciferin analogs.	D-luciferin	159-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
18034618-2	2007	Our primary objective was to determine whether the genes for cytochrome P450 (CYP) 2C9, nicotinamide adenine dinucleotide phosphate, reduced, quinone oxidoreductase (NQO1) and vitamin K epoxide reductase complex subunit 1 (VKORC1) are associated with warfarin dose requirements in African-Americans.	Warfarin	251-259	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-86
18034619-7	2007	Also, CYP2C9*2 (Arg144Cys) and CYP2C9*3 (Ile359Leu) variant alleles were significantly associated with low MWWD (p = 0.003 and 0.027, respectively).	ile359leu	41-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
17686967-1	2007	CYP2C9 catalyzes the demethylation of the biphasic kinetics substrate (S)-naproxen, and the CYP2C9*2 (R144C) and CYP2C9*3 (I359L) variants are associated with lower rates of (S)-naproxen demethylation.	Naproxen	70-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
17686967-1	2007	CYP2C9 catalyzes the demethylation of the biphasic kinetics substrate (S)-naproxen, and the CYP2C9*2 (R144C) and CYP2C9*3 (I359L) variants are associated with lower rates of (S)-naproxen demethylation.	Naproxen	70-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
17686967-1	2007	CYP2C9 catalyzes the demethylation of the biphasic kinetics substrate (S)-naproxen, and the CYP2C9*2 (R144C) and CYP2C9*3 (I359L) variants are associated with lower rates of (S)-naproxen demethylation.	Naproxen	70-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
17686967-1	2007	CYP2C9 catalyzes the demethylation of the biphasic kinetics substrate (S)-naproxen, and the CYP2C9*2 (R144C) and CYP2C9*3 (I359L) variants are associated with lower rates of (S)-naproxen demethylation.	Naproxen	174-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
17686967-1	2007	CYP2C9 catalyzes the demethylation of the biphasic kinetics substrate (S)-naproxen, and the CYP2C9*2 (R144C) and CYP2C9*3 (I359L) variants are associated with lower rates of (S)-naproxen demethylation.	Naproxen	174-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
17686967-1	2007	CYP2C9 catalyzes the demethylation of the biphasic kinetics substrate (S)-naproxen, and the CYP2C9*2 (R144C) and CYP2C9*3 (I359L) variants are associated with lower rates of (S)-naproxen demethylation.	Naproxen	174-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
17686967-4	2007	Uncoupling in CYP2C9.1 and CYP2C9.3 was primarily to H(2)O(2).	Hydrogen Peroxide	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
17686967-4	2007	Uncoupling in CYP2C9.1 and CYP2C9.3 was primarily to H(2)O(2).	Hydrogen Peroxide	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
17686967-5	2007	In contrast, CYP2C9.2 uncoupled to excess water preferentially.	Water	42-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
18034618-5	2007	Possession of a CYP2C9*2, *3 or *5 allele was associated with a 38% lower warfarin dose compared with the *1/*1 genotype (30 +/- 13 vs 48 +/- 18 mg/week; p = 0.003).	Warfarin	74-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
18034618-7	2007	Multiple regression analysis revealed that CYP2C9 genotype (p = 0.015), age (p < 0.001) and body surface area (p < 0.001) were jointly associated with warfarin dose requirements, and together explained 33% of the variability in warfarin dose requirements among African-Americans.	Warfarin	157-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
18034618-7	2007	Multiple regression analysis revealed that CYP2C9 genotype (p = 0.015), age (p < 0.001) and body surface area (p < 0.001) were jointly associated with warfarin dose requirements, and together explained 33% of the variability in warfarin dose requirements among African-Americans.	Warfarin	234-242	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
18034618-8	2007	DISCUSSION: Our data suggest that CYP2C9 genotype, age and body size are important determinants of warfarin dose requirements in African-Americans.	Warfarin	99-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
18034619-0	2007	Allelic variants in the CYP2C9 and VKORC1 loci and interindividual variability in the anticoagulant dose effect of warfarin in Italians.	Warfarin	115-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
18034619-3	2007	We investigated the influence of variants of the VKORC1 and CYP2C9 loci on the mean weekly warfarin dose (MWWD) required to reach stabilized therapeutic international normalized ratio, in order to confirm and to estimate the contribution of common genetic variability of these two genes in an Italian population and to search for novel rare VKORC1 alleles.	Warfarin	91-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
18040121-0	2007	Severe phenytoin toxicity in a CYP2C9*3*3 homozygous mutant from India.	Phenytoin	7-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
17517049-7	2007	Recombinant CYP2C9, CYP2C18 and CYP2C19 catalysed all hydroxylation pathways, whereas CYP2C8 formed only 6beta-OHGz and 7beta-OHGz.	6beta-ohgz	105-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
17517049-7	2007	Recombinant CYP2C9, CYP2C18 and CYP2C19 catalysed all hydroxylation pathways, whereas CYP2C8 formed only 6beta-OHGz and 7beta-OHGz.	7beta-ohgz	120-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
17517049-8	2007	CONCLUSION: Taken together, the results indicate that CYP2C9 is the major contributor to Gz metabolic clearance, although CYP2C19 may also be involved in MeOH-Gz formation (the major metabolic pathway).	gz	89-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
17646413-9	2007	The decrease in voriconazole exposure was probably due to the induction of CYP2C19 and CYP2C9 by ritonavir.	Voriconazole	16-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
17646413-9	2007	The decrease in voriconazole exposure was probably due to the induction of CYP2C19 and CYP2C9 by ritonavir.	Ritonavir	97-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
17925902-6	2007	Similarly, genetic testing for variants in cytochrome CYP2C9 and vitamin K epoxide reductase could inform decisions about prescribing warfarin.	Warfarin	134-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
18958736-3	2007	Both human CYP 2C9 and rat CYP 2C11 metabolize TA to a reactive metabolite that was reported to bind exclusively to these enzymes.	Ticrynafen	47-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-18
17979511-3	2007	In humans, functionally relevant polymorphisms, which may significantly modulate epoxyeicosatrienoic acid levels in vivo, have been identified in the genes encoding CYP2J2, CYP2C8, CYP2C9 and soluble epoxide hydrolase.	epoxyeicosatrienoic acid	81-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
17898651-1	2007	Cytochrome P450 2C9 (CYP4502C9) genotyping is useful in dosage adjustments for several critical drug therapies, including warfarin.	Warfarin	122-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
17898651-1	2007	Cytochrome P450 2C9 (CYP4502C9) genotyping is useful in dosage adjustments for several critical drug therapies, including warfarin.	Warfarin	122-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-30
17955831-1	2007	Single nucleotide polymorphisms (SNPs) in genes encoding cytochrome P450 enzyme 2C9 (CYP2C9) and Vitamin K epoxide reductase subunit I (VKORC1) make a significant contribution to the inter-individual variability in the maintenance dose of vitamin K antagonists (warfarin, acenocoumarol, phenprocoumon).	Vitamin K	239-248	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-83
17955831-4	2007	CYP2C9 and VKORC1 account for up to half the variability in vitamin K antagonists requirements and incorporating genotying data for these two genes into dosing algorithms could lead to a safer anticoagulation therapy.	Vitamin K	60-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
17955831-1	2007	Single nucleotide polymorphisms (SNPs) in genes encoding cytochrome P450 enzyme 2C9 (CYP2C9) and Vitamin K epoxide reductase subunit I (VKORC1) make a significant contribution to the inter-individual variability in the maintenance dose of vitamin K antagonists (warfarin, acenocoumarol, phenprocoumon).	Vitamin K	239-248	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
17955831-1	2007	Single nucleotide polymorphisms (SNPs) in genes encoding cytochrome P450 enzyme 2C9 (CYP2C9) and Vitamin K epoxide reductase subunit I (VKORC1) make a significant contribution to the inter-individual variability in the maintenance dose of vitamin K antagonists (warfarin, acenocoumarol, phenprocoumon).	Warfarin	262-270	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-83
17955831-1	2007	Single nucleotide polymorphisms (SNPs) in genes encoding cytochrome P450 enzyme 2C9 (CYP2C9) and Vitamin K epoxide reductase subunit I (VKORC1) make a significant contribution to the inter-individual variability in the maintenance dose of vitamin K antagonists (warfarin, acenocoumarol, phenprocoumon).	Warfarin	262-270	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
17955831-1	2007	Single nucleotide polymorphisms (SNPs) in genes encoding cytochrome P450 enzyme 2C9 (CYP2C9) and Vitamin K epoxide reductase subunit I (VKORC1) make a significant contribution to the inter-individual variability in the maintenance dose of vitamin K antagonists (warfarin, acenocoumarol, phenprocoumon).	Acenocoumarol	272-285	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-83
17955831-1	2007	Single nucleotide polymorphisms (SNPs) in genes encoding cytochrome P450 enzyme 2C9 (CYP2C9) and Vitamin K epoxide reductase subunit I (VKORC1) make a significant contribution to the inter-individual variability in the maintenance dose of vitamin K antagonists (warfarin, acenocoumarol, phenprocoumon).	Acenocoumarol	272-285	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
17955831-1	2007	Single nucleotide polymorphisms (SNPs) in genes encoding cytochrome P450 enzyme 2C9 (CYP2C9) and Vitamin K epoxide reductase subunit I (VKORC1) make a significant contribution to the inter-individual variability in the maintenance dose of vitamin K antagonists (warfarin, acenocoumarol, phenprocoumon).	Phenprocoumon	287-300	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-83
17955831-1	2007	Single nucleotide polymorphisms (SNPs) in genes encoding cytochrome P450 enzyme 2C9 (CYP2C9) and Vitamin K epoxide reductase subunit I (VKORC1) make a significant contribution to the inter-individual variability in the maintenance dose of vitamin K antagonists (warfarin, acenocoumarol, phenprocoumon).	Phenprocoumon	287-300	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
17591676-3	2007	DHEA treatment elevated the expression and activities of CYP3A4, CYP2C9, CYP2C19, and CYP2B6 in primary cultures of human hepatocytes.	Dehydroepiandrosterone	0-4	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
17696334-4	2007	The model compound for the study is the nonsteroidal anti-inflammatory drug celecoxib, a COX-2 selective inhibitor and known CYP2C9 substrate.	Celecoxib	76-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
17721328-7	2007	CYP2C9*2 C/T, CYP2C9*3 A/C, VKORC1 (-1639) G/A genotyping might be necessary for patients with Factor V Leiden and/or prothrombin G2021A mutation before warfarin anticoagulant therapy.	Warfarin	153-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
17960328-0	2007	Effective virtual screening protocol for CYP2C9 ligands using a screening site constructed from flurbiprofen and S-warfarin pockets.	Flurbiprofen	96-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
17576809-5	2007	Human CYP2C9 metabolized esfenvalerate but not deltamethrin.	fenvalerate	25-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
17960328-0	2007	Effective virtual screening protocol for CYP2C9 ligands using a screening site constructed from flurbiprofen and S-warfarin pockets.	Sulfur	113-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
17960328-0	2007	Effective virtual screening protocol for CYP2C9 ligands using a screening site constructed from flurbiprofen and S-warfarin pockets.	Warfarin	115-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
17960328-1	2007	An effective virtual screening protocol was developed against an extended active site of CYP2C9, which was derived from X-ray structures complexed with flubiprofen and S-warfarin.	Flurbiprofen	152-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
17960328-1	2007	An effective virtual screening protocol was developed against an extended active site of CYP2C9, which was derived from X-ray structures complexed with flubiprofen and S-warfarin.	Warfarin	168-178	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
17542019-2	2007	Probe substrates were phenacetin, diclofenac, S-mephenytoin, and dextromethorphan for CYP1A2, CYP2C9, CYP2C19, and CYP2D6, respectively.	Dextromethorphan	65-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
17542019-2	2007	Probe substrates were phenacetin, diclofenac, S-mephenytoin, and dextromethorphan for CYP1A2, CYP2C9, CYP2C19, and CYP2D6, respectively.	Phenacetin	22-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
17496208-1	2007	The elimination process of the endothelin receptor antagonist bosentan (Tracleer) in humans is entirely dependent on metabolism mediated by two cytochrome P450 (P450) enzymes, i.e., CYP3A4 and CYP2C9.	Bosentan	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	193-199
19356039-1	2007	Three neurotransmitters, namely adrenaline, serotonin and tryptamine inhibit the in vitro activity of several cytochrome P450 (CYP) isozymes (CYP1A2, CYP2C9, CYP2D6 and CYP3A).	Epinephrine	32-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
19356039-1	2007	Three neurotransmitters, namely adrenaline, serotonin and tryptamine inhibit the in vitro activity of several cytochrome P450 (CYP) isozymes (CYP1A2, CYP2C9, CYP2D6 and CYP3A).	Serotonin	44-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
19356039-1	2007	Three neurotransmitters, namely adrenaline, serotonin and tryptamine inhibit the in vitro activity of several cytochrome P450 (CYP) isozymes (CYP1A2, CYP2C9, CYP2D6 and CYP3A).	tryptamine	58-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
19356039-4	2007	However, the effect became negligible when adrenaline concentration was decreased to 100 microM: whereas a high inhibitory effect was observed in CYP2D6, CYP2C9 and CYP3A4 enzyme activities, the NADPH reductase activity remains unchanged.	Epinephrine	43-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
17827781-5	2007	A three-dimensional model for docking between EXP-3174 and CYP2C9 indicated that the chloro group of EXP-3174 is oriented to a hydrophobic pocket in the CYP2C9 active site, indicating that the lipophilicity of the group present in ARBs at the position corresponding to that of the hydroxyisopropyl group in olmesartan is important in inhibiting CYP2C9 activity.	olmesartan	307-317	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
17572144-5	2007	METHODS AND RESULTS: FMD of the radial artery was determined in 12 healthy volunteers by high-resolution ultrasound and analyzed before and after intra-arterial infusion of sulfaphenazole, a specific CYP 2C9 inhibitor, L-NMMA (NO synthase inhibitor) and co-infusion of both.	Sulfaphenazole	173-187	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	200-207
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.	Fluconazole	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-40
17496169-5	2007	A strong association was found between genetic polymorphisms in six genes, including VKORC1, CYP2C9, PROC, EPHX1, GGCX, and ORM1, and interindividual variability in the anticoagulant effect of warfarin; the strongest predictors were VKORC1 and CYP2C9.	Warfarin	193-201	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
17496169-5	2007	A strong association was found between genetic polymorphisms in six genes, including VKORC1, CYP2C9, PROC, EPHX1, GGCX, and ORM1, and interindividual variability in the anticoagulant effect of warfarin; the strongest predictors were VKORC1 and CYP2C9.	Warfarin	193-201	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	244-250
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.	Fluconazole	39-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-146
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
17332144-1	2007	CYP2C9 is one of the major drug-metabolizing enzymes, and it is involved in the oxidative metabolism of approximately 10% of clinically important drugs, among which some, such as the anticoagulant warfarin, have a narrow therapeutic index.	Warfarin	197-205	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
17298483-0	2007	Influence of CYP2C9 and CYP2C19 genetic polymorphisms on pharmacokinetics of gliclazide MR in Chinese subjects.	Gliclazide	77-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
17298483-1	2007	AIMS: To investigate the influence of CYP2C9 and CYP2C19 genetic polymorphisms on the pharmacokinetics of gliclazide modified release (MR) in healthy Chinese subjects.	Gliclazide	106-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
17298483-11	2007	CONCLUSIONS: The pharmacokinetics of gliclazide MR are affected mainly by CYP2C19 genetic polymorphism instead of CYP2C9 genetic polymorphism.	Gliclazide	37-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
17446262-4	2007	In the present study with CYP2C9, cyt b5 exerted complex actions upon P450 oxidative reactions by affecting the rate of metabolite formation, the consumption of NADPH by cytochrome P450 reductase, and uncoupling of the reaction cycle to hydrogen peroxide and water.	NADP	161-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
17446262-4	2007	In the present study with CYP2C9, cyt b5 exerted complex actions upon P450 oxidative reactions by affecting the rate of metabolite formation, the consumption of NADPH by cytochrome P450 reductase, and uncoupling of the reaction cycle to hydrogen peroxide and water.	Hydrogen Peroxide	237-254	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
17446262-4	2007	In the present study with CYP2C9, cyt b5 exerted complex actions upon P450 oxidative reactions by affecting the rate of metabolite formation, the consumption of NADPH by cytochrome P450 reductase, and uncoupling of the reaction cycle to hydrogen peroxide and water.	Water	259-264	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
17446262-7	2007	The major effects of cyt b5 are hypothesized to result from a cyt b5-induced conformational change in CYP2C9 that results in an increased collision frequency between the iron-oxygen species (Cpd I) and the substrate, and a decrease in the oxidase activity.	Iron	170-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
17446262-7	2007	The major effects of cyt b5 are hypothesized to result from a cyt b5-induced conformational change in CYP2C9 that results in an increased collision frequency between the iron-oxygen species (Cpd I) and the substrate, and a decrease in the oxidase activity.	Oxygen	175-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
23055851-6	2007	Ibuprofen is primarily metabolized by cytochrome P450 (CYP) 2C9.	Ibuprofen	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-63
23055851-7	2007	The immaturity of neonatal biotransformation pathways has a pronounced effect on the pharmacokinetic parameters of ibuprofen, particularly because CYP2C9 enzyme activity is known to be very low at birth and to increase rapidly over the first several days of life.	Ibuprofen	115-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
23055851-10	2007	Factors such as gestational age and CYP2C9 polymorphism may affect ibuprofen metabolism and therefore optimal dosing, but further clinical investigation is needed in these areas.	Ibuprofen	67-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
17510308-0	2007	Estimation of warfarin maintenance dose based on VKORC1 (-1639 G>A) and CYP2C9 genotypes.	Warfarin	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
17510308-1	2007	BACKGROUND: CYP2C9 polymorphisms are associated with decreased S-warfarin clearance and lower maintenance dosage.	Warfarin	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
17510308-6	2007	RESULTS: Eighty percent of CYP2C9*1/*1 patients stabilized on <4.0 mg/day warfarin had at least 1 VKORC1 -1639A allele.	Warfarin	77-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
17510308-9	2007	A model including VKORC1 and CYP2C9 genotypes, age, sex, and body weight accounted for 61% of the variance in warfarin daily maintenance dose.	Warfarin	110-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
17510308-12	2007	VKORC1 and CYP2C9 genotypes, age, sex, and body weight account for the majority of variance in warfarin dose among our study population.	Warfarin	95-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
17611042-4	2007	Secondly, SNPs of cytochrome P450 2C9 (CYP2C9) gene have been shown to decrease the catabolism of coumarin derivatives (acenocoumarol, warfarin).	coumarin	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-37
17611042-4	2007	Secondly, SNPs of cytochrome P450 2C9 (CYP2C9) gene have been shown to decrease the catabolism of coumarin derivatives (acenocoumarol, warfarin).	coumarin	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
17611042-4	2007	Secondly, SNPs of cytochrome P450 2C9 (CYP2C9) gene have been shown to decrease the catabolism of coumarin derivatives (acenocoumarol, warfarin).	Acenocoumarol	120-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-37
17611042-4	2007	Secondly, SNPs of cytochrome P450 2C9 (CYP2C9) gene have been shown to decrease the catabolism of coumarin derivatives (acenocoumarol, warfarin).	Acenocoumarol	120-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
17611042-4	2007	Secondly, SNPs of cytochrome P450 2C9 (CYP2C9) gene have been shown to decrease the catabolism of coumarin derivatives (acenocoumarol, warfarin).	Warfarin	135-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-37
17611042-4	2007	Secondly, SNPs of cytochrome P450 2C9 (CYP2C9) gene have been shown to decrease the catabolism of coumarin derivatives (acenocoumarol, warfarin).	Warfarin	135-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
17611042-7	2007	Finally, the combined analysis of VKORC1 and CYP2C9 SNPs with age may account for more than 50% of the individual variability of the warfarin maintenance dosage.	Warfarin	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
18240910-4	2007	Recently, polymorphisms in two genes, cytochrome P450 2C9 and vitamin K epoxide reductase complex 1, have been shown to affect warfarin"s pharmacogenomics and pharmacodynamics, respectively.	Warfarin	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-57
17433521-4	2007	Curcumin inhibited CYP1A2 (IC(50), 40.0 microM), CYP3A4 (IC(50), 16.3 microM), CYP2D6 (IC(50), 50.3 microM), CYP2C9 (IC(50), 4.3 microM) and CYP2B6 (IC(50), 24.5 microM).	Curcumin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
17516991-0	2007	Inhibitory effect of valproic acid on cytochrome P450 2C9 activity in epilepsy patients.	Valproic Acid	21-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-57
17516991-4	2007	The aim of this study was to evaluate the inhibitory effect of valproic acid on cytochrome P450 2C9 (CYP2C9) activity by using losartan oxidation as a probe in epilepsy patients.	Valproic Acid	63-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-99
17516991-4	2007	The aim of this study was to evaluate the inhibitory effect of valproic acid on cytochrome P450 2C9 (CYP2C9) activity by using losartan oxidation as a probe in epilepsy patients.	Valproic Acid	63-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
17516991-4	2007	The aim of this study was to evaluate the inhibitory effect of valproic acid on cytochrome P450 2C9 (CYP2C9) activity by using losartan oxidation as a probe in epilepsy patients.	Losartan	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-99
17516991-4	2007	The aim of this study was to evaluate the inhibitory effect of valproic acid on cytochrome P450 2C9 (CYP2C9) activity by using losartan oxidation as a probe in epilepsy patients.	Losartan	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
17516991-7	2007	Losartan and E3174, the CYP2C9-derived carboxylic acid metabolite of losartan in 8 hr urine were assayed by using high pressure liquid chromatography.	Carboxylic Acids	39-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
17516991-7	2007	Losartan and E3174, the CYP2C9-derived carboxylic acid metabolite of losartan in 8 hr urine were assayed by using high pressure liquid chromatography.	Losartan	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
17516991-10	2007	The results suggest an inhibitory effect of valproic acid on CYP2C9 enzyme activity in epilepsy patients at steady state.	Valproic Acid	44-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
17332144-3	2007	We found a new sequence variation in exon 7 of the CYP2C9 gene (1060G>A) resulting in a substitution of acidic amino acid glutamate to basic lysine (E354K) when translated.	amino acid glutamate	114-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
17332144-3	2007	We found a new sequence variation in exon 7 of the CYP2C9 gene (1060G>A) resulting in a substitution of acidic amino acid glutamate to basic lysine (E354K) when translated.	Lysine	144-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
17332144-4	2007	The allele, designated CYP2C9(*)24, was present in heterozygous state in one warfarin-treated patient.	Warfarin	77-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
17332144-9	2007	These results suggest that CYP2C9.24 may be improperly folded, both in yeast and mammalian cells, resulting in improper heme incorporation and rapid intracellular degradation.	Heme	120-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
17468864-10	2007	Furthermore, BTC was found to be a potent inhibitor of CYP3A4 and CYP2C9 activity in vitro.	Benzethonium	13-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
17612953-11	2007	Tienilic acid is activated by and covalently bound to CYP2C9, and the neoantigens thus formed activate immune systems, resulting in the formation of an autoantibodydirected against CYP2C9, named anti-liver/kidney microsomal autoantibody type 2, whereas the pathological role of the autoantibodies in drug-induced hepatitis remains largely unknown.	Ticrynafen	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
17612953-11	2007	Tienilic acid is activated by and covalently bound to CYP2C9, and the neoantigens thus formed activate immune systems, resulting in the formation of an autoantibodydirected against CYP2C9, named anti-liver/kidney microsomal autoantibody type 2, whereas the pathological role of the autoantibodies in drug-induced hepatitis remains largely unknown.	Ticrynafen	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
17596671-0	2007	A case report of a patient carrying CYP2C9*3/4 genotype with extremely low warfarin dose requirement.	Warfarin	75-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
17596671-1	2007	We report a case of intolerance to warfarin dosing due to impaired drug metabolism in a patient with CYP2C9*3/*4.	Warfarin	35-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
17562299-0	2007	Contributions of CYP2C9/CYP2C19 genotypes and drug interaction to the phenytoin treatment in the Korean epileptic patients in the clinical setting.	Phenytoin	70-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
16969365-0	2007	Genetic variation at the CYP2C locus and its association with torsemide biotransformation.	Torsemide	62-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-30
16969365-2	2007	Torsemide total oral clearance was linearly associated with the number of CYP2C9(*)3 alleles (geometric mean: 59, 40 and 20 ml/min in carriers of no, one and two alleles) and so were the methyl- and ring-hydroxylation but not the carboxylation clearance.	Torsemide	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
16969365-5	2007	Torsemide total oral clearance was predictable with r(2)=82.1% using plasma concentrations at 0.5, 1, 2 and 24 h. In conclusion, torsemide"s biotransformation strongly depended on the CYP2C9(*)3 variant but no other.	Torsemide	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	184-190
16969365-5	2007	Torsemide total oral clearance was predictable with r(2)=82.1% using plasma concentrations at 0.5, 1, 2 and 24 h. In conclusion, torsemide"s biotransformation strongly depended on the CYP2C9(*)3 variant but no other.	Torsemide	129-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	184-190
17562299-2	2007	The CYP2C9 polymorphism is a wellknown major genetic factor responsible for phenytoin metabolism.	Phenytoin	76-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
17562299-4	2007	Using a multiple regression model for evaluation of the CYP2C9 and CYP2C19 genotypes, together with other non-genetic variables, we explained 39.6% of the variance in serum phenytoin levels.	Phenytoin	173-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
17562299-5	2007	Incorporation of genotyping for CYP2C9 and CYP2C19 into a clinical practice may be of some help in the determination of phenytoin dosage.	Phenytoin	120-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
17442686-1	2007	This study assessed the effects of clopidogrel, a CYP 2C9 inhibitor, on fluvastatin pharmacokinetics in healthy volunteers.	Clopidogrel	35-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-57
17504998-4	2007	The purposes of this study were to evaluate the effect of genetic variants of CYP2C9 and CYP2C19 on the pharmacokinetics of indisulam and on clinical outcome and to assess the need for pharmacogenetically guided dose adaptation.	N-(3-chloro-7-indolyl)-1,4-benzenedisulphonamide	124-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
17361128-3	2007	Clopidogrel"s activation involves two sequential steps by CYP3A, CYP1A2, CYP2C9, CYP2C19, and/or CYP2B6.	Clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
17513950-9	2007	Treatment of endothelial cells with lovastatin increased CYP2C9 expression.	Lovastatin	36-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
17513950-10	2007	After 96 hours of treatment, fluvastatin and lovastatin clearly increased CYP2C9 protein level.	Fluvastatin	29-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
17513950-10	2007	After 96 hours of treatment, fluvastatin and lovastatin clearly increased CYP2C9 protein level.	Lovastatin	45-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
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
17442935-7	2007	The enzymes CYP2C9, CYP2C8, and myeloperoxidase catalyzed the conversion of sulfamethoxazole to sulfamethoxazole hydroxylamine.	sulfamethoxazole hydroxylamine	96-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
19802360-0	2007	Influence of CYP2C9 Genotype on warfarin dose among African American and European Americans.	Warfarin	32-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
19802360-4	2007	Herein we report the influence of CYP2C9 genotype on warfarin dose among European American and African American patients.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
19802360-16	2007	Warfarin dose was significantly related to CYP2C9 genotype (p<0.0001) both in univariate and multivariate analyses.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
19802360-20	2007	CYP2C9 genotype predicts warfarin dose in European Americans, but not in African Americans.	Warfarin	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
17479200-0	2007	Any effect of CYP2C9 variants on warfarin clearance in Chinese patients?	Warfarin	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
17307149-2	2007	In order to gain insights for developing personalized drugs, the 3D (dimensional) structure of CYP2C19 has been developed based on the crystal structure of CYP2C9 (PDB code 1R90), and its structure-activity relationship with the ligands of CEC, Fluvoxamine, Lescol, and Ticlopidine investigated through the structure-activity relationship approach.	chlorethylclonidine	240-243	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
17307149-2	2007	In order to gain insights for developing personalized drugs, the 3D (dimensional) structure of CYP2C19 has been developed based on the crystal structure of CYP2C9 (PDB code 1R90), and its structure-activity relationship with the ligands of CEC, Fluvoxamine, Lescol, and Ticlopidine investigated through the structure-activity relationship approach.	Fluvoxamine	245-256	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
17307149-2	2007	In order to gain insights for developing personalized drugs, the 3D (dimensional) structure of CYP2C19 has been developed based on the crystal structure of CYP2C9 (PDB code 1R90), and its structure-activity relationship with the ligands of CEC, Fluvoxamine, Lescol, and Ticlopidine investigated through the structure-activity relationship approach.	Fluvastatin	258-264	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
17307149-2	2007	In order to gain insights for developing personalized drugs, the 3D (dimensional) structure of CYP2C19 has been developed based on the crystal structure of CYP2C9 (PDB code 1R90), and its structure-activity relationship with the ligands of CEC, Fluvoxamine, Lescol, and Ticlopidine investigated through the structure-activity relationship approach.	Ticlopidine	270-281	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
17054666-0	2007	Evaluation of flurbiprofen urinary ratios as in vivo indices for CYP2C9 activity.	Flurbiprofen	14-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
17301738-5	2007	CYP2C9 genotype and age were identified as predictors for S-warfarin clearance, and VKORC1 genotype as a predictor for warfarin sensitivity.	Warfarin	60-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
17220242-1	2007	The cytochrome P450 (P450) enzymes CYP2C8, CYP2C9, and CYP2J2 metabolize arachidonic acid to epoxyeicosatrienoic acids, which are known to be vital in regulation of vascular tone and cardiovascular homeostasis.	Arachidonic Acid	73-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
17220242-1	2007	The cytochrome P450 (P450) enzymes CYP2C8, CYP2C9, and CYP2J2 metabolize arachidonic acid to epoxyeicosatrienoic acids, which are known to be vital in regulation of vascular tone and cardiovascular homeostasis.	epoxyeicosatrienoic acids	93-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
17251307-5	2007	Therefore, the three nitrogenous ligands aniline, imidazole, and triazole were used as binding spectra standards with purified human CYP3A4 and CYP2C9, because their small size should not present any steric limitations in their accessing the heme prosthetic group.	aniline	41-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
17251307-5	2007	Therefore, the three nitrogenous ligands aniline, imidazole, and triazole were used as binding spectra standards with purified human CYP3A4 and CYP2C9, because their small size should not present any steric limitations in their accessing the heme prosthetic group.	imidazole	50-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
17251307-5	2007	Therefore, the three nitrogenous ligands aniline, imidazole, and triazole were used as binding spectra standards with purified human CYP3A4 and CYP2C9, because their small size should not present any steric limitations in their accessing the heme prosthetic group.	Triazoles	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
17377945-0	2007	Study of recombinant cytochrome P450 2C9 activity with diclofenac by MEKC.	Diclofenac	55-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-40
17377945-2	2007	The aim of this paper is to demonstrate the applicability of CE for the determination of the enzymatic activity of CYP2C9 with diclofenac as a probe substrate.	Diclofenac	127-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
17603219-4	2007	The CYP2C9SV protein showed a typical reduced CO-difference spectrum, indicating that the translated protein binds a heme moiety.	Heme	117-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
17391071-6	2007	There were statistically significant differences in warfarin dose between the CYP2C9*1/*1 (4.3 +/- 1.6 mg/day; p < 0.001) and those with the other two genotypes including CYP2C9*1/*3 and CYP2C9*3/*4 (2.7 +/- 0.9 mg/day).	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
16983400-4	2007	The most important genes affecting the pharmacokinetic and pharmacodynamic parameters of warfarin are CYP2C9 (cytochrome P(450) 2C9) and VKORC1 (vitamin K epoxide reductase complex subunit 1).	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
16983400-4	2007	The most important genes affecting the pharmacokinetic and pharmacodynamic parameters of warfarin are CYP2C9 (cytochrome P(450) 2C9) and VKORC1 (vitamin K epoxide reductase complex subunit 1).	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-131
17391071-6	2007	There were statistically significant differences in warfarin dose between the CYP2C9*1/*1 (4.3 +/- 1.6 mg/day; p < 0.001) and those with the other two genotypes including CYP2C9*1/*3 and CYP2C9*3/*4 (2.7 +/- 0.9 mg/day).	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	174-180
17391071-6	2007	There were statistically significant differences in warfarin dose between the CYP2C9*1/*1 (4.3 +/- 1.6 mg/day; p < 0.001) and those with the other two genotypes including CYP2C9*1/*3 and CYP2C9*3/*4 (2.7 +/- 0.9 mg/day).	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	174-180
17303175-4	2007	Human CYP2C9-Arg expressed in the microsomes of human B lymphoblastoid cells efficiently catalyzed the 11-hydroxylation of Delta(8)-THC (7.60 nmol/min/nmol CYP), Delta(9)-THC (19.2 nmol/min/nmol CYP) and CBN (6.62 nmol/min/nmol CYP).	Arginine	13-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
17311370-3	2007	We have used analogues of the prototypical CYP2C9 heteroactivator dapsone to validate a simple docking method that can be used to predict heteroactivators based on ligand binding location in a P450 crystal structure.	Dapsone	66-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
17311370-5	2007	One of the top-scoring compounds identified was verified to be a CYP2C9 heteroactivator in vitro, and it possessed activity similar to dapsone.	Dapsone	135-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
17303175-4	2007	Human CYP2C9-Arg expressed in the microsomes of human B lymphoblastoid cells efficiently catalyzed the 11-hydroxylation of Delta(8)-THC (7.60 nmol/min/nmol CYP), Delta(9)-THC (19.2 nmol/min/nmol CYP) and CBN (6.62 nmol/min/nmol CYP).	delta-8-tetrahydrocannabinol	123-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
17110455-1	2007	CYP2C9 and VKORC1 genetic variants are associated with low and intermediate warfarin dose requirements, but markers of high doses are less well characterized.	Warfarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
17303175-4	2007	Human CYP2C9-Arg expressed in the microsomes of human B lymphoblastoid cells efficiently catalyzed the 11-hydroxylation of Delta(8)-THC (7.60 nmol/min/nmol CYP), Delta(9)-THC (19.2 nmol/min/nmol CYP) and CBN (6.62 nmol/min/nmol CYP).	Dronabinol	162-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
17322161-5	2007	Specifically, cranberry juice may inhibit the activity of CYP2C9, the primary isoenzyme involved in the metabolism of S-warfarin.	Warfarin	118-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
17456829-6	2007	RESULTS: Of genetic factors evaluated in the model, CYP2C9 and VKORC1 each contributed substantially to dose variability, and together with clinical factors explained 56% of the individual variability in stable warfarin dose.	Warfarin	211-219	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
17456829-8	2007	CONCLUSION: The importance of CYP2C9 and VKORC1 to patient-specific dose of warfarin has been confirmed, while polymorphisms of gamma carboxylase, factor VII and Apo E genes did not substantially contribute to predictive models for stable warfarin dose.	Warfarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
17324110-0	2007	Warfarin and cytochrome P450 2C9 genotype: possible ethnic variation in warfarin sensitivity.	Warfarin	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-32
17305793-0	2007	CYP2C9 variant modifies blood pressure-lowering response to losartan in Type 1 diabetic patients with nephropathy.	Losartan	60-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
17577464-0	2007	Warfarin metabolism and anticoagulant effect: a prospective, observational study of the impact of CYP2C9 genetic polymorphism in the presence of drug-disease and drug-drug interactions.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
17577464-1	2007	BACKGROUND: Cytocbrome P450 (CYP) 2C9 polymorphism affects the warfarin dosage requirement in stable outpatients.	Warfarin	63-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-37
17577464-3	2007	OBJECTIVE: The aim of this study was to examine the effects of CYP2C9 genetic polymorphism on warfarin dosage requirements in patients with severe comorbid conditions and those treated with medications that potentially interact with warfarin.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
17577464-3	2007	OBJECTIVE: The aim of this study was to examine the effects of CYP2C9 genetic polymorphism on warfarin dosage requirements in patients with severe comorbid conditions and those treated with medications that potentially interact with warfarin.	Warfarin	233-241	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
17577464-14	2007	CONCLUSIONS: In this study population of patients with severe comorbid conditions and those treated with medications that potentially interact with warfarin, CYP2C9 *1/*3 genotype, older age, CHF, and the use of antibiotics were associated with lower warfarin dosage requirements.	Warfarin	251-259	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
17577464-15	2007	The CYP2C9*1/*3 genotype, compared with CYP2C9 *1/*1, was associated with 33% lower mean warfarin dosage requirements and higher INR values, which were higher than the upper therapeutic range of INR (ie, 3).	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
17577464-15	2007	The CYP2C9*1/*3 genotype, compared with CYP2C9 *1/*1, was associated with 33% lower mean warfarin dosage requirements and higher INR values, which were higher than the upper therapeutic range of INR (ie, 3).	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
17577464-16	2007	Genetic CYP2C9 polymorphism contributed to the variability in warfarin dosage requirements in the presence of drug-disease and drug-drug interactions.	Warfarin	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
17048007-7	2007	A multiple regression model with VKORC1, CYP2C9, PROC and the non-genetic predictors age, bodyweight, drug interactions and indication for treatment jointly accounted for 62% of variance in warfarin dose.	Warfarin	190-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
17324110-3	2007	The aim was to evaluate the influence of two CYP2C9 functional polymorphisms (*2 and *3) on warfarin dose in African-Americans, an unstudied population and Caucasians, and also to assess the effect of these polymorphisms on anticoagulation response after accounting for nongenetic factors and genetic factors that might also impact the dose-response relationship of warfarin.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
29793299-2	2007	: A warfarin-dosing model in Asians that uses single nucleotide polymorphisms in vitamin K epoxide reductase complex and cytochrome P450 2C9.	Warfarin	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-140
17284505-3	2007	CYP2C9 is responsible for the irreversible metabolism of ibuprofen.	Ibuprofen	57-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
17132763-5	2007	In addition, we investigated the effect of pomegranate juice on the pharmacokinetics of tolbutamide (substrate for CYP2C9) in rats.	Tolbutamide	88-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
29793299-8	2007	Tham and colleagues used specific CYP2C9 and VKORC1 polymorphisms, along with clinical factors, to build an algorithm to accurately estimate warfarin doses in a multi-ethnic Asian population.	Warfarin	141-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
29793302-4	2007	In particular, the variability in warfarin dose requirement is now recognized to be due, in large part, to polymorphisms in two genes: cytochrome P450 2C9 and the vitamin K epoxide reductase complex subunit 1.	Warfarin	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-154
17304159-0	2007	Population estimation of the effects of cytochrome P450 2C9 and 2C19 polymorphisms on phenobarbital clearance in Japanese.	Phenobarbital	86-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-59
17304159-1	2007	A nonlinear mixed-effect modeling (NONMEM) program was used to evaluate the effects of cytochrome P450 (CYP) 2C9 and CYP2C19 polymorphisms on the phenobarbital (PB) population clearance for Japanese epileptics.	Phenobarbital	146-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-112
17304159-5	2007	The total clearance of PB decreased by 48% in patients with CYP2C9*1/*3 genotype in comparison with those with CYP2C9*1/*1 genotype (P < 0.001).	Phenobarbital	23-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
17304159-5	2007	The total clearance of PB decreased by 48% in patients with CYP2C9*1/*3 genotype in comparison with those with CYP2C9*1/*1 genotype (P < 0.001).	Phenobarbital	23-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
17304159-7	2007	To our knowledge, this is the first report to demonstrate that the CYP2C9 genotype affects the PB metabolism in routine care, but the results should be further verified in other ethnic populations.	Phenobarbital	95-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
17375979-8	2007	CYP2C19 contributes to the metabolism of diazepam and phenytoin, the latter drug also representing a substrate of CYP2C9, with its predominant variants being defined as *2 and *3.	Diazepam	41-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
16822276-9	2007	CONCLUSIONS: Coadministration of potent inhibitors of CYP3A4/5 and CYP2D6, but not CYP2C9, resulted in a moderate increase in lasofoxifene exposure.	Lasofoxifene	126-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
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 9	Homo sapiens	151-157
17375979-8	2007	CYP2C19 contributes to the metabolism of diazepam and phenytoin, the latter drug also representing a substrate of CYP2C9, with its predominant variants being defined as *2 and *3.	Phenytoin	54-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
17375979-9	2007	For both AEDs, there is maximally a 2-fold difference in the hepatic elimination rate (e.g. clearance) or the AUC between the extremes of EMs and PMs which, in the case of phenytoin (an AED with a narrow "therapeutic window"), would suggest a dosage reduction only for patients who are carriers of mutated alleles of both CYP2C19 and CYP2C9, a subgroup that is very rare among Caucasians (about 1% of the population) but more frequent in Asians (about 10%).	Phenytoin	172-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	334-340
17167248-0	2007	Frequency of CYP2C9 genotypes among Omani patients receiving warfarin and its correlation with warfarin dose.	Warfarin	61-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
17167248-0	2007	Frequency of CYP2C9 genotypes among Omani patients receiving warfarin and its correlation with warfarin dose.	Warfarin	95-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
17167248-1	2007	OBJECTIVES: This study was conducted to determine the frequency of CYP2C9 alleles in Omani patients receiving warfarin and to correlate genotyping data with warfarin dosage.	Warfarin	110-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
17167248-1	2007	OBJECTIVES: This study was conducted to determine the frequency of CYP2C9 alleles in Omani patients receiving warfarin and to correlate genotyping data with warfarin dosage.	Warfarin	157-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
17284096-3	2007	In particular, two polymorphisms of cytochrome P450 2C9 are known to slow down the metabolism of phenytoin to a degree that increases the risk of the neurotoxic adverse effects of this drug among carriers of these polymorphisms.	Phenytoin	97-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-55
18690851-2	2007	Consistent with in vitro data, clinical studies have demonstrated that CYP2C9 polymorphisms significantly influence warfarin pharmacokinetics by reducing (S)-warfarin metabolic clearance, consequently lowering maintenance dose requirements and increasing the risk over-anticoagulation during the initiation phase of therapy.	Warfarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
18690851-2	2007	Consistent with in vitro data, clinical studies have demonstrated that CYP2C9 polymorphisms significantly influence warfarin pharmacokinetics by reducing (S)-warfarin metabolic clearance, consequently lowering maintenance dose requirements and increasing the risk over-anticoagulation during the initiation phase of therapy.	Warfarin	158-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
19356015-2	2007	The CYP form with the lowest in vitro K(i) is evaluated first clinically, employing a suitable probe drug like midazolam (CYP3A4), theophylline (CYP1A2), (S)-warfarin (CYP2C9) and desipramine (CYP2D6), and the NCE is classified as a "none", "weak", "moderate", or "strong" inhibitor.	Warfarin	156-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
17708066-11	2007	Diosmin might have inhibited the microsomal CYP2C9 mediated oxidation of diclofenac sodium.	Diosmin	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
17708066-11	2007	Diosmin might have inhibited the microsomal CYP2C9 mediated oxidation of diclofenac sodium.	Diclofenac	73-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
17253883-8	2007	In addition to CYP3A4, repaglinide is metabolised via CYP2C8, while nateglinide metabolism also involves CYP2C9.	Nateglinide	68-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
17020955-7	2007	In human liver microsomes, involvement of CYP2D6, CYP1A2, CYP2C9, and CYP2C19 in diphenhydramine N-demethylation was confirmed by using P450 isozyme-specific inhibitors.	Diphenhydramine	81-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
17020955-7	2007	In human liver microsomes, involvement of CYP2D6, CYP1A2, CYP2C9, and CYP2C19 in diphenhydramine N-demethylation was confirmed by using P450 isozyme-specific inhibitors.	Nitrogen	97-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
17020955-11	2007	In addition, large differences in the metabolic activities of CYP2D6 and those of CYP1A2, CYP2C9, and CYP2C19 could cause the individual differences in anti-allergic efficacy and the sedative effect of diphenhydramine.	Diphenhydramine	202-217	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
17419358-5	2007	Basing on the results of the study, the authors propose an algorithm of choosing the initial warfarin dose depending on CYP2C9 genotype.	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
17192504-7	2007	These data demonstrate a CYP2C9-mediated pharmacokinetic interaction with pharmacodynamic, clinically relevant consequences, which might require warfarin dose adjustment.	Warfarin	145-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
17344941-4	2007	Losartan metabolism has been suggested as a marker for determination of CYP2C9 activity.	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
17419358-0	2007	[The influence of CYP2C9 genetic polymorphism on the pharmacokinetics and pharmacodynamics of warfarin in patients with constant atrial fibrillation].	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
17419358-1	2007	CYP2C9 is the main enzyme participating in warfarin metabolism, of which genetic polymorphism is typical.	Warfarin	43-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
17419358-2	2007	The aim of the study was to investigate the influence of having allelic variants CYP2C9*2 and CYP2C9*3 on the pharmacokinetics, dosage regimen, and the rate of hemorrhage in patients with constant atrial fibrillation taking warfarin.	Warfarin	224-232	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
17419358-4	2007	It was shown that in patients with CYP2C9*2 and CYP2C9*3 the clearance of warfarin and its dose were lower, while the episodes of excessive hypocoagulation and hemorrhage associated with warfarin were more frequent than in patients without these allelic variants.	Warfarin	74-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
17419358-4	2007	It was shown that in patients with CYP2C9*2 and CYP2C9*3 the clearance of warfarin and its dose were lower, while the episodes of excessive hypocoagulation and hemorrhage associated with warfarin were more frequent than in patients without these allelic variants.	Warfarin	74-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
17419358-4	2007	It was shown that in patients with CYP2C9*2 and CYP2C9*3 the clearance of warfarin and its dose were lower, while the episodes of excessive hypocoagulation and hemorrhage associated with warfarin were more frequent than in patients without these allelic variants.	Warfarin	187-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
17419358-4	2007	It was shown that in patients with CYP2C9*2 and CYP2C9*3 the clearance of warfarin and its dose were lower, while the episodes of excessive hypocoagulation and hemorrhage associated with warfarin were more frequent than in patients without these allelic variants.	Warfarin	187-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
17049586-0	2007	Genotypes of vitamin K epoxide reductase, gamma-glutamyl carboxylase, and cytochrome P450 2C9 as determinants of daily warfarin dose in Japanese patients.	Warfarin	119-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-93
17397249-0	2007	The influence of NSAIDs on coumarin sensitivity in patients with CYP2C9 polymorphism after total hip replacement surgery.	coumarin	27-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
17397249-1	2007	OBJECTIVE: To determine the influence of NSAIDs on the international normalized ratio (INR) in patients with cytochrome P450 (CYP)-2C9 enzyme variants starting acenocoumarol (an oral coumarin) therapy during the first 7 days after total hip replacement surgery.	Acenocoumarol	160-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-134
17672075-17	2007	Episodes of MHO rise > 5.0 in warfarin therapy were observed in 50% carriers of CYP2C9*3 and in none homozygous carriers of CYP2C9*1 (p = 0.024).	Warfarin	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
17672075-17	2007	Episodes of MHO rise > 5.0 in warfarin therapy were observed in 50% carriers of CYP2C9*3 and in none homozygous carriers of CYP2C9*1 (p = 0.024).	Warfarin	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-133
17672075-18	2007	CYP2C9*3 patients needed lower maintenance doses of warfarin, in CYP2C9*1 and CYP2C9*2 patients anticoagulant doses were comparable.	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
17672075-21	2007	Determination of CYP2C9 genotype in APS patients before treatment with oral anticoagulants may help in planning individual policy and in reducing the risk of warfarin overdosage at the start of therapy.	Warfarin	158-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
17963417-6	2007	Multiple studies indicated that the CYP2C9 *3 allele (Ile359Leu polymorphism) was associated with decreased clearance of sulfonylurea drugs.	Sulfonylurea Compounds	121-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
17963417-7	2007	Supporting this, one study reported an increased insulin secretion in CYP2C9*3 allele carriers when using the sulfonylurea agent glyburide.	Glyburide	129-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
17963417-8	2007	The CYP2C9*3 allele was also associated with a decreased clearance of meglitinides, whereas the CYP2C8*3 (Arg139Lys; Lys399Arg) variant increased the clearance of meglitinides.	meglitinide	70-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
17963417-8	2007	The CYP2C9*3 allele was also associated with a decreased clearance of meglitinides, whereas the CYP2C8*3 (Arg139Lys; Lys399Arg) variant increased the clearance of meglitinides.	meglitinide	163-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
17279482-6	2007	Among them, tanshinone IIA and cryptotanshinone are found to be potent inhibitors to CYP1A2, while artemisinin is a marginal inhibitor to CYP1A2 and glycyrrhetic acid is a weak inhibitor to CYP2C9.	tanshinone	12-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
17279482-6	2007	Among them, tanshinone IIA and cryptotanshinone are found to be potent inhibitors to CYP1A2, while artemisinin is a marginal inhibitor to CYP1A2 and glycyrrhetic acid is a weak inhibitor to CYP2C9.	cryptotanshinone	31-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
17279482-6	2007	Among them, tanshinone IIA and cryptotanshinone are found to be potent inhibitors to CYP1A2, while artemisinin is a marginal inhibitor to CYP1A2 and glycyrrhetic acid is a weak inhibitor to CYP2C9.	Glycyrrhetinic Acid	149-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
17049586-4	2007	We genotyped eleven representative single nucleotide polymorphisms (SNPs) in the three genes involved in vitamin K cycle and the 42613A>C SNP in CYP2C9, known as CYP2C93, and then examined an association of these genotypes with warfarin maintenance doses (mean+/-SD=2.96+/-1.06 mg/day).	Warfarin	231-239	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
17049586-5	2007	We found an association of effective warfarin dose with the -1639G>A (p=0.004) and 3730G>A genotypes (p=0.006) in VKORC1, the 8016G>A genotype in GGCX (p=0.022), and the 42613A>C genotype in CYP2C9 (p=0.015).	Warfarin	37-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	203-209
17049586-7	2007	The contribution to inter-individual variation in warfarin dose was 5.9% for VKORC1 -1639G>A, 5.2% for CYP2C9 42613A>C, and 4.6% for GGCX 8016G>A.	Warfarin	50-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
17097122-9	2006	The CYP2C9 inhibitor sulphaphenazole (10 microM) protected from diclofenac-induced cell injury and prevented increases in [Ca(2+)](c), while it had no effect on the dissipation of the DeltaPsi(m).	Sulfaphenazole	21-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
17010942-3	2006	The P450 M-2C enzyme expressed in yeast cells catalyzed p-methylhydroxylation of only tolbutamide among four substrates tested, paclitaxel as a CYP2C8 substrate, diclofenac and tolbutamide as CYP2C9 substrates and S-mephenytoin as a CYP2C19 substrate.	Tolbutamide	86-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	192-198
17010942-5	2006	Although all of the recombinant human CYP2C8, CYP2C9 and CYP2C19 expressed in yeast cells catalyzed tolbutamide p-methylhydroxylation, the kinetic profile of CYP2C8 was most similar to that of P450 M-2C.	Tolbutamide	100-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
17010942-6	2006	Tolbutamide oxidation by the marmoset liver microsomes and the recombinant P450 M-2C was inhibited most effectively by quercetin, a CYP2C8 inhibitor, followed by omeprazole, a CYP2C19 inhibitor, whereas sulfaphenazole, a CYP2C9 inhibitor, was less potent under the conditions used.	Tolbutamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	221-227
17010942-6	2006	Tolbutamide oxidation by the marmoset liver microsomes and the recombinant P450 M-2C was inhibited most effectively by quercetin, a CYP2C8 inhibitor, followed by omeprazole, a CYP2C19 inhibitor, whereas sulfaphenazole, a CYP2C9 inhibitor, was less potent under the conditions used.	Quercetin	119-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	221-227
17161452-3	2007	Pharmacogenetic analysis of two genes, the warfarin metabolic enzyme CYP2C9 and warfarin target enzyme, vitamin K epoxide reductase complex 1 VKORC1, confirmed their influence on warfarin maintenance dose.	Warfarin	43-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
17161452-4	2007	Possession of CYP2C9*2 or CYP2C9*3 variant alleles, which result in decreased enzyme activity, is associated with a significant decrease in the mean warfarin dose.	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
17161452-4	2007	Possession of CYP2C9*2 or CYP2C9*3 variant alleles, which result in decreased enzyme activity, is associated with a significant decrease in the mean warfarin dose.	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
17161452-6	2007	Haplotypes based on these SNPs explain a large fraction of the interindividual variation in warfarin dose, and VKORC1 has an approximately three-fold greater effect than CYP2C9.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-176
17161452-7	2007	Algorithms incorporating genetic (CYP2C9 and VKORC1), demographic, and clinical factors to estimate the warfarin dosage, could potentially minimize the risk of over dose during warfarin induction.	Warfarin	104-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
17161452-7	2007	Algorithms incorporating genetic (CYP2C9 and VKORC1), demographic, and clinical factors to estimate the warfarin dosage, could potentially minimize the risk of over dose during warfarin induction.	Warfarin	177-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
17097122-9	2006	The CYP2C9 inhibitor sulphaphenazole (10 microM) protected from diclofenac-induced cell injury and prevented increases in [Ca(2+)](c), while it had no effect on the dissipation of the DeltaPsi(m).	Diclofenac	64-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
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 9	Homo sapiens	77-83
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.	triphenyltin	174-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
17178259-6	2006	Cerivastatin is metabolized by CYP2C8 and CYP3A4, and fluvastatin is metabolized by CYP2C9.	Fluvastatin	54-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
17178259-7	2006	The exposure to fluvastatin is increased by less than 2-fold by inhibitors of CYP2C9.	Fluvastatin	16-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
16963489-3	2006	The most abundant isoform of this subfamily is CYP2C9, which is the major clearance pathway for the low therapeutic index drugs warfarin and phenytoin.	Warfarin	128-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
16963489-3	2006	The most abundant isoform of this subfamily is CYP2C9, which is the major clearance pathway for the low therapeutic index drugs warfarin and phenytoin.	Phenytoin	141-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
17042764-7	2006	A number of factors such as patient age, body weight, co-morbidity, frailty, warfarin daily dose and CYP2C9 and VKORC1 polymorphism could affect response to vitamin K and thus the rate and extent of INR reversal.	Vitamin K	157-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
17111199-0	2006	Genotypes of the cytochrome p450 isoform, CYP2C9, and the vitamin K epoxide reductase complex subunit 1 conjointly determine stable warfarin dose: a prospective study.	Warfarin	132-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
17111199-1	2006	BACKGROUND: Warfarin has a narrow therapeutic range and wide inter-individual dosing requirements that may be related to functional variants of genes affecting warfarin metabolism (i.e., CYP2C9) and activity (i.e., vitamin K epoxide reductase complex subunit 1-VKORC1).	Warfarin	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	187-193
17111199-1	2006	BACKGROUND: Warfarin has a narrow therapeutic range and wide inter-individual dosing requirements that may be related to functional variants of genes affecting warfarin metabolism (i.e., CYP2C9) and activity (i.e., vitamin K epoxide reductase complex subunit 1-VKORC1).	Warfarin	160-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	187-193
17111199-11	2006	CONCLUSION: In this large prospective study of warfarin genetic dose-determinants, carriage of a single or double CYP2C9 variant, reduced warfarin dose 18-72%, and of a VKORC1 variant by 65%.	Warfarin	47-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
17111199-11	2006	CONCLUSION: In this large prospective study of warfarin genetic dose-determinants, carriage of a single or double CYP2C9 variant, reduced warfarin dose 18-72%, and of a VKORC1 variant by 65%.	Warfarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
17162464-5	2006	Adefovir and its prodrug inhibited CYP2C9 at concentrations below 100 microM; inhibition by adefovir was of the uncompetitive (at the lower inhibitor concentrations) or of the competitive nature with a Ki = 420 microM.	adefovir	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
16945988-0	2006	Contribution of CYP2C9, CYP2A6, and CYP2B6 to valproic acid metabolism in hepatic microsomes from individuals with the CYP2C9*1/*1 genotype.	Valproic Acid	46-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
16945988-0	2006	Contribution of CYP2C9, CYP2A6, and CYP2B6 to valproic acid metabolism in hepatic microsomes from individuals with the CYP2C9*1/*1 genotype.	Valproic Acid	46-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
16945988-2	2006	cDNA-expressed CYP2C9*1, CYP2A6, and CYP2B6 were the most active catalysts of 4-ene-VPA, 4-OH-VPA, and 5-OH-VPA formation.	2-propyl-4-pentenoic acid	78-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
16945988-2	2006	cDNA-expressed CYP2C9*1, CYP2A6, and CYP2B6 were the most active catalysts of 4-ene-VPA, 4-OH-VPA, and 5-OH-VPA formation.	4-Hydroxyvalproic acid	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
16945988-2	2006	cDNA-expressed CYP2C9*1, CYP2A6, and CYP2B6 were the most active catalysts of 4-ene-VPA, 4-OH-VPA, and 5-OH-VPA formation.	5-Hydroxyvalproic acid	103-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
16945988-9	2006	Overall, our novel findings indicate that in human hepatic microsomes, CYP2C9*1 is the predominant catalyst in the formation of 4-ene-VPA, 4-OH-VPA, and 5-OH-VPA, whereas CYP2A6 contributes partially to 3-OH-VPA formation.	2-propyl-4-pentenoic acid	128-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
16945988-9	2006	Overall, our novel findings indicate that in human hepatic microsomes, CYP2C9*1 is the predominant catalyst in the formation of 4-ene-VPA, 4-OH-VPA, and 5-OH-VPA, whereas CYP2A6 contributes partially to 3-OH-VPA formation.	4-Hydroxyvalproic acid	139-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
16945988-9	2006	Overall, our novel findings indicate that in human hepatic microsomes, CYP2C9*1 is the predominant catalyst in the formation of 4-ene-VPA, 4-OH-VPA, and 5-OH-VPA, whereas CYP2A6 contributes partially to 3-OH-VPA formation.	5-Hydroxyvalproic acid	153-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
16945988-9	2006	Overall, our novel findings indicate that in human hepatic microsomes, CYP2C9*1 is the predominant catalyst in the formation of 4-ene-VPA, 4-OH-VPA, and 5-OH-VPA, whereas CYP2A6 contributes partially to 3-OH-VPA formation.	3-Hydroxyvalproic acid	203-211	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
17213583-6	2006	The activities of CYP1A2 and CYP2C9 were significantly reduced in the present of TMX.	1,3,8-trihydroxy-5-methoxyxanthone	81-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
17213583-7	2006	CONCLUSION: TMX (10 micromol/L) has significant inhibitive effect on the activities of CYP1A2 and CYP2C9, but no significant inhibitive effect on the activities of CYP2C19, CYP2E1 and CYP3A4.	1,3,8-trihydroxy-5-methoxyxanthone	12-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
16978661-8	2006	Incubation of PUFAs with CYP2C9 or CYP2C19 in the presence of NADPH resulted in the decrease of PUFA concentrations in the incubation mixtures.	NADP	62-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
17162464-6	2006	Tenofovir and tenofovir disoproxil influenced the activity of CYP2C9, and competitive inhibition was found with Ki = 580 and 395 microM, respectively.	Tenofovir	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
17162464-6	2006	Tenofovir and tenofovir disoproxil influenced the activity of CYP2C9, and competitive inhibition was found with Ki = 580 and 395 microM, respectively.	Tenofovir	14-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
16869821-4	2006	Results The acenocoumarol-sensitive patient was found to possess, in addition to CYP2C9*3 allele, a CYP2C9*11 allele and the VKORC1 AA diplotype which were all traced back through the parental lines.	Acenocoumarol	12-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
16928789-3	2006	We measured the Michaelis-Menten kinetic parameters for four CYP2C9 substrates (diclofenac, (S)-warfarin, tolbutamide, and (S)-flurbiprofen) using four recombinant CYP2C9 enzyme systems (Supersomes, Baculosomes, RECO system, and in-house purified, reconstituted enzyme) to determine whether the enzyme systems exhibited kinetic differences in metabolic product formation rates under uniform experimental conditions.	Diclofenac	80-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
16928789-3	2006	We measured the Michaelis-Menten kinetic parameters for four CYP2C9 substrates (diclofenac, (S)-warfarin, tolbutamide, and (S)-flurbiprofen) using four recombinant CYP2C9 enzyme systems (Supersomes, Baculosomes, RECO system, and in-house purified, reconstituted enzyme) to determine whether the enzyme systems exhibited kinetic differences in metabolic product formation rates under uniform experimental conditions.	Warfarin	92-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
16753237-1	2006	Biotransformation of deoxypodophyllotoxin to epipodophyllotoxin by three major human hepatic enzymes, CYP1A2, CYP2C9 and CYP3A4, heterologously expressed in E. coli DH5alpha, was investigated.	deoxypodophyllotoxin	21-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
16753237-1	2006	Biotransformation of deoxypodophyllotoxin to epipodophyllotoxin by three major human hepatic enzymes, CYP1A2, CYP2C9 and CYP3A4, heterologously expressed in E. coli DH5alpha, was investigated.	Podophyllotoxin	45-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
17085674-2	2006	Functional polymorphisms of UGT1A6 (T181A and R184S) and CYP2C9 (R144C and I359L) have been reported to modify the protective effect of aspirin on colorectal adenoma risk.	Aspirin	136-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
16784736-13	2006	CONCLUSIONS: The BCRP 421C>A polymorphism may play an important role in the pharmacokinetics of rosuvastatin in healthy Chinese males after the exclusion of impact of SLCO1B1 and CYP2C9 genetic polymorphism.	Rosuvastatin Calcium	99-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	182-188
17112811-0	2006	Impact of CYP2C9*3/*3 genotype on the pharmacokinetics and pharmacodynamics of piroxicam.	Piroxicam	79-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
17112813-0	2006	Warfarin dose requirement for patients with both VKORC1 3673A/A and CYP2C9*3/*3 genotypes.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
16928789-7	2006	In addition, when (S)-flurbiprofen was used as a substrate probe to determine CYP2C9 inhibition with a set of 12 inhibitors, decreased inhibition potency was observed across 11 of those inhibitors in the RECO purified, reconstituted enzyme compared with the Supersomes baculovirus microsomal preparation and pooled human liver microsomes.	Flurbiprofen	18-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
16869821-4	2006	Results The acenocoumarol-sensitive patient was found to possess, in addition to CYP2C9*3 allele, a CYP2C9*11 allele and the VKORC1 AA diplotype which were all traced back through the parental lines.	Acenocoumarol	12-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
16869821-5	2006	Conclusions Acenocoumarol sensitivity in this subject is the consequence of inheritance of multiple functionally defective alleles in both the CYP2C9 and VKORC1 genes.	Acenocoumarol	12-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
17015052-0	2006	A warfarin-dosing model in Asians that uses single-nucleotide polymorphisms in vitamin K epoxide reductase complex and cytochrome P450 2C9.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-138
17064211-9	2006	Warfarin undergoes hepatic metabolism through cytochrome P450 2C9, and carbamazepine induces this isoenzyme.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-65
16740353-4	2006	CYP2C9*13, firstly identified by some of the present authors in a Chinese poor metabolizer of lornoxicam, is characterized by mutation encoding Leu90Pro substitution.	lornoxicam	94-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16740353-4	2006	CYP2C9*13, firstly identified by some of the present authors in a Chinese poor metabolizer of lornoxicam, is characterized by mutation encoding Leu90Pro substitution.	leu90pro	144-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16740353-5	2006	Kinetic experiments show that CYP2C9*13 has less catalytic activity in elimination of diclofenac and lornoxicam in vitro.	Diclofenac	86-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
16740353-5	2006	Kinetic experiments show that CYP2C9*13 has less catalytic activity in elimination of diclofenac and lornoxicam in vitro.	lornoxicam	101-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
16740353-7	2006	The structure change caused by Leu90Pro replacement is revealed and used to explain the dramatic decrease of the enzymatic activity in clearance of the two CYP2C9 substrates: diclofenac and lornoxicam.	leu90pro	31-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
16740353-7	2006	The structure change caused by Leu90Pro replacement is revealed and used to explain the dramatic decrease of the enzymatic activity in clearance of the two CYP2C9 substrates: diclofenac and lornoxicam.	Diclofenac	175-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
16740353-7	2006	The structure change caused by Leu90Pro replacement is revealed and used to explain the dramatic decrease of the enzymatic activity in clearance of the two CYP2C9 substrates: diclofenac and lornoxicam.	lornoxicam	190-200	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
16815961-0	2006	Amiodarone analog-dependent effects on CYP2C9-mediated metabolism and kinetic profiles.	Amiodarone	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
17015052-1	2006	INTRODUCTION: Because of the unique lack of genetic diversity despite the multiethnicity in the Asian population, we hypothesize that single-nucleotide polymorphisms in cytochrome P450 (CYP) 2C9 (CYP2C9*3) and vitamin K epoxide reductase complex subunit 1 (VKORC1) at position 381, used to infer VKORC1haplotype in combination with demographic factors, can accurately predict warfarin doses.	Warfarin	376-384	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-194
16815961-5	2006	Amiodarone activated naproxen demethylation at lower concentrations, regardless of the CYP2C9 allele, and inhibited metabolism at higher concentrations without altering the kinetic profile.	Amiodarone	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
17015052-1	2006	INTRODUCTION: Because of the unique lack of genetic diversity despite the multiethnicity in the Asian population, we hypothesize that single-nucleotide polymorphisms in cytochrome P450 (CYP) 2C9 (CYP2C9*3) and vitamin K epoxide reductase complex subunit 1 (VKORC1) at position 381, used to infer VKORC1haplotype in combination with demographic factors, can accurately predict warfarin doses.	Warfarin	376-384	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
16815961-7	2006	Benzbromarone altered naproxen demethylation kinetics from a biphasic profile to that of a hyperbolic form in CYP2C9.1 and CYP2C9.3, resulting in inhibition and activation, respectively.	Benzbromarone	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
16815961-7	2006	Benzbromarone altered naproxen demethylation kinetics from a biphasic profile to that of a hyperbolic form in CYP2C9.1 and CYP2C9.3, resulting in inhibition and activation, respectively.	Benzbromarone	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
16815961-7	2006	Benzbromarone altered naproxen demethylation kinetics from a biphasic profile to that of a hyperbolic form in CYP2C9.1 and CYP2C9.3, resulting in inhibition and activation, respectively.	Naproxen	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
17015052-8	2006	CONCLUSION: Warfarin dose requirements in Asians can be accurately predicted by use of a combination of patient demographics and a simplified genotyping approach for single variants in CYP2C9 and VKORC1.	Warfarin	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	185-191
16946524-4	2006	Glimepiride also inhibited 7-hydroxylation of S-warfarin in a competitive manner by microsomes from human liver which showed the genotypes of CYP2C9, as CYP2C9*1/*1 or CYP2C9*1/*3.	Sulfur	46-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
16815961-8	2006	In contrast, benz(meth)arone activated naproxen demethylation in both CYP2C9.1 and CYP2C9.3.	benz(meth)arone	13-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
16815961-8	2006	In contrast, benz(meth)arone activated naproxen demethylation in both CYP2C9.1 and CYP2C9.3.	benz(meth)arone	13-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
16815961-8	2006	In contrast, benz(meth)arone activated naproxen demethylation in both CYP2C9.1 and CYP2C9.3.	Naproxen	39-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
16815961-8	2006	In contrast, benz(meth)arone activated naproxen demethylation in both CYP2C9.1 and CYP2C9.3.	Naproxen	39-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
16862439-2	2006	Presented here are the results on the construction and characterization of three fusion proteins containing the N-terminally modified human cytochrome P450s CYP2C9, CY2C19 and CYP3A4 fused to the soluble NADPH-dependent oxidoreductase domain of CYP102A1 from Bacillus megaterium.	NADP	204-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
16946524-2	2006	S-Warfarin 7-hydroxylation by recombinant CYP2C9.1 and CYP2C9.3 was inhibited by glimepiride competitively.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
16714062-6	2006	Among the statins, simvastatin, lovastatin and atorvastatin are metabolized by cytochrome P450 3A4 (CYP3A4) while fluvastatin is metabolized by CYP2C9.	Atorvastatin	47-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
16714062-6	2006	Among the statins, simvastatin, lovastatin and atorvastatin are metabolized by cytochrome P450 3A4 (CYP3A4) while fluvastatin is metabolized by CYP2C9.	Fluvastatin	114-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
16946524-2	2006	S-Warfarin 7-hydroxylation by recombinant CYP2C9.1 and CYP2C9.3 was inhibited by glimepiride competitively.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
16946524-4	2006	Glimepiride also inhibited 7-hydroxylation of S-warfarin in a competitive manner by microsomes from human liver which showed the genotypes of CYP2C9, as CYP2C9*1/*1 or CYP2C9*1/*3.	Sulfur	46-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
16946524-2	2006	S-Warfarin 7-hydroxylation by recombinant CYP2C9.1 and CYP2C9.3 was inhibited by glimepiride competitively.	glimepiride	81-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
16946524-4	2006	Glimepiride also inhibited 7-hydroxylation of S-warfarin in a competitive manner by microsomes from human liver which showed the genotypes of CYP2C9, as CYP2C9*1/*1 or CYP2C9*1/*3.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
16946524-2	2006	S-Warfarin 7-hydroxylation by recombinant CYP2C9.1 and CYP2C9.3 was inhibited by glimepiride competitively.	glimepiride	81-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
16946524-3	2006	The apparent K(i) value of glimepiride was lower at CYP2C9.3 than at CYP2C9.1.	glimepiride	27-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
16946524-4	2006	Glimepiride also inhibited 7-hydroxylation of S-warfarin in a competitive manner by microsomes from human liver which showed the genotypes of CYP2C9, as CYP2C9*1/*1 or CYP2C9*1/*3.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
16946524-3	2006	The apparent K(i) value of glimepiride was lower at CYP2C9.3 than at CYP2C9.1.	glimepiride	27-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
16952492-1	2006	BACKGROUND: We have previously shown that flurbiprofen metabolism to 4"-hydroxyflurbiprofen provides an in vivo measure of cytochrome P450 (CYP) 2C9 activity.	Flurbiprofen	42-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-148
16946524-4	2006	Glimepiride also inhibited 7-hydroxylation of S-warfarin in a competitive manner by microsomes from human liver which showed the genotypes of CYP2C9, as CYP2C9*1/*1 or CYP2C9*1/*3.	glimepiride	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
16946524-4	2006	Glimepiride also inhibited 7-hydroxylation of S-warfarin in a competitive manner by microsomes from human liver which showed the genotypes of CYP2C9, as CYP2C9*1/*1 or CYP2C9*1/*3.	glimepiride	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
16946524-4	2006	Glimepiride also inhibited 7-hydroxylation of S-warfarin in a competitive manner by microsomes from human liver which showed the genotypes of CYP2C9, as CYP2C9*1/*1 or CYP2C9*1/*3.	glimepiride	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
16940139-0	2006	Safety of voriconazole in a patient with CYP2C9*2/CYP2C9*2 genotype.	Voriconazole	10-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
16940139-0	2006	Safety of voriconazole in a patient with CYP2C9*2/CYP2C9*2 genotype.	Voriconazole	10-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
16952496-0	2006	Is celecoxib an inducer of cytochrome P450 3A4 in subjects carrying the CYP2C9*3 allele?	Celecoxib	3-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
16952492-1	2006	BACKGROUND: We have previously shown that flurbiprofen metabolism to 4"-hydroxyflurbiprofen provides an in vivo measure of cytochrome P450 (CYP) 2C9 activity.	4'-hydroxyflurbiprofen	69-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-148
16847664-2	2006	The CYP2C9 genotype has been shown to influence the response to warfarin therapy, but such an effect on phenprocoumon therapy remains uncertain.	Warfarin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
16763015-7	2006	Hepatocytes exposed to 1 mM FFA for 14 h showed lower activity values of CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2D6, CYP2E1, and CYP3A4 enzymes than nontreated hepatocytes (about 45-65% reduction).	Fatty Acids, Nonesterified	28-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
16815679-3	2006	CYP2C9 catalyses the prochiral formation of (R) and (S)-p-HPPH, and is approximately 40 times more stereoselective towards the formation of the (S) isomer whereas CYP2C19 is not stereoselective.	Ranolazine	44-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16815679-3	2006	CYP2C9 catalyses the prochiral formation of (R) and (S)-p-HPPH, and is approximately 40 times more stereoselective towards the formation of the (S) isomer whereas CYP2C19 is not stereoselective.	(s)-p-hpph	52-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16888441-4	2006	RECENT FINDINGS: Single-nucleotide polymorphisms in cytochrome P450 2C9 and vitamin K epoxide reductase have been shown to make significant contributions to the variability in warfarin dose requirements.	Warfarin	176-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-71
16611750-3	2006	OBJECTIVE: We tested for association between single nucleotide polymorphisms (SNPs) in VKORC1 and CYP2C9 and average weekly warfarin dose required to maintain patients at their desired anticoagulation target.	Warfarin	124-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
16611750-10	2006	CYP2C9*3 was significantly (p = 0.05) associated with average warfarin dosage after adjustment for VKORC1*1173.	Warfarin	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16611750-12	2006	The consistent findings regarding the role of VKORC1 and CYP2C9 in warfarin metabolism and maintenance dosage represent a clinically useful proof of principal for the use of pharmacogenomic information in medicine and may lead to improved understanding of warfarin"s actions.	Warfarin	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
16918308-4	2006	Potential mechanisms for oxazaphosphorine resistance include decreased activation by cytochrome P450s (e.g. CYP3A4, CYP2C9 and CYP2B6), increased deactivation of the agents by deactivating enzymes such as aldehyde dehydrogenases (ALDHs), increased cellular thiol level, increased DNA repair capacity, and altered cellular apoptotic response to DNA repair, e.g. deficient apoptosis due to lack of cellular mechanisms to result in cell death following DNA damage.	oxazaphosphorine	25-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
16890578-10	2006	The mean daily dose of warfarin was lower in subjects with CYP2C9*1/*3 (1.86 +/- 0.80 mg/d, P = .007) than in subjects with CYP2C9*1/*1 (3.36 +/- 1.43 mg/d).	Warfarin	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
16890578-10	2006	The mean daily dose of warfarin was lower in subjects with CYP2C9*1/*3 (1.86 +/- 0.80 mg/d, P = .007) than in subjects with CYP2C9*1/*1 (3.36 +/- 1.43 mg/d).	Warfarin	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
16679385-4	2006	Using a substrate-cassette approach, P450 activities were determined after incubation with the prototypic inhibitors tienilic acid (CYP2C9), erythromycin, troleandomycin, and fluoxetine (CYP3A4).	Ticrynafen	117-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
16679385-6	2006	Tienilic acid selectively inhibited CYP2C9-dependent diclofenac 4"-hydroxylation activity, and erythromycin, troleandomycin, and fluoxetine inhibited CYP3A4-dependent midazolam 1"-hydroxylation in a time- and concentration-dependent manner.	Ticrynafen	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
16679385-6	2006	Tienilic acid selectively inhibited CYP2C9-dependent diclofenac 4"-hydroxylation activity, and erythromycin, troleandomycin, and fluoxetine inhibited CYP3A4-dependent midazolam 1"-hydroxylation in a time- and concentration-dependent manner.	Diclofenac	53-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
16580879-1	2006	Polymorphisms in the CYP2C9 gene can have a significant impact on drug therapy by affecting the pharmacokinetics of frequently prescribed drugs, such as phenprocoumon and warfarin.	Phenprocoumon	153-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
16698161-6	2006	Sulphaphenazole, a specific human CYP2C9 inhibitor, showed a Ki value of 30.8 microM and IC50 at 44.0 microM in the test system.	Sulfaphenazole	0-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
16580879-1	2006	Polymorphisms in the CYP2C9 gene can have a significant impact on drug therapy by affecting the pharmacokinetics of frequently prescribed drugs, such as phenprocoumon and warfarin.	Warfarin	171-179	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
16875977-1	2006	OBJECTIVES: We assessed the role of cytochrome P450 2C9 (CYP 2C9)-derived endothelium-derived hyperpolarizing factor (EDHF) in the forearm microcirculation of essential hypertensive patients (EH) by utilizing sulfaphenazole (SUL), a selective CYP 2C9 inhibitor.	endothelium-derived hyperpolarizing factor	74-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-55
16875977-1	2006	OBJECTIVES: We assessed the role of cytochrome P450 2C9 (CYP 2C9)-derived endothelium-derived hyperpolarizing factor (EDHF) in the forearm microcirculation of essential hypertensive patients (EH) by utilizing sulfaphenazole (SUL), a selective CYP 2C9 inhibitor.	endothelium-derived hyperpolarizing factor	74-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-64
16875977-1	2006	OBJECTIVES: We assessed the role of cytochrome P450 2C9 (CYP 2C9)-derived endothelium-derived hyperpolarizing factor (EDHF) in the forearm microcirculation of essential hypertensive patients (EH) by utilizing sulfaphenazole (SUL), a selective CYP 2C9 inhibitor.	edhf	118-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-55
16875977-1	2006	OBJECTIVES: We assessed the role of cytochrome P450 2C9 (CYP 2C9)-derived endothelium-derived hyperpolarizing factor (EDHF) in the forearm microcirculation of essential hypertensive patients (EH) by utilizing sulfaphenazole (SUL), a selective CYP 2C9 inhibitor.	edhf	118-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-64
16875977-1	2006	OBJECTIVES: We assessed the role of cytochrome P450 2C9 (CYP 2C9)-derived endothelium-derived hyperpolarizing factor (EDHF) in the forearm microcirculation of essential hypertensive patients (EH) by utilizing sulfaphenazole (SUL), a selective CYP 2C9 inhibitor.	Sulfaphenazole	209-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-55
16875977-1	2006	OBJECTIVES: We assessed the role of cytochrome P450 2C9 (CYP 2C9)-derived endothelium-derived hyperpolarizing factor (EDHF) in the forearm microcirculation of essential hypertensive patients (EH) by utilizing sulfaphenazole (SUL), a selective CYP 2C9 inhibitor.	Sulfaphenazole	209-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-64
16875977-1	2006	OBJECTIVES: We assessed the role of cytochrome P450 2C9 (CYP 2C9)-derived endothelium-derived hyperpolarizing factor (EDHF) in the forearm microcirculation of essential hypertensive patients (EH) by utilizing sulfaphenazole (SUL), a selective CYP 2C9 inhibitor.	Sulfaphenazole	225-228	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-55
16875977-1	2006	OBJECTIVES: We assessed the role of cytochrome P450 2C9 (CYP 2C9)-derived endothelium-derived hyperpolarizing factor (EDHF) in the forearm microcirculation of essential hypertensive patients (EH) by utilizing sulfaphenazole (SUL), a selective CYP 2C9 inhibitor.	Sulfaphenazole	225-228	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-64
16875977-3	2006	Cytochrome P450 2C9 is a possible source of EDHF.	edhf	44-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
17024799-0	2006	Tamoxifen inhibits cytochrome P450 2C9 activity in breast cancer patients.	Tamoxifen	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-38
17024799-1	2006	Tamoxifen has been reported to potentiate the anticoagulant effect of warfarin and also to increase the plasma level of phenytoin, which are mainly metabolized by CYP2C9.	Tamoxifen	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-169
17024799-1	2006	Tamoxifen has been reported to potentiate the anticoagulant effect of warfarin and also to increase the plasma level of phenytoin, which are mainly metabolized by CYP2C9.	Phenytoin	120-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-169
17024799-2	2006	The aim of this study was to determine the influence of tamoxifen on CYP2C9 activity in vivo in humans.	Tamoxifen	56-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
17024799-7	2006	Tamoxifen inhibited CYP2C9 activity in breast cancer patients within two weeks of its administration.	Tamoxifen	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
17024799-8	2006	The inhibition of CYP2C9 activity may be a possible explanation for the drug-drug interaction of tamoxifen with CYP2C9 substrates.	Tamoxifen	97-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
17024799-8	2006	The inhibition of CYP2C9 activity may be a possible explanation for the drug-drug interaction of tamoxifen with CYP2C9 substrates.	Tamoxifen	97-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
29788657-5	2006	Thus, cytochrome P450 (CYP)2D6 polymorphism influences codeine and tramadol analgesic effects, CYP2C9 has an impact on the disposition of some nonsteroidal anti-inflammatory drugs, and opioid receptor polymorphism (118A>G) may reduce morphine potency.	Morphine	237-245	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
16960144-3	2006	It is now clear that genetic polymorphisms in genes influencing metabolism (CYP2C9) and pharmacodynamic response (VKORC1) are strongly associated with warfarin responsiveness.	Warfarin	151-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
16847429-6	2006	Multivariate regression analysis showed that patient age, height and CYP2C9, VKORC1 and APOE genotypes significantly contributed to warfarin dose requirement (R = 57%).	Warfarin	132-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
16802783-4	2006	Here, we have attached CYP2C9 to gold substrates such that the resulting construct maintains the ability to bind and metabolize substrates in the presence of NADPH and cytochrome P450 reductase.	NADP	158-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
16867169-4	2006	In detail these selective substrates were caffeine (CYP1A2), coumarin (CYP2A6), tolbutamide (CYP2C9), S-(+)-mephenytoin (CYP2C19), dextromethorphane (CYP2D6), chlorzoxazone (CYP2E1) and testosterone (CYP3A4).	Tolbutamide	80-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
16867170-3	2006	The metabolism of pioglitazone by CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4 and CYP3A5 was investigated using human recombinant CYP isoforms.	Pioglitazone	18-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
16818632-6	2006	In NHFs cultured in low versus normal serum, MYC induced increased expression of CYP2C9, a gene product well known to be associated with ROS production.	Reactive Oxygen Species	137-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
16818632-7	2006	Specific inhibition of CYP2C9 by small interfering RNA was shown to partially inhibit MYC-induced ROS production.	Reactive Oxygen Species	98-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
16797247-5	2006	RESULTS: Variant CYP2C9 genotypes enhanced the protective effect of ibuprofen on the prevention of colorectal cancer, and a dose-response relationship with respect to increasing numbers of variant alleles was seen (P interaction = .02).	Ibuprofen	68-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
16797247-8	2006	CONCLUSIONS: In this study, the major effect seen was an enhancement by slower-metabolizing CYP2C9 variants of the chemopreventive activity of ibuprofen against colorectal cancer.	Ibuprofen	143-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
16783563-0	2006	Amodiaquine, its desethylated metabolite, or both, inhibit the metabolism of debrisoquine (CYP2D6) and losartan (CYP2C9) in vivo.	Amodiaquine	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
16783563-0	2006	Amodiaquine, its desethylated metabolite, or both, inhibit the metabolism of debrisoquine (CYP2D6) and losartan (CYP2C9) in vivo.	Debrisoquin	77-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
16783563-0	2006	Amodiaquine, its desethylated metabolite, or both, inhibit the metabolism of debrisoquine (CYP2D6) and losartan (CYP2C9) in vivo.	Losartan	103-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
16783563-1	2006	OBJECTIVE: To study the extent of in vivo inhibition by the antimalarial drug amodiaquine, its active metabolite N-desethylamodiaquine, or both, of the metabolism of four probe drugs of the enzymes CYP2D6, CYP2C19, CYP2C9 and CYP1A2.	Amodiaquine	78-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	215-221
16783563-8	2006	The CYP2D6 and CYP2C9 activities of the subjects were measured by debrisoquine and losartan phenotyping tests, respectively.	Debrisoquin	66-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
16783563-8	2006	The CYP2D6 and CYP2C9 activities of the subjects were measured by debrisoquine and losartan phenotyping tests, respectively.	Losartan	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
16783563-10	2006	The effects on CYP2D6 and CYP2C9 activities subsided within a week after intake of amodiaquine as tested by the phenotyping cocktail.	Amodiaquine	83-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
16783563-12	2006	CONCLUSION: A single dose of amodiaquine decreased CYP2D6 and CYP2C9 activities significantly compared to baseline values.	Amodiaquine	29-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
16723553-11	2006	This was likely caused by inhibition of the cytochrome P450 2C9-mediated metabolism of S-(+)-ibuprofen.	Ibuprofen	87-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-63
17022718-11	2006	The risk for digestive hemorrhage associated with the CYP2C9 genotype is particularly relevant when using aceclofenac, celecoxib, diclofenac, ibuprofen, indomethacin, lornoxicam, piroxicam, or naproxen.	aceclofenac	106-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
17022718-11	2006	The risk for digestive hemorrhage associated with the CYP2C9 genotype is particularly relevant when using aceclofenac, celecoxib, diclofenac, ibuprofen, indomethacin, lornoxicam, piroxicam, or naproxen.	Celecoxib	119-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
17022718-11	2006	The risk for digestive hemorrhage associated with the CYP2C9 genotype is particularly relevant when using aceclofenac, celecoxib, diclofenac, ibuprofen, indomethacin, lornoxicam, piroxicam, or naproxen.	Diclofenac	130-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
17022718-11	2006	The risk for digestive hemorrhage associated with the CYP2C9 genotype is particularly relevant when using aceclofenac, celecoxib, diclofenac, ibuprofen, indomethacin, lornoxicam, piroxicam, or naproxen.	Ibuprofen	142-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
17022718-11	2006	The risk for digestive hemorrhage associated with the CYP2C9 genotype is particularly relevant when using aceclofenac, celecoxib, diclofenac, ibuprofen, indomethacin, lornoxicam, piroxicam, or naproxen.	Indomethacin	153-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
17022718-11	2006	The risk for digestive hemorrhage associated with the CYP2C9 genotype is particularly relevant when using aceclofenac, celecoxib, diclofenac, ibuprofen, indomethacin, lornoxicam, piroxicam, or naproxen.	lornoxicam	167-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
17022718-11	2006	The risk for digestive hemorrhage associated with the CYP2C9 genotype is particularly relevant when using aceclofenac, celecoxib, diclofenac, ibuprofen, indomethacin, lornoxicam, piroxicam, or naproxen.	Piroxicam	179-188	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
17022718-11	2006	The risk for digestive hemorrhage associated with the CYP2C9 genotype is particularly relevant when using aceclofenac, celecoxib, diclofenac, ibuprofen, indomethacin, lornoxicam, piroxicam, or naproxen.	Naproxen	193-201	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
16788382-1	2006	Genetic variations in cytochrome P450 2C9 (CYP2C9) are known to contribute to interindividual and interethnic variability in response to clinical drugs such as warfarin.	Warfarin	160-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-41
16788382-1	2006	Genetic variations in cytochrome P450 2C9 (CYP2C9) are known to contribute to interindividual and interethnic variability in response to clinical drugs such as warfarin.	Warfarin	160-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
16639745-0	2006	Multiple molecular dynamics simulations of human p450 monooxygenase CYP2C9: the molecular basis of substrate binding and regioselectivity toward warfarin.	Warfarin	145-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
16639745-4	2006	Besides the nonproductive state of the CYP2C9 warfarin complex captured in the crystal structure, three additional states were observed.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
16722840-7	2006	More recently, single nucleotide polymorphisms in the 2C9 isoform of cytochrome P450 (CYP2C9) and vitamin K epoxide reductase (VKOR) have been shown to make significant contributions to the variability in coumarin dosage requirements.	coumarin	205-213	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
16630605-0	2006	Frequency of CYP2C9 polymorphisms affecting warfarin metabolism in a large anticoagulant clinic cohort.	Warfarin	44-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
16630605-7	2006	CONCLUSIONS: Allele frequencies and genotypes for CYP2C9*2 and *3 variants in patients on warfarin are not statistically different from controls whether or not they are stratified for ethnicity.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
16630605-9	2006	CYP2C9 genotype predicts warfarin dosage even in an uncontrolled, retrospective survey of unselected patients on warfarin therapy.	Warfarin	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16630605-9	2006	CYP2C9 genotype predicts warfarin dosage even in an uncontrolled, retrospective survey of unselected patients on warfarin therapy.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16501008-9	2006	The K(i) values for CYP2C9 and CYP2C19 were 1.7 and 3.3 microM, respectively, and those for CYP3A4 were 8.3 and 2.9 microM, using two substrates, testosterone and midazolam, respectively.	Testosterone	146-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
16325295-0	2006	Effect of CYP2C9 genetic polymorphisms on the efficacy and pharmacokinetics of glimepiride in subjects with type 2 diabetes.	glimepiride	79-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
16325295-1	2006	Glimepiride, a sulfonylurea hypoglycemic agent, is metabolized by cytochrome P450 2C9 (CYP2C9) which is known to have genetic polymorphisms.	glimepiride	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-85
16325295-1	2006	Glimepiride, a sulfonylurea hypoglycemic agent, is metabolized by cytochrome P450 2C9 (CYP2C9) which is known to have genetic polymorphisms.	glimepiride	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
16325295-4	2006	The long-term observations of 2 patients with a CYP2C9*1/*3 suggested that subjects with a CYP2C9*1/*3 respond well to glimepiride during the initial phase of treatment, but 1 patient have shown the weight gain over the long-term treatment.	glimepiride	119-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
16325295-4	2006	The long-term observations of 2 patients with a CYP2C9*1/*3 suggested that subjects with a CYP2C9*1/*3 respond well to glimepiride during the initial phase of treatment, but 1 patient have shown the weight gain over the long-term treatment.	glimepiride	119-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
16325295-5	2006	The pharmacokinetic study showed that the area under the concentration-time curve for glimepiride in the CYP2C9*1/*3 subjects was approximately 2.5-fold higher than that of the CYP2C9*1/*1 subjects.	glimepiride	86-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
16325295-5	2006	The pharmacokinetic study showed that the area under the concentration-time curve for glimepiride in the CYP2C9*1/*3 subjects was approximately 2.5-fold higher than that of the CYP2C9*1/*1 subjects.	glimepiride	86-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	177-183
16325295-6	2006	The intrinsic clearance of glimepiride by the CYP2C9*3 enzyme was lower than that by the CYP2C9*1 enzyme.	glimepiride	27-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
16325295-6	2006	The intrinsic clearance of glimepiride by the CYP2C9*3 enzyme was lower than that by the CYP2C9*1 enzyme.	glimepiride	27-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
16325295-7	2006	These results suggested that the lower hydroxylation activity of glimepiride in the subject with type 2 diabetes and CYP2C9*1/*3 led to a marked elevation in the plasma concentrations of glimepiride and a stronger pharmacological effect of glimepiride.	glimepiride	65-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
16325295-7	2006	These results suggested that the lower hydroxylation activity of glimepiride in the subject with type 2 diabetes and CYP2C9*1/*3 led to a marked elevation in the plasma concentrations of glimepiride and a stronger pharmacological effect of glimepiride.	glimepiride	187-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
16325295-7	2006	These results suggested that the lower hydroxylation activity of glimepiride in the subject with type 2 diabetes and CYP2C9*1/*3 led to a marked elevation in the plasma concentrations of glimepiride and a stronger pharmacological effect of glimepiride.	glimepiride	187-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
16639344-0	2006	Lopinavir/ritonavir induces the hepatic activity of cytochrome P450 enzymes CYP2C9, CYP2C19, and CYP1A2 but inhibits the hepatic and intestinal activity of CYP3A as measured by a phenotyping drug cocktail in healthy volunteers.	Lopinavir	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
16639344-0	2006	Lopinavir/ritonavir induces the hepatic activity of cytochrome P450 enzymes CYP2C9, CYP2C19, and CYP1A2 but inhibits the hepatic and intestinal activity of CYP3A as measured by a phenotyping drug cocktail in healthy volunteers.	Ritonavir	10-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
16676068-1	2006	The degree of interpatient variability in the warfarin dose required to achieve the desired anticoagulant response can only partly be explained by polymorphisms in the CYP2C9 gene, suggesting that additional genetic factors such as polymorphisms in genes involved in blood coagulation may influence warfarin dose requirement.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
16676068-1	2006	The degree of interpatient variability in the warfarin dose required to achieve the desired anticoagulant response can only partly be explained by polymorphisms in the CYP2C9 gene, suggesting that additional genetic factors such as polymorphisms in genes involved in blood coagulation may influence warfarin dose requirement.	Warfarin	299-307	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
16676068-8	2006	With a regression model we explained 60.0% of variability in warfarin dose, which was due to gene polymorphisms (CYP2C9, VKORC1), age and body-surface-area.	Warfarin	61-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
16627267-2	2006	We developed and verified a melting analysis assay for common single nucleotide polymorphisms of cytochrome P-450 (CYP) 2C9 that affect warfarin metabolism.	Warfarin	136-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-123
16580898-0	2006	Influence of coagulation factor, vitamin K epoxide reductase complex subunit 1, and cytochrome P450 2C9 gene polymorphisms on warfarin dose requirements.	Warfarin	126-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-103
16580898-1	2006	INTRODUCTION: The primary objective of this study was to determine whether variability in warfarin dose requirements is determined by common polymorphisms in genes whose products are involved in the pharmacodynamics and pharmacokinetics of warfarin, namely, the coagulation factors, vitamin K epoxide reductase complex subunit 1 (VKORC1), and cytochrome P450 (CYP) 2C9.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	343-368
16580898-1	2006	INTRODUCTION: The primary objective of this study was to determine whether variability in warfarin dose requirements is determined by common polymorphisms in genes whose products are involved in the pharmacodynamics and pharmacokinetics of warfarin, namely, the coagulation factors, vitamin K epoxide reductase complex subunit 1 (VKORC1), and cytochrome P450 (CYP) 2C9.	Warfarin	240-248	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	343-368
16552506-2	2006	We have previously shown that warfarin dose is influenced by cytochrome P450 (CYP) 2C9 genotype, age, body weight and co-treatment with drugs that interfere with warfarin metabolism.	Warfarin	30-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-86
16552506-2	2006	We have previously shown that warfarin dose is influenced by cytochrome P450 (CYP) 2C9 genotype, age, body weight and co-treatment with drugs that interfere with warfarin metabolism.	Warfarin	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-86
16556082-7	2006	The systemic azoles, such as ketoconazole, itraconazole, fluconazole and voriconazole, are inhibitors of CYP isoenzymes, such as CYP3A4, CYP2C9 and CYP2C19, to varying degrees.	Azoles	13-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
16556082-7	2006	The systemic azoles, such as ketoconazole, itraconazole, fluconazole and voriconazole, are inhibitors of CYP isoenzymes, such as CYP3A4, CYP2C9 and CYP2C19, to varying degrees.	Ketoconazole	29-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
16556082-7	2006	The systemic azoles, such as ketoconazole, itraconazole, fluconazole and voriconazole, are inhibitors of CYP isoenzymes, such as CYP3A4, CYP2C9 and CYP2C19, to varying degrees.	Itraconazole	43-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
16556082-7	2006	The systemic azoles, such as ketoconazole, itraconazole, fluconazole and voriconazole, are inhibitors of CYP isoenzymes, such as CYP3A4, CYP2C9 and CYP2C19, to varying degrees.	Fluconazole	57-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
16556082-7	2006	The systemic azoles, such as ketoconazole, itraconazole, fluconazole and voriconazole, are inhibitors of CYP isoenzymes, such as CYP3A4, CYP2C9 and CYP2C19, to varying degrees.	Voriconazole	73-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
16505204-5	2006	Aerosol gene transfer of recombinant adenovirus containing the human CYP2C9 significantly elevated mean pulmonary artery pressure and total pulmonary resistance indices, both of which were sensitive to the inhibitor sulfaphenazole.	Sulfaphenazole	216-230	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
16765138-0	2006	CYP2C9 genotyping in acenocoumarol treatment: is it a cost-effective addition to international normalized ratio monitoring?	Acenocoumarol	21-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16793587-4	2006	CYP2C9, for instance, was involved in the conversion of estrogen sulfate to 16-hydroxy sulfate metabolite, DDC in estrogen-dependent pathogenesis of endometrial carcinoma possibly by DDC interaction with AR to enhance steroid receptor transcription.	estrogen sulfate	56-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16793587-4	2006	CYP2C9, for instance, was involved in the conversion of estrogen sulfate to 16-hydroxy sulfate metabolite, DDC in estrogen-dependent pathogenesis of endometrial carcinoma possibly by DDC interaction with AR to enhance steroid receptor transcription.	16-hydroxy sulfate	76-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16793587-4	2006	CYP2C9, for instance, was involved in the conversion of estrogen sulfate to 16-hydroxy sulfate metabolite, DDC in estrogen-dependent pathogenesis of endometrial carcinoma possibly by DDC interaction with AR to enhance steroid receptor transcription.	Zalcitabine	107-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16793587-4	2006	CYP2C9, for instance, was involved in the conversion of estrogen sulfate to 16-hydroxy sulfate metabolite, DDC in estrogen-dependent pathogenesis of endometrial carcinoma possibly by DDC interaction with AR to enhance steroid receptor transcription.	Zalcitabine	183-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16547074-5	2006	It is noteworthy that Compound K, protopanaxadiol (Ppd), and protopanaxatriol (Ppt) all exhibited moderate inhibition against CYP2C9 activity, and Ppd and Ppt also exhibited potent competitive inhibition against CYP3A4 activity.	protopanaxadiol	34-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
16547074-5	2006	It is noteworthy that Compound K, protopanaxadiol (Ppd), and protopanaxatriol (Ppt) all exhibited moderate inhibition against CYP2C9 activity, and Ppd and Ppt also exhibited potent competitive inhibition against CYP3A4 activity.	protopanaxatriol	61-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
16547074-5	2006	It is noteworthy that Compound K, protopanaxadiol (Ppd), and protopanaxatriol (Ppt) all exhibited moderate inhibition against CYP2C9 activity, and Ppd and Ppt also exhibited potent competitive inhibition against CYP3A4 activity.	protopanaxatriol	79-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
16413010-2	2006	Cytochrome P4502C9 (CYP2C9) is polymorphic in human and is principally responsible for the metabolism of warfarin.	Warfarin	105-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-18
16413010-2	2006	Cytochrome P4502C9 (CYP2C9) is polymorphic in human and is principally responsible for the metabolism of warfarin.	Warfarin	105-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
16413010-4	2006	We screened a new polymorphism of CYP2C9 and investigated its role in warfarin sensitivity.	Warfarin	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
16413010-10	2006	The association between warfarin dose requirement and genetic polymorphism of CYP2C9 was also analysed.	Warfarin	24-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
16501008-8	2006	Using cDNA-expressed enzymes, clevidipine inhibited CYP2C9, CYP2C19, and CYP3A4 activities with IC(50) values below 10 microM, whereas CYP1A2, CYP2D6, and CYP2E1 activities were not substantially inhibited (IC(50) values >70 microM).	clevidipine	30-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
16873909-0	2006	Influence of the CYP2C9 AND CYP2C19 polymorphisms on phenytoin hydroxylation in healthy individuals from south India.	Phenytoin	53-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
16873909-1	2006	BACKGROUND AND OBJECTIVES: Phenytoin, a widely used anti-epileptic drug, is metabolized mainly by CYP2C9 (90%) and partly by CYP2C19 (10%) to its major metabolite 5-(para-hydroxyphenyl)-5- phenylhydantoin (p-HPPH).	Phenytoin	27-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
16873909-8	2006	RESULTS: A significant correlation was observed between the CYP2C9 genotype and metabolic ratio of phenytoin/p-HPPH (r = 0.472, 95% CI 0.100 to 0.728; P = 0.01).	Phenytoin	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
16873909-9	2006	While no association was found with CYP2C19 alone, a significant correlation was observed between the combined CYP2C9 and CYP2C19 genotypes and phenytoin metabolic ratio (r = 0.507, 95% CI 0.146 to 0.749; P< 0.01).	Phenytoin	144-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
16873909-10	2006	INTERPRETATION AND CONCLUSION: CYP2C9*2 and *3 mutant alleles caused decreased hydroxylation of phenytoin in vivo, whereas the mutant alleles of CYP2C19 played only a minor role in the metabolism of phenytoin in subjects of our study.	Phenytoin	96-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
16873909-10	2006	INTERPRETATION AND CONCLUSION: CYP2C9*2 and *3 mutant alleles caused decreased hydroxylation of phenytoin in vivo, whereas the mutant alleles of CYP2C19 played only a minor role in the metabolism of phenytoin in subjects of our study.	Phenytoin	199-208	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
16639344-6	2006	CYP2C9 and CYP2C19 activities were quantified by S-WARF AUC0-inf and OMP/5-hydroxy OMP ratio, respectively.	5-hydroxymethylomeprazole	73-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16318905-6	2006	CYP1A2 and CYP2C9 played minor roles in the metabolism of rutaecarpine.	rutecarpine	58-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
16708125-2	2006	One of several factors underlying the variability in warfarin dose response in the patients receiving this oral anticoagulant is a genetic predisposition, especially the CYP2C9 polymorphisms.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-176
16708125-7	2006	The clinical correlation between CYP2C9 polymorphism and warfarin metabolism was also assessed.	Warfarin	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
16708125-9	2006	CYP2C9 variants are strongly associated with low-dose warfarin requirement.	Warfarin	54-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16708125-10	2006	In summary, the CYP2C9 variants strongly affect the warfarin dose requirement.	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
16415119-7	2006	A monoclonal antibody to CYP2B6 and the CYP3A inhibitor ketoconazole substantially inhibited R-138727 formation, whereas inhibitors of CYP2C9 (sulfaphenazole) and CYP2C19 (omeprazole) did not.	Sulfaphenazole	143-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-141
16501008-9	2006	The K(i) values for CYP2C9 and CYP2C19 were 1.7 and 3.3 microM, respectively, and those for CYP3A4 were 8.3 and 2.9 microM, using two substrates, testosterone and midazolam, respectively.	Midazolam	163-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
16699986-3	2006	AIM: To investigate the influence of CYP2C9 polymorphism on the occurrence of bleeding complications related to acenocoumarol therapy.	Acenocoumarol	112-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
16635054-1	2006	BACKGROUND: CYP2C9 is one of the major drug metabolizing enzymes for many drugs including warfarin, NSAIDs and losartan.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
16635054-1	2006	BACKGROUND: CYP2C9 is one of the major drug metabolizing enzymes for many drugs including warfarin, NSAIDs and losartan.	Losartan	111-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
16513453-0	2006	Accumulation of celecoxib with a 7-fold higher drug exposure in individuals homozygous for CYP2C9*3.	Celecoxib	16-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
16490777-1	2006	7-Methoxy-4-trifluoromethylcoumarin (MFC) has been used extensively in high-throughput screens for the identification of potential CYP2C9 interactions.	7-methoxy-4-trifluoromethylcoumarin	0-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
16490777-1	2006	7-Methoxy-4-trifluoromethylcoumarin (MFC) has been used extensively in high-throughput screens for the identification of potential CYP2C9 interactions.	7-methoxy-4-trifluoromethylcoumarin	37-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
16513444-5	2006	CYP2C9*2 and VKORC1 coding region variants were rare (<2%), whereas CYP2C9*3 associated with lower warfarin requirements was less common in Chinese and Malays (7% and 9%, respectively) than in Indians (18%) and could not account for their lower warfarin requirements.	Warfarin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
16699986-6	2006	RESULTS: In 145 patients bearing alleles with reduced activity (CYP2C9*2 and/or *3), the optimal dose of acenocoumarol was significantly (p<0.001) lower than in patients with the wild type allele (2.12+/-0.96 mg/day and 2.90+/-1.46 mg/day, respectively).	Acenocoumarol	105-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
16699986-7	2006	In comparison with wild type allele patients, the mean daily acenocoumarol dose was lower in the CYP2C9*2 group, and the lowest in *3 bearers.	Acenocoumarol	61-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
16699986-9	2006	CONCLUSIONS: Patients bearing CYP2C9 alleles with reduced enzymatic activity have a lower acenocoumarol requirement.	Acenocoumarol	90-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
16445595-0	2006	Inhibitory effect of 5-fluorouracil on cytochrome P450 2C9 activity in cancer patients.	Fluorouracil	21-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-58
16388406-5	2006	RESULTS: The acid forms had minimal inhibitory effects on all CYP activities tested, except for fluvastatin on CYP2C9-mediated tolbutamide 4-hydroxylation (IC50 = 1.7 microM) and simvastatin on CYP3A4/5-mediated paclitaxel 3-hydroxylation (12.0 microM).	Fluvastatin	96-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
16388406-5	2006	RESULTS: The acid forms had minimal inhibitory effects on all CYP activities tested, except for fluvastatin on CYP2C9-mediated tolbutamide 4-hydroxylation (IC50 = 1.7 microM) and simvastatin on CYP3A4/5-mediated paclitaxel 3-hydroxylation (12.0 microM).	Tolbutamide	127-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
16479536-6	2006	Tagging technology is shown to supersede conventional methods for P450 profiling in terms of discriminatory power and throughput, exemplified by the simultaneous detection of distinct induction profiles for cyp2c subfamily members in response to phenobarbitone: cyp2c29 expression, but not cyp2c40 or cyp2c50, was induced threefold by treatment.	Phenobarbital	246-260	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	207-212
16445595-1	2006	Drug interactions have been reported between 5-fluorouracil and cytochrome P450 2C9 (CYP2C9) substrates, S-warfarin and phenytoin.	Fluorouracil	45-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-83
16445595-1	2006	Drug interactions have been reported between 5-fluorouracil and cytochrome P450 2C9 (CYP2C9) substrates, S-warfarin and phenytoin.	Fluorouracil	45-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
16445595-1	2006	Drug interactions have been reported between 5-fluorouracil and cytochrome P450 2C9 (CYP2C9) substrates, S-warfarin and phenytoin.	Phenytoin	120-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
16445595-2	2006	This study was performed to determine the influence of 5-fluorouracil on cytochrome P450 2C9 (CYP2C9) activity in colorectal cancer patients (n=17) receiving 5-fluorouracil.	Fluorouracil	55-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-92
16445595-2	2006	This study was performed to determine the influence of 5-fluorouracil on cytochrome P450 2C9 (CYP2C9) activity in colorectal cancer patients (n=17) receiving 5-fluorouracil.	Fluorouracil	55-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
16445595-2	2006	This study was performed to determine the influence of 5-fluorouracil on cytochrome P450 2C9 (CYP2C9) activity in colorectal cancer patients (n=17) receiving 5-fluorouracil.	Fluorouracil	158-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-92
16445595-2	2006	This study was performed to determine the influence of 5-fluorouracil on cytochrome P450 2C9 (CYP2C9) activity in colorectal cancer patients (n=17) receiving 5-fluorouracil.	Fluorouracil	158-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
16445595-3	2006	Losartan was used as a marker to assess CYP2C9 activity.	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
16445595-9	2006	The results suggest that in most patients 5-fluorouracil inhibited CYP2C9 activity.	Fluorouracil	42-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
16445595-11	2006	This finding may help explain the mechanism of interaction between 5-fluorouracil and CYP2C9 substrates.	Fluorouracil	67-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
16356485-3	2006	CI-1034 moderately inhibited CYP2C9 (IC(50) 39.6 microM) and CYP3A4 activity (IC(50) 21.6 microM); CYP3A4 inhibition was metabolism-dependent.	PD 180988	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
16802848-10	2006	Clearance is hepatic via N-oxidation by the hepatic cytochrome P450 (CYP) isoenzymes, CYP2C19, CYP2C9 and CYP3A4.	Nitrogen	25-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
16550733-1	2006	OBJECTIVE: Bosentan has been shown in vitro and in vivo to induce the cytochrome P450 enzymes CYP2C9 and CYP3A4.	Bosentan	11-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
16863464-0	2006	Contribution of CYP2C9 to variability in vitamin K antagonist metabolism.	Vitamin K	41-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
16863464-3	2006	CYP2C9 makes a very important contribution to metabolism of vitamin K antagonist anticoagulants, and is the main oxidising enzyme for S-warfarin and S-acenocoumarol as well as contributing to phenprocoumon metabolism.	Vitamin K	60-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16863464-3	2006	CYP2C9 makes a very important contribution to metabolism of vitamin K antagonist anticoagulants, and is the main oxidising enzyme for S-warfarin and S-acenocoumarol as well as contributing to phenprocoumon metabolism.	Warfarin	134-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16863464-3	2006	CYP2C9 makes a very important contribution to metabolism of vitamin K antagonist anticoagulants, and is the main oxidising enzyme for S-warfarin and S-acenocoumarol as well as contributing to phenprocoumon metabolism.	Acenocoumarol	149-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16863464-4	2006	A large number of studies have now shown that CYP2C9 genotype predicts dose requirement for both warfarin and acenocoumarol, with a possible contribution for phenprocoumon.	Warfarin	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
16863464-4	2006	A large number of studies have now shown that CYP2C9 genotype predicts dose requirement for both warfarin and acenocoumarol, with a possible contribution for phenprocoumon.	Acenocoumarol	110-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
16863464-6	2006	Although CYP2C9 genotype is clearly a predictor of vitamin K antagonist dose requirement, especially in Caucasian populations in whom variant alleles are common, a number of recent studies have shown that age, genotype for the gene encoding the target gene vitamin K epoxide reductase and concomitant drugs are equally important factors in determining dose.	Vitamin K	51-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
16424822-0	2006	Different contributions of polymorphisms in VKORC1 and CYP2C9 to intra- and inter-population differences in maintenance dose of warfarin in Japanese, Caucasians and African-Americans.	Warfarin	128-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
16424822-10	2006	Furthermore, VKORC1 1173C > T and CYP2C9 (*2/*3/*11) genotypes, age and weight were identified as independent covariates contributing to interpatient variability in warfarin dosage.	Warfarin	168-176	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
16424822-11	2006	CONCLUSIONS: Both VKORC1 and CYP2C9 polymorphisms contribute to inter-population difference in warfarin doses among the three populations, but their contribution to intra-population variability may differ within each population.	Warfarin	95-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
16359930-12	2006	Currently, the best example of avoiding side effects is determining genotype at the CYP2C9 locus with respect of warfarin treatment, since carriers for functional variants (>20% of the population) require lower doses for optimal anticoagulation, and homozygotes, although rare, may well experience serious bleeding if given a usual dose.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
16493479-4	2006	Warfarin daily dose was predominantly determined by VKORC1 and CYP2C9 genotypes (partial r(2) = 0.21; 0.20, respectively).	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
16493479-7	2006	Combined genotype analysis revealed that CYP2C9 andVKORC1 wild type and CALU mutant patients required the highest warfarin doses (7.8 +/- 1.5mg/day; n = 9) as compared to the CYP2C9 and VKORC1 mutant and CALU wild type genotypes (2.8 +/- 0.3 mg/day; n = 18; p < 0.01).	Warfarin	114-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
16493479-9	2006	Compound genetic profiles comprising VKORC1, CALU and CYP2C9 improve categorization of individual warfarin dose requirements in more than 25% of patients at steady-state anticoagulation.	Warfarin	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
16137701-2	2006	In this study the inhibitory effect of chamomile essential oil and its major constituents on four selected human cytochrome P450 enzymes (CYP1A2, CYP2C9, CYP2D6 and CYP3A4) was investigated.	chamomile essential oil	39-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
16401082-6	2006	The oxidation of alpha-thujone by human CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 occurs with up to 80% C-4 methyl inversion, in agreement with a dominant radical hydroxylation mechanism.	beta-thujone	17-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
16286479-1	2006	To determine the efficacy of cytochrome P450 2C9 metabolites of arachidonic acid, viz.	Arachidonic Acid	64-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-48
16428919-3	2006	Therefore, in vitro and in vivo inhibition studies were done to ascertain the influence of ginkgo on CYP2C9, the P-450 isozyme responsible for the metabolism of the most potent warfarin enantiomer, (S)-warfarin.	Warfarin	177-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
16428919-3	2006	Therefore, in vitro and in vivo inhibition studies were done to ascertain the influence of ginkgo on CYP2C9, the P-450 isozyme responsible for the metabolism of the most potent warfarin enantiomer, (S)-warfarin.	Warfarin	198-210	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
16475710-1	2006	The oxazaphosphorines cyclophosphamide (CP) and ifosfamide (IF) are alkylating agents that require bioactivation via cytochrome (CYP) P450 isoenzymes including CYP2C9 enzymes.	oxazaphosphorines	4-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
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
16475710-1	2006	The oxazaphosphorines cyclophosphamide (CP) and ifosfamide (IF) are alkylating agents that require bioactivation via cytochrome (CYP) P450 isoenzymes including CYP2C9 enzymes.	Ifosfamide	48-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
16475710-3	2006	The mutant alleles of CYP2C9 were residue 144 (Arg (*1)/Cys (*2)), residue 358 (Tyr/Cys), residue 359 (Ile/Leu (*3)) and residue 417 (Gly/Asp).	Arginine	47-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
16475710-3	2006	The mutant alleles of CYP2C9 were residue 144 (Arg (*1)/Cys (*2)), residue 358 (Tyr/Cys), residue 359 (Ile/Leu (*3)) and residue 417 (Gly/Asp).	Cysteine	56-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
16475710-3	2006	The mutant alleles of CYP2C9 were residue 144 (Arg (*1)/Cys (*2)), residue 358 (Tyr/Cys), residue 359 (Ile/Leu (*3)) and residue 417 (Gly/Asp).	Glycine	134-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
16475710-3	2006	The mutant alleles of CYP2C9 were residue 144 (Arg (*1)/Cys (*2)), residue 358 (Tyr/Cys), residue 359 (Ile/Leu (*3)) and residue 417 (Gly/Asp).	Aspartic Acid	138-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
17112294-8	2006	Systemic clearance of dexloxiglumide is moderate and cytochrome P450 (CYP) 3A4/5 and CYP2C9 have been implicated in the metabolism of dexloxiglumide to produce O-demethyl dexloxi-glumide.	dexloxiglumide	22-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
17112294-8	2006	Systemic clearance of dexloxiglumide is moderate and cytochrome P450 (CYP) 3A4/5 and CYP2C9 have been implicated in the metabolism of dexloxiglumide to produce O-demethyl dexloxi-glumide.	dexloxiglumide	134-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
17112294-8	2006	Systemic clearance of dexloxiglumide is moderate and cytochrome P450 (CYP) 3A4/5 and CYP2C9 have been implicated in the metabolism of dexloxiglumide to produce O-demethyl dexloxi-glumide.	o-demethyl dexloxi-glumide	160-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
17124101-3	2006	SNPs in the cytochrome P450 complex (CYP2C9) affect coumarin metabolism.	coumarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
16413247-1	2006	OBJECTIVES: Recent anecdotal, unvalidated case reports have suggested potentiation of warfarin-induced anticoagulation by cranberry juice, possibly through inhibition of human cytochrome P450 (CYP) 2C9, the enzyme responsible for the clearance of the active S-enantiomer of warfarin.	Warfarin	86-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-201
16413247-1	2006	OBJECTIVES: Recent anecdotal, unvalidated case reports have suggested potentiation of warfarin-induced anticoagulation by cranberry juice, possibly through inhibition of human cytochrome P450 (CYP) 2C9, the enzyme responsible for the clearance of the active S-enantiomer of warfarin.	Warfarin	274-282	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-201
16299161-1	2006	Gemfibrozil more potently inhibits CYP2C9 than CYP2C8 in vitro, and yet the opposite inhibitory potency is observed in the clinic.	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
16299161-3	2006	Gemfibrozil most potently inhibited CYP2C9 (IC50 of 30 microM), whereas gemfibrozil glucuronide most potently inhibited CYP2C8 (IC50 of 24 microM).	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
17124101-4	2006	Patients with either of two common variants, CYP2C9*2 or CYP2C9*3, metabolize coumarins slowly and are twice as likely to have a laboratory or clinical adverse event, unless their initial coumarin doses are reduced.	Coumarins	78-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
17124101-4	2006	Patients with either of two common variants, CYP2C9*2 or CYP2C9*3, metabolize coumarins slowly and are twice as likely to have a laboratory or clinical adverse event, unless their initial coumarin doses are reduced.	Coumarins	78-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
17124101-4	2006	Patients with either of two common variants, CYP2C9*2 or CYP2C9*3, metabolize coumarins slowly and are twice as likely to have a laboratory or clinical adverse event, unless their initial coumarin doses are reduced.	coumarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
17124101-4	2006	Patients with either of two common variants, CYP2C9*2 or CYP2C9*3, metabolize coumarins slowly and are twice as likely to have a laboratory or clinical adverse event, unless their initial coumarin doses are reduced.	coumarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
16432637-0	2006	Association of VKORC1 and CYP2C9 polymorphisms with warfarin dose requirements in Japanese patients.	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
16379042-2	2006	To assess the biotransformation and CYP reaction phenotype and their potential implications for human pharmacology and toxicology, the in vitro metabolism of ET-743 was characterized using incubations with human liver preparations, cytochrome P450 (CYP) and uridine diphosphoglucuronosyl transferase (UGT) supersomes.CYP supersomes and liver microsomes showed that ET-743 was metabolized mainly by CYP3A4, but also by CYP2C9, 2C19, 2D6, and 2E1.	Trabectedin	158-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	418-424
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
17827526-9	2006	It was located in the amino acid number 144 of CYP2C9 protein with the change of normal amino acid arginine into cysteine, which is the same as identified in poor metabolism patients as homozygous CYP2C9*2.	amino acid arginine	88-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
17827526-9	2006	It was located in the amino acid number 144 of CYP2C9 protein with the change of normal amino acid arginine into cysteine, which is the same as identified in poor metabolism patients as homozygous CYP2C9*2.	amino acid arginine	88-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
17827526-9	2006	It was located in the amino acid number 144 of CYP2C9 protein with the change of normal amino acid arginine into cysteine, which is the same as identified in poor metabolism patients as homozygous CYP2C9*2.	Cysteine	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
17827526-9	2006	It was located in the amino acid number 144 of CYP2C9 protein with the change of normal amino acid arginine into cysteine, which is the same as identified in poor metabolism patients as homozygous CYP2C9*2.	Cysteine	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
16432637-5	2006	We then genotyped the CYP2C9 gene for the Japanese common genetic variant, CYP2C9*3 and, based on the genotype of these two genes, classified patients into three categories, which we call "warfarin-responsive index."	Warfarin	189-197	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
16432637-5	2006	We then genotyped the CYP2C9 gene for the Japanese common genetic variant, CYP2C9*3 and, based on the genotype of these two genes, classified patients into three categories, which we call "warfarin-responsive index."	Warfarin	189-197	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
16432637-7	2006	Thus, analysis of the combination of VKORC1 and CYP2C9 genotypes should identify warfarin-sensitive patients who require a lower dose of drug, allowing personalized warfarin treatment.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
16924387-0	2006	The high prevalence of the poor and ultrarapid metabolite alleles of CYP2D6, CYP2C9, CYP2C19, CYP3A4, and CYP3A5 in Taiwanese population.	ultrarapid	36-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
16432637-7	2006	Thus, analysis of the combination of VKORC1 and CYP2C9 genotypes should identify warfarin-sensitive patients who require a lower dose of drug, allowing personalized warfarin treatment.	Warfarin	165-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
16719380-0	2006	Determination of CYP2C9-catalyzed diclofenac 4"-hydroxylation by high-performance liquid chromatography.	diclofenac 4"	34-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
16719380-1	2006	A reverse-phase, high-performance liquid chromatography method is described for quantification of diclofenac 4"-hydroxylation catalyzed by human liver microsomes or cDNA-expressed CYP2C9.	Diclofenac	98-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	180-186
16719380-3	2006	This method is applicable to enzymatic studies for determination of CYP2C9-catalyzed diclofenac 4"-hydroxylation activity.	Diclofenac	85-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
16543980-0	2006	A novel sequence variant in exon 7 of CYP2C9 gene (CYP2C9*24) in a patient on warfarin therapy.	Warfarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
16541193-0	2006	CYP2C9 Ile359Leu polymorphism, plasma irbesartan concentration and acute blood pressure reductions in response to irbesartan treatment in Chinese hypertensive patients.	ile359leu	7-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16541193-0	2006	CYP2C9 Ile359Leu polymorphism, plasma irbesartan concentration and acute blood pressure reductions in response to irbesartan treatment in Chinese hypertensive patients.	Irbesartan	114-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16541193-1	2006	Our previous study demonstrated that the CYP2C9*3 gene variant was significantly associated with elevated plasma irbesartan concentration and blood pressure decline, assessed by a 4-week follow-up and revisit following daily administration of irbesartan.	Irbesartan	113-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
16541193-1	2006	Our previous study demonstrated that the CYP2C9*3 gene variant was significantly associated with elevated plasma irbesartan concentration and blood pressure decline, assessed by a 4-week follow-up and revisit following daily administration of irbesartan.	Irbesartan	243-253	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
16541193-8	2006	Subjects with the CYP2C9*1/CYP2C9*3 genotype had significantly higher plasma irbesartan concentrations when compared with those with the CYP2C9*1/CYP2C9*1 genotype (beta +/- SE = 81 +/- 36) and greater DBP response (beta +/- SE = 5.6 +/- 2.5 mmHg) at the 6-h time point after adjusting for important confounders.	Irbesartan	77-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
16541193-8	2006	Subjects with the CYP2C9*1/CYP2C9*3 genotype had significantly higher plasma irbesartan concentrations when compared with those with the CYP2C9*1/CYP2C9*1 genotype (beta +/- SE = 81 +/- 36) and greater DBP response (beta +/- SE = 5.6 +/- 2.5 mmHg) at the 6-h time point after adjusting for important confounders.	Irbesartan	77-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
16541193-8	2006	Subjects with the CYP2C9*1/CYP2C9*3 genotype had significantly higher plasma irbesartan concentrations when compared with those with the CYP2C9*1/CYP2C9*1 genotype (beta +/- SE = 81 +/- 36) and greater DBP response (beta +/- SE = 5.6 +/- 2.5 mmHg) at the 6-h time point after adjusting for important confounders.	Irbesartan	77-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
16541193-8	2006	Subjects with the CYP2C9*1/CYP2C9*3 genotype had significantly higher plasma irbesartan concentrations when compared with those with the CYP2C9*1/CYP2C9*1 genotype (beta +/- SE = 81 +/- 36) and greater DBP response (beta +/- SE = 5.6 +/- 2.5 mmHg) at the 6-h time point after adjusting for important confounders.	Irbesartan	77-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
16541193-9	2006	Our finding suggests that the CYP2C9*3 gene variant significantly alters the plasma concentration and acute DBP response at the 6-h point following irbesartan treatment in Chinese hypertensive patients.	Irbesartan	148-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
16543980-0	2006	A novel sequence variant in exon 7 of CYP2C9 gene (CYP2C9*24) in a patient on warfarin therapy.	Warfarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
16601787-1	2005	Enzyme activities of the CYP enzymes (CYP3A4, CYP2C9 and CYP2A6) were determined using classical substrates (testosterone, diclofenac and coumarin, respectively) as well as with luminogenic or fluorogenic substrates in micromethod arrangement.	Testosterone	109-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
16188404-0	2005	Down-regulation of astroglial CYP2C, glucocorticoid receptor and constitutive androstane receptor genes in response to cocaine in human U373 MG astrocytoma cells.	Cocaine	119-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-35
16188404-2	2005	Cytochromes P450 (CYP), especially the astrocytic members of the CYP2C subfamily may play an important role in the modulation of cerebrovascular functions, by generating vasodilatator metabolites from arachidonic acid (AA).	Arachidonic Acid	201-217	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-70
16188404-3	2005	Our study examined the regulation of CYP2C genes in response to cocaine or amphetamine in the human astrocyte-like U373 MG cells, using reverse transcription-polymerase chain reaction (RT-PCR) and western-blot analysis.	Cocaine	64-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-42
16188404-3	2005	Our study examined the regulation of CYP2C genes in response to cocaine or amphetamine in the human astrocyte-like U373 MG cells, using reverse transcription-polymerase chain reaction (RT-PCR) and western-blot analysis.	Amphetamine	75-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-42
16188404-4	2005	A treatment for 48h with increasing concentrations of cocaine caused a significant down-regulation of CYP2C8 and CYP2C9 genes and decreased the protein level.	Cocaine	54-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
16188404-7	2005	Effects of cocaine on CYP2C were accompanied by a decrease in the GR and CAR gene expression suggesting that these nuclear receptors could be involved in the CYP2C repression by cocaine in the U373 MG cell line.	Cocaine	11-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-27
16188404-7	2005	Effects of cocaine on CYP2C were accompanied by a decrease in the GR and CAR gene expression suggesting that these nuclear receptors could be involved in the CYP2C repression by cocaine in the U373 MG cell line.	Cocaine	11-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-163
16188404-7	2005	Effects of cocaine on CYP2C were accompanied by a decrease in the GR and CAR gene expression suggesting that these nuclear receptors could be involved in the CYP2C repression by cocaine in the U373 MG cell line.	Cocaine	178-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-27
16385662-0	2005	A case of intolerance to warfarin dosing in an intermediate metabolizer of CYP2C9.	Warfarin	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
16385662-1	2005	We report a case of intolerance to warfarin dosing due to impaired drug metabolism in a patient heterozygous for the CYP2C9*3 allele.	Warfarin	35-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
16188404-7	2005	Effects of cocaine on CYP2C were accompanied by a decrease in the GR and CAR gene expression suggesting that these nuclear receptors could be involved in the CYP2C repression by cocaine in the U373 MG cell line.	Cocaine	178-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-163
16601787-1	2005	Enzyme activities of the CYP enzymes (CYP3A4, CYP2C9 and CYP2A6) were determined using classical substrates (testosterone, diclofenac and coumarin, respectively) as well as with luminogenic or fluorogenic substrates in micromethod arrangement.	Diclofenac	123-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
16305586-1	2005	BACKGROUND: As acetylsalicylic acid is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6) and cytochrome P450 2C9 (CYP2C9), interindividual differences in activity of these enzymes may modulate the effects and side-effects of acetylsalicylic acid.	Aspirin	15-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-118
16601787-1	2005	Enzyme activities of the CYP enzymes (CYP3A4, CYP2C9 and CYP2A6) were determined using classical substrates (testosterone, diclofenac and coumarin, respectively) as well as with luminogenic or fluorogenic substrates in micromethod arrangement.	coumarin	138-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
16305586-1	2005	BACKGROUND: As acetylsalicylic acid is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6) and cytochrome P450 2C9 (CYP2C9), interindividual differences in activity of these enzymes may modulate the effects and side-effects of acetylsalicylic acid.	Aspirin	15-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
16305586-1	2005	BACKGROUND: As acetylsalicylic acid is metabolized by UDP-glucuronosyltransferase 1A6 (UGT1A6) and cytochrome P450 2C9 (CYP2C9), interindividual differences in activity of these enzymes may modulate the effects and side-effects of acetylsalicylic acid.	Aspirin	231-251	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
16305586-2	2005	The objective of this study was to assess whether polymorphisms in UGT1A6 and CYP2C9 genes are related to the prevalence of upper gastrointestinal symptoms in cardiovascular patients using acetylsalicylic acid for secondary prevention of ischaemic heart disease.	Aspirin	189-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
16601787-2	2005	The luciferin-based luminogenic substrates for CYP3A4 and CYP2C9 as well as coumarin in micromethod for assay of CYP2A6 activity gave results well comparable with the classical methods with determination of reaction products by the HPLC.	D-luciferin	4-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
16111713-1	2005	CYP2C9 is a major P450 2C enzyme, which hydroxylates about 16% of drugs that are in current clinical use and contributes to the metabolism of a number of clinically important substrate drugs such as warfarin.	Warfarin	199-207	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16183781-1	2005	The present study was conducted to assess a possible in vivo effect of propiverine, an anticholinergic drug to treat urinary incontinence and related disorders, on the activity of intestinal CYP3A4 and of hepatic CYP3A4, CYP2C9, CYP2C19, and CYP1A2.	propiverine	71-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	221-227
16192747-3	2005	The risk of such interactions is increased if voriconazole and, much less pronounced caspofungin, are co-administered with drugs which have an inducing or inhibiting effect on the CYP 450 system, primarily on the isoenzymes CYP2C19, CYP2C9 and CYP3A4.	Voriconazole	46-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	233-239
16338275-2	2005	We aimed to determine the influence of CYP2B6, CYP2C9, and CYP2C19 genetic polymorphism on methadone pharmacokinetics and on the response to treatment.	Methadone	91-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
16291720-4	2005	In Transwell assays, the migration of endothelial cells pre-exposed to hypoxia to increase CYP expression was abolished by CYP 2C antisense oligonucleotides as well as by the CYP inhibitor MS-PPOH and the EET antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (EEZE).	Oligonucleotides	140-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
16291720-4	2005	In Transwell assays, the migration of endothelial cells pre-exposed to hypoxia to increase CYP expression was abolished by CYP 2C antisense oligonucleotides as well as by the CYP inhibitor MS-PPOH and the EET antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (EEZE).	14,15-episulfide eicosatrienoic acid	220-253	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
16291720-7	2005	Matrix metalloprotease (MMP) activity was increased in CYP-2C9-overexpressing cells and correlated with increased invasion through Matrigel-coated Transwell chambers: an effect sensitive to the CYP 2C9 inhibitor sulfaphenazole as well as to EEZE and the MMP inhibitor GM6001.	Sulfaphenazole	212-226	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-62
16291720-7	2005	Matrix metalloprotease (MMP) activity was increased in CYP-2C9-overexpressing cells and correlated with increased invasion through Matrigel-coated Transwell chambers: an effect sensitive to the CYP 2C9 inhibitor sulfaphenazole as well as to EEZE and the MMP inhibitor GM6001.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	268-274	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-62
16237546-9	2005	The minor role of CYP2C9 in 4"-hydroxy-PPC formation and the effect of CYP2C9 genotype for (S)-6- and (S)-7-hydroxy-PPC were confirmed.	S 6	91-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
16237546-9	2005	The minor role of CYP2C9 in 4"-hydroxy-PPC formation and the effect of CYP2C9 genotype for (S)-6- and (S)-7-hydroxy-PPC were confirmed.	(s)-7-hydroxy-ppc	102-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
16236141-3	2005	In vitro and in vivo data suggest that the metabolism of fluoxetine to norfluoxetine is stereoselective and mediated, at least in part, by the polymorphic cytochrome P450 (CYP) isoenzymes CYP2D6, CYP2C9 and CYP2C19.	Fluoxetine	57-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
16236141-3	2005	In vitro and in vivo data suggest that the metabolism of fluoxetine to norfluoxetine is stereoselective and mediated, at least in part, by the polymorphic cytochrome P450 (CYP) isoenzymes CYP2D6, CYP2C9 and CYP2C19.	norfluoxetine	71-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
16236141-9	2005	Among homozygous extensive metabolizers for CYP2D6, patients homozygous for CYP2C9*1 had lower dose-normalized R-fluoxetine concentrations and lower active moiety levels compared with those carrying detrimental CYP2C9 alleles (P<0.05).	(R)-Fluoxetine	111-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
16081671-2	2005	There was an excellent correlation between IC(50, apparent) values determined using diclofenac and naproxen as CYP2C9 substrates (r2 = 0.82, p < 0.0001), with values being generally higher in the naproxen assay.	Naproxen	99-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
16236141-10	2005	These results suggest that CYP2D6 and CYP2C9 polymorphisms contribute to the interindividual variability in fluoxetine pharmacokinetics at steady-state.	Fluoxetine	108-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
16321620-1	2005	OBJECTIVE: Our objective was to prospectively study the impact of CYP2C9 polymorphism (*2 and *3) on the risk of overanticoagulation during the induction phase of warfarin therapy.	Warfarin	163-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
16321620-8	2005	CONCLUSIONS: The CYP2C9*2 and *3 single-nucleotide polymorphisms significantly increase the risk of overanticoagulation during the first 2 weeks of warfarin treatment, with increased INR levels evident after only 4 days" treatment in *2 carriers.	Warfarin	148-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
16321620-9	2005	Our prospective data are consistent with results from previous retrospective studies and indicate that CYP2C9 genotyping may be a means of improving safety during warfarin induction.	Warfarin	163-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
16236040-1	2005	AIMS: Dexloxiglumide is a new CCK(1) receptor antagonist under investigation for treatment of functional gastrointestinal disorders and is metabolized by CYP3A4 and CYP2C9.	dexloxiglumide	6-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	165-171
16303885-0	2005	Impact of age, CYP2C9 genotype and concomitant medication on the rate of rise for prothrombin time during the first 30 days of warfarin therapy.	Warfarin	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
16118328-6	2005	Therefore, a number of COX inhibitors were surveyed and it was determined that CYP2C9 plays a relatively minor role in the overall clearance (<or=20% of the dose) of sulindac, naproxen, ketoprofen, diclofenac, rofecoxib, and etoricoxib.	Sulindac	169-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
16118328-6	2005	Therefore, a number of COX inhibitors were surveyed and it was determined that CYP2C9 plays a relatively minor role in the overall clearance (<or=20% of the dose) of sulindac, naproxen, ketoprofen, diclofenac, rofecoxib, and etoricoxib.	Diclofenac	201-211	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
16118328-8	2005	In contrast, CYP2C9 genotype is expected to impact the clearance of ibuprofen, indomethacin, flurbiprofen, celecoxib, valdecoxib, lornoxicam, tenoxicam, meloxicam, and piroxicam.	Ibuprofen	68-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
16118328-8	2005	In contrast, CYP2C9 genotype is expected to impact the clearance of ibuprofen, indomethacin, flurbiprofen, celecoxib, valdecoxib, lornoxicam, tenoxicam, meloxicam, and piroxicam.	Indomethacin	79-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
16118328-8	2005	In contrast, CYP2C9 genotype is expected to impact the clearance of ibuprofen, indomethacin, flurbiprofen, celecoxib, valdecoxib, lornoxicam, tenoxicam, meloxicam, and piroxicam.	Flurbiprofen	93-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
16118328-8	2005	In contrast, CYP2C9 genotype is expected to impact the clearance of ibuprofen, indomethacin, flurbiprofen, celecoxib, valdecoxib, lornoxicam, tenoxicam, meloxicam, and piroxicam.	Celecoxib	107-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
16118328-8	2005	In contrast, CYP2C9 genotype is expected to impact the clearance of ibuprofen, indomethacin, flurbiprofen, celecoxib, valdecoxib, lornoxicam, tenoxicam, meloxicam, and piroxicam.	valdecoxib	118-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
16118328-8	2005	In contrast, CYP2C9 genotype is expected to impact the clearance of ibuprofen, indomethacin, flurbiprofen, celecoxib, valdecoxib, lornoxicam, tenoxicam, meloxicam, and piroxicam.	lornoxicam	130-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
16118328-8	2005	In contrast, CYP2C9 genotype is expected to impact the clearance of ibuprofen, indomethacin, flurbiprofen, celecoxib, valdecoxib, lornoxicam, tenoxicam, meloxicam, and piroxicam.	Meloxicam	153-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
16118328-8	2005	In contrast, CYP2C9 genotype is expected to impact the clearance of ibuprofen, indomethacin, flurbiprofen, celecoxib, valdecoxib, lornoxicam, tenoxicam, meloxicam, and piroxicam.	Piroxicam	168-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
16248835-5	2005	Further study conducted in cDNA-expressed cytochrome P450s (CYPs) demonstrates that the inhibition of the in-vitro biotransformation of warfarin enantiomers by omeprazole is attributed to its inhibitory effect on the activities of CYP1A2, CYP3A4, CYP2C9 and CYP2C19.	Warfarin	136-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	247-253
16112652-0	2005	CYP2C-catalyzed delta9-tetrahydrocannabinol metabolism: kinetics, pharmacogenetics and interaction with phenytoin.	Dronabinol	16-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-5
16112652-0	2005	CYP2C-catalyzed delta9-tetrahydrocannabinol metabolism: kinetics, pharmacogenetics and interaction with phenytoin.	Phenytoin	104-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-5
16220110-2	2005	Among them, phenytoin has been used as a probe to determine CYP2C9 phenotype by measuring the urinary excretion of its major metabolite, S-enantiomer of 5-(4-hydroxyphenyl)-5-phenylhydantoin (p-HPPH).	Phenytoin	12-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
16220110-2	2005	Among them, phenytoin has been used as a probe to determine CYP2C9 phenotype by measuring the urinary excretion of its major metabolite, S-enantiomer of 5-(4-hydroxyphenyl)-5-phenylhydantoin (p-HPPH).	hydroxyphenytoin	153-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
16220110-2	2005	Among them, phenytoin has been used as a probe to determine CYP2C9 phenotype by measuring the urinary excretion of its major metabolite, S-enantiomer of 5-(4-hydroxyphenyl)-5-phenylhydantoin (p-HPPH).	p-hpph	192-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
16220110-10	2005	On the other hand, only CYP2C9 was predictive for the urinary excretion of (S)-p-HPPH and PMR (r=0.21, P=0.001 and r=0.25, P<0.001, respectively).	(s)-p-hpph	75-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
16220110-11	2005	Furthermore, significant relation was found between urinary excretion of (R)-p-HPPH and CYP2C9 genotype (P=0.035) and levels significantly increased in the genotype order: CYP2C9*1/*9, CYP2C9*1/*1, CYP2C9*9/*11, CYP2C9*1/*8 and CYP2C9*1/*5 (P<0.001, Jonckheere-Terpstra test).	(r)-p-hpph	73-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
16220110-11	2005	Furthermore, significant relation was found between urinary excretion of (R)-p-HPPH and CYP2C9 genotype (P=0.035) and levels significantly increased in the genotype order: CYP2C9*1/*9, CYP2C9*1/*1, CYP2C9*9/*11, CYP2C9*1/*8 and CYP2C9*1/*5 (P<0.001, Jonckheere-Terpstra test).	(r)-p-hpph	73-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
16220110-11	2005	Furthermore, significant relation was found between urinary excretion of (R)-p-HPPH and CYP2C9 genotype (P=0.035) and levels significantly increased in the genotype order: CYP2C9*1/*9, CYP2C9*1/*1, CYP2C9*9/*11, CYP2C9*1/*8 and CYP2C9*1/*5 (P<0.001, Jonckheere-Terpstra test).	(r)-p-hpph	73-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
16220110-11	2005	Furthermore, significant relation was found between urinary excretion of (R)-p-HPPH and CYP2C9 genotype (P=0.035) and levels significantly increased in the genotype order: CYP2C9*1/*9, CYP2C9*1/*1, CYP2C9*9/*11, CYP2C9*1/*8 and CYP2C9*1/*5 (P<0.001, Jonckheere-Terpstra test).	(r)-p-hpph	73-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
16220110-11	2005	Furthermore, significant relation was found between urinary excretion of (R)-p-HPPH and CYP2C9 genotype (P=0.035) and levels significantly increased in the genotype order: CYP2C9*1/*9, CYP2C9*1/*1, CYP2C9*9/*11, CYP2C9*1/*8 and CYP2C9*1/*5 (P<0.001, Jonckheere-Terpstra test).	(r)-p-hpph	73-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
16220110-11	2005	Furthermore, significant relation was found between urinary excretion of (R)-p-HPPH and CYP2C9 genotype (P=0.035) and levels significantly increased in the genotype order: CYP2C9*1/*9, CYP2C9*1/*1, CYP2C9*9/*11, CYP2C9*1/*8 and CYP2C9*1/*5 (P<0.001, Jonckheere-Terpstra test).	(r)-p-hpph	73-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
16220110-12	2005	In summary, the present study demonstrates that, in a Black population, CYP2C9*5, *6, *8 and *11 variants, but not CYP2C9*9, are associated with a decreased phenytoin metabolism.	Phenytoin	157-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
15947090-5	2005	The mean warfarin daily dose requirement was highest in CYP2C9 homozygous wild-type patients, compared with those with the variant *2 and *3 alleles (P < .001) and highest in patients with the VKORC1 (position -1639) GG genotype compared with those with the GA genotype and the AA genotype (P < .001).	Warfarin	9-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
15947090-7	2005	Age, height, and CYP2C9 genotype significantly contributed to S-warfarin and total warfarin clearance, whereas only age and body size significantly contributed to R-warfarin clearance.	Warfarin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
15947090-7	2005	Age, height, and CYP2C9 genotype significantly contributed to S-warfarin and total warfarin clearance, whereas only age and body size significantly contributed to R-warfarin clearance.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
15947090-7	2005	Age, height, and CYP2C9 genotype significantly contributed to S-warfarin and total warfarin clearance, whereas only age and body size significantly contributed to R-warfarin clearance.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
15947090-8	2005	The multivariate regression model including the variables of age, CYP2C9 and VKORC1 genotype, and height produced the best model for estimating warfarin dose (R2 = 55%).	Warfarin	144-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
16198655-0	2005	Influence of CYP2C9 genotypes on the pharmacokinetics and pharmacodynamics of piroxicam.	Piroxicam	78-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
16198655-1	2005	OBJECTIVE: Our objective was to evaluate the influence of cytochrome P450 (CYP) 2C9 polymorphisms on the pharmacokinetics and pharmacodynamics of the nonsteroidal anti-inflammatory drug piroxicam.	Piroxicam	186-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-83
16198655-8	2005	CONCLUSION: Piroxicam"s oral clearance was impaired and its inhibitory effect on cyclooxygenase 1 activity was increased in CYP2C9*1/*2 or CYP2C9*1/*3 individuals, as compared with CYP2C 9*1 homozygous individuals.	Piroxicam	12-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
16198655-8	2005	CONCLUSION: Piroxicam"s oral clearance was impaired and its inhibitory effect on cyclooxygenase 1 activity was increased in CYP2C9*1/*2 or CYP2C9*1/*3 individuals, as compared with CYP2C 9*1 homozygous individuals.	Piroxicam	12-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	139-145
16198655-8	2005	CONCLUSION: Piroxicam"s oral clearance was impaired and its inhibitory effect on cyclooxygenase 1 activity was increased in CYP2C9*1/*2 or CYP2C9*1/*3 individuals, as compared with CYP2C 9*1 homozygous individuals.	Piroxicam	12-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-188
16198656-0	2005	CYP2C9, but not CYP2C19, polymorphisms affect the pharmacokinetics and pharmacodynamics of glyburide in Chinese subjects.	Glyburide	91-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16198656-1	2005	BACKGROUND: Although cytochrome P450 (CYP) 2C9 was thought to be the main pathway for glyburide (INN, glibenclamide) metabolism in vivo, studies in vitro indicated that CYP2C19 had a more dominant effect.	Glyburide	86-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-46
16198656-1	2005	BACKGROUND: Although cytochrome P450 (CYP) 2C9 was thought to be the main pathway for glyburide (INN, glibenclamide) metabolism in vivo, studies in vitro indicated that CYP2C19 had a more dominant effect.	Glyburide	102-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-46
16198656-11	2005	CONCLUSION: CYP2C9, but not CYP2C19, polymorphism appears to exert a dominant influence on glyburide pharmacokinetics and pharmacodynamics in vivo.	Glyburide	91-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
16248835-5	2005	Further study conducted in cDNA-expressed cytochrome P450s (CYPs) demonstrates that the inhibition of the in-vitro biotransformation of warfarin enantiomers by omeprazole is attributed to its inhibitory effect on the activities of CYP1A2, CYP3A4, CYP2C9 and CYP2C19.	Omeprazole	160-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	247-253
16112652-4	2005	The present study was designed to address the kinetics and pharmacogenetics of CYP2C-mediated metabolism of (delta9)-THC by studying its metabolism in human liver microsomes and expressed enzymes.	Dronabinol	108-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-84
16112652-5	2005	Expressed CYP2C9.1 exhibited high affinity for the hydroxylation of delta9-THC (apparent Km, 2 microM), similar to that observed in human liver microsomes (apparent Km 0.8 microM).	Dronabinol	68-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
16112652-7	2005	Given the high affinity of CYP2C9 for the hydroxylation of delta9-THC, we evaluated the potential for an interaction between delta9-THC, 11-hydroxy-delta9-THC, or 11-nor-9-carboxy-delta9-THC and the CYP2C9 substrate, phenytoin.	Dronabinol	59-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
16112652-7	2005	Given the high affinity of CYP2C9 for the hydroxylation of delta9-THC, we evaluated the potential for an interaction between delta9-THC, 11-hydroxy-delta9-THC, or 11-nor-9-carboxy-delta9-THC and the CYP2C9 substrate, phenytoin.	11-nor-delta(9)-tetrahydrocannabinol-9-carboxylic acid	163-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	199-205
16112652-8	2005	Surprisingly, delta9-THC increased the rate of phenytoin hydroxylation in human liver microsomes and expressed CYP2C9 enzyme.	Dronabinol	14-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
16094537-0	2005	CYP2C9*3 allelic variant is associated with metabolism of irbesartan in Chinese population.	Irbesartan	58-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16094537-2	2005	The objective of this study was to test the presence of the CYP2C9*3 allelic variant in the Chinese population and to investigate the association of this variant with both metabolism and therapeutic efficacy of irbesartan on essential hypertension.	Irbesartan	211-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
16094537-9	2005	Multiple linear regression analyses revealed that the CYP2C9*3 allele carriers had significantly higher irbesartan concentrations in plasma at 6 h (Taihu: P < 0.0001; Dongzhi: P = 0.03) and 24 h (Taihu: P < 0.0001; Dongzhi: P = 0.00013) after dosing.	Irbesartan	104-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
16094537-11	2005	CONCLUSION: Our study suggests that the CYP2C9*3 plays an important role in the metabolism of irbesartan and/or is in linkage disequilibrium with another potential CYP2C9 allele, both of which possibly modify the pharmacokinetics of irbesartan.	Irbesartan	94-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
16094537-11	2005	CONCLUSION: Our study suggests that the CYP2C9*3 plays an important role in the metabolism of irbesartan and/or is in linkage disequilibrium with another potential CYP2C9 allele, both of which possibly modify the pharmacokinetics of irbesartan.	Irbesartan	94-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	164-170
16094537-11	2005	CONCLUSION: Our study suggests that the CYP2C9*3 plays an important role in the metabolism of irbesartan and/or is in linkage disequilibrium with another potential CYP2C9 allele, both of which possibly modify the pharmacokinetics of irbesartan.	Irbesartan	233-243	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
16094537-11	2005	CONCLUSION: Our study suggests that the CYP2C9*3 plays an important role in the metabolism of irbesartan and/or is in linkage disequilibrium with another potential CYP2C9 allele, both of which possibly modify the pharmacokinetics of irbesartan.	Irbesartan	233-243	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	164-170
16141794-9	2005	In multivariate analysis, VKORC1 and CYP2C9 explained 31% and 7.9% of the variability in warfarin dose, respectively.	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
16205037-3	2005	Fluconazole, micafungin, and voriconazole have lower inhibitory effects on CYP3A4 activities than itraconazole and miconazole, and IC(50) and/or K(i) values against CYP2C9 and CYP2C19 activities are the lowest for miconazole, followed by voriconazole and fluconazole.	Fluconazole	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	165-171
16270629-7	2005	Since hereditary pharmacodynamic (VKORC1) and pharmacokinetic (CYP2C9) factors account for up to 50% of the inter-individual variability of the warfarin response, these genetic markers may serve as clinically relevant predictors of warfarin dosing in future studies.	Warfarin	144-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
16270629-7	2005	Since hereditary pharmacodynamic (VKORC1) and pharmacokinetic (CYP2C9) factors account for up to 50% of the inter-individual variability of the warfarin response, these genetic markers may serve as clinically relevant predictors of warfarin dosing in future studies.	Warfarin	232-240	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
16205037-6	2005	Miconazole is a potent inhibitor of all CYPs investigated in vitro, although there are few detailed studies on the clinical significance of this except for CYP2C9.	Miconazole	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
16205037-3	2005	Fluconazole, micafungin, and voriconazole have lower inhibitory effects on CYP3A4 activities than itraconazole and miconazole, and IC(50) and/or K(i) values against CYP2C9 and CYP2C19 activities are the lowest for miconazole, followed by voriconazole and fluconazole.	Micafungin	13-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	165-171
16205037-3	2005	Fluconazole, micafungin, and voriconazole have lower inhibitory effects on CYP3A4 activities than itraconazole and miconazole, and IC(50) and/or K(i) values against CYP2C9 and CYP2C19 activities are the lowest for miconazole, followed by voriconazole and fluconazole.	Voriconazole	29-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	165-171
16205037-4	2005	In in vivo pharmacokinetic studies, it is well known that itraconazole is a potent clinically important inhibitor of the clearance of CYP3A4 substrates, and fluconazole and voriconazole are reported to increase the blood or plasma concentrations of not only midazolam and cyclosporine (CYP3A4 substrates) but also of phenytoin (CYP2C9 substrate) and/or omeprazole (CYP2C19/CYP3A4 substrate).	Itraconazole	58-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	328-334
16205037-4	2005	In in vivo pharmacokinetic studies, it is well known that itraconazole is a potent clinically important inhibitor of the clearance of CYP3A4 substrates, and fluconazole and voriconazole are reported to increase the blood or plasma concentrations of not only midazolam and cyclosporine (CYP3A4 substrates) but also of phenytoin (CYP2C9 substrate) and/or omeprazole (CYP2C19/CYP3A4 substrate).	Fluconazole	157-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	328-334
16408808-4	2005	RESULTS: Imrecoxib is metabolized by CYP2C9, CYP2D6 and CYP3A4, with the rate of 62.5%, 21.1% and 16.4%, respectively.	Imrecoxib	9-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
16205037-4	2005	In in vivo pharmacokinetic studies, it is well known that itraconazole is a potent clinically important inhibitor of the clearance of CYP3A4 substrates, and fluconazole and voriconazole are reported to increase the blood or plasma concentrations of not only midazolam and cyclosporine (CYP3A4 substrates) but also of phenytoin (CYP2C9 substrate) and/or omeprazole (CYP2C19/CYP3A4 substrate).	Voriconazole	173-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	328-334
16141567-1	2005	The effects of five antifungal drugs, fluconazole, itraconazole, micafungin, miconazole, and voriconazole, on cytochrome P450 (CYP) 2C9-mediated tolbutamide hydroxylation, CYP2C19-mediated S-mephenytoin 4"-hydroxylation, and CYP3A4-mediated nifedipine oxidation activities in human liver microsomes were compared.	Miconazole	77-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-135
16408808-5	2005	CONCLUSION: CYP2C9 is the major enzyme involved in imrecoxib hydroxylation metabolism.	Imrecoxib	51-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
16014372-7	2005	The mechanism of action for the interaction is not clear, but may be related to down-regulation of CYP2C9 by capecitabine or its metabolites or a pharmacodynamic interaction with warfarin.	Capecitabine	109-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
16197363-8	2005	Recent drug-drug interaction studies have demonstrated that meloxicam interacts with some medications, including cholestyramine, lithium and some inhibitors of cytochrome P450 -2C9 and -3A4.	Meloxicam	60-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-180
16141567-1	2005	The effects of five antifungal drugs, fluconazole, itraconazole, micafungin, miconazole, and voriconazole, on cytochrome P450 (CYP) 2C9-mediated tolbutamide hydroxylation, CYP2C19-mediated S-mephenytoin 4"-hydroxylation, and CYP3A4-mediated nifedipine oxidation activities in human liver microsomes were compared.	Voriconazole	93-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-135
16141567-1	2005	The effects of five antifungal drugs, fluconazole, itraconazole, micafungin, miconazole, and voriconazole, on cytochrome P450 (CYP) 2C9-mediated tolbutamide hydroxylation, CYP2C19-mediated S-mephenytoin 4"-hydroxylation, and CYP3A4-mediated nifedipine oxidation activities in human liver microsomes were compared.	Tolbutamide	145-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-135
15924351-1	2005	Microsomal epoxide hydrolase (mEH) and cytochrome P450 2C9 (CYP2C9) are involved in the bioactivation and detoxification of polycyclic aromatic hydrocarbons (PAHs) derived from tobacco smoke.	Polycyclic Aromatic Hydrocarbons	124-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
15856231-8	2005	The effect of paclitaxel treatment on hepatic expression of PGP and P450 isoforms (CYP2C and CYP3A) was determined to elucidate the mechanism by which paclitaxel disposition is altered by previous drug exposure.	Paclitaxel	14-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-88
15856231-8	2005	The effect of paclitaxel treatment on hepatic expression of PGP and P450 isoforms (CYP2C and CYP3A) was determined to elucidate the mechanism by which paclitaxel disposition is altered by previous drug exposure.	Paclitaxel	151-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-88
15856231-11	2005	Activity and protein levels for CYP2C in liver were elevated at 24 and 96 h after paclitaxel dosing.	Paclitaxel	82-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-37
15856231-12	2005	Cremophor EL, a carrier solvent for paclitaxel, also caused elevated CYP2C activity.	cremophor EL	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-74
15856231-12	2005	Cremophor EL, a carrier solvent for paclitaxel, also caused elevated CYP2C activity.	Paclitaxel	36-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-74
15919766-2	2005	Recent studies in our laboratory have shown that the nuclear receptor pregnane X receptor (PXR) is important in the transcriptional activation of the CYP2C9 promoter by drugs such as rifampicin and that the essential element is a constitutive androstane receptor (CAR)/PXR site -1839 bp upstream of the translation start site.	Rifampin	183-193	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
15919766-8	2005	Mutation of the two HNF4alpha binding sites differentially prevented up-regulation of CYP2C9 promoter by both CAR as well as HNF4alpha, synergy between the two receptors, and essentially abolished induction by rifampicin in HepG2 cells transfected with PXR.	Rifampin	210-220	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
16153401-0	2005	Cytochrome P450 2C9 genotype: impact on celecoxib safety and pharmacokinetics in a pediatric patient.	Celecoxib	40-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
15924351-1	2005	Microsomal epoxide hydrolase (mEH) and cytochrome P450 2C9 (CYP2C9) are involved in the bioactivation and detoxification of polycyclic aromatic hydrocarbons (PAHs) derived from tobacco smoke.	Polycyclic Aromatic Hydrocarbons	158-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
15955872-0	2005	CYP2C9 genotype-dependent effects on in vitro drug-drug interactions: switching of benzbromarone effect from inhibition to activation in the CYP2C9.3 variant.	Benzbromarone	83-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16308280-2	2005	CYP2C9*13 is an allele identified in a Chinese poor metabolizer of lornoxicam which has a Leu90Pro amino acid substitution.	lornoxicam	67-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16308280-3	2005	This paper reports on a study aimed at comparing the catalytic properties of CYP2C9*13 with those of the wild-type CYP2C9*1 and mutant CYP2C9*3 (Ile359Leu) in the COS-7 expression system using various substrates.	carbonyl sulfide	163-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
16308280-3	2005	This paper reports on a study aimed at comparing the catalytic properties of CYP2C9*13 with those of the wild-type CYP2C9*1 and mutant CYP2C9*3 (Ile359Leu) in the COS-7 expression system using various substrates.	carbonyl sulfide	163-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
16308280-3	2005	This paper reports on a study aimed at comparing the catalytic properties of CYP2C9*13 with those of the wild-type CYP2C9*1 and mutant CYP2C9*3 (Ile359Leu) in the COS-7 expression system using various substrates.	carbonyl sulfide	163-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
16308280-4	2005	CYP2C9*3 and *13 produced far lower luminescence than CYP2C9*1 in luciferin H metabolism.	luciferin h	66-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16308280-4	2005	CYP2C9*3 and *13 produced far lower luminescence than CYP2C9*1 in luciferin H metabolism.	luciferin h	66-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
16308280-5	2005	CYP2C9*13 exhibited an 11-fold increase in Km but no change in Vmax with tolbutamide as the substrate, a five-fold increase in Km and an 88.8% reduction in Vmax with diclofenac.	Diclofenac	166-176	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
16042675-3	2005	Our aim was to investigate the effects of the gemfibrozil-itraconazole combination on the pharmacokinetics and pharmacodynamics of another meglitinide analogue, nateglinide, which is metabolized by CYP2C9 and CYP3A4.	Nateglinide	161-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	198-204
16042675-11	2005	The findings suggest that in vivo gemfibrozil, probably due to its metabolites, is a much more potent inhibitor of CYP2C8 than of CYP2C9.	Gemfibrozil	34-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
16268502-0	2005	[Influence of cytochrom P450 CYP2C9 polymorphism on the pharmacokinetics of tolbutamide metabolism using oligonucleotide genotyping microarray].	Tolbutamide	76-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
16268502-0	2005	[Influence of cytochrom P450 CYP2C9 polymorphism on the pharmacokinetics of tolbutamide metabolism using oligonucleotide genotyping microarray].	Oligonucleotides	105-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
16268502-1	2005	AIM: To investigate the influence of cytochrom P450 CYP2C9 polymorphism on the pharmacokinetics of tolbutamide.	Tolbutamide	99-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
16268502-9	2005	Pharmacokinetic outcome showed that the individuals with CYP2C9 *1/*3 or CYP2C9 *3/*3 had slower metabolic elimination of tolbutamide than those with CYP2C9 *1/*1.	Tolbutamide	122-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
16268502-9	2005	Pharmacokinetic outcome showed that the individuals with CYP2C9 *1/*3 or CYP2C9 *3/*3 had slower metabolic elimination of tolbutamide than those with CYP2C9 *1/*1.	Tolbutamide	122-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
16268502-9	2005	Pharmacokinetic outcome showed that the individuals with CYP2C9 *1/*3 or CYP2C9 *3/*3 had slower metabolic elimination of tolbutamide than those with CYP2C9 *1/*1.	Tolbutamide	122-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
16268502-10	2005	CONCLUSION: CYP2C9 genetic polymorphism has a significant influence on the pharmacokinetics of tolbutamide.	Tolbutamide	95-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
16278191-3	2005	The formation of norketobemidone from ketobemidone (1 microM) correlated best with CYP2C9 activity, measured as losartan oxidation (rs = 0.82, n = 19, p < 0.001), but there was also a strong correlation with CYP3A4 activity.	norketobemidone	17-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
16278191-3	2005	The formation of norketobemidone from ketobemidone (1 microM) correlated best with CYP2C9 activity, measured as losartan oxidation (rs = 0.82, n = 19, p < 0.001), but there was also a strong correlation with CYP3A4 activity.	ketobemidone	20-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
16278191-3	2005	The formation of norketobemidone from ketobemidone (1 microM) correlated best with CYP2C9 activity, measured as losartan oxidation (rs = 0.82, n = 19, p < 0.001), but there was also a strong correlation with CYP3A4 activity.	Losartan	112-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
16278191-5	2005	Inhibition studies confirmed the involvement of CYP2C9 and CTP3A4 in the formation of norketobemidone.	norketobemidone	86-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
16278191-6	2005	The formation rate of norketobemidone was three times higher in the CYP2C9*1*1 genotype group compared with the CYP2C9*1*2, CYP2C9*1*3 and CYP2C9*3*3 genotypes (p < 0.01).	norketobemidone	22-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
16278191-6	2005	The formation rate of norketobemidone was three times higher in the CYP2C9*1*1 genotype group compared with the CYP2C9*1*2, CYP2C9*1*3 and CYP2C9*3*3 genotypes (p < 0.01).	norketobemidone	22-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
16278191-6	2005	The formation rate of norketobemidone was three times higher in the CYP2C9*1*1 genotype group compared with the CYP2C9*1*2, CYP2C9*1*3 and CYP2C9*3*3 genotypes (p < 0.01).	norketobemidone	22-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
16278191-6	2005	The formation rate of norketobemidone was three times higher in the CYP2C9*1*1 genotype group compared with the CYP2C9*1*2, CYP2C9*1*3 and CYP2C9*3*3 genotypes (p < 0.01).	norketobemidone	22-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
16278191-8	2005	The data suggest that CYP2C9 and CYP3A4 play a major role in the formation of norketobemidone at clinically relevant concentrations.	norketobemidone	78-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
15790782-0	2005	Cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1) genotypes as determinants of acenocoumarol sensitivity.	Acenocoumarol	99-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
15790782-0	2005	Cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1) genotypes as determinants of acenocoumarol sensitivity.	Acenocoumarol	99-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
15955872-3	2005	Although benzbromarone inhibited CYP2C9.1 activity as expected, CYP2C9.3-mediated flurbiprofen 4"-hydroxylation was activated in the presence of benzbromarone.	Flurbiprofen	82-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
15955872-3	2005	Although benzbromarone inhibited CYP2C9.1 activity as expected, CYP2C9.3-mediated flurbiprofen 4"-hydroxylation was activated in the presence of benzbromarone.	Benzbromarone	145-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
16342679-0	2005	[Impact of cytochrome P450 CYP2C9 variant allele CYP2C9 * 3 on the pharmacokinetics of glibenclamide and lornoxicam in Chinese subjects].	Glyburide	87-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
16342679-0	2005	[Impact of cytochrome P450 CYP2C9 variant allele CYP2C9 * 3 on the pharmacokinetics of glibenclamide and lornoxicam in Chinese subjects].	Glyburide	87-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
16342679-0	2005	[Impact of cytochrome P450 CYP2C9 variant allele CYP2C9 * 3 on the pharmacokinetics of glibenclamide and lornoxicam in Chinese subjects].	lornoxicam	105-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
16342679-0	2005	[Impact of cytochrome P450 CYP2C9 variant allele CYP2C9 * 3 on the pharmacokinetics of glibenclamide and lornoxicam in Chinese subjects].	lornoxicam	105-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
16342679-1	2005	AIM: To investigate the impact of CYP2C9 * 3 on the pharmacokinetics of glibenclamide and lornoxicam.	Glyburide	72-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
16342679-1	2005	AIM: To investigate the impact of CYP2C9 * 3 on the pharmacokinetics of glibenclamide and lornoxicam.	lornoxicam	90-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
16342679-5	2005	RESULTS: After a single oral dose of 2.5 mg glibenclamide, C(max) was (70.0 +/- 11.5) microg x L(-1) in CYP2C9 * 1/ * 3 subjects and (51.9 +/- 12.3) microg x L(-1) in * 1/ *1 subjects.	Glyburide	44-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
16342679-7	2005	Statistic analysis results indicated that glibenclamide AUC(0-infinity) was significantly higher (1.5-fold) and subsequently CL/F was significantly lower (40%) in CYP2C9 * 1/ * 3 subjects than those in * 1/ * 1 subjects (P < 0.01).	Glyburide	42-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-169
16342679-7	2005	Statistic analysis results indicated that glibenclamide AUC(0-infinity) was significantly higher (1.5-fold) and subsequently CL/F was significantly lower (40%) in CYP2C9 * 1/ * 3 subjects than those in * 1/ * 1 subjects (P < 0.01).	Fluorine	128-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-169
16342679-8	2005	After a single oral dose of 8 mg lornoxicam, C(max) was (1.54 +/- 0.24) mg x L(-1) in CYP2C9 * 1/ * 3 subjects and (1.19 +/- 0.37) mg x L(-1) in * 1/ * 1 subjects.	lornoxicam	33-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
16342679-11	2005	2-fold) and subsequently CL/F was significantly lower (55% ) in CYP2C9 * 1/ * 3 subjects than those in * 1/ * 1 subjects (P < 0.001).	Fluorine	28-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
16342679-12	2005	CONCLUSION: CYP2C9 * 3 greatly affects both the pharmacokinetic profiles of glibenclamide and lornoxicam.	Glyburide	76-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
16342679-12	2005	CONCLUSION: CYP2C9 * 3 greatly affects both the pharmacokinetic profiles of glibenclamide and lornoxicam.	lornoxicam	94-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
16342679-13	2005	The elimination of these drugs significantly decreased in subjects with CYP2C9 * 1/ * 3 genotype, especially lornoxicam.	lornoxicam	109-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
16042675-0	2005	Coadministration of gemfibrozil and itraconazole has only a minor effect on the pharmacokinetics of the CYP2C9 and CYP3A4 substrate nateglinide.	Gemfibrozil	20-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
16042675-0	2005	Coadministration of gemfibrozil and itraconazole has only a minor effect on the pharmacokinetics of the CYP2C9 and CYP3A4 substrate nateglinide.	Itraconazole	36-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
16042675-2	2005	In vitro, gemfibrozil is a more potent inhibitor of CYP2C9 than of CYP2C8.	Gemfibrozil	10-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
16042675-3	2005	Our aim was to investigate the effects of the gemfibrozil-itraconazole combination on the pharmacokinetics and pharmacodynamics of another meglitinide analogue, nateglinide, which is metabolized by CYP2C9 and CYP3A4.	Gemfibrozil	46-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	198-204
16042675-3	2005	Our aim was to investigate the effects of the gemfibrozil-itraconazole combination on the pharmacokinetics and pharmacodynamics of another meglitinide analogue, nateglinide, which is metabolized by CYP2C9 and CYP3A4.	Itraconazole	58-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	198-204
16042675-3	2005	Our aim was to investigate the effects of the gemfibrozil-itraconazole combination on the pharmacokinetics and pharmacodynamics of another meglitinide analogue, nateglinide, which is metabolized by CYP2C9 and CYP3A4.	meglitinide	139-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	198-204
16160068-0	2005	A prospective, randomized pilot trial of model-based warfarin dose initiation using CYP2C9 genotype and clinical data.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
16160068-1	2005	BACKGROUND: Rapid genetic screening for cytochrome P450 (CYP) 2C9 variants may play a role in improving the efficacy and safety of warfarin in individuals with CYP2C9 variants.	Warfarin	131-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-65
16160068-1	2005	BACKGROUND: Rapid genetic screening for cytochrome P450 (CYP) 2C9 variants may play a role in improving the efficacy and safety of warfarin in individuals with CYP2C9 variants.	Warfarin	131-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
16160068-2	2005	The feasibility of prospective CYP2C9 model-based warfarin dosing has not yet been assessed.	Warfarin	50-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
16160068-3	2005	OBJECTIVES: To evaluate the feasibility of applying a CYP2C9 gene-based warfarin dosing model in clinical practice.	Warfarin	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
16160068-20	2005	CONCLUSIONS: Prospective application of a multivariate CYP2C9 gene-based warfarin dosing model is feasible.	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
15914520-10	2005	Voriconazole is metabolized primarily by CYP2C19, as well as CYP2C9 and CYP3A4.	Voriconazole	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
15963101-0	2005	Association between CYP2C9 slow metabolizer genotypes and severe hypoglycaemia on medication with sulphonylurea hypoglycaemic agents.	Sulfonylurea Compounds	98-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
15963101-1	2005	AIMS: The genetically polymorphic cytochrome P450 (CYP) enzyme CYP2C9 metabolizes most sulphonylurea oral hypoglycaemic agents.	Sulfonylurea Compounds	87-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
15843486-1	2005	Recently, two new classes of reversible inhibitors, the benzbromarones (BZBRs) and the N-3 substituted phenobarbitals (PBs), were used to study the active site characteristics of CYP2C9 and 2C19, respectively.	Benzbromarone	56-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	179-185
15843486-1	2005	Recently, two new classes of reversible inhibitors, the benzbromarones (BZBRs) and the N-3 substituted phenobarbitals (PBs), were used to study the active site characteristics of CYP2C9 and 2C19, respectively.	Benzbromarone	72-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	179-185
15843486-1	2005	Recently, two new classes of reversible inhibitors, the benzbromarones (BZBRs) and the N-3 substituted phenobarbitals (PBs), were used to study the active site characteristics of CYP2C9 and 2C19, respectively.	n-3 substituted phenobarbitals	87-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	179-185
15843486-1	2005	Recently, two new classes of reversible inhibitors, the benzbromarones (BZBRs) and the N-3 substituted phenobarbitals (PBs), were used to study the active site characteristics of CYP2C9 and 2C19, respectively.	Phenobarbital	119-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	179-185
15843491-6	2005	Significant (p < 0.05) inhibition by selective P450 isoform inhibitor sulfaphenazole (2.1 microM; CYP2C9) indicated a role for CYP2C9 in the formation of the hydroxylamine.	Sulfaphenazole	73-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
15843491-6	2005	Significant (p < 0.05) inhibition by selective P450 isoform inhibitor sulfaphenazole (2.1 microM; CYP2C9) indicated a role for CYP2C9 in the formation of the hydroxylamine.	Sulfaphenazole	73-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
15843491-6	2005	Significant (p < 0.05) inhibition by selective P450 isoform inhibitor sulfaphenazole (2.1 microM; CYP2C9) indicated a role for CYP2C9 in the formation of the hydroxylamine.	Hydroxylamine	161-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
15843491-6	2005	Significant (p < 0.05) inhibition by selective P450 isoform inhibitor sulfaphenazole (2.1 microM; CYP2C9) indicated a role for CYP2C9 in the formation of the hydroxylamine.	Hydroxylamine	161-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
15843491-8	2005	Fluconazole (CYP2C9/19 and CYP3A4 inhibitor at clinical concentrations) inhibited hydroxylamine formation, with one-enzyme model K(i) estimates ranging from 9 to 40 microM.	Fluconazole	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
15843491-8	2005	Fluconazole (CYP2C9/19 and CYP3A4 inhibitor at clinical concentrations) inhibited hydroxylamine formation, with one-enzyme model K(i) estimates ranging from 9 to 40 microM.	Hydroxylamine	82-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
15952022-10	2005	APOE genotype explains 6% of warfarin dose variance among CYP2C9 extensive metabolisers (analysis of variance, P=0.009).	Warfarin	29-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
15983826-14	2005	CONCLUSION: These data are consistent with a significant induction of CYP2C9 metabolism of S(-) warfarin by aprepitant.	Sulfur	6-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
15983826-14	2005	CONCLUSION: These data are consistent with a significant induction of CYP2C9 metabolism of S(-) warfarin by aprepitant.	Warfarin	92-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
15888487-4	2005	We identified three CYP2C9 variants, CYP2C9*3, T299A and P382L, in four warfarin-sensitive patients.	Warfarin	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
15888487-4	2005	We identified three CYP2C9 variants, CYP2C9*3, T299A and P382L, in four warfarin-sensitive patients.	Warfarin	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
15970795-0	2005	In-vitro and in-vivo effects of the CYP2C9*11 polymorphism on warfarin metabolism and dose.	Warfarin	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
15970795-1	2005	OBJECTIVE: To determine the in-vitro and in-vivo effects of the CYP2C9*11 polymorphism on (S)-warfarin metabolism.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
15970795-7	2005	Metabolic studies demonstrated that functional CYP2C9.11 possessed similar (S)-warfarin hydroxylation regioselectivity and modestly reduced catalytic efficiency relative to the wild-type enzyme.	Warfarin	75-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
15970795-8	2005	CONCLUSIONS: In-vivo reduction in CYP2C9 (S)-warfarin activity due to the CYP2C9*11 polymorphism may largely be a consequence of decreased enzyme stability resulting in compromised expression of holo-enzyme.	Warfarin	45-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
15970795-8	2005	CONCLUSIONS: In-vivo reduction in CYP2C9 (S)-warfarin activity due to the CYP2C9*11 polymorphism may largely be a consequence of decreased enzyme stability resulting in compromised expression of holo-enzyme.	Warfarin	45-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
15970795-9	2005	Increased enzyme lability of CYP2C9.11 may be related to improper folding due to the disruption of conserved salt-bridge and hydrogen bonding contacts in the loop region between the J and J" helices of the protein.	Hydrogen	125-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
15955872-0	2005	CYP2C9 genotype-dependent effects on in vitro drug-drug interactions: switching of benzbromarone effect from inhibition to activation in the CYP2C9.3 variant.	Benzbromarone	83-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
15955872-2	2005	To examine this possibility, the effect of the potent CYP2C9 inhibitor, benzbromarone, was studied with regard to CYP2C9.1- and CYP2C9.3-mediated flurbiprofen metabolism to evaluate whether the variant enzyme exhibits differential inhibition kinetics.	Benzbromarone	72-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
15955872-2	2005	To examine this possibility, the effect of the potent CYP2C9 inhibitor, benzbromarone, was studied with regard to CYP2C9.1- and CYP2C9.3-mediated flurbiprofen metabolism to evaluate whether the variant enzyme exhibits differential inhibition kinetics.	Benzbromarone	72-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
15955872-2	2005	To examine this possibility, the effect of the potent CYP2C9 inhibitor, benzbromarone, was studied with regard to CYP2C9.1- and CYP2C9.3-mediated flurbiprofen metabolism to evaluate whether the variant enzyme exhibits differential inhibition kinetics.	Benzbromarone	72-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
15955872-3	2005	Although benzbromarone inhibited CYP2C9.1 activity as expected, CYP2C9.3-mediated flurbiprofen 4"-hydroxylation was activated in the presence of benzbromarone.	Benzbromarone	9-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
15764711-0	2005	Role of CYP2C9 and its variants (CYP2C9*3 and CYP2C9*13) in the metabolism of lornoxicam in humans.	lornoxicam	78-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
15764713-9	2005	Using cDNA-expressed cytochrome P450 isoenzymes, it was determined that several isoforms contributed to the metabolism of bortezomib, including CYP3A4, CYP2C19, CYP1A2, CYP2D6, and CYP2C9.	Bortezomib	122-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
15764711-0	2005	Role of CYP2C9 and its variants (CYP2C9*3 and CYP2C9*13) in the metabolism of lornoxicam in humans.	lornoxicam	78-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
15764717-0	2005	Detection of a novel reactive metabolite of diclofenac: evidence for CYP2C9-mediated bioactivation via arene oxides.	Diclofenac	44-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
15764711-0	2005	Role of CYP2C9 and its variants (CYP2C9*3 and CYP2C9*13) in the metabolism of lornoxicam in humans.	lornoxicam	78-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
15764711-2	2005	Recently, we identified a new CYP2C9 allele with a Leu90Pro mutation in a Chinese poor metabolizer of lornoxicam [Si D, Guo Y, Zhang Y, Yang L, Zhou H, and Zhong D (2004) Pharmacogenetics 14:465-469].	lornoxicam	102-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
15764717-0	2005	Detection of a novel reactive metabolite of diclofenac: evidence for CYP2C9-mediated bioactivation via arene oxides.	arene oxides	103-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
15764711-4	2005	To examine enzymatic activity of the CYP2C9*13 allele, kinetic parameters for lornoxicam 5"-hydroxylation were determined in COS-7 cells transiently transfected with pcDNA3.1 plasmids carrying wild-type CYP2C9*1, variant CYP2C9*3, and CYP2C9*13 cDNA.	lornoxicam	78-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
15764717-3	2005	Formation of M4 was mediated specifically by CYP2C9 in human liver microsomes, as evidenced by the following observations: 1) cDNA-expressed CYP2C9-catalyzing formation of M4; 2) inhibition of M4 formation by sulfaphenazole, a CYP2C9-selective inhibitor; and 3) strong correlation between the production of M4 and CYP2C9-mediated tolbutamide 4-hydroxylase activities in a panel of human liver microsome samples.	Sulfaphenazole	209-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
15764717-3	2005	Formation of M4 was mediated specifically by CYP2C9 in human liver microsomes, as evidenced by the following observations: 1) cDNA-expressed CYP2C9-catalyzing formation of M4; 2) inhibition of M4 formation by sulfaphenazole, a CYP2C9-selective inhibitor; and 3) strong correlation between the production of M4 and CYP2C9-mediated tolbutamide 4-hydroxylase activities in a panel of human liver microsome samples.	Sulfaphenazole	209-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
15764717-3	2005	Formation of M4 was mediated specifically by CYP2C9 in human liver microsomes, as evidenced by the following observations: 1) cDNA-expressed CYP2C9-catalyzing formation of M4; 2) inhibition of M4 formation by sulfaphenazole, a CYP2C9-selective inhibitor; and 3) strong correlation between the production of M4 and CYP2C9-mediated tolbutamide 4-hydroxylase activities in a panel of human liver microsome samples.	Sulfaphenazole	209-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
15764711-8	2005	In a subsequent clinical study, the AUC of lornoxicam was increased by 1.9-fold and its oral clearance (CL/F) decreased by 44% in three CYP2C9*1/*13 subjects, compared with CYP2C9*1/*1 individuals.	lornoxicam	43-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
15764717-7	2005	This mechanism is consistent with the structural modeling of the CYP2C9-diclofenac complex, which reveals that both the C-3" and C-4" of the dichlorophenyl ring are proximate to the heme group.	Heme	182-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
15875171-0	2005	Twenty-four hour tolbutamide plasma concentration as a phenotypic measure of CYP2C9 activity.	Tolbutamide	17-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
15764717-3	2005	Formation of M4 was mediated specifically by CYP2C9 in human liver microsomes, as evidenced by the following observations: 1) cDNA-expressed CYP2C9-catalyzing formation of M4; 2) inhibition of M4 formation by sulfaphenazole, a CYP2C9-selective inhibitor; and 3) strong correlation between the production of M4 and CYP2C9-mediated tolbutamide 4-hydroxylase activities in a panel of human liver microsome samples.	Sulfaphenazole	209-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
15764717-7	2005	This mechanism is consistent with the structural modeling of the CYP2C9-diclofenac complex, which reveals that both the C-3" and C-4" of the dichlorophenyl ring are proximate to the heme group.	Diclofenac	72-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
16192110-6	2005	There was good correlation between the formation rates of 4-OH valsartan and diclofenac 4"-hydroxylase activities (representative CYP2C9 activity) of 11 individual microsomes (r = 0.889).	4-oh valsartan	58-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
16192110-10	2005	These results showed that CYP2C9 is the only form responsible for 4-hydroxylation of valsartan in human liver microsomes.	Valsartan	85-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
16192110-11	2005	Although CYP2C9 is involved in valsartan metabolism, CYP-mediated drug-drug interaction between valsartan and other co-administered drugs would be negligible.	Valsartan	31-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
15901588-8	2005	Rosuvastatin undergoes only minor metabolism (10% of the administered dose) by the cytochrome P-450 2C9 isoenzyme.	Rosuvastatin Calcium	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-103
15857618-5	2005	A range of substrates was investigated to determine the effect of the heme-substrate interaction on CYP2C9 redox potential.	Heme	70-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
15842554-0	2005	Chlorpropamide 2-hydroxylation is catalysed by CYP2C9 and CYP2C19 in vitro: chlorpropamide disposition is influenced by CYP2C9, but not by CYP2C19 genetic polymorphism.	Chlorpropamide	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
15961979-2	2005	Because CYP2C9 is a genetically polymorphic enzyme, genetic variability could play an important role in the potential interaction between NSAIDs and coumarins.	Coumarins	149-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
15961979-10	2005	The risk of overanticoagulation was 2.98 (95% confidence interval, 1.09-7.02) in coumarin-treated patients taking NSAIDs with a CYP2C9*2 allele and 10.8 (95% confidence interval, 2.57-34.6) in those with a CYP2C9*3 allele.	coumarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
15961979-10	2005	The risk of overanticoagulation was 2.98 (95% confidence interval, 1.09-7.02) in coumarin-treated patients taking NSAIDs with a CYP2C9*2 allele and 10.8 (95% confidence interval, 2.57-34.6) in those with a CYP2C9*3 allele.	coumarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	206-212
15842554-5	2005	In incubation studies using human recombinant CYP isoforms, however, 2-OH-chlorpropamide was formed by both CYP2C9 and CYP2C19 with similar intrinsic clearances (CYP2C9 vs. CYP2C19: 0.26 vs. 0.22 microl min(-1) nmol(-1) protein).	CHEBI:143296	69-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
15842554-0	2005	Chlorpropamide 2-hydroxylation is catalysed by CYP2C9 and CYP2C19 in vitro: chlorpropamide disposition is influenced by CYP2C9, but not by CYP2C19 genetic polymorphism.	Chlorpropamide	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
15842554-0	2005	Chlorpropamide 2-hydroxylation is catalysed by CYP2C9 and CYP2C19 in vitro: chlorpropamide disposition is influenced by CYP2C9, but not by CYP2C19 genetic polymorphism.	Chlorpropamide	76-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
15842554-7	2005	In in vivo clinical trials, eight subjects with the CYP2C9*1/*3 genotype exhibited significantly lower nonrenal clearance [*1/*3 vs.*1/*1: 1.8 +/- 0.2 vs. 2.4 +/- 0.1 ml h(-1) kg(-1), P < 0.05; 95% confidence interval (CI) on the difference 0.2, 1.0] and higher metabolic ratios (of chlorpropamide/2-OH-chlorpropamide in urine: *1/*3 vs.*1/*1: 1.01 +/- 0.19 vs. 0.56 +/- 0.08, P < 0.05; 95% CI on the difference - 0.9, - 0.1) than did 13 subjects with CYP2C9*1/*1 genotype.	Chlorpropamide	286-300	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
15842554-7	2005	In in vivo clinical trials, eight subjects with the CYP2C9*1/*3 genotype exhibited significantly lower nonrenal clearance [*1/*3 vs.*1/*1: 1.8 +/- 0.2 vs. 2.4 +/- 0.1 ml h(-1) kg(-1), P < 0.05; 95% confidence interval (CI) on the difference 0.2, 1.0] and higher metabolic ratios (of chlorpropamide/2-OH-chlorpropamide in urine: *1/*3 vs.*1/*1: 1.01 +/- 0.19 vs. 0.56 +/- 0.08, P < 0.05; 95% CI on the difference - 0.9, - 0.1) than did 13 subjects with CYP2C9*1/*1 genotype.	Chlorpropamide	286-300	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	458-464
15842554-0	2005	Chlorpropamide 2-hydroxylation is catalysed by CYP2C9 and CYP2C19 in vitro: chlorpropamide disposition is influenced by CYP2C9, but not by CYP2C19 genetic polymorphism.	Chlorpropamide	76-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
15842554-7	2005	In in vivo clinical trials, eight subjects with the CYP2C9*1/*3 genotype exhibited significantly lower nonrenal clearance [*1/*3 vs.*1/*1: 1.8 +/- 0.2 vs. 2.4 +/- 0.1 ml h(-1) kg(-1), P < 0.05; 95% confidence interval (CI) on the difference 0.2, 1.0] and higher metabolic ratios (of chlorpropamide/2-OH-chlorpropamide in urine: *1/*3 vs.*1/*1: 1.01 +/- 0.19 vs. 0.56 +/- 0.08, P < 0.05; 95% CI on the difference - 0.9, - 0.1) than did 13 subjects with CYP2C9*1/*1 genotype.	CHEBI:143296	301-320	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
15842554-3	2005	To evaluate whether genetic polymorphisms of CYP2C9 and/or CYP2C19 influence the disposition of chlorpropamide, a single oral dose of 250 mg chlorpropamide was administered to 21 healthy subjects pregenotyped for CYP2C9 and CYP2C19.	Chlorpropamide	96-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
15842554-7	2005	In in vivo clinical trials, eight subjects with the CYP2C9*1/*3 genotype exhibited significantly lower nonrenal clearance [*1/*3 vs.*1/*1: 1.8 +/- 0.2 vs. 2.4 +/- 0.1 ml h(-1) kg(-1), P < 0.05; 95% confidence interval (CI) on the difference 0.2, 1.0] and higher metabolic ratios (of chlorpropamide/2-OH-chlorpropamide in urine: *1/*3 vs.*1/*1: 1.01 +/- 0.19 vs. 0.56 +/- 0.08, P < 0.05; 95% CI on the difference - 0.9, - 0.1) than did 13 subjects with CYP2C9*1/*1 genotype.	CHEBI:143296	301-320	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	458-464
15842554-9	2005	CONCLUSIONS: These results suggest that chlorpropamide disposition is principally determined by CYP2C9 activity in vivo, although both CYP2C9 and CYP2C19 have a catalysing activity of chlorpropamide 2-hydroxylation pathway.	Chlorpropamide	40-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
15842554-9	2005	CONCLUSIONS: These results suggest that chlorpropamide disposition is principally determined by CYP2C9 activity in vivo, although both CYP2C9 and CYP2C19 have a catalysing activity of chlorpropamide 2-hydroxylation pathway.	Chlorpropamide	184-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-141
15842554-5	2005	In incubation studies using human recombinant CYP isoforms, however, 2-OH-chlorpropamide was formed by both CYP2C9 and CYP2C19 with similar intrinsic clearances (CYP2C9 vs. CYP2C19: 0.26 vs. 0.22 microl min(-1) nmol(-1) protein).	CHEBI:143296	69-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
15900281-0	2005	CYP2C9 haplotype structure in European American warfarin patients and association with clinical outcomes.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15900281-9	2005	CONCLUSION: These data establish a whole-gene, high-resolution haplotype structure for CYP2C9 in a European American patient population and suggest that genetic variation in exons, rather than the promoter or other regulatory regions, is largely responsible for warfarin sensitivity associated with CYP2C9 variants in this population.	Warfarin	262-270	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
15900282-1	2005	BACKGROUND: Warfarin dose response is partially explained by the polymorphisms in the cytochrome P450 (CYP) 2C9 gene, affecting S -warfarin clearance, as well as by age and body weight.	Warfarin	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-111
15900282-1	2005	BACKGROUND: Warfarin dose response is partially explained by the polymorphisms in the cytochrome P450 (CYP) 2C9 gene, affecting S -warfarin clearance, as well as by age and body weight.	Warfarin	131-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-111
15840038-2	2005	Recent studies suggest that an endothelial cytochrome P450 (CYP) epoxygenase (CYP 2C9) can modulate endothelium-dependent vasodilatation in two different ways: (1) by the production of epoxyeicosatrienoic acids (EETs), which elicit hyperpolarization and relaxation; and (2) by the release of oxygen-derived free radicals, which compromise the bioavailability of nitric oxide.	epoxyeicosatrienoic acids	185-210	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-85
15840038-2	2005	Recent studies suggest that an endothelial cytochrome P450 (CYP) epoxygenase (CYP 2C9) can modulate endothelium-dependent vasodilatation in two different ways: (1) by the production of epoxyeicosatrienoic acids (EETs), which elicit hyperpolarization and relaxation; and (2) by the release of oxygen-derived free radicals, which compromise the bioavailability of nitric oxide.	eets	212-216	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-85
15840038-2	2005	Recent studies suggest that an endothelial cytochrome P450 (CYP) epoxygenase (CYP 2C9) can modulate endothelium-dependent vasodilatation in two different ways: (1) by the production of epoxyeicosatrienoic acids (EETs), which elicit hyperpolarization and relaxation; and (2) by the release of oxygen-derived free radicals, which compromise the bioavailability of nitric oxide.	oxygen-derived free radicals	292-320	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-85
15840038-2	2005	Recent studies suggest that an endothelial cytochrome P450 (CYP) epoxygenase (CYP 2C9) can modulate endothelium-dependent vasodilatation in two different ways: (1) by the production of epoxyeicosatrienoic acids (EETs), which elicit hyperpolarization and relaxation; and (2) by the release of oxygen-derived free radicals, which compromise the bioavailability of nitric oxide.	Nitric Oxide	362-374	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-85
15840038-5	2005	In HD patients, ACh infusions were repeated together with sulfaphenazole (SPZ, 6 mg/min), a highly selective inhibitor of CYP 2C9 with and without concomitant blockade of the nitric oxide synthase (NOS) by N(omega)monomethyl L-arginine (L-NMMA, 16 microumol/min).	Sulfaphenazole	58-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-129
16012074-3	2005	Recombinant human CYP3A4 and CYP2C9 both exhibited catalytic activity with respect to the formation of rotameric O-deethylated metabolites (M12, M13), the metabolites resulting from aromatization (M22/M24) and N-oxide reduction (M31).	n-oxide	210-217	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
16012077-5	2005	When estazolam was incubated with expressed human CYP enzymes (CYP1A2, CYP2A6, CYP2C9, CYP2C19, CYP2D6, CYP2E1 and CYP3A4), it was metabolized only by CYP3A4.	Estazolam	5-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
15889670-0	2005	[Significance of cytochrome P450 2C9 genotype for the bleeding complications in patients treated with acenocoumarol].	Acenocoumarol	102-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-36
15766564-0	2005	Eicosapentaenoic acid metabolism by cytochrome P450 enzymes of the CYP2C subfamily.	Eicosapentaenoic Acid	0-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-72
15766564-1	2005	CYP2C enzymes epoxidize arachidonic acid (AA) to metabolites involved in the regulation of vascular and renal function.	Arachidonic Acid	24-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-5
15766564-7	2005	These results demonstrate that EPA is an efficient substrate of CYP2C enzymes and suggest that n-3 PUFA-rich diets may shift the CYP2C-dependent generation of physiologically active eicosanoids from AA- to EPA-derived metabolites.	Eicosapentaenoic Acid	31-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-69
15766564-7	2005	These results demonstrate that EPA is an efficient substrate of CYP2C enzymes and suggest that n-3 PUFA-rich diets may shift the CYP2C-dependent generation of physiologically active eicosanoids from AA- to EPA-derived metabolites.	Eicosapentaenoic Acid	31-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-134
15766564-7	2005	These results demonstrate that EPA is an efficient substrate of CYP2C enzymes and suggest that n-3 PUFA-rich diets may shift the CYP2C-dependent generation of physiologically active eicosanoids from AA- to EPA-derived metabolites.	Fatty Acids, Unsaturated	99-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-69
15766564-7	2005	These results demonstrate that EPA is an efficient substrate of CYP2C enzymes and suggest that n-3 PUFA-rich diets may shift the CYP2C-dependent generation of physiologically active eicosanoids from AA- to EPA-derived metabolites.	Fatty Acids, Unsaturated	99-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-134
15766564-7	2005	These results demonstrate that EPA is an efficient substrate of CYP2C enzymes and suggest that n-3 PUFA-rich diets may shift the CYP2C-dependent generation of physiologically active eicosanoids from AA- to EPA-derived metabolites.	Eicosanoids	182-193	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-69
15766564-7	2005	These results demonstrate that EPA is an efficient substrate of CYP2C enzymes and suggest that n-3 PUFA-rich diets may shift the CYP2C-dependent generation of physiologically active eicosanoids from AA- to EPA-derived metabolites.	Eicosanoids	182-193	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-134
15766564-7	2005	These results demonstrate that EPA is an efficient substrate of CYP2C enzymes and suggest that n-3 PUFA-rich diets may shift the CYP2C-dependent generation of physiologically active eicosanoids from AA- to EPA-derived metabolites.	Eicosapentaenoic Acid	206-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-69
15766564-7	2005	These results demonstrate that EPA is an efficient substrate of CYP2C enzymes and suggest that n-3 PUFA-rich diets may shift the CYP2C-dependent generation of physiologically active eicosanoids from AA- to EPA-derived metabolites.	Eicosapentaenoic Acid	206-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-134
15889670-4	2005	AIM: The influence of CYP2C9 polymorphism on the effectiveness of the--in Hungary for oral anticoagulation exclusively used--acenocoumarol therapy and on the occurrence of bleeding complications was investigated.	Acenocoumarol	125-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
15889670-8	2005	In the 145 patients bearing the alleles with reduced activity (CYP2C9*2 and/or *3), the optimised dose of the acenocoumarol was significantly (p < 0.001) lower than in patients with the wild type allele (2.12 +/- 0.96 mg/day and 2.90 +/- 1.45 mg/day, respectively).	Acenocoumarol	110-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
15805193-5	2005	Phenytoin is principally metabolized by CYP2C9, and both are probable substrates of the drug transporter P-glycoprotein.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
15805193-7	2005	We report that a known functional polymorphism in CYP2C9 is highly associated with the maximum dose of phenytoin (P = 0.0066).	Phenytoin	103-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
15801938-2	2005	Because gemfibrozil inhibits CYP2C9 in vitro, we studied its effects on the pharmacokinetics and pharmacodynamics of racemic warfarin.	Gemfibrozil	8-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
15841315-0	2005	Prospective dosing of warfarin based on cytochrome P-450 2C9 genotype.	Warfarin	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-60
15855721-1	2005	Two research groups have reported the effect of genetic polymorphisms of CYP2C9 and CYP2C19 on the pharmacokinetic parameters of phenytoin in Japanese epileptic patients.	Phenytoin	129-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
15841315-1	2005	Cytochrome P-450 2C9 (CYP2C9) polymorphisms (CYP2C9*2 and CYP2C9*3) reduce the clearance of warfarin, increase the risk of bleeding, and prolong the time to stable dosing.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-20
15841315-1	2005	Cytochrome P-450 2C9 (CYP2C9) polymorphisms (CYP2C9*2 and CYP2C9*3) reduce the clearance of warfarin, increase the risk of bleeding, and prolong the time to stable dosing.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
15841315-1	2005	Cytochrome P-450 2C9 (CYP2C9) polymorphisms (CYP2C9*2 and CYP2C9*3) reduce the clearance of warfarin, increase the risk of bleeding, and prolong the time to stable dosing.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
15841315-1	2005	Cytochrome P-450 2C9 (CYP2C9) polymorphisms (CYP2C9*2 and CYP2C9*3) reduce the clearance of warfarin, increase the risk of bleeding, and prolong the time to stable dosing.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
15841315-3	2005	We initiated warfarin therapy in 48 orthopedic patients tailored to the following variables: CYP2C9 genotype, age, weight, height, gender, race, and use of simvastatin or amiodarone.	Warfarin	13-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
15841315-4	2005	By using pharmacogenetics-based dosing, patients with a CYP2C9 variant achieved a stable, therapeutic warfarin dose without excessive delay.	Warfarin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
15608129-0	2005	Development and validation of a high-throughput radiometric cyp2c9 inhibition assay using tritiated diclofenac.	tritiated diclofenac	90-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
15608129-3	2005	The assay is based on the release of tritium as tritiated water that occurs upon CYP2C9-mediated 4"-hydroxylation of diclofenac labeled with tritium in the 4" position.	Tritium	37-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
15608129-3	2005	The assay is based on the release of tritium as tritiated water that occurs upon CYP2C9-mediated 4"-hydroxylation of diclofenac labeled with tritium in the 4" position.	Water	58-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
15608129-3	2005	The assay is based on the release of tritium as tritiated water that occurs upon CYP2C9-mediated 4"-hydroxylation of diclofenac labeled with tritium in the 4" position.	Diclofenac	117-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
15608129-3	2005	The assay is based on the release of tritium as tritiated water that occurs upon CYP2C9-mediated 4"-hydroxylation of diclofenac labeled with tritium in the 4" position.	Tritium	141-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
15608129-5	2005	The reaction is NADPH-dependent, and sensitive to CYP2C9 inhibitors and inhibitory monoclonal antibodies, but not to inhibitors of or antibodies against other P450 enzymes.	NADP	16-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
15608129-6	2005	Competition experiments using tritiated and unlabeled diclofenac indicated that CYP2C9-mediated diclofenac 4"-hydroxylation exhibits positive cooperativity and no significant kinetic isotope effect or NIH shift.	Diclofenac	54-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
15608129-6	2005	Competition experiments using tritiated and unlabeled diclofenac indicated that CYP2C9-mediated diclofenac 4"-hydroxylation exhibits positive cooperativity and no significant kinetic isotope effect or NIH shift.	Diclofenac	96-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
15608129-9	2005	This assay thus represents a high-throughput version of the classic diclofenac 4"-hydroxylation assay, which is one of the most widely used methods to assess the potential for CYP2C9 inhibition of new chemical entities.	diclofenac 4"	68-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
15703368-5	2005	Oxymorphone ER exhibits a minimal potential for causing metabolic drug-drug interactions mediated by CYP2C9 or CYP3A4.	Oxymorphone	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
15660356-3	2005	The transgenic rice plant 2C9-57R2 expressing CYP2C9 gene showed resistance to sulfonylureas, and the transgenic rice plant 2C19-12R1 expressing CYP2C19 gene showed cross-resistance to certain herbicides with different structures and modes of action.	Sulfonylurea Compounds	79-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
15855725-3	2005	This formation was completely blocked by both sulfaphenazole, a selective CYP2C9 inhibitor, and CYP2C9 antibody, whereas potent inhibitors selective for other CYPs exhibited little effects.	Sulfaphenazole	46-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
15855725-4	2005	Of 12 recombinant CYPs examined, O-desmethyl metabolite was principally formed by CYP2C9.	o-desmethyl	33-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
15855726-7	2005	Phenytoin is metabolized to 4"-HPPH by CYP2C9 and CYP2C19 in which there are genetic polymorphisms.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
15855726-7	2005	Phenytoin is metabolized to 4"-HPPH by CYP2C9 and CYP2C19 in which there are genetic polymorphisms.	hydroxyphenytoin	28-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
15676042-1	2005	AIMS: To investigate the potential induction by rifampicin of intestinal CYP2C8, CYP2C9, CYP2D6 and CYP3A4 using preparations of human enterocytes.	Rifampin	48-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
15652503-0	2005	Biosynthesis of epoxyeicosatrienoic acids varies between polymorphic CYP2C enzymes.	epoxyeicosatrienoic acids	16-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-74
15652503-1	2005	Arachidonic acid is oxidized by cytochromes P450 2C (CYP2C) to epoxyeicosatrienoic acids (EETs), possessing vasoactive properties, with 11,12-EET as the endothelium derived hyperpolarization factor.	Arachidonic Acid	0-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-51
15652503-1	2005	Arachidonic acid is oxidized by cytochromes P450 2C (CYP2C) to epoxyeicosatrienoic acids (EETs), possessing vasoactive properties, with 11,12-EET as the endothelium derived hyperpolarization factor.	Arachidonic Acid	0-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-58
15652503-1	2005	Arachidonic acid is oxidized by cytochromes P450 2C (CYP2C) to epoxyeicosatrienoic acids (EETs), possessing vasoactive properties, with 11,12-EET as the endothelium derived hyperpolarization factor.	epoxyeicosatrienoic acids	63-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-51
15652503-1	2005	Arachidonic acid is oxidized by cytochromes P450 2C (CYP2C) to epoxyeicosatrienoic acids (EETs), possessing vasoactive properties, with 11,12-EET as the endothelium derived hyperpolarization factor.	epoxyeicosatrienoic acids	63-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-58
15652503-1	2005	Arachidonic acid is oxidized by cytochromes P450 2C (CYP2C) to epoxyeicosatrienoic acids (EETs), possessing vasoactive properties, with 11,12-EET as the endothelium derived hyperpolarization factor.	eets	90-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-58
15652503-1	2005	Arachidonic acid is oxidized by cytochromes P450 2C (CYP2C) to epoxyeicosatrienoic acids (EETs), possessing vasoactive properties, with 11,12-EET as the endothelium derived hyperpolarization factor.	11,12-epoxy-5,8,14-eicosatrienoic acid	136-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-51
15652503-1	2005	Arachidonic acid is oxidized by cytochromes P450 2C (CYP2C) to epoxyeicosatrienoic acids (EETs), possessing vasoactive properties, with 11,12-EET as the endothelium derived hyperpolarization factor.	11,12-epoxy-5,8,14-eicosatrienoic acid	136-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-58
15652503-9	2005	In conclusion, there are genetic differences in the CYP2C-dependent oxidation of arachidonic acid to vasoactive metabolites, of which the relevance to cardiovascular pathophysiology is still unclear.	Arachidonic Acid	81-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-57
15569819-5	2005	Overexpression of CYP2C9 increased COX-2 promoter activity, an effect accompanied by a significant increase in COX-2 protein expression and elevated prostacyclin production.	Epoprostenol	149-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
15569819-6	2005	The CYP2C9-induced expression of COX-2 was inhibited by the CYP2C9 inhibitor, sulfaphenazole, whereas 11,12-EET increased COX-2 expression.	Sulfaphenazole	78-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
15569819-6	2005	The CYP2C9-induced expression of COX-2 was inhibited by the CYP2C9 inhibitor, sulfaphenazole, whereas 11,12-EET increased COX-2 expression.	Sulfaphenazole	78-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
15569819-7	2005	Overexpression of CYP2C9 and stimulation with 11,12-EET increased intracellular cAMP levels and stimulated DNA-binding of the cAMP-response element-binding protein.	Cyclic AMP	80-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
15569819-7	2005	Overexpression of CYP2C9 and stimulation with 11,12-EET increased intracellular cAMP levels and stimulated DNA-binding of the cAMP-response element-binding protein.	Cyclic AMP	126-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
15569819-8	2005	The protein kinase A inhibitor, KT5720, attenuated the CYP2C9-induced increase in COX-2 promoter activity and protein expression.	KT 5720	32-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
15569819-9	2005	Overexpression of CYP2C9 stimulated endothelial tube formation, an effect that was attenuated by the COX-2 inhibitor celecoxib.	Celecoxib	117-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
15569819-11	2005	CONCLUSIONS: These data indicate that CYP2C9-derived EETs induce the expression of COX-2 in endothelial cells via a cAMP-dependent pathway and that this mechanism contributes to CYP2C9-induced angiogenesis.	Cyclic AMP	116-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
15569819-11	2005	CONCLUSIONS: These data indicate that CYP2C9-derived EETs induce the expression of COX-2 in endothelial cells via a cAMP-dependent pathway and that this mechanism contributes to CYP2C9-induced angiogenesis.	Cyclic AMP	116-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	178-184
15569819-12	2005	Overexpression of cytochrome P450 (CYP) 2C9 in endothelial cells increased cAMP levels, stimulated the cAMP-response element-binding protein, and enhanced cyclooxygenase-2 (COX-2) promoter activity, protein expression, and prostacyclin production.	Cyclic AMP	75-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-43
15569819-12	2005	Overexpression of cytochrome P450 (CYP) 2C9 in endothelial cells increased cAMP levels, stimulated the cAMP-response element-binding protein, and enhanced cyclooxygenase-2 (COX-2) promoter activity, protein expression, and prostacyclin production.	Cyclic AMP	103-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-43
15569819-12	2005	Overexpression of cytochrome P450 (CYP) 2C9 in endothelial cells increased cAMP levels, stimulated the cAMP-response element-binding protein, and enhanced cyclooxygenase-2 (COX-2) promoter activity, protein expression, and prostacyclin production.	Epoprostenol	223-235	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-43
15569819-13	2005	CYP2C9 overexpression stimulated endothelial tube formation, which was attenuated by the COX-2 inhibitor celecoxib.	Celecoxib	105-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15676042-11	2005	Induction of intestinal CYP2C8 and CYP2C9 might contribute in part to rifampicin - mediated drug interactions, in addition to their hepatic counterparts and intestinal and hepatic CYP3A4.	Rifampin	70-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
15537834-5	2005	R-Lansoprazole increased the Michaelis-Menten-derived V(max) of phenytoin 4-hydroxylation from 0.024 to 0.121 pmol/min/pmol P450, and lowered its K(m) from 20.5 to 15.0 microM, suggesting that R-lansoprazole activates CYP2C9-mediated phenytoin metabolism without displacing phenytoin from the active site.	Dexlansoprazole	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
15537834-0	2005	Lansoprazole enantiomer activates human liver microsomal CYP2C9 catalytic activity in a stereospecific and substrate-specific manner.	Lansoprazole	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
15537834-1	2005	We recently proposed a possible stereoselective activation by lansoprazole of CYP2C9-catalyzed tolbutamide hydroxylation, as well as stereoselective inhibition of several cytochrome P450 (P450) isoforms.	Lansoprazole	62-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
15537834-1	2005	We recently proposed a possible stereoselective activation by lansoprazole of CYP2C9-catalyzed tolbutamide hydroxylation, as well as stereoselective inhibition of several cytochrome P450 (P450) isoforms.	Tolbutamide	95-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
15537834-2	2005	This study evaluated the effects of lansoprazole enantiomers on CYP2C9 activity in vitro, using several probe substrates.	Lansoprazole	36-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
15537834-4	2005	R-Lansoprazole-mediated activation of the formation of 4-hydroxyphenytoin was also seen with recombinant human CYP2C9.	Dexlansoprazole	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
15537834-4	2005	R-Lansoprazole-mediated activation of the formation of 4-hydroxyphenytoin was also seen with recombinant human CYP2C9.	hydroxyphenytoin	55-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
15714076-0	2005	CYP2C9 gene variants, drug dose, and bleeding risk in warfarin-treated patients: a HuGEnet systematic review and meta-analysis.	Warfarin	54-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15714076-1	2005	PURPOSE: Two common variant alleles of the cytochrome CYP2C9 (CYP2C9*2 and CYP2C9*3) lead to reduced warfarin metabolism in vitro and in vivo.	Warfarin	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
15714076-1	2005	PURPOSE: Two common variant alleles of the cytochrome CYP2C9 (CYP2C9*2 and CYP2C9*3) lead to reduced warfarin metabolism in vitro and in vivo.	Warfarin	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
15714076-1	2005	PURPOSE: Two common variant alleles of the cytochrome CYP2C9 (CYP2C9*2 and CYP2C9*3) lead to reduced warfarin metabolism in vitro and in vivo.	Warfarin	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
15714076-2	2005	The study objective was to examine the strength and quality of existing evidence about CYP2C9 gene variants and clinical outcomes in warfarin-treated patients.	Warfarin	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
15714076-11	2005	Mean difference in daily warfarin dose: for CYP2C9*2, the reduction was 0.85 mg (0.60-1.11 mg), a 17% reduction.	Warfarin	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
15714076-16	2005	CONCLUSIONS: Patients with CYP2C9*2 and CYP2C9*3 alleles have lower mean daily warfarin doses and a greater risk of bleeding.	Warfarin	79-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
15714076-16	2005	CONCLUSIONS: Patients with CYP2C9*2 and CYP2C9*3 alleles have lower mean daily warfarin doses and a greater risk of bleeding.	Warfarin	79-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
15854203-3	2005	Metabolism of pitavastatin by the cytochrome P450 (CYP) system is minimal, principally through CYP 2C9, with little involvement of the CYP 3A4 isoenzyme, potentially reducing the risk of drug-drug interactions between pitavastatin and other drugs known to inhibit CYP enzymes.	pitavastatin	14-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-102
15537834-5	2005	R-Lansoprazole increased the Michaelis-Menten-derived V(max) of phenytoin 4-hydroxylation from 0.024 to 0.121 pmol/min/pmol P450, and lowered its K(m) from 20.5 to 15.0 microM, suggesting that R-lansoprazole activates CYP2C9-mediated phenytoin metabolism without displacing phenytoin from the active site.	michaelis-menten	29-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
15537834-5	2005	R-Lansoprazole increased the Michaelis-Menten-derived V(max) of phenytoin 4-hydroxylation from 0.024 to 0.121 pmol/min/pmol P450, and lowered its K(m) from 20.5 to 15.0 microM, suggesting that R-lansoprazole activates CYP2C9-mediated phenytoin metabolism without displacing phenytoin from the active site.	Phenytoin	64-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
15537834-10	2005	Overall, these results suggest that R-lansoprazole activates CYP2C9 in a stereospecific and substrate-specific manner, possibly by binding within the active site and inducing positive cooperativity.	Dexlansoprazole	36-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
15547048-3	2005	Using P450 isoform-selective inhibitors and recombinant heterologously expressed enzymes, it was demonstrated that several P450 enzymes catalyzed sertraline N-demethylation, with CYP2B6 contributing the greatest extent, and lesser contributions from CYP2C19, CYP2C9, CYP3A4, and CYP2D6.	sertraline n	146-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	259-265
15711768-0	2005	Retrospective analyses of acenocoumarol doses and bleeding complications in patients with wild type or variant cytochrome P450 CYP2C9 alleles.	Acenocoumarol	26-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-133
15585365-6	2005	The results show that CYP3A4 contributes to the oxidation of KR-60436 to pyrrole-KR-60436, O-demethylpyrrole-KR-60436 and N-dehydroxyethyl-KR-60436, and CYP2C9 and CYP2D6 play roles in demethylation of KR-60436 to form the active metabolite, O-demethyl-KR-60436.	Krypton	61-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
15585365-6	2005	The results show that CYP3A4 contributes to the oxidation of KR-60436 to pyrrole-KR-60436, O-demethylpyrrole-KR-60436 and N-dehydroxyethyl-KR-60436, and CYP2C9 and CYP2D6 play roles in demethylation of KR-60436 to form the active metabolite, O-demethyl-KR-60436.	pyrrole-kr	73-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
15585365-6	2005	The results show that CYP3A4 contributes to the oxidation of KR-60436 to pyrrole-KR-60436, O-demethylpyrrole-KR-60436 and N-dehydroxyethyl-KR-60436, and CYP2C9 and CYP2D6 play roles in demethylation of KR-60436 to form the active metabolite, O-demethyl-KR-60436.	o-demethylpyrrole-kr	91-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
15585365-6	2005	The results show that CYP3A4 contributes to the oxidation of KR-60436 to pyrrole-KR-60436, O-demethylpyrrole-KR-60436 and N-dehydroxyethyl-KR-60436, and CYP2C9 and CYP2D6 play roles in demethylation of KR-60436 to form the active metabolite, O-demethyl-KR-60436.	Nitrogen	122-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
15585365-6	2005	The results show that CYP3A4 contributes to the oxidation of KR-60436 to pyrrole-KR-60436, O-demethylpyrrole-KR-60436 and N-dehydroxyethyl-KR-60436, and CYP2C9 and CYP2D6 play roles in demethylation of KR-60436 to form the active metabolite, O-demethyl-KR-60436.	Krypton	80-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
15585365-6	2005	The results show that CYP3A4 contributes to the oxidation of KR-60436 to pyrrole-KR-60436, O-demethylpyrrole-KR-60436 and N-dehydroxyethyl-KR-60436, and CYP2C9 and CYP2D6 play roles in demethylation of KR-60436 to form the active metabolite, O-demethyl-KR-60436.	Krypton	81-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
15585365-6	2005	The results show that CYP3A4 contributes to the oxidation of KR-60436 to pyrrole-KR-60436, O-demethylpyrrole-KR-60436 and N-dehydroxyethyl-KR-60436, and CYP2C9 and CYP2D6 play roles in demethylation of KR-60436 to form the active metabolite, O-demethyl-KR-60436.	o-demethyl-kr	242-255	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
15675511-2	2005	In this approach, single-stranded DNA (ssDNA)-polyacrylamide (polyAAm) conjugate was used as a pseudo-immobilized affinity ligand to separate the target DNA, cytochrome P450 2C9 (CYP2C9), and its point mutant.	polyacrylamide	46-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-177
15675511-2	2005	In this approach, single-stranded DNA (ssDNA)-polyacrylamide (polyAAm) conjugate was used as a pseudo-immobilized affinity ligand to separate the target DNA, cytochrome P450 2C9 (CYP2C9), and its point mutant.	polyacrylamide	46-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	179-185
15675511-2	2005	In this approach, single-stranded DNA (ssDNA)-polyacrylamide (polyAAm) conjugate was used as a pseudo-immobilized affinity ligand to separate the target DNA, cytochrome P450 2C9 (CYP2C9), and its point mutant.	polyacrylamide	62-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-177
15675511-2	2005	In this approach, single-stranded DNA (ssDNA)-polyacrylamide (polyAAm) conjugate was used as a pseudo-immobilized affinity ligand to separate the target DNA, cytochrome P450 2C9 (CYP2C9), and its point mutant.	polyacrylamide	62-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	179-185
15665498-2	2005	The modified CDs inhibited the activities of CYP2C19 and CYP3A4 while enhancing CYP2C9 activity by 140 to 176% relative to the control values at lower concentrations.	Cyclodextrins	13-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
15606435-0	2005	Lornoxicam pharmacokinetics in relation to cytochrome P450 2C9 genotype.	lornoxicam	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-62
15606435-1	2005	AIMS: To investigate the pharmacokinetics of lornoxicam and the relationship with CYP2C9 polymorphism in healthy Chinese subjects.	lornoxicam	45-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
15606435-5	2005	RESULTS: Of the 18 subjects, one subject was found to be a very poor metabolizer of lornoxicam with a long t(1/2) of 106 h, a low CL/F of 0.71 ml min(-1), and a high AUC(0-infinity) of 187.6 microg ml(-1) h. Genotyping studies revealed that this subject was heterozygous for CYP2C9*3 and a new variant CYP2C9 allele.	lornoxicam	84-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	275-281
15606435-5	2005	RESULTS: Of the 18 subjects, one subject was found to be a very poor metabolizer of lornoxicam with a long t(1/2) of 106 h, a low CL/F of 0.71 ml min(-1), and a high AUC(0-infinity) of 187.6 microg ml(-1) h. Genotyping studies revealed that this subject was heterozygous for CYP2C9*3 and a new variant CYP2C9 allele.	lornoxicam	84-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	302-308
15606435-8	2005	CONCLUSIONS: The results show that the pharmacokinetics of lornoxicam are dependent on CYP2C9 polymorphism.	lornoxicam	59-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
15606435-9	2005	In particular, the presence of the CYP2C9*3 allele impairs the oral clearance of lornoxicam.	lornoxicam	81-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
15637526-8	2005	In addition to its role in pharmacokinetics, CYP2C9 contributes to the metabolism of fatty acids, prostanoids, and steroid hormones, and it may catalyze potentially toxic bioactivation reactions.	Fatty Acids	85-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
15637526-8	2005	In addition to its role in pharmacokinetics, CYP2C9 contributes to the metabolism of fatty acids, prostanoids, and steroid hormones, and it may catalyze potentially toxic bioactivation reactions.	Prostaglandins	98-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
15637526-8	2005	In addition to its role in pharmacokinetics, CYP2C9 contributes to the metabolism of fatty acids, prostanoids, and steroid hormones, and it may catalyze potentially toxic bioactivation reactions.	Steroids	115-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
16372821-6	2005	Total oral clearance of all studied sulphonylureas (tolbutamide, glibenclamide [glyburide], glimepiride, glipizide) was only about 20% in persons with the CYP2C9*3/*3 genotype compared with carriers of the wild-type genotype CYP2C9*1/*1, and clearance in the heterozygous carriers was between 50% and 80% of that of the wild-type genotypes.	Sulfonylurea Compounds	36-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
16372821-6	2005	Total oral clearance of all studied sulphonylureas (tolbutamide, glibenclamide [glyburide], glimepiride, glipizide) was only about 20% in persons with the CYP2C9*3/*3 genotype compared with carriers of the wild-type genotype CYP2C9*1/*1, and clearance in the heterozygous carriers was between 50% and 80% of that of the wild-type genotypes.	Tolbutamide	52-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
16372821-6	2005	Total oral clearance of all studied sulphonylureas (tolbutamide, glibenclamide [glyburide], glimepiride, glipizide) was only about 20% in persons with the CYP2C9*3/*3 genotype compared with carriers of the wild-type genotype CYP2C9*1/*1, and clearance in the heterozygous carriers was between 50% and 80% of that of the wild-type genotypes.	Glyburide	65-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
16372821-6	2005	Total oral clearance of all studied sulphonylureas (tolbutamide, glibenclamide [glyburide], glimepiride, glipizide) was only about 20% in persons with the CYP2C9*3/*3 genotype compared with carriers of the wild-type genotype CYP2C9*1/*1, and clearance in the heterozygous carriers was between 50% and 80% of that of the wild-type genotypes.	Glyburide	80-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
16372821-6	2005	Total oral clearance of all studied sulphonylureas (tolbutamide, glibenclamide [glyburide], glimepiride, glipizide) was only about 20% in persons with the CYP2C9*3/*3 genotype compared with carriers of the wild-type genotype CYP2C9*1/*1, and clearance in the heterozygous carriers was between 50% and 80% of that of the wild-type genotypes.	glimepiride	92-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
16372821-6	2005	Total oral clearance of all studied sulphonylureas (tolbutamide, glibenclamide [glyburide], glimepiride, glipizide) was only about 20% in persons with the CYP2C9*3/*3 genotype compared with carriers of the wild-type genotype CYP2C9*1/*1, and clearance in the heterozygous carriers was between 50% and 80% of that of the wild-type genotypes.	Glipizide	105-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
16372821-10	2005	The meglitinide-class drug nateglinide is metabolised by CYP2C9.	meglitinide	4-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
16372821-10	2005	The meglitinide-class drug nateglinide is metabolised by CYP2C9.	Nateglinide	27-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
16372821-11	2005	According to the pharmacokinetic data, moderate dose adjustments based on CYP2C9 genotypes may help in reducing interindividual variability in the antihyperglycaemic effects of nateglinide.	Nateglinide	177-188	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
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 9	Homo sapiens	165-171
16372822-8	2005	More recently, CYP2C9 has also been reported to catalyse the hydroxylation of phenprocoumon and acenocoumarol.	Phenprocoumon	78-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
16372822-8	2005	More recently, CYP2C9 has also been reported to catalyse the hydroxylation of phenprocoumon and acenocoumarol.	Acenocoumarol	96-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
16372822-10	2005	Overall, the CYP2C9 isoenzyme appears to be most important for the clearance of warfarin, followed by acenocoumarol and, lastly, phenprocoumon.	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
16372822-10	2005	Overall, the CYP2C9 isoenzyme appears to be most important for the clearance of warfarin, followed by acenocoumarol and, lastly, phenprocoumon.	Acenocoumarol	102-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
15486075-0	2005	Interactions between CYP2C9 and CYP2C19 in reconstituted binary systems influence their catalytic activity: possible rationale for the inability of CYP2C19 to catalyze methoxychlor demethylation in human liver microsomes.	Methoxychlor	168-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
15486075-5	2005	When reconstituted with CPR, cytochrome b(5), and lipid, purified CYP2C19 and CYP2C9 catalyzed methoxychlor-O-demethylation.	methoxychlor-o	95-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
15486075-6	2005	However, whereas equimolar CPR to CYP2C9 supported maximal rates of methoxychlor demethylation and diclofenac hydroxylation, the rate of methoxychlor demethylation by CYP2C19 was not fully saturated, even with a 9-fold molar excess of CPR over CYP2C19.	Methoxychlor	68-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
15486075-6	2005	However, whereas equimolar CPR to CYP2C9 supported maximal rates of methoxychlor demethylation and diclofenac hydroxylation, the rate of methoxychlor demethylation by CYP2C19 was not fully saturated, even with a 9-fold molar excess of CPR over CYP2C19.	Diclofenac	99-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
15486075-10	2005	By contrast, in the incubation containing CYP2C9, diclofenac hydroxylation was activated by the presence of CYP2C19.	Diclofenac	50-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
15617742-0	2005	The frequency of cytochrome P450 2C9 genetic variants in the Russian population and their associations with individual sensitivity to warfarin therapy.	Warfarin	134-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-36
15940194-0	2005	[Clinical value of allele variants of cytochrome CYP2C9 gene for anticoagulation therapy with warfarin].	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
15940194-1	2005	Warfarin is metabolized by cytochrome CYP2C9 and its pharmacokinetic properties depend on structural polymorphisms of CYP2C9 gene.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
15940194-1	2005	Warfarin is metabolized by cytochrome CYP2C9 and its pharmacokinetic properties depend on structural polymorphisms of CYP2C9 gene.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
15940194-2	2005	We studied frequencies of allele variants of CYP2C9 gene and associations of individual reaction to warfarin intake with genotype of CYP2C9 gene.	Warfarin	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
15940194-4	2005	Carriers of CYP2C9x2 and CYP2C9x3 alleles more rapidly achieved therapeutic levels of hypocoagulation and required significantly lower weekly doses of warfarin.	Warfarin	151-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
15824753-0	2005	Influence of CYP2C9 polymorphisms, demographic factors and concomitant drug therapy on warfarin metabolism and maintenance dose.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
15824753-2	2005	S-warfarin is metabolized mainly by polymorphic cytochrome P450 (CYP) 2C9.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-73
15824753-3	2005	We systematically quantified the influence of CYP2C9 genotype, demographic factors and concomitant drug treatment on warfarin metabolism and maintenance dose.	Warfarin	117-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
15824753-5	2005	Multiple regression analysis demonstrated that CYP2C9 genotype, age, concomitant treatment with warfarin metabolism inducers and lean body weight contributed significantly to interindividual variability in warfarin dose requirement (adjusted R(2)=0.37).	Warfarin	206-214	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
15578879-0	2004	Effect of polymorphisms in the cytochrome P450 CYP2C9 gene on warfarin anticoagulation.	Warfarin	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
15578879-3	2004	Warfarin metabolism is under genetic control, involving primarily the CYP2C9 gene encoding the enzyme that catalyzes the conversion of warfarin to inactive metabolites.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
15578879-3	2004	Warfarin metabolism is under genetic control, involving primarily the CYP2C9 gene encoding the enzyme that catalyzes the conversion of warfarin to inactive metabolites.	Warfarin	135-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
15578879-5	2004	The objective of this case study is to investigate the relationship between CYP2C9 genotype and warfarin anticoagulation.	Warfarin	96-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
15578879-6	2004	DESIGN: A case of deep vein thrombosis treated with the standard warfarin dose is investigated for intensity of anticoagulation and CYP2C9 genotype; the case illustrates the relationship between CYP2C9 variant and overanticoagulation with subsequent bleeding complication.	Warfarin	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
15578879-6	2004	DESIGN: A case of deep vein thrombosis treated with the standard warfarin dose is investigated for intensity of anticoagulation and CYP2C9 genotype; the case illustrates the relationship between CYP2C9 variant and overanticoagulation with subsequent bleeding complication.	Warfarin	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
15578879-7	2004	RESULTS: The patient"s genotype, CYP2C9*1*3, correlated with an exaggerated anticoagulant response during the initiation of warfarin therapy at standard dose, and a bleeding episode ensued.	Warfarin	124-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
15578879-10	2004	Genotype knowledge of the CYP2C9 variant alleles may help the clinician to individualize warfarin therapy with the ultimate goals of shortening the initial period of induction therapy, reaching a stable maintenance dose earlier, and minimizing bleeding complications in patients who are high responders and need lower warfarin doses.	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
15578879-10	2004	Genotype knowledge of the CYP2C9 variant alleles may help the clinician to individualize warfarin therapy with the ultimate goals of shortening the initial period of induction therapy, reaching a stable maintenance dose earlier, and minimizing bleeding complications in patients who are high responders and need lower warfarin doses.	Warfarin	318-326	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
15333513-8	2004	Avasimibe inhibited CYP2C9 (IC50 2.9 microM), CYP1A2 (IC50 13.9 microM), and CYP2C19 (IC50 26.5 microM).	avasimibe	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
15333513-9	2004	A clinical drug interaction study was conducted to determine whether avasimibe might interact with the CYP2C9 substrate warfarin.	Warfarin	120-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
15342469-8	2004	Gomisin C, however, inhibited CYP1A2-, CYP2C9-, CYP2C19-, and CYP2D6-dependent activities only to a limited extent (IC50 values >10 microM).	schizandrer A	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
15592327-0	2004	CYP2C9 polymorphisms and the interindividual variability in pharmacokinetics and pharmacodynamics of the loop diuretic drug torsemide.	Torsemide	124-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15592327-1	2004	INTRODUCTION: According to in vitro data, torsemide (INN, torasemide) is a substrate of the genetically polymorphic enzyme cytochrome P450 (CYP) 2C9, but the impact of CYP2C9 polymorphisms on torsemide pharmacokinetics and pharmacodynamics has not been studied in humans.	Torsemide	42-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-148
15592327-1	2004	INTRODUCTION: According to in vitro data, torsemide (INN, torasemide) is a substrate of the genetically polymorphic enzyme cytochrome P450 (CYP) 2C9, but the impact of CYP2C9 polymorphisms on torsemide pharmacokinetics and pharmacodynamics has not been studied in humans.	Torsemide	42-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
15592327-1	2004	INTRODUCTION: According to in vitro data, torsemide (INN, torasemide) is a substrate of the genetically polymorphic enzyme cytochrome P450 (CYP) 2C9, but the impact of CYP2C9 polymorphisms on torsemide pharmacokinetics and pharmacodynamics has not been studied in humans.	inn	53-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-148
15592327-1	2004	INTRODUCTION: According to in vitro data, torsemide (INN, torasemide) is a substrate of the genetically polymorphic enzyme cytochrome P450 (CYP) 2C9, but the impact of CYP2C9 polymorphisms on torsemide pharmacokinetics and pharmacodynamics has not been studied in humans.	inn	53-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
15592327-1	2004	INTRODUCTION: According to in vitro data, torsemide (INN, torasemide) is a substrate of the genetically polymorphic enzyme cytochrome P450 (CYP) 2C9, but the impact of CYP2C9 polymorphisms on torsemide pharmacokinetics and pharmacodynamics has not been studied in humans.	Torsemide	58-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-148
15592327-1	2004	INTRODUCTION: According to in vitro data, torsemide (INN, torasemide) is a substrate of the genetically polymorphic enzyme cytochrome P450 (CYP) 2C9, but the impact of CYP2C9 polymorphisms on torsemide pharmacokinetics and pharmacodynamics has not been studied in humans.	Torsemide	58-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
15592327-3	2004	The effects of the CYP2C9 polymorphism on torsemide-induced urine volume and urinary elimination of sodium, potassium, chloride, and uric acid were measured during a salt-restricted diet.	Torsemide	42-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
15592327-4	2004	RESULTS: Median torsemide total oral clearance values were 3.4, 2.2, and 1.2 L/h in carriers of the CYP2C9 genotypes *1/*1 , *1/*3 , and *3/*3 , respectively, but there was no significant difference related to CYP2C9*2 .	Torsemide	16-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
15592327-6	2004	From 0 to 8 hours after torsemide administration, Na + , K + , and Cl - elimination was higher in carriers of CYP2C9*3 alleles than in carriers of the homozygous wild-type genotype, and 24-hour uric acid elimination values in urine were 451, 350, and 249 mg in carriers of 0, 1, and 2 CYP2C9*3 alleles, respectively (P = .003).	Torsemide	24-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
15592327-7	2004	CONCLUSION: Torsemide pharmacokinetics differed significantly between subgroups with different CYP2C9 genotypes, and diuretic effects were slightly more exaggerated in carriers of CYP2C9*3 alleles.	Torsemide	12-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
15592327-7	2004	CONCLUSION: Torsemide pharmacokinetics differed significantly between subgroups with different CYP2C9 genotypes, and diuretic effects were slightly more exaggerated in carriers of CYP2C9*3 alleles.	Torsemide	12-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	180-186
15592335-2	2004	METHODS: The frequency of coadministration between losartan and well-established cytochrome P450 (CYP) 2C9 inhibitors, as well as codeine and tramadol and CYP2D6 inhibitors, was studied by use of data from a university hospital medication database.	Losartan	51-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-106
15608560-0	2004	Upstream and coding region CYP2C9 polymorphisms: correlation with warfarin dose and metabolism.	Warfarin	66-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
15585441-12	2004	As with other protease inhibitors, atazanavir is also a substrate and moderate inhibitor of the cytochrome P450 (CYP) system, in particular CYP3A4 and CYP2C9.	Atazanavir Sulfate	35-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	151-157
15608560-1	2004	OBJECTIVES: To assess whether CYP2C9 alleles other than CYP2C9*2 and *3 are associated with a low-warfarin dose requirement and the relevance of upstream CYP2C9 polymorphisms to dose requirement and metabolism.	Warfarin	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
15608560-3	2004	PCR-based genotyping assays for novel upstream and other known polymorphisms were used to screen a larger patient population of known CYP2C9*2 and *3 genotype requiring a range of warfarin doses.	Warfarin	180-188	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
15608560-10	2004	CONCLUSIONS: The coding region non-synonymous polymorphisms associated with the CYP2C9*2 and CYP2C9*3 alleles are the major CYP2C9-related factor affecting warfarin dose in UK Caucasians.	Warfarin	156-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
15608560-10	2004	CONCLUSIONS: The coding region non-synonymous polymorphisms associated with the CYP2C9*2 and CYP2C9*3 alleles are the major CYP2C9-related factor affecting warfarin dose in UK Caucasians.	Warfarin	156-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
15608560-10	2004	CONCLUSIONS: The coding region non-synonymous polymorphisms associated with the CYP2C9*2 and CYP2C9*3 alleles are the major CYP2C9-related factor affecting warfarin dose in UK Caucasians.	Warfarin	156-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
15536456-11	2004	Carriers of the CYP2C9*2 or *3 allele needed a significantly lower phenprocoumon dosage compared with homozygous CYP2C9*1/*1 subjects.	Phenprocoumon	67-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
29793229-5	2004	CYP2C9 metabolizes several oral hypoglycemics, oral anticoagulants, non-steroidal anti-inflammatory drugs and other drugs, including phenytoin, losartan, fluvastatin, and torsemide.	Phenytoin	133-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
29793229-5	2004	CYP2C9 metabolizes several oral hypoglycemics, oral anticoagulants, non-steroidal anti-inflammatory drugs and other drugs, including phenytoin, losartan, fluvastatin, and torsemide.	Losartan	144-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
29793229-5	2004	CYP2C9 metabolizes several oral hypoglycemics, oral anticoagulants, non-steroidal anti-inflammatory drugs and other drugs, including phenytoin, losartan, fluvastatin, and torsemide.	Fluvastatin	154-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
29793229-5	2004	CYP2C9 metabolizes several oral hypoglycemics, oral anticoagulants, non-steroidal anti-inflammatory drugs and other drugs, including phenytoin, losartan, fluvastatin, and torsemide.	Torsemide	171-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
29793229-8	2004	Several studies demonstrated that the CYP2C9 polymorphisms are medically important for non-steroidal anti-inflammatory drugs, for oral hypoglycemics, vitamin K antagonistic oral anticoagulants, and phenytoin.	Vitamin K	150-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
29793229-8	2004	Several studies demonstrated that the CYP2C9 polymorphisms are medically important for non-steroidal anti-inflammatory drugs, for oral hypoglycemics, vitamin K antagonistic oral anticoagulants, and phenytoin.	Phenytoin	198-207	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
29793229-11	2004	Data appear mature enough for the routine consideration of CYP2C9 genotypes in therapy with acenocoumarol, phenytoin, warfarin, and some other drugs.	Acenocoumarol	92-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
29793229-11	2004	Data appear mature enough for the routine consideration of CYP2C9 genotypes in therapy with acenocoumarol, phenytoin, warfarin, and some other drugs.	Phenytoin	107-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
29793229-11	2004	Data appear mature enough for the routine consideration of CYP2C9 genotypes in therapy with acenocoumarol, phenytoin, warfarin, and some other drugs.	Warfarin	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
15557548-8	2004	Phenytoin and phenobarbital are metabolized by cytochrome P450 isozymes, with activity dependent on genetic polymorphism (CYP2C9, CYP2C19).	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
15557548-8	2004	Phenytoin and phenobarbital are metabolized by cytochrome P450 isozymes, with activity dependent on genetic polymorphism (CYP2C9, CYP2C19).	Phenobarbital	14-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
15543094-9	2004	Chronic hypoxia, increased amounts of nonheme iron in the liver and adrenals of these infants, enhanced activity of CYP2C9 regarded as the functional source of reactive oxygen species (ROS) in some endothelial cells, and nicotine accumulation in tissues also intensified production of ROS.	Reactive Oxygen Species	160-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
15543094-9	2004	Chronic hypoxia, increased amounts of nonheme iron in the liver and adrenals of these infants, enhanced activity of CYP2C9 regarded as the functional source of reactive oxygen species (ROS) in some endothelial cells, and nicotine accumulation in tissues also intensified production of ROS.	Reactive Oxygen Species	185-188	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
15543094-9	2004	Chronic hypoxia, increased amounts of nonheme iron in the liver and adrenals of these infants, enhanced activity of CYP2C9 regarded as the functional source of reactive oxygen species (ROS) in some endothelial cells, and nicotine accumulation in tissues also intensified production of ROS.	Reactive Oxygen Species	285-288	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
15304426-0	2004	The involvement of CYP3A4 and CYP2C9 in the metabolism of 17 alpha-ethinylestradiol.	Ethinyl Estradiol	58-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
15536456-13	2004	Similar to warfarin and acenocoumarol, phenprocoumon had a lower dosage requirement in carriers of CYP2C9*2 or *3 compared with that in CYP2C9 wild-type subjects.	Phenprocoumon	39-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
15304426-6	2004	The involvement of CYP3A4 and CYP2C9 was further confirmed by using selective chemical inhibitors (i.e., ketoconazole and sulfaphenazole).	Ketoconazole	105-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
15304426-6	2004	The involvement of CYP3A4 and CYP2C9 was further confirmed by using selective chemical inhibitors (i.e., ketoconazole and sulfaphenazole).	Sulfaphenazole	122-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
15304427-10	2004	Aprepitant was a very weak inhibitor of CYP2C9 and CYP2C19, with Ki values of 108 and 66 microM for the 7-hydroxylation of warfarin and the 4"-hydroxylation of S-mephenytoin, respectively.	Warfarin	123-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
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 9	Homo sapiens	114-120
15304427-10	2004	Aprepitant was a very weak inhibitor of CYP2C9 and CYP2C19, with Ki values of 108 and 66 microM for the 7-hydroxylation of warfarin and the 4"-hydroxylation of S-mephenytoin, respectively.	Mephenytoin	160-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
15528841-5	2004	In contrast, in addition to the reported inhibitory effect of isoniazid on CYP1A2, CYP2A6, CYP2C19, and CYP3A activities, our results newly showed its effect on CYP2C9 and CYP2E1 activities.	Isoniazid	62-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
15569425-0	2004	[Association between genetic polymorphisms of CYP2C19 and CYP2C9 and phenytoin serum concentration].	Phenytoin	69-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
15569425-1	2004	OBJECTIVE: To investigate the relationship between the genetic polymorphism of cytochrome CYP2C19 and CYP2C9 and the serum concentration of phenytoin (PHT) in patients with epilepsy.	Phenytoin	140-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
15569425-1	2004	OBJECTIVE: To investigate the relationship between the genetic polymorphism of cytochrome CYP2C19 and CYP2C9 and the serum concentration of phenytoin (PHT) in patients with epilepsy.	Phenytoin	151-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
15569425-11	2004	CONCLUSION: Phenytoin is metabolized via CYP2C19 and CYP2C9.	Phenytoin	12-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
15373932-2	2004	Rosiglitazone is a novel thiazolidinedione antidiabetic drug, mainly metabolized by CYP2C8 and to a lesser extent CYP2C9.	2,4-thiazolidinedione	25-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
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.	Ketoconazole	38-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
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 9	Homo sapiens	145-151
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 9	Homo sapiens	145-151
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 9	Homo sapiens	145-151
15382119-4	2004	We show that IL-1beta decreases CAR expression and decreases phenobarbital- or bilirubin-mediated induction of CYP2B6, CYP2C9, CYP3A4, UGT1A1, GSTA1, GSTA2, and SLC21A6 messenger RNA.	Phenobarbital	61-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
15382119-4	2004	We show that IL-1beta decreases CAR expression and decreases phenobarbital- or bilirubin-mediated induction of CYP2B6, CYP2C9, CYP3A4, UGT1A1, GSTA1, GSTA2, and SLC21A6 messenger RNA.	Bilirubin	79-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
15540908-0	2004	Genetic polymorphism of the CYP2C9 subfamily of 3 different races in warfarin maintenance dose.	Warfarin	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
15454736-0	2004	A novel CYP2C9 variant that caused erroneous genotyping in a patient on warfarin therapy.	Warfarin	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
15385837-0	2004	Dosage recommendation of phenytoin for patients with epilepsy with different CYP2C9/CYP2C19 polymorphisms.	Phenytoin	25-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
15325841-1	2004	The effect of human serum albumin (HSA), in its endogenous, free fatty acid free (FAF) and globulin free (GF) form, on the activity of CYP2C9 was studied in human liver microsomes using tolbutamide as the substrate.	Fatty Acids, Nonesterified	60-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-141
15325841-1	2004	The effect of human serum albumin (HSA), in its endogenous, free fatty acid free (FAF) and globulin free (GF) form, on the activity of CYP2C9 was studied in human liver microsomes using tolbutamide as the substrate.	Fatty Acids, Nonesterified	82-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-141
15325841-1	2004	The effect of human serum albumin (HSA), in its endogenous, free fatty acid free (FAF) and globulin free (GF) form, on the activity of CYP2C9 was studied in human liver microsomes using tolbutamide as the substrate.	Tolbutamide	186-197	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-141
15325841-4	2004	HSA(FAF) and BSA showed a concentration-dependent and biphasic (activation and inhibition) interaction with CYP2C9 activity.	Fatty Acids, Nonesterified	4-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
15325841-10	2004	The FDH Test ratio for HSA was about 1, indicating that HSA binding of tolbutamide reduced the CYP2C9 activity in accord with the free-drug hypothesis.	Tolbutamide	71-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
15325841-13	2004	As revealed by their removal, free fatty acids and globulins, significantly alter the interaction of HSA with CYP2C9.	Fatty Acids, Nonesterified	30-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
15325841-14	2004	In addition, HSA and BSA showed different effects on the oxidation of tolbutamide by CYP2C9.	Tolbutamide	70-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
15364537-8	2004	Primary cultures of hepatocytes were treated with beta-naphthoflavone, an inducer of CYP1A2, phenobarbital or rifampin, both of which induce CYP2B6, CYP2C9, CYP2C19, and CYP3A4, albeit it to different extents.	beta-Naphthoflavone	50-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
15364537-8	2004	Primary cultures of hepatocytes were treated with beta-naphthoflavone, an inducer of CYP1A2, phenobarbital or rifampin, both of which induce CYP2B6, CYP2C9, CYP2C19, and CYP3A4, albeit it to different extents.	Rifampin	110-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
15288804-0	2004	Active-site characteristics of CYP2C19 and CYP2C9 probed with hydantoin and barbiturate inhibitors.	Hydantoins	62-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
15288804-0	2004	Active-site characteristics of CYP2C19 and CYP2C9 probed with hydantoin and barbiturate inhibitors.	barbituric acid	76-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
15288804-5	2004	(S)-(+)-N-3-Benzylnirvanol and (R)-(-)-N-3-benzylphenobarbital emerged as the most potent and selective CYP2C19 inhibitors, with K(i) values of < 250nM--at least two orders of magnitude greater inhibitor potency than towards CYP2C9.	N-3-benzylnirvanol	0-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	228-234
15288804-5	2004	(S)-(+)-N-3-Benzylnirvanol and (R)-(-)-N-3-benzylphenobarbital emerged as the most potent and selective CYP2C19 inhibitors, with K(i) values of < 250nM--at least two orders of magnitude greater inhibitor potency than towards CYP2C9.	(r)-(-)-n-3-benzylphenobarbital	31-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	228-234
15371982-0	2004	Novel CYP2C9 genetic variants in Asian subjects and their influence on maintenance warfarin dose.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
15371982-1	2004	BACKGROUND: Commonly occurring genetic variants in CYP2C9 are known to reduce catalytic activity and are associated with enhanced patient sensitivity to warfarin.	Warfarin	153-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
15371982-2	2004	Interethnic differences in warfarin dose requirement have been described in the Asian population, and we postulate that this could be related to genetic variants of CYP2C9 that are unique to ethnic groups.	Warfarin	27-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	165-171
15371982-3	2004	METHODS: We prospectively genotyped 125 patients who were receiving a stable daily warfarin dose to maintain international normalized ratio values between 2 and 3 through comprehensive sequencing of the promoter and coding regions of the CYP2C9 gene.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	238-244
15371982-7	2004	CYP2C9*3, but not CYP2C9*2, was found in Chinese and Malay patients, and carriers of the CYP2C9*3 variant in Chinese ( P <.01) and Indian ( P <.01) patients, but not Malay patients ( P =.77), required less warfarin.	Warfarin	206-214	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15341704-1	2004	Warfarin, the principal oral anticoagulant used in the treatment and prevention of thromboembolic disease, is primarily metabolized by CYP2C9, one of the hepatic microsomal enzymes.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-141
15319344-5	2004	Other metabolites formed in NADPH-fortified liver microsomes included the TZD-5-OH derivative (M24), also catalyzed by CYP3A4, and the O-desmethyl derivative (M28), whose formation was catalyzed by CYP2C9 and CYP2C19.	NADP	28-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	198-204
15350166-6	2004	The demonstration of the safe use of fluvastatin in a wide range of patients may be associated with the predominant acid form of the drug in vivo, as well as its predominant metabolism via the cytochrome P450 2C9 pathway.	Fluvastatin	37-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	193-212
15378224-2	2004	METHODS: The inhibitory potency of memantine on CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 activities was examined with specific probe drugs in HLM and recombinant P450s.	Memantine	35-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
15295798-2	2004	Torasemide was reported to be mainly metabolized via hepatic CYP2C9 in humans, and human CYP2C9 and male rat CYP2C11 proteins have 77% homology.	Torsemide	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
15742978-0	2004	Genetic polymorphisms of cytochrome P450 2C9 causing reduced phenprocoumon (S)-7-hydroxylation in vitro and in vivo.	ethyl-2-methylthio-4-methyl-5-pyrimidine carboxylate	75-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-44
15351856-1	2004	Variant cytochrome P450 (CYP) 2C9 genotypes are associated with low maintenance dose requirement of warfarin therapy and increased risk of major bleeding events.	Warfarin	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-33
15742978-1	2004	The effect of cytochrome P450 (CYP) 2C9 polymorphisms on the stereoselective biotransformation of the oral anticoagulant phenprocoumon (PPC) to inactive, monohydroxylated metabolites was studied in vitro and in vivo.	Phenprocoumon	121-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-39
15742978-2	2004	In human liver microsomes, the (S)-7-hydroxylation--being the major metabolic pathway--was significantly compromised in a gene-dose-dependent manner in samples expressing the CYP2C9*2 or CYP2C9*3 allele.	Sulfur	32-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	175-181
15742978-2	2004	In human liver microsomes, the (S)-7-hydroxylation--being the major metabolic pathway--was significantly compromised in a gene-dose-dependent manner in samples expressing the CYP2C9*2 or CYP2C9*3 allele.	Sulfur	32-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	187-193
15742978-3	2004	The CYP2C9*3/*3 genotype corresponded to an almost fourfold lower (S)-7-hydroxylation rate than CYP2C9*1/*1 (wild-type).	Sulfur	67-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
15742978-4	2004	The intrinsic clearance of human recombinant CYP2C9*2 and CYP2C9*3 for the (S)-7-hydroxylation was 28.9 and 50.9% lower than of CYP2C9*1, respectively.	Sulfur	75-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
15742978-4	2004	The intrinsic clearance of human recombinant CYP2C9*2 and CYP2C9*3 for the (S)-7-hydroxylation was 28.9 and 50.9% lower than of CYP2C9*1, respectively.	Sulfur	75-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
15742978-4	2004	The intrinsic clearance of human recombinant CYP2C9*2 and CYP2C9*3 for the (S)-7-hydroxylation was 28.9 and 50.9% lower than of CYP2C9*1, respectively.	Sulfur	75-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
15742978-6	2004	Increasing plasma AUC metabolic ratios (parent compound/metabolite) in CYP2C9*2 and CYP2C9*3 variant allele carriers were found for each hydroxylation reaction and the CYP2C9*3/*3 genotype corresponded to an about 10-fold higher metabolic ratio of PPC (S)-7-hydroxylation relative to CYP2C9*1/*1.	Sulfur	252-255	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
15742978-6	2004	Increasing plasma AUC metabolic ratios (parent compound/metabolite) in CYP2C9*2 and CYP2C9*3 variant allele carriers were found for each hydroxylation reaction and the CYP2C9*3/*3 genotype corresponded to an about 10-fold higher metabolic ratio of PPC (S)-7-hydroxylation relative to CYP2C9*1/*1.	Sulfur	252-255	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
15742978-6	2004	Increasing plasma AUC metabolic ratios (parent compound/metabolite) in CYP2C9*2 and CYP2C9*3 variant allele carriers were found for each hydroxylation reaction and the CYP2C9*3/*3 genotype corresponded to an about 10-fold higher metabolic ratio of PPC (S)-7-hydroxylation relative to CYP2C9*1/*1.	Sulfur	252-255	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
15742978-6	2004	Increasing plasma AUC metabolic ratios (parent compound/metabolite) in CYP2C9*2 and CYP2C9*3 variant allele carriers were found for each hydroxylation reaction and the CYP2C9*3/*3 genotype corresponded to an about 10-fold higher metabolic ratio of PPC (S)-7-hydroxylation relative to CYP2C9*1/*1.	Sulfur	252-255	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
15306208-4	2004	On the other hand, cisapride strongly inhibited CYP3A4 and markedly inhibited CYP2C9.	Cisapride	19-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
15247556-2	2004	Phenytoin (PHT) is a CYP3A4 inducer and CYP2C9/CYP2C19 substrate.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
15181000-0	2004	The structure of human cytochrome P450 2C9 complexed with flurbiprofen at 2.0-A resolution.	Flurbiprofen	58-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-42
15247556-2	2004	Phenytoin (PHT) is a CYP3A4 inducer and CYP2C9/CYP2C19 substrate.	Phenytoin	11-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
15310247-8	2004	The liver microsomal SOH activity showed significant correlations with tolbutamide hydroxylation (r = 0.569) and chlorzoxazone hydroxylation (r = 0.770) activities, which were the model reactions catalyzed by CYP2C9 and CYP2E1, respectively.	Tolbutamide	71-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	209-215
15310247-8	2004	The liver microsomal SOH activity showed significant correlations with tolbutamide hydroxylation (r = 0.569) and chlorzoxazone hydroxylation (r = 0.770) activities, which were the model reactions catalyzed by CYP2C9 and CYP2E1, respectively.	Chlorzoxazone	113-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	209-215
15290664-2	2004	The cytochrome P-450 (CYP) 2C9 (CYP2C9) enzyme is involved in the metabolism of several drugs, including possibly aspirin, and such carcinogens as smoking-related polycyclic aromatic hydrocarbons.	Aspirin	114-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-30
15289788-1	2004	UNLABELLED: Background and aim Previous data indicate that the urinary losartan/E-3174 ratio is a marker for cytochrome P450 (CYP) 2C9 activity in vivo.	Losartan	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-134
15289788-1	2004	UNLABELLED: Background and aim Previous data indicate that the urinary losartan/E-3174 ratio is a marker for cytochrome P450 (CYP) 2C9 activity in vivo.	losartan carboxylic acid	80-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-134
15289788-3	2004	METHODS: A single oral dose of losartan (25 mg) was given to 19 Beninese subjects with CYP2C9*1/*1 (n = 9), *1/*5 (n = 1), *1/*6 (n = 1), *1/*8 (n = 2), *1/*11 (n = 3), *5/*6 (n = 1), *5/*8 (n = 1), and *8/*11 (n = 1) genotypes.	Losartan	31-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
15289788-6	2004	RESULTS: The urinary losartan/E-3174 ratio in the various genotypes was as follows: 1.85 +/- 2.4 (mean +/- SD) for CYP2C9*1/*1, 14.6 for CYP2C9*1/*5, 4.2 for CYP2C9*1/*6, 188 for CYP2C9*5/*6, 11.6 for CYP2C9*5/*8, 0.44 +/- 0.13 (mean +/- SD) for CYP2C9*1/*8, 2.2 for CYP2C9*8/*11, and 5.72 +/- 4.5 (mean +/- SD) for CYP2C9*1/*11.	Losartan	21-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
15289788-6	2004	RESULTS: The urinary losartan/E-3174 ratio in the various genotypes was as follows: 1.85 +/- 2.4 (mean +/- SD) for CYP2C9*1/*1, 14.6 for CYP2C9*1/*5, 4.2 for CYP2C9*1/*6, 188 for CYP2C9*5/*6, 11.6 for CYP2C9*5/*8, 0.44 +/- 0.13 (mean +/- SD) for CYP2C9*1/*8, 2.2 for CYP2C9*8/*11, and 5.72 +/- 4.5 (mean +/- SD) for CYP2C9*1/*11.	losartan carboxylic acid	30-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
15289788-8	2004	The urinary losartan/E-3174 ratio of the single CYP2C9*1/*6 subject was higher than the 95% confidence interval of the mean of the CYP2C9*1/*1 group (0.0-3.7), whereas the metabolic ratio of the CYP2C9*8/*11 carrier was inside the 95% confidence interval of the means of the CYP2C9*1/*1 and CYP2C9*1/*11 groups (0.0-18).	Losartan	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
15289788-8	2004	The urinary losartan/E-3174 ratio of the single CYP2C9*1/*6 subject was higher than the 95% confidence interval of the mean of the CYP2C9*1/*1 group (0.0-3.7), whereas the metabolic ratio of the CYP2C9*8/*11 carrier was inside the 95% confidence interval of the means of the CYP2C9*1/*1 and CYP2C9*1/*11 groups (0.0-18).	Losartan	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
15289788-8	2004	The urinary losartan/E-3174 ratio of the single CYP2C9*1/*6 subject was higher than the 95% confidence interval of the mean of the CYP2C9*1/*1 group (0.0-3.7), whereas the metabolic ratio of the CYP2C9*8/*11 carrier was inside the 95% confidence interval of the means of the CYP2C9*1/*1 and CYP2C9*1/*11 groups (0.0-18).	Losartan	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
15289788-8	2004	The urinary losartan/E-3174 ratio of the single CYP2C9*1/*6 subject was higher than the 95% confidence interval of the mean of the CYP2C9*1/*1 group (0.0-3.7), whereas the metabolic ratio of the CYP2C9*8/*11 carrier was inside the 95% confidence interval of the means of the CYP2C9*1/*1 and CYP2C9*1/*11 groups (0.0-18).	Losartan	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
15289788-8	2004	The urinary losartan/E-3174 ratio of the single CYP2C9*1/*6 subject was higher than the 95% confidence interval of the mean of the CYP2C9*1/*1 group (0.0-3.7), whereas the metabolic ratio of the CYP2C9*8/*11 carrier was inside the 95% confidence interval of the means of the CYP2C9*1/*1 and CYP2C9*1/*11 groups (0.0-18).	Losartan	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
15289788-8	2004	The urinary losartan/E-3174 ratio of the single CYP2C9*1/*6 subject was higher than the 95% confidence interval of the mean of the CYP2C9*1/*1 group (0.0-3.7), whereas the metabolic ratio of the CYP2C9*8/*11 carrier was inside the 95% confidence interval of the means of the CYP2C9*1/*1 and CYP2C9*1/*11 groups (0.0-18).	losartan carboxylic acid	21-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
15289789-6	2004	The main genetic factor for reduced clearance of R-(-)-ibuprofen is the CYP2C8*3 allele, whereas the clearance for S-(+)-ibuprofen is influenced by CYP2C8*3 and CYP2C9*3 alleles to a similar extent.	Ibuprofen	49-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
15289789-6	2004	The main genetic factor for reduced clearance of R-(-)-ibuprofen is the CYP2C8*3 allele, whereas the clearance for S-(+)-ibuprofen is influenced by CYP2C8*3 and CYP2C9*3 alleles to a similar extent.	Ibuprofen	115-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
15289789-8	2004	As compared with individuals with no mutations, individuals with the common genotype CYP2C8*1/*3 plus CYP2C9*1/*2 (19% of the population) displayed decreased ibuprofen clearance (mean, 65% [95% CI, 42%-89%]; P &lt;.001).	Ibuprofen	158-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
15289789-9	2004	Individuals homozygous or double-heterozygous for CYP2C8*3 and CYP2C9*3 variant alleles (8% of the population) had extremely low ibuprofen clearance rates, with values ranging from 7% to 27% of the mean clearance rates among noncarriers of mutations (P &lt;.001).	Ibuprofen	129-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
15289789-11	2004	CONCLUSION: Low ibuprofen clearance occurs in a substantial proportion of healthy subjects, is not enantiospecific, and is strongly linked to CYP2C8 and CYP2C9 polymorphisms.	Ibuprofen	16-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
15258107-5	2004	Pantoprazole was a competitive inhibitor of both CYP2C9-catalyzed diclofenac 4"-hydroxylation and CYP3A4-catalyzed midazolam 1"-hydroxylation (K(i) of 6 and 22 microM, respectively), which were at least 2 times more potent than the other PPIs.	Pantoprazole	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
15258107-5	2004	Pantoprazole was a competitive inhibitor of both CYP2C9-catalyzed diclofenac 4"-hydroxylation and CYP3A4-catalyzed midazolam 1"-hydroxylation (K(i) of 6 and 22 microM, respectively), which were at least 2 times more potent than the other PPIs.	Diclofenac	66-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
15258107-7	2004	The inhibitory potency of a nonenzymatically formed product of rabeprazole, rabeprazole thioether, was also investigated and showed potent, competitive inhibition with K(i) values of 6 microM for CYP2C9, 2 to 8 microM for CYP2C19, 12 microM for CYP2D6, and 15 microM for CYP3A4.	Rabeprazole	63-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
15258107-7	2004	The inhibitory potency of a nonenzymatically formed product of rabeprazole, rabeprazole thioether, was also investigated and showed potent, competitive inhibition with K(i) values of 6 microM for CYP2C9, 2 to 8 microM for CYP2C19, 12 microM for CYP2D6, and 15 microM for CYP3A4.	rabeprazole-thioether	76-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
15258107-8	2004	The inhibitory potency of R-omeprazole on the four studied P450 enzymes was also studied and showed higher inhibitory potency than its S-isomer on CYP2C9 and 2C19 activities.	r-omeprazole	26-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
15258107-9	2004	Our data suggest that, although the inhibitory profiles of the five studied PPIs were similar, lansoprazole and pantoprazole are the most potent in vitro inhibitors of CYP2C19 and CYP2C9, respectively.	Lansoprazole	95-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	180-186
15258107-9	2004	Our data suggest that, although the inhibitory profiles of the five studied PPIs were similar, lansoprazole and pantoprazole are the most potent in vitro inhibitors of CYP2C19 and CYP2C9, respectively.	Pantoprazole	112-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	180-186
15290664-2	2004	The cytochrome P-450 (CYP) 2C9 (CYP2C9) enzyme is involved in the metabolism of several drugs, including possibly aspirin, and such carcinogens as smoking-related polycyclic aromatic hydrocarbons.	Aspirin	114-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
15290664-2	2004	The cytochrome P-450 (CYP) 2C9 (CYP2C9) enzyme is involved in the metabolism of several drugs, including possibly aspirin, and such carcinogens as smoking-related polycyclic aromatic hydrocarbons.	Polycyclic Aromatic Hydrocarbons	163-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-30
15290664-2	2004	The cytochrome P-450 (CYP) 2C9 (CYP2C9) enzyme is involved in the metabolism of several drugs, including possibly aspirin, and such carcinogens as smoking-related polycyclic aromatic hydrocarbons.	Polycyclic Aromatic Hydrocarbons	163-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
15122071-4	2004	Using CYP supersomes it was shown that thiocoraline is mainly metabolized by CYP3A4, with CYP1A1, CYP2C8 and CYP2C9 playing a minor role in the biotransformation (&lt;3%).	thiocoraline	39-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
15197517-0	2004	Effect of a selective CYP2C9 inhibitor on the pharmacokinetics of nateglinide in healthy subjects.	Nateglinide	66-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
15197517-1	2004	PURPOSE: The objective of the study was to determine the effect of a potent and selective CYP2C9 inhibitor, sulfinpyrazone (Anturane), on the pharmacokinetics of nateglinide (Starlix), a novel antidiabetic drug which is primarily (approximately 70%) metabolized via CYP2C9.	Sulfinpyrazone	108-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
15197517-1	2004	PURPOSE: The objective of the study was to determine the effect of a potent and selective CYP2C9 inhibitor, sulfinpyrazone (Anturane), on the pharmacokinetics of nateglinide (Starlix), a novel antidiabetic drug which is primarily (approximately 70%) metabolized via CYP2C9.	Sulfinpyrazone	108-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	266-272
15197517-1	2004	PURPOSE: The objective of the study was to determine the effect of a potent and selective CYP2C9 inhibitor, sulfinpyrazone (Anturane), on the pharmacokinetics of nateglinide (Starlix), a novel antidiabetic drug which is primarily (approximately 70%) metabolized via CYP2C9.	Sulfinpyrazone	124-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
15197517-1	2004	PURPOSE: The objective of the study was to determine the effect of a potent and selective CYP2C9 inhibitor, sulfinpyrazone (Anturane), on the pharmacokinetics of nateglinide (Starlix), a novel antidiabetic drug which is primarily (approximately 70%) metabolized via CYP2C9.	Sulfinpyrazone	124-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	266-272
15197517-1	2004	PURPOSE: The objective of the study was to determine the effect of a potent and selective CYP2C9 inhibitor, sulfinpyrazone (Anturane), on the pharmacokinetics of nateglinide (Starlix), a novel antidiabetic drug which is primarily (approximately 70%) metabolized via CYP2C9.	Nateglinide	162-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
15197517-1	2004	PURPOSE: The objective of the study was to determine the effect of a potent and selective CYP2C9 inhibitor, sulfinpyrazone (Anturane), on the pharmacokinetics of nateglinide (Starlix), a novel antidiabetic drug which is primarily (approximately 70%) metabolized via CYP2C9.	Nateglinide	162-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	266-272
15197517-1	2004	PURPOSE: The objective of the study was to determine the effect of a potent and selective CYP2C9 inhibitor, sulfinpyrazone (Anturane), on the pharmacokinetics of nateglinide (Starlix), a novel antidiabetic drug which is primarily (approximately 70%) metabolized via CYP2C9.	Nateglinide	175-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
15197517-1	2004	PURPOSE: The objective of the study was to determine the effect of a potent and selective CYP2C9 inhibitor, sulfinpyrazone (Anturane), on the pharmacokinetics of nateglinide (Starlix), a novel antidiabetic drug which is primarily (approximately 70%) metabolized via CYP2C9.	Nateglinide	175-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	266-272
15285849-4	2004	Quercetin, the biflavone amentoflavone, sesamin, as well as (Z,Z)-4,4"-(1,4-pentadiene-1,5-diyl)diphenol and 3-nonadec-8-enyl-benzene-1,2-diol, were also inhibitors of CYP2C9.	(z,z)-4,4"-(1,4-pentadiene-1,5-diyl)diphenol	60-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
15285849-5	2004	The IC50 of amentoflavone for CYP2C9 was 0.019 microg mL(-1) (0.035 microM).	amentoflavone	12-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
15284535-6	2004	CYP2C9*11 appeared to be a putative poor metabolizer allele, exhibiting a three-fold increase in the Km and more than a two-fold decrease in the intrinsic clearance for tolbutamide.	Tolbutamide	169-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15284535-7	2004	Examination of the crystal structure of human CYP2C9 reveals that R335 is located in the turn between the J and J" helices and forms a hydrogen-bonding ion pair with D341 from the J" helix.	Hydrogen	135-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
15284535-7	2004	Examination of the crystal structure of human CYP2C9 reveals that R335 is located in the turn between the J and J" helices and forms a hydrogen-bonding ion pair with D341 from the J" helix.	d341	166-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
15284535-10	2004	A second potentially PM allele CYP2C9*12 found in a racially unidentified sample also exhibited a modest decrease in the Vmax and the intrinsic clearance for tolbutamide in a recombinant system.	Tolbutamide	158-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
15284536-0	2004	Relative impact of covariates in prescribing warfarin according to CYP2C9 genotype.	Warfarin	45-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
15229460-9	2004	After 7 simulated daily doses, significant differences were observed between CYP2C9*1/*1 and CYP2C9*1/*3 individuals in relation to the minimum plasma (trough) tenoxicam concentration (Cmin, 5.2 +/- 1.3 microg x mL(-1) versus 7.6 +/- 2.6 microg x mL(-1); P = .021), maximum tenoxicam plasma concentration (Cmax, 7.4 +/- 1.9 microg x mL(-1) versus 10.5 +/- 3.0 microg x mL(-1); P = .020), and 24-hour AUC (152 +/- 39 microg x mL(-1) x h versus 219 +/- 72 microg x mL(-1) x h).	tenoxicam	160-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
15229460-0	2004	CYP2C9 genotypes and the pharmacokinetics of tenoxicam in Brazilians.	tenoxicam	45-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15229460-1	2004	OBJECTIVE: Cytochrome P450 (CYP) 2C9, the product of the polymorphic gene CYP2C9, provides the major catabolic pathway for several anti-inflammatory drugs, including tenoxicam.	tenoxicam	166-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-36
15229460-1	2004	OBJECTIVE: Cytochrome P450 (CYP) 2C9, the product of the polymorphic gene CYP2C9, provides the major catabolic pathway for several anti-inflammatory drugs, including tenoxicam.	tenoxicam	166-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
15229460-8	2004	After a single dose of tenoxicam, the area under the plasma concentration-time curve (AUC) from time 0 to infinity and the oral clearance of tenoxicam were 190 +/- 48 microg x mL(-1) x h and 113 +/- 30 mL x h(-1), respectively, in wild-type homozygous subjects (CYP2C9*1/*1), as compared with 261 +/- 14 microg x mL(-1) x h (P = .013) and 77 +/- 4 mL x h(-1) (P = .036), respectively, in CYP2C9*1/*2 heterozygous subjects and 335 +/- 126 microg x mL(-1) x h (P = .003) and 67 +/- 23 mL x h(-1) (P = .008) in CYP2C9*1/*3, respectively, heterozygous subjects.	tenoxicam	23-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	262-268
15229460-8	2004	After a single dose of tenoxicam, the area under the plasma concentration-time curve (AUC) from time 0 to infinity and the oral clearance of tenoxicam were 190 +/- 48 microg x mL(-1) x h and 113 +/- 30 mL x h(-1), respectively, in wild-type homozygous subjects (CYP2C9*1/*1), as compared with 261 +/- 14 microg x mL(-1) x h (P = .013) and 77 +/- 4 mL x h(-1) (P = .036), respectively, in CYP2C9*1/*2 heterozygous subjects and 335 +/- 126 microg x mL(-1) x h (P = .003) and 67 +/- 23 mL x h(-1) (P = .008) in CYP2C9*1/*3, respectively, heterozygous subjects.	tenoxicam	23-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	388-394
15229460-8	2004	After a single dose of tenoxicam, the area under the plasma concentration-time curve (AUC) from time 0 to infinity and the oral clearance of tenoxicam were 190 +/- 48 microg x mL(-1) x h and 113 +/- 30 mL x h(-1), respectively, in wild-type homozygous subjects (CYP2C9*1/*1), as compared with 261 +/- 14 microg x mL(-1) x h (P = .013) and 77 +/- 4 mL x h(-1) (P = .036), respectively, in CYP2C9*1/*2 heterozygous subjects and 335 +/- 126 microg x mL(-1) x h (P = .003) and 67 +/- 23 mL x h(-1) (P = .008) in CYP2C9*1/*3, respectively, heterozygous subjects.	tenoxicam	23-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	388-394
15205386-3	2004	In the present study, in vitro enzyme kinetic data were used to predict the in vivo clearance and drug-drug interaction potential of four well known CYP2C9 substrates (tolbutamide, fluvastatin, ibuprofen and diclofenac) that are frequently used as benchmark substances in screening programs.	Tolbutamide	168-179	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
15205386-3	2004	In the present study, in vitro enzyme kinetic data were used to predict the in vivo clearance and drug-drug interaction potential of four well known CYP2C9 substrates (tolbutamide, fluvastatin, ibuprofen and diclofenac) that are frequently used as benchmark substances in screening programs.	Fluvastatin	181-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
15205386-3	2004	In the present study, in vitro enzyme kinetic data were used to predict the in vivo clearance and drug-drug interaction potential of four well known CYP2C9 substrates (tolbutamide, fluvastatin, ibuprofen and diclofenac) that are frequently used as benchmark substances in screening programs.	Ibuprofen	194-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
15205386-3	2004	In the present study, in vitro enzyme kinetic data were used to predict the in vivo clearance and drug-drug interaction potential of four well known CYP2C9 substrates (tolbutamide, fluvastatin, ibuprofen and diclofenac) that are frequently used as benchmark substances in screening programs.	Diclofenac	208-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
15197523-2	2004	Losartan has recently been suggested as a selective probe for CYP2C9 metabolic activity.	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
15197523-3	2004	The aim of the study was to determine the activity of CYP2C9, using losartan as a probe drug, in relation to CYP2C9 genotype in healthy Turkish subjects.	Losartan	68-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
15197523-3	2004	The aim of the study was to determine the activity of CYP2C9, using losartan as a probe drug, in relation to CYP2C9 genotype in healthy Turkish subjects.	Losartan	68-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
15197523-6	2004	Losartan oxidation was also studied in vitro, using human CYP2C8 and CYP2C9 enzymes expressed in yeast.	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
15197523-8	2004	The urinary losartan/E3174 ratio was significantly higher in subjects with CYP2C9*1/*3 genotype (median 2.35, n=12) than in subjects with CYP2C9*1/*1 (0.71, n=58) and *1/*2 (0.85, n=10) genotypes ( P&lt;0.05).	Losartan	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
15197523-8	2004	The urinary losartan/E3174 ratio was significantly higher in subjects with CYP2C9*1/*3 genotype (median 2.35, n=12) than in subjects with CYP2C9*1/*1 (0.71, n=58) and *1/*2 (0.85, n=10) genotypes ( P&lt;0.05).	Losartan	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
15197523-8	2004	The urinary losartan/E3174 ratio was significantly higher in subjects with CYP2C9*1/*3 genotype (median 2.35, n=12) than in subjects with CYP2C9*1/*1 (0.71, n=58) and *1/*2 (0.85, n=10) genotypes ( P&lt;0.05).	losartan carboxylic acid	21-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
15197523-10	2004	CONCLUSION: The urinary losartan to E3174 metabolic ratio after a 25-mg losartan dose was found to be a safe and useful phenotyping assay for CYP2C9 activity in vivo.	Losartan	24-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
15197523-11	2004	CYP2C9*3 variant allele is a major determinant of the enzyme activity, and it decreases losartan metabolism significantly, while CYP2C9*2 allele has less impact on enzyme function.	Losartan	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15197523-11	2004	CYP2C9*3 variant allele is a major determinant of the enzyme activity, and it decreases losartan metabolism significantly, while CYP2C9*2 allele has less impact on enzyme function.	Losartan	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
15349140-2	2004	CYP2C9*2 (Arg144Cys) and *3 (Ile359Leu) have been the most widely studied alleles.	ile359leu	29-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15349140-5	2004	In addition, multiple human studies have demonstrated significant associations between CYP2C9 genotype and the disposition of substrates such as warfarin, phenytoin and various sulfonylureas, angiotensin II receptor blockers and non-steroidal antiinflammatory agents.	Warfarin	145-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
15349140-5	2004	In addition, multiple human studies have demonstrated significant associations between CYP2C9 genotype and the disposition of substrates such as warfarin, phenytoin and various sulfonylureas, angiotensin II receptor blockers and non-steroidal antiinflammatory agents.	Phenytoin	155-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
15349140-5	2004	In addition, multiple human studies have demonstrated significant associations between CYP2C9 genotype and the disposition of substrates such as warfarin, phenytoin and various sulfonylureas, angiotensin II receptor blockers and non-steroidal antiinflammatory agents.	Sulfonylurea Compounds	177-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
15349140-6	2004	Individuals carrying the CYP2C9*2 and *3 alleles also have lower warfarin and phenytoin daily dose requirements, and appear more susceptible to adverse events during the initiation of therapy.	Warfarin	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
15349140-6	2004	Individuals carrying the CYP2C9*2 and *3 alleles also have lower warfarin and phenytoin daily dose requirements, and appear more susceptible to adverse events during the initiation of therapy.	Phenytoin	78-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
15226678-1	2004	OBJECTIVES: Cytochrome P450 (CYP) 2C9 metabolizes about 16% of drugs in current clinical use, including lornoxicam and tolbutamide.	lornoxicam	104-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-37
15226678-1	2004	OBJECTIVES: Cytochrome P450 (CYP) 2C9 metabolizes about 16% of drugs in current clinical use, including lornoxicam and tolbutamide.	Tolbutamide	119-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-37
15213846-0	2004	The risk of bleeding complications in patients with cytochrome P450 CYP2C9*2 or CYP2C9*3 alleles on acenocoumarol or phenprocoumon.	Acenocoumarol	100-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
15213846-0	2004	The risk of bleeding complications in patients with cytochrome P450 CYP2C9*2 or CYP2C9*3 alleles on acenocoumarol or phenprocoumon.	Acenocoumarol	100-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
15213846-0	2004	The risk of bleeding complications in patients with cytochrome P450 CYP2C9*2 or CYP2C9*3 alleles on acenocoumarol or phenprocoumon.	Phenprocoumon	117-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
15213846-1	2004	The principal enzyme involved in coumarin metabolism is CYP2C9.	coumarin	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
15213846-4	2004	It was, therefore, our objective to study the effect of the CYP2C9 polymorphisms on bleeding complications during initiation and maintenance phases of coumarin anticoagulant therapy.	coumarin	151-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
15213846-15	2004	In this study among outpatients of an anticoagulation clinic using acenocoumarol or phenprocoumon, having a variant allele of CYP2C9 was associated with an increased risk of major bleeding events in patients on acenocoumarol, but not in patients on phenprocoumon.	Acenocoumarol	67-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
15213846-15	2004	In this study among outpatients of an anticoagulation clinic using acenocoumarol or phenprocoumon, having a variant allele of CYP2C9 was associated with an increased risk of major bleeding events in patients on acenocoumarol, but not in patients on phenprocoumon.	Phenprocoumon	84-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
15213846-15	2004	In this study among outpatients of an anticoagulation clinic using acenocoumarol or phenprocoumon, having a variant allele of CYP2C9 was associated with an increased risk of major bleeding events in patients on acenocoumarol, but not in patients on phenprocoumon.	Acenocoumarol	211-224	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
15213846-15	2004	In this study among outpatients of an anticoagulation clinic using acenocoumarol or phenprocoumon, having a variant allele of CYP2C9 was associated with an increased risk of major bleeding events in patients on acenocoumarol, but not in patients on phenprocoumon.	Phenprocoumon	249-262	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
15213846-16	2004	Although one might consider the assessment of the CYP2C9 genotype of a patient for dose adjustment before starting treatment with acenocoumarol, a prospective randomised trial should demonstrate whether this reduces the increased risk of major bleeding events.	Acenocoumarol	130-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
15229460-9	2004	After 7 simulated daily doses, significant differences were observed between CYP2C9*1/*1 and CYP2C9*1/*3 individuals in relation to the minimum plasma (trough) tenoxicam concentration (Cmin, 5.2 +/- 1.3 microg x mL(-1) versus 7.6 +/- 2.6 microg x mL(-1); P = .021), maximum tenoxicam plasma concentration (Cmax, 7.4 +/- 1.9 microg x mL(-1) versus 10.5 +/- 3.0 microg x mL(-1); P = .020), and 24-hour AUC (152 +/- 39 microg x mL(-1) x h versus 219 +/- 72 microg x mL(-1) x h).	tenoxicam	160-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
15229460-12	2004	Heterozygosis for CYP2C9*3, and to a lesser degree CYP2C9*2, increases the exposure to tenoxicam during single and repeated doses.	tenoxicam	87-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
15229460-12	2004	Heterozygosis for CYP2C9*3, and to a lesser degree CYP2C9*2, increases the exposure to tenoxicam during single and repeated doses.	tenoxicam	87-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
15180495-4	2004	With in vivo animal models, acute moderate hypoxia (PaO2 of around 35-50 mm Hg) reduces the clearance of drugs biotransformed by CYP1A1, CYP1A2, CYP2B6, CYP2C9, CYP2C19 and CYP2E1, although hypoxia does not affect the clearance of drugs biotransformed by CYP3A6.	pao2	52-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
15672756-6	2004	The relative activity factor approach assumed that NE-098 formation is predominantly catalysed by CYP3A4 and CYP2C9 and the NE-152+163mix (a mixture of two hydroxylated metabolites, NE-152 and NE-163) formation is only catalysed by CYP3A4.	CHEMBL542786	51-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
15196026-5	2004	Torsemide is preferentially metabolized by CYP2C9, and it was anticipated that the mutations in CYP2C8 might increase activity.	Torsemide	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
15196026-9	2004	Mutation of CYP2C8 at position 359 (S359I), a site of genetic polymorphism in CYP2C9, resulted in relatively minor changes in paclitaxel- and torsemide-hydroxylase activities.	Paclitaxel	126-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
15170332-0	2004	Quantitative binding models for CYP2C9 based on benzbromarone analogues.	Benzbromarone	48-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
15170332-2	2004	To uncover the determinants of specificity for cytochrome CYP2C9, a novel library of benzbromarone (bzbr) inhibitors was used to reevaluate its pharmacophore.	Benzbromarone	85-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
15170332-2	2004	To uncover the determinants of specificity for cytochrome CYP2C9, a novel library of benzbromarone (bzbr) inhibitors was used to reevaluate its pharmacophore.	Benzbromarone	100-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
15170358-1	2004	Cytochrome P450 2C9 (CYP2C9)-mediated flurbiprofen 4"-hydroxylation is activated by the presence of dapsone resulting in reduction of the K(m) for flurbiprofen hydroxylation and an increase in V(m).	Flurbiprofen	38-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
15170358-1	2004	Cytochrome P450 2C9 (CYP2C9)-mediated flurbiprofen 4"-hydroxylation is activated by the presence of dapsone resulting in reduction of the K(m) for flurbiprofen hydroxylation and an increase in V(m).	Flurbiprofen	38-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
15170358-1	2004	Cytochrome P450 2C9 (CYP2C9)-mediated flurbiprofen 4"-hydroxylation is activated by the presence of dapsone resulting in reduction of the K(m) for flurbiprofen hydroxylation and an increase in V(m).	Dapsone	100-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
15170358-1	2004	Cytochrome P450 2C9 (CYP2C9)-mediated flurbiprofen 4"-hydroxylation is activated by the presence of dapsone resulting in reduction of the K(m) for flurbiprofen hydroxylation and an increase in V(m).	Dapsone	100-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
15170358-1	2004	Cytochrome P450 2C9 (CYP2C9)-mediated flurbiprofen 4"-hydroxylation is activated by the presence of dapsone resulting in reduction of the K(m) for flurbiprofen hydroxylation and an increase in V(m).	Flurbiprofen	147-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
15170358-1	2004	Cytochrome P450 2C9 (CYP2C9)-mediated flurbiprofen 4"-hydroxylation is activated by the presence of dapsone resulting in reduction of the K(m) for flurbiprofen hydroxylation and an increase in V(m).	Flurbiprofen	147-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
15170358-2	2004	Previous spectral binding studies have demonstrated that the binding of flurbiprofen with CYP2C9 is increased (decrease in K(S)) by the presence of dapsone.	Flurbiprofen	72-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
15170358-2	2004	Previous spectral binding studies have demonstrated that the binding of flurbiprofen with CYP2C9 is increased (decrease in K(S)) by the presence of dapsone.	Dapsone	148-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
15170358-9	2004	Molecular modeling studies were also performed to corroborate the relative orientations of flurbiprofen and dapsone in the active site of CYP2C9.	Flurbiprofen	91-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
15170358-9	2004	Molecular modeling studies were also performed to corroborate the relative orientations of flurbiprofen and dapsone in the active site of CYP2C9.	Dapsone	108-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
15170358-10	2004	Shift of the 4" proton of flurbiprofen closer to the heme iron of CYP2C9 in the presence of dapsone may play a role in activation.	Flurbiprofen	26-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
15170358-10	2004	Shift of the 4" proton of flurbiprofen closer to the heme iron of CYP2C9 in the presence of dapsone may play a role in activation.	Heme	53-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
15170358-10	2004	Shift of the 4" proton of flurbiprofen closer to the heme iron of CYP2C9 in the presence of dapsone may play a role in activation.	Iron	58-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
15170358-10	2004	Shift of the 4" proton of flurbiprofen closer to the heme iron of CYP2C9 in the presence of dapsone may play a role in activation.	Dapsone	92-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
15145963-2	2004	In addition, warfarin S/R ratios are used to assess CYP2C9 activity.	Warfarin	13-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
15145963-11	2004	Single-point and two-point S-warfarin concentrations, but not warfarin S/R ratios, were predictive of S-warfarin AUC(0- infinity ) during CYP2C9 baseline activity and inhibition.	Warfarin	29-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
15145963-14	2004	LSS using S-warfarin concentrations is an efficient and accurate technique to evaluate S-warfarin AUC(0- infinity ) when using warfarin as a CYP2C9 probe drug.	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
15145963-14	2004	LSS using S-warfarin concentrations is an efficient and accurate technique to evaluate S-warfarin AUC(0- infinity ) when using warfarin as a CYP2C9 probe drug.	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
15046773-6	2004	Following exposure to OTA, cells expressing CYP2C9 showed a significant reduction in neutral red (NR) uptake but not in Alamar blue (AB) reduction, as compared to the control LNCX cells which do not express CYP450 enzymes.	Neutral Red	85-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
15046773-8	2004	When pre-treated with l-buthionine S,R-sulphoximine (BSO) to deplete GSH, CYP2C9-expressing cells showed also a loss of cell viability as compared to LNCX cells, although to a lesser extent as compared to non-depleted CYP2C9-expressing cells.	L-Buthionine	22-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
15046773-8	2004	When pre-treated with l-buthionine S,R-sulphoximine (BSO) to deplete GSH, CYP2C9-expressing cells showed also a loss of cell viability as compared to LNCX cells, although to a lesser extent as compared to non-depleted CYP2C9-expressing cells.	L-Buthionine	22-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
15046773-8	2004	When pre-treated with l-buthionine S,R-sulphoximine (BSO) to deplete GSH, CYP2C9-expressing cells showed also a loss of cell viability as compared to LNCX cells, although to a lesser extent as compared to non-depleted CYP2C9-expressing cells.	r-sulphoximine	37-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
15046773-8	2004	When pre-treated with l-buthionine S,R-sulphoximine (BSO) to deplete GSH, CYP2C9-expressing cells showed also a loss of cell viability as compared to LNCX cells, although to a lesser extent as compared to non-depleted CYP2C9-expressing cells.	r-sulphoximine	37-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
15046773-8	2004	When pre-treated with l-buthionine S,R-sulphoximine (BSO) to deplete GSH, CYP2C9-expressing cells showed also a loss of cell viability as compared to LNCX cells, although to a lesser extent as compared to non-depleted CYP2C9-expressing cells.	Buthionine Sulfoximine	53-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
15046773-8	2004	When pre-treated with l-buthionine S,R-sulphoximine (BSO) to deplete GSH, CYP2C9-expressing cells showed also a loss of cell viability as compared to LNCX cells, although to a lesser extent as compared to non-depleted CYP2C9-expressing cells.	Buthionine Sulfoximine	53-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
15046773-8	2004	When pre-treated with l-buthionine S,R-sulphoximine (BSO) to deplete GSH, CYP2C9-expressing cells showed also a loss of cell viability as compared to LNCX cells, although to a lesser extent as compared to non-depleted CYP2C9-expressing cells.	Glutathione	69-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
15175798-1	2004	Two cytochrome P450 2C9 (CYP2C9) polymorphisms, CYP2C9*2 and *3, metabolize warfarin inefficiently.	Warfarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-23
15175798-1	2004	Two cytochrome P450 2C9 (CYP2C9) polymorphisms, CYP2C9*2 and *3, metabolize warfarin inefficiently.	Warfarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
15175798-1	2004	Two cytochrome P450 2C9 (CYP2C9) polymorphisms, CYP2C9*2 and *3, metabolize warfarin inefficiently.	Warfarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
15175798-6	2004	The CYP2C9 polymorphisms independently predicted low warfarin requirements after adjusting for Body Mass Index, age, acetaminophen use, and race (OR 24.80; 95% CI 3.83-160.78).	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
15175798-6	2004	The CYP2C9 polymorphisms independently predicted low warfarin requirements after adjusting for Body Mass Index, age, acetaminophen use, and race (OR 24.80; 95% CI 3.83-160.78).	Acetaminophen	117-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
15175798-10	2004	In conclusion, CYP2C9*2 or *3 compound heterozygotes and homozygotes have low warfarin requirements even after excluding liver disease, excessive alcohol or acetaminophen consumption, low body weight, advancing age, and drug interactions.	Warfarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
15175798-10	2004	In conclusion, CYP2C9*2 or *3 compound heterozygotes and homozygotes have low warfarin requirements even after excluding liver disease, excessive alcohol or acetaminophen consumption, low body weight, advancing age, and drug interactions.	Alcohols	146-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
15175798-10	2004	In conclusion, CYP2C9*2 or *3 compound heterozygotes and homozygotes have low warfarin requirements even after excluding liver disease, excessive alcohol or acetaminophen consumption, low body weight, advancing age, and drug interactions.	Acetaminophen	157-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
15056479-7	2004	CYP2C9, CYP2E1 CYP2C19 and CYP2D6 are engaged to a lesser degree in 5-sulphoxidation, while CYP1A2, CYP3A4 and CYP2D6 in perazine N-demethylation (6-10%, depending on the isoform).	Perazine	121-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15130760-0	2004	Differential activation of CYP2C9 variants by dapsone.	Dapsone	46-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
15130760-1	2004	Studies have shown that CYP2C9.1 mediated metabolism of flurbiprofen or naproxen is activated by co-incubation with dapsone.	Flurbiprofen	56-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
15130760-1	2004	Studies have shown that CYP2C9.1 mediated metabolism of flurbiprofen or naproxen is activated by co-incubation with dapsone.	Naproxen	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
15130760-1	2004	Studies have shown that CYP2C9.1 mediated metabolism of flurbiprofen or naproxen is activated by co-incubation with dapsone.	Dapsone	116-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
15130760-4	2004	Dapsone increased the efficiency (V(m)/K(m)) of flurbiprofen 4"-hydroxylation by CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5 by 8-, 31-, 47-, and 22-fold, respectively.	Dapsone	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
15130760-4	2004	Dapsone increased the efficiency (V(m)/K(m)) of flurbiprofen 4"-hydroxylation by CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5 by 8-, 31-, 47-, and 22-fold, respectively.	Dapsone	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
15130760-4	2004	Dapsone increased the efficiency (V(m)/K(m)) of flurbiprofen 4"-hydroxylation by CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5 by 8-, 31-, 47-, and 22-fold, respectively.	Dapsone	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
15130760-4	2004	Dapsone increased the efficiency (V(m)/K(m)) of flurbiprofen 4"-hydroxylation by CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5 by 8-, 31-, 47-, and 22-fold, respectively.	Dapsone	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
15130760-4	2004	Dapsone increased the efficiency (V(m)/K(m)) of flurbiprofen 4"-hydroxylation by CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5 by 8-, 31-, 47-, and 22-fold, respectively.	Flurbiprofen	48-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
15130760-4	2004	Dapsone increased the efficiency (V(m)/K(m)) of flurbiprofen 4"-hydroxylation by CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5 by 8-, 31-, 47-, and 22-fold, respectively.	Flurbiprofen	48-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
15130760-4	2004	Dapsone increased the efficiency (V(m)/K(m)) of flurbiprofen 4"-hydroxylation by CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5 by 8-, 31-, 47-, and 22-fold, respectively.	Flurbiprofen	48-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
15130760-4	2004	Dapsone increased the efficiency (V(m)/K(m)) of flurbiprofen 4"-hydroxylation by CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5 by 8-, 31-, 47-, and 22-fold, respectively.	Flurbiprofen	48-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
15130760-5	2004	In similar experiments using the substrate naproxen, dapsone increased the efficiency of naproxen demethylation 7-, 15-, 13-, and 22-fold, in CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5, respectively.	Naproxen	43-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
15130760-5	2004	In similar experiments using the substrate naproxen, dapsone increased the efficiency of naproxen demethylation 7-, 15-, 13-, and 22-fold, in CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5, respectively.	Dapsone	53-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
15130760-5	2004	In similar experiments using the substrate naproxen, dapsone increased the efficiency of naproxen demethylation 7-, 15-, 13-, and 22-fold, in CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5, respectively.	Dapsone	53-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	152-158
15130760-5	2004	In similar experiments using the substrate naproxen, dapsone increased the efficiency of naproxen demethylation 7-, 15-, 13-, and 22-fold, in CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5, respectively.	Dapsone	53-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	152-158
15130760-5	2004	In similar experiments using the substrate naproxen, dapsone increased the efficiency of naproxen demethylation 7-, 15-, 13-, and 22-fold, in CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5, respectively.	Dapsone	53-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	152-158
15130760-5	2004	In similar experiments using the substrate naproxen, dapsone increased the efficiency of naproxen demethylation 7-, 15-, 13-, and 22-fold, in CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5, respectively.	Naproxen	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
15130760-5	2004	In similar experiments using the substrate naproxen, dapsone increased the efficiency of naproxen demethylation 7-, 15-, 13-, and 22-fold, in CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5, respectively.	Naproxen	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	152-158
15130760-5	2004	In similar experiments using the substrate naproxen, dapsone increased the efficiency of naproxen demethylation 7-, 15-, 13-, and 22-fold, in CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5, respectively.	Naproxen	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	152-158
15130760-5	2004	In similar experiments using the substrate naproxen, dapsone increased the efficiency of naproxen demethylation 7-, 15-, 13-, and 22-fold, in CYP2C9.1, CYP2C9.2, CYP2C9.3, and CYP2C9.5, respectively.	Naproxen	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	152-158
15130760-6	2004	Also, dapsone normalized naproxen"s kinetic profile from biphasic (CYP2C9.1 and CYP2C9.2) or linear (CYP2C9.3 and CYP2C9.5) to hyperbolic for all variant forms.	Dapsone	6-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
15130760-6	2004	Also, dapsone normalized naproxen"s kinetic profile from biphasic (CYP2C9.1 and CYP2C9.2) or linear (CYP2C9.3 and CYP2C9.5) to hyperbolic for all variant forms.	Dapsone	6-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
15130760-6	2004	Also, dapsone normalized naproxen"s kinetic profile from biphasic (CYP2C9.1 and CYP2C9.2) or linear (CYP2C9.3 and CYP2C9.5) to hyperbolic for all variant forms.	Dapsone	6-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
15130760-6	2004	Also, dapsone normalized naproxen"s kinetic profile from biphasic (CYP2C9.1 and CYP2C9.2) or linear (CYP2C9.3 and CYP2C9.5) to hyperbolic for all variant forms.	Dapsone	6-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
15130760-6	2004	Also, dapsone normalized naproxen"s kinetic profile from biphasic (CYP2C9.1 and CYP2C9.2) or linear (CYP2C9.3 and CYP2C9.5) to hyperbolic for all variant forms.	Naproxen	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
15130760-6	2004	Also, dapsone normalized naproxen"s kinetic profile from biphasic (CYP2C9.1 and CYP2C9.2) or linear (CYP2C9.3 and CYP2C9.5) to hyperbolic for all variant forms.	Naproxen	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
15130760-6	2004	Also, dapsone normalized naproxen"s kinetic profile from biphasic (CYP2C9.1 and CYP2C9.2) or linear (CYP2C9.3 and CYP2C9.5) to hyperbolic for all variant forms.	Naproxen	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
15130760-6	2004	Also, dapsone normalized naproxen"s kinetic profile from biphasic (CYP2C9.1 and CYP2C9.2) or linear (CYP2C9.3 and CYP2C9.5) to hyperbolic for all variant forms.	Naproxen	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
15130760-7	2004	Thus, amino acid substitutions of CYP2C9 variants affect the degree of dapsone activation in a genotype-dependent fashion.	Dapsone	71-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
15133536-3	2004	Tolbutamide 4-methylhydroxylation and testosterone 6beta-hydroxylation were used as index reactions of CYP2C9 or CYP3A4 catalytic activities, respectively.	Tolbutamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
15133536-8	2004	Ginsenoside Rd also had significant inhibitory potency on both CYP2C9- and CYP3A4-mediated index reactions with IC(50) values of 105 and 62 micromol/L, respectively.	Ginsenosides	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
15133536-11	2004	Our findings suggest that quercetin and ginsenoside Rd have the potential to interact with conventional medicines that are metabolized by CYP2C9 and CYP3A4 in vivo.	Quercetin	26-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
15133536-11	2004	Our findings suggest that quercetin and ginsenoside Rd have the potential to interact with conventional medicines that are metabolized by CYP2C9 and CYP3A4 in vivo.	Ginsenosides	40-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
15039471-0	2004	Warfarin resistance with poor CYP2C9 activity and CYP2C9*1*2 genotype.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
15039471-0	2004	Warfarin resistance with poor CYP2C9 activity and CYP2C9*1*2 genotype.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
15108219-8	2004	Thus, DEX interacts with CYP2C9 both as inhibitor (K(i)=69.0 microM) and as substrate in vitro.	dexloxiglumide	6-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
15116049-0	2004	CYP2C9 and oral anticoagulation therapy with acenocoumarol and warfarin: similarities yet differences.	Warfarin	63-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15116052-1	2004	OBJECTIVE: Our objective was to assess whether there is an association between the presence of allelic variants of the gene for cytochrome P450 (CYP) 2C9 and anticoagulation problems during the initial 3 to 6 months of acenocoumarol treatment.	Acenocoumarol	219-232	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-153
15116052-10	2004	CYP2C9 genotyping could be useful to identify potential candidates for more frequent INR controls to minimize problems with acenocoumarol anticoagulation status.	Acenocoumarol	124-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15116053-1	2004	OBJECTIVE: The aim of this study was to investigate the respective contribution of the different cytochrome P450 (CYP) 2C9 genetic polymorphisms to the interindividual variability of acenocoumarol pharmacodynamic response.	Acenocoumarol	183-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-122
15116053-4	2004	Finally, CYP2C9 phenotype was evaluated after a single oral dose of 4 mg of acenocoumarol.	Acenocoumarol	76-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
15116053-6	2004	RESULTS: The CYP2C9*3 allele was the only nonsynonymous single nucleotide polymorphism (SNP) influencing acenocoumarol pharmacodynamics; the percentages of remaining factor VII were 60% +/- 19%, 39% +/- 17%, and 17% for CYP2C9*1/CYP2C9*1, CYP2C9*1/CYP2C9*3, and CYP2C9*3/CYP2C9*3 subjects, respectively (P =.001).	Acenocoumarol	105-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
15116053-9	2004	The haplotype that contains the CYP2C9*3 allele was the only one influencing acenocoumarol pharmacodynamics, explaining 14.3% of its interindividual variability.	Acenocoumarol	77-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
15116053-11	2004	CONCLUSION: Overall, CYP2C9-related genetic variability accounts for 14% of the interindividual variability in acenocoumarol pharmacodynamic response.	Acenocoumarol	111-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
15100169-5	2004	In CYP2C9 phenotyping with losartan, three subpopulations were distinguished that differed in the number of CYP2C9*3 alleles (0, 1, or 2).	Losartan	27-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	3-9
15100169-6	2004	A three-fold higher metabolic ratio (MR; urinary losartan/carboxymetabolite) was found comparing CYP2C9*1/*3 (n = 20) to CYP2C9*1/*1 (n = 81), but there was considerable variation within each genotype.	Losartan	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
15100169-6	2004	A three-fold higher metabolic ratio (MR; urinary losartan/carboxymetabolite) was found comparing CYP2C9*1/*3 (n = 20) to CYP2C9*1/*1 (n = 81), but there was considerable variation within each genotype.	Losartan	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
15100169-7	2004	Subjects genotyped as CYP2C9*1/*1, but with an unexpectedly slow oxidation of losartan, were selected for DNA-sequencing analysis of the CYP2C9 gene.	Losartan	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
15100169-9	2004	However, sequencing of the CYP2C9 gene was also carried out in patients genotyped as CYP2C9*1/*1 but with an exceptionally low steady-state clearance of S-warfarin.	Warfarin	155-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
15100169-9	2004	However, sequencing of the CYP2C9 gene was also carried out in patients genotyped as CYP2C9*1/*1 but with an exceptionally low steady-state clearance of S-warfarin.	Warfarin	155-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
15370959-6	2004	Both pranlukast and zafirlukast showed moderate inhibition of CYP2C9-catalysed tolbutamide 4-methylhydroxylation, competitively inhibiting tolbutamide 4-methylhydroxylation with estimated mean K(i) values of 3.82 +/- 0.50 and 5.86 +/- 0.08 microM, respectively.	pranlukast	5-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
15024534-0	2004	Genetic polymorphism of cytochrome P450 2C9 in diphenylhydantoin-induced cutaneous adverse drug reactions.	Phenytoin	47-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-43
15024534-3	2004	Genetic polymorphisms leading to altered metabolic processes of cytochrome P(450) (CYP) 2C9, a main metabolic enzyme for DPH, may be the pathological mechanism for certain cases of DPH-induced CADRs.	Phenytoin	121-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-91
15024534-3	2004	Genetic polymorphisms leading to altered metabolic processes of cytochrome P(450) (CYP) 2C9, a main metabolic enzyme for DPH, may be the pathological mechanism for certain cases of DPH-induced CADRs.	Phenytoin	181-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-91
15024534-4	2004	OBJECTIVE: To examine the effects of an altered CYP2C9 variant, CYP2C9*3, on DPH-induced CADRs.	Phenytoin	77-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
15024534-4	2004	OBJECTIVE: To examine the effects of an altered CYP2C9 variant, CYP2C9*3, on DPH-induced CADRs.	Phenytoin	77-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
15024534-5	2004	METHODS: Ten patients with DPH-induced CADRs were examined for CYP2C9 genetic polymorphisms.	Phenytoin	27-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
15024534-8	2004	RESULTS: A heterozygous CYP2C9*3 variant was found in three of the 10 DPH-induced CADR patients.	Phenytoin	70-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
15024534-13	2004	CONCLUSION: A CYP2C9*3 variant could play a role in the proportion of patients with DPH-induced CADRs that differ from patients with DPH-induced CADRs showing positive patch-test results.	Phenytoin	84-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
15024534-13	2004	CONCLUSION: A CYP2C9*3 variant could play a role in the proportion of patients with DPH-induced CADRs that differ from patients with DPH-induced CADRs showing positive patch-test results.	Phenytoin	133-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
15045499-0	2004	Cytochrome P450 2C9 phenotyping using low-dose tolbutamide.	Tolbutamide	47-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
15045499-1	2004	OBJECTIVES: The hypoglycaemic drug tolbutamide is used for assessment of CYP2C9 activity in vivo.	Tolbutamide	35-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
15045499-2	2004	However, therapeutically active doses of 500 mg bear the risk of hypoglycaemia, and a tolbutamide-derived parameter based on a single plasma or urine concentration reflecting CYP2C9 activity accurately is lacking.	Tolbutamide	86-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	175-181
15045499-9	2004	CONCLUSIONS: A low dose of 125 mg tolbutamide can safely and accurately be used for CYP2C9 phenotyping.	Tolbutamide	34-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
15045499-10	2004	As a simple metric for CYP2C9 activity, we propose to determine tolbutamide in plasma 24 h after drug intake.	Tolbutamide	64-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
15118259-6	2004	(14)C-Pitavastatin is metabolized with CYP2C9 to 8-hydroxy derivative, but its Vmax /Km was about 2 micro l/min/mg, about 1/8 to 1/100 in comparison to the reported values of other statins, indicating that pitavastatin is hardly metabolized.	c-pitavastatin	4-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
15370959-6	2004	Both pranlukast and zafirlukast showed moderate inhibition of CYP2C9-catalysed tolbutamide 4-methylhydroxylation, competitively inhibiting tolbutamide 4-methylhydroxylation with estimated mean K(i) values of 3.82 +/- 0.50 and 5.86 +/- 0.08 microM, respectively.	zafirlukast	20-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
15370959-6	2004	Both pranlukast and zafirlukast showed moderate inhibition of CYP2C9-catalysed tolbutamide 4-methylhydroxylation, competitively inhibiting tolbutamide 4-methylhydroxylation with estimated mean K(i) values of 3.82 +/- 0.50 and 5.86 +/- 0.08 microM, respectively.	Tolbutamide	79-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
15370959-6	2004	Both pranlukast and zafirlukast showed moderate inhibition of CYP2C9-catalysed tolbutamide 4-methylhydroxylation, competitively inhibiting tolbutamide 4-methylhydroxylation with estimated mean K(i) values of 3.82 +/- 0.50 and 5.86 +/- 0.08 microM, respectively.	Tolbutamide	139-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
15370959-12	2004	The results suggest that like zafirlukast, pranlukast also has the potential moderately to inhibit CYP2C9-catalysed tolbutamide 4-methylhydroxylation.	pranlukast	43-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
15370959-12	2004	The results suggest that like zafirlukast, pranlukast also has the potential moderately to inhibit CYP2C9-catalysed tolbutamide 4-methylhydroxylation.	Tolbutamide	116-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
15370959-13	2004	Therefore, the inhibitory potential of pranlukast should be considered when it is co-administered with CYP2C9 substrates with narrow therapeutic ranges (e.g. S-warfarin, phenytoin).	pranlukast	39-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
15370961-0	2004	Stereoselective glucuronidation and hydroxylation of etodolac by UGT1A9 and CYP2C9 in man.	Etodolac	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
15370961-8	2004	Of several human P450 enzymes, CYP2C9 had the greatest activity for hydroxylation of R-etodolac.	Etodolac	85-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
15370961-9	2004	Sulfaphenazole, an inhibitor of CYP2C9, and anti-CYP2C9 antibody inhibited the hydroxylation of R-etodolac in human liver microsomes.	Sulfaphenazole	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
15370961-9	2004	Sulfaphenazole, an inhibitor of CYP2C9, and anti-CYP2C9 antibody inhibited the hydroxylation of R-etodolac in human liver microsomes.	Etodolac	96-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
15370961-9	2004	Sulfaphenazole, an inhibitor of CYP2C9, and anti-CYP2C9 antibody inhibited the hydroxylation of R-etodolac in human liver microsomes.	Etodolac	96-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
15370961-10	2004	CYP2C9 therefore contributes to the stereoselective hydroxylation of R-etodolac.	Etodolac	69-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
14656880-0	2004	Association of pharmacokinetic (CYP2C9) and pharmacodynamic (factors II, VII, IX, and X; proteins S and C; and gamma-glutamyl carboxylase) gene variants with warfarin sensitivity.	Warfarin	158-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
15070684-0	2004	5"-Flanking region polymorphisms of CYP2C9 and their relationship to S-warfarin metabolism in white and Japanese patients.	Warfarin	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
15070684-1	2004	White and Japanese patients require different warfarin dosages to achieve therapeutic anticoagulation, but this can be only partly explained by genetic variability in the coding region of CYP2C9-a critical enzyme in the drug"s metabolism.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	188-194
15070684-2	2004	Accordingly, analysis of the -2.1-kb 5"-flanking region of CYP2C9 was undertaken in 22 white and 38 Japanese patients whose unbound oral clearance of S-warfarin had been previously determined.	Warfarin	150-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
15135088-11	2004	Diclofenac efficiently inhibited CYP2C9 and to a less extent CYP3A4 enzyme.	Diclofenac	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
15094935-1	2004	The objective of this study was to report 2 cases of CYP2C9 genetic polymorphism and elevated warfarin S:R ratios in patients taking low doses of warfarin, and compare the observed characteristics with those in published reports.	Warfarin	146-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
15094935-6	2004	This report of a CYP2C9*3 heterozygous individual taking a low dose of warfarin is consistent with previous reports in the literature.	Warfarin	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
15094935-7	2004	This summary of a CYP2C9*6 homozygous individual taking a low dose of warfarin is the first such published report.	Warfarin	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
15094935-8	2004	CYP2C9 genotyping in these patients provided a likely explanation for their continued low warfarin dosage requirements.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15094935-9	2004	Awareness of a patient"s CYP2C9 genotype may provide an explanation for low warfarin dosage requirements in stable patients and may help in determining the optimal dose in patients being initiated on warfarin.	Warfarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
15094935-9	2004	Awareness of a patient"s CYP2C9 genotype may provide an explanation for low warfarin dosage requirements in stable patients and may help in determining the optimal dose in patients being initiated on warfarin.	Warfarin	200-208	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
14656880-6	2004	Multiple regression analysis revealed that warfarin sensitivity was independently associated with -402G-->A, (CAA repeat)n, CYP2C9*3, and 165Thr-->Met, which accounted for 50% of variance.	Warfarin	43-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
15051744-12	2004	Since this isozyme had the lowest in vitro IC(50) values for the cytochrome P450s most commonly involved with the metabolism of drugs (CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4), azimilide-related drug interactions mediated via these isozymes are not anticipated.	azimilide	181-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
15039296-0	2004	Assessment of arginine 97 and lysine 72 as determinants of substrate specificity in cytochrome P450 2C9 (CYP2C9).	Arginine	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-103
15039296-0	2004	Assessment of arginine 97 and lysine 72 as determinants of substrate specificity in cytochrome P450 2C9 (CYP2C9).	Arginine	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
15039296-0	2004	Assessment of arginine 97 and lysine 72 as determinants of substrate specificity in cytochrome P450 2C9 (CYP2C9).	Lysine	30-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-103
15039296-0	2004	Assessment of arginine 97 and lysine 72 as determinants of substrate specificity in cytochrome P450 2C9 (CYP2C9).	Lysine	30-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
14739663-4	2004	The major enzyme involved in the metabolism of acenocoumarol in man is CYP2C9.	Acenocoumarol	47-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
15050794-1	2004	PURPOSE: Allelic variants of the gene coding for cytochrome P450 isoform 2C9 (CYP2C9), 2C9*2 and 2C9*3, were shown to increase sensitivity to warfarin in adults.	Warfarin	142-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-76
14722322-9	2004	Treatment with 10 microM rifampin resulted in increases in CYP3A4 mRNA (17-fold) and activity (6-beta-hydroxytestoterone formation, 9-fold); and in CYP2C9 mRNA (4-fold) and activity (4"-hydroxydiclofenac formation, 2-fold).	Rifampin	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
15050794-1	2004	PURPOSE: Allelic variants of the gene coding for cytochrome P450 isoform 2C9 (CYP2C9), 2C9*2 and 2C9*3, were shown to increase sensitivity to warfarin in adults.	Warfarin	142-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
15050794-3	2004	The aim of our purpose was to investigate whether a genetic factor, such as cyp2c9 genotype, does influence the warfarin maintenance dose in very elderly patients.	Warfarin	112-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
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.	Rifampin	35-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	177-183
15268978-10	2004	Recombinant CYP3A4, CYP3A5, CYP2C9 and CYP2D6, but not CYP1A2, catalysed norhydromorphone formation, whereas none of these enzymes was active in dihydroisomorphine formation.	norhydromorphone	73-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
15268978-10	2004	Recombinant CYP3A4, CYP3A5, CYP2C9 and CYP2D6, but not CYP1A2, catalysed norhydromorphone formation, whereas none of these enzymes was active in dihydroisomorphine formation.	Dihydroisomorphine	145-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
15268978-12	2004	In summary, CYP3A and, to a lesser extent, CYP2C9 catalysed hydromorphone N-demethylation in human liver microsomes.	Hydromorphone	60-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
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 9	Homo sapiens	177-183
15001971-1	2004	OBJECTIVE: Variant alleles of the CYP2C9 gene encoding the cytochrome P450 (CYP) enzyme (2C9*2 [Arg144Cys] and 2C9*3 [Ile359Leu]) are known to increase the anticoagulant effect of warfarin and decrease the mean daily dose required to maintain the international normalized ratio (INR) of the prothrombin time within the target therapeutic range.	Warfarin	180-188	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
15001971-7	2004	CONCLUSIONS: The requirement of smaller doses of warfarin in relation to CYP2C9 polymorphisms is already manifest on the fourth day of treatment, at the time of the first INR estimate.	Warfarin	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
15001972-0	2004	Contribution of age, body size, and CYP2C9 genotype to anticoagulant response to warfarin.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
15001972-1	2004	OBJECTIVE: Our objective was to assess the contribution of CYP2C9 genotype, age, body size, and vitamin K and lipid status to warfarin dose requirements.	Warfarin	126-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
15001972-10	2004	CYP2C9 genotype had a significant effect on S-warfarin clearance (r = 0.34, P &lt;.0001) but none on R-warfarin clearance.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15001972-11	2004	CONCLUSION: This study showed that age and CYP2C9 polymorphism affect warfarin dose requirements in patients receiving long-term therapy and having stable control of anticoagulation.	Warfarin	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
15001972-12	2004	It is anticipated that using dosing regimens modified to take into account the contribution of age and CYP2C9 genotype has the potential to improve the safety of warfarin therapy.	Warfarin	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
15058617-6	2004	Other dental therapeutic agents are substrates for CYP2C9 (celecoxib, ibuprofen and naproxen), CYP2D6 (codeine and tramadol), CYP3A4 (methylprednisolone) and CYP2E1 (acetaminophen).	Celecoxib	59-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
14977868-7	2004	Moreover, sulfaphenazole, a CYP2C9 competitive inhibitor, inhibited disulfoton sulfoxidation by CYP2C9 (IC50 0.84 microM) as well as in HLMs.	Sulfaphenazole	10-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
14977868-7	2004	Moreover, sulfaphenazole, a CYP2C9 competitive inhibitor, inhibited disulfoton sulfoxidation by CYP2C9 (IC50 0.84 microM) as well as in HLMs.	Sulfaphenazole	10-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
14977868-7	2004	Moreover, sulfaphenazole, a CYP2C9 competitive inhibitor, inhibited disulfoton sulfoxidation by CYP2C9 (IC50 0.84 microM) as well as in HLMs.	Disulfoton	68-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
14977868-7	2004	Moreover, sulfaphenazole, a CYP2C9 competitive inhibitor, inhibited disulfoton sulfoxidation by CYP2C9 (IC50 0.84 microM) as well as in HLMs.	Disulfoton	68-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
15048614-3	2004	The present study was aimed to evaluate the possible inhibition of CYP2D6 during haloperidol treatment, and to determine the effect of CYP2D6 and CYP2C9 genotypes on the plasma concentration of haloperidol.	Haloperidol	194-205	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
14718257-0	2004	5-Hydroxytryptamine is biotransformed by CYP2C9, 2C19 and 2B6 to hydroxylamine, which is converted into nitric oxide.	Serotonin	0-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
14970873-8	2004	In conclusion, the detected presence of CYP3A4 and CYP2C9 in breast tumours offers the possibility of intratumoral turnover of ifosfamide.	Ifosfamide	127-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
14717783-6	2004	There was no correlation between warfarin daily dose and average daily dietary vitamin K intake when calculated over 28 d. The regression model for warfarin dose showed that, while dietary vitamin K had no effect, CYP2C9 genotype (P = 2%) and age (P &lt; 1%) significantly contributed to inter-patient variability in warfarin dose requirements.	Warfarin	148-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	214-220
14717783-6	2004	There was no correlation between warfarin daily dose and average daily dietary vitamin K intake when calculated over 28 d. The regression model for warfarin dose showed that, while dietary vitamin K had no effect, CYP2C9 genotype (P = 2%) and age (P &lt; 1%) significantly contributed to inter-patient variability in warfarin dose requirements.	Warfarin	148-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	214-220
15049511-0	2004	Inhibitory effects of the monoamine oxidase inhibitor tranylcypromine on the cytochrome P450 enzymes CYP2C19, CYP2C9, and CYP2D6.	Tranylcypromine	54-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
15049511-2	2004	The inhibitory effects of tranylcypromine, a nonselective irreversible inhibitor of monoamine oxidase (MAO), on three cytochrome P450 (CYP) enzymes, namely CYP2C9, CYP2C19, and CYP2D6, have been evaluated in vitro.	Tranylcypromine	26-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
15049511-9	2004	The results demonstrated that tranylcypromine is a competitive inhibitor of CYP2C19 (Ki = 32 microM) and CYP2D6 (Ki = 367 microM) and a noncompetitive inhibitor of CYP2C9 (Ki = 56 microM).	Tranylcypromine	30-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	164-170
14718257-0	2004	5-Hydroxytryptamine is biotransformed by CYP2C9, 2C19 and 2B6 to hydroxylamine, which is converted into nitric oxide.	Hydroxylamine	65-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
14718257-0	2004	5-Hydroxytryptamine is biotransformed by CYP2C9, 2C19 and 2B6 to hydroxylamine, which is converted into nitric oxide.	Nitric Oxide	104-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
15499170-10	2004	On the other hand, bergamottin showed time-dependent decreases in IC(50) for CYP1A2, CYP 2C9, CYP 2C19, CYP 2D6 and CYP 3A4, suggesting that bergamottin is a quasi-irrversible or an irreversible inhibitor of the 5 CYP isoforms.	bergamottin	19-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-92
15499170-10	2004	On the other hand, bergamottin showed time-dependent decreases in IC(50) for CYP1A2, CYP 2C9, CYP 2C19, CYP 2D6 and CYP 3A4, suggesting that bergamottin is a quasi-irrversible or an irreversible inhibitor of the 5 CYP isoforms.	bergamottin	141-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-92
14726986-9	2004	Among patients with two CYP2D6 active genes, the dose-corrected plasma concentrations of fluoxetine and active moiety (fluoxetine plus norfluoxetine) were significantly ( P&lt;0.05) higher in the CYP2C9*1/*2 and CYP2C9*1/*3 genotype groups than in CYP2C9*1/*1.	norfluoxetine	135-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
14726986-9	2004	Among patients with two CYP2D6 active genes, the dose-corrected plasma concentrations of fluoxetine and active moiety (fluoxetine plus norfluoxetine) were significantly ( P&lt;0.05) higher in the CYP2C9*1/*2 and CYP2C9*1/*3 genotype groups than in CYP2C9*1/*1.	norfluoxetine	135-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
14726986-2	2004	CYP2C9 has also been shown to influence the metabolism of fluoxetine in vitro; however, this relationship has not been studied in humans.	Fluoxetine	58-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
14726986-9	2004	Among patients with two CYP2D6 active genes, the dose-corrected plasma concentrations of fluoxetine and active moiety (fluoxetine plus norfluoxetine) were significantly ( P&lt;0.05) higher in the CYP2C9*1/*2 and CYP2C9*1/*3 genotype groups than in CYP2C9*1/*1.	norfluoxetine	135-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
14726986-3	2004	The aim of the present study was to evaluate the influence of CYP2D6 and CYP2C9 genotypes on the plasma concentration of fluoxetine and norfluoxetine in psychiatric patients during steady-state conditions.	Fluoxetine	121-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
14726986-11	2004	CONCLUSION: The present results show that CYP2D6 and potentially CYP2C9 genotypes seem to influence fluoxetine plasma concentration during steady-state conditions in patients.	Fluoxetine	100-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
14726986-3	2004	The aim of the present study was to evaluate the influence of CYP2D6 and CYP2C9 genotypes on the plasma concentration of fluoxetine and norfluoxetine in psychiatric patients during steady-state conditions.	norfluoxetine	136-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
14747429-9	2004	As fluconazole is a strong inhibitor of cytochrome P450 (CYP) 2C9, other CYP2C9 inhibitors are unlikely to affect lumiracoxib pharmacokinetics with clinical relevance, making dosage adjustment unnecessary.	Fluconazole	3-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-65
14726986-9	2004	Among patients with two CYP2D6 active genes, the dose-corrected plasma concentrations of fluoxetine and active moiety (fluoxetine plus norfluoxetine) were significantly ( P&lt;0.05) higher in the CYP2C9*1/*2 and CYP2C9*1/*3 genotype groups than in CYP2C9*1/*1.	Fluoxetine	89-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
14726986-9	2004	Among patients with two CYP2D6 active genes, the dose-corrected plasma concentrations of fluoxetine and active moiety (fluoxetine plus norfluoxetine) were significantly ( P&lt;0.05) higher in the CYP2C9*1/*2 and CYP2C9*1/*3 genotype groups than in CYP2C9*1/*1.	Fluoxetine	89-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
14726986-9	2004	Among patients with two CYP2D6 active genes, the dose-corrected plasma concentrations of fluoxetine and active moiety (fluoxetine plus norfluoxetine) were significantly ( P&lt;0.05) higher in the CYP2C9*1/*2 and CYP2C9*1/*3 genotype groups than in CYP2C9*1/*1.	Fluoxetine	89-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
14726986-9	2004	Among patients with two CYP2D6 active genes, the dose-corrected plasma concentrations of fluoxetine and active moiety (fluoxetine plus norfluoxetine) were significantly ( P&lt;0.05) higher in the CYP2C9*1/*2 and CYP2C9*1/*3 genotype groups than in CYP2C9*1/*1.	Fluoxetine	119-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
14726986-9	2004	Among patients with two CYP2D6 active genes, the dose-corrected plasma concentrations of fluoxetine and active moiety (fluoxetine plus norfluoxetine) were significantly ( P&lt;0.05) higher in the CYP2C9*1/*2 and CYP2C9*1/*3 genotype groups than in CYP2C9*1/*1.	Fluoxetine	119-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
14726986-9	2004	Among patients with two CYP2D6 active genes, the dose-corrected plasma concentrations of fluoxetine and active moiety (fluoxetine plus norfluoxetine) were significantly ( P&lt;0.05) higher in the CYP2C9*1/*2 and CYP2C9*1/*3 genotype groups than in CYP2C9*1/*1.	Fluoxetine	119-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
15066644-0	2004	Warfarin therapy is feasible in CYP2C9*3 homozygous patients.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
15066644-1	2004	Background: Patients carrying variant CYP2C9 alleles are prone to bleeding complications under standard warfarin treatment.	Warfarin	104-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
14600250-8	2004	This is the first report to demonstrate that the nuclear receptor PXR mediates induction of CYP2C9 with rifampicin, phenobarbital, and hyperforin.	hyperforin	135-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
14600250-0	2004	Induction of human CYP2C9 by rifampicin, hyperforin, and phenobarbital is mediated by the pregnane X receptor.	Rifampin	29-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
14610241-2	2004	Initially, the potential of atomoxetine and its two metabolites, N-desmethylatomoxetine and 4-hydroxyatomoxetine, to inhibit the metabolism of probe substrates for CYP1A2, CYP2C9, CYP2D6, and CYP3A was evaluated in human hepatic microsomes.	Atomoxetine Hydrochloride	28-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
14600250-0	2004	Induction of human CYP2C9 by rifampicin, hyperforin, and phenobarbital is mediated by the pregnane X receptor.	hyperforin	41-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
14600250-0	2004	Induction of human CYP2C9 by rifampicin, hyperforin, and phenobarbital is mediated by the pregnane X receptor.	Phenobarbital	57-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
14600250-1	2004	Human CYP2C9 is important in the metabolism of numerous clinically used drugs such as the anticoagulant warfarin, the anticonvulsant phenytoin, antidiabetic drugs such as tolbutamide and glipizide, the hypertensive agent losartan, and numerous nonsteroidal anti-inflammatory drugs.	Warfarin	104-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
14600250-1	2004	Human CYP2C9 is important in the metabolism of numerous clinically used drugs such as the anticoagulant warfarin, the anticonvulsant phenytoin, antidiabetic drugs such as tolbutamide and glipizide, the hypertensive agent losartan, and numerous nonsteroidal anti-inflammatory drugs.	Phenytoin	133-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
14600250-1	2004	Human CYP2C9 is important in the metabolism of numerous clinically used drugs such as the anticoagulant warfarin, the anticonvulsant phenytoin, antidiabetic drugs such as tolbutamide and glipizide, the hypertensive agent losartan, and numerous nonsteroidal anti-inflammatory drugs.	Tolbutamide	171-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
14600250-1	2004	Human CYP2C9 is important in the metabolism of numerous clinically used drugs such as the anticoagulant warfarin, the anticonvulsant phenytoin, antidiabetic drugs such as tolbutamide and glipizide, the hypertensive agent losartan, and numerous nonsteroidal anti-inflammatory drugs.	Glipizide	187-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
14600250-1	2004	Human CYP2C9 is important in the metabolism of numerous clinically used drugs such as the anticoagulant warfarin, the anticonvulsant phenytoin, antidiabetic drugs such as tolbutamide and glipizide, the hypertensive agent losartan, and numerous nonsteroidal anti-inflammatory drugs.	Losartan	221-229	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
14600250-2	2004	Several studies have reported that certain drugs such as rifampicin and phenobarbital induce CYP2C9, but the molecular basis for this induction remains unknown.	Rifampin	57-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
14600250-2	2004	Several studies have reported that certain drugs such as rifampicin and phenobarbital induce CYP2C9, but the molecular basis for this induction remains unknown.	Phenobarbital	72-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
14600250-3	2004	In the present study, we demonstrate that the human pregnane X receptor (hPXR) mediates induction of CYP2C9 by the prototype drugs rifampicin, hyperforin (found in St. John"s Wart), and phenobarbital.	Rifampin	131-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
14600250-3	2004	In the present study, we demonstrate that the human pregnane X receptor (hPXR) mediates induction of CYP2C9 by the prototype drugs rifampicin, hyperforin (found in St. John"s Wart), and phenobarbital.	hyperforin	143-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
14600250-3	2004	In the present study, we demonstrate that the human pregnane X receptor (hPXR) mediates induction of CYP2C9 by the prototype drugs rifampicin, hyperforin (found in St. John"s Wart), and phenobarbital.	Phenobarbital	186-199	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
14600250-4	2004	Deletion and mutagenesis studies with luciferase reporter constructs showed that a functional PXR-responsive element located -1839/-1824 base pairs upstream from the translation start site was the primary binding site mediating the rifampicin induction of CYP2C9.	Rifampin	232-242	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	256-262
14610241-2	2004	Initially, the potential of atomoxetine and its two metabolites, N-desmethylatomoxetine and 4-hydroxyatomoxetine, to inhibit the metabolism of probe substrates for CYP1A2, CYP2C9, CYP2D6, and CYP3A was evaluated in human hepatic microsomes.	N-desmethylatomoxetine	65-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
14600250-6	2004	Mutational analysis of 3- and 12-kilobase CYP2C9 promoter fragments indicated that this proximal binding site was essential for rifampicin inducibility, although a cooperative effect could be attributed to a second CAR-RE located at -2899/-2883.	Rifampin	128-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
14600250-7	2004	In summary, we have demonstrated rifampicin induction of CYP2C9 promoter constructs that is consistent with the magnitude of induction of CYP2C9 protein and mRNA reported in vivo and in primary human hepatocytes, and we have identified the cis-element essential for this response.	Rifampin	33-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
14600250-7	2004	In summary, we have demonstrated rifampicin induction of CYP2C9 promoter constructs that is consistent with the magnitude of induction of CYP2C9 protein and mRNA reported in vivo and in primary human hepatocytes, and we have identified the cis-element essential for this response.	Rifampin	33-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
14600250-8	2004	This is the first report to demonstrate that the nuclear receptor PXR mediates induction of CYP2C9 with rifampicin, phenobarbital, and hyperforin.	Rifampin	104-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
14610241-2	2004	Initially, the potential of atomoxetine and its two metabolites, N-desmethylatomoxetine and 4-hydroxyatomoxetine, to inhibit the metabolism of probe substrates for CYP1A2, CYP2C9, CYP2D6, and CYP3A was evaluated in human hepatic microsomes.	4-hydroxyatomoxetine	92-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
14600250-8	2004	This is the first report to demonstrate that the nuclear receptor PXR mediates induction of CYP2C9 with rifampicin, phenobarbital, and hyperforin.	Phenobarbital	116-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
14985143-0	2004	CYP2C subfamily, primarily CYP2C9, catalyses the enantioselective demethylation of the endocrine disruptor pesticide methoxychlor in human liver microsomes: use of inhibitory monoclonal antibodies in P450 identification.	Methoxychlor	117-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
14970301-0	2004	Warfarin and celecoxib interaction in the setting of cytochrome P450 (CYP2C9) polymorphism with bleeding complication.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
14970301-0	2004	Warfarin and celecoxib interaction in the setting of cytochrome P450 (CYP2C9) polymorphism with bleeding complication.	Celecoxib	13-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
14970301-3	2004	As the CYP2C9 enzyme metabolises these drugs, it was determined whether variant alleles were responsible for altering warfarin handling.	Warfarin	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	7-13
14662709-0	2004	Inhibition of cytochrome P450 2C9 improves endothelium-dependent, nitric oxide-mediated vasodilatation in patients with coronary artery disease.	Nitric Oxide	66-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-33
14662709-10	2004	CONCLUSIONS: The CYP 2C9 inhibitor sulfaphenazole enhances endothelium-dependent vasodilator responses in patients with manifest coronary artery disease.	Sulfaphenazole	35-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-24
14662709-11	2004	This effect seems to be related to an increase in the bioavailability of NO, probably as a consequence of an attenuated generation of reactive oxygen species by CYP 2C9 in endothelial cells.	Reactive Oxygen Species	134-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-168
14659971-2	2004	Cytochrome P450 2C (CYP2C) plays an important role in phenytoin metabolism.	Phenytoin	54-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-18
14659971-2	2004	Cytochrome P450 2C (CYP2C) plays an important role in phenytoin metabolism.	Phenytoin	54-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-25
14659971-3	2004	Recently, single nucleotide polymorphisms in the coding region of CYP 2C influencing phenytoin metabolism were identified.	Phenytoin	85-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
14659971-4	2004	The purpose of the present study was to see if CYP 2C polymorphisms might relate to the onset and severity of phenytoin-induced gingival overgrowth.	Phenytoin	110-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
14628297-7	2004	At 10 microg/ml of methadone, CYP2C9 and CYP2D6 also generated EDDP, but in at least 10-fold lower quantities than CYP2B6.	Methadone	19-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
14628297-7	2004	At 10 microg/ml of methadone, CYP2C9 and CYP2D6 also generated EDDP, but in at least 10-fold lower quantities than CYP2B6.	2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine	63-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
15061384-3	2004	The aim of the study was to determine the frequency of the CYP2C9 polymorphism in a representative sample of the Croatian population (n = 177) and to assess the association between the CYP2C9 polymorphism and the warfarin dose in patients with thromboembolism (n = 181).	Warfarin	213-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	185-191
15061384-16	2004	These preliminary results suggest a significant association of the CYP2C9 polymorphism with the warfarin dose and underline the importance of pre-therapeutic genotyping to identify the subjects likely to develop undesirable drug effects.	Warfarin	96-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
14748619-7	2004	Nateglinide is extensively metabolised, primarily by cytochrome P450 2C9, and eliminated primarily by the kidney.	Nateglinide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-72
15005635-0	2004	Influence of CYP2C9 and CYP2D6 polymorphisms on the pharmacokinetics of nateglinide in genotyped healthy volunteers.	Nateglinide	72-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
15005635-2	2004	According to in vitro data, about 70% of nateglinide intrinsic clearance may be mediated by cytochrome P450 (CYP) 2C9 and a smaller fraction by CYP3A4 and CYP2D6.	Nateglinide	41-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-117
15005635-7	2004	RESULTS: Significantly reduced oral nateglinide clearance was found in carriers of CYP2C9*3 alleles, (p &lt; 0.01), whereas carriers of CYP2C9*2 alleles had kinetic parameters similar to those of carriers of the wild-type allele (p = nonsignificant).	Nateglinide	36-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
15005635-10	2004	These differences in nateglinide kinetics due to CYP2C9 genotypes did not result in statistically significant differences in plasma glucose, insulin and glucagon.	Nateglinide	21-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
15005635-11	2004	Pharmacokinetic-pharmacodynamic modelling revealed a minor effect of CYP2C9 genotype on insulin and glucose, and extrapolations indicated that carriers of the CYP2C9*3/*3 genotype may be at a slightly higher risk of hypoglycaemia compared with carriers of CYP2C9*1, particularly when taking nateglinide doses above 120 mg.	Glucose	100-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
15005635-11	2004	Pharmacokinetic-pharmacodynamic modelling revealed a minor effect of CYP2C9 genotype on insulin and glucose, and extrapolations indicated that carriers of the CYP2C9*3/*3 genotype may be at a slightly higher risk of hypoglycaemia compared with carriers of CYP2C9*1, particularly when taking nateglinide doses above 120 mg.	Glucose	100-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
14741071-1	2004	OBJECTIVE: The potential for a drug interaction was investigated between nateglinide, an oral antidiabetic agent, and acenocoumarol, an oral anticoagulant, as these drugs are primarily metabolized via CYP2C9.	Nateglinide	73-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	201-207
15005635-11	2004	Pharmacokinetic-pharmacodynamic modelling revealed a minor effect of CYP2C9 genotype on insulin and glucose, and extrapolations indicated that carriers of the CYP2C9*3/*3 genotype may be at a slightly higher risk of hypoglycaemia compared with carriers of CYP2C9*1, particularly when taking nateglinide doses above 120 mg.	Nateglinide	291-302	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
15005635-11	2004	Pharmacokinetic-pharmacodynamic modelling revealed a minor effect of CYP2C9 genotype on insulin and glucose, and extrapolations indicated that carriers of the CYP2C9*3/*3 genotype may be at a slightly higher risk of hypoglycaemia compared with carriers of CYP2C9*1, particularly when taking nateglinide doses above 120 mg.	Nateglinide	291-302	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
15005635-12	2004	CONCLUSION: The effect of CYP2C9 polymorphisms on nateglinide kinetics may cause a slightly increased risk for hypoglycaemia, which may become relevant in diabetic patients.	Nateglinide	50-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
15509184-13	2004	In vitro data suggest that (R)-bicalutamide has the potential to inhibit CYP3A4 and, to a lesser extent, CYP2C9, 2C19 and 2D6.	(R)-Bicalutamide	27-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
15568889-16	2004	Bosentan decreases exposure to ciclosporin, glibenclamide, simvastatin (and beta-hydroxyacid simvastatin) and (R)- and (S)-warfarin by up to 50% because of induction of CYP3A4 and/or CYP2C9.	Bosentan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	183-189
15568889-20	2004	The possibility of reduced efficacy of CYP2C9 and 3A4 substrates should be considered when coadministered with bosentan.	Bosentan	111-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
14971821-4	2004	The patient was homozygous for the rare CYP2C9*3 allele, which determines the slowest metabolic rate for CYP2C9 enzymatic activity, that is probably involved in the metabolism of leflunomide.	Leflunomide	179-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
14971821-4	2004	The patient was homozygous for the rare CYP2C9*3 allele, which determines the slowest metabolic rate for CYP2C9 enzymatic activity, that is probably involved in the metabolism of leflunomide.	Leflunomide	179-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
14709627-5	2004	The reference inhibitor ketoconazole was less selective and exhibited potent inhibition (IC(50) values &lt;10 microM) for CYP1A1, CYP1B1, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP4F2, and CYP4F12.	Ketoconazole	24-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
14709614-0	2004	Catalytic roles of CYP2C9 and its variants (CYP2C9*2 and CYP2C9*3) in lornoxicam 5"-hydroxylation.	lornoxicam	70-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
14709614-0	2004	Catalytic roles of CYP2C9 and its variants (CYP2C9*2 and CYP2C9*3) in lornoxicam 5"-hydroxylation.	lornoxicam	70-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
14709614-0	2004	Catalytic roles of CYP2C9 and its variants (CYP2C9*2 and CYP2C9*3) in lornoxicam 5"-hydroxylation.	lornoxicam	70-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
14563790-5	2004	Clopidogrel also inhibited CYP2C9, and ticlopidine also inhibited CYP1A2, with lower potency.	Clopidogrel	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
14709614-1	2004	The effects of allelic variants of CYP2C9 (CYP2C9*2 and CYP2C9*3) on lornoxicam 5"-hydroxylation were studied using the corresponding variant protein expressed in baculovirus-infected insect cells and human liver microsomes of known genotypes of CYP2C9.	lornoxicam	69-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
14709614-1	2004	The effects of allelic variants of CYP2C9 (CYP2C9*2 and CYP2C9*3) on lornoxicam 5"-hydroxylation were studied using the corresponding variant protein expressed in baculovirus-infected insect cells and human liver microsomes of known genotypes of CYP2C9.	lornoxicam	69-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
14709614-1	2004	The effects of allelic variants of CYP2C9 (CYP2C9*2 and CYP2C9*3) on lornoxicam 5"-hydroxylation were studied using the corresponding variant protein expressed in baculovirus-infected insect cells and human liver microsomes of known genotypes of CYP2C9.	lornoxicam	69-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
14709614-1	2004	The effects of allelic variants of CYP2C9 (CYP2C9*2 and CYP2C9*3) on lornoxicam 5"-hydroxylation were studied using the corresponding variant protein expressed in baculovirus-infected insect cells and human liver microsomes of known genotypes of CYP2C9.	lornoxicam	69-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
14709614-2	2004	The results of the baculovirus expression system showed that CYP2C9.3 gives higher K(m) and lower V(max) values for lornoxicam 5"-hydroxylation than does CYP2C9.1.	lornoxicam	116-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
14709614-8	2004	In conclusion, this study showed that lornoxicam 5"-hydroxylation via CYP2C9 was markedly decreased by the substitution of Ile359Leu (CYP2C9.3), whereas the effect of the substitution of Arg144Cys (CYP2C9.2) was nonexistent or negligible.	lornoxicam	38-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
14709614-8	2004	In conclusion, this study showed that lornoxicam 5"-hydroxylation via CYP2C9 was markedly decreased by the substitution of Ile359Leu (CYP2C9.3), whereas the effect of the substitution of Arg144Cys (CYP2C9.2) was nonexistent or negligible.	lornoxicam	38-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
14709614-8	2004	In conclusion, this study showed that lornoxicam 5"-hydroxylation via CYP2C9 was markedly decreased by the substitution of Ile359Leu (CYP2C9.3), whereas the effect of the substitution of Arg144Cys (CYP2C9.2) was nonexistent or negligible.	lornoxicam	38-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
14709614-8	2004	In conclusion, this study showed that lornoxicam 5"-hydroxylation via CYP2C9 was markedly decreased by the substitution of Ile359Leu (CYP2C9.3), whereas the effect of the substitution of Arg144Cys (CYP2C9.2) was nonexistent or negligible.	ile359leu	123-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
14709614-8	2004	In conclusion, this study showed that lornoxicam 5"-hydroxylation via CYP2C9 was markedly decreased by the substitution of Ile359Leu (CYP2C9.3), whereas the effect of the substitution of Arg144Cys (CYP2C9.2) was nonexistent or negligible.	ile359leu	123-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
14709614-8	2004	In conclusion, this study showed that lornoxicam 5"-hydroxylation via CYP2C9 was markedly decreased by the substitution of Ile359Leu (CYP2C9.3), whereas the effect of the substitution of Arg144Cys (CYP2C9.2) was nonexistent or negligible.	ile359leu	123-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
14709614-9	2004	Additional in vivo studies are required to confirm that individuals with homologous CYP2C9*3 allele exhibit impaired lornoxicam clearance.	lornoxicam	117-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
14676821-2	2004	Warfarin is metabolised by cytochrome P450 enzymes CYP2C9, CYP1A2 and CYP3A.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
14676821-4	2004	Genetic variability in CYP2C9, CYP3A5 and ABCB1 was analysed in 201 stable warfarin-treated patients using solid-phase minisequencing, pyrosequencing and SNaPshot.	Warfarin	75-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
14676821-5	2004	CYP2C9 variants, age, weight, concurrent drug treatment and indication for treatment significantly influenced warfarin dosing in these patients, explaining 29% of the variation in dose.	Warfarin	110-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15128047-1	2004	CYP2C9 catalyses the biotransformation of the oral anticoagulants S-warfarin and R- and S-acenocoumarol.	Sulfur	66-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15128047-1	2004	CYP2C9 catalyses the biotransformation of the oral anticoagulants S-warfarin and R- and S-acenocoumarol.	Warfarin	68-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15128047-1	2004	CYP2C9 catalyses the biotransformation of the oral anticoagulants S-warfarin and R- and S-acenocoumarol.	r- and s-acenocoumarol	81-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15128047-2	2004	According to data obtained in vitro, phenprocoumon is also metabolized by CYP2C9 but the impact of the CYP2C9 polymorphism on phenprocoumon pharmacokinetics has not been studied.	Phenprocoumon	37-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
15128047-3	2004	Twenty-six healthy heterozygous and homozygous carriers of the CYP2C9 alleles *1 (wild-type), *2 (Arg144Cys), and *3 (Ile359Leu) received a single oral dose of 12 mg of racemic phenprocoumon.	ile359leu	118-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
15128047-3	2004	Twenty-six healthy heterozygous and homozygous carriers of the CYP2C9 alleles *1 (wild-type), *2 (Arg144Cys), and *3 (Ile359Leu) received a single oral dose of 12 mg of racemic phenprocoumon.	Phenprocoumon	177-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
15128047-7	2004	Plasma and urine concentrations of 4"-, 6- and 7-hydroxyphenprocoumon were significantly lower in homozygous carriers of the CYP2C9*2 and *3 variants compared to CYP2C9*1/*1.	4"-, 6- and 7-hydroxyphenprocoumon	35-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
15128047-8	2004	Carriers of CYP2C9*3/*3 had a median AUC of (R,S) 7-OH-phenprocoumon of only approximately 25% compared to the wild-type genotype.	(r,s) 7-oh-phenprocoumon	44-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
15128047-9	2004	The AUC of (R,S) 6-OH-phenprocoumon was only approximately 50% in CYP2C9*3/*3 compared to the homozygous wild-type genotype.	(r,s) 6-oh-phenprocoumon	11-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
15128048-0	2004	The risk of overanticoagulation in patients with cytochrome P450 CYP2C9*2 or CYP2C9*3 alleles on acenocoumarol or phenprocoumon.	Acenocoumarol	97-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
15128048-0	2004	The risk of overanticoagulation in patients with cytochrome P450 CYP2C9*2 or CYP2C9*3 alleles on acenocoumarol or phenprocoumon.	Acenocoumarol	97-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
15128048-1	2004	Cytochrome P4502C9 (CYP2C9) is the main enzyme implicated in coumarin anticoagulant metabolism.	coumarin	61-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-18
15128048-1	2004	Cytochrome P4502C9 (CYP2C9) is the main enzyme implicated in coumarin anticoagulant metabolism.	coumarin	61-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
15128048-2	2004	The variant alleles CYP2C9*2 and CYP2C9*3 are associated with an increased response to warfarin.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
15128048-2	2004	The variant alleles CYP2C9*2 and CYP2C9*3 are associated with an increased response to warfarin.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
15128048-4	2004	We investigated CYP2C9 polymorphisms in relation to the international normalized ratio (INR) during the first 6 weeks of treatment and its effect on the maintenance dose in a cohort of 1124 patients from the Rotterdam Study who were treated with acenocoumarol or phenprocoumon.	Acenocoumarol	246-259	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
15128048-4	2004	We investigated CYP2C9 polymorphisms in relation to the international normalized ratio (INR) during the first 6 weeks of treatment and its effect on the maintenance dose in a cohort of 1124 patients from the Rotterdam Study who were treated with acenocoumarol or phenprocoumon.	Phenprocoumon	263-276	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
15128048-9	2004	Individuals with one or more CYP2C9*2 or CYP2C9*3 allele(s) require a significantly lower dose of acenocoumarol compared to wild-type patients.	Acenocoumarol	98-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
15128048-9	2004	Individuals with one or more CYP2C9*2 or CYP2C9*3 allele(s) require a significantly lower dose of acenocoumarol compared to wild-type patients.	Acenocoumarol	98-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
14691573-6	2004	Advanced age, lower body surface area (BSA), and the presence of cytochrome P450 2C9 *2 or *3 single nucleotide polymorphisms were strongly associated (P &lt; 0.001) with lower warfarin dose: the maintenance dose decreased by 8% per decade of age, by 13% per standard deviation decrease in BSA, by 19% per 2C9*2 allele, and by 30% per 2C9*3 allele.	Warfarin	177-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-84
14676821-0	2004	Warfarin sensitivity related to CYP2C9, CYP3A5, ABCB1 (MDR1) and other factors.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
14691574-4	2004	We also determined the role of cytochrome P450 2C9 (CYP2C9) polymorphism on coumarin dosage and INR in NSAID users.	coumarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-50
14691574-4	2004	We also determined the role of cytochrome P450 2C9 (CYP2C9) polymorphism on coumarin dosage and INR in NSAID users.	coumarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
14642736-7	2003	Incubations of tamoxifen with recombinant human cytochrome P-450s (CYPs) found that CYP2C9 and CYP2D6 produced all three of the above tamoxifen metabolites, while CYP1A1 and CYP3A4 catalyzed the formation of alpha-hydroxytamoxifen and N-desmethyltamoxifen, and CYP1A2 and CYP1B1 only formed the alpha-hydroxy metabolite.	Tamoxifen	15-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
15199661-5	2004	Fluvoxamine is a potent inhibitor of CYP1A2 and CYP2C19 and a moderate inhibitor of CYP2C9.	Fluvoxamine	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
14614357-0	2003	Early overanticoagulation with acenocoumarol due to a genetic polymorphism of cytochrome P450 CYP2C9.	Acenocoumarol	31-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
14642736-7	2003	Incubations of tamoxifen with recombinant human cytochrome P-450s (CYPs) found that CYP2C9 and CYP2D6 produced all three of the above tamoxifen metabolites, while CYP1A1 and CYP3A4 catalyzed the formation of alpha-hydroxytamoxifen and N-desmethyltamoxifen, and CYP1A2 and CYP1B1 only formed the alpha-hydroxy metabolite.	Tamoxifen	134-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
14614357-3	2003	This case illustrates the role of the *3 polymorphism of the cytochrome P450 CYP2C9 as an independent risk factor modulating the sensitivity of patients to the anticoagulant effect of acenocoumarol.	Acenocoumarol	184-197	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
14616412-1	2003	AIMS: Voriconazole is a new triazole antifungal agent, and is metabolized by the cytochrome P450 isoenzymes CYP2C9, CYP2C19, and, to a lesser extent, by CYP3A4.	Voriconazole	6-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
14642736-7	2003	Incubations of tamoxifen with recombinant human cytochrome P-450s (CYPs) found that CYP2C9 and CYP2D6 produced all three of the above tamoxifen metabolites, while CYP1A1 and CYP3A4 catalyzed the formation of alpha-hydroxytamoxifen and N-desmethyltamoxifen, and CYP1A2 and CYP1B1 only formed the alpha-hydroxy metabolite.	alpha-hydroxytamoxifen	208-230	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
14642736-7	2003	Incubations of tamoxifen with recombinant human cytochrome P-450s (CYPs) found that CYP2C9 and CYP2D6 produced all three of the above tamoxifen metabolites, while CYP1A1 and CYP3A4 catalyzed the formation of alpha-hydroxytamoxifen and N-desmethyltamoxifen, and CYP1A2 and CYP1B1 only formed the alpha-hydroxy metabolite.	N-desmethyltamoxifen	235-255	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
14616412-1	2003	AIMS: Voriconazole is a new triazole antifungal agent, and is metabolized by the cytochrome P450 isoenzymes CYP2C9, CYP2C19, and, to a lesser extent, by CYP3A4.	Triazoles	28-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
14616412-2	2003	Phenytoin is an inducer of CYP3A4 activity, and a substrate and inducer of CYP2C9 and CYP2C19.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
14616414-1	2003	AIMS: Voriconazole, a new triazole antifungal agent, is metabolized mainly by cytochrome P450s CYP2C19 and CYP2C9, and also by CYP3A4.	Voriconazole	6-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
14616414-1	2003	AIMS: Voriconazole, a new triazole antifungal agent, is metabolized mainly by cytochrome P450s CYP2C19 and CYP2C9, and also by CYP3A4.	Triazoles	26-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
14616415-1	2003	AIMS: Voriconazole, a novel triazole antifungal agent, is metabolized by the cytochrome P450 isoenzymes CYP2C19, CYP2C9, and to a lesser extent by CYP3A4.	Voriconazole	6-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
14616416-1	2003	AIMS: Voriconazole is a new triazole antifungal agent, and is metabolized by the cytochrome P450 isoenzymes CYP2C9, CYP2C19 and to a lesser extent by CYP3A4.	Voriconazole	6-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
14616416-1	2003	AIMS: Voriconazole is a new triazole antifungal agent, and is metabolized by the cytochrome P450 isoenzymes CYP2C9, CYP2C19 and to a lesser extent by CYP3A4.	Triazoles	28-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
14703066-9	2003	CYP2C9 is involved in the conversion of estrone sulfate to the 16-hydroxy sulfate metabolite.	estrone sulfate	40-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
14703066-9	2003	CYP2C9 is involved in the conversion of estrone sulfate to the 16-hydroxy sulfate metabolite.	16-hydroxy sulfate	63-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
14575648-4	2003	Among these are metabolic factors (bioactivation by hCYP2C9 or hCYP3A4 to thiol-reactive quinone imines, activation by hUGT2B7 to protein-reactive acyl glucuronides and iso-glucuronides, and 4"-hydroxylation secondary to diclofenac glucuronidation), as well as kinetic factors (Mrp2-mediated concentrative transport of diclofenac metabolites into bile).	Sulfhydryl Compounds	74-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-59
14684755-0	2003	Involvement of CYP 2C9 in mediating the proinflammatory effects of linoleic acid in vascular endothelial cells.	Linoleic Acid	67-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-22
14684755-3	2003	CYP 2C9 is involved in linoleic acid epoxygenation, and the major product of this reaction is leukotoxin (LTX).	Linoleic Acid	23-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-7
14684755-5	2003	METHODS: The effect of linoleic acid on CYP 2C9 gene expression was studied by RT-PCR.	Linoleic Acid	23-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-47
14684755-8	2003	RESULTS: Linoleic acid treatment for six hours increased the expression of CYP 2C9 in endothelial cells.	Linoleic Acid	9-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-82
14684755-9	2003	Linoleic acid-mediated increase in oxidative stress and activation of AP-1 were blocked by sulfaphenazole, a specific inhibitor of CYP 2C9.	Linoleic Acid	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-138
14684755-9	2003	Linoleic acid-mediated increase in oxidative stress and activation of AP-1 were blocked by sulfaphenazole, a specific inhibitor of CYP 2C9.	Sulfaphenazole	91-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-138
14684755-11	2003	CONCLUSION: Our data show that CYP 2C9 plays a key role in linoleic acid-induced oxidative stress and subsequent proinflammatory events in vascular endothelial cells by possibly causing superoxide generation through uncoupling processes.	Linoleic Acid	59-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-38
14684755-11	2003	CONCLUSION: Our data show that CYP 2C9 plays a key role in linoleic acid-induced oxidative stress and subsequent proinflammatory events in vascular endothelial cells by possibly causing superoxide generation through uncoupling processes.	Superoxides	186-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-38
14651673-0	2003	Involvement of cytochrome P450 2C9, 2E1 and 3A4 in trimethadione N-demethylation in human microsomes.	Trimethadione	51-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-34
14651673-3	2003	In this study, we determined the percentage contribution of the three CYPs (CYP2C9, CYP2E1 and CYP3A4) to TMO N-demethylation.	Nitrogen	110-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
14651673-9	2003	CONCLUSION: TMO is metabolized not only by CYP2E1 but also CYP3A4 and CYP2C9.	Trimethadione	12-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
14557374-3	2003	Several potent heteroactivators of CYP2C9-mediated 7-methoxy-4-trifluoromethyl-coumarin metabolism are marketed drugs or endogenous compounds (amiodarone, niclosamide, liothyronine, meclofenemate, zafirlukast, estropipate, and dichlorphenamide, yielding 150% control reaction velocity at 0.04, 0.09, 0.5, 1, 1.2, 1.5, and 2.5 microM, respectively).	7-methoxy-4-trifluoromethylcoumarin	51-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
14557374-3	2003	Several potent heteroactivators of CYP2C9-mediated 7-methoxy-4-trifluoromethyl-coumarin metabolism are marketed drugs or endogenous compounds (amiodarone, niclosamide, liothyronine, meclofenemate, zafirlukast, estropipate, and dichlorphenamide, yielding 150% control reaction velocity at 0.04, 0.09, 0.5, 1, 1.2, 1.5, and 2.5 microM, respectively).	Amiodarone	143-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
14557374-3	2003	Several potent heteroactivators of CYP2C9-mediated 7-methoxy-4-trifluoromethyl-coumarin metabolism are marketed drugs or endogenous compounds (amiodarone, niclosamide, liothyronine, meclofenemate, zafirlukast, estropipate, and dichlorphenamide, yielding 150% control reaction velocity at 0.04, 0.09, 0.5, 1, 1.2, 1.5, and 2.5 microM, respectively).	Niclosamide	155-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
14557374-3	2003	Several potent heteroactivators of CYP2C9-mediated 7-methoxy-4-trifluoromethyl-coumarin metabolism are marketed drugs or endogenous compounds (amiodarone, niclosamide, liothyronine, meclofenemate, zafirlukast, estropipate, and dichlorphenamide, yielding 150% control reaction velocity at 0.04, 0.09, 0.5, 1, 1.2, 1.5, and 2.5 microM, respectively).	Triiodothyronine	168-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
14557374-3	2003	Several potent heteroactivators of CYP2C9-mediated 7-methoxy-4-trifluoromethyl-coumarin metabolism are marketed drugs or endogenous compounds (amiodarone, niclosamide, liothyronine, meclofenemate, zafirlukast, estropipate, and dichlorphenamide, yielding 150% control reaction velocity at 0.04, 0.09, 0.5, 1, 1.2, 1.5, and 2.5 microM, respectively).	meclofenemate	182-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
14557374-3	2003	Several potent heteroactivators of CYP2C9-mediated 7-methoxy-4-trifluoromethyl-coumarin metabolism are marketed drugs or endogenous compounds (amiodarone, niclosamide, liothyronine, meclofenemate, zafirlukast, estropipate, and dichlorphenamide, yielding 150% control reaction velocity at 0.04, 0.09, 0.5, 1, 1.2, 1.5, and 2.5 microM, respectively).	zafirlukast	197-208	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
14557374-3	2003	Several potent heteroactivators of CYP2C9-mediated 7-methoxy-4-trifluoromethyl-coumarin metabolism are marketed drugs or endogenous compounds (amiodarone, niclosamide, liothyronine, meclofenemate, zafirlukast, estropipate, and dichlorphenamide, yielding 150% control reaction velocity at 0.04, 0.09, 0.5, 1, 1.2, 1.5, and 2.5 microM, respectively).	estropipate	210-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
14557374-3	2003	Several potent heteroactivators of CYP2C9-mediated 7-methoxy-4-trifluoromethyl-coumarin metabolism are marketed drugs or endogenous compounds (amiodarone, niclosamide, liothyronine, meclofenemate, zafirlukast, estropipate, and dichlorphenamide, yielding 150% control reaction velocity at 0.04, 0.09, 0.5, 1, 1.2, 1.5, and 2.5 microM, respectively).	Dichlorphenamide	227-243	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
14576103-4	2003	The mechanism of the drug interaction reported between chloramphenicol and phenytoin, which results in the elevation of plasma phenytoin concentrations, is clinically assumed to result from the inhibition of CYP2C9 by chloramphenicol.	Chloramphenicol	55-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	208-214
14576103-4	2003	The mechanism of the drug interaction reported between chloramphenicol and phenytoin, which results in the elevation of plasma phenytoin concentrations, is clinically assumed to result from the inhibition of CYP2C9 by chloramphenicol.	Phenytoin	75-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	208-214
14576103-4	2003	The mechanism of the drug interaction reported between chloramphenicol and phenytoin, which results in the elevation of plasma phenytoin concentrations, is clinically assumed to result from the inhibition of CYP2C9 by chloramphenicol.	Phenytoin	127-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	208-214
14576103-4	2003	The mechanism of the drug interaction reported between chloramphenicol and phenytoin, which results in the elevation of plasma phenytoin concentrations, is clinically assumed to result from the inhibition of CYP2C9 by chloramphenicol.	Chloramphenicol	218-233	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	208-214
14661864-0	2003	Polymorphism in CYP2C9 as a non-critical factor of warfarin dosage adjustment in Korean patients.	Warfarin	51-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
14661864-1	2003	Cytochrome P4502C9(CYP2C9) is largely responsible for terminating anticoagulant effect by hydroxylation of S-warfarin to inactive metabolites.	Warfarin	107-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
14661864-3	2003	The aim of this study was to assess relationship between requirement of warfarin dose and polymorphism in CYP2C9 in Korean population.	Warfarin	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
14586384-2	2003	Data suggest that warfarin can be used as a safe and accurate biomarker for CYP2C9, and if warfarin is administered with vitamin K, the pharmacodynamic effect is ablated.	Warfarin	18-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
14586391-6	2003	These results suggest that the CYP2C9*1/*3 genotype could be associated with decreased clearance and increased plasma concentration of candesartan, potentially enhancing its hypotensive effect.	candesartan	135-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
14678248-8	2003	Cytochrome P450 (CYP) isoform-specific chemical and monoclonal antibody inhibition studies have demonstrated that CYP2B6, CYP2C9, CYP2D6 and CYP3A4 all mediate the formation of Z-4-OH-tam.	z-4-oh-tam	177-187	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
14678248-10	2003	Significant associations between the percentage inhibition of Z-4-OH-tam by CYP isoform-specific inhibitors and the rate of metabolism of CYP isoform-specific index reactions and between individual expression of CYP2B6, CYP2C9 and CYP2D6 and Z-4-OH-tam formation rates indicate predominant roles for these isoforms in this pathway.	z-4-oh-tam	62-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	220-226
14678248-12	2003	Genotyping of patients with regards to CYP2B6, CYP2C9 and CYP2D6 may play a role in prediction of Z-4-OH-tam formation and, consequently, ultimate therapeutic benefit of tamoxifen treatment.	z-4-oh-tam	98-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
14678248-12	2003	Genotyping of patients with regards to CYP2B6, CYP2C9 and CYP2D6 may play a role in prediction of Z-4-OH-tam formation and, consequently, ultimate therapeutic benefit of tamoxifen treatment.	Tamoxifen	170-179	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
14504849-0	2003	Effect of the single CYP2C9*3 allele on pharmacokinetics and pharmacodynamics of losartan in healthy Japanese subjects.	Losartan	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
14504849-1	2003	OBJECTIVE: Losartan is metabolized to the active carboxylic acid metabolite EXP3174 by CYP2C9.	Losartan	11-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
14504849-1	2003	OBJECTIVE: Losartan is metabolized to the active carboxylic acid metabolite EXP3174 by CYP2C9.	Carboxylic Acids	49-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
14504849-2	2003	In this study, we determined the effects of the single CYP2C9*3 variant on the pharmacokinetics and pharmacodynamics of losartan.	Losartan	120-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
14504849-11	2003	CONCLUSION: The single CYP2C9*3 variant reduces the metabolism of losartan and its hypotensive effect.	Losartan	66-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
14641553-2	2003	Of special interest are those with a narrow therapeutic index, such as S-warfarin, tolbutamide and phenytoin, where impairment in CYP2C9 metabolic activity might cause difficulties in dose adjustment as well as toxicity.	Sulfur	71-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
14641553-2	2003	Of special interest are those with a narrow therapeutic index, such as S-warfarin, tolbutamide and phenytoin, where impairment in CYP2C9 metabolic activity might cause difficulties in dose adjustment as well as toxicity.	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
14641553-2	2003	Of special interest are those with a narrow therapeutic index, such as S-warfarin, tolbutamide and phenytoin, where impairment in CYP2C9 metabolic activity might cause difficulties in dose adjustment as well as toxicity.	Tolbutamide	83-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
14641553-2	2003	Of special interest are those with a narrow therapeutic index, such as S-warfarin, tolbutamide and phenytoin, where impairment in CYP2C9 metabolic activity might cause difficulties in dose adjustment as well as toxicity.	Phenytoin	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
14641553-8	2003	Furthermore in Japanese a CYP2C9 promotor variant of four linked SNPs was correlated with reduced intrinsic clearance of phenytoin in vitro.	Phenytoin	121-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
12826020-2	2003	The cytochrome P450 (CYP) 2C9 inhibitor sulphaphenazole was recently identified as a potent inhibitor of NO- and prostacyclin (PGI2)-independent relaxation in porcine coronary arteries.	Sulfaphenazole	40-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-29
12826020-2	2003	The cytochrome P450 (CYP) 2C9 inhibitor sulphaphenazole was recently identified as a potent inhibitor of NO- and prostacyclin (PGI2)-independent relaxation in porcine coronary arteries.	Epoprostenol	113-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-29
12826020-2	2003	The cytochrome P450 (CYP) 2C9 inhibitor sulphaphenazole was recently identified as a potent inhibitor of NO- and prostacyclin (PGI2)-independent relaxation in porcine coronary arteries.	Epoprostenol	127-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-29
14520122-0	2003	Effects of polymorphisms in CYP2D6, CYP2C9, and CYP2C19 on trimipramine pharmacokinetics.	Trimipramine	59-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
14520122-2	2003	A single oral dose of 75 mg trimipramine was given to 42 healthy volunteers selected according to their CYP2D6, CYP2C19, and CYP2C9 genotypes.	Trimipramine	28-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
14520122-8	2003	The desmethyltrimipramine area under the concentration-time curve was 40-fold greater in CYP2D6 PMs than in the reference group (1.7 vs. 0.04 mg/L x h in EMs), but below the quantification limit in most carriers of deficiencies of CYP2C19 or CYP2C9.	desmethyltrimipramine	4-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	242-248
15647404-3	2005	Anticoagulant response is also influenced by a number of drugs that induce or inhibit warfarin metabolism, as well as by genetic polymorphisms that may modulate expression or activity of CYP2C9, the isoform mediating clearance of S-warfarin.	Sulfur	230-231	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	187-193
15647404-3	2005	Anticoagulant response is also influenced by a number of drugs that induce or inhibit warfarin metabolism, as well as by genetic polymorphisms that may modulate expression or activity of CYP2C9, the isoform mediating clearance of S-warfarin.	Warfarin	232-240	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	187-193
15647404-5	2005	St. John"s wort and possibly some ginseng formulations may have the potential to diminish warfarin anticoagulation, apparently by inducing CYP2C9 activity.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	139-145
14534520-8	2003	CONCLUSION: The effect of rifampin on the pharmacokinetics and pharmacodynamics of gliclazide suggests that rifampin affects the disposition of gliclazide in humans, possibly by the induction of cytochrome P450 2C9.	Gliclazide	83-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-214
14534520-8	2003	CONCLUSION: The effect of rifampin on the pharmacokinetics and pharmacodynamics of gliclazide suggests that rifampin affects the disposition of gliclazide in humans, possibly by the induction of cytochrome P450 2C9.	Rifampin	108-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-214
14534520-8	2003	CONCLUSION: The effect of rifampin on the pharmacokinetics and pharmacodynamics of gliclazide suggests that rifampin affects the disposition of gliclazide in humans, possibly by the induction of cytochrome P450 2C9.	Gliclazide	144-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-214
14521618-0	2003	Warfarin and acenocoumarol dose requirements according to CYP2C9 genotyping in North-Italian patients.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
14521618-0	2003	Warfarin and acenocoumarol dose requirements according to CYP2C9 genotyping in North-Italian patients.	Acenocoumarol	13-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
12904931-4	2003	METHODS: The inhibitory effect of 5-FU on CYP1A2, CYP2C9, CYP2C19, CYP2C8, CYP2E1, CYP2D6, and CYP3A4 activities was examined with specific probe drugs in human liver microsomes.	Fluorouracil	34-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
12972955-6	2003	The CLint for the formation of D-703 from verapamil (marker of CYP2C8 activity) was 7.6-fold higher (P &lt; 0.001) and that for the diclofenac 4"-hydroxylation (marker of CYP2C9 activity) was 6.1-fold higher (P &lt; 0.001) in the liver than in the intestine.	D 703	31-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
12867493-2	2003	Inhibition of the CYP2C9-dependent formation of (S)-7-hydroxy-warfarin from (S)-warfarin was measured in seven healthy subjects at three different doses of fluconazole.	7-hydroxywarfarin	48-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
12920163-1	2003	The inhibitory effect of glyburide [International Nonproprietary Name (INN), glibenclamide] on CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 activities was evaluated using pooled human liver microsomes.	Glyburide	25-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
12920163-2	2003	Glyburide strongly inhibited CYP2C9-catalyzed S-warfarin and phenytoin metabolism in a competitive manner, with Ki (IC50) values of 2.4 (11.3) microM and 3.1 (9.4) microM, respectively.	Glyburide	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
12920163-2	2003	Glyburide strongly inhibited CYP2C9-catalyzed S-warfarin and phenytoin metabolism in a competitive manner, with Ki (IC50) values of 2.4 (11.3) microM and 3.1 (9.4) microM, respectively.	Sulfur	46-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
12920163-2	2003	Glyburide strongly inhibited CYP2C9-catalyzed S-warfarin and phenytoin metabolism in a competitive manner, with Ki (IC50) values of 2.4 (11.3) microM and 3.1 (9.4) microM, respectively.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
12920163-2	2003	Glyburide strongly inhibited CYP2C9-catalyzed S-warfarin and phenytoin metabolism in a competitive manner, with Ki (IC50) values of 2.4 (11.3) microM and 3.1 (9.4) microM, respectively.	Phenytoin	61-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
12920163-5	2003	In summary, glyburide showed potent inhibition on CYP2C9 and weak inhibition on CYP3A4, whereas it had minimal or no inhibitory effect on the other cytochromes p450 examined.	Glyburide	12-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
12920163-6	2003	It is anticipated that clinically significant drug-drug interactions will ensue when glyburide is coadministered with agents that are cleared primarily by the CYP2C9-mediated pathway and those with narrow therapeutic ranges.	Glyburide	85-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
12867493-2	2003	Inhibition of the CYP2C9-dependent formation of (S)-7-hydroxy-warfarin from (S)-warfarin was measured in seven healthy subjects at three different doses of fluconazole.	Warfarin	76-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
12867493-2	2003	Inhibition of the CYP2C9-dependent formation of (S)-7-hydroxy-warfarin from (S)-warfarin was measured in seven healthy subjects at three different doses of fluconazole.	Fluconazole	156-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
12900870-2	2003	Mephenytoin (MEPH), dextromethorphan, diclofenac, caffeine, and methadone (MET) were successfully applied as test substrates for CYP2C19, CYP2D6*1, CYP2C9*1, CYP1A2, and CYP3A4, respectively.	Mephenytoin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
12900870-2	2003	Mephenytoin (MEPH), dextromethorphan, diclofenac, caffeine, and methadone (MET) were successfully applied as test substrates for CYP2C19, CYP2D6*1, CYP2C9*1, CYP1A2, and CYP3A4, respectively.	Dextromethorphan	20-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
12900870-2	2003	Mephenytoin (MEPH), dextromethorphan, diclofenac, caffeine, and methadone (MET) were successfully applied as test substrates for CYP2C19, CYP2D6*1, CYP2C9*1, CYP1A2, and CYP3A4, respectively.	Diclofenac	38-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
12900870-2	2003	Mephenytoin (MEPH), dextromethorphan, diclofenac, caffeine, and methadone (MET) were successfully applied as test substrates for CYP2C19, CYP2D6*1, CYP2C9*1, CYP1A2, and CYP3A4, respectively.	Methadone	64-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
12900870-2	2003	Mephenytoin (MEPH), dextromethorphan, diclofenac, caffeine, and methadone (MET) were successfully applied as test substrates for CYP2C19, CYP2D6*1, CYP2C9*1, CYP1A2, and CYP3A4, respectively.	Methadone	75-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
12900870-7	2003	CYP2C9 and CYP2C19 provided enhanced formation of R-EDDP and CYP2D6 incubation resulted in the preferential conversion to S-EDDP.	r-eddp	50-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
12900870-7	2003	CYP2C9 and CYP2C19 provided enhanced formation of R-EDDP and CYP2D6 incubation resulted in the preferential conversion to S-EDDP.	2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine	122-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15199455-3	2003	The most important of these is CYP2C9, which 7-hydroxylates S-warfarin.	Warfarin	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
12871048-2	2003	As a result, the metabolism of diclofenac in humans partitions between acyl glucuronidation and phenyl hydroxylation, with the former reaction catalyzed primarily by uridine 5"-diphosphoglucuronosyl transferase 2B7 while the latter is catalyzed by cytochrome P450 (CYP)2C9 and 3A4.	Diclofenac	31-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	248-272
12871048-4	2003	The 4"-hydroxylation of the drug appears to represent a feature reaction for CYP2C9 catalysis, and this regioselective oxidation is presumably dictated by interactions of the carboxylate moiety of the substrate with a putative cationic residue of the enzyme.	carboxylate	175-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
14760217-1	2003	Warfarin and other coumarins are metabolized by the cytochrome P450 2C9 complex.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-71
14760217-1	2003	Warfarin and other coumarins are metabolized by the cytochrome P450 2C9 complex.	Coumarins	19-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-71
12893985-0	2003	Influence of CYP2C9 genetic polymorphisms on pharmacokinetics of celecoxib and its metabolites.	Celecoxib	65-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
12893985-1	2003	In-vitro data indicate major effects of the genetically polymorphic cytochrome P450 enzyme 2C9 (CYP2C9) on the pharmacokinetics of celecoxib, a nonsteroidal anti-inflammatory drug acting as selective cyclooxygenase-2 inhibitor.	Celecoxib	131-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-94
12893985-1	2003	In-vitro data indicate major effects of the genetically polymorphic cytochrome P450 enzyme 2C9 (CYP2C9) on the pharmacokinetics of celecoxib, a nonsteroidal anti-inflammatory drug acting as selective cyclooxygenase-2 inhibitor.	Celecoxib	131-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
12893985-2	2003	Human studies report decreased clearance in heterozygous carriers of the CYP2C9 variant Ile359Leu (*3), but results appeared controversial and only data on single subjects carrying the homozygous CYP2C9*3/*3 genotype have been published.	ile359leu	88-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
12891229-0	2003	Influence of CYP2C9 polymorphisms on the pharmacokinetics and cholesterol-lowering activity of (-)-3S,5R-fluvastatin and (+)-3R,5S-fluvastatin in healthy volunteers.	Cholesterol	62-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
12891229-0	2003	Influence of CYP2C9 polymorphisms on the pharmacokinetics and cholesterol-lowering activity of (-)-3S,5R-fluvastatin and (+)-3R,5S-fluvastatin in healthy volunteers.	(-)-3s,5r-fluvastatin	95-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
12891229-2	2003	The consequences of CYP2C9 genetic polymorphisms on fluvastatin pharmacokinetics and on its efficacy have not been investigated in humans thus far.	Fluvastatin	52-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
12891229-9	2003	Mean (and SD) values for area under the curve of the active (+)-3R,5S-fluvastatin in carriers of the genotype CYP2C9*1/*1, *1/*3, and *3/*3 were 173 (85) micro g. L(-1).	5s-fluvastatin	67-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
12891229-19	2003	CONCLUSIONS: The pharmacokinetics of both enantiomers of fluvastatin depended on the CYP2C9 genotype, with a 3-fold group mean difference in the active enantiomer and even greater differences in the inactive enantiomer, but differences in plasma concentrations were not reflected in cholesterol lowering after 14 days of fluvastatin intake in healthy volunteers.	Fluvastatin	57-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
12891229-19	2003	CONCLUSIONS: The pharmacokinetics of both enantiomers of fluvastatin depended on the CYP2C9 genotype, with a 3-fold group mean difference in the active enantiomer and even greater differences in the inactive enantiomer, but differences in plasma concentrations were not reflected in cholesterol lowering after 14 days of fluvastatin intake in healthy volunteers.	Cholesterol	283-294	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
12891229-19	2003	CONCLUSIONS: The pharmacokinetics of both enantiomers of fluvastatin depended on the CYP2C9 genotype, with a 3-fold group mean difference in the active enantiomer and even greater differences in the inactive enantiomer, but differences in plasma concentrations were not reflected in cholesterol lowering after 14 days of fluvastatin intake in healthy volunteers.	Fluvastatin	321-332	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
15199455-4	2003	In clinical studies, possession of the CYP2C9*2 or CYP2C9*3 variant alleles, which result in decreased enzyme activity, has been associated with a significant decrease in mean warfarin dose requirement in at least eight studies.	Warfarin	176-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
15199455-4	2003	In clinical studies, possession of the CYP2C9*2 or CYP2C9*3 variant alleles, which result in decreased enzyme activity, has been associated with a significant decrease in mean warfarin dose requirement in at least eight studies.	Warfarin	176-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
15199455-7	2003	The molecular basis of warfarin resistance remains unclear but could be due to unusually high CYP2C9 activity (pharmacokinetic resistance) or to abnormal vitamin K epoxide reductase (pharmacodynamic resistance).	Warfarin	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
15199455-8	2003	There is less information available on genetic factors affecting other anticoagulants, but the CYP2C9 genotype is also relevant to acenocoumarol dose.	Acenocoumarol	131-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
12861225-0	2003	Crystal structure of human cytochrome P450 2C9 with bound warfarin.	Warfarin	58-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-46
12899669-0	2003	A screening study on the liability of eight different female sex steroids to inhibit CYP2C9, 2C19 and 3A4 activities in human liver microsomes.	Steroids	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
12899669-3	2003	Aethinyloestradiol was found to be a potent inhibitor (55% mean inhibition; 95% CI 32% to 79%) of losartan oxidation (CYP2C9) and R-omeprazole 5-hydroxylation (70%; 63% to 77%) (CYP2C19), while it had little effect on R-omeprazole sulphoxidation (CYP3A4) activity.	aethinyloestradiol	0-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
12899669-3	2003	Aethinyloestradiol was found to be a potent inhibitor (55% mean inhibition; 95% CI 32% to 79%) of losartan oxidation (CYP2C9) and R-omeprazole 5-hydroxylation (70%; 63% to 77%) (CYP2C19), while it had little effect on R-omeprazole sulphoxidation (CYP3A4) activity.	Losartan	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
12899669-5	2003	Of the progestin hormones studied, gestodene and 3-ketodesogestrel were potent inhibitors of CYP2C19 (57%; 47% to 67% and 51%; 29% to 45%) and CYP3A4 (45%; 30% to 59% and 40%; 19% to 62%), but had little effect on the CYP2C9 activity.	Gestodene	35-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
12899669-5	2003	Of the progestin hormones studied, gestodene and 3-ketodesogestrel were potent inhibitors of CYP2C19 (57%; 47% to 67% and 51%; 29% to 45%) and CYP3A4 (45%; 30% to 59% and 40%; 19% to 62%), but had little effect on the CYP2C9 activity.	etonogestrel	49-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
12899669-6	2003	In addition, medroxyprogesterone acetate was found to inhibit CYP2C9 (55%; 45% to 65%), while not having significant effect on 2C19 or 3A4.	Medroxyprogesterone Acetate	13-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
12899669-7	2003	In conclusion, the liability of clinically used female sex steroids to inhibit CYP2C9, 2C19 and 3A4 activities in human liver microsomes is very distinctive and these differences among both the oestrogen and progestin hormones may, at least in part, explain the variable results from clinical trials examining inhibitory effects of hormone replacement therapy and oral contraceptives on drug metabolism.	Steroids	59-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
12861225-6	2003	Here we describe the crystal structure of a human CYP450, CYP2C9, both unliganded and in complex with the anti-coagulant drug warfarin.	Warfarin	126-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
12861225-7	2003	The structure defines unanticipated interactions between CYP2C9 and warfarin, and reveals a new binding pocket.	Warfarin	68-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
12861225-8	2003	The binding mode of warfarin suggests that CYP2C9 may undergo an allosteric mechanism during its function.	Warfarin	20-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
12814975-0	2003	A new class of CYP2C9 inhibitors: probing 2C9 specificity with high-affinity benzbromarone derivatives.	Benzbromarone	77-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
12844133-1	2003	AIM: Our goal was to investigate whether artemisinin autoinduction is caused by an increase in cytochrome P450 (CYP) 2B6 or CYP2C9 activities, we evaluated the effects of multiple-dose artemisinin administration on S-mephenytoin N-demethylation in healthy subjects.	artemisinin	41-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
12844133-4	2003	The CYP2C9 in vivo marker tolbutamide was administered on day -28 and on days 7, 12, and 17 to monitor the minor involvement of CYP2C9 in S-mephenytoin N-demethylation.	Tolbutamide	26-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
12893985-5	2003	A more than two-fold reduced oral clearance in homozygous carriers of CYP2C9*3 was seen for celecoxib compared to carriers of the wild-type genotype CYP2C9*1/*1 and heterozygous carriers of one *3 allele were in-between (P = 0.003 for trend), whereas CYP2C9*2 had no significant influence on celecoxib pharmacokinetics.	Celecoxib	92-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
12893985-5	2003	A more than two-fold reduced oral clearance in homozygous carriers of CYP2C9*3 was seen for celecoxib compared to carriers of the wild-type genotype CYP2C9*1/*1 and heterozygous carriers of one *3 allele were in-between (P = 0.003 for trend), whereas CYP2C9*2 had no significant influence on celecoxib pharmacokinetics.	Celecoxib	292-301	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
12893985-6	2003	Decreased concentrations of carboxy- and hydroxy-celecoxib in heterozygous and homozygous carriers of CYP2C9*3 were detected which supported the influence of CYP2C9 polymorphisms on celecoxib pharmacokinetic variability.	carboxy- and hydroxy-celecoxib	28-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
12893985-6	2003	Decreased concentrations of carboxy- and hydroxy-celecoxib in heterozygous and homozygous carriers of CYP2C9*3 were detected which supported the influence of CYP2C9 polymorphisms on celecoxib pharmacokinetic variability.	carboxy- and hydroxy-celecoxib	28-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
12893985-6	2003	Decreased concentrations of carboxy- and hydroxy-celecoxib in heterozygous and homozygous carriers of CYP2C9*3 were detected which supported the influence of CYP2C9 polymorphisms on celecoxib pharmacokinetic variability.	Celecoxib	49-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
12893985-6	2003	Decreased concentrations of carboxy- and hydroxy-celecoxib in heterozygous and homozygous carriers of CYP2C9*3 were detected which supported the influence of CYP2C9 polymorphisms on celecoxib pharmacokinetic variability.	Celecoxib	49-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
12893985-7	2003	Approximately 0.5% of Caucasians carrying the genotype CYP2C9*3/*3 will have greatly increased internal exposure to celecoxib.	Celecoxib	116-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
12814975-2	2003	The CYP2C9 pharmacophore is proposed to include either an anionic group or hydrogen bond donor in addition to its hydrophobic groups.	Hydrogen	75-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
12734606-1	2003	OBJECTIVE: This study analyzed the frequency of CYP2C9 variant alleles and evaluated the impact of CYP2C9 genotype on diclofenac metabolism in a Spanish population.	Diclofenac	118-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
12844136-0	2003	Acenocoumarol pharmacokinetics in relation to cytochrome P450 2C9 genotype.	Acenocoumarol	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-65
12844136-1	2003	BACKGROUND AND OBJECTIVES: Cytochrome P450 (CYP) 2C9 is one of the major CYP enzymes involved in the biotransformation of drugs, among others, the oral anticoagulant acenocoumarol.	Acenocoumarol	166-179	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-52
12844136-3	2003	Patients with the CYP2C9*3 variant are known to require a lower maintenance dose of racemic acenocoumarol.	Acenocoumarol	92-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
12844136-4	2003	We investigated the impact of the polymorphisms CYP2C9*2 and CYP2C9*3 on the pharmacokinetics of R- and S-acenocoumarol.	r- and s-acenocoumarol	97-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
12844136-4	2003	We investigated the impact of the polymorphisms CYP2C9*2 and CYP2C9*3 on the pharmacokinetics of R- and S-acenocoumarol.	r- and s-acenocoumarol	97-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
12844136-9	2003	The mean oral clearance of S-acenocoumarol was 45% lower in the CYP2C9*1/*3 genotypes (10.9 +/- 3.0 L/h versus 19.8 +/- 3.1 L/h, P =.02).	Acenocoumarol	27-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
12844136-16	2003	CONCLUSION: The results show S-acenocoumarol pharmacokinetics to be dependent on CYP2C9 polymorphism.	Acenocoumarol	29-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
12844136-17	2003	In particular, the presence of the CYP2C9*3 allele impairs oral clearance of the coumarin.	coumarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
14527094-1	2003	Diclofenac has been used for the evaluation of CYP2C9 activity in vitro as well as in vivo with varying results.	Diclofenac	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
14527094-5	2003	The mean (+/- SD) of diclofenac/4"-OH diclofenac ratio was 1.5 times higher among subjects carrying CYP2C9*3 allele (CYP2C9*1/*3 and CYP2C9*2/*3 genotypes) (0.91 +/- 0.28), compared to CYP2C9*1/*1 subjects (0.60 +/- 0.11).	Diclofenac	21-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
14527094-5	2003	The mean (+/- SD) of diclofenac/4"-OH diclofenac ratio was 1.5 times higher among subjects carrying CYP2C9*3 allele (CYP2C9*1/*3 and CYP2C9*2/*3 genotypes) (0.91 +/- 0.28), compared to CYP2C9*1/*1 subjects (0.60 +/- 0.11).	Diclofenac	21-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
14527094-5	2003	The mean (+/- SD) of diclofenac/4"-OH diclofenac ratio was 1.5 times higher among subjects carrying CYP2C9*3 allele (CYP2C9*1/*3 and CYP2C9*2/*3 genotypes) (0.91 +/- 0.28), compared to CYP2C9*1/*1 subjects (0.60 +/- 0.11).	Diclofenac	21-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
14527094-5	2003	The mean (+/- SD) of diclofenac/4"-OH diclofenac ratio was 1.5 times higher among subjects carrying CYP2C9*3 allele (CYP2C9*1/*3 and CYP2C9*2/*3 genotypes) (0.91 +/- 0.28), compared to CYP2C9*1/*1 subjects (0.60 +/- 0.11).	Diclofenac	21-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
14527094-5	2003	The mean (+/- SD) of diclofenac/4"-OH diclofenac ratio was 1.5 times higher among subjects carrying CYP2C9*3 allele (CYP2C9*1/*3 and CYP2C9*2/*3 genotypes) (0.91 +/- 0.28), compared to CYP2C9*1/*1 subjects (0.60 +/- 0.11).	4"-oh diclofenac	32-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
14527094-5	2003	The mean (+/- SD) of diclofenac/4"-OH diclofenac ratio was 1.5 times higher among subjects carrying CYP2C9*3 allele (CYP2C9*1/*3 and CYP2C9*2/*3 genotypes) (0.91 +/- 0.28), compared to CYP2C9*1/*1 subjects (0.60 +/- 0.11).	4"-oh diclofenac	32-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
14527094-5	2003	The mean (+/- SD) of diclofenac/4"-OH diclofenac ratio was 1.5 times higher among subjects carrying CYP2C9*3 allele (CYP2C9*1/*3 and CYP2C9*2/*3 genotypes) (0.91 +/- 0.28), compared to CYP2C9*1/*1 subjects (0.60 +/- 0.11).	4"-oh diclofenac	32-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
14527094-5	2003	The mean (+/- SD) of diclofenac/4"-OH diclofenac ratio was 1.5 times higher among subjects carrying CYP2C9*3 allele (CYP2C9*1/*3 and CYP2C9*2/*3 genotypes) (0.91 +/- 0.28), compared to CYP2C9*1/*1 subjects (0.60 +/- 0.11).	4"-oh diclofenac	32-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
14527094-6	2003	The results show that the urinary diclofenac/4"-OH diclofenac ratio might be used to study CYP2C9 in humans.	Diclofenac	34-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
14527094-6	2003	The results show that the urinary diclofenac/4"-OH diclofenac ratio might be used to study CYP2C9 in humans.	4"-oh diclofenac	45-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
12742136-0	2003	Analysis of diclofenac and its metabolites by high-performance liquid chromatography: relevance of CYP2C9 genotypes in diclofenac urinary metabolic ratios.	Diclofenac	119-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
12742136-2	2003	The polymorphic CYP2C9 is involved in the metabolism of diclofenac to 4"-OH diclofenac and 3"-OH diclofenac.	Diclofenac	56-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
12742136-2	2003	The polymorphic CYP2C9 is involved in the metabolism of diclofenac to 4"-OH diclofenac and 3"-OH diclofenac.	4"-oh diclofenac	70-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
12742136-2	2003	The polymorphic CYP2C9 is involved in the metabolism of diclofenac to 4"-OH diclofenac and 3"-OH diclofenac.	3"-oh diclofenac	91-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
12742136-7	2003	The relationship between diclofenac metabolic ratios among different CYP2C9 genotypes is reported.	Diclofenac	25-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
12742136-8	2003	The CYP2C9*3/*3 subject had the highest diclofenac/4"-OH ratios.	Diclofenac	40-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
12742136-8	2003	The CYP2C9*3/*3 subject had the highest diclofenac/4"-OH ratios.	4"-oh	51-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
12728288-15	2003	CONCLUSIONS: CYP2C9*3 variants are associated with an increased bleeding risk in patients anticoagulated with phenprocoumon.	Phenprocoumon	110-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
12734606-6	2003	The diclofenac/4"-OH diclofenac urinary ratio, but not the diclofenac/3"-OH diclofenac and diclofenac/5-OH diclofenac ratios, was related to CYP2C9 genotype.	Diclofenac	4-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
12734606-6	2003	The diclofenac/4"-OH diclofenac urinary ratio, but not the diclofenac/3"-OH diclofenac and diclofenac/5-OH diclofenac ratios, was related to CYP2C9 genotype.	4"-oh diclofenac	15-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
12734606-6	2003	The diclofenac/4"-OH diclofenac urinary ratio, but not the diclofenac/3"-OH diclofenac and diclofenac/5-OH diclofenac ratios, was related to CYP2C9 genotype.	Diclofenac	21-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
12734606-6	2003	The diclofenac/4"-OH diclofenac urinary ratio, but not the diclofenac/3"-OH diclofenac and diclofenac/5-OH diclofenac ratios, was related to CYP2C9 genotype.	Diclofenac	21-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
12734606-9	2003	CYP2C9*3 allele seems to influence the 4"-hydroxylation of diclofenac, although there is a large overlapping in the urinary metabolic ratio between the genotype groups studied	Diclofenac	59-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
12695341-10	2003	These data indicate that voriconazole is a substrate for CYP2C9, CYP2C19, and CYP3A4, with CYP2C9 involvement being minimal in human liver microsomes.	Voriconazole	25-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
14739630-3	2003	Genetic variants associated with the metabolism of (S)-warfarin by cytochrome P450 2C9 may have specific implications on untoward effects.	Warfarin	51-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-86
14739630-5	2003	Studies have demonstrated that initial dosing of warfarin with CYP2C9*3 with a five-milligram dose caused an increase in the international normalized ratio and significant risk of bleeding.	Warfarin	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
12800253-0	2003	Rapid detection of the known SNPs of CYP2C9 using oligonucleotide microarray.	Oligonucleotides	50-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
12800253-3	2003	In order to facilitate the detection of the known SNPs of CYP2C9, an allele-specific oligonucleotide (ASO) based microarray was made.	Oligonucleotides	85-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
12800253-3	2003	In order to facilitate the detection of the known SNPs of CYP2C9, an allele-specific oligonucleotide (ASO) based microarray was made.	1,5-anhydroglucitol	102-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
12800253-4	2003	METHODS: An oligonucleotide microarray was made to facilitate the SNP (single nucleotide polymorphism) screening and was applied for the detection of CYP2C9 polymorphism in 62 high blood pressure (HBP) patients who received Irbesartan for treatment.	Oligonucleotides	12-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
12800253-6	2003	And the relation between CYP2C9 polymorphism and therapeutic outcome of Irbesartan was statistically analyzed.	Irbesartan	72-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
12800253-11	2003	CONCLUSION: The oligonucleotide microarray made in this study is a reliable assay for detecting the CYP2C9 known alleles and the heterozygous CYP2C9*1/*3 has no significant effects on the therapeutic outcome of Irbesartan.	Oligonucleotides	16-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
12800253-11	2003	CONCLUSION: The oligonucleotide microarray made in this study is a reliable assay for detecting the CYP2C9 known alleles and the heterozygous CYP2C9*1/*3 has no significant effects on the therapeutic outcome of Irbesartan.	Irbesartan	211-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
12867215-12	2003	However, as 80% of voriconazole is hepatically eliminated, primarily via the cytochrome P450 (CYP) isozymes CYP2C19, CYP3A4, and CYP2C9, voriconazole has a high potential for drug interactions, and dose reduction is recommended in patients with mild to moderate hepatic dysfunction (Child-Pugh class A or B).	Voriconazole	19-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
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
12684728-7	2003	No correlation was found between 4-hydroxylation of cyclophosphamide and the formation rate of hydroxycelecoxib, mainly catalysed by CYP2C9 ( r(s)=0.17, P=0.55, n=32).	Hydroxy Celecoxib	95-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
12820813-0	2003	Losartan and E3174 pharmacokinetics in cytochrome P450 2C9*1/*1, *1/*2, and *1/*3 individuals.	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-58
12820813-0	2003	Losartan and E3174 pharmacokinetics in cytochrome P450 2C9*1/*1, *1/*2, and *1/*3 individuals.	losartan carboxylic acid	13-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-58
12820813-8	2003	A significant association between CYP2C9 genotype and losartan to E3174 formation clearance was observed, such that 50% of the variability was accounted for by the genotype.	Losartan	54-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
12820813-8	2003	A significant association between CYP2C9 genotype and losartan to E3174 formation clearance was observed, such that 50% of the variability was accounted for by the genotype.	losartan carboxylic acid	66-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
12820813-11	2003	Alterations in losartan dosing in CYP2C9*1/*2 and *1/*3 individuals does not appear necessary.	Losartan	15-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
12708941-12	2003	Phenytoin induces the metabolism of drugs that are substrates of CYP2C, CYP2D, and CYP3A; however, phenytoin is eliminated predominantly by CYP2C9- and CYP2C19-dependent hepatic metabolism.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
12708941-12	2003	Phenytoin induces the metabolism of drugs that are substrates of CYP2C, CYP2D, and CYP3A; however, phenytoin is eliminated predominantly by CYP2C9- and CYP2C19-dependent hepatic metabolism.	Phenytoin	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
12708941-16	2003	CONCLUSIONS: Phenytoin is a known inducer of drugs metabolized by CYP2C, CYP2D, and CYP3A, but its own metabolism may be altered by drugs influencing CYP2C9 or CYP2C19, such as diazepam.	Phenytoin	13-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
12708941-16	2003	CONCLUSIONS: Phenytoin is a known inducer of drugs metabolized by CYP2C, CYP2D, and CYP3A, but its own metabolism may be altered by drugs influencing CYP2C9 or CYP2C19, such as diazepam.	Diazepam	177-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
12695341-10	2003	These data indicate that voriconazole is a substrate for CYP2C9, CYP2C19, and CYP3A4, with CYP2C9 involvement being minimal in human liver microsomes.	Voriconazole	25-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
12724615-3	2003	The most important of these is CYP2C9, which hydroxylates the S-enantiomers of warfarin, acenocoumarol and phenprocoumon with high catalytic activity.	Warfarin	79-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
12682803-3	2003	The present study aimed to evaluate the influence of CYP2D6 and CYP2C9 genotypes, and tobacco smoking on steady-state thioridazine plasma levels.	Thioridazine	118-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
12724615-3	2003	The most important of these is CYP2C9, which hydroxylates the S-enantiomers of warfarin, acenocoumarol and phenprocoumon with high catalytic activity.	Acenocoumarol	89-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
12724615-3	2003	The most important of these is CYP2C9, which hydroxylates the S-enantiomers of warfarin, acenocoumarol and phenprocoumon with high catalytic activity.	Phenprocoumon	107-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
12724615-4	2003	In at least eight separate clinical studies, possession of the CYP2C9*2 or CYP2C9*3 variant alleles, which result in decreased enzyme activity, has been associated with a significant decrease in a mean warfarin dose requirement.	Warfarin	202-210	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
12724615-4	2003	In at least eight separate clinical studies, possession of the CYP2C9*2 or CYP2C9*3 variant alleles, which result in decreased enzyme activity, has been associated with a significant decrease in a mean warfarin dose requirement.	Warfarin	202-210	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
12724615-6	2003	Possession of the CYP2C9*3 variant also appears to be associated with a low acenocoumarol dose requirement.	Acenocoumarol	76-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
12721102-22	2003	Of the other isoforms studied, CYP2C9 and CYP3A4 contribute to a lesser degree to promazine 5-sulphoxidation and N-demethylation, respectively.	Promazine	82-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
12698304-0	2003	Differences in flurbiprofen pharmacokinetics between CYP2C9*1/*1, *1/*2, and *1/*3 genotypes.	Flurbiprofen	15-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
12642470-7	2003	Inhibition studies conducted for CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP3A4, CYP2A6, and CYP2E1 showed troglitazone to be the most nonselective and potent inhibitor followed by rosiglitazone and pioglitazone.	Troglitazone	108-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
12642470-9	2003	Troglitazone, in addition, inhibited CYP2C9 (K(i) 0.6 microM).	Troglitazone	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
12698304-4	2003	RESULTS: CYP2C9 genotype was a significant predictor of flurbiprofen metabolism and accounted for 59% of the variability in flurbiprofen AUC(0- infinity ), and approximately 50% of the variability in flurbiprofen oral clearance, formation clearance to 4"-hydroxyflurbiprofen, and the 0 to 24-h urinary metabolic ratio of flurbiprofen to 4"-hydroxyflurbiprofen.	4'-hydroxyflurbiprofen	252-274	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
12698304-1	2003	OBJECTIVE: This study was conducted to examine differences in flurbiprofen metabolism among individuals with the CYP2C9*1/*1, *1/*2, and *1/*3 genotypes.	Flurbiprofen	62-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
12698304-4	2003	RESULTS: CYP2C9 genotype was a significant predictor of flurbiprofen metabolism and accounted for 59% of the variability in flurbiprofen AUC(0- infinity ), and approximately 50% of the variability in flurbiprofen oral clearance, formation clearance to 4"-hydroxyflurbiprofen, and the 0 to 24-h urinary metabolic ratio of flurbiprofen to 4"-hydroxyflurbiprofen.	Flurbiprofen	124-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
12698304-4	2003	RESULTS: CYP2C9 genotype was a significant predictor of flurbiprofen metabolism and accounted for 59% of the variability in flurbiprofen AUC(0- infinity ), and approximately 50% of the variability in flurbiprofen oral clearance, formation clearance to 4"-hydroxyflurbiprofen, and the 0 to 24-h urinary metabolic ratio of flurbiprofen to 4"-hydroxyflurbiprofen.	4'-hydroxyflurbiprofen	337-359	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
12698304-5	2003	Flurbiprofen AUC(0- infinity )was significantly higher and all measures of flurbiprofen clearance were significantly lower in the CYP2C9*1/*3 individuals than in those with *1/*1.	Flurbiprofen	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
12698304-5	2003	Flurbiprofen AUC(0- infinity )was significantly higher and all measures of flurbiprofen clearance were significantly lower in the CYP2C9*1/*3 individuals than in those with *1/*1.	Flurbiprofen	75-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
12698304-7	2003	CONCLUSIONS: CYP2C9 genotype is a significant predictor of flurbiprofen disposition in humans by altering CYP2C9-mediated metabolism and reducing systemic clearance.	Flurbiprofen	59-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
12698304-4	2003	RESULTS: CYP2C9 genotype was a significant predictor of flurbiprofen metabolism and accounted for 59% of the variability in flurbiprofen AUC(0- infinity ), and approximately 50% of the variability in flurbiprofen oral clearance, formation clearance to 4"-hydroxyflurbiprofen, and the 0 to 24-h urinary metabolic ratio of flurbiprofen to 4"-hydroxyflurbiprofen.	Flurbiprofen	56-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
12698304-4	2003	RESULTS: CYP2C9 genotype was a significant predictor of flurbiprofen metabolism and accounted for 59% of the variability in flurbiprofen AUC(0- infinity ), and approximately 50% of the variability in flurbiprofen oral clearance, formation clearance to 4"-hydroxyflurbiprofen, and the 0 to 24-h urinary metabolic ratio of flurbiprofen to 4"-hydroxyflurbiprofen.	Flurbiprofen	124-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
12698304-4	2003	RESULTS: CYP2C9 genotype was a significant predictor of flurbiprofen metabolism and accounted for 59% of the variability in flurbiprofen AUC(0- infinity ), and approximately 50% of the variability in flurbiprofen oral clearance, formation clearance to 4"-hydroxyflurbiprofen, and the 0 to 24-h urinary metabolic ratio of flurbiprofen to 4"-hydroxyflurbiprofen.	Flurbiprofen	124-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
12586744-4	2003	CYP 2C9 overexpression was associated with the activation of Akt and an increase in cyclin D1 expression, effects that were abolished by the epidermal growth factor (EGF) receptor inhibitor, AG1478, which also prevented the CYP 2C9-induced increase in cell proliferation.	RTKI cpd	191-197	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	224-231
12698304-7	2003	CONCLUSIONS: CYP2C9 genotype is a significant predictor of flurbiprofen disposition in humans by altering CYP2C9-mediated metabolism and reducing systemic clearance.	Flurbiprofen	59-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
12586744-0	2003	Cytochrome P450 2C9-derived epoxyeicosatrienoic acids induce angiogenesis via cross-talk with the epidermal growth factor receptor (EGFR).	epoxyeicosatrienoic acids	28-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
12586744-5	2003	Stimulation of EGF receptor overexpressing cells with 11,12-EET or transfection of these cells with CYP 2C9 enhanced the tyrosine phosphorylation of the EGF receptor.	Tyrosine	121-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-107
12586744-3	2003	In human endothelial cells overexpressing CYP 2C9, cell number was increased compared with control cells and was inhibited by the CYP 2C9 inhibitor, sulfaphenazole.	Sulfaphenazole	149-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-49
12621390-0	2003	Population differences in S-warfarin metabolism between CYP2C9 genotype-matched Caucasian and Japanese patients.	Warfarin	28-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
12586744-3	2003	In human endothelial cells overexpressing CYP 2C9, cell number was increased compared with control cells and was inhibited by the CYP 2C9 inhibitor, sulfaphenazole.	Sulfaphenazole	149-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-137
12586744-4	2003	CYP 2C9 overexpression was associated with the activation of Akt and an increase in cyclin D1 expression, effects that were abolished by the epidermal growth factor (EGF) receptor inhibitor, AG1478, which also prevented the CYP 2C9-induced increase in cell proliferation.	RTKI cpd	191-197	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-7
12649384-2	2003	Cytochromes P450 1A1 (18.5), 1A2 (20), and 2D6 (100) catalyzed the O-demethylation of harmaline, and CYP1A1 (98.5), CYP1A2 (35), CYP2C9 (16), CYP2C19 (30), and CYP2D6 (115) catalyzed that of harmine (relative activities).	Harmaline	86-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
12649384-5	2003	K(cat) (min(-1)) and K(m) Awake M) values for harmaline were: CYP1A1, 10.8 and 11.8; CYP1A2, 12.3 and 13.3; CYP2C9, 5.3 and 175; CYP2C19, 10.3 and 160; and CYP2D6, 39.9 and 1.4.	Harmaline	46-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
12649384-6	2003	Values for harmine were: CYP1A1, 45.2 and 52.2; CYP1A2, 9.2 and 14.7; CYP2C9, 11.9 and 117; CYP2C19, 21.4 and 121; and CYP2D6, 29.7 and 7.4.	Harmine	11-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
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 9	Homo sapiens	170-176
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.	BINOL, naphthol	139-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-176
12482324-1	2003	Human cytochrome P450 2C9 (CYP2C9) is important in the metabolism of non-steroidal anti-inflammatory compounds such as diclofenac, the antidiabetic agent tolbutamide and other clinically important drugs, many of which are weakly acidic.	Diclofenac	119-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-25
12482324-1	2003	Human cytochrome P450 2C9 (CYP2C9) is important in the metabolism of non-steroidal anti-inflammatory compounds such as diclofenac, the antidiabetic agent tolbutamide and other clinically important drugs, many of which are weakly acidic.	Diclofenac	119-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
12482324-1	2003	Human cytochrome P450 2C9 (CYP2C9) is important in the metabolism of non-steroidal anti-inflammatory compounds such as diclofenac, the antidiabetic agent tolbutamide and other clinically important drugs, many of which are weakly acidic.	Tolbutamide	154-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-25
12482324-1	2003	Human cytochrome P450 2C9 (CYP2C9) is important in the metabolism of non-steroidal anti-inflammatory compounds such as diclofenac, the antidiabetic agent tolbutamide and other clinically important drugs, many of which are weakly acidic.	Tolbutamide	154-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
12482324-2	2003	Multiple sequence alignment of CYPs identified CYP2C9 Asp(293) as corresponding to Asp(301) of CYP2D6, which has been suggested to play a role in the binding of basic substrates to the latter enzyme.	Aspartic Acid	54-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
12482324-2	2003	Multiple sequence alignment of CYPs identified CYP2C9 Asp(293) as corresponding to Asp(301) of CYP2D6, which has been suggested to play a role in the binding of basic substrates to the latter enzyme.	Aspartic Acid	83-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
12482324-8	2003	Our analysis suggests a structural role for the carboxyl side chain of Asp(293) in CYP2C9 substrate binding and catalysis.	Aspartic Acid	71-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
12615570-4	2003	DISCUSSION: adverse outcomes with warfarin therapy could be explained and possibly avoided by identifying patients with variant alleles for CYP2C9 before initiation of therapy.	Warfarin	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
12621390-1	2003	OBJECTIVE: Our objective was to investigate population differences in the metabolic activity of cytochrome P450 (CYP) 2C9 between genotypically matched Caucasian and Japanese patients by using the unbound oral clearance of S-warfarin as an in vivo phenotypic trait measure.	Sulfur	223-224	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-121
12621390-1	2003	OBJECTIVE: Our objective was to investigate population differences in the metabolic activity of cytochrome P450 (CYP) 2C9 between genotypically matched Caucasian and Japanese patients by using the unbound oral clearance of S-warfarin as an in vivo phenotypic trait measure.	Warfarin	225-233	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-121
12621390-9	2003	In addition, Japanese patients heterozygous for the CYP2C9*3 genotype (n = 4) showed a significantly (P &lt;.05) reduced unbound oral clearance for S-warfarin, by 63%, as compared with Japanese patients possessing the homozygous CYP2C9*1 genotype.	Warfarin	150-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
12637241-18	2003	Correlation analysis suggested that CYP2B11 catalyses the N-demethylation of dextromethorphan (mediated in humans by CYP3A) and the 4"-hydroxylation of mephenytoin (mediated in humans by CYP2C19) in the dog, and that this enzyme and CYP3A12 contribute to S-warfarin 7-hydroxylation (mediated in humans by CYP2C9).	Nitrogen	58-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	305-311
12639175-8	2003	Drug interactions occur through inhibition of the CYP2C9, CYP2C19, and CYP3A4 isoenzymes, resulting in alterations in kinetic parameters of either voriconazole or the interacting agent.	Voriconazole	147-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
12713683-7	2003	In addition, bosentan is not only a substrate but also an inducer of CYP3A4 and CYP2C9.	Bosentan	13-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
12637241-5	2003	The rate of 7-hydroxylation of S-warfarin (CYP2C9 in humans) by dog liver microsomes (mean +/- SD from 12 (six male and six female) dogs = 10.8 +/- 1.9 fmol mg(-1) protein min(-1)) was 1.5-2 orders of magnitude lower than that in humans.	Warfarin	31-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
12573493-2	2003	There is strong evidence suggesting that the activation of a CYP 2C epoxygenase in endothelial cells is an essential step in nitric oxide (NO)- and prostacyclin (PGI(2))-independent vasodilatation of several vascular beds, particularly in the heart and kidney.	Nitric Oxide	125-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
12573493-2	2003	There is strong evidence suggesting that the activation of a CYP 2C epoxygenase in endothelial cells is an essential step in nitric oxide (NO)- and prostacyclin (PGI(2))-independent vasodilatation of several vascular beds, particularly in the heart and kidney.	Epoprostenol	148-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
12573493-2	2003	There is strong evidence suggesting that the activation of a CYP 2C epoxygenase in endothelial cells is an essential step in nitric oxide (NO)- and prostacyclin (PGI(2))-independent vasodilatation of several vascular beds, particularly in the heart and kidney.	Epoprostenol	162-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
12573493-6	2003	Cerivastatin and fluvastatin increase CYP 2C mRNA and protein in native and cultured endothelial cells, and enhance the bradykinin-induced NO/PGI(2)-independent relaxation of arterial segments as well as the generation of reactive oxygen species.	cerivastatin	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
12573493-6	2003	Cerivastatin and fluvastatin increase CYP 2C mRNA and protein in native and cultured endothelial cells, and enhance the bradykinin-induced NO/PGI(2)-independent relaxation of arterial segments as well as the generation of reactive oxygen species.	Fluvastatin	17-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
12446689-9	2003	Intriguingly, removal of the negative charge from either 216 or 301 produced enzymes (E216A, E216K, and D301Q) with elevated levels (50-75-fold) of catalytic activity toward diclofenac, a carboxylate-containing CYP2C9 substrate that lacks a basic nitrogen atom.	Diclofenac	174-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	211-217
12446689-9	2003	Intriguingly, removal of the negative charge from either 216 or 301 produced enzymes (E216A, E216K, and D301Q) with elevated levels (50-75-fold) of catalytic activity toward diclofenac, a carboxylate-containing CYP2C9 substrate that lacks a basic nitrogen atom.	Nitrogen	247-255	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	211-217
12446689-11	2003	The kinetic parameters for diclofenac (K(m) 108 microm, k(cat) 5 min(-1)) along with nifedipine (K(m) 28 microm, k(cat) 2 min(-1)) and tolbutamide (K(m) 315 microm, k(cat) 1 min(-1)), which are not normally substrates for CYP2D6, were within an order of magnitude of those observed with CYP3A4 or CYP2C9.	Diclofenac	27-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	297-303
12549950-10	2003	Fenofibrate is also a mild to moderate inhibitor of CYP2C9, the enzyme responsible for warfarin metabolism.	Fenofibrate	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
12549950-10	2003	Fenofibrate is also a mild to moderate inhibitor of CYP2C9, the enzyme responsible for warfarin metabolism.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
12559973-1	2003	Studies were designed to investigate the possible mechanisms associated with the kinetic observation of CYP2C9 activation by dapsone and its phase I metabolite, N-hydroxydapsone.	Dapsone	125-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
12559973-1	2003	Studies were designed to investigate the possible mechanisms associated with the kinetic observation of CYP2C9 activation by dapsone and its phase I metabolite, N-hydroxydapsone.	4-amino-4'-hydroxylaminodiphenylsulfone	161-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
12559973-2	2003	Kinetic studies suggested that dapsone activated CYP2C9-mediated flurbiprofen 4(")-hydroxylation by decreasing the K(m) (alpha=0.2) and increasing the V(max) (beta=1.9).	Dapsone	31-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
12559973-2	2003	Kinetic studies suggested that dapsone activated CYP2C9-mediated flurbiprofen 4(")-hydroxylation by decreasing the K(m) (alpha=0.2) and increasing the V(max) (beta=1.9).	Flurbiprofen	65-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
12559973-5	2003	In the presence of dapsone, the spectral binding constant (K(s)) for flurbiprofen was reduced from 14.1 to 2.1 microM, while in the presence of N-hydroxydapsone, the K(s) remained unchanged (14.0 microM), which suggests that dapsone causes an increase in the affinity of flurbiprofen for CYP2C9, whereas N-hydroxydapsone does not.	Dapsone	19-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	288-294
12559973-5	2003	In the presence of dapsone, the spectral binding constant (K(s)) for flurbiprofen was reduced from 14.1 to 2.1 microM, while in the presence of N-hydroxydapsone, the K(s) remained unchanged (14.0 microM), which suggests that dapsone causes an increase in the affinity of flurbiprofen for CYP2C9, whereas N-hydroxydapsone does not.	Flurbiprofen	69-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	288-294
12559973-7	2003	Interestingly, the presence of N-hydroxydapsone generally caused the same effects on stoichiometry as those of flurbiprofen 4(")-hydroxylation but failed to reduce excess water formation, which suggests that, while N-hydroxydapsone activates CYP2C9, it does so less efficiently and possibly through a mechanism different from that of dapsone.	Dapsone	40-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	242-248
12450521-8	2003	This result suggests the implication of genetically polymorphic enzymes, presumably CYP2D6, CYP2C9 and CYP2C19 in the metabolism of fluoxetine to norfluoxetine.	Fluoxetine	132-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
12450521-8	2003	This result suggests the implication of genetically polymorphic enzymes, presumably CYP2D6, CYP2C9 and CYP2C19 in the metabolism of fluoxetine to norfluoxetine.	norfluoxetine	146-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
12388259-5	2003	Finally, we tested the most abundant arachidonic acid metabolite of CYP2C9, 14,15-epoxyeicosatrienoic acid, which induced angiogenesis in vivo when embedded in Matrigel plugs and implanted in adult rats.	Arachidonic Acid	37-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
12388259-5	2003	Finally, we tested the most abundant arachidonic acid metabolite of CYP2C9, 14,15-epoxyeicosatrienoic acid, which induced angiogenesis in vivo when embedded in Matrigel plugs and implanted in adult rats.	14,15-epoxy-5,8,11-eicosatrienoic acid	76-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
12464242-2	2003	From a consideration of specific interactions between drug substrates for human CYP2 family enzymes and the putative active sites of CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, and CYP2E1, it is likely that the number and disposition of hydrogen bond donor/acceptors and aromatic rings within the various P450 substrate molecules determines their enzyme selectivity and binding affinity, together with directing their preferred routes of metabolism by the CYP2 enzymes concerned.	Hydrogen	242-250	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
12464247-0	2003	Substrate selectivity of human cytochrome P450 2C9: importance of residues 476, 365, and 114 in recognition of diclofenac and sulfaphenazole and in mechanism-based inactivation by tienilic acid.	Diclofenac	111-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-50
12464247-0	2003	Substrate selectivity of human cytochrome P450 2C9: importance of residues 476, 365, and 114 in recognition of diclofenac and sulfaphenazole and in mechanism-based inactivation by tienilic acid.	Sulfaphenazole	126-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-50
12464247-0	2003	Substrate selectivity of human cytochrome P450 2C9: importance of residues 476, 365, and 114 in recognition of diclofenac and sulfaphenazole and in mechanism-based inactivation by tienilic acid.	Ticrynafen	180-193	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-50
12464247-1	2003	A series of six site-directed mutants of CYP 2C9 were constructed with the aim to better define the amino acid residues that play a critical role in substrate selectivity of CYP 2C9, particularly in three distinctive properties of this enzyme: (i) its selective mechanism-based inactivation by tienilic acid (TA), (ii) its high affinity and hydroxylation regioselectivity toward diclofenac, and (iii) its high affinity for the competitive inhibitor sulfaphenazole (SPA).	Ticrynafen	294-307	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-48
12464247-1	2003	A series of six site-directed mutants of CYP 2C9 were constructed with the aim to better define the amino acid residues that play a critical role in substrate selectivity of CYP 2C9, particularly in three distinctive properties of this enzyme: (i) its selective mechanism-based inactivation by tienilic acid (TA), (ii) its high affinity and hydroxylation regioselectivity toward diclofenac, and (iii) its high affinity for the competitive inhibitor sulfaphenazole (SPA).	Ticrynafen	294-307	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	174-181
12464247-1	2003	A series of six site-directed mutants of CYP 2C9 were constructed with the aim to better define the amino acid residues that play a critical role in substrate selectivity of CYP 2C9, particularly in three distinctive properties of this enzyme: (i) its selective mechanism-based inactivation by tienilic acid (TA), (ii) its high affinity and hydroxylation regioselectivity toward diclofenac, and (iii) its high affinity for the competitive inhibitor sulfaphenazole (SPA).	Ticrynafen	309-311	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-48
12464247-1	2003	A series of six site-directed mutants of CYP 2C9 were constructed with the aim to better define the amino acid residues that play a critical role in substrate selectivity of CYP 2C9, particularly in three distinctive properties of this enzyme: (i) its selective mechanism-based inactivation by tienilic acid (TA), (ii) its high affinity and hydroxylation regioselectivity toward diclofenac, and (iii) its high affinity for the competitive inhibitor sulfaphenazole (SPA).	Ticrynafen	309-311	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	174-181
12464247-1	2003	A series of six site-directed mutants of CYP 2C9 were constructed with the aim to better define the amino acid residues that play a critical role in substrate selectivity of CYP 2C9, particularly in three distinctive properties of this enzyme: (i) its selective mechanism-based inactivation by tienilic acid (TA), (ii) its high affinity and hydroxylation regioselectivity toward diclofenac, and (iii) its high affinity for the competitive inhibitor sulfaphenazole (SPA).	Diclofenac	379-389	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-48
12464247-1	2003	A series of six site-directed mutants of CYP 2C9 were constructed with the aim to better define the amino acid residues that play a critical role in substrate selectivity of CYP 2C9, particularly in three distinctive properties of this enzyme: (i) its selective mechanism-based inactivation by tienilic acid (TA), (ii) its high affinity and hydroxylation regioselectivity toward diclofenac, and (iii) its high affinity for the competitive inhibitor sulfaphenazole (SPA).	Diclofenac	379-389	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	174-181
12464247-1	2003	A series of six site-directed mutants of CYP 2C9 were constructed with the aim to better define the amino acid residues that play a critical role in substrate selectivity of CYP 2C9, particularly in three distinctive properties of this enzyme: (i) its selective mechanism-based inactivation by tienilic acid (TA), (ii) its high affinity and hydroxylation regioselectivity toward diclofenac, and (iii) its high affinity for the competitive inhibitor sulfaphenazole (SPA).	Sulfaphenazole	449-463	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-48
12464247-1	2003	A series of six site-directed mutants of CYP 2C9 were constructed with the aim to better define the amino acid residues that play a critical role in substrate selectivity of CYP 2C9, particularly in three distinctive properties of this enzyme: (i) its selective mechanism-based inactivation by tienilic acid (TA), (ii) its high affinity and hydroxylation regioselectivity toward diclofenac, and (iii) its high affinity for the competitive inhibitor sulfaphenazole (SPA).	Sulfaphenazole	449-463	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	174-181
12464247-5	2003	At the opposite end, the F94L and F110I mutants showed properties very similar to those of CYP 2C9 toward TA and diclofenac.	Ticrynafen	106-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-98
12464247-5	2003	At the opposite end, the F94L and F110I mutants showed properties very similar to those of CYP 2C9 toward TA and diclofenac.	Diclofenac	113-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-98
12464247-7	2003	These data indicate that Phe 114 plays an important role in recognition of aromatic substrates of CYP 2C9, presumably via Pi-stacking interactions.	Phenylalanine	25-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-105
12464247-8	2003	They also provide the first experimental evidence showing that Phe 476 plays a crucial role in substrate recognition and hydroxylation by CYP 2C9.	Phenylalanine	63-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-145
14558433-8	2003	Likewise, fluconazole interferes with the CYP2C9-mediated hepatic elimination of fluvastatin.	Fluconazole	10-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
14558433-8	2003	Likewise, fluconazole interferes with the CYP2C9-mediated hepatic elimination of fluvastatin.	Fluvastatin	81-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
14650362-6	2003	The cytochrome P (CYP) enzyme CYP2C9 plays a major role in the metabolism of gemfibrozil.	Gemfibrozil	77-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
12634980-1	2003	BACKGROUND: Cytochrome P450 2C9 (CYP2C9) allelic variant carriers have been shown to experience hyper-responsiveness to small doses of oral anticoagulants (OAs) (warfarin or acenocoumarol) and a higher bleeding rate.	Warfarin	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-31
12634980-1	2003	BACKGROUND: Cytochrome P450 2C9 (CYP2C9) allelic variant carriers have been shown to experience hyper-responsiveness to small doses of oral anticoagulants (OAs) (warfarin or acenocoumarol) and a higher bleeding rate.	Warfarin	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
12634980-1	2003	BACKGROUND: Cytochrome P450 2C9 (CYP2C9) allelic variant carriers have been shown to experience hyper-responsiveness to small doses of oral anticoagulants (OAs) (warfarin or acenocoumarol) and a higher bleeding rate.	Acenocoumarol	174-187	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-31
12634980-1	2003	BACKGROUND: Cytochrome P450 2C9 (CYP2C9) allelic variant carriers have been shown to experience hyper-responsiveness to small doses of oral anticoagulants (OAs) (warfarin or acenocoumarol) and a higher bleeding rate.	Acenocoumarol	174-187	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
12637241-18	2003	Correlation analysis suggested that CYP2B11 catalyses the N-demethylation of dextromethorphan (mediated in humans by CYP3A) and the 4"-hydroxylation of mephenytoin (mediated in humans by CYP2C19) in the dog, and that this enzyme and CYP3A12 contribute to S-warfarin 7-hydroxylation (mediated in humans by CYP2C9).	Dextromethorphan	77-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	305-311
12637241-18	2003	Correlation analysis suggested that CYP2B11 catalyses the N-demethylation of dextromethorphan (mediated in humans by CYP3A) and the 4"-hydroxylation of mephenytoin (mediated in humans by CYP2C19) in the dog, and that this enzyme and CYP3A12 contribute to S-warfarin 7-hydroxylation (mediated in humans by CYP2C9).	Mephenytoin	152-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	305-311
12637241-18	2003	Correlation analysis suggested that CYP2B11 catalyses the N-demethylation of dextromethorphan (mediated in humans by CYP3A) and the 4"-hydroxylation of mephenytoin (mediated in humans by CYP2C19) in the dog, and that this enzyme and CYP3A12 contribute to S-warfarin 7-hydroxylation (mediated in humans by CYP2C9).	Warfarin	257-265	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	305-311
12603175-0	2003	Influence of age and cytochrome P450 2C9 genotype on the steady-state disposition of diclofenac and celecoxib.	Diclofenac	85-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-40
12485954-5	2003	The metabolism of NE-100 was mediated with recombinant CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4.	N,N-dipropyl-2-(4-methoxy-3-(2-phenylethoxy)phenyl)ethylamine monohydrochloride	18-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
12534640-1	2003	AIMS: The cytochrome P450 enzyme CYP2C9 catalyses the 4"-hydroxylation of the nonsteroidal analgesic drug diclofenac in humans.	Diclofenac	106-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
12534640-2	2003	We studied the influences of the known amino acid variants, CYP2C9*2 (Arg144Cys) and CYP2C9*3 (Ile359Leu), on diclofenac pharmacokinetics after a 50-mg oral dose of diclofenac in healthy volunteers.	Diclofenac	110-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
12534640-2	2003	We studied the influences of the known amino acid variants, CYP2C9*2 (Arg144Cys) and CYP2C9*3 (Ile359Leu), on diclofenac pharmacokinetics after a 50-mg oral dose of diclofenac in healthy volunteers.	Diclofenac	110-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
12882588-10	2003	Rifampicin also induces CYP2C-mediated metabolism and thus reduces the plasma concentrations of, for example, the CYP2C9 substrate (S)-warfarin and the sulfonylurea antidiabetic drugs.	Rifampin	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
12882588-10	2003	Rifampicin also induces CYP2C-mediated metabolism and thus reduces the plasma concentrations of, for example, the CYP2C9 substrate (S)-warfarin and the sulfonylurea antidiabetic drugs.	Warfarin	135-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
14768975-8	2003	This may be due to increased metabolism of celecoxib due to the induction of cytochrome P4502C9 (CYP2C9) in liver.	Celecoxib	43-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-95
14768975-8	2003	This may be due to increased metabolism of celecoxib due to the induction of cytochrome P4502C9 (CYP2C9) in liver.	Celecoxib	43-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
15618748-8	2003	ABT exhibited the highest Ki value for CYP2C9-dependent diclofenac 4"-hydroxylation among those determined by this assay (Ki=3500 microM).	diclofenac 4"	56-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
12603175-0	2003	Influence of age and cytochrome P450 2C9 genotype on the steady-state disposition of diclofenac and celecoxib.	Celecoxib	100-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-40
12603176-1	2003	BACKGROUND: In vitro, bosentan has been shown to be a mild inducer of cytochrome P450 (CYP) 2C9 and 3A4.	Bosentan	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-95
14586772-4	2003	Aspirin-induced asthma (AIA) is a typical drug-induced phenotype due to aspirin or nonsteroidal antiinflammatory drugs, and these drugs are metabolized by CYP2C9 and UGT1A6, which are regulated by PXR.	Aspirin	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
12558459-7	2003	Cyclosporin-treated patients on the other hand show several-fold higher systemic exposure of all statins, both those that are metabolised by CYP3A4 and fluvastatin (metabolised by CYP2C9).	Cyclosporine	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	180-186
12558459-7	2003	Cyclosporin-treated patients on the other hand show several-fold higher systemic exposure of all statins, both those that are metabolised by CYP3A4 and fluvastatin (metabolised by CYP2C9).	Fluvastatin	152-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	180-186
12520632-0	2003	Tolbutamide, flurbiprofen, and losartan as probes of CYP2C9 activity in humans.	Tolbutamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
12520632-0	2003	Tolbutamide, flurbiprofen, and losartan as probes of CYP2C9 activity in humans.	Losartan	31-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
12520632-5	2003	The formation clearance of tolbutamide to its CYP2C9-mediated metabolites demonstrated a stronger association with genotype compared to flurbiprofen and losartan, respectively (r2 = 0.64 vs. 0.53 vs. 0.42).	Tolbutamide	27-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
12520632-5	2003	The formation clearance of tolbutamide to its CYP2C9-mediated metabolites demonstrated a stronger association with genotype compared to flurbiprofen and losartan, respectively (r2 = 0.64 vs. 0.53 vs. 0.42).	Losartan	153-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
12520632-8	2003	Tolbutamide is a better CYP2C9 probe than flurbiprofen and losartan, and the 0- to 12-hour amount of 4"-hydroxytolbutamide and carboxytolbutamide is the best urinary measure of its metabolism.	Tolbutamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
14682608-5	2003	In the presence of gemfibrozil, a focal point was obtained in Dixon plots, demonstrating that there was inhibition of CYP2C8-, CYP2C9- and CYP3A4-mediated metabolism.	Gemfibrozil	19-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-133
12509498-0	2003	Cytochrome P450 2C9 plays an important role in the regulation of exercise-induced skeletal muscle blood flow and oxygen uptake in humans.	Oxygen	113-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
12509498-9	2003	The results demonstrate that CYP 2C9 plays an important role in the regulation of hyperaemia and oxygen uptake during exercise.	Oxygen	97-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-36
12426520-6	2002	RESULTS: Tolbutamide area under the plasma concentration-time curve from time zero to infinity [AUC(0- infinity )] significantly increased by 1.5-fold and 1.9-fold, respectively, in subjects expressing the CYP2C9(*)1/(*)2 and (*)1/(*)3 genotypes compared with (*)1/(*)1 subjects.	Tolbutamide	9-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	206-212
14583800-1	2003	Alteration of monoaminergic neurotransmission has been implicated in the pathophysiology of mood disorders, and CYP2C9 enzyme activity has been shown to be modulated by serotonin in vitro.	Serotonin	169-178	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
14597963-0	2003	Influence of CYP2C9 genotypes on the formation of a hepatotoxic metabolite of valproic acid in human liver microsomes.	Valproic Acid	78-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
14597963-1	2003	The present study investigated the effect of cytochrome P450 2C9 (CYP2C9) genetic polymorphism on the biotransformation of valproic acid (VPA) to its hepatotoxic metabolite, 4-ene-VPA, and compared that to the formation of the inactive 4-OH-VPA and 5-OH-VPA.	Valproic Acid	123-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-64
14597963-1	2003	The present study investigated the effect of cytochrome P450 2C9 (CYP2C9) genetic polymorphism on the biotransformation of valproic acid (VPA) to its hepatotoxic metabolite, 4-ene-VPA, and compared that to the formation of the inactive 4-OH-VPA and 5-OH-VPA.	Valproic Acid	123-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
14597963-1	2003	The present study investigated the effect of cytochrome P450 2C9 (CYP2C9) genetic polymorphism on the biotransformation of valproic acid (VPA) to its hepatotoxic metabolite, 4-ene-VPA, and compared that to the formation of the inactive 4-OH-VPA and 5-OH-VPA.	Valproic Acid	138-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-64
14597963-1	2003	The present study investigated the effect of cytochrome P450 2C9 (CYP2C9) genetic polymorphism on the biotransformation of valproic acid (VPA) to its hepatotoxic metabolite, 4-ene-VPA, and compared that to the formation of the inactive 4-OH-VPA and 5-OH-VPA.	Valproic Acid	138-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
14597963-4	2003	The formation rates of 4-ene-VPA, 4-OH-VPA, and 5-OH-VPA in human liver microsomes were reduced by 29, 28, and 31%, respectively, in samples with one mutated CYP2C9 allele, and by 61, 73, and 58%, respectively, in samples with two mutated CYP2C9 alleles.	2-propyl-4-pentenoic acid	23-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
14597963-4	2003	The formation rates of 4-ene-VPA, 4-OH-VPA, and 5-OH-VPA in human liver microsomes were reduced by 29, 28, and 31%, respectively, in samples with one mutated CYP2C9 allele, and by 61, 73, and 58%, respectively, in samples with two mutated CYP2C9 alleles.	2-propyl-4-pentenoic acid	23-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	239-245
14597963-4	2003	The formation rates of 4-ene-VPA, 4-OH-VPA, and 5-OH-VPA in human liver microsomes were reduced by 29, 28, and 31%, respectively, in samples with one mutated CYP2C9 allele, and by 61, 73, and 58%, respectively, in samples with two mutated CYP2C9 alleles.	4-Hydroxyvalproic acid	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
14597963-4	2003	The formation rates of 4-ene-VPA, 4-OH-VPA, and 5-OH-VPA in human liver microsomes were reduced by 29, 28, and 31%, respectively, in samples with one mutated CYP2C9 allele, and by 61, 73, and 58%, respectively, in samples with two mutated CYP2C9 alleles.	4-Hydroxyvalproic acid	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	239-245
14597963-4	2003	The formation rates of 4-ene-VPA, 4-OH-VPA, and 5-OH-VPA in human liver microsomes were reduced by 29, 28, and 31%, respectively, in samples with one mutated CYP2C9 allele, and by 61, 73, and 58%, respectively, in samples with two mutated CYP2C9 alleles.	5-Hydroxyvalproic acid	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
14597963-4	2003	The formation rates of 4-ene-VPA, 4-OH-VPA, and 5-OH-VPA in human liver microsomes were reduced by 29, 28, and 31%, respectively, in samples with one mutated CYP2C9 allele, and by 61, 73, and 58%, respectively, in samples with two mutated CYP2C9 alleles.	5-Hydroxyvalproic acid	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	239-245
12433806-8	2002	In addition, the selectivity of (-)-OSU6162 to inhibit six human p450 enzymes (CYP1A2, CYP2C9, CYP2C19, CYP2E1, CYP2D6 and CYP3A4) was evaluated using an in vitro inhibition screen.	OSU 6162	32-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
12386124-0	2002	Activation of CYP2C9-mediated metabolism by a series of dapsone analogs: kinetics and structural requirements.	Dapsone	56-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
12386124-1	2002	Cytochrome P450 2C9-mediated metabolism has been shown to be activated in the presence of the effector dapsone.	Dapsone	103-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
12386124-9	2002	Overall, it is apparent from these studies that a sulfone group in direct association with two benzene rings with para-electron-donating groups represents the most efficient activator of CYP2C9.	Sulfones	50-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	187-193
12386124-9	2002	Overall, it is apparent from these studies that a sulfone group in direct association with two benzene rings with para-electron-donating groups represents the most efficient activator of CYP2C9.	Benzene	95-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	187-193
12386132-2	2002	Phenytoin is oxidized to 4"-HPPH by CYP2C9 and to a minor extent by CYP2C19, and then 4"-HPPH is metabolized to 4"-HPPH O-glucuronide by UDP-glucuronosyltransferase (UGT).	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
12386132-2	2002	Phenytoin is oxidized to 4"-HPPH by CYP2C9 and to a minor extent by CYP2C19, and then 4"-HPPH is metabolized to 4"-HPPH O-glucuronide by UDP-glucuronosyltransferase (UGT).	hydroxyphenytoin	25-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
12451430-1	2002	OBJECTIVE: To examine the effect of fluconazole, a potent inhibitor of CYP2C9 and CYP2C19, on the pharmacokinetics of rosuvastatin in healthy volunteers.	Fluconazole	36-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
12451430-1	2002	OBJECTIVE: To examine the effect of fluconazole, a potent inhibitor of CYP2C9 and CYP2C19, on the pharmacokinetics of rosuvastatin in healthy volunteers.	Rosuvastatin Calcium	118-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
12451434-3	2002	The lower activity of CYP2C9*5 encoded enzyme than *1 has been reported for the S-warfarin 7-hydroxylation in vitro.	Warfarin	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
12822205-5	2003	Fluvastatin has a low potential for drug interactions due to its CYP2C9-dependant metabolism.	Fluvastatin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
12452751-7	2002	DISCUSSION: The metabolism of warfarin involves several cytochrome P450 isoenzymes, including CYP1A2, CYP2C9, CYP2C19, and CYP3A4.	Warfarin	30-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
12452751-8	2002	Fluvoxamine has the potential to inhibit CYP1A2, CYP2C9, CYP2C19, and CYP3A4 to a significant degree.	Fluvoxamine	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
12496751-0	2002	Influence of CYP2C9 and CYP2C19 genetic polymorphisms on warfarin maintenance dose and metabolic clearance.	Warfarin	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
12496751-1	2002	OBJECTIVE: Our objective was to determine the influence of cytochrome P450 (CYP) 2C9 and CYP2C19 genetic polymorphisms on warfarin dose requirement and metabolic clearance.	Warfarin	122-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-84
12496751-8	2002	The mean S-warfarin CL(free) values varied significantly among the CYP2C9 genotype groups (P &lt;.0001), although most patients (72%) with no mutated alleles showed S-warfarin CL(free) values in the same range as those carrying mutated alleles (58-777 mL/min).	warfarin cl	11-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
12496751-8	2002	The mean S-warfarin CL(free) values varied significantly among the CYP2C9 genotype groups (P &lt;.0001), although most patients (72%) with no mutated alleles showed S-warfarin CL(free) values in the same range as those carrying mutated alleles (58-777 mL/min).	s-warfarin cl	9-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
12496751-10	2002	CONCLUSION: CYP2C9 genetic polymorphisms markedly influence warfarin dose requirements and metabolic clearance of the S-warfarin enantiomer, although nongenetic factors may also contribute to their large interindividual variability.	Warfarin	60-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
12496751-10	2002	CONCLUSION: CYP2C9 genetic polymorphisms markedly influence warfarin dose requirements and metabolic clearance of the S-warfarin enantiomer, although nongenetic factors may also contribute to their large interindividual variability.	Warfarin	120-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
12913403-0	2002	Warfarin dose adjustments based on CYP2C9 genetic polymorphisms.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
12913403-3	2002	The purpose of this study was to further characterize the relationship between CYP2C9 genotype and phenotype and to develop a basis for guidelines to interpret CYP2C9 genotype for warfarin dosing.	Warfarin	180-188	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
12913403-3	2002	The purpose of this study was to further characterize the relationship between CYP2C9 genotype and phenotype and to develop a basis for guidelines to interpret CYP2C9 genotype for warfarin dosing.	Warfarin	180-188	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
12913403-9	2002	Both CYP2C9*2 and *3 alleles were associated with lower maintenance dosages, lower total and R-warfarin plasma concentrations, decreased oral clearance of S-warfarin, increased plasma S:R-warfarin ratio and extended S-warfarin elimination half-life.	Warfarin	93-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	5-11
12913403-9	2002	Both CYP2C9*2 and *3 alleles were associated with lower maintenance dosages, lower total and R-warfarin plasma concentrations, decreased oral clearance of S-warfarin, increased plasma S:R-warfarin ratio and extended S-warfarin elimination half-life.	Sulfur	155-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	5-11
12913403-9	2002	Both CYP2C9*2 and *3 alleles were associated with lower maintenance dosages, lower total and R-warfarin plasma concentrations, decreased oral clearance of S-warfarin, increased plasma S:R-warfarin ratio and extended S-warfarin elimination half-life.	Warfarin	95-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	5-11
12913403-9	2002	Both CYP2C9*2 and *3 alleles were associated with lower maintenance dosages, lower total and R-warfarin plasma concentrations, decreased oral clearance of S-warfarin, increased plasma S:R-warfarin ratio and extended S-warfarin elimination half-life.	Warfarin	157-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	5-11
12913403-9	2002	Both CYP2C9*2 and *3 alleles were associated with lower maintenance dosages, lower total and R-warfarin plasma concentrations, decreased oral clearance of S-warfarin, increased plasma S:R-warfarin ratio and extended S-warfarin elimination half-life.	Warfarin	157-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	5-11
12913403-12	2002	The warfarin dose required to maintain a consistent target INR between subjects differs as a function of S-warfarin clearance which is decreased by both CYP2C9*2 and or CYP2C9*3 variant alleles.	Warfarin	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
12913403-12	2002	The warfarin dose required to maintain a consistent target INR between subjects differs as a function of S-warfarin clearance which is decreased by both CYP2C9*2 and or CYP2C9*3 variant alleles.	Warfarin	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
12913403-12	2002	The warfarin dose required to maintain a consistent target INR between subjects differs as a function of S-warfarin clearance which is decreased by both CYP2C9*2 and or CYP2C9*3 variant alleles.	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
12913403-12	2002	The warfarin dose required to maintain a consistent target INR between subjects differs as a function of S-warfarin clearance which is decreased by both CYP2C9*2 and or CYP2C9*3 variant alleles.	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
12426514-3	2002	Rifampin (INN, rifampicin), a potent enzyme inducer of CYP-mediated metabolism (especially CYP2C9, CYP2C19, and CYP3A4), is known to markedly decrease plasma concentrations and effects of a number coadministered drugs.	Rifampin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
12426514-3	2002	Rifampin (INN, rifampicin), a potent enzyme inducer of CYP-mediated metabolism (especially CYP2C9, CYP2C19, and CYP3A4), is known to markedly decrease plasma concentrations and effects of a number coadministered drugs.	inn	10-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
12426514-3	2002	Rifampin (INN, rifampicin), a potent enzyme inducer of CYP-mediated metabolism (especially CYP2C9, CYP2C19, and CYP3A4), is known to markedly decrease plasma concentrations and effects of a number coadministered drugs.	Rifampin	15-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
12426520-10	2002	With tolbutamide used as a CYP2C9 probe, CYP2C9 genotype was the major determinant of CYP2C9 phenotype (r(2) = 0.77).	Tolbutamide	5-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
12426520-10	2002	With tolbutamide used as a CYP2C9 probe, CYP2C9 genotype was the major determinant of CYP2C9 phenotype (r(2) = 0.77).	Tolbutamide	5-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
12426520-10	2002	With tolbutamide used as a CYP2C9 probe, CYP2C9 genotype was the major determinant of CYP2C9 phenotype (r(2) = 0.77).	Tolbutamide	5-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
12392591-2	2002	The aims of the present in vitro investigation were 1) to compare the rate of celecoxib hydroxylation by different genetic variants of cytochrome P450 2C9 (CYP2C9), and 2) to identify the enzyme(s) involved in the formation of the major metabolite carboxycelecoxib.	Celecoxib	78-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-154
12414349-6	2002	Out of 170 patients requiring a low-dose of acenocoumarol (&lt;or= 2 mg/day), 27.1% carried the CYP2C9*3 allele, while among the patients requiring higher doses, 8.4% had CYP2C9*3 (OR=4.77, 95% CI = 2.40-9.48, p&lt;0.001 vs. 2C9*1/*1 patients).	Acenocoumarol	44-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
12414349-6	2002	Out of 170 patients requiring a low-dose of acenocoumarol (&lt;or= 2 mg/day), 27.1% carried the CYP2C9*3 allele, while among the patients requiring higher doses, 8.4% had CYP2C9*3 (OR=4.77, 95% CI = 2.40-9.48, p&lt;0.001 vs. 2C9*1/*1 patients).	Acenocoumarol	44-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
12414349-7	2002	In the multivariate analysis, independent predictive variables for low-dose acenocoumarol requirements were age &gt;70 years (OR=3.73, 95%CI=2.29-6.08, p&lt;0.001), and the CYP2C9*3 allele (OR=4.75, 95%CI=2.36-9.55, p &lt;0.001).	Acenocoumarol	76-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	173-179
12414349-9	2002	INTERPRETATION AND CONCLUSIONS: CYP2C9*3 is related to lower acenocoumarol dose requirements, a higher frequency of over-anticoagulation at the initiation of therapy and an unstable anticoagulant response.	Acenocoumarol	61-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
12414349-0	2002	Pharmacogenetics of acenocoumarol: cytochrome P450 CYP2C9 polymorphisms influence dose requirements and stability of anticoagulation.	Acenocoumarol	20-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
12414349-2	2002	Variant alleles, CYP2C9*2 and CYP2C9*3, have been related to decreased enzymatic activity, but their clinical relevance in acenocoumarol metabolism has not been established.	Acenocoumarol	123-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
12414349-2	2002	Variant alleles, CYP2C9*2 and CYP2C9*3, have been related to decreased enzymatic activity, but their clinical relevance in acenocoumarol metabolism has not been established.	Acenocoumarol	123-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
12414349-3	2002	We investigated CYP2C9 polymorphisms in relation to acenocoumarol dose requirement, stability of anticoagulation and bleeding.	Acenocoumarol	52-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
12414349-4	2002	DESIGN AND METHODS: CYP2C9 genotyping was performed in 325 acenocoumarol-treated patients (INR target between 2.0 and 3.0) and in an additional group of 84 patients with repeated bleeding.	Acenocoumarol	59-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
12414349-5	2002	RESULTS: Patients with the wild-type CYP2C9*1/*1 genotype (n=169) required a higher maintenance dose of acenocoumarol (17.1 8.7 mg/week) than did patients with the CYP2C9*2 (14.6 6.4 mg/week, p&lt;0.05, N=97) or the CYP2C9*3 allele (11.2 6.2 mg/week, p&lt;0.001, n=59).	Acenocoumarol	104-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
12392591-2	2002	The aims of the present in vitro investigation were 1) to compare the rate of celecoxib hydroxylation by different genetic variants of cytochrome P450 2C9 (CYP2C9), and 2) to identify the enzyme(s) involved in the formation of the major metabolite carboxycelecoxib.	Celecoxib	78-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
12392591-2	2002	The aims of the present in vitro investigation were 1) to compare the rate of celecoxib hydroxylation by different genetic variants of cytochrome P450 2C9 (CYP2C9), and 2) to identify the enzyme(s) involved in the formation of the major metabolite carboxycelecoxib.	carboxycelecoxib	248-264	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-154
12392591-2	2002	The aims of the present in vitro investigation were 1) to compare the rate of celecoxib hydroxylation by different genetic variants of cytochrome P450 2C9 (CYP2C9), and 2) to identify the enzyme(s) involved in the formation of the major metabolite carboxycelecoxib.	carboxycelecoxib	248-264	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
12392591-7	2002	RESULTS: The intrinsic clearance of celecoxib hydroxylation was significantly lower for yeast-expressed CYP2C9.3 (0.14 ml min-1 nmol-1 enzyme) compared with CYP2C9.1 (0.44 ml min-1 nmol-1 enzyme).	Celecoxib	36-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
12392591-7	2002	RESULTS: The intrinsic clearance of celecoxib hydroxylation was significantly lower for yeast-expressed CYP2C9.3 (0.14 ml min-1 nmol-1 enzyme) compared with CYP2C9.1 (0.44 ml min-1 nmol-1 enzyme).	Celecoxib	36-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
12392591-8	2002	In human liver microsomes, a significant 2-fold decrease in the rate of hydroxycelecoxib formation was evident in CYP2C9*1/*3 samples compared with CYP2C9*1/*1 samples.	Hydroxy Celecoxib	72-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
12392591-8	2002	In human liver microsomes, a significant 2-fold decrease in the rate of hydroxycelecoxib formation was evident in CYP2C9*1/*3 samples compared with CYP2C9*1/*1 samples.	Hydroxy Celecoxib	72-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
12392591-9	2002	There was also a marked reduction (up to 5.3 times) of hydroxycelecoxib formation in a liver sample genotyped as CYP2C9*3/*3.	Hydroxy Celecoxib	55-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
12392591-11	2002	Inhibition experiments with sulphaphenazole (SPZ) or triacetyloleandomycin indicated that celecoxib hydroxylation in human liver microsomes was mainly dependent on CYP2C9 and not CYP3A4.	Celecoxib	90-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	164-170
12392591-14	2002	CONCLUSIONS: The results confirm that CYP2C9 is the major enzyme for celecoxib hydroxylation in vitro and further indicate that the CYP2C9*3 allelic variant is associated with markedly slower metabolism.	Celecoxib	69-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
12392591-14	2002	CONCLUSIONS: The results confirm that CYP2C9 is the major enzyme for celecoxib hydroxylation in vitro and further indicate that the CYP2C9*3 allelic variant is associated with markedly slower metabolism.	Celecoxib	69-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
12359989-1	2002	BACKGROUND: The cytochrome P450 CYP2C9 enzyme (CYP2C9) metabolizes many clinically important drugs, for example, phenytoin, warfarin and the angiotensin II type 1 (AT(1)) receptor antagonists, losartan and irbesartan.	Irbesartan	206-216	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
12392591-0	2002	Oxidation of celecoxib by polymorphic cytochrome P450 2C9 and alcohol dehydrogenase.	Celecoxib	13-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-57
12228186-5	2002	In the incubation study using cDNA-expressed P450s, both CYP2C9 and CYP2C19 catalyzed phenytoin p-hydroxylation, whereas TCAs inhibited only the CYP2C19 pathway.	Phenytoin	86-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
12359989-0	2002	The CYP2C9 genotype predicts the blood pressure response to irbesartan: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA) trial.	Irbesartan	60-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
12359989-0	2002	The CYP2C9 genotype predicts the blood pressure response to irbesartan: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA) trial.	Atenolol	154-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
12359989-1	2002	BACKGROUND: The cytochrome P450 CYP2C9 enzyme (CYP2C9) metabolizes many clinically important drugs, for example, phenytoin, warfarin and the angiotensin II type 1 (AT(1)) receptor antagonists, losartan and irbesartan.	Phenytoin	113-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
12359989-1	2002	BACKGROUND: The cytochrome P450 CYP2C9 enzyme (CYP2C9) metabolizes many clinically important drugs, for example, phenytoin, warfarin and the angiotensin II type 1 (AT(1)) receptor antagonists, losartan and irbesartan.	Phenytoin	113-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
12359989-1	2002	BACKGROUND: The cytochrome P450 CYP2C9 enzyme (CYP2C9) metabolizes many clinically important drugs, for example, phenytoin, warfarin and the angiotensin II type 1 (AT(1)) receptor antagonists, losartan and irbesartan.	Warfarin	124-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
12359989-1	2002	BACKGROUND: The cytochrome P450 CYP2C9 enzyme (CYP2C9) metabolizes many clinically important drugs, for example, phenytoin, warfarin and the angiotensin II type 1 (AT(1)) receptor antagonists, losartan and irbesartan.	Warfarin	124-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
12359989-1	2002	BACKGROUND: The cytochrome P450 CYP2C9 enzyme (CYP2C9) metabolizes many clinically important drugs, for example, phenytoin, warfarin and the angiotensin II type 1 (AT(1)) receptor antagonists, losartan and irbesartan.	Losartan	193-201	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
12359989-1	2002	BACKGROUND: The cytochrome P450 CYP2C9 enzyme (CYP2C9) metabolizes many clinically important drugs, for example, phenytoin, warfarin and the angiotensin II type 1 (AT(1)) receptor antagonists, losartan and irbesartan.	Losartan	193-201	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
12236850-0	2002	Involvement of CYP2C9 and UGT2B7 in the metabolism of zaltoprofen, a nonsteroidal anti-inflammatory drug, and its lack of clinically significant CYP inhibition potential.	pyranoprofen	54-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
12236850-4	2002	The inhibitory effects of zaltoprofen on the metabolism of selective probe substrates for CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1 and CYP3A4 were also determined in human liver microsomes.	pyranoprofen	26-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
12236850-5	2002	RESULTS: Zaltoprofen was extensively metabolized by CYP2C9 and UGT2B7.	pyranoprofen	9-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
12236850-7	2002	In the human liver microsomal metabolism study, zaltoprofen metabolism was markedly inhibited by sulphaphenazole, a selective inhibitor of CYP2C9.	pyranoprofen	48-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	139-145
12236850-7	2002	In the human liver microsomal metabolism study, zaltoprofen metabolism was markedly inhibited by sulphaphenazole, a selective inhibitor of CYP2C9.	Sulfaphenazole	97-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	139-145
12236850-9	2002	However, zaltoprofen inhibited CYP2C9 by 26% at 5 micro g ml(-1).	pyranoprofen	9-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
12236850-10	2002	At higher concentrations, zaltoprofen produced some inhibition of CYP2C9 (IC50 = 19.2 micro g ml(-1); 64.4 micro m) and CYP3A4 (IC50 = 53.9 micro g ml(-1); 181 micro m).	pyranoprofen	26-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
12236850-12	2002	Furthermore, the maximum free drug concentrations in the hepatic intracellular was calculated to be 0.068 micro g ml(-1) and the increase in the AUC in the presence of zaltoprofen was estimated to be only 0.4% for CYP2C9 substrates and 0.1% for CYP3A4 substrates, respectively.	pyranoprofen	168-179	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	214-220
12236850-13	2002	CONCLUSIONS: Zaltoprofen is predominantly metabolized by CYP2C9 and UGT2B7, and is considered unlikely to cause significant drug interactions in vivo when coadministered with CYP substrates at clinically effective doses.	pyranoprofen	13-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
12231541-8	2002	ET743 was metabolized by cDNA-expressed human CYP3A4 and to a much lesser extent by CYP2C9, CYP2D6, and CYP2E1 preparations.	Trabectedin	0-5	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
12235454-1	2002	OBJECTIVES: Our objective was to investigate the effects of genetic polymorphisms of cytochrome P450 (CYP) 2C9 on the pharmacokinetics of glyburide (INN, glibenclamide) and glimepiride, two widely used sulfonylurea antidiabetic drugs.	Glyburide	154-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-110
12235454-5	2002	However, in individuals heterozygous for the CYP2C9*3 allele, the median total area under the plasma concentration-time curve of glyburide (n = 2) was 280% (P &lt; or = .05) and that of glimepiride (n = 3) was 267% (P &lt; or = .01) of the respective values in subjects with the CYP2C9*1/*1 genotype (n = 5 and n = 12, respectively).	Glyburide	129-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
12235454-5	2002	However, in individuals heterozygous for the CYP2C9*3 allele, the median total area under the plasma concentration-time curve of glyburide (n = 2) was 280% (P &lt; or = .05) and that of glimepiride (n = 3) was 267% (P &lt; or = .01) of the respective values in subjects with the CYP2C9*1/*1 genotype (n = 5 and n = 12, respectively).	Glyburide	129-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	279-285
12235454-5	2002	However, in individuals heterozygous for the CYP2C9*3 allele, the median total area under the plasma concentration-time curve of glyburide (n = 2) was 280% (P &lt; or = .05) and that of glimepiride (n = 3) was 267% (P &lt; or = .01) of the respective values in subjects with the CYP2C9*1/*1 genotype (n = 5 and n = 12, respectively).	glimepiride	186-197	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
12698985-3	2002	MATERIALS AND METHODS: We chose 3 model drugs that are metabolized by distinct cytochrome P450 (CYP) isoforms (theophylline, phenytoin and cyclosporine for CYPIA2, CYP2C9/2C19 and CYP3A4, respectively).	Cyclosporine	139-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	164-170
12360109-0	2002	Contributions of CYP2D6, CYP2C9 and CYP2C19 to the biotransformation of E- and Z-doxepin in healthy volunteers.	e- and z-doxepin	72-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
12360109-2	2002	We studied the effects of genetic polymorphisms in CYP2D6, CYP2C9 and CYP2C19 on E- and Z-doxepin pharmacokinetics in humans.	e- and z-doxepin	81-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
12360109-8	2002	E-doxepin oral clearance was also significantly lower in carriers of CYP2C9*3/*3 (238 l h(-1) ).	Doxepin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
12235454-7	2002	CONCLUSIONS: Genetic polymorphisms of CYP2C9 markedly affect the pharmacokinetics of both glyburide and glimepiride.	Glyburide	90-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
12235454-7	2002	CONCLUSIONS: Genetic polymorphisms of CYP2C9 markedly affect the pharmacokinetics of both glyburide and glimepiride.	glimepiride	104-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
12235454-8	2002	The influence of the CYP2C9*3 variant allele on glyburide and glimepiride pharmacokinetics may be clinically significant.	Glyburide	48-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
12359989-1	2002	BACKGROUND: The cytochrome P450 CYP2C9 enzyme (CYP2C9) metabolizes many clinically important drugs, for example, phenytoin, warfarin and the angiotensin II type 1 (AT(1)) receptor antagonists, losartan and irbesartan.	Irbesartan	206-216	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
12359989-3	2002	The CYP2C9 genotype is known to determine sensitivity to and dose requirements for both warfarin and phenytoin, and also the rate of metabolism of losartan.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
12359989-3	2002	The CYP2C9 genotype is known to determine sensitivity to and dose requirements for both warfarin and phenytoin, and also the rate of metabolism of losartan.	Phenytoin	101-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
12359989-3	2002	The CYP2C9 genotype is known to determine sensitivity to and dose requirements for both warfarin and phenytoin, and also the rate of metabolism of losartan.	Losartan	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
12359989-5	2002	OBJECTIVE: To determine whether the CYP2C9genotype influences the blood pressure-decreasing response to antihypertensive treatment with irbesartan.	Irbesartan	136-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
12359989-9	2002	RESULTS: The diastolic blood pressure (DBP) response differed in relation to the CYP2C9 genotype in patients given irbesartan: the reduction in patients with genotype CYP2C9*1/CYP2C9*1 (n = 33) was 7.5% and that with CYP2C9*1/CYP2C9*2 (n = 12) was 14.4% ( P= 0.036).	Irbesartan	115-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
12359989-9	2002	RESULTS: The diastolic blood pressure (DBP) response differed in relation to the CYP2C9 genotype in patients given irbesartan: the reduction in patients with genotype CYP2C9*1/CYP2C9*1 (n = 33) was 7.5% and that with CYP2C9*1/CYP2C9*2 (n = 12) was 14.4% ( P= 0.036).	Irbesartan	115-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
12359989-9	2002	RESULTS: The diastolic blood pressure (DBP) response differed in relation to the CYP2C9 genotype in patients given irbesartan: the reduction in patients with genotype CYP2C9*1/CYP2C9*1 (n = 33) was 7.5% and that with CYP2C9*1/CYP2C9*2 (n = 12) was 14.4% ( P= 0.036).	Irbesartan	115-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
12359989-9	2002	RESULTS: The diastolic blood pressure (DBP) response differed in relation to the CYP2C9 genotype in patients given irbesartan: the reduction in patients with genotype CYP2C9*1/CYP2C9*1 (n = 33) was 7.5% and that with CYP2C9*1/CYP2C9*2 (n = 12) was 14.4% ( P= 0.036).	Irbesartan	115-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
12359989-9	2002	RESULTS: The diastolic blood pressure (DBP) response differed in relation to the CYP2C9 genotype in patients given irbesartan: the reduction in patients with genotype CYP2C9*1/CYP2C9*1 (n = 33) was 7.5% and that with CYP2C9*1/CYP2C9*2 (n = 12) was 14.4% ( P= 0.036).	Irbesartan	115-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
12359989-12	2002	CONCLUSIONS: The CYP2C9 genotype seems to predict the DBP response to irbesartan, but not to atenolol, in patients with essential hypertension.	Irbesartan	70-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
12167559-9	2002	LY333531 and N-desmethyl LY333531 were also examined for their ability to inhibit metabolism mediated by CYP2D6, CYP2C9, CYP3A, and CYP1A2.	ruboxistaurin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
12167559-9	2002	LY333531 and N-desmethyl LY333531 were also examined for their ability to inhibit metabolism mediated by CYP2D6, CYP2C9, CYP3A, and CYP1A2.	18-(methylaminomethyl)-17-oxa-4,14,21-triazahexacyclo[19.6.1.17,14.02,6.08,13.022,27]nonacosa-1(28),2(6),7(29),8,10,12,22,24,26-nonaene-3,5-dione	13-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
12167570-11	2002	Thus, a phenolic group seems essential for efficient ortho-hydroxylation, forming catechol-M and tris-OH-M. Inhibition studies with HLM and P450s indicate that CYP2C9 and likely 2C19 are catalysts of methoxychlor-mono-demethylation.	catechol	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
12167570-11	2002	Thus, a phenolic group seems essential for efficient ortho-hydroxylation, forming catechol-M and tris-OH-M. Inhibition studies with HLM and P450s indicate that CYP2C9 and likely 2C19 are catalysts of methoxychlor-mono-demethylation.	tris-oh	97-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
12181452-3	2002	This report examines the regulation of CYP2C9 with respect to two specific receptors thought to be involved in phenobarbital (PB) induction, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR).	Phenobarbital	111-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
12235454-8	2002	The influence of the CYP2C9*3 variant allele on glyburide and glimepiride pharmacokinetics may be clinically significant.	glimepiride	62-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
12235444-1	2002	BACKGROUND: Phenytoin, a cytochrome P450 (CYP) 2C9 substrate, has a narrow therapeutic index and nonlinear pharmacokinetics.	Phenytoin	12-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-50
12235444-2	2002	Therefore there is the potential for significant concentration-related adverse effects when phenytoin is coadministered with other CYP2C9 substrates.	Phenytoin	92-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
12235444-3	2002	Losartan, an antihypertensive agent, is also a substrate for CYP2C9.	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
12235444-10	2002	In the 14 CYP2C9*1/*1 subjects, the mean AUC(0-24) of losartan was increased by 29% (284 +/- 84 ng x h/mL versus 402 +/- 128 ng x h/mL; P =.008).	Losartan	54-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
12235444-12	2002	CONCLUSIONS: Losartan, a CYP2C9 substrate, had no effect on the pharmacokinetics of phenytoin.	Losartan	13-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
12235444-13	2002	However, phenytoin inhibited the CYP2C9-mediated conversion of losartan to E3174.	Phenytoin	9-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
12235444-13	2002	However, phenytoin inhibited the CYP2C9-mediated conversion of losartan to E3174.	Losartan	63-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
12235444-13	2002	However, phenytoin inhibited the CYP2C9-mediated conversion of losartan to E3174.	losartan carboxylic acid	75-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
12235454-1	2002	OBJECTIVES: Our objective was to investigate the effects of genetic polymorphisms of cytochrome P450 (CYP) 2C9 on the pharmacokinetics of glyburide (INN, glibenclamide) and glimepiride, two widely used sulfonylurea antidiabetic drugs.	Glyburide	138-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-110
12181452-3	2002	This report examines the regulation of CYP2C9 with respect to two specific receptors thought to be involved in phenobarbital (PB) induction, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR).	Phenobarbital	126-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
12181452-11	2002	In summary, a new CAR/PXR binding site was identified in the CYP2C9 promoter, and this site seems to constitutively regulate transcription via a CAR-dependent mechanism; however, it could not be shown to account for PB inducibility of the gene.	Phenobarbital	216-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
12207635-0	2002	The influence of CYP2B6, CYP2C9 and CYP2D6 genotypes on the formation of the potent antioestrogen Z-4-hydroxy-tamoxifen in human liver.	z-4-hydroxy-tamoxifen	98-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
12207635-1	2002	AIMS: To investigate in a large panel of 50 human liver samples the contribution of CYP2C9, CYP2D6, and CYP3A4 to the overall formation of the potent antioestrogen Z-4-hydroxy-tamoxifen, and how various genotypes affect its formation from tamoxifen.	z-4-hydroxy-tamoxifen	164-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
12207635-5	2002	RESULTS: Z-4-hydroxy-tamoxifen was formed by supersomes expressing CYP2B6, CYP2C9, CYP2C19 and CYP2D6, but not CYP3A4.	z-4-hydroxy-tamoxifen	9-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
12207635-7	2002	Furthermore, Z-4-hydroxy-tamoxifen formation significantly correlated with both CYP2C9 expression (r(s)=0.256, P&lt;0.05) and CYP2D6 expression (r(s)=0.309, P&lt;0.05).	z-4-hydroxy-tamoxifen	13-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
12207635-9	2002	CYP2D6 and CYP2C9 contribute on average 45 and 46%, respectively, to the overall formation of Z-4-hydroxy-tamoxifen.	z-4-hydroxy-tamoxifen	94-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
12207635-10	2002	CONCLUSIONS: CYP2B6, CYP2C9 and CYP2D6 genotypes all affected Z-4-hydroxy-tamoxifen formation and can predict individual ability to catalyse this reaction.	z-4-hydroxy-tamoxifen	62-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
12207635-1	2002	AIMS: To investigate in a large panel of 50 human liver samples the contribution of CYP2C9, CYP2D6, and CYP3A4 to the overall formation of the potent antioestrogen Z-4-hydroxy-tamoxifen, and how various genotypes affect its formation from tamoxifen.	Tamoxifen	176-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
12207639-0	2002	Intra-individual variability in urinary losartan oxidation ratio, an in vivo marker of CYP2C9 activity.	Losartan	40-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
12207635-2	2002	METHODS: The formation of Z-4-hydroxy-tamoxifen from 10 microm tamoxifen was studied in human liver microsomes (n=50), characterized for CYP2B6, CYP2C9, CYP2D6 and CYP3A4 expression, and CYP2B6, CYP2C9 and CYP2D6 genotype.	z-4-hydroxy-tamoxifen	26-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
12124312-5	2002	For the 4"-hydroxylation of diclofenac, CYP2C9 had a lower K(m) and a higher V(max) than CYP2C19.	Diclofenac	28-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
11991950-1	2002	The fully active dihydroxylated metabolite of vitamin D(3) induces the expression of CYP3A4 and, to a lesser extent, CYP2B6 and CYP2C9 genes in normal differentiated primary human hepatocytes.	Vitamin D	46-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
12130704-5	2002	Parallel increases in CYP2C mRNAs, measured by Northern blotting and/or RNase protection, were found in rifampicin-treated hepatocytes, with CYP2C8, CYP2C9, and CYP2C19 transcripts exhibiting increases of 688 +/- 635, 207 +/- 49, and 230 +/- 60%, respectively, versus an 8.8-fold enhancement of CYP3A4 mRNA levels.	Rifampin	104-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
12130704-7	2002	Phenobarbital (100 microM) was a powerful inducer of CYP2C9 (850%) and CYP2C19 (735%) mRNA content, and also increased CYP2C8 (610%) and CYP3A4 (205%) transcripts.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
12123234-0	2002	Leu208Val and Ile181Leu variants of cytochrome P450 CYP2C9 are not related to the acenocoumarol dose requirement in a Spanish population.	ile181leu	14-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
12152005-0	2002	Enantiospecific effects of cytochrome P450 2C9 amino acid variants on ibuprofen pharmacokinetics and on the inhibition of cyclooxygenases 1 and 2.	Ibuprofen	70-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-46
12065445-11	2002	The present study demonstrates that CYP3A4 is the principal enzyme responsible for ketamine N-demethylation in human liver microsomes and that CYP2B6 and CYP2C9 have a minor contribution to ketamine N-demethylation at therapeutic concentrations of the drug.	ketamine n	190-200	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
12136253-11	2002	The application of the relative substrate-activity factor (RSF)-approach and the calculation of the contribution of various isoforms in the ifosfamide 4-hydroxylation yielded the following results: CYP 3A4: 58+/-31%, CYP 2A6: 25+/-15%, and CYP 2C9: 5+/-2% of the total measured 4-hydroxylation.	Ifosfamide	140-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	240-247
12136253-12	2002	A correlation between 4-hydroxylation and the N-dechloroethylation rates of ifosfamide and the activities of isoenzymes indicates the involvement of both CYP 3A4 ( P=0.026) and CYP 2C9 ( P=0.012) in the 4-hydroxylation reaction and of CYP 3A4 ( P&lt;0.01) in the N-dechloroethylation reaction.	Ifosfamide	76-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	177-184
12065442-4	2002	The reactions examined were CYP2C9-catalyzed diclofenac 4"-hydroxylation, CYP2D6-catalyzed dextromethorphan O-demethylation and thioridazine S-oxidation, CYP2C19-catalyzed imipramine N-demethylation, CYP3A4-catalyzed midazolam 1"-hydroxylation, and CYP1A2-catalyzed tacrine 1-hydroxylation.	Diclofenac	45-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
12065445-0	2002	Contribution of CYP3A4, CYP2B6, and CYP2C9 isoforms to N-demethylation of ketamine in human liver microsomes.	Nitrogen	55-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
12065445-0	2002	Contribution of CYP3A4, CYP2B6, and CYP2C9 isoforms to N-demethylation of ketamine in human liver microsomes.	Ketamine	74-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
12065445-9	2002	In human lymphoblast-expressed P450, the activities of CYP2B6 were higher than those of CYP3A4 and CYP2C9 at three concentrations of ketamine, 0.005, 0.05, and 0.5 mM.	Ketamine	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
12065698-0	2002	Effect of albumin and cytosol on enzyme kinetics of tolbutamide hydroxylation and on inhibition of CYP2C9 by gemfibrozil in human liver microsomes.	Gemfibrozil	109-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
12152005-9	2002	Ex vivo formation of thromboxane B(2), reflecting cyclooxygenase type 1 inhibition, depended significantly on the CYP2C9 polymorphism.	thromboxane b	21-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
12065698-1	2002	The effect of human serum albumin (Hsa) and human liver cytosol (Hlc) on the in vitro enzyme kinetics of the formation of hydroxytolbutamide (CYP2C9 marker reaction) and the inhibitory effect of gemfibrozil on tolbutamide hydroxylation were examined using human liver microsomes.	hydroxymethyltolbutamide	122-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
12065698-1	2002	The effect of human serum albumin (Hsa) and human liver cytosol (Hlc) on the in vitro enzyme kinetics of the formation of hydroxytolbutamide (CYP2C9 marker reaction) and the inhibitory effect of gemfibrozil on tolbutamide hydroxylation were examined using human liver microsomes.	Tolbutamide	129-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
12065698-6	2002	The K(i) (6 microM) of gemfibrozil for CYP2C9, calculated using total drug concentrations, was increased by Hlc (8 microM), Hsa (40 microM), or both (72 microM).	Gemfibrozil	23-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
12152005-10	2002	The maximal inhibition of thromboxane B(2) formation and the area under the effect-time curve were larger in carriers of the slow CYP2C9 genotypes *1/*3, *2/*3, and *3/*3 than in *1/*1 carriers; the same trend was observed for prostaglandin E(2), reflecting cyclooxygenase type 2 inhibition.	thromboxane b	26-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
12152005-10	2002	The maximal inhibition of thromboxane B(2) formation and the area under the effect-time curve were larger in carriers of the slow CYP2C9 genotypes *1/*3, *2/*3, and *3/*3 than in *1/*1 carriers; the same trend was observed for prostaglandin E(2), reflecting cyclooxygenase type 2 inhibition.	Prostaglandins E	227-242	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
12180536-5	2002	Rh-CYP2C19, -CYP1A2, and -CYP2C9 were able to N-demethylate cis- and trans-doxepin.	n-demethylate	46-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
12180536-4	2002	Furafylline (CYP1A2) and sulfaphenazole (CYP2C9) inhibited the N-demethylation to a lesser extent while quinidine (CYP2D6) or troleandomycine (CYP3A4) had no effect.	Sulfaphenazole	25-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
12180536-5	2002	Rh-CYP2C19, -CYP1A2, and -CYP2C9 were able to N-demethylate cis- and trans-doxepin.	cis- and trans-doxepin	60-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
12180536-4	2002	Furafylline (CYP1A2) and sulfaphenazole (CYP2C9) inhibited the N-demethylation to a lesser extent while quinidine (CYP2D6) or troleandomycine (CYP3A4) had no effect.	Nitrogen	63-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
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
12084621-3	2002	Isozymes selective for imidazolidine oxidation in order of decreasing overall activity are CYP3A4&gt;CYP2C19 or CYP2A6&gt;CYP2C9, while those selective for nitroimine reduction are CYP1A2, CYP2B6, CYP2D6 and CYP2E1.	Imidazolidines	23-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
12084621-3	2002	Isozymes selective for imidazolidine oxidation in order of decreasing overall activity are CYP3A4&gt;CYP2C19 or CYP2A6&gt;CYP2C9, while those selective for nitroimine reduction are CYP1A2, CYP2B6, CYP2D6 and CYP2E1.	nitroimine	156-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
12110367-7	2002	In reconstituted systems containing CYP2C9, CYP2C19, and CYP3A4, the formation of 3",4"-diHPPH was also enhanced by catalase to different extents.	3",4"-dihpph	82-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
12019187-0	2002	Trimethoprim and sulfamethoxazole are selective inhibitors of CYP2C8 and CYP2C9, respectively.	Trimethoprim, Sulfamethoxazole Drug Combination	0-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
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
12019187-4	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.	Tolbutamide	113-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
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.	Trimethoprim	248-260	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	227-233
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
12019187-7	2002	In conclusion, trimethoprim and sulfamethoxazole can be used as selective inhibitors of CYP2C8 and CYP2C9 in in vitro studies.	Trimethoprim, Sulfamethoxazole Drug Combination	15-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
12019187-8	2002	In humans, trimethoprim and sulfamethoxazole may inhibit the activities of CYP2C8 and CYP2C9, respectively.	Trimethoprim, Sulfamethoxazole Drug Combination	11-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
12160484-14	2002	Lower rates of V11294 metabolism to some V11294 metabolites were also observed with cDNA-expressed CYP2C9, CYP2C19 and CYP2D6, whereas only very low or undetectable rates of V11294 metabolism were observed with cDNA-expressed CYP1A2, CYP2A6, CYP2B6, CYP2C8 and CYP2E1.	3-(3-cyclopentyloxy-4-methoxybenzyl)-6-ethylamino-8-isopropyl-3H-purine	15-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
12081638-3	2002	The aim of this pilot study was to clarify if PR has an effect on losartan oxidation used as a measure of CYP2C9 activity.	Losartan	66-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
12160484-14	2002	Lower rates of V11294 metabolism to some V11294 metabolites were also observed with cDNA-expressed CYP2C9, CYP2C19 and CYP2D6, whereas only very low or undetectable rates of V11294 metabolism were observed with cDNA-expressed CYP1A2, CYP2A6, CYP2B6, CYP2C8 and CYP2E1.	3-(3-cyclopentyloxy-4-methoxybenzyl)-6-ethylamino-8-isopropyl-3H-purine	41-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
12044584-4	2002	In contrast, fluvastatin (mainly metabolized by CYP 2C9) and pravastatin (eliminated by other metabolic routes) are less subject to this interaction.	Fluvastatin	13-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-55
11867622-5	2002	The specific CYP 2C9 inhibitor, sulfaphenazole, prevented both the enhanced cell proliferation and up-regulation of cyclin D1.	Sulfaphenazole	32-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-20
11867622-10	2002	Overexpression of CYP 2C9 significantly increased the expression of MKP-1, as did incubation with 11,12-EET.	11,12-epoxy-5,8,14-eicosatrienoic acid	98-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-25
11955666-6	2002	CYP2C9 catalyzed the 4"-demethylation of tamarixetin, whereas CYP2D6 did not seem to play any role in the metabolism of the selected flavonoids.	tamarixetin	41-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11950794-0	2002	Metabolism of (+)- and (-)-limonenes to respective carveols and perillyl alcohols by CYP2C9 and CYP2C19 in human liver microsomes.	(+)- and (-)-limonenes	14-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
11950794-0	2002	Metabolism of (+)- and (-)-limonenes to respective carveols and perillyl alcohols by CYP2C9 and CYP2C19 in human liver microsomes.	carveol	51-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
11950794-0	2002	Metabolism of (+)- and (-)-limonenes to respective carveols and perillyl alcohols by CYP2C9 and CYP2C19 in human liver microsomes.	perillyl alcohol	64-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
11950794-4	2002	Sulfaphenazole, flavoxamine, and antibodies raised against purified liver cytochrome P450 (P450) 2C9 that inhibit both CYP2C9- and 2C19-dependent activities, significantly inhibited microsomal oxidations of (+)- and (-)-limonene enantiomers.	Sulfaphenazole	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
11950794-4	2002	Sulfaphenazole, flavoxamine, and antibodies raised against purified liver cytochrome P450 (P450) 2C9 that inhibit both CYP2C9- and 2C19-dependent activities, significantly inhibited microsomal oxidations of (+)- and (-)-limonene enantiomers.	flavoxamine	16-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
11950794-4	2002	Sulfaphenazole, flavoxamine, and antibodies raised against purified liver cytochrome P450 (P450) 2C9 that inhibit both CYP2C9- and 2C19-dependent activities, significantly inhibited microsomal oxidations of (+)- and (-)-limonene enantiomers.	(+)- and (-)-limonene	207-228	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
11950794-5	2002	The limonene oxidation activities correlated well with contents of CYP2C9 and activities of tolbutamide methyl hydroxylation in liver microsomes of 62 human samples, whereas these activities did not correlate with contents of CYP2C19 and activities of S-mephenytoin 4-hydroxylation.	Limonene	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
11950794-8	2002	These results suggest that both (+)- and (-)-limonene enantiomers are oxidized at 6- and 7-positions by CYP2C9 and CYP2C19 in human liver microsomes.	(+)- and (-)-limonene	32-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
11950794-9	2002	CYP2C9 may be more important than CYP2C19 in catalyzing limonene oxidations in human liver microsomes, since levels of the former protein are more abundant than CYP2C19 in these human samples.	Limonene	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11964373-2	2002	Here, we assessed the mechanisms by which the epoxyeicosatrienoic acids (EETs) generated by a CYP 2C enzyme control interendothelial gap junctional communication.	epoxyeicosatrienoic acids	46-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
11964373-4	2002	The initial phase was sensitive to the CYP 2C9 inhibitor sulfaphenazole and the protein kinase A (PKA) inhibitors Rp-cAMPS and KT5720 and could be mimicked by forskolin and caged cAMP as well as by the PKA activators 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole 3",5"-cyclic monophosphorothioate sodium salt and Sp-cAMPS.	Sulfaphenazole	57-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-46
11964373-2	2002	Here, we assessed the mechanisms by which the epoxyeicosatrienoic acids (EETs) generated by a CYP 2C enzyme control interendothelial gap junctional communication.	eets	73-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
11956508-9	2002	Results of in vitro experiments showed that glyburide is metabolized by cytochrome P450 (CYP) 2C9, 2C19, and 3A4.	Glyburide	44-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-97
11964373-4	2002	The initial phase was sensitive to the CYP 2C9 inhibitor sulfaphenazole and the protein kinase A (PKA) inhibitors Rp-cAMPS and KT5720 and could be mimicked by forskolin and caged cAMP as well as by the PKA activators 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole 3",5"-cyclic monophosphorothioate sodium salt and Sp-cAMPS.	5,6-dichloro-1-beta-d-ribofuranosylbenzimidazole 3",5"-cyclic monophosphorothioate sodium salt	217-311	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-46
11964373-4	2002	The initial phase was sensitive to the CYP 2C9 inhibitor sulfaphenazole and the protein kinase A (PKA) inhibitors Rp-cAMPS and KT5720 and could be mimicked by forskolin and caged cAMP as well as by the PKA activators 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole 3",5"-cyclic monophosphorothioate sodium salt and Sp-cAMPS.	adenosine-3',5'-cyclic phosphorothioate	316-324	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-46
11956512-0	2002	Impact of CYP2C9 amino acid polymorphisms on glyburide kinetics and on the insulin and glucose response in healthy volunteers.	Glyburide	45-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
11956512-2	2002	We hypothesized that glyburide may be a substrate of cytochrome P450 2C9 (CYP2C9), an enzyme that has two low-activity amino acid variants-Arg144Cys (CYP2C9*2) and Ile359Leu (CYP2C9*3).	Glyburide	21-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-72
11956512-2	2002	We hypothesized that glyburide may be a substrate of cytochrome P450 2C9 (CYP2C9), an enzyme that has two low-activity amino acid variants-Arg144Cys (CYP2C9*2) and Ile359Leu (CYP2C9*3).	Glyburide	21-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
11956512-2	2002	We hypothesized that glyburide may be a substrate of cytochrome P450 2C9 (CYP2C9), an enzyme that has two low-activity amino acid variants-Arg144Cys (CYP2C9*2) and Ile359Leu (CYP2C9*3).	Glyburide	21-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
11956512-2	2002	We hypothesized that glyburide may be a substrate of cytochrome P450 2C9 (CYP2C9), an enzyme that has two low-activity amino acid variants-Arg144Cys (CYP2C9*2) and Ile359Leu (CYP2C9*3).	Glyburide	21-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
11956512-2	2002	We hypothesized that glyburide may be a substrate of cytochrome P450 2C9 (CYP2C9), an enzyme that has two low-activity amino acid variants-Arg144Cys (CYP2C9*2) and Ile359Leu (CYP2C9*3).	ile359leu	164-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-72
11956512-2	2002	We hypothesized that glyburide may be a substrate of cytochrome P450 2C9 (CYP2C9), an enzyme that has two low-activity amino acid variants-Arg144Cys (CYP2C9*2) and Ile359Leu (CYP2C9*3).	ile359leu	164-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
11956512-2	2002	We hypothesized that glyburide may be a substrate of cytochrome P450 2C9 (CYP2C9), an enzyme that has two low-activity amino acid variants-Arg144Cys (CYP2C9*2) and Ile359Leu (CYP2C9*3).	ile359leu	164-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
11956512-2	2002	We hypothesized that glyburide may be a substrate of cytochrome P450 2C9 (CYP2C9), an enzyme that has two low-activity amino acid variants-Arg144Cys (CYP2C9*2) and Ile359Leu (CYP2C9*3).	ile359leu	164-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
11956512-8	2002	RESULTS: Pharmacokinetics of glyburide depended significantly on CYP2C9 genotypes.	Glyburide	29-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
11956512-11	2002	CONCLUSIONS: Carriers of the CYP2C9 variant *3 had decreased oral clearances of glyburide.	Glyburide	80-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
11956512-12	2002	This confirms that glyburide is metabolized by CYP2C9.	Glyburide	19-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
11926893-0	2002	Association between CYP2C9 genetic variants and anticoagulation-related outcomes during warfarin therapy.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
11926893-2	2002	The principal enzyme involved in warfarin metabolism is CYP2C9, and 2 relatively common variant forms with reduced activity have been identified, CYP2C9*2 and CYP2C9*3.	Warfarin	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
11926893-2	2002	The principal enzyme involved in warfarin metabolism is CYP2C9, and 2 relatively common variant forms with reduced activity have been identified, CYP2C9*2 and CYP2C9*3.	Warfarin	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
11926893-2	2002	The principal enzyme involved in warfarin metabolism is CYP2C9, and 2 relatively common variant forms with reduced activity have been identified, CYP2C9*2 and CYP2C9*3.	Warfarin	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
11926893-4	2002	OBJECTIVE: To determine if CYP2C9*2 and CYP2C9*3 variants are associated with overanticoagulation and bleeding events during warfarin therapy.	Warfarin	125-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
11926893-4	2002	OBJECTIVE: To determine if CYP2C9*2 and CYP2C9*3 variants are associated with overanticoagulation and bleeding events during warfarin therapy.	Warfarin	125-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
11926893-14	2002	CONCLUSIONS: The results of our study suggest that the CYP2C9*2 and CYP2C9*3 polymorphisms are associated with an increased risk of overanticoagulation and of bleeding events among patients in a warfarin anticoagulation clinic setting, although small numbers in some cases would suggest the need for caution in interpretation.	Warfarin	195-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
11926893-14	2002	CONCLUSIONS: The results of our study suggest that the CYP2C9*2 and CYP2C9*3 polymorphisms are associated with an increased risk of overanticoagulation and of bleeding events among patients in a warfarin anticoagulation clinic setting, although small numbers in some cases would suggest the need for caution in interpretation.	Warfarin	195-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
11926893-15	2002	Screening for CYP2C9 variants may allow clinicians to develop dosing protocols and surveillance techniques to reduce the risk of adverse drug reactions in patients receiving warfarin.	Warfarin	174-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
11918509-5	2002	DISCUSSION: RTV is an inducer of the hepatic isoenzymes CYP1A2, CYP1A4, and CYP2C9/19 and leads to extensive metabolism of acenocoumarol that cannot be balanced by dose increases.	Ritonavir	12-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
11918509-5	2002	DISCUSSION: RTV is an inducer of the hepatic isoenzymes CYP1A2, CYP1A4, and CYP2C9/19 and leads to extensive metabolism of acenocoumarol that cannot be balanced by dose increases.	Acenocoumarol	123-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
11901091-3	2002	To this end, the kinetic profiles of three model CYP2C9 substrates (flurbiprofen, naproxen, and piroxicam) were studied using purified CYP2C9*1 (wild-type) and variants involving active site amino acid changes, including the naturally occurring variants CYP2C9*3 (Leu359) and CYP2C9*5 (Glu360) and the man-made mutant CYP2C9 F114L.	Flurbiprofen	68-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
11901091-3	2002	To this end, the kinetic profiles of three model CYP2C9 substrates (flurbiprofen, naproxen, and piroxicam) were studied using purified CYP2C9*1 (wild-type) and variants involving active site amino acid changes, including the naturally occurring variants CYP2C9*3 (Leu359) and CYP2C9*5 (Glu360) and the man-made mutant CYP2C9 F114L.	Naproxen	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
11901091-3	2002	To this end, the kinetic profiles of three model CYP2C9 substrates (flurbiprofen, naproxen, and piroxicam) were studied using purified CYP2C9*1 (wild-type) and variants involving active site amino acid changes, including the naturally occurring variants CYP2C9*3 (Leu359) and CYP2C9*5 (Glu360) and the man-made mutant CYP2C9 F114L.	Piroxicam	96-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
11901091-4	2002	CYP2C9*1 (wild-type) metabolized each of the three compounds with a distinctive profile reflective of typical hyperbolic (flurbiprofen), biphasic (naproxen), and substrate inhibition (piroxicam) kinetics.	Flurbiprofen	122-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11901091-4	2002	CYP2C9*1 (wild-type) metabolized each of the three compounds with a distinctive profile reflective of typical hyperbolic (flurbiprofen), biphasic (naproxen), and substrate inhibition (piroxicam) kinetics.	Naproxen	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11901091-4	2002	CYP2C9*1 (wild-type) metabolized each of the three compounds with a distinctive profile reflective of typical hyperbolic (flurbiprofen), biphasic (naproxen), and substrate inhibition (piroxicam) kinetics.	Piroxicam	184-193	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11901091-5	2002	CYP2C9*3 metabolism was again hyperbolic for flurbiprofen, of a linear form for naproxen (no saturation noted), and exhibited substrate inhibition with piroxicam.	Flurbiprofen	45-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11901091-5	2002	CYP2C9*3 metabolism was again hyperbolic for flurbiprofen, of a linear form for naproxen (no saturation noted), and exhibited substrate inhibition with piroxicam.	Naproxen	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11901091-5	2002	CYP2C9*3 metabolism was again hyperbolic for flurbiprofen, of a linear form for naproxen (no saturation noted), and exhibited substrate inhibition with piroxicam.	Piroxicam	152-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11901091-6	2002	CYP2C9*5-mediated metabolism was hyperbolic for flurbiprofen and piroxicam but linear with respect to naproxen turnover.	Flurbiprofen	48-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11901091-6	2002	CYP2C9*5-mediated metabolism was hyperbolic for flurbiprofen and piroxicam but linear with respect to naproxen turnover.	Piroxicam	65-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11901091-6	2002	CYP2C9*5-mediated metabolism was hyperbolic for flurbiprofen and piroxicam but linear with respect to naproxen turnover.	Naproxen	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11901092-4	2002	CYP2A6 (coumarin 7-hydroxylation) and CYP2C9 (diclofenac 4"-hydroxylation) activities exhibited a mixed type of inhibition comprising competitive and noncompetitive components in response to SN-38, the K(i) values being 181 and 156 microM, respectively.	Diclofenac	46-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
11901092-4	2002	CYP2A6 (coumarin 7-hydroxylation) and CYP2C9 (diclofenac 4"-hydroxylation) activities exhibited a mixed type of inhibition comprising competitive and noncompetitive components in response to SN-38, the K(i) values being 181 and 156 microM, respectively.	Irinotecan	191-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	24-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	35-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	180-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
11901092-9	2002	These results mean that CPT-11 and SN-38 interact with human P450 isoforms, such as CYP2A6, CYP2C9, and CYP3A4, in vitro and imply that the significant drug interactions involving CPT-11 may be caused by a mechanism-based inactivation of CYP3A4 by SN-38 as an active metabolite of CPT-11 rather than competitive inhibition.	Irinotecan	180-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
11910269-6	2002	Because paroxetine is a mild inhibitor of CYP1A2, CYP2C9, CYP2C19, and CYP3A4, increase of (S)-methadone concentrations in both EMs and PMs could be mediated by inhibition of any of these isozymes.	Paroxetine	8-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
11854151-6	2002	Ketoconazole seemed to be the most selective for CYP3A4, although it also inhibited CYP2C9.	Ketoconazole	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
11956677-0	2002	Inhibition by atovaquone of CYP2C9-mediated sulphamethoxazole hydroxylamine formation.	Atovaquone	14-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
11956677-0	2002	Inhibition by atovaquone of CYP2C9-mediated sulphamethoxazole hydroxylamine formation.	sulfamethoxazole hydroxylamine	44-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
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 hydroxylamine	23-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
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
11956677-7	2002	Compared with human liver microsomes, CYP2C9*1 showed an eightfold greater specific activity for SMX-HA generation; as for liver microsomes, CYP2C9*1 activity was inhibited by atovaquone.	Atovaquone	176-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
11956677-7	2002	Compared with human liver microsomes, CYP2C9*1 showed an eightfold greater specific activity for SMX-HA generation; as for liver microsomes, CYP2C9*1 activity was inhibited by atovaquone.	Atovaquone	176-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
11956677-8	2002	CONCLUSIONS: Atovaquone is a relatively weak inhibitor of CYP2C9-mediated SMX-HA formation in vitro.	Atovaquone	13-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
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
11925616-8	2002	The enzyme activity of CYP2C9 catalyzing oxidation of tolbutamide to hydroxy tolbutamide in S9 fraction of the cell was determined by high performance liquid chromatography(HPLC).	Tolbutamide	54-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
11925616-8	2002	The enzyme activity of CYP2C9 catalyzing oxidation of tolbutamide to hydroxy tolbutamide in S9 fraction of the cell was determined by high performance liquid chromatography(HPLC).	hydroxymethyltolbutamide	69-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
11875362-0	2002	CYP2C9 polymorphism: impact on tolbutamide pharmacokinetics and response.	Tolbutamide	31-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11893129-0	2002	The frequency and effects of cytochrome P450 (CYP) 2C9 polymorphisms in patients receiving warfarin.	Warfarin	91-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-54
11893129-3	2002	To better understand the interaction between genotype and response to warfarin therapy, we determined the frequency and functional effects of polymorphisms of the predominant cytochrome P450 subfamily responsible for warfarin metabolism (eg, CYP2C9) in an ethnically defined U.S. patient population.	Warfarin	217-225	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	242-248
11893129-13	2002	CONCLUSIONS: CYP2C9 polymorphisms are common, associated with significant reductions in warfarin dose, and partly account for interpatient variability in warfarin sensitivity.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
11893129-13	2002	CONCLUSIONS: CYP2C9 polymorphisms are common, associated with significant reductions in warfarin dose, and partly account for interpatient variability in warfarin sensitivity.	Warfarin	154-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
11907487-12	2002	Consistent with expression data, formation of verapamil metabolites catalyzed by CYP3A4 and CYP2C was shown.	Verapamil	46-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-97
11936218-4	2002	Oroxylin A inhibited diclofenac 4-hydroxylation (CYP2C9) activity with a IC50 of 6.7 microM.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
11936218-4	2002	Oroxylin A inhibited diclofenac 4-hydroxylation (CYP2C9) activity with a IC50 of 6.7 microM.	Diclofenac	21-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
11875364-9	2002	Tolbutamide was confirmed as a substrate of the genetically polymorphic enzyme CYP2C9.	Tolbutamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
11875364-0	2002	Impact of CYP2C9 and CYP2C19 polymorphisms on tolbutamide kinetics and the insulin and glucose response in healthy volunteers.	Tolbutamide	46-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
11875365-0	2002	Effects of CYP2C19 and CYP2C9 genetic polymorphisms on the disposition of and blood glucose lowering response to tolbutamide in humans.	Glucose	84-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
11875365-0	2002	Effects of CYP2C19 and CYP2C9 genetic polymorphisms on the disposition of and blood glucose lowering response to tolbutamide in humans.	Tolbutamide	113-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
11875365-1	2002	Several recent in-vitro data have revealed that CYP2C19, in addition to CYP2C9, is also involved in the 4-methylhydroxylation of tolbutamide.	Tolbutamide	129-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
11875365-7	2002	In subjects heterozygous for the CYP2C9*3 allele, C(max) and AUC of tolbutamide were significantly greater and the plasma half-life significantly longer than those in homozygous CYP2C9*1 subjects.	Tolbutamide	68-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
11875365-7	2002	In subjects heterozygous for the CYP2C9*3 allele, C(max) and AUC of tolbutamide were significantly greater and the plasma half-life significantly longer than those in homozygous CYP2C9*1 subjects.	Tolbutamide	68-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	178-184
11875365-9	2002	The estimated AUC of the increase in serum glucose after oral intake of 100 g dextrose was 2.7-fold higher in subjects with the wild-type CYP2C9 genotype than in those with CYP2C9*1/*3, but CYP2C19 genetic polymorphism did not alter the blood glucose lowering effect of tolbutamide.	Glucose	43-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
11875365-9	2002	The estimated AUC of the increase in serum glucose after oral intake of 100 g dextrose was 2.7-fold higher in subjects with the wild-type CYP2C9 genotype than in those with CYP2C9*1/*3, but CYP2C19 genetic polymorphism did not alter the blood glucose lowering effect of tolbutamide.	Glucose	43-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	173-179
11875365-9	2002	The estimated AUC of the increase in serum glucose after oral intake of 100 g dextrose was 2.7-fold higher in subjects with the wild-type CYP2C9 genotype than in those with CYP2C9*1/*3, but CYP2C19 genetic polymorphism did not alter the blood glucose lowering effect of tolbutamide.	Glucose	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
11875365-9	2002	The estimated AUC of the increase in serum glucose after oral intake of 100 g dextrose was 2.7-fold higher in subjects with the wild-type CYP2C9 genotype than in those with CYP2C9*1/*3, but CYP2C19 genetic polymorphism did not alter the blood glucose lowering effect of tolbutamide.	Glucose	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	173-179
11875365-9	2002	The estimated AUC of the increase in serum glucose after oral intake of 100 g dextrose was 2.7-fold higher in subjects with the wild-type CYP2C9 genotype than in those with CYP2C9*1/*3, but CYP2C19 genetic polymorphism did not alter the blood glucose lowering effect of tolbutamide.	Glucose	243-250	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
11875365-9	2002	The estimated AUC of the increase in serum glucose after oral intake of 100 g dextrose was 2.7-fold higher in subjects with the wild-type CYP2C9 genotype than in those with CYP2C9*1/*3, but CYP2C19 genetic polymorphism did not alter the blood glucose lowering effect of tolbutamide.	Tolbutamide	270-281	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
11875364-1	2002	Tolbutamide is known to be metabolized by cytochrome P450 2C9 (CYP2C9), and the effects of the CYP2C9 amino acid polymorphisms *2 (Arg144Cys) and *3 (Ile359Leu) could be important for drug treatment with tolbutamide and for use of tolbutamide as a CYP2C9 test drug.	Tolbutamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-61
11875365-11	2002	Our results strongly suggest that the disposition and hypoglycemic effect of tolbutamide are affected mainly by CYP2C9 genetic polymorphism, but not by CYP2C19 polymorphism.	Tolbutamide	77-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
11875365-13	2002	This suggests that, at least in vivo, tolbutamide remains a selective probe for measuring CYP2C9 activity in humans.	Tolbutamide	38-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
11875364-1	2002	Tolbutamide is known to be metabolized by cytochrome P450 2C9 (CYP2C9), and the effects of the CYP2C9 amino acid polymorphisms *2 (Arg144Cys) and *3 (Ile359Leu) could be important for drug treatment with tolbutamide and for use of tolbutamide as a CYP2C9 test drug.	Tolbutamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
11853173-3	2002	Additionally, nonylphenol competitively inhibited diclofenac 4"-hydroxylation by CYP2C9 and S-mephenytoin 4"-hydroxylation by CYP2C19 with Ki values of 5.3 and 37 microM, respectively.	nonylphenol	14-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
11853173-3	2002	Additionally, nonylphenol competitively inhibited diclofenac 4"-hydroxylation by CYP2C9 and S-mephenytoin 4"-hydroxylation by CYP2C19 with Ki values of 5.3 and 37 microM, respectively.	diclofenac 4"	50-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
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 9	Homo sapiens	126-132
11853173-5	2002	These results suggest that nonylphenol inhibits human hepatic CYPs, especially CYP2C9 and CYP2C19, and steroidogenic CYP17 activities.	nonylphenol	27-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
11936702-2	2002	METHODS: Bufuralol 1"-hydroxylation and tolbutamide 4-methylhydroxylation were used as index reactions for CYP2D6 and CYP2C9, respectively.	bufuralol	9-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
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%.	aminopyrine n	95-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
11816012-7	2002	Since celecoxib should be metabolized primarily by cytochrome 2C9 (CYP2C9), a poor metabolizer (PM) for this cytochrome P450 enzyme was included in the study.	Celecoxib	6-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
11792677-9	2002	Using human microsomes, tibolone, 3alpha-hydroxy tibolone, 3beta-hydroxy tibolone, and Delta(4)-tibolone appeared to be at least 50-fold less potent inhibitors of CYP1A2, CYP2C9, CYP2E1, and CYP3A4 compared with enzyme-selective inhibitors.	tibolone	24-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
11792677-9	2002	Using human microsomes, tibolone, 3alpha-hydroxy tibolone, 3beta-hydroxy tibolone, and Delta(4)-tibolone appeared to be at least 50-fold less potent inhibitors of CYP1A2, CYP2C9, CYP2E1, and CYP3A4 compared with enzyme-selective inhibitors.	3-hydroxytibolone	34-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
11792677-9	2002	Using human microsomes, tibolone, 3alpha-hydroxy tibolone, 3beta-hydroxy tibolone, and Delta(4)-tibolone appeared to be at least 50-fold less potent inhibitors of CYP1A2, CYP2C9, CYP2E1, and CYP3A4 compared with enzyme-selective inhibitors.	3-hydroxytibolone	59-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
11792677-9	2002	Using human microsomes, tibolone, 3alpha-hydroxy tibolone, 3beta-hydroxy tibolone, and Delta(4)-tibolone appeared to be at least 50-fold less potent inhibitors of CYP1A2, CYP2C9, CYP2E1, and CYP3A4 compared with enzyme-selective inhibitors.	delta(4)-tibolone	87-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
11936702-7	2002	CONCLUSION: All five H1-antihistamines studied inhibited CYP2D6 markedly, but only cyclizine and promethazine inhibited CYP2C9 at concentrations above that usually seen in plasma.	Cyclizine	83-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
11936702-7	2002	CONCLUSION: All five H1-antihistamines studied inhibited CYP2D6 markedly, but only cyclizine and promethazine inhibited CYP2C9 at concentrations above that usually seen in plasma.	Promethazine	97-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
11875991-0	2002	Warfarin therapy in a patient homozygous for the CYP2C9 3 allele.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
11876575-6	2002	Fluvoxamine is a potent CYP1A2 and CYP2C19 inhibitor, and a moderate CYP2C9, CYP2D6, and CYP3A4 inhibitor.	Fluvoxamine	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
11925850-0	2002	[Relationship of polymorphism in CYP2C9 to genetic susceptibility to diclofenac-induced influenza-virus-associated encephalopathy].	Diclofenac	69-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
11831544-1	2002	Modafinil has been reported to produce a concentration-related suppression of CYP2C9 activity in vitro in primary cultures of human hepatocytes.	Modafinil	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
11831544-5	2002	Since (S)-warfarin is predominantly metabolized via CYP2C9, the results indicate that the marked suppression of CYP2C9 activity in vitro does not translate into a similar effect clinically.	Warfarin	6-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
11831544-5	2002	Since (S)-warfarin is predominantly metabolized via CYP2C9, the results indicate that the marked suppression of CYP2C9 activity in vitro does not translate into a similar effect clinically.	Warfarin	6-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
11925850-2	2002	CYP2C9 is known as the major cytochrome P450 gene product that catalyzes diclofenac in human liver.	Diclofenac	73-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11925850-6	2002	We suggest that this mutation in the CYP2C9 gene may be related to diclofenac-induced influenza-virus-associated encephalopathy.	Diclofenac	67-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
11823761-0	2002	Pharmacokinetics of losartan and its metabolite E-3174 in relation to the CYP2C9 genotype.	Losartan	20-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
11679585-3	2002	In previous work, we have shown that CYP2C9 is inducible in primary human hepatocytes by xenobiotics including dexamethasone, rifampicin, and phenobarbital.	Dexamethasone	111-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
11679585-3	2002	In previous work, we have shown that CYP2C9 is inducible in primary human hepatocytes by xenobiotics including dexamethasone, rifampicin, and phenobarbital.	Rifampin	126-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
11679585-3	2002	In previous work, we have shown that CYP2C9 is inducible in primary human hepatocytes by xenobiotics including dexamethasone, rifampicin, and phenobarbital.	Phenobarbital	142-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
11679585-8	2002	Identification of these functional elements provides rational mechanistic basis for CYP2C9 induction by dexamethasone (submicromolar concentrations), and by phenobarbital and rifampicin, respectively.	Dexamethasone	104-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
11679585-8	2002	Identification of these functional elements provides rational mechanistic basis for CYP2C9 induction by dexamethasone (submicromolar concentrations), and by phenobarbital and rifampicin, respectively.	Phenobarbital	157-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
11679585-8	2002	Identification of these functional elements provides rational mechanistic basis for CYP2C9 induction by dexamethasone (submicromolar concentrations), and by phenobarbital and rifampicin, respectively.	Rifampin	175-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
11753007-2	2002	Both parecoxib and valdecoxib inhibit human cytochrome P450 2C9 (CYP2C9) activity in vitro.	parecoxib	5-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-63
11753007-2	2002	Both parecoxib and valdecoxib inhibit human cytochrome P450 2C9 (CYP2C9) activity in vitro.	parecoxib	5-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
11753007-2	2002	Both parecoxib and valdecoxib inhibit human cytochrome P450 2C9 (CYP2C9) activity in vitro.	valdecoxib	19-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-63
11753007-2	2002	Both parecoxib and valdecoxib inhibit human cytochrome P450 2C9 (CYP2C9) activity in vitro.	valdecoxib	19-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
11753007-3	2002	Thus, a potential exists for in vivo interactions with other CYP2C9 substrates, including propofol.	Propofol	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
12405866-17	2002	Sulfonylurea drugs utilise mainly CYP2C9 for metabolism, and this isoenzyme may be induced by ritonavir and nelfinavir with a resulting decrease in efficacy of the sulfonylurea.	Sulfonylurea Compounds	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
12405866-17	2002	Sulfonylurea drugs utilise mainly CYP2C9 for metabolism, and this isoenzyme may be induced by ritonavir and nelfinavir with a resulting decrease in efficacy of the sulfonylurea.	Sulfonylurea Compounds	164-176	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
12405866-18	2002	Losartan may have increased effect when coadministered with ritonavir and nelfinavir because of the induction of CYP2C9 and the expected increase in formation of the active metabolite, E-3174.	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
12405866-18	2002	Losartan may have increased effect when coadministered with ritonavir and nelfinavir because of the induction of CYP2C9 and the expected increase in formation of the active metabolite, E-3174.	Ritonavir	60-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
12405866-18	2002	Losartan may have increased effect when coadministered with ritonavir and nelfinavir because of the induction of CYP2C9 and the expected increase in formation of the active metabolite, E-3174.	Nelfinavir	74-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
11823761-0	2002	Pharmacokinetics of losartan and its metabolite E-3174 in relation to the CYP2C9 genotype.	losartan carboxylic acid	48-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
11823761-1	2002	BACKGROUND AND AIM: Losartan is metabolized by polymorphic CYP2C9 to E-3174.	Losartan	20-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
11823761-2	2002	Our aim was to evaluate the pharmacokinetics of losartan and E-3174 in relation to the CYP2C9 genotype.	Losartan	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
11823761-2	2002	Our aim was to evaluate the pharmacokinetics of losartan and E-3174 in relation to the CYP2C9 genotype.	losartan carboxylic acid	61-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
11823761-3	2002	METHODS: A 50-mg oral dose of losartan was given to 22 Swedish volunteers with different CYP2C9 genotypes.	Losartan	30-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
11888331-15	2002	Inhibition of the CYP2C9 and CYP3A isoenzymes by zafirlukast has been reported in vitro.	zafirlukast	49-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
11823761-6	2002	RESULTS: The maximum plasma concentration of E-3174 was significantly (P &lt;.05) lower in the CYP2C9*1/*3 (n = 5) and CYP2C9*2/*3 (n = 4) groups compared with the CYP2C9*1/*1 (n = 6) and CYP2C9*1/*2 (n = 3) groups and extremely low in 1 subject with the CYP2C9*3/*3 genotype.	losartan carboxylic acid	45-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
11823761-6	2002	RESULTS: The maximum plasma concentration of E-3174 was significantly (P &lt;.05) lower in the CYP2C9*1/*3 (n = 5) and CYP2C9*2/*3 (n = 4) groups compared with the CYP2C9*1/*1 (n = 6) and CYP2C9*1/*2 (n = 3) groups and extremely low in 1 subject with the CYP2C9*3/*3 genotype.	losartan carboxylic acid	45-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
11823761-6	2002	RESULTS: The maximum plasma concentration of E-3174 was significantly (P &lt;.05) lower in the CYP2C9*1/*3 (n = 5) and CYP2C9*2/*3 (n = 4) groups compared with the CYP2C9*1/*1 (n = 6) and CYP2C9*1/*2 (n = 3) groups and extremely low in 1 subject with the CYP2C9*3/*3 genotype.	losartan carboxylic acid	45-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
11823761-6	2002	RESULTS: The maximum plasma concentration of E-3174 was significantly (P &lt;.05) lower in the CYP2C9*1/*3 (n = 5) and CYP2C9*2/*3 (n = 4) groups compared with the CYP2C9*1/*1 (n = 6) and CYP2C9*1/*2 (n = 3) groups and extremely low in 1 subject with the CYP2C9*3/*3 genotype.	losartan carboxylic acid	45-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
11823761-6	2002	RESULTS: The maximum plasma concentration of E-3174 was significantly (P &lt;.05) lower in the CYP2C9*1/*3 (n = 5) and CYP2C9*2/*3 (n = 4) groups compared with the CYP2C9*1/*1 (n = 6) and CYP2C9*1/*2 (n = 3) groups and extremely low in 1 subject with the CYP2C9*3/*3 genotype.	losartan carboxylic acid	45-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
11823761-7	2002	The ratio of the total losartan area under the plasma concentration-time curve (AUC) to the total E-3174 AUC (AUC(losartan)/AUC(E-3174)) was higher in the subject with the CYP2C9*3/*3 genotype (30-fold) and also in the CYP2C9*1/*3 and *2/*3 groups (approximately 2- and 3-fold, respectively) compared with the CYP2C9*1/*1 group.	Losartan	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
11823761-7	2002	The ratio of the total losartan area under the plasma concentration-time curve (AUC) to the total E-3174 AUC (AUC(losartan)/AUC(E-3174)) was higher in the subject with the CYP2C9*3/*3 genotype (30-fold) and also in the CYP2C9*1/*3 and *2/*3 groups (approximately 2- and 3-fold, respectively) compared with the CYP2C9*1/*1 group.	Losartan	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	219-225
11823761-7	2002	The ratio of the total losartan area under the plasma concentration-time curve (AUC) to the total E-3174 AUC (AUC(losartan)/AUC(E-3174)) was higher in the subject with the CYP2C9*3/*3 genotype (30-fold) and also in the CYP2C9*1/*3 and *2/*3 groups (approximately 2- and 3-fold, respectively) compared with the CYP2C9*1/*1 group.	Losartan	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	219-225
11823761-7	2002	The ratio of the total losartan area under the plasma concentration-time curve (AUC) to the total E-3174 AUC (AUC(losartan)/AUC(E-3174)) was higher in the subject with the CYP2C9*3/*3 genotype (30-fold) and also in the CYP2C9*1/*3 and *2/*3 groups (approximately 2- and 3-fold, respectively) compared with the CYP2C9*1/*1 group.	Losartan	114-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
11823761-10	2002	CONCLUSION: The CYP2C9*3 allele was shown to be associated with decreased formation of E-3174 from losartan.	losartan carboxylic acid	87-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
11823761-10	2002	CONCLUSION: The CYP2C9*3 allele was shown to be associated with decreased formation of E-3174 from losartan.	Losartan	99-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
11823761-11	2002	The significant differences between genotypes in plasma and urine losartan/E-3174 ratios and the good correlation between the plasma and urine ratios suggest that the losartan/E-3174 ratio in 0- to 8-hour urine specimens may serve as a phenotyping assay for CYP2C9 activity.	Losartan	167-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	258-264
15618707-5	2002	Addition of HSA resulted in smaller Km,u values for diclofenac and terfenadine metabolism by CYP2C9 and CYP3A4, respectively, and the Ki,u value for ketoconazole inhibition of CYP3A4 was also reduced.	Diclofenac	52-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
15618695-7	2002	In contrast, the inhibitory effects of phenacetin, diclofenac, S-mephenytoin, dextromethorphan, bufuralol and terfenadine, typical substrates for CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4, respectively, on each recombinant CYP activity decreased after preincubation.	Phenacetin	39-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
12036392-9	2002	The CYP3A family metabolises lovastatin, simvastatin, atorvastatin and cerivastatin, whereas CYP2C9 metabolises fluvastatin.	Fluvastatin	112-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
11794436-6	2002	Genetic analysis of the cytochrome P450 (CYP) isoenzyme 2C9, which mediates the major deactivating pathway of S-warfarin, revealed that the patient was a compound heterozygote carrying two variant alleles: CYP2C9*2 and CYP2C9*3.	Warfarin	110-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	206-212
15618705-11	2002	CYP2C enzymes were suggested to play major roles in metabolizing (+)-carveol to (+)-carvone and (+)-carvone to (+)-carveol by liver microsomes, since the activities were inhibited significantly by anti-human CYP2C9 antibodies in these animal species.	carveol	65-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	208-214
15618705-11	2002	CYP2C enzymes were suggested to play major roles in metabolizing (+)-carveol to (+)-carvone and (+)-carvone to (+)-carveol by liver microsomes, since the activities were inhibited significantly by anti-human CYP2C9 antibodies in these animal species.	carvone	80-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	208-214
15618705-11	2002	CYP2C enzymes were suggested to play major roles in metabolizing (+)-carveol to (+)-carvone and (+)-carvone to (+)-carveol by liver microsomes, since the activities were inhibited significantly by anti-human CYP2C9 antibodies in these animal species.	carvone	96-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	208-214
15618705-11	2002	CYP2C enzymes were suggested to play major roles in metabolizing (+)-carveol to (+)-carvone and (+)-carvone to (+)-carveol by liver microsomes, since the activities were inhibited significantly by anti-human CYP2C9 antibodies in these animal species.	carveol	111-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	208-214
15618705-12	2002	Studies with recombinant P450 enzymes suggested that CYP2C9 and 2C19 in humans and CYP2C11 in untreated male rats were the major enzymes in metabolizing (+)-carvone.	carvone	153-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
15618706-5	2002	CYP2C9 expressed in human B-lymphoblastoid cells catalyzed efficiently the MALDO activity for 11-oxo-Delta(8)-tetrahydrocannabinol (10.1 nmol/min/nmol P450), while the catalytic activities of other human CYPs expressed in the cells were lesser extents.	11-oxo-delta(8)-tetrahydrocannabinol	94-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
15618706-7	2002	These results indicate that CYP2C9 and CYP3A4 are major enzymes responsible for the MALDO activity in human liver for 11-oxo-Delta(8)-tetrahydrocannabinol and 9-anthraldehyde, respectively.	11-oxo-delta(8)-tetrahydrocannabinol	118-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
15618706-7	2002	These results indicate that CYP2C9 and CYP3A4 are major enzymes responsible for the MALDO activity in human liver for 11-oxo-Delta(8)-tetrahydrocannabinol and 9-anthraldehyde, respectively.	9-anthraldehyde	159-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
15618707-2	2002	The effect of addition of rat liver cytosol to an in vitro system using human liver microsomes was examined by measuring the catalytic activities of CYP2C9 (tolbutamide and diclofenac) and CYP3A4 (terfenadine).	Tolbutamide	157-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
15618707-4	2002	After addition of rat liver cytosol, the unbound Km value (Km,u) for terfenadine metabolism by CYP3A4, and the unbound Ki value of miconazole (Ki,u) for CYP2C9 were smaller than for the controls.	Miconazole	131-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
15618707-5	2002	Addition of HSA resulted in smaller Km,u values for diclofenac and terfenadine metabolism by CYP2C9 and CYP3A4, respectively, and the Ki,u value for ketoconazole inhibition of CYP3A4 was also reduced.	Terfenadine	67-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
15618695-7	2002	In contrast, the inhibitory effects of phenacetin, diclofenac, S-mephenytoin, dextromethorphan, bufuralol and terfenadine, typical substrates for CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4, respectively, on each recombinant CYP activity decreased after preincubation.	bufuralol	96-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
15618695-7	2002	In contrast, the inhibitory effects of phenacetin, diclofenac, S-mephenytoin, dextromethorphan, bufuralol and terfenadine, typical substrates for CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4, respectively, on each recombinant CYP activity decreased after preincubation.	Terfenadine	110-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
11794436-6	2002	Genetic analysis of the cytochrome P450 (CYP) isoenzyme 2C9, which mediates the major deactivating pathway of S-warfarin, revealed that the patient was a compound heterozygote carrying two variant alleles: CYP2C9*2 and CYP2C9*3.	Warfarin	110-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	219-225
11794436-7	2002	The patient"s enhanced sensitivity to warfarin 5 mg/day can be ascribed to decreased clearance of S-warfarin secondary to genetic alteration of the gene encoding CYP2C9, resulting in a life-threatening complication.	Warfarin	38-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
11794436-7	2002	The patient"s enhanced sensitivity to warfarin 5 mg/day can be ascribed to decreased clearance of S-warfarin secondary to genetic alteration of the gene encoding CYP2C9, resulting in a life-threatening complication.	Sulfur	98-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
11794436-7	2002	The patient"s enhanced sensitivity to warfarin 5 mg/day can be ascribed to decreased clearance of S-warfarin secondary to genetic alteration of the gene encoding CYP2C9, resulting in a life-threatening complication.	Warfarin	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
11717174-3	2001	At higher concentrations, DDB marginally inhibited caffeine N(3)-demethylation (CYP1A2), diclofenac 4"-hydroxylation (CYP2C9), and dextromethorphan O-demethylation (CYP2D6) activities, but this compound had no effect on CYP2A6-, CYP2C19-, and CYP2E1-mediated reactions.	ddb	26-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
11724084-9	2001	DISCUSSION: Phenytoin is principally metabolized by CYP2C9.	Phenytoin	12-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
11708911-6	2001	The selectivity analysis singled out CYP2C8 as the most different of the four CYP2C enzymes with amino acids with distinct properties in positions 114, 205, and 476 (Ser, Phe, and Ile, respectively) compared to the other enzymes.	Serine	166-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-42
11708911-6	2001	The selectivity analysis singled out CYP2C8 as the most different of the four CYP2C enzymes with amino acids with distinct properties in positions 114, 205, and 476 (Ser, Phe, and Ile, respectively) compared to the other enzymes.	Phenylalanine	171-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-42
11708911-6	2001	The selectivity analysis singled out CYP2C8 as the most different of the four CYP2C enzymes with amino acids with distinct properties in positions 114, 205, and 476 (Ser, Phe, and Ile, respectively) compared to the other enzymes.	Isoleucine	180-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-42
11708911-7	2001	An inverse pharmacophore model for CYP2C9 was constructed from the selective regions, and the model agreed with the docking of diclofenac where the properties of the ligand overlapped with the pharmacophoric points in the model.	Diclofenac	127-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
11829203-0	2001	The role of CYP2C9 genotype in the metabolism of diclofenac in vivo and in vitro.	Diclofenac	49-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
11829203-1	2001	INTRODUCTION: The polymorphic cytochrome P450 enzyme 2C9 (CYP2C9) catalyses the metabolism of many drugs including S-warfarin, acenocoumarol, phenytoin, tolbutamide, losartan and most of the non-steroidal anti-inflammatory drugs.	Warfarin	115-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-56
11829203-1	2001	INTRODUCTION: The polymorphic cytochrome P450 enzyme 2C9 (CYP2C9) catalyses the metabolism of many drugs including S-warfarin, acenocoumarol, phenytoin, tolbutamide, losartan and most of the non-steroidal anti-inflammatory drugs.	Warfarin	115-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
11829203-1	2001	INTRODUCTION: The polymorphic cytochrome P450 enzyme 2C9 (CYP2C9) catalyses the metabolism of many drugs including S-warfarin, acenocoumarol, phenytoin, tolbutamide, losartan and most of the non-steroidal anti-inflammatory drugs.	Acenocoumarol	127-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-56
11829203-1	2001	INTRODUCTION: The polymorphic cytochrome P450 enzyme 2C9 (CYP2C9) catalyses the metabolism of many drugs including S-warfarin, acenocoumarol, phenytoin, tolbutamide, losartan and most of the non-steroidal anti-inflammatory drugs.	Acenocoumarol	127-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
11829203-1	2001	INTRODUCTION: The polymorphic cytochrome P450 enzyme 2C9 (CYP2C9) catalyses the metabolism of many drugs including S-warfarin, acenocoumarol, phenytoin, tolbutamide, losartan and most of the non-steroidal anti-inflammatory drugs.	Phenytoin	142-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-56
11829203-1	2001	INTRODUCTION: The polymorphic cytochrome P450 enzyme 2C9 (CYP2C9) catalyses the metabolism of many drugs including S-warfarin, acenocoumarol, phenytoin, tolbutamide, losartan and most of the non-steroidal anti-inflammatory drugs.	Phenytoin	142-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
11829203-1	2001	INTRODUCTION: The polymorphic cytochrome P450 enzyme 2C9 (CYP2C9) catalyses the metabolism of many drugs including S-warfarin, acenocoumarol, phenytoin, tolbutamide, losartan and most of the non-steroidal anti-inflammatory drugs.	Tolbutamide	153-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-56
11829203-1	2001	INTRODUCTION: The polymorphic cytochrome P450 enzyme 2C9 (CYP2C9) catalyses the metabolism of many drugs including S-warfarin, acenocoumarol, phenytoin, tolbutamide, losartan and most of the non-steroidal anti-inflammatory drugs.	Tolbutamide	153-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
11829203-1	2001	INTRODUCTION: The polymorphic cytochrome P450 enzyme 2C9 (CYP2C9) catalyses the metabolism of many drugs including S-warfarin, acenocoumarol, phenytoin, tolbutamide, losartan and most of the non-steroidal anti-inflammatory drugs.	Losartan	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-56
11829203-1	2001	INTRODUCTION: The polymorphic cytochrome P450 enzyme 2C9 (CYP2C9) catalyses the metabolism of many drugs including S-warfarin, acenocoumarol, phenytoin, tolbutamide, losartan and most of the non-steroidal anti-inflammatory drugs.	Losartan	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
11829203-2	2001	Diclofenac is metabolised to 4"-hydroxy (OH), the major diclofenac metabolite, 3"-OH and 3"-OH-4"-methoxy metabolites by CYP2C9.	Diclofenac	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
11829203-2	2001	Diclofenac is metabolised to 4"-hydroxy (OH), the major diclofenac metabolite, 3"-OH and 3"-OH-4"-methoxy metabolites by CYP2C9.	4-hydroxyphenylacetic acid	29-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
11829203-2	2001	Diclofenac is metabolised to 4"-hydroxy (OH), the major diclofenac metabolite, 3"-OH and 3"-OH-4"-methoxy metabolites by CYP2C9.	3"-oh	79-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
11829203-2	2001	Diclofenac is metabolised to 4"-hydroxy (OH), the major diclofenac metabolite, 3"-OH and 3"-OH-4"-methoxy metabolites by CYP2C9.	3"-oh-4"	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
11829203-3	2001	The aim of the present study was to clarify the impact of the CYP2C9 polymorphism on the metabolism of diclofenac both in vivo and in vitro.	Diclofenac	103-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
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 9	Homo sapiens	207-213
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 9	Homo sapiens	207-213
11740344-0	2001	Identification of a null allele of CYP2C9 in an African-American exhibiting toxicity to phenytoin.	Phenytoin	88-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
11740344-2	2001	Two polymorphic alleles CYP2C9*2 and CYP2C9*3 have been documented which affect the metabolism and clinical toxicity of drugs such as phenytoin, warfarin, glipizide, and tolbutamide.	Phenytoin	134-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
11740344-2	2001	Two polymorphic alleles CYP2C9*2 and CYP2C9*3 have been documented which affect the metabolism and clinical toxicity of drugs such as phenytoin, warfarin, glipizide, and tolbutamide.	Phenytoin	134-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
11740344-2	2001	Two polymorphic alleles CYP2C9*2 and CYP2C9*3 have been documented which affect the metabolism and clinical toxicity of drugs such as phenytoin, warfarin, glipizide, and tolbutamide.	Warfarin	145-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
11740344-2	2001	Two polymorphic alleles CYP2C9*2 and CYP2C9*3 have been documented which affect the metabolism and clinical toxicity of drugs such as phenytoin, warfarin, glipizide, and tolbutamide.	Warfarin	145-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
11740344-2	2001	Two polymorphic alleles CYP2C9*2 and CYP2C9*3 have been documented which affect the metabolism and clinical toxicity of drugs such as phenytoin, warfarin, glipizide, and tolbutamide.	Glipizide	155-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
11740344-2	2001	Two polymorphic alleles CYP2C9*2 and CYP2C9*3 have been documented which affect the metabolism and clinical toxicity of drugs such as phenytoin, warfarin, glipizide, and tolbutamide.	Glipizide	155-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
11740344-2	2001	Two polymorphic alleles CYP2C9*2 and CYP2C9*3 have been documented which affect the metabolism and clinical toxicity of drugs such as phenytoin, warfarin, glipizide, and tolbutamide.	Tolbutamide	170-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
11740344-2	2001	Two polymorphic alleles CYP2C9*2 and CYP2C9*3 have been documented which affect the metabolism and clinical toxicity of drugs such as phenytoin, warfarin, glipizide, and tolbutamide.	Tolbutamide	170-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
11740344-9	2001	Sequencing studies revealed that the individual was homozygous for a new CYP2C9 allele (CYP2C9*6) with the deletion of an adenine at base pair 818 of the cDNA.	Adenine	122-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
11740344-9	2001	Sequencing studies revealed that the individual was homozygous for a new CYP2C9 allele (CYP2C9*6) with the deletion of an adenine at base pair 818 of the cDNA.	Adenine	122-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
11740344-12	2001	The study also demonstrates the severe clinical consequences to patients with a null mutation in CYP2C9 after treatment with normal doses of phenytoin.	Phenytoin	141-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
11736863-0	2001	In vitro evaluation of valproic acid as an inhibitor of human cytochrome P450 isoforms: preferential inhibition of cytochrome P450 2C9 (CYP2C9).	Valproic Acid	23-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-134
11736863-0	2001	In vitro evaluation of valproic acid as an inhibitor of human cytochrome P450 isoforms: preferential inhibition of cytochrome P450 2C9 (CYP2C9).	Valproic Acid	23-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
11736863-3	2001	RESULTS: Valproic acid competitively inhibited CYP2C9 activity with a Ki value of 600 microM.	Valproic Acid	9-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
11736863-7	2001	CONCLUSIONS: Valproic acid inhibits the activity of CYP2C9 at clinically relevant concentrations in human liver microsomes.	Valproic Acid	13-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
11736863-8	2001	Inhibition of CYP2C9 can explain some of the effects of valproic acid on the pharmacokinetics of other drugs, such as phenytoin.	Valproic Acid	56-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
11736863-8	2001	Inhibition of CYP2C9 can explain some of the effects of valproic acid on the pharmacokinetics of other drugs, such as phenytoin.	Phenytoin	118-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
11736863-9	2001	Co-administration of high doses of valproic acid with drugs that are primarily metabolized by CYP2C9 may result in significant drug interactions.	Valproic Acid	35-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
11594733-0	2001	Interaction of new sulfaphenazole derivatives with human liver cytochrome p450 2Cs: structural determinants required for selective recognition by CYP 2C9 and for inhibition of human CYP 2Cs.	Sulfaphenazole	19-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-153
11719730-1	2001	OBJECTIVE: Our objective was to study the effects of gemfibrozil on the pharmacokinetics and pharmacodynamics of glimepiride, a new sulfonylurea antidiabetic drug and a substrate of cytochrome P4502C9 (CYP2C9).	Gemfibrozil	53-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	182-200
11719730-1	2001	OBJECTIVE: Our objective was to study the effects of gemfibrozil on the pharmacokinetics and pharmacodynamics of glimepiride, a new sulfonylurea antidiabetic drug and a substrate of cytochrome P4502C9 (CYP2C9).	glimepiride	113-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	182-200
11719730-1	2001	OBJECTIVE: Our objective was to study the effects of gemfibrozil on the pharmacokinetics and pharmacodynamics of glimepiride, a new sulfonylurea antidiabetic drug and a substrate of cytochrome P4502C9 (CYP2C9).	glimepiride	113-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	202-208
11692083-0	2001	Early acenocoumarol overanticoagulation among cytochrome P450 2C9 poor metabolizers.	Acenocoumarol	6-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-65
11692083-1	2001	Cytochrome P450 2C9 (CYP2C9) is the enzyme that terminates the anticoagulant effect of warfarin.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
11692083-1	2001	Cytochrome P450 2C9 (CYP2C9) is the enzyme that terminates the anticoagulant effect of warfarin.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
11692083-2	2001	The heterozygous carriers of the two allelic variants CYP2C9*2 and CYP2C9*3 have been associated with impaired warfarin metabolism and a higher risk of haemorrhage.	Warfarin	111-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
11692083-2	2001	The heterozygous carriers of the two allelic variants CYP2C9*2 and CYP2C9*3 have been associated with impaired warfarin metabolism and a higher risk of haemorrhage.	Warfarin	111-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
11692083-3	2001	Only three CYP2C9 poor metabolizers (CYP2C9*3/CYP2C9*3) initiating warfarin treatment have so far been identified, all of them with a dramatic overdose occurring a few days after treatment initiation.	Warfarin	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
11588061-0	2001	Genetic polymorphism in exon 4 of cytochrome P450 CYP2C9 may be associated with warfarin sensitivity in Chinese patients.	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
11588061-1	2001	CYP2C9 polymorphisms reported in Caucasians (Arg144Cys in exon 3 and Ile359Leu in exon 7) are extremely uncommon in Chinese persons.	ile359leu	69-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11588061-2	2001	The genotype of CYP2C9 in this population was characterized to investigate its relation with the interindividual variation in warfarin dosages.	Warfarin	126-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
11602509-0	2001	Gemfibrozil is a potent inhibitor of human cytochrome P450 2C9.	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-62
11602509-3	2001	Gemfibrozil strongly and competitively inhibited CYP2C9 activity, with a K(i) (IC(50)) value of 5.8 (9.6) microM.	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
11602509-7	2001	In conclusion, gemfibrozil inhibits the activity of CYP2C9 at clinically relevant concentrations, and this is the likely mechanism by which gemfibrozil interacts with CYP2C9 substrate drugs, such as warfarin and glyburide.	Gemfibrozil	15-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
11602509-7	2001	In conclusion, gemfibrozil inhibits the activity of CYP2C9 at clinically relevant concentrations, and this is the likely mechanism by which gemfibrozil interacts with CYP2C9 substrate drugs, such as warfarin and glyburide.	Gemfibrozil	15-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
11602509-7	2001	In conclusion, gemfibrozil inhibits the activity of CYP2C9 at clinically relevant concentrations, and this is the likely mechanism by which gemfibrozil interacts with CYP2C9 substrate drugs, such as warfarin and glyburide.	Gemfibrozil	140-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
11602509-7	2001	In conclusion, gemfibrozil inhibits the activity of CYP2C9 at clinically relevant concentrations, and this is the likely mechanism by which gemfibrozil interacts with CYP2C9 substrate drugs, such as warfarin and glyburide.	Gemfibrozil	140-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
11602509-7	2001	In conclusion, gemfibrozil inhibits the activity of CYP2C9 at clinically relevant concentrations, and this is the likely mechanism by which gemfibrozil interacts with CYP2C9 substrate drugs, such as warfarin and glyburide.	Warfarin	199-207	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
11602509-7	2001	In conclusion, gemfibrozil inhibits the activity of CYP2C9 at clinically relevant concentrations, and this is the likely mechanism by which gemfibrozil interacts with CYP2C9 substrate drugs, such as warfarin and glyburide.	Glyburide	212-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
11602509-7	2001	In conclusion, gemfibrozil inhibits the activity of CYP2C9 at clinically relevant concentrations, and this is the likely mechanism by which gemfibrozil interacts with CYP2C9 substrate drugs, such as warfarin and glyburide.	Glyburide	212-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
11692083-3	2001	Only three CYP2C9 poor metabolizers (CYP2C9*3/CYP2C9*3) initiating warfarin treatment have so far been identified, all of them with a dramatic overdose occurring a few days after treatment initiation.	Warfarin	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
11692083-3	2001	Only three CYP2C9 poor metabolizers (CYP2C9*3/CYP2C9*3) initiating warfarin treatment have so far been identified, all of them with a dramatic overdose occurring a few days after treatment initiation.	Warfarin	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
11692083-4	2001	Acenocoumarol, another coumarinic anticoagulant, has recently been shown to be metabolized by CYP2C9.	Acenocoumarol	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
11594733-3	2001	This indicates that the CYP 2C9-iron(III)-NH(2)R bond previously described to exist in the CYP 2C9-SPA complex does not play a key role in the high affinity of SPA for CYP 2C9.	ferric sulfate	32-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-31
11594733-3	2001	This indicates that the CYP 2C9-iron(III)-NH(2)R bond previously described to exist in the CYP 2C9-SPA complex does not play a key role in the high affinity of SPA for CYP 2C9.	ferric sulfate	32-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-98
11594733-3	2001	This indicates that the CYP 2C9-iron(III)-NH(2)R bond previously described to exist in the CYP 2C9-SPA complex does not play a key role in the high affinity of SPA for CYP 2C9.	ferric sulfate	32-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-98
11594733-3	2001	This indicates that the CYP 2C9-iron(III)-NH(2)R bond previously described to exist in the CYP 2C9-SPA complex does not play a key role in the high affinity of SPA for CYP 2C9.	galactose-1-phosphate	45-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-31
11594733-3	2001	This indicates that the CYP 2C9-iron(III)-NH(2)R bond previously described to exist in the CYP 2C9-SPA complex does not play a key role in the high affinity of SPA for CYP 2C9.	galactose-1-phosphate	45-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-98
11594733-3	2001	This indicates that the CYP 2C9-iron(III)-NH(2)R bond previously described to exist in the CYP 2C9-SPA complex does not play a key role in the high affinity of SPA for CYP 2C9.	galactose-1-phosphate	45-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-98
11580286-10	2001	The effects of ticlopidine on CYP 2C19 are very analogous with those previously described for the inactivation of CYP 2C9 by tienilic acid.	Ticlopidine	15-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-121
11580286-10	2001	The effects of ticlopidine on CYP 2C19 are very analogous with those previously described for the inactivation of CYP 2C9 by tienilic acid.	Ticrynafen	125-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-121
11580286-11	2001	This suggests that a similar electrophilic intermediate, possibly a thiophene S-oxide, is involved in the inactivation of CYP 2C19 and CYP 2C9 by ticlopidine and tienilic acid, respectively.	thiophene s-oxide	68-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-142
11580286-11	2001	This suggests that a similar electrophilic intermediate, possibly a thiophene S-oxide, is involved in the inactivation of CYP 2C19 and CYP 2C9 by ticlopidine and tienilic acid, respectively.	Ticlopidine	146-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-142
11580286-11	2001	This suggests that a similar electrophilic intermediate, possibly a thiophene S-oxide, is involved in the inactivation of CYP 2C19 and CYP 2C9 by ticlopidine and tienilic acid, respectively.	Ticrynafen	162-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-142
11560876-8	2001	Finally, 10 microM CCM induced both CYP2C9 and CYP2B6, strengthening the evidence that hPXR is involved in the regulation of these genes.	Fruitcal	19-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
11673755-0	2001	Severe phenytoin intoxication in a subject homozygous for CYP2C9*3.	Phenytoin	7-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
11673755-5	2001	In the absence of any acquired predisposing factor for phenytoin toxicity, genetic mutations in the cytochrome P450 (CYP) enzymes responsible for phenytoin metabolism (CYP2C9 and CYP2C19) were suspected.	Phenytoin	146-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
11673755-7	2001	In view of the markedly reduced metabolic activity of CYP2C*3 in comparison with the wild-type enzyme (about one fifth) and of the minor role of CYP2C19 in phenytoin metabolism, it is likely that CYP2C9*3 mutation was largely responsible for drug overdose.	Phenytoin	156-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
11560876-0	2001	Calcium channel modulators of the dihydropyridine family are human pregnane X receptor activators and inducers of CYP3A, CYP2B, and CYP2C in human hepatocytes.	1,4-dihydropyridine	34-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-137
11907638-1	2001	BACKGROUND: The concurrent use of amiodarone and warfarin inhibits metabolism of S-warfarinby cytochrome P450 (CYP) 2C9, thereby increasing the anticoagulant effect of warfarin.	Amiodarone	34-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-119
11678778-11	2001	CYP2C9 metabolizes a wide variety of drugs including the anticoagulant warfarin, antidiabetic agents such as tolbutamide, anticonvulsants such as phenytoin, and nonsteroidal anti-inflammatory drugs.	Warfarin	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11678778-11	2001	CYP2C9 metabolizes a wide variety of drugs including the anticoagulant warfarin, antidiabetic agents such as tolbutamide, anticonvulsants such as phenytoin, and nonsteroidal anti-inflammatory drugs.	Tolbutamide	109-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11678778-14	2001	Severe and life-threatening bleeding episodes have been reported in CYP2C9 PMs exposed to warfarin.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
11907638-6	2001	CONCLUSIONS: It was suggested that inhibition of CYP2C9 by desethylamiodarone, the active metabolite of amiodarone, plays an important role in the interaction of warfarin and amiodarone.	Amiodarone	104-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
11907638-1	2001	BACKGROUND: The concurrent use of amiodarone and warfarin inhibits metabolism of S-warfarinby cytochrome P450 (CYP) 2C9, thereby increasing the anticoagulant effect of warfarin.	Warfarin	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-119
11907638-1	2001	BACKGROUND: The concurrent use of amiodarone and warfarin inhibits metabolism of S-warfarinby cytochrome P450 (CYP) 2C9, thereby increasing the anticoagulant effect of warfarin.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-119
11907638-2	2001	Amiodarone primarily inhibits CYP1A2 and CYP3A4, and desethylamiodarone primarily inhibits CYP2C9.	desethylamiodarone	53-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
11907638-6	2001	CONCLUSIONS: It was suggested that inhibition of CYP2C9 by desethylamiodarone, the active metabolite of amiodarone, plays an important role in the interaction of warfarin and amiodarone.	desethylamiodarone	59-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
11907638-6	2001	CONCLUSIONS: It was suggested that inhibition of CYP2C9 by desethylamiodarone, the active metabolite of amiodarone, plays an important role in the interaction of warfarin and amiodarone.	Amiodarone	67-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
11907638-6	2001	CONCLUSIONS: It was suggested that inhibition of CYP2C9 by desethylamiodarone, the active metabolite of amiodarone, plays an important role in the interaction of warfarin and amiodarone.	Warfarin	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
11668218-0	2001	Phenytoin metabolic ratio: a putative marker of CYP2C9 activity in vivo.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
11601668-6	2001	Celecoxib is metabolized by CYP2C9 and may be increased or decreased by CYP2C9 modifiers.	Celecoxib	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
11601668-6	2001	Celecoxib is metabolized by CYP2C9 and may be increased or decreased by CYP2C9 modifiers.	Celecoxib	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
11668218-8	2001	The CYP2C9-mediated production of (S)-p-HPPH represented the major metabolic pathway of phenytoin biotransformation as its excretion accounted for 95.6 + 0.9% of "total" p-HPPH excretion over the 96 h collection interval.	Phosphorus	34-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
11668218-8	2001	The CYP2C9-mediated production of (S)-p-HPPH represented the major metabolic pathway of phenytoin biotransformation as its excretion accounted for 95.6 + 0.9% of "total" p-HPPH excretion over the 96 h collection interval.	Phenytoin	88-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
11668218-11	2001	CYP2C9 genotyping and several phenytoin metabolic indices are correlated with CYP2C9 activity in vivo.	Phenytoin	30-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
11668218-12	2001	The utility of phenytoin to predict the metabolism of other CYP2C9 substrates justifies further evaluation.	Phenytoin	15-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
11557918-9	2001	CONCLUSION: The presence of even one copy of CYP2C9*3 reduces profoundly the metabolic clearance of S -acenocoumarol.	Acenocoumarol	100-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
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 9	Homo sapiens	75-81
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 9	Homo sapiens	0-6
11557918-0	2001	Altered pharmacokinetics of R- and S-acenocoumarol in a subject heterozygous for CYP2C9*3.	r-	28-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
11557918-0	2001	Altered pharmacokinetics of R- and S-acenocoumarol in a subject heterozygous for CYP2C9*3.	Acenocoumarol	35-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
11551516-6	2001	Importantly, we show elevated levels of CYP2C9 protein to be associated with cadmium accumulation in liver.	Cadmium	77-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
11551516-8	2001	One is that variation in CYP2C9 protein levels may be, in part, attributed to an individual"s non-workplace exposure to cadmium, or an individual"s CYP2C9 genotype may be a risk factor for cadmium accumulation.	Cadmium	120-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
11551516-8	2001	One is that variation in CYP2C9 protein levels may be, in part, attributed to an individual"s non-workplace exposure to cadmium, or an individual"s CYP2C9 genotype may be a risk factor for cadmium accumulation.	Cadmium	189-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
11551516-8	2001	One is that variation in CYP2C9 protein levels may be, in part, attributed to an individual"s non-workplace exposure to cadmium, or an individual"s CYP2C9 genotype may be a risk factor for cadmium accumulation.	Cadmium	189-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
11470765-9	2001	The association of the CYP2C9 polymorphism to colorectal cancer risk could be related to CYP2C9-mediated metabolic activation of polycyclic aromatic hydrocarbons and heterocyclic aromatic amines.	Polycyclic Aromatic Hydrocarbons	129-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
11583336-0	2001	Reply to rebuttal: Gene variants of the cytochrome P450 CYP2C9 affect oral anticoagulation with warfarin.	Warfarin	96-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
11470765-9	2001	The association of the CYP2C9 polymorphism to colorectal cancer risk could be related to CYP2C9-mediated metabolic activation of polycyclic aromatic hydrocarbons and heterocyclic aromatic amines.	Polycyclic Aromatic Hydrocarbons	129-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
11470765-9	2001	The association of the CYP2C9 polymorphism to colorectal cancer risk could be related to CYP2C9-mediated metabolic activation of polycyclic aromatic hydrocarbons and heterocyclic aromatic amines.	heterocyclic aromatic amines	166-194	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
11470765-9	2001	The association of the CYP2C9 polymorphism to colorectal cancer risk could be related to CYP2C9-mediated metabolic activation of polycyclic aromatic hydrocarbons and heterocyclic aromatic amines.	heterocyclic aromatic amines	166-194	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
11503010-1	2001	BACKGROUND: Interindividual variability in responses to warfarin is attributed to dietary vitamin K, drug interactions, age, or genetic polymorphism in the cytochrome P4502C9 enzyme (CYP2C9) (allelic variants 2C9*2 and 2C9*3 ) linked with impaired metabolism of the potent enantiomere S-warfarin.	Warfarin	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-181
11503010-1	2001	BACKGROUND: Interindividual variability in responses to warfarin is attributed to dietary vitamin K, drug interactions, age, or genetic polymorphism in the cytochrome P4502C9 enzyme (CYP2C9) (allelic variants 2C9*2 and 2C9*3 ) linked with impaired metabolism of the potent enantiomere S-warfarin.	Warfarin	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	183-189
11503010-1	2001	BACKGROUND: Interindividual variability in responses to warfarin is attributed to dietary vitamin K, drug interactions, age, or genetic polymorphism in the cytochrome P4502C9 enzyme (CYP2C9) (allelic variants 2C9*2 and 2C9*3 ) linked with impaired metabolism of the potent enantiomere S-warfarin.	Warfarin	287-295	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-181
11503010-1	2001	BACKGROUND: Interindividual variability in responses to warfarin is attributed to dietary vitamin K, drug interactions, age, or genetic polymorphism in the cytochrome P4502C9 enzyme (CYP2C9) (allelic variants 2C9*2 and 2C9*3 ) linked with impaired metabolism of the potent enantiomere S-warfarin.	Warfarin	287-295	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	183-189
11457649-0	2001	Minimal in vivo activation of CYP2C9-mediated flurbiprofen metabolism by dapsone.	Flurbiprofen	46-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
11454729-5	2001	PEITC noncompetitively inhibited S-warfarin 7-hydroxylase activity catalyzed by CYP2C9 (K(i) = 6.5 +/- 0.9 microM), S-mephenytoin 4"-hydroxylase activity catalyzed by CYP2C19 (K(i) = 12.0 +/- 3.2 microM), bufuralol 1"-hydroxylase activity catalyzed by CYP2D6 (K(i) = 28.4 +/- 7.9 microM), and chlorzoxazone 6-hydroxylase activity catalyzed by CYP2E1 (K(i) = 21.5 +/- 3.4 microM).	phenethyl isothiocyanate	0-5	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
11457649-0	2001	Minimal in vivo activation of CYP2C9-mediated flurbiprofen metabolism by dapsone.	Dapsone	73-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
11457649-1	2001	Dapsone has been shown to activate flurbiprofen 4"-hydroxylation by expressed CYP2C9 enzyme and in human liver microsomes.	Dapsone	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
11457649-1	2001	Dapsone has been shown to activate flurbiprofen 4"-hydroxylation by expressed CYP2C9 enzyme and in human liver microsomes.	Flurbiprofen	35-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
11457649-9	2001	These dapsone plasma concentrations were within the range of concentrations producing activation of flurbiprofen metabolism by CYP2C9 in vitro.	Dapsone	6-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-133
11457649-9	2001	These dapsone plasma concentrations were within the range of concentrations producing activation of flurbiprofen metabolism by CYP2C9 in vitro.	Flurbiprofen	100-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-133
11452703-1	2001	Evidence for the selectivity of S-warfarin metabolism by CYP2C9 is substantial, suggesting that warfarin may be a potential CYP2C9 phenotyping probe.	Warfarin	32-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
11455026-7	2001	The major effect of the Asp360Glu mutation was to increase the K(m) value relative to that of CYP2C9*1 for all three substrates: 12-fold higher for (S)-warfarin 7-hydroxylation, 5-fold higher for the 4"-hydroxylation of diclofenac, and 3-fold higher for the omega-1 hydroxylation of lauric acid.	lauric acid	283-294	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
11408373-6	2001	In comparison to the CYP2C9.1 variant, oxidation of losartan was significantly reduced in yeast expressing the rare CYP2C9.2 or CYP2C9.3 variants.	Losartan	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
11408373-7	2001	Moreover, the rate of losartan oxidation was lower in liver microsomes from individuals hetero- or homozygous for the CYP2C9*3 allele, or homozygous for the CYP2C9*2 allele.	Losartan	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
11408373-7	2001	Moreover, the rate of losartan oxidation was lower in liver microsomes from individuals hetero- or homozygous for the CYP2C9*3 allele, or homozygous for the CYP2C9*2 allele.	Losartan	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
11408373-9	2001	In summary, these in vitro results indicate that CYP2C9 is the major human P450 isoenzyme responsible for losartan oxidation and that the CYP2C9 genotype contributes to interindividual differences in losartan oxidation and activation.	Losartan	106-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
11408373-9	2001	In summary, these in vitro results indicate that CYP2C9 is the major human P450 isoenzyme responsible for losartan oxidation and that the CYP2C9 genotype contributes to interindividual differences in losartan oxidation and activation.	Losartan	200-208	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
11408373-9	2001	In summary, these in vitro results indicate that CYP2C9 is the major human P450 isoenzyme responsible for losartan oxidation and that the CYP2C9 genotype contributes to interindividual differences in losartan oxidation and activation.	Losartan	200-208	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
11455026-7	2001	The major effect of the Asp360Glu mutation was to increase the K(m) value relative to that of CYP2C9*1 for all three substrates: 12-fold higher for (S)-warfarin 7-hydroxylation, 5-fold higher for the 4"-hydroxylation of diclofenac, and 3-fold higher for the omega-1 hydroxylation of lauric acid.	Warfarin	148-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
11455026-7	2001	The major effect of the Asp360Glu mutation was to increase the K(m) value relative to that of CYP2C9*1 for all three substrates: 12-fold higher for (S)-warfarin 7-hydroxylation, 5-fold higher for the 4"-hydroxylation of diclofenac, and 3-fold higher for the omega-1 hydroxylation of lauric acid.	Diclofenac	220-230	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
11408370-0	2001	Dapsone activation of CYP2C9-mediated metabolism: evidence for activation of multiple substrates and a two-site model.	Dapsone	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
11408370-1	2001	Dapsone activates CYP2C9-mediated metabolism in various expression systems and is itself metabolized by CYP2C9 to its hydroxylamine metabolite.	Dapsone	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
11408370-1	2001	Dapsone activates CYP2C9-mediated metabolism in various expression systems and is itself metabolized by CYP2C9 to its hydroxylamine metabolite.	Dapsone	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
11408370-1	2001	Dapsone activates CYP2C9-mediated metabolism in various expression systems and is itself metabolized by CYP2C9 to its hydroxylamine metabolite.	Hydroxylamine	118-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
11408370-4	2001	Dapsone increased the Michaelis-Menten-derived V(max) of flurbiprofen 4"-hydroxylation from 12.6 to 20.6 pmol/min/pmol P450, and lowered its K(m) from 28.9 to 10.0 microM, suggesting that dapsone activates CYP2C9-mediated flurbiprofen metabolism without displacing flurbiprofen from the active site, supporting a two-site model describing activation.	Dapsone	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	206-212
11408370-4	2001	Dapsone increased the Michaelis-Menten-derived V(max) of flurbiprofen 4"-hydroxylation from 12.6 to 20.6 pmol/min/pmol P450, and lowered its K(m) from 28.9 to 10.0 microM, suggesting that dapsone activates CYP2C9-mediated flurbiprofen metabolism without displacing flurbiprofen from the active site, supporting a two-site model describing activation.	Flurbiprofen	57-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	206-212
11408370-9	2001	Overall, these results suggest that dapsone activates the metabolism of multiple substrates of CYP2C9 by binding within the active site and causing positive cooperativity, thus lending further support to a two-site binding model of P450-mediated metabolism.	Dapsone	36-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
11408373-0	2001	Role of CYP2C9 polymorphism in losartan oxidation.	Losartan	31-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
11408373-2	2001	The aim of the present investigation was to study the contribution of CYP2C9 and CYP3A4 in losartan oxidation in vitro and to evaluate the role of CYP2C9 polymorphism.	Losartan	91-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
11452703-1	2001	Evidence for the selectivity of S-warfarin metabolism by CYP2C9 is substantial, suggesting that warfarin may be a potential CYP2C9 phenotyping probe.	Warfarin	32-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
11452703-1	2001	Evidence for the selectivity of S-warfarin metabolism by CYP2C9 is substantial, suggesting that warfarin may be a potential CYP2C9 phenotyping probe.	Warfarin	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
11452703-1	2001	Evidence for the selectivity of S-warfarin metabolism by CYP2C9 is substantial, suggesting that warfarin may be a potential CYP2C9 phenotyping probe.	Warfarin	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
11452703-4	2001	The objective of this study was to investigate the pharmacokinetics and pharmacodynamics of S- and R-warfarin in plasma following the administration of warfarin alone versus warfarin and vitamin K in CYP2C9*1 homozygotes.	Warfarin	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	200-206
11452703-4	2001	The objective of this study was to investigate the pharmacokinetics and pharmacodynamics of S- and R-warfarin in plasma following the administration of warfarin alone versus warfarin and vitamin K in CYP2C9*1 homozygotes.	Vitamin K	187-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	200-206
11452703-14	2001	Warfarin 10 mg may be safely used as a CYP2C9 probe in *1 homozygotes when given concomitantly with 10 mg of oral vitamin K.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
11353758-5	2001	Among the 12 cDNA-expressed CYP enzymes examined, CYP2B6, CYP2C9, and CYP3A4 showed high activities for the N-demethylation of both enantiomers at the substrate concentration of 1 mM.	Nitrogen	15-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
11408373-5	2001	Sulfaphenazole, a CYP2C9 inhibitor, blocked the formation of E-3174 at low losartan concentrations (&lt;1 microM), whereas the inhibitory effect of triacetyloleandomycin, a CYP3A4 inhibitor, was significant only at high concentrations of losartan (&gt;25 microM).	Sulfaphenazole	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
11408373-5	2001	Sulfaphenazole, a CYP2C9 inhibitor, blocked the formation of E-3174 at low losartan concentrations (&lt;1 microM), whereas the inhibitory effect of triacetyloleandomycin, a CYP3A4 inhibitor, was significant only at high concentrations of losartan (&gt;25 microM).	losartan carboxylic acid	61-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
11408373-6	2001	In comparison to the CYP2C9.1 variant, oxidation of losartan was significantly reduced in yeast expressing the rare CYP2C9.2 or CYP2C9.3 variants.	Losartan	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
11408373-6	2001	In comparison to the CYP2C9.1 variant, oxidation of losartan was significantly reduced in yeast expressing the rare CYP2C9.2 or CYP2C9.3 variants.	Losartan	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
11353758-7	2001	Also, the intrinsic clearance (CL(int): V(max)/K(m)) of CYP2B6 for the N-demethylation of both enantiomers were 7 to 13 times higher than those of CYP2C9 and CYP3A4.	Nitrogen	71-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
11353758-8	2001	Orphenadrine (CYP2B6 inhibitor, 500 microM) and sulfaphenazole (CYP2C9 inhibitor, 100 microM) inhibited the N-demethylase activities for both enantiomers (5 microM) in human liver microsomes by 60 to 70%, whereas cyclosporin A (CYP3A4 inhibitor, 100 microM) failed to inhibit these activities.	Sulfaphenazole	48-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
11325819-0	2001	CYP2C9 and UGT1A6 genotypes modulate the protective effect of aspirin on colon adenoma risk.	Aspirin	62-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11353749-10	2001	Moreover, etoricoxib (0.1-100 microM) was found to be a relatively weak inhibitor (IC(50) &gt; 100 microM) of multiple P450s (CYP1A2, CYP2D6, CYP3A, CYP2E1, CYP2C9, and CYP2C19) in human liver microsomes.	Etoricoxib	10-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
11353755-7	2001	SCH 66712 also inhibited HL microsomal CYP3A4, CYP2C9, and CYP2C19; however, the concentrations required to inhibit those isoforms were 5- to 10-fold higher than those required to inhibit CYP2D6.	SCH 66712	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
11356927-3	2001	R-Norfluoxetine formation rates in a characterized microsomal bank correlated with the catalytic activities for cytochrome P450 (CYP) 2D6, CYP2C9, and CYP2C8.	(R)-Norfluoxetine	0-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	139-145
11356927-4	2001	Expressed CYP2C9, CYP2C19, and CYP2D6 formed R-norfluoxetine following incubation with 1 microM R-fluoxetine and exhibited apparent K(m) values of 9.7, 8.5, and 1.8 microM, respectively.	(R)-Norfluoxetine	45-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
11356927-4	2001	Expressed CYP2C9, CYP2C19, and CYP2D6 formed R-norfluoxetine following incubation with 1 microM R-fluoxetine and exhibited apparent K(m) values of 9.7, 8.5, and 1.8 microM, respectively.	(R)-Fluoxetine	96-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
11356927-5	2001	Multivariate correlation analysis identified CYP2C9 and CYP2D6 as significant regressors with R-norfluoxetine formation.	(R)-Norfluoxetine	94-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
11406737-12	2001	The mechanism underlying the interaction between rifampin and glyburide is probably induction of either CYP2C9 or P-glycoprotein or both.	Rifampin	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
11406737-12	2001	The mechanism underlying the interaction between rifampin and glyburide is probably induction of either CYP2C9 or P-glycoprotein or both.	Glyburide	62-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
11406737-13	2001	Induction of CYP2C9 would explain the increased systemic elimination of glipizide.	Glipizide	72-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
11356927-9	2001	Thus, it would appear that both CYP2D6 and CYP2C9 contribute to the formation of R-norfluoxetine, whereas only CYP2D6 is responsible for the conversion to S-norfluoxetine.	(R)-Norfluoxetine	81-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
11356927-10	2001	Since the enantiomers of fluoxetine and norfluoxetine are inhibitors of CYP2D6, upon chronic dosing, the CYP2D6-mediated metabolism of the fluoxetine enantiomers would likely be inhibited, resulting in R-norfluoxetine formation being mediated by CYP2C9 and S-norfluoxetine formation being mediated by multiple high K(m) enzymes.	Fluoxetine	25-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	246-252
11356927-10	2001	Since the enantiomers of fluoxetine and norfluoxetine are inhibitors of CYP2D6, upon chronic dosing, the CYP2D6-mediated metabolism of the fluoxetine enantiomers would likely be inhibited, resulting in R-norfluoxetine formation being mediated by CYP2C9 and S-norfluoxetine formation being mediated by multiple high K(m) enzymes.	norfluoxetine	40-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	246-252
11356927-10	2001	Since the enantiomers of fluoxetine and norfluoxetine are inhibitors of CYP2D6, upon chronic dosing, the CYP2D6-mediated metabolism of the fluoxetine enantiomers would likely be inhibited, resulting in R-norfluoxetine formation being mediated by CYP2C9 and S-norfluoxetine formation being mediated by multiple high K(m) enzymes.	Fluoxetine	43-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	246-252
11434505-0	2001	The effect of genetic polymorphism of cytochrome P450 CYP2C9 on phenytoin dose requirement.	Phenytoin	64-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
11434505-1	2001	The cytochrome P450 enzyme CYP2C9 catalyses the metabolism of numerous therapeutic agents, including the anti-epileptic drug phenytoin.	Phenytoin	125-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
11434505-4	2001	Because this may be relevant in treatment with phenytoin, we studied the effect of CYP2C9 genotype on phenytoin dose requirement in a group of 60 epileptic patients on long-term phenytoin therapy.	Phenytoin	102-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
11434505-4	2001	Because this may be relevant in treatment with phenytoin, we studied the effect of CYP2C9 genotype on phenytoin dose requirement in a group of 60 epileptic patients on long-term phenytoin therapy.	Phenytoin	102-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
11434505-6	2001	For patients carrying at least one mutant CYP2C9 allele (n = 17), the mean phenytoin dose required to achieve a therapeutic serum concentration was about 37% lower than the mean dose required by wild-type individuals (199 mg/day versus 314 mg/day; P &lt; 0.01).	Phenytoin	75-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
11434505-8	2001	The results show that there is a strong association between CYP2C9 allelic variants and phenytoin dose requirement.	Phenytoin	88-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
11325819-3	2001	NSAIDs, particularly aspirin, are glucuronidated by UGT1A6 and some classes of NSAIDs are also metabolized by cytochrome P450 (CYP) 2C9.	Aspirin	21-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-135
11325819-8	2001	However, this association was absent in aspirin users who carried the CYP2C9 variant alleles (OR, 0.88; 95% CI, 0.51-1.53) or who were homozygous wild-type UGT1A6 (OR, 0.86; 95% CI, 0.50-1.50).	Aspirin	40-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
11309547-11	2001	This was probably caused by inhibition of the cytochrome P-450 2C9-mediated biotransformation of glimepiride by fluconazole.	glimepiride	97-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-66
11573629-7	2001	These results indicate that only CYP3A4, but not CYP2B6 or CYP2C, is involved in the metabolism of midazolam in vitro.	Midazolam	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-64
11309547-11	2001	This was probably caused by inhibition of the cytochrome P-450 2C9-mediated biotransformation of glimepiride by fluconazole.	Fluconazole	112-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-66
11372587-1	2001	OBJECTIVES: To determine the relative contribution of cytochromes P450 (CYP) 2C9 and 2C19 to the formation of 5-(-4-hydroxyphenyl)-5-phenylhydantion (HPPH) from phenytoin (PPH).	5-(-4-hydroxyphenyl)-5-phenylhydantion	110-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-89
11255075-2	2001	The mechanism of this drug-drug interaction has been attributed to inhibition of CYP2C9-catalyzed hydroxylation of phenytoin to its major oxidative metabolite in humans, para-hydroxyphenyl phenyl hydantoin (HPPH).	Phenytoin	115-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
11255075-2	2001	The mechanism of this drug-drug interaction has been attributed to inhibition of CYP2C9-catalyzed hydroxylation of phenytoin to its major oxidative metabolite in humans, para-hydroxyphenyl phenyl hydantoin (HPPH).	para-hydroxyphenyl phenyl hydantoin	170-205	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
11372587-1	2001	OBJECTIVES: To determine the relative contribution of cytochromes P450 (CYP) 2C9 and 2C19 to the formation of 5-(-4-hydroxyphenyl)-5-phenylhydantion (HPPH) from phenytoin (PPH).	2-(1-hexyloxyethyl)-2-devinyl pyropheophorbide-a	150-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-89
11255075-2	2001	The mechanism of this drug-drug interaction has been attributed to inhibition of CYP2C9-catalyzed hydroxylation of phenytoin to its major oxidative metabolite in humans, para-hydroxyphenyl phenyl hydantoin (HPPH).	2-(1-hexyloxyethyl)-2-devinyl pyropheophorbide-a	207-211	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
11372587-1	2001	OBJECTIVES: To determine the relative contribution of cytochromes P450 (CYP) 2C9 and 2C19 to the formation of 5-(-4-hydroxyphenyl)-5-phenylhydantion (HPPH) from phenytoin (PPH).	Phenytoin	161-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-89
11255075-9	2001	Diclofenac hydroxylation to 4"-OH diclofenac, a specific marker for CYP2C9 activity, was determined in HLM1-HLM6 and was highly correlated with HPPH formation in HLM1-HLM6, indicating that phenytoin hydroxylation in human liver microsomes is largely due to CYP2C9.	Diclofenac	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
11255075-9	2001	Diclofenac hydroxylation to 4"-OH diclofenac, a specific marker for CYP2C9 activity, was determined in HLM1-HLM6 and was highly correlated with HPPH formation in HLM1-HLM6, indicating that phenytoin hydroxylation in human liver microsomes is largely due to CYP2C9.	Diclofenac	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	257-263
11372587-4	2001	Coincubation with the CYP2C9 inhibitor, sulfaphenazole (SPA), at 5 mumol/l reduced reaction velocity to less than 15% of control values.	Sulfaphenazole	40-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
11372587-4	2001	Coincubation with the CYP2C9 inhibitor, sulfaphenazole (SPA), at 5 mumol/l reduced reaction velocity to less than 15% of control values.	Sulfaphenazole	56-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
11255075-9	2001	Diclofenac hydroxylation to 4"-OH diclofenac, a specific marker for CYP2C9 activity, was determined in HLM1-HLM6 and was highly correlated with HPPH formation in HLM1-HLM6, indicating that phenytoin hydroxylation in human liver microsomes is largely due to CYP2C9.	4"-oh diclofenac	28-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
11255075-9	2001	Diclofenac hydroxylation to 4"-OH diclofenac, a specific marker for CYP2C9 activity, was determined in HLM1-HLM6 and was highly correlated with HPPH formation in HLM1-HLM6, indicating that phenytoin hydroxylation in human liver microsomes is largely due to CYP2C9.	4"-oh diclofenac	28-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	257-263
11465405-12	2001	While 10O microM BFBFC was metabolized to HFC by cDNA-expressed CYP3A4, little or no metabolism was observed with cDNA-expressed CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 and CYP2E1.	2,5-bis(trifluoromethyl)-7-benzyloxy-4-trifluoromethylcoumarin	17-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
11255075-9	2001	Diclofenac hydroxylation to 4"-OH diclofenac, a specific marker for CYP2C9 activity, was determined in HLM1-HLM6 and was highly correlated with HPPH formation in HLM1-HLM6, indicating that phenytoin hydroxylation in human liver microsomes is largely due to CYP2C9.	Phenytoin	189-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
11255075-9	2001	Diclofenac hydroxylation to 4"-OH diclofenac, a specific marker for CYP2C9 activity, was determined in HLM1-HLM6 and was highly correlated with HPPH formation in HLM1-HLM6, indicating that phenytoin hydroxylation in human liver microsomes is largely due to CYP2C9.	Phenytoin	189-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	257-263
11255075-10	2001	This work presents direct evidence that the effect of fluoxetine on phenytoin blood levels may be explained by inhibition of CYP2C9-catalyzed phenytoin hydroxylation.	Fluoxetine	54-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
11255075-10	2001	This work presents direct evidence that the effect of fluoxetine on phenytoin blood levels may be explained by inhibition of CYP2C9-catalyzed phenytoin hydroxylation.	Phenytoin	68-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
11255075-10	2001	This work presents direct evidence that the effect of fluoxetine on phenytoin blood levels may be explained by inhibition of CYP2C9-catalyzed phenytoin hydroxylation.	Phenytoin	142-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
11304902-2	2001	Alosetron is extensively metabolized by multiple cytochrome P450 (CYP) enzymes, including CYP 2C9 and 3A4.	alosetron	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-97
11304903-2	2001	Alosetron is extensively metabolized by multiple cytochrome P450 (CYP) enzymes, including CYP2C9 and CYP3A4.	alosetron	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
11304903-4	2001	Fluoxetine metabolism involves CYP2D6 and CYP2C9 in the formation of its major metabolite, norfluoxetine.	Fluoxetine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
11304903-4	2001	Fluoxetine metabolism involves CYP2D6 and CYP2C9 in the formation of its major metabolite, norfluoxetine.	norfluoxetine	91-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
11465405-19	2001	While 80 microM 7BQ was metabolized to 7HQ by cDNA-expressed CYP3A4, only low rates of metabolism were observed with cDNA-expressed CYPIA2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 and CYP2E1.	7-benzyloxyquinoline	16-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	164-170
11181490-4	2001	Compounds known to activate the pregnane X receptor (PXR) such as rifampicin, or the constitutively activated receptor (CAR) such as phenobarbital, induced CYP2C8, CYP2C9, and to a lesser extent CYP2C19 mRNAs and proteins.	Rifampin	66-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	164-170
11337938-0	2001	In-vitro metabolism of celecoxib, a cyclooxygenase-2 inhibitor, by allelic variant forms of human liver microsomal cytochrome P450 2C9: correlation with CYP2C9 genotype and in-vivo pharmacokinetics.	Celecoxib	23-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-134
11337938-0	2001	In-vitro metabolism of celecoxib, a cyclooxygenase-2 inhibitor, by allelic variant forms of human liver microsomal cytochrome P450 2C9: correlation with CYP2C9 genotype and in-vivo pharmacokinetics.	Celecoxib	23-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
11337938-1	2001	In-vitro studies were conducted to assess the impact of CYP2C9 genotype on the metabolism (methyl hydroxylation) and pharmacokinetics of celecoxib, a novel cyclooxygenase-2 inhibitor and CYP2C9 substrate.	Celecoxib	137-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
11337938-2	2001	When compared to cDNA-expressed wild-type CYP2C9 (CYP2C9*1), the Vmax/Km ratio for celecoxib methyl hydroxylation was reduced by 34% and 90% in the presence of recombinant CYP2C9*2 and CYP2C9*3, respectively.	Celecoxib	83-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
11337938-2	2001	When compared to cDNA-expressed wild-type CYP2C9 (CYP2C9*1), the Vmax/Km ratio for celecoxib methyl hydroxylation was reduced by 34% and 90% in the presence of recombinant CYP2C9*2 and CYP2C9*3, respectively.	Celecoxib	83-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-58
11337938-2	2001	When compared to cDNA-expressed wild-type CYP2C9 (CYP2C9*1), the Vmax/Km ratio for celecoxib methyl hydroxylation was reduced by 34% and 90% in the presence of recombinant CYP2C9*2 and CYP2C9*3, respectively.	Celecoxib	83-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
11337938-2	2001	When compared to cDNA-expressed wild-type CYP2C9 (CYP2C9*1), the Vmax/Km ratio for celecoxib methyl hydroxylation was reduced by 34% and 90% in the presence of recombinant CYP2C9*2 and CYP2C9*3, respectively.	Celecoxib	83-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
11337938-6	2001	Based on simulations of the in-vitro data obtained with the recombinant CYP2C9 proteins, it was anticipated that the pharmacokinetics of celecoxib (as a much as a five-fold increase in plasma AUC) would be altered (versus CYP2C9*1/*1 subjects) in subjects genotyped heterozygous or homozygous for the CYP2C9*2 (Cys144) or CYP2C9*3 (Leu359) allele.	Celecoxib	137-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
11337938-6	2001	Based on simulations of the in-vitro data obtained with the recombinant CYP2C9 proteins, it was anticipated that the pharmacokinetics of celecoxib (as a much as a five-fold increase in plasma AUC) would be altered (versus CYP2C9*1/*1 subjects) in subjects genotyped heterozygous or homozygous for the CYP2C9*2 (Cys144) or CYP2C9*3 (Leu359) allele.	Celecoxib	137-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	222-228
11337938-6	2001	Based on simulations of the in-vitro data obtained with the recombinant CYP2C9 proteins, it was anticipated that the pharmacokinetics of celecoxib (as a much as a five-fold increase in plasma AUC) would be altered (versus CYP2C9*1/*1 subjects) in subjects genotyped heterozygous or homozygous for the CYP2C9*2 (Cys144) or CYP2C9*3 (Leu359) allele.	Celecoxib	137-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	222-228
11337938-6	2001	Based on simulations of the in-vitro data obtained with the recombinant CYP2C9 proteins, it was anticipated that the pharmacokinetics of celecoxib (as a much as a five-fold increase in plasma AUC) would be altered (versus CYP2C9*1/*1 subjects) in subjects genotyped heterozygous or homozygous for the CYP2C9*2 (Cys144) or CYP2C9*3 (Leu359) allele.	Celecoxib	137-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	222-228
11337938-7	2001	In a subsequent clinical study, the AUC of celecoxib was increased (versus CYP2C9*1/*1 subjects) approximately 2.2-fold (range, 1.6-3-fold) in two CYP2C9*1/*3 subjects and one CYP2C9*3/*3 subject receiving a single oral dose (200 mg) of the drug.	Celecoxib	43-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
11337938-7	2001	In a subsequent clinical study, the AUC of celecoxib was increased (versus CYP2C9*1/*1 subjects) approximately 2.2-fold (range, 1.6-3-fold) in two CYP2C9*1/*3 subjects and one CYP2C9*3/*3 subject receiving a single oral dose (200 mg) of the drug.	Celecoxib	43-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
11337938-7	2001	In a subsequent clinical study, the AUC of celecoxib was increased (versus CYP2C9*1/*1 subjects) approximately 2.2-fold (range, 1.6-3-fold) in two CYP2C9*1/*3 subjects and one CYP2C9*3/*3 subject receiving a single oral dose (200 mg) of the drug.	Celecoxib	43-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
11298070-11	2001	Sildenafil metabolism was inhibited by potent CYP3A4 inhibitors which are used clinically, but was found to be only a weak inhibitor of drug metabolizing enzymes itself, the strongest inhibition occurring against CYP2C9 (Ki = 80 microM).	Sildenafil Citrate	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	213-219
11298070-12	2001	CONCLUSIONS: Evidence is provided for CYP3A4 and to a lesser extent CYP2C9-mediated metabolism of sildenafil.	Sildenafil Citrate	98-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
11298070-13	2001	There is the possibility that elevated plasma concentrations of sildenafil could occur with coadministration of known inhibitors of CYP2C9 or CYP3A4.	Sildenafil Citrate	64-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
11181490-6	2001	The concentration dependence of CYP2C8 and CYP2C9 mRNAs in response to rifampicin and phenobarbital paralleled that of CYP3A4 and CYP2B6, the maximum accumulation being reached with 10 microM rifampicin and 100 microM phenobarbital.	Rifampin	71-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
11181490-6	2001	The concentration dependence of CYP2C8 and CYP2C9 mRNAs in response to rifampicin and phenobarbital paralleled that of CYP3A4 and CYP2B6, the maximum accumulation being reached with 10 microM rifampicin and 100 microM phenobarbital.	Phenobarbital	86-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
11181490-6	2001	The concentration dependence of CYP2C8 and CYP2C9 mRNAs in response to rifampicin and phenobarbital paralleled that of CYP3A4 and CYP2B6, the maximum accumulation being reached with 10 microM rifampicin and 100 microM phenobarbital.	Rifampin	192-202	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
11181490-6	2001	The concentration dependence of CYP2C8 and CYP2C9 mRNAs in response to rifampicin and phenobarbital paralleled that of CYP3A4 and CYP2B6, the maximum accumulation being reached with 10 microM rifampicin and 100 microM phenobarbital.	Phenobarbital	218-231	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
11181490-7	2001	In contrast, dexamethasone produced maximum induction of CYP2C8 and CYP2C9 mRNAs at 0.1 microM while in these conditions neither CYP3A4 nor CYP2B6 was significantly induced.	Dexamethasone	13-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
11181490-8	2001	Moreover, the concentration dependence of CYP2C8 and CYP2C9 mRNAs in response to dexamethasone paralleled that of tyrosine aminotransferase.	Dexamethasone	81-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
11181490-9	2001	Furthermore, dexamethasone, which has been recently shown to up-regulate PXR and CAR expression through the glucocorticoid receptor, potentiated CYP2C8 and CYP2C9 mRNA induction in response to rifampicin and phenobarbital.	Dexamethasone	13-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
11181490-9	2001	Furthermore, dexamethasone, which has been recently shown to up-regulate PXR and CAR expression through the glucocorticoid receptor, potentiated CYP2C8 and CYP2C9 mRNA induction in response to rifampicin and phenobarbital.	Rifampin	193-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
11181490-9	2001	Furthermore, dexamethasone, which has been recently shown to up-regulate PXR and CAR expression through the glucocorticoid receptor, potentiated CYP2C8 and CYP2C9 mRNA induction in response to rifampicin and phenobarbital.	Phenobarbital	208-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
11465391-11	2001	The specificity of inhibition by 8-phenyltheophylline was assessed by measuring its effect on debrisoquine 4-hydroxylase (CYP2D6), terfenadine hydroxylase (CYP3A4), chlorzoxazone 6-hydroxylase (CYP2E1) and tolbutamide 4-hydroxylase (CYP2C9) activities in human liver microsomal fraction.	8-phenyltheophylline	33-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	233-239
11181505-9	2001	The metabolic activities of CYP2C9 and CYP2C19 were confirmed by inhibition by sulfaphenazole for CYP2C9 and ticlopidine for CYP2C19.	Sulfaphenazole	79-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
11181505-9	2001	The metabolic activities of CYP2C9 and CYP2C19 were confirmed by inhibition by sulfaphenazole for CYP2C9 and ticlopidine for CYP2C19.	Sulfaphenazole	79-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
11181505-9	2001	The metabolic activities of CYP2C9 and CYP2C19 were confirmed by inhibition by sulfaphenazole for CYP2C9 and ticlopidine for CYP2C19.	Ticlopidine	109-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
11307788-5	2001	Gene typing of cytochrome P450 CYP2C9, a liver enzyme responsible for warfarin metabolism, showed that the patient was a carrier of both the mutant alleles (CYP2C9*2/*3) of this enzyme.	Warfarin	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
11307788-5	2001	Gene typing of cytochrome P450 CYP2C9, a liver enzyme responsible for warfarin metabolism, showed that the patient was a carrier of both the mutant alleles (CYP2C9*2/*3) of this enzyme.	Warfarin	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
11231472-0	2001	Mutations of the CYP2C9 gene and the response to warfarin.	Warfarin	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
11207028-0	2001	Inhibition of cytochrome P450 2C9 activity in vitro by 5-hydroxytryptamine and adrenaline.	Serotonin	55-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-33
11329260-0	2001	Identification of human CYP2C19 residues that confer S-mephenytoin 4"-hydroxylation activity to CYP2C9.	Mephenytoin	53-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
11234294-3	2001	METHOD: In 60 patients on long-term phenytoin therapy the concentration of phenytoin in serum was measured and CYP2C9 genotyping was performed (mutant alleles of CYP2C9 are associated with impaired phenytoin metabolism).	Phenytoin	36-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
11234294-3	2001	METHOD: In 60 patients on long-term phenytoin therapy the concentration of phenytoin in serum was measured and CYP2C9 genotyping was performed (mutant alleles of CYP2C9 are associated with impaired phenytoin metabolism).	Phenytoin	75-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
11234294-3	2001	METHOD: In 60 patients on long-term phenytoin therapy the concentration of phenytoin in serum was measured and CYP2C9 genotyping was performed (mutant alleles of CYP2C9 are associated with impaired phenytoin metabolism).	Phenytoin	75-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
11234294-5	2001	CYP2C9 genotype and comedication were connected to phenytoin daily dose requirement.	Phenytoin	51-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11741520-5	2001	RESULT: CYP1A2, CYP3A4, and CYP2C9 catalyze the estradiol 2-hydroxylation.	Estradiol	48-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
11741520-6	2001	CYP2C9, CYP2C19, and CYP2C8 have high activity in catalyzing 17beta-hydroxy dehydrogenation in cDNA expressed P450, but CYP1A2 is the most important enzyme in catalyzing estradiol 2-hydroxylation.	17beta	61-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11741520-6	2001	CYP2C9, CYP2C19, and CYP2C8 have high activity in catalyzing 17beta-hydroxy dehydrogenation in cDNA expressed P450, but CYP1A2 is the most important enzyme in catalyzing estradiol 2-hydroxylation.	Estradiol	170-179	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11159803-4	2001	DMSO was found to inhibit CYP2C9 and CYP2C19, CYP2E1, and CYP3A4 in a concentration-dependent manner.	Dimethyl Sulfoxide	0-4	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
11159803-5	2001	At 2% DMSO, the activities for the four isoforms were approximately 40% (CYP2C9), 23% (CYP2C19), and 11% (CYP2E1) of that observed for 0.1% acetonitrile and 45% (CYP3A4) of that observed for 1% acetonitrile.	Dimethyl Sulfoxide	6-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
11159803-5	2001	At 2% DMSO, the activities for the four isoforms were approximately 40% (CYP2C9), 23% (CYP2C19), and 11% (CYP2E1) of that observed for 0.1% acetonitrile and 45% (CYP3A4) of that observed for 1% acetonitrile.	acetonitrile	140-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
11159803-5	2001	At 2% DMSO, the activities for the four isoforms were approximately 40% (CYP2C9), 23% (CYP2C19), and 11% (CYP2E1) of that observed for 0.1% acetonitrile and 45% (CYP3A4) of that observed for 1% acetonitrile.	acetonitrile	194-206	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
11159803-7	2001	Methanol was found to inhibit CYP2C9 and CYP2E1 activities, but to a lesser extent than DMSO.	Methanol	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
11207028-1	2001	In the present study, the occurrence of a modulatory effect of 14 neurotransmitters, precursors and metabolites on the cytochrome P450 2C9 (CYP2C9) enzyme activity, as determined by diclofenac 4-hydroxylation, was studied in human liver microsomes.	Diclofenac	182-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
11213860-0	2001	Implications of cytochrome P450 2C9 polymorphism on warfarin metabolism and dosing.	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-35
11213860-3	2001	S-Warfarin, the more potent isomer, is metabolized primarily by CYP2C9.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
11213860-6	2001	Clinical studies showed an increased plasma level of S-warfarin, decreased clearance of S-warfarin, increased frequency of bleeding, and prolongation of hospitalization in patients with variant CYP2C9 alleles.	Warfarin	53-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	194-200
11213860-6	2001	Clinical studies showed an increased plasma level of S-warfarin, decreased clearance of S-warfarin, increased frequency of bleeding, and prolongation of hospitalization in patients with variant CYP2C9 alleles.	Sulfur	53-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	194-200
11213860-6	2001	Clinical studies showed an increased plasma level of S-warfarin, decreased clearance of S-warfarin, increased frequency of bleeding, and prolongation of hospitalization in patients with variant CYP2C9 alleles.	Warfarin	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	194-200
11206048-4	2001	The genotypes of CYP2C9 and 2C19, the enzymes responsible for phenytoin metabolism, were homozygous for the wild-type alleles (CYP2C9*1/*1 and 2C19*1/ *1).	Phenytoin	62-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
11206048-4	2001	The genotypes of CYP2C9 and 2C19, the enzymes responsible for phenytoin metabolism, were homozygous for the wild-type alleles (CYP2C9*1/*1 and 2C19*1/ *1).	Phenytoin	62-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-133
11206048-5	2001	The interaction may be a result of inhibition of both CYP2C9 and 2C19 by fluvoxamine.	Fluvoxamine	73-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
11207028-0	2001	Inhibition of cytochrome P450 2C9 activity in vitro by 5-hydroxytryptamine and adrenaline.	Epinephrine	79-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-33
11207028-1	2001	In the present study, the occurrence of a modulatory effect of 14 neurotransmitters, precursors and metabolites on the cytochrome P450 2C9 (CYP2C9) enzyme activity, as determined by diclofenac 4-hydroxylation, was studied in human liver microsomes.	Diclofenac	182-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-138
11139472-4	2001	The selective CYP 2C9 inhibitor sulfaphenazole and the superoxide anion (O(2-)) scavengers Tiron and nordihydroguaretic acid also induced a leftward shift in the NO-mediated concentration-relaxation curve to bradykinin.	Sulfaphenazole	32-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-21
11139472-4	2001	The selective CYP 2C9 inhibitor sulfaphenazole and the superoxide anion (O(2-)) scavengers Tiron and nordihydroguaretic acid also induced a leftward shift in the NO-mediated concentration-relaxation curve to bradykinin.	1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt	91-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-21
11139472-0	2001	Endothelium-derived hyperpolarizing factor synthase (Cytochrome P450 2C9) is a functionally significant source of reactive oxygen species in coronary arteries.	Reactive Oxygen Species	114-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-72
11139472-4	2001	The selective CYP 2C9 inhibitor sulfaphenazole and the superoxide anion (O(2-)) scavengers Tiron and nordihydroguaretic acid also induced a leftward shift in the NO-mediated concentration-relaxation curve to bradykinin.	Masoprocol	101-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-21
11139472-5	2001	CYP activity and O(2-) production, determined in microsomes prepared from cells overexpressing CYP 2C9, were almost completely inhibited by sulfaphenazole.	Superoxides	17-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-102
11139472-5	2001	CYP activity and O(2-) production, determined in microsomes prepared from cells overexpressing CYP 2C9, were almost completely inhibited by sulfaphenazole.	Sulfaphenazole	140-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-102
11139472-11	2001	These results suggest that a CYP isozyme homologous to CYP 2C9 is a physiologically relevant generator of ROS in coronary endothelial cells and modulates both vascular tone and homeostasis.	Reactive Oxygen Species	106-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-62
11730569-0	2001	Effects of CYP2C19 genotype and CYP2C9 on fluoxetine N-demethylation in human liver microsomes.	Fluoxetine	42-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
11475198-9	2001	Interactions associated with CYP2C9-interference may, however, be present for fluvastatin.	Fluvastatin	78-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
11730569-10	2001	CONCLUSION: Cytochrome P-450 CYP2C9 is likely to be a major CYP isoform catalyzing fluoxetine N-demethylation in human liver microsomes at a substrate concentration close to the therapeutic level, while polymorphic CYP2C19 may play a more important role in this metabolic pathway at high substrate concentration.	fluoxetine n	83-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
11180037-0	2001	Fluvoxamine inhibits the CYP2C9 catalyzed biotransformation of tolbutamide.	Fluvoxamine	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
11135730-8	2001	All of the CYPs evaluated were capable of hydroxylating propofol; however, CYP2B6 and CYP2C9 were most active.	Propofol	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
11135730-11	2001	CONCLUSIONS: Cytochrome P-450 2B6, and to a lesser extent CYP2C9, contribute to the oxidative metabolism of propofol.	Propofol	108-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
11180037-0	2001	Fluvoxamine inhibits the CYP2C9 catalyzed biotransformation of tolbutamide.	Tolbutamide	63-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
11180037-1	2001	OBJECTIVE: Our objective was to examine the interaction between fluvoxamine and tolbutamide to confirm that fluvoxamine inhibits CYP2C9.	Tolbutamide	80-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
11180037-1	2001	OBJECTIVE: Our objective was to examine the interaction between fluvoxamine and tolbutamide to confirm that fluvoxamine inhibits CYP2C9.	Fluvoxamine	108-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
11368292-5	2001	The 6-hydroxy and N-desisopropyl fluvastatin metabolites are exclusively generated by cytochrome P450 (CYP) 2C9 and do not accumulate in the blood.	6-hydroxy and n-desisopropyl fluvastatin	4-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-111
11180037-13	2001	CONCLUSION: Fluvoxamine is a moderate inhibitor of CYP2C9 in vivo.	Fluvoxamine	12-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
11735605-5	2001	On the other hand, rifampicin is a nonspecific inducer of CYP-mediated metabolism (especially of CYP2C9, CYP2C19 and CYP3A4) and may therefore cause therapeutic failure of other coadministered drugs by increasing their clearance.	Rifampin	19-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
11368292-6	2001	CYP2C9, CYP3A4, CYP2C8 and CYP2D6 form the 5-hydroxy fluvastatin metabolite.	5-hydroxy fluvastatin	43-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11368292-13	2001	In addition to being a CYP2C9 substrate, fluvastatin demonstrates inhibitory effects on this isoenzyme in vitro and in vivo.	Fluvastatin	41-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
11368292-14	2001	In human liver microsomes, fluvastatin significantly inhibits the hydroxylation of 2 CYP2C9 substrates, tolbutamide and diclofenac.	Fluvastatin	27-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
11368292-15	2001	The oral clearances of the CYP2C9 substrates diclofenac, tolbutamide, glibenclamide (glyburide) and losartan are reduced by 15 to 25% when coadministered with fluvastatin.	Diclofenac	45-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
11368292-15	2001	The oral clearances of the CYP2C9 substrates diclofenac, tolbutamide, glibenclamide (glyburide) and losartan are reduced by 15 to 25% when coadministered with fluvastatin.	Tolbutamide	57-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
11523725-12	2001	Human liver microsomes obtained from individuals heterozygous for CYP2C9*3 showed significantly reduced (S)-warfarin 7-hydroxylation as compared with those obtained from individuals genotyped as CYP2C9*1.	Warfarin	104-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
11523725-13	2001	The influence of the CYP2C9*3 allele on the in vivo pharmacokinetics of (S)-warfarin has been studied in Japanese patients.	Warfarin	72-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
11523725-14	2001	Patients with the homozygous CYP2C9*3 genotype, as well as those with the heterozygous CYP2C9*1/*3 genotype, had significantly reduced clearance of (S)-warfarin (by 90 and 60%, respectively) compared with those with homozygous CYP2C9*1.	Warfarin	148-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
11523725-14	2001	Patients with the homozygous CYP2C9*3 genotype, as well as those with the heterozygous CYP2C9*1/*3 genotype, had significantly reduced clearance of (S)-warfarin (by 90 and 60%, respectively) compared with those with homozygous CYP2C9*1.	Warfarin	148-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
11523725-14	2001	Patients with the homozygous CYP2C9*3 genotype, as well as those with the heterozygous CYP2C9*1/*3 genotype, had significantly reduced clearance of (S)-warfarin (by 90 and 60%, respectively) compared with those with homozygous CYP2C9*1.	Warfarin	148-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
11523725-15	2001	The maintenance dosages of warfarin required in Japanese patients with heterozygous and homozygous CYP2C9*3 mutations were significantly lower than those in patients with CYP2C9*1/*1.	Warfarin	27-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
11523725-16	2001	In addition, 86% of British patients exhibiting adequate therapeutic responses with lower maintenance dosages of warfarin (&lt;1.5 mg/day) had either the CYP2C9*2 or CYP2C9*3 mutation singly or in combination, whereas only 38% of randomly selected patients receiving warfarin carried the corresponding mutations.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
11368292-15	2001	The oral clearances of the CYP2C9 substrates diclofenac, tolbutamide, glibenclamide (glyburide) and losartan are reduced by 15 to 25% when coadministered with fluvastatin.	Glyburide	70-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
11368292-15	2001	The oral clearances of the CYP2C9 substrates diclofenac, tolbutamide, glibenclamide (glyburide) and losartan are reduced by 15 to 25% when coadministered with fluvastatin.	Glyburide	85-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
11368292-15	2001	The oral clearances of the CYP2C9 substrates diclofenac, tolbutamide, glibenclamide (glyburide) and losartan are reduced by 15 to 25% when coadministered with fluvastatin.	Losartan	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
11368292-15	2001	The oral clearances of the CYP2C9 substrates diclofenac, tolbutamide, glibenclamide (glyburide) and losartan are reduced by 15 to 25% when coadministered with fluvastatin.	Fluvastatin	159-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
11523725-18	2001	These data indicate that the CYP2C9*3 allele may be associated with retarded elimination of (S)-warfarin and the resulting clinical effects.	Warfarin	92-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
11523726-2	2001	Although irbesartan does not require biotransformation for its pharmacological activity, it does undergo metabolism via the cytochrome P450 (CYP) 2C9 isoenzyme and negligible metabolism by the CYP3A4 isoenzyme.	Irbesartan	9-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-149
11124226-5	2001	Niclosamide had substrate-dependent contrasting effects on CYP2C9 activity with an apparent activation (400%) of 7-methoxy-4-trifluoromethylcoumarin demethylase activity and potent inhibition (K(i) = 6.00 microM) of diclofenac 4-hydroxylase activity.	Niclosamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
11124228-0	2001	Interaction of delavirdine with human liver microsomal cytochrome P450: inhibition of CYP2C9, CYP2C19, and CYP2D6.	Delavirdine	15-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
11124228-3	2001	The interaction of delavirdine with CYP2C9 was examined with pooled human liver microsomes using diclofenac 4"-hydroxylation as a reporter of CYP2C9 catalytic activity.	Delavirdine	19-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
11124228-3	2001	The interaction of delavirdine with CYP2C9 was examined with pooled human liver microsomes using diclofenac 4"-hydroxylation as a reporter of CYP2C9 catalytic activity.	Delavirdine	19-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
11124228-8	2001	Several analogs of delavirdine showed similar inhibition of CYP2C9.	Delavirdine	19-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
11124228-12	2001	These results, along with previously reported experiments, indicate that delavirdine can partially inhibit CYP2C9, -2C19, -2D6, and -3A4, although the degree of inhibition in vivo would be subject to a variety of additional factors.	Delavirdine	73-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
11887965-3	2001	Differential response to phenytoin, for example, is related to interindividual genetic differences in the metabolic enzyme CYP2C9, and to a lesser extent, CYP2C19.	Phenytoin	25-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
11294368-0	2001	Is diclofenac a valuable CYP2C9 probe in humans?	diclofenac a	3-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
11294368-2	2001	The in vitro CYP2C9-specific substrate diclofenac might be a valuable, well-tolerated probe candidate.	Diclofenac	39-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
11294368-3	2001	In order to validate diclofenac as an in vivo CYP2C9 probe, we planned to show that urinary 4"-hydroxydiclofenac/diclofenac metabolic ratio (MR) would correlate to the apparent partial metabolic clearance of diclofenac into 4"-hydroxydiclofenac (Clmet).	Diclofenac	21-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
11294368-10	2001	However, since we found a lower metabolic clearance of diclofenac in heterozygous CYP2C9 subjects, as observed with other CYP2C9 substrates, diclofenac, in another galenic form, might be a potential probe to quantify CYP2C9 activity in humans.	Diclofenac	55-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
11294368-10	2001	However, since we found a lower metabolic clearance of diclofenac in heterozygous CYP2C9 subjects, as observed with other CYP2C9 substrates, diclofenac, in another galenic form, might be a potential probe to quantify CYP2C9 activity in humans.	Diclofenac	55-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
11294368-10	2001	However, since we found a lower metabolic clearance of diclofenac in heterozygous CYP2C9 subjects, as observed with other CYP2C9 substrates, diclofenac, in another galenic form, might be a potential probe to quantify CYP2C9 activity in humans.	Diclofenac	55-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
11294368-10	2001	However, since we found a lower metabolic clearance of diclofenac in heterozygous CYP2C9 subjects, as observed with other CYP2C9 substrates, diclofenac, in another galenic form, might be a potential probe to quantify CYP2C9 activity in humans.	Diclofenac	141-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
11908757-0	2001	The predictive value of MDR1, CYP2C9, and CYP2C19 polymorphisms for phenytoin plasma levels.	Phenytoin	68-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
11908757-8	2001	A combined analysis of variable alleles of CYP2C9, 2C19 and MDR1 revealed that the number of mutant CYP2C9 alleles is a major determinant, the number of MDR1*T alleles further contributes to the prediction of phenytoin plasma levels and CYP2C19*2 does not explain individual variability.	Phenytoin	209-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
11334262-2	2001	The inhibitory effects of cimetidine, nizatidine and omeprazole on the metabolic activity of CYP2C9, 2C19, 2D6 and 3A were investigated in human liver microsomes.	Cimetidine	26-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
11334262-2	2001	The inhibitory effects of cimetidine, nizatidine and omeprazole on the metabolic activity of CYP2C9, 2C19, 2D6 and 3A were investigated in human liver microsomes.	Nizatidine	38-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
12579866-7	2001	CONCLUSION: There were significant individual differences in the pharmacokinetics of meloxicam in Chinese volunteers, which may be due to the genetic polymorphism of CYP2C9.	Meloxicam	85-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	166-172
11908757-8	2001	A combined analysis of variable alleles of CYP2C9, 2C19 and MDR1 revealed that the number of mutant CYP2C9 alleles is a major determinant, the number of MDR1*T alleles further contributes to the prediction of phenytoin plasma levels and CYP2C19*2 does not explain individual variability.	Phenytoin	209-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
11334262-2	2001	The inhibitory effects of cimetidine, nizatidine and omeprazole on the metabolic activity of CYP2C9, 2C19, 2D6 and 3A were investigated in human liver microsomes.	Omeprazole	53-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
11908757-9	2001	The regression equation that fitted the data best included the number of mutant CYP2C9 and MDR*T alleles as predictory variables and explained 15.4% of the variability of phenytoin data (r2 = 0.154, P = 0.0002).	Phenytoin	171-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
11908757-10	2001	Furthermore, analysis of CYP2C9 and MDR1 genotypes in 35 phenytoin-treated patients recruited from therapeutic drug monitoring showed that combined CYP2C9 and MDR1 analysis has some predictive value not only in the controlled settings of a clinical trial, but also in the daily clinical practice.	Phenytoin	57-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
11908757-10	2001	Furthermore, analysis of CYP2C9 and MDR1 genotypes in 35 phenytoin-treated patients recruited from therapeutic drug monitoring showed that combined CYP2C9 and MDR1 analysis has some predictive value not only in the controlled settings of a clinical trial, but also in the daily clinical practice.	Phenytoin	57-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
11908770-0	2001	CYP2C9*3 influences the metabolism and the drug-interaction of candesartan in vitro.	candesartan	63-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11908770-1	2001	Candesartan cilexetil is an angiotensin II receptor antagonist, and candesartan, its active metabolite, is metabolized by CYP2C9.	candesartan	68-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
11908770-3	2001	We characterized the kinetics of candesartan by CYP2C9*1/*1 and CYP2C9*1/*3 in human liver microsomes.	candesartan	33-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
11908770-3	2001	We characterized the kinetics of candesartan by CYP2C9*1/*1 and CYP2C9*1/*3 in human liver microsomes.	candesartan	33-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
11908770-5	2001	Subsequently, CYP2C9*1 and CYP2C9*3 (Leu359) were expressed in yeast, and the kinetics of candesartan were determined.	candesartan	90-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
11908770-5	2001	Subsequently, CYP2C9*1 and CYP2C9*3 (Leu359) were expressed in yeast, and the kinetics of candesartan were determined.	candesartan	90-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
11136298-7	2000	CONCLUSIONS: The effects of rifampicin on the pharmacokinetics of glimepiride suggest that rifampicin induced the CYP2C9-mediated metabolism of glimepiride and thereby slightly increased its systemic clearance.	Rifampin	28-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
11136298-7	2000	CONCLUSIONS: The effects of rifampicin on the pharmacokinetics of glimepiride suggest that rifampicin induced the CYP2C9-mediated metabolism of glimepiride and thereby slightly increased its systemic clearance.	glimepiride	66-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
11136298-7	2000	CONCLUSIONS: The effects of rifampicin on the pharmacokinetics of glimepiride suggest that rifampicin induced the CYP2C9-mediated metabolism of glimepiride and thereby slightly increased its systemic clearance.	Rifampin	91-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
11136298-7	2000	CONCLUSIONS: The effects of rifampicin on the pharmacokinetics of glimepiride suggest that rifampicin induced the CYP2C9-mediated metabolism of glimepiride and thereby slightly increased its systemic clearance.	glimepiride	144-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
11095582-6	2000	The involvement of CYP1A2 in DMXAA metabolism by human livers was demonstrated by the following: 1) the potent inhibition of DMXAA metabolism by furafylline (k(inact) = 0.23 +/- 0.04 min(-1), K"(app) = 15.6 +/- 6.7 microM) and alpha-naphthoflavone (K(i) = 0.036 microM), but not by cimetidine, ketoconazole, tolbutamide, quinidine, chlorzoxazone, diethyldithiocarbamate, troleandomycin, and sulfaphenazole; 2) when incubated with human lymphoblastoid cell microsomes containing cDNA-expressed CYP isoenzymes, DMXAA was metabolized only by CYP1A2, with an apparent K(m) of 6.2 +/- 1.5 microM and V(max) of 0.014 +/- 0.001 nmol/min/mg, but not by CYP2A6, CYP2B6, CYP2C9 (Arg(144)), CYP2C19, CYP2D6 (Val(374)), CYP2E1, and CYP3A4; 3) a significant correlation (r = 0.90; P &lt;.001) between 6-methylhydroxylation of DMXAA and 7-ethoxyresorufin O-deethylation; and 4) a significant correlation (r = 0.75; P &lt;.01) between the CYP1A protein level determined by Western blots and DMXAA 6-methylhydroxylation.	furafylline	145-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	661-667
11095582-6	2000	The involvement of CYP1A2 in DMXAA metabolism by human livers was demonstrated by the following: 1) the potent inhibition of DMXAA metabolism by furafylline (k(inact) = 0.23 +/- 0.04 min(-1), K"(app) = 15.6 +/- 6.7 microM) and alpha-naphthoflavone (K(i) = 0.036 microM), but not by cimetidine, ketoconazole, tolbutamide, quinidine, chlorzoxazone, diethyldithiocarbamate, troleandomycin, and sulfaphenazole; 2) when incubated with human lymphoblastoid cell microsomes containing cDNA-expressed CYP isoenzymes, DMXAA was metabolized only by CYP1A2, with an apparent K(m) of 6.2 +/- 1.5 microM and V(max) of 0.014 +/- 0.001 nmol/min/mg, but not by CYP2A6, CYP2B6, CYP2C9 (Arg(144)), CYP2C19, CYP2D6 (Val(374)), CYP2E1, and CYP3A4; 3) a significant correlation (r = 0.90; P &lt;.001) between 6-methylhydroxylation of DMXAA and 7-ethoxyresorufin O-deethylation; and 4) a significant correlation (r = 0.75; P &lt;.01) between the CYP1A protein level determined by Western blots and DMXAA 6-methylhydroxylation.	vadimezan	29-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	661-667
11129071-8	2000	This method provides a sensitive and specific assay for the detection of flurbiprofen and 4"-hydoxyflurbiprofen in urine and plasma and is suitable for use in in vivo studies evaluating the regulation of CYP2C9 activity.	Flurbiprofen	73-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	204-210
11038165-0	2000	Formation of a dihydroxy metabolite of phenytoin in human liver microsomes/cytosol: roles of cytochromes P450 2C9, 2C19, and 3A4.	Phenytoin	39-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-119
11038154-4	2000	Of various cDNA-expressed human CYPs, only CYP2C9 hydroxylated (S)-acenocoumarol.	Acenocoumarol	63-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
11038165-7	2000	Of 10 cDNA-expressed human P450 enzymes examined, CYP2C19, CYP2C9, and CYP3A4 catalyzed 3",4"-diHPPH formation from the primary hydroxylated metabolites (3"-hydroxy-DPH and 4"-HPPH).	3",4"-dihpph	88-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
11038154-6	2000	CYP2C9 also mediated the 6-, 7-, and 8-hydroxylations of (R)-acenocoumarol with K(m) values three to four times and V(max) values one-sixth times those of (S)-acenocoumarol.	(R)-Acenocoumarol	57-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11038161-7	2000	Tolbutamide was metabolized by CYP2C9 (70%) and CYP2C19 (30%), diazepam by CYP2C19 (100%), ibuprofen by CYP2C9 (90%) and CYP2C19 (10%), and omeprazole by CYP2C19 (68%) and CYP3A4 (32%).	Tolbutamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
11038161-7	2000	Tolbutamide was metabolized by CYP2C9 (70%) and CYP2C19 (30%), diazepam by CYP2C19 (100%), ibuprofen by CYP2C9 (90%) and CYP2C19 (10%), and omeprazole by CYP2C19 (68%) and CYP3A4 (32%).	Tolbutamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
11038154-6	2000	CYP2C9 also mediated the 6-, 7-, and 8-hydroxylations of (R)-acenocoumarol with K(m) values three to four times and V(max) values one-sixth times those of (S)-acenocoumarol.	Acenocoumarol	155-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11038165-7	2000	Of 10 cDNA-expressed human P450 enzymes examined, CYP2C19, CYP2C9, and CYP3A4 catalyzed 3",4"-diHPPH formation from the primary hydroxylated metabolites (3"-hydroxy-DPH and 4"-HPPH).	3"-hydroxy-dph	154-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
11038154-14	2000	The results demonstrate that (S)-acenocoumarol is hydroxylated by a single enzyme, namely CYP2C9.	Acenocoumarol	29-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
11038154-15	2000	CYP2C9 is also the main enzyme in the 7-hydroxylation of (R)-acenocoumarol.	(R)-Acenocoumarol	57-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
11038161-7	2000	Tolbutamide was metabolized by CYP2C9 (70%) and CYP2C19 (30%), diazepam by CYP2C19 (100%), ibuprofen by CYP2C9 (90%) and CYP2C19 (10%), and omeprazole by CYP2C19 (68%) and CYP3A4 (32%).	Ibuprofen	91-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
11038165-7	2000	Of 10 cDNA-expressed human P450 enzymes examined, CYP2C19, CYP2C9, and CYP3A4 catalyzed 3",4"-diHPPH formation from the primary hydroxylated metabolites (3"-hydroxy-DPH and 4"-HPPH).	hydroxyphenytoin	173-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
11038165-9	2000	These results suggest that CYP2C9, CYP2C19, and CYP3A4 all have catalytic activities in 3",4"-diHPPH formation from primary hydroxylated metabolites in human liver and that the hepatic contents of these three P450 forms determine which P450 enzymes play major roles of DPH oxidation in individual humans.	3",4"-dihpph	88-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
11038165-9	2000	These results suggest that CYP2C9, CYP2C19, and CYP3A4 all have catalytic activities in 3",4"-diHPPH formation from primary hydroxylated metabolites in human liver and that the hepatic contents of these three P450 forms determine which P450 enzymes play major roles of DPH oxidation in individual humans.	Phenytoin	269-272	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
11186138-0	2000	The possession of the CYP2C9*3 allele is associated with low dose requirement of acenocoumarol.	Acenocoumarol	81-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
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
11127854-1	2000	Cytochrome P450 CYP2C9 gene variants have been associated with hyperresponsiveness to small doses of warfarin and a higher bleeding complication rate.	Warfarin	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
11127854-4	2000	The adjusted dose required of warfarin was higher among patients with the CYP2C9*1 haplotype (5.6 mg) than those of patients carrying the CYP2C9*2 (4.7 mg; p = 0.007, Scheffe"s test) or the CYP2C9*3 haplotype (4.0 mg; p &lt;0.001, Scheffe"s test).	Warfarin	30-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
11127854-4	2000	The adjusted dose required of warfarin was higher among patients with the CYP2C9*1 haplotype (5.6 mg) than those of patients carrying the CYP2C9*2 (4.7 mg; p = 0.007, Scheffe"s test) or the CYP2C9*3 haplotype (4.0 mg; p &lt;0.001, Scheffe"s test).	Warfarin	30-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
11127854-4	2000	The adjusted dose required of warfarin was higher among patients with the CYP2C9*1 haplotype (5.6 mg) than those of patients carrying the CYP2C9*2 (4.7 mg; p = 0.007, Scheffe"s test) or the CYP2C9*3 haplotype (4.0 mg; p &lt;0.001, Scheffe"s test).	Warfarin	30-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
11127854-8	2000	CYP2C9 gene variants modulate the anticoagulant effect of the dose of warfarin prescribed.	Warfarin	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10991840-5	2000	Cytotoxicity was studied by exposing the cells to 0.01 to 4 mM CPA in the presence or absence of sulfaphenazole, a CYP2C9-specific inhibitor.	Sulfaphenazole	97-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
10991840-7	2000	H2C9 cells quickly metabolized diclofenac, indicating the presence of high levels of CYP2C9.	Diclofenac	31-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
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
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
10991840-3	2000	The catalytic activity present in cell lines was examined by measuring the conversion of diclofenac, a CYP2C9-specific substrate, to its 4"-hydroxy metabolite by high-pressure liquid chromatography.	Diclofenac	89-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
11317178-3	2000	The clinical significance of this event as well as a possible interaction between clopidogrel and other drugs metabolized by the cytochrome P450 2C9 pathways coadministered to this patient are discussed.	Clopidogrel	82-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-148
10997938-6	2000	Scaling the intrinsic clearance values for the individual CYP enzymes to estimate contributions of each in human liver microsomes suggested that CYP2D6, CYP2C9, and CYP3A4 contribute the greatest amount of fluoxetine N-demethylation in human liver microsomes.	Fluoxetine	206-216	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
10997938-7	2000	These data were corroborated with the examination of the effects of CYP-specific inhibitors quinidine (CYP2D6), sulfaphenazole (CYP2C9), and ketoconazole (CYP3A4) on fluoxetine N-demethylation in pooled human liver microsomes.	Sulfaphenazole	112-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
10997938-7	2000	These data were corroborated with the examination of the effects of CYP-specific inhibitors quinidine (CYP2D6), sulfaphenazole (CYP2C9), and ketoconazole (CYP3A4) on fluoxetine N-demethylation in pooled human liver microsomes.	Fluoxetine	166-176	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
11315104-10	2000	Using human beta-lymphoblastoid cell microsomes containing cDNA-expressed CYP isoforms, 20 microM BFC was metabolized by CYP1A2 and CYP3A4, with lower rates of metabolism being observed with CYP2C9 and CYP2C19.	7-benzyloxy-4-trifluoromethylcoumarin	98-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
11315104-19	2000	BFC metabolism appears to be primarily catalysed by CYP1A2 and CYP3A4, with possibly some contribution by CYP2C9, CYP2C19 and perhaps other CYP isoforms.	7-benzyloxy-4-trifluoromethylcoumarin	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
10961881-0	2000	Influence of cytochrome P-450 CYP2C9 polymorphisms on warfarin sensitivity and risk of over-anticoagulation in patients on long-term treatment.	Warfarin	54-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
10961881-1	2000	Cytochrome P-450 2C9 is the principle enzyme that terminates the anticoagulant effect of warfarin.	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-20
10961881-11	2000	This study confirmed an association between CYP2C9 genotype and warfarin sensitivity.	Warfarin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
10960410-10	2000	CYP2C9 showed a significantly rapid metabolism of R(+)-enantiomer, suggesting that CYP2C9 is mainly involved in the enantioselective metabolism of thiamylal.	Thiamylal	147-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10960410-10	2000	CYP2C9 showed a significantly rapid metabolism of R(+)-enantiomer, suggesting that CYP2C9 is mainly involved in the enantioselective metabolism of thiamylal.	Thiamylal	147-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
10955816-9	2000	Although sulfaphenazole (an inhibitor of CYP2C9) and S-mephenytoin (an inhibitor of CYP2C19) partially inhibited the disappearance of MPA, no effect of the anti-CYP2C antibody was observed.	Sulfaphenazole	9-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
11026737-4	2000	At 10 microM PER, a concentration consistent with anticipated in vivo liver concentrations, CYP3A4 and CYP2C9 contributed 50% and 35%, respectively, to PER-N-demethylation.	Nitrogen	156-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
11026737-14	2000	CONCLUSIONS: Alterations in the activity of CYP3A4, CYP2C9 and FMO3 through genetic polymorphisms, enzyme induction or inhibition bear the potential to cause clinically significant changes in perazine clearance.	Perazine	192-200	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
10924340-4	2000	In parallel, IL-6 decreases both rifampicin- and phenobarbital-mediated induction of CYP2B6, CYP2C8, CYP2C9, and CYP3A4.	Rifampin	33-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
10924340-4	2000	In parallel, IL-6 decreases both rifampicin- and phenobarbital-mediated induction of CYP2B6, CYP2C8, CYP2C9, and CYP3A4.	Phenobarbital	49-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
10930961-15	2000	The more pronounced effect of ritonavir may be attributed to its additional potent inhibition of CYP2C9.	Ritonavir	30-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
11029845-8	2000	Lovastatin, simvastatin, and atorvastatin are substrates of CYP3A4, whereas fluvastatin is metabolized by CYP2C9.	Fluvastatin	76-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
11029845-10	2000	Compared with other statins, pravastatin thus has a reduced potential for drug interactions with other substrates, inhibitors, or inducers of the CYP3A4 and CYP2C9 systems.	Pravastatin	29-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
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 9	Homo sapiens	48-54
10976551-3	2000	We studied the possible correlation of the formation clearance of 3-hydroxyquinidine with probe-based assays for CYP1A2, CYP2C9, CYP2C19, and CYP2D6.	3-hydroxyquinidine	66-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
10901692-2	2000	Sulfaphenazole (2.16 microM) and tolbutamide (500 microM), selective inhibitors of CYP2C9 (or 2C8/9), inhibited DDS-NHY by 48 +/- 14 and 41 +/- 15%, respectively.	Sulfaphenazole	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
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 9	Homo sapiens	48-54
10901692-2	2000	Sulfaphenazole (2.16 microM) and tolbutamide (500 microM), selective inhibitors of CYP2C9 (or 2C8/9), inhibited DDS-NHY by 48 +/- 14 and 41 +/- 15%, respectively.	Tolbutamide	33-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
10901707-6	2000	Although the CYP2C9 inhibitor sulfaphenazole (100 microM) inhibited MEGX formation by about 30%, recombinant human CYP2C9 showed very low catalytic activity, suggesting a negligible role for this enzyme in lidocaine N-deethylation.	Sulfaphenazole	30-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
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 9	Homo sapiens	147-153
10901712-3	2000	The Catalyst models generated from multiple conformers of competitive inhibitors of CYP2C9 activities contained at least one hydrophobic and two hydrogen bond acceptor/donor regions.	Hydrogen	145-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
10901692-2	2000	Sulfaphenazole (2.16 microM) and tolbutamide (500 microM), selective inhibitors of CYP2C9 (or 2C8/9), inhibited DDS-NHY by 48 +/- 14 and 41 +/- 15%, respectively.	dds-nhy	112-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
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 9	Homo sapiens	70-76
10948089-4	2000	The CYP inducer beta-naphthoflavone and the Ca(2+) antagonist nifedipine significantly increased CYP2C mRNA but did not change the expression of CYP2J or CYP2B.	beta-Naphthoflavone	16-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-102
10948089-4	2000	The CYP inducer beta-naphthoflavone and the Ca(2+) antagonist nifedipine significantly increased CYP2C mRNA but did not change the expression of CYP2J or CYP2B.	Nifedipine	62-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-102
10948089-5	2000	To determine the relationship between CYP2C expression and EDHF production in native endothelial cells, we incubated porcine coronary arteries with nifedipine.	edhf	59-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-43
10948089-6	2000	Nifedipine enhanced endothelial CYP2C protein expression, as well as the generation of 11,12-epoxyeicosatrienoic acid.	Nifedipine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-37
10948089-8	2000	The specific CYP2C9 inhibitor sulfaphenazole, on the other hand, significantly attenuated EDHF-mediated hyperpolarization and relaxation.	Sulfaphenazole	30-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
10948089-8	2000	The specific CYP2C9 inhibitor sulfaphenazole, on the other hand, significantly attenuated EDHF-mediated hyperpolarization and relaxation.	edhf	90-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
10871299-7	2000	The flavonoid compound I3,II8-biapigenin was shown to be a potent, competitive inhibitor of CYP3A4, CYP2C9, and CYP1A2 activities with K(i) values of 0.038, 0.32, and 0.95 microM, respectively.	Flavonoids	4-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
10975605-0	2000	Relationship of polymorphism in CYP2C9 to genetic susceptibility to diclofenac-induced hepatitis.	Diclofenac	68-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
10975605-2	2000	Adduct formation may be due to metabolism of diclofenac via an alternative pathway rather than via its major 4"-hydroxylation pathway mediated by the cytochrome P450 CYP2C9.	Diclofenac	45-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	166-172
10975605-3	2000	We hypothesized that possession of variant CYP2C9 alleles might be a risk factor for diclofenac-induced hepatotoxicity, since the allelic variants CYP2C9*2 and CYP2C9*3 may be associated with impaired metabolism compared to the wild-type (CYP2C9*1).	Diclofenac	85-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
10975605-3	2000	We hypothesized that possession of variant CYP2C9 alleles might be a risk factor for diclofenac-induced hepatotoxicity, since the allelic variants CYP2C9*2 and CYP2C9*3 may be associated with impaired metabolism compared to the wild-type (CYP2C9*1).	Diclofenac	85-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
10975605-3	2000	We hypothesized that possession of variant CYP2C9 alleles might be a risk factor for diclofenac-induced hepatotoxicity, since the allelic variants CYP2C9*2 and CYP2C9*3 may be associated with impaired metabolism compared to the wild-type (CYP2C9*1).	Diclofenac	85-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
10975605-3	2000	We hypothesized that possession of variant CYP2C9 alleles might be a risk factor for diclofenac-induced hepatotoxicity, since the allelic variants CYP2C9*2 and CYP2C9*3 may be associated with impaired metabolism compared to the wild-type (CYP2C9*1).	Diclofenac	85-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
10975605-7	2000	The relationship between CYP2C9 genotype and susceptibility to diclofenac-induced hepatotoxicity was further examined by genotyping 24 patients with diclofenac-induced hepatotoxicity together with 100 healthy controls for the CYP2C9*2 and CYP2C9*3 alleles.	Diclofenac	63-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
10923005-8	2000	Compared to a wild-type genotype, the presence of the CYP2C9*2, CYP2C9*3, or CYP2A6*2 allele was associated with a significant reduction in weekly warfarin dose (mean weekly warfarin dose [+/- SE] for wild-type genotype was 0.397 +/- 0.024 mg/kg/wk vs 0.307 +/- 0.03 mg/kg/wk for carriers of CYP2C9*2, CYP2C9*3, or CYP2A6*2 polymorphism; P =.03).	Warfarin	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
10923005-8	2000	Compared to a wild-type genotype, the presence of the CYP2C9*2, CYP2C9*3, or CYP2A6*2 allele was associated with a significant reduction in weekly warfarin dose (mean weekly warfarin dose [+/- SE] for wild-type genotype was 0.397 +/- 0.024 mg/kg/wk vs 0.307 +/- 0.03 mg/kg/wk for carriers of CYP2C9*2, CYP2C9*3, or CYP2A6*2 polymorphism; P =.03).	Warfarin	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
10923005-8	2000	Compared to a wild-type genotype, the presence of the CYP2C9*2, CYP2C9*3, or CYP2A6*2 allele was associated with a significant reduction in weekly warfarin dose (mean weekly warfarin dose [+/- SE] for wild-type genotype was 0.397 +/- 0.024 mg/kg/wk vs 0.307 +/- 0.03 mg/kg/wk for carriers of CYP2C9*2, CYP2C9*3, or CYP2A6*2 polymorphism; P =.03).	Warfarin	174-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
10923005-8	2000	Compared to a wild-type genotype, the presence of the CYP2C9*2, CYP2C9*3, or CYP2A6*2 allele was associated with a significant reduction in weekly warfarin dose (mean weekly warfarin dose [+/- SE] for wild-type genotype was 0.397 +/- 0.024 mg/kg/wk vs 0.307 +/- 0.03 mg/kg/wk for carriers of CYP2C9*2, CYP2C9*3, or CYP2A6*2 polymorphism; P =.03).	Warfarin	174-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
10923005-8	2000	Compared to a wild-type genotype, the presence of the CYP2C9*2, CYP2C9*3, or CYP2A6*2 allele was associated with a significant reduction in weekly warfarin dose (mean weekly warfarin dose [+/- SE] for wild-type genotype was 0.397 +/- 0.024 mg/kg/wk vs 0.307 +/- 0.03 mg/kg/wk for carriers of CYP2C9*2, CYP2C9*3, or CYP2A6*2 polymorphism; P =.03).	Warfarin	174-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
10923005-8	2000	Compared to a wild-type genotype, the presence of the CYP2C9*2, CYP2C9*3, or CYP2A6*2 allele was associated with a significant reduction in weekly warfarin dose (mean weekly warfarin dose [+/- SE] for wild-type genotype was 0.397 +/- 0.024 mg/kg/wk vs 0.307 +/- 0.03 mg/kg/wk for carriers of CYP2C9*2, CYP2C9*3, or CYP2A6*2 polymorphism; P =.03).	Warfarin	174-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
10923005-8	2000	Compared to a wild-type genotype, the presence of the CYP2C9*2, CYP2C9*3, or CYP2A6*2 allele was associated with a significant reduction in weekly warfarin dose (mean weekly warfarin dose [+/- SE] for wild-type genotype was 0.397 +/- 0.024 mg/kg/wk vs 0.307 +/- 0.03 mg/kg/wk for carriers of CYP2C9*2, CYP2C9*3, or CYP2A6*2 polymorphism; P =.03).	Warfarin	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
10923005-8	2000	Compared to a wild-type genotype, the presence of the CYP2C9*2, CYP2C9*3, or CYP2A6*2 allele was associated with a significant reduction in weekly warfarin dose (mean weekly warfarin dose [+/- SE] for wild-type genotype was 0.397 +/- 0.024 mg/kg/wk vs 0.307 +/- 0.03 mg/kg/wk for carriers of CYP2C9*2, CYP2C9*3, or CYP2A6*2 polymorphism; P =.03).	Warfarin	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
10871299-7	2000	The flavonoid compound I3,II8-biapigenin was shown to be a potent, competitive inhibitor of CYP3A4, CYP2C9, and CYP1A2 activities with K(i) values of 0.038, 0.32, and 0.95 microM, respectively.	ii8-biapigenin	26-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
10871299-8	2000	Hyperforin was a potent noncompetitive inhibitor of CYP2D6 activity (K(i) = 1.5 microM) and competitive inhibitor of CYP2C9 and CYP3A4 activities (K(i) = 1.8 and 0.48 microM, respectively).	hyperforin	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
10820139-9	2000	At high concentrations of modafinil (&gt;/=100 microM), the mean activity of CYP2C9 was decreased (up to 60%) relative to that in the solvent controls.	Modafinil	26-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
10820139-10	2000	Overall, modafinil was shown to have effects on human hepatic CYP1A2, CYP2B6, CYP2C9, CYP2C19, and CYP3A4/5 activities in vitro.	Modafinil	9-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
10895987-8	2000	Clear inhibition was found for denitronifedipine oxidation (CYP3A4; IC50=29 microM and 46 microM) and S(-)-warfarin 7-hydroxylation (CYP2C9; IC50=43 microM and 45 microM).	Warfarin	103-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
10952477-8	2000	The mechanism of the increased plasma concentrations and prolonged elimination of fluvastatin is probably inhibition of the CYP2C9-mediated metabolism of fluvastatin by fluconazole.	Fluvastatin	82-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
10952477-8	2000	The mechanism of the increased plasma concentrations and prolonged elimination of fluvastatin is probably inhibition of the CYP2C9-mediated metabolism of fluvastatin by fluconazole.	Fluvastatin	154-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
10952477-8	2000	The mechanism of the increased plasma concentrations and prolonged elimination of fluvastatin is probably inhibition of the CYP2C9-mediated metabolism of fluvastatin by fluconazole.	Fluconazole	169-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
10952477-9	2000	Care should be taken if fluconazole or other potent inhibitors of CYP2C9 are prescribed to patients using fluvastatin.	Fluconazole	24-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
10952477-9	2000	Care should be taken if fluconazole or other potent inhibitors of CYP2C9 are prescribed to patients using fluvastatin.	Fluvastatin	106-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
10895987-11	2000	With therapeutic silibinin peak plasma concentrations of 0.6 microM and biliary concentrations up to 200 microM, metabolic interactions with xenobiotics metabolised by CYP3A4 or CYP2C9 cannot be excluded.	Silybin	17-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	178-184
10850388-0	2000	Catalytic activity of three variants (Ile, Leu, and Thr) at amino acid residue 359 in human CYP2C9 gene and simultaneous detection using single-strand conformation polymorphism analysis.	Threonine	52-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
10850388-1	2000	This study evaluated the catalytic activity of three variants (Ile, Leu, and Thr) at codon 359 of CYP2C9 enzymes expressed in a yeast cDNA expression system, and then established single-strand conformation polymorphism (PCR-SSCP) analysis for simultaneous detection as a screening method.	Isoleucine	63-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
10850388-0	2000	Catalytic activity of three variants (Ile, Leu, and Thr) at amino acid residue 359 in human CYP2C9 gene and simultaneous detection using single-strand conformation polymorphism analysis.	Isoleucine	38-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
10850388-1	2000	This study evaluated the catalytic activity of three variants (Ile, Leu, and Thr) at codon 359 of CYP2C9 enzymes expressed in a yeast cDNA expression system, and then established single-strand conformation polymorphism (PCR-SSCP) analysis for simultaneous detection as a screening method.	Leucine	68-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
10850388-0	2000	Catalytic activity of three variants (Ile, Leu, and Thr) at amino acid residue 359 in human CYP2C9 gene and simultaneous detection using single-strand conformation polymorphism analysis.	Leucine	43-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
10850388-1	2000	This study evaluated the catalytic activity of three variants (Ile, Leu, and Thr) at codon 359 of CYP2C9 enzymes expressed in a yeast cDNA expression system, and then established single-strand conformation polymorphism (PCR-SSCP) analysis for simultaneous detection as a screening method.	Threonine	77-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
10877007-5	2000	Losartan and irbesartan inhibited the CYP2C9-associated tolbutamide methylhydroxylation more potently (Ki values 4.1 microM and 24.5 microM), than valsartan, candesartan or eprosartan (Ki values 135 microM, 155 microM and &gt; 1000 microM, respectively).	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
10772636-0	2000	Substrate-dependent effect of acetonitrile on human liver microsomal cytochrome P450 2C9 (CYP2C9) activity.	acetonitrile	30-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-88
10772636-0	2000	Substrate-dependent effect of acetonitrile on human liver microsomal cytochrome P450 2C9 (CYP2C9) activity.	acetonitrile	30-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
10772636-6	2000	The presence of acetonitrile (3%, v/v) gave rise to a lower K(m) and a higher V(max) for diclofenac hydroxylase in both liver microsomes and recombinant CYP2C9 preparations (87 and 52% increase in V(max)/K(m) ratio, respectively).	acetonitrile	16-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
10877007-5	2000	Losartan and irbesartan inhibited the CYP2C9-associated tolbutamide methylhydroxylation more potently (Ki values 4.1 microM and 24.5 microM), than valsartan, candesartan or eprosartan (Ki values 135 microM, 155 microM and &gt; 1000 microM, respectively).	Irbesartan	13-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
10877007-5	2000	Losartan and irbesartan inhibited the CYP2C9-associated tolbutamide methylhydroxylation more potently (Ki values 4.1 microM and 24.5 microM), than valsartan, candesartan or eprosartan (Ki values 135 microM, 155 microM and &gt; 1000 microM, respectively).	Tolbutamide	56-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
10877007-5	2000	Losartan and irbesartan inhibited the CYP2C9-associated tolbutamide methylhydroxylation more potently (Ki values 4.1 microM and 24.5 microM), than valsartan, candesartan or eprosartan (Ki values 135 microM, 155 microM and &gt; 1000 microM, respectively).	Valsartan	147-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
10877007-5	2000	Losartan and irbesartan inhibited the CYP2C9-associated tolbutamide methylhydroxylation more potently (Ki values 4.1 microM and 24.5 microM), than valsartan, candesartan or eprosartan (Ki values 135 microM, 155 microM and &gt; 1000 microM, respectively).	candesartan	158-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
10877007-5	2000	Losartan and irbesartan inhibited the CYP2C9-associated tolbutamide methylhydroxylation more potently (Ki values 4.1 microM and 24.5 microM), than valsartan, candesartan or eprosartan (Ki values 135 microM, 155 microM and &gt; 1000 microM, respectively).	eprosartan	173-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
10877007-8	2000	CONCLUSION: All sartans except eprosartan have at least some affinity for CYP2C9, but only losartan has an affinity for CYP2C19.	eprosartan	31-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
10877007-10	2000	This would suggest that the theoretical potential for drug interactions is likely to be quite low, with the possible exceptions of losartan and irbesartan for CYP2C9.	Irbesartan	144-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
10725317-13	2000	It is concluded that some of these sulfonamides have to be carefully coadministered with CYP2C9 substrates such as tolbutamide although coadministration of sulfaphenazole needs the greatest care.	Sulfonamides	35-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
10806608-1	2000	To assess the effect of tolcapone (an inhibitor of cytochrome P450 [CYP] 2C9 in vitro) on the pharmacokinetics and hypoglycemic effect of the CYP 2C9 substrate tolbutamide, 12 healthy male volunteers were randomized to receive a single dose of tolbutamide 500 mg plus either placebo or tolcapone 200 mg after an overnight fast and 30 minutes after the start of a 6.5-hour 5% glucose infusion (150 mL/h).	Tolcapone	24-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-149
10813596-0	2000	Ontogenesis of CYP2C-dependent arachidonic acid metabolism in the human liver: relationship with sudden infant death syndrome.	Arachidonic Acid	31-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-20
10813596-2	2000	To determine the possible consequence of the up-regulation of CYP2C in SIDS, we examined the metabolism of arachidonic acid (AA) an endogenous substrate of CYP2C involved in the physiologic regulation of vascular tone.	Arachidonic Acid	107-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-161
10813596-4	2000	In SIDS, the accumulation of CYP2C proteins was associated with a significant increase in the formation of 14,15 and 11,12 diHETE, which were shown to be supported by individually expressed CYP2C8 and 2C9 and HETE1 (presumably 15 HETE).	dihete	123-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-34
10813596-5	2000	This increase was markedly inhibited by addition of sulfaphenazole, a selective inhibitor of CYP2C9.	Sulfaphenazole	52-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
10813596-6	2000	So, we propose that the higher CYP2C content in SIDS stimulates the production of EETs and diHETEs and might have severe pathologic consequences in children.	eets	82-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-36
10813596-6	2000	So, we propose that the higher CYP2C content in SIDS stimulates the production of EETs and diHETEs and might have severe pathologic consequences in children.	dihetes	91-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-36
10773015-0	2000	Major role of human liver microsomal cytochrome P450 2C9 (CYP2C9) in the oxidative metabolism of celecoxib, a novel cyclooxygenase-II inhibitor.	Celecoxib	97-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-56
10773015-0	2000	Major role of human liver microsomal cytochrome P450 2C9 (CYP2C9) in the oxidative metabolism of celecoxib, a novel cyclooxygenase-II inhibitor.	Celecoxib	97-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
10773015-3	2000	The treatment of a panel of human liver microsomal samples (n = 16 subjects) with antibodies against CYP2C9 and CYP3A4 inhibited the formation of hydroxy celecoxib by 72 to 92% and 0 to 27%, respectively.	Hydroxy Celecoxib	146-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
10773015-5	2000	In addition, the formation of hydroxy celecoxib significantly correlated with CYP2C9-selective tolbutamide methyl hydroxylation (r = 0.92, P &lt;.	Hydroxy Celecoxib	30-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
10773015-5	2000	In addition, the formation of hydroxy celecoxib significantly correlated with CYP2C9-selective tolbutamide methyl hydroxylation (r = 0.92, P &lt;.	Tolbutamide	95-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
10773015-10	2000	It is concluded that methyl hydroxylation of celecoxib is primarily catalyzed by human liver microsomal CYP2C9, although CYP3A4 also plays a role.	Celecoxib	45-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
10772937-0	2000	Arginines 97 and 108 in CYP2C9 are important determinants of the catalytic function.	Arginine	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
10772937-3	2000	To elucidate the function of the B-C loop we used homology modelling based on the Cyp102 structure in combination with functional studies of mutants using diclofenac as a model substrate for CYP2C9.	Diclofenac	155-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
10729206-7	2000	Correlation analysis was performed using individual samples of human liver microsomes, and the best correlation of linoleic acid epoxidation activity was with tolbutamide hydroxylase activity, CYP2C9.	Linoleic Acid	115-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	193-199
10729206-8	2000	Recombinant CYP2C9 was the most active in linoleic acid epoxygenation, and antibody and chemical inhibition also indicated the importance of CYP2C9.	Linoleic Acid	42-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
10725303-6	2000	Tolbutamide hydroxylation tended to be lower in children versus adults (P =.047) (CYP2C9), but did not reach statistical significance after correcting for multiple comparisons.	Tolbutamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
10725317-13	2000	It is concluded that some of these sulfonamides have to be carefully coadministered with CYP2C9 substrates such as tolbutamide although coadministration of sulfaphenazole needs the greatest care.	Tolbutamide	115-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
10774639-6	2000	Although phenytoin is metabolized predominantly by CYP2C9 with a minor contribution of CYP2C19, patients with the Leu359 variant should be monitored closely when treated with a moderate to high daily dose of phenytoin.	Phenytoin	9-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
10853880-0	2000	Lack of differences in diclofenac (a substrate for CYP2C9) pharmacokinetics in healthy volunteers with respect to the single CYP2C9*3 allele.	Diclofenac	23-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
10853880-1	2000	OBJECTIVES: Evidence exists to suggest that diclofenac is metabolised by CYP2C9.	Diclofenac	44-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
10853880-2	2000	The present study was undertaken in order to evaluate the effect of the single CYP2C9*3 variant on drug metabolism using diclofenac as a probe drug.	Diclofenac	121-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
10853880-3	2000	METHODS: A single dose of diclofenac was administered orally to 12 healthy subjects in whom the genotype of CYP2C9 had been determined previously.	Diclofenac	26-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
10853880-5	2000	RESULTS: For diclofenac, the following kinetic parameters were observed in the CYP2C9*1/*1 and CYP2C9*1/*3 subjects, respectively (mean +/- SD): apparent oral clearance (ml/kg/h) 355.8 +/- 56.9 and 484.4 +/- 155.3; area under plasma concentration time curve (microg h/ml) 2.7 +/- 0.7 and 1.9 +/- 0.6.	Diclofenac	13-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
10853880-5	2000	RESULTS: For diclofenac, the following kinetic parameters were observed in the CYP2C9*1/*1 and CYP2C9*1/*3 subjects, respectively (mean +/- SD): apparent oral clearance (ml/kg/h) 355.8 +/- 56.9 and 484.4 +/- 155.3; area under plasma concentration time curve (microg h/ml) 2.7 +/- 0.7 and 1.9 +/- 0.6.	Diclofenac	13-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
10853880-6	2000	The formation clearance of 4"-hydroxydiclofenac (ml/kg/h) was 63.6 +/- 19.1 in the CYP2C9*1/*1 subjects compared with 75.9 +/- 27.6 in the CYP2C9*1/*3 subjects.	4'-hydroxydiclofenac	27-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
10853880-6	2000	The formation clearance of 4"-hydroxydiclofenac (ml/kg/h) was 63.6 +/- 19.1 in the CYP2C9*1/*1 subjects compared with 75.9 +/- 27.6 in the CYP2C9*1/*3 subjects.	4'-hydroxydiclofenac	27-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	139-145
10853880-8	2000	CONCLUSION: Since the disposition kinetics of diclofenac does not change in subjects with the single CYP2C9*3 mutant allele, it is suggested that the effects of CYP2C9 polymorphisms on the drug metabolism tend to be substrate specific.	Diclofenac	46-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
10759690-7	2000	TCL was also a moderate inhibitor of CYP1A2 (Ki = 49 +/- 19 microM) and a weak inhibitor of CYP2C9 (Ki &gt; 75 microM), but its effect on the activities of CYP2E1 (Ki = 584 +/- 48 microM) and CYP3A (&gt; 1000 microM) was marginal.	Ticlopidine	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
10821163-3	2000	The results indicate that sulphaphenazole, quinidine and alpha-naphthoflavone are selective inhibitors of CYP2C9 (IC50 = 0.5-0.7 microM), CYP2D6 (0.3-0.4 microM) and CYP1A (0.05-5 microM) respectively on the basis of the IC50, which are much lower than those of other P450 isoforms (&gt; 10-fold).	Sulfaphenazole	26-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
10821163-3	2000	The results indicate that sulphaphenazole, quinidine and alpha-naphthoflavone are selective inhibitors of CYP2C9 (IC50 = 0.5-0.7 microM), CYP2D6 (0.3-0.4 microM) and CYP1A (0.05-5 microM) respectively on the basis of the IC50, which are much lower than those of other P450 isoforms (&gt; 10-fold).	Quinidine	43-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
10821163-3	2000	The results indicate that sulphaphenazole, quinidine and alpha-naphthoflavone are selective inhibitors of CYP2C9 (IC50 = 0.5-0.7 microM), CYP2D6 (0.3-0.4 microM) and CYP1A (0.05-5 microM) respectively on the basis of the IC50, which are much lower than those of other P450 isoforms (&gt; 10-fold).	alpha-naphthoflavone	57-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
10640513-1	2000	CYP2C9 is involved in the metabolism of the oral anticoagulants warfarin, phenprocoumon, and acenocoumarol.	Warfarin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10803683-0	2000	Torsemide metabolism by CYP2C9 variants and other human CYP2C subfamily enzymes.	Torsemide	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
10718780-4	2000	RESULTS: Amiodarone weakly inhibited CYP2C9, CYP2D6, and CYP3A4-mediated activities with Ki values of 45.1-271.6 microm.	Amiodarone	9-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
10718780-6	2000	The catalytic activities of CYP1A1 (Ki=1.5 microm, alpha=5.7), CYP1A2 (Ki=18.8 microm, alpha=2.6), CYP2C9 (Ki=2.3 microm, alpha=5.9), and CYP2C19 (Ki=15.7 microm, alpha=4.5) were inhibited by desethylamiodarone with mixed type.	desethylamiodarone	192-210	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
10681382-2	2000	Although most studies have implicated CYP2C9 as the exclusive catalyst of hepatic tolbutamide hydroxylation in humans, there is evidence that other CYP2C enzymes (e.g., CYP2C19) may also participate.	Tolbutamide	82-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
10681382-7	2000	Monospecific anti-CYP2C9 was also found to inhibit rates of tolbutamide hydroxylation by 93 +/- 4 and 78 +/- 6% in CYP2C19-deficient and CYP2C19-containing human liver microsomes, respectively.	Tolbutamide	60-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
10681382-8	2000	Taken together, our results indicate that both CYP2C9 and CYP2C19 are involved in tolbutamide hydroxylation by human liver microsomes, and that CYP2C19 underlies at least 14 to 22% of tolbutamide metabolism.	Tolbutamide	82-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
10681382-8	2000	Taken together, our results indicate that both CYP2C9 and CYP2C19 are involved in tolbutamide hydroxylation by human liver microsomes, and that CYP2C19 underlies at least 14 to 22% of tolbutamide metabolism.	Tolbutamide	184-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
10709776-11	2000	Fluconazole, miconazole and sulfamethoxazole are potent inhibitors of CYP2C9.	Fluconazole	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
10709776-11	2000	Fluconazole, miconazole and sulfamethoxazole are potent inhibitors of CYP2C9.	Miconazole	13-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
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
10749518-9	2000	Celecoxib is metabolised primarily by the cytochrome P450 (CYP) 2C9 isoenzyme and has an elimination half-life of about 11 hours in healthy individuals.	Celecoxib	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-67
10749518-14	2000	As celecoxib is metabolised by CYP2C9, increased clinical vigilance is required during the coadministration of other substrates or inhibitors of this enzyme.	Celecoxib	3-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
10801223-7	2000	CONCLUSIONS: Although I(inlet,u,max) overestimated the unbound concentration in the liver, the tolbutamide/sulfaphenazole interaction could be successfully predicted by using a fixed value of I(inlet,u,max) indicating that the unbound concentration of sulfaphenazole in the liver after its clinical dose is by far larger than the concentration to inhibit CYP2C9-mediated metabolism and that care should be taken when it is co-administered with drugs that are substrates of CYP2C9.	Tolbutamide	95-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	355-361
10801223-7	2000	CONCLUSIONS: Although I(inlet,u,max) overestimated the unbound concentration in the liver, the tolbutamide/sulfaphenazole interaction could be successfully predicted by using a fixed value of I(inlet,u,max) indicating that the unbound concentration of sulfaphenazole in the liver after its clinical dose is by far larger than the concentration to inhibit CYP2C9-mediated metabolism and that care should be taken when it is co-administered with drugs that are substrates of CYP2C9.	Tolbutamide	95-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	473-479
10801223-7	2000	CONCLUSIONS: Although I(inlet,u,max) overestimated the unbound concentration in the liver, the tolbutamide/sulfaphenazole interaction could be successfully predicted by using a fixed value of I(inlet,u,max) indicating that the unbound concentration of sulfaphenazole in the liver after its clinical dose is by far larger than the concentration to inhibit CYP2C9-mediated metabolism and that care should be taken when it is co-administered with drugs that are substrates of CYP2C9.	Sulfaphenazole	107-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	355-361
10801223-7	2000	CONCLUSIONS: Although I(inlet,u,max) overestimated the unbound concentration in the liver, the tolbutamide/sulfaphenazole interaction could be successfully predicted by using a fixed value of I(inlet,u,max) indicating that the unbound concentration of sulfaphenazole in the liver after its clinical dose is by far larger than the concentration to inhibit CYP2C9-mediated metabolism and that care should be taken when it is co-administered with drugs that are substrates of CYP2C9.	Sulfaphenazole	107-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	473-479
10640508-2	2000	All six compounds reversibly inhibited CYP2D6 (bufuralol 1"-hydroxylation) and CYP2C9 (tolbutamide methyl hydroxylation) activities.	Tolbutamide	87-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
10640508-3	2000	The IC(50) values for the inhibition of CYP2D6 and CYP2C9 for nicardipine were 3 to 9 microM, whereas those for all others ranged from 14 to &gt;150 microM.	Nicardipine	62-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
10640513-1	2000	CYP2C9 is involved in the metabolism of the oral anticoagulants warfarin, phenprocoumon, and acenocoumarol.	Phenprocoumon	74-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10640513-1	2000	CYP2C9 is involved in the metabolism of the oral anticoagulants warfarin, phenprocoumon, and acenocoumarol.	Acenocoumarol	93-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10640513-11	2000	The degree of pharmacokinetic interactions exhibited by oral anticoagulants and lornoxicam is dependent on the respective contribution of CYP2C9 to their total clearance.	lornoxicam	80-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
11144118-4	2000	Colchicine caused an increase of CYP2E1 protein content, colchiceine and N-deacetylcolchiceine induced isoforms CYP2C9, 2E1 and 3A4 whereas colchicoside induced CYP2C9 and 2E1.	Colchicine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
10805063-9	2000	Nicardipine, benidipine, manidipine and barnidipine competitively inhibited the CYP2C9 and CYP2D6 activities.	Nicardipine	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
10805063-9	2000	Nicardipine, benidipine, manidipine and barnidipine competitively inhibited the CYP2C9 and CYP2D6 activities.	benidipine	13-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
10805063-9	2000	Nicardipine, benidipine, manidipine and barnidipine competitively inhibited the CYP2C9 and CYP2D6 activities.	manidipine	25-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
10805063-9	2000	Nicardipine, benidipine, manidipine and barnidipine competitively inhibited the CYP2C9 and CYP2D6 activities.	mepirodipine	40-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
10805063-12	2000	Among the human CYP isoforms investigated, the inhibitory effects of 1,4-dihydropyridine calcium antagonists were potent on human CYP1A2, CYP2B6, CYP2C9, CYP2C19 and CYP2D6 as well as CYP3A4.	1,4-dihydropyridine calcium	69-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
10678291-4	2000	Losartan is distinguished from other ARBs by cytochrome P450 (CYP) 3A4- and CYP2C9-mediated biotransformation to its active metabolite EXP-3174.	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
10673364-4	2000	Using an RT-competitive PCR (RT-cPCR) with beta-actin as the standard in this study, the constitutive and rifampicin (RFP)-induced expression of CYP3A4, CYP2C9, CYP2E1, and CYP1A2 mRNA in the HepG2 cells could be quantitatively and reproducibly determined.	Rifampin	106-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
10805063-14	2000	CONCLUSIONS: In consideration of the Ki values obtained in the in vitro inhibition study and the concentration of 1,4-dihydropyridine calcium antagonists in human liver, the possibility of in vivo drug interactions of nicardipine and other drugs which are mainly metabolised by CYP2C9 and/or CYP3A4 was suggested.	Nicardipine	218-229	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	278-284
11144118-4	2000	Colchicine caused an increase of CYP2E1 protein content, colchiceine and N-deacetylcolchiceine induced isoforms CYP2C9, 2E1 and 3A4 whereas colchicoside induced CYP2C9 and 2E1.	Colchicine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
11144118-4	2000	Colchicine caused an increase of CYP2E1 protein content, colchiceine and N-deacetylcolchiceine induced isoforms CYP2C9, 2E1 and 3A4 whereas colchicoside induced CYP2C9 and 2E1.	trimethylcolchicinic acid methyl ether	73-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
11144118-4	2000	Colchicine caused an increase of CYP2E1 protein content, colchiceine and N-deacetylcolchiceine induced isoforms CYP2C9, 2E1 and 3A4 whereas colchicoside induced CYP2C9 and 2E1.	colchicoside	140-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
10659951-4	2000	Troglitazone (5 microM) significantly inhibited CYP2C8-dependent paclitaxel 6alpha-hydroxylation and CYP2C9-dependent S-warfarin 7-hydroxylation.	Troglitazone	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
10712746-0	2000	Phenobarbital increases DNA adduct and metabolites formed by ochratoxin A: role of CYP 2C9 and microsomal glutathione-S-transferase.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-90
10711629-2	2000	In this study, we examined the extent of thalidomide metabolism by preparations of pooled human microsomes, microsomes containing cloned human CYP isozymes (CYPIA2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4), and Hansen"s disease patients.	Thalidomide	41-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
10771452-5	2000	IC50 values for the inhibition of specific probe substrates for CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4, by ziprasidone, risperidone and 9-hydroxyrisperidone were also determined using human liver microsomes from three subjects.	ziprasidone	111-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
10771452-5	2000	IC50 values for the inhibition of specific probe substrates for CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4, by ziprasidone, risperidone and 9-hydroxyrisperidone were also determined using human liver microsomes from three subjects.	Risperidone	124-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
10771452-5	2000	IC50 values for the inhibition of specific probe substrates for CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4, by ziprasidone, risperidone and 9-hydroxyrisperidone were also determined using human liver microsomes from three subjects.	Paliperidone Palmitate	140-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
10668851-8	2000	CYP2C9 activity was significantly (P &lt; or = .005) increased by 38% +/- 35%, as reflected by the tolbutamide urinary metabolic ratio and oral clearance.	Tolbutamide	99-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10611138-0	2000	Stimulation of tolbutamide hydroxylation by acetone and acetonitrile in human liver microsomes and in a cytochrome P-450 2C9-reconstituted system.	Tolbutamide	15-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-124
10611138-3	2000	This study was initiated to evaluate the effect of acetonitrile and acetone, in addition to other organic solvents, on the tolbutamide hydroxylation activity of CYP2C9 in both human liver microsomes and a CYP2C9-reconstituted system.	acetonitrile	51-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
10611138-3	2000	This study was initiated to evaluate the effect of acetonitrile and acetone, in addition to other organic solvents, on the tolbutamide hydroxylation activity of CYP2C9 in both human liver microsomes and a CYP2C9-reconstituted system.	acetonitrile	51-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	205-211
10611138-3	2000	This study was initiated to evaluate the effect of acetonitrile and acetone, in addition to other organic solvents, on the tolbutamide hydroxylation activity of CYP2C9 in both human liver microsomes and a CYP2C9-reconstituted system.	Acetone	68-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
10611138-3	2000	This study was initiated to evaluate the effect of acetonitrile and acetone, in addition to other organic solvents, on the tolbutamide hydroxylation activity of CYP2C9 in both human liver microsomes and a CYP2C9-reconstituted system.	Acetone	68-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	205-211
10611138-3	2000	This study was initiated to evaluate the effect of acetonitrile and acetone, in addition to other organic solvents, on the tolbutamide hydroxylation activity of CYP2C9 in both human liver microsomes and a CYP2C9-reconstituted system.	Tolbutamide	123-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
10611138-3	2000	This study was initiated to evaluate the effect of acetonitrile and acetone, in addition to other organic solvents, on the tolbutamide hydroxylation activity of CYP2C9 in both human liver microsomes and a CYP2C9-reconstituted system.	Tolbutamide	123-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	205-211
10611138-4	2000	Both acetonitrile and acetone significantly stimulated the NADPH-dependent tolbutamide hydroxylation by nearly 2- to 3-fold in human liver microsomes and CYP2C9-reconstituted system when incubated at 2 and 4% final solvent concentrations.	acetonitrile	5-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
10611138-4	2000	Both acetonitrile and acetone significantly stimulated the NADPH-dependent tolbutamide hydroxylation by nearly 2- to 3-fold in human liver microsomes and CYP2C9-reconstituted system when incubated at 2 and 4% final solvent concentrations.	Acetone	22-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
10611138-4	2000	Both acetonitrile and acetone significantly stimulated the NADPH-dependent tolbutamide hydroxylation by nearly 2- to 3-fold in human liver microsomes and CYP2C9-reconstituted system when incubated at 2 and 4% final solvent concentrations.	NADP	59-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
10611138-4	2000	Both acetonitrile and acetone significantly stimulated the NADPH-dependent tolbutamide hydroxylation by nearly 2- to 3-fold in human liver microsomes and CYP2C9-reconstituted system when incubated at 2 and 4% final solvent concentrations.	Tolbutamide	75-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
10611138-9	2000	Overall, the stimulatory effect of both acetonitrile and acetone on tolbutamide hydroxylation was found to be primarily due to a consistent increase in V(max), whereas K(m) was unchanged in both human liver microsomes and the reconstituted CYP2C9 system.	acetonitrile	40-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	240-246
10611138-9	2000	Overall, the stimulatory effect of both acetonitrile and acetone on tolbutamide hydroxylation was found to be primarily due to a consistent increase in V(max), whereas K(m) was unchanged in both human liver microsomes and the reconstituted CYP2C9 system.	Acetone	57-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	240-246
10611138-9	2000	Overall, the stimulatory effect of both acetonitrile and acetone on tolbutamide hydroxylation was found to be primarily due to a consistent increase in V(max), whereas K(m) was unchanged in both human liver microsomes and the reconstituted CYP2C9 system.	Tolbutamide	68-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	240-246
10659951-4	2000	Troglitazone (5 microM) significantly inhibited CYP2C8-dependent paclitaxel 6alpha-hydroxylation and CYP2C9-dependent S-warfarin 7-hydroxylation.	Warfarin	120-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
10659951-7	2000	The inhibitory potential of troglitazone (50% inhibition concentration, IC50) was approximately 5 microM for drug oxidations catalyzed by CYP2C9 and CYP2C8 and approximately 20 microM for activities catalyzed by CYP2C19 and CYP3A4 respectively.	Troglitazone	28-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
10562412-0	1999	Structural forms of phenprocoumon and warfarin that are metabolized at the active site of CYP2C9.	Phenprocoumon	20-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
10562412-0	1999	Structural forms of phenprocoumon and warfarin that are metabolized at the active site of CYP2C9.	Warfarin	38-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
10562412-4	1999	The conclusion that (S)-warfarin and (S)-phenprocoumon interact with CYP2C9 in very different structural states provides a clear basis for the significant differences observed in their metabolic profiles.	Warfarin	20-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
10562412-4	1999	The conclusion that (S)-warfarin and (S)-phenprocoumon interact with CYP2C9 in very different structural states provides a clear basis for the significant differences observed in their metabolic profiles.	Phenprocoumon	37-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
10562412-6	1999	An additional electrostatic binding site also appears to contribute to the orientation of coumarin analogs in the CYP2C9 active site by interacting with the C2-carbonyl group of the coumarin nucleus.	coumarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
10562412-6	1999	An additional electrostatic binding site also appears to contribute to the orientation of coumarin analogs in the CYP2C9 active site by interacting with the C2-carbonyl group of the coumarin nucleus.	coumarin	182-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
10630892-2	1999	Metabolism of steroid hormones with anabolic properties was studied in vitro using human recombinant CYP3A4, CYP2C9 and 2B6 enzymes.	Steroids	14-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-123
10613612-3	1999	In vitro inhibition constants (K(i)) of benzbromarone for (S)-warfarin 7-hydroxylation were determined with use of human CYP2C9 and liver microsomes.	Benzbromarone	40-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
10613612-4	1999	The magnitude of changes in the formation clearance for 7-hydroxylation (CLf), the unbound oral clearance (CL(oral,u)), and the oral clearance (CL(oral)) for (S)-warfarin were predicted by equations incorporating the in vitro Ki, the theoretical maximum unbound hepatic benzbromarone concentration, and the fractions of warfarin eliminated through metabolism and of CYP2C9-mediated metabolic reaction susceptible to inhibition by benzbromarone.	Warfarin	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	366-372
10613612-7	1999	Benzbromarone was found to be a potent competitive inhibitor (Ki &lt; 0.01 micromol/L) for (S)-warfarin 7-hydroxylation mediated by CYP2C9.	Benzbromarone	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
10613612-7	1999	Benzbromarone was found to be a potent competitive inhibitor (Ki &lt; 0.01 micromol/L) for (S)-warfarin 7-hydroxylation mediated by CYP2C9.	Warfarin	91-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
10613612-9	1999	CONCLUSION: Benzbromarone would intensify anticoagulant response of warfarin through an enantioselective inhibition of CYP2C9-mediated metabolism of pharmacologically more potent (S)-warfarin.	Benzbromarone	12-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
10613612-9	1999	CONCLUSION: Benzbromarone would intensify anticoagulant response of warfarin through an enantioselective inhibition of CYP2C9-mediated metabolism of pharmacologically more potent (S)-warfarin.	Warfarin	68-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
10613612-9	1999	CONCLUSION: Benzbromarone would intensify anticoagulant response of warfarin through an enantioselective inhibition of CYP2C9-mediated metabolism of pharmacologically more potent (S)-warfarin.	Warfarin	179-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
10665838-9	1999	In contrast, fluvastatin (mainly metabolized by cytochrome P450-2C9) and pravastatin (eliminated by other metabolic routes) are less subject to this interaction.	Fluvastatin	13-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-67
10647906-4	1999	Methylenedioxyphenyl compounds which possess a bulky structure such as 1,4-benzothiazine showed substantial inhibition of S-warfarin 7-hydroxylation catalysed by CYP2C9, S-mephenytoin 4"-hydroxylation by CYP2C19, bufuralol 1"-hydroxylation by CYP2D6, and testosterone 6beta-hydroxylation by CYP3A4.	1,4-benzothiazine	71-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
10647906-4	1999	Methylenedioxyphenyl compounds which possess a bulky structure such as 1,4-benzothiazine showed substantial inhibition of S-warfarin 7-hydroxylation catalysed by CYP2C9, S-mephenytoin 4"-hydroxylation by CYP2C19, bufuralol 1"-hydroxylation by CYP2D6, and testosterone 6beta-hydroxylation by CYP3A4.	Warfarin	124-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
10647906-4	1999	Methylenedioxyphenyl compounds which possess a bulky structure such as 1,4-benzothiazine showed substantial inhibition of S-warfarin 7-hydroxylation catalysed by CYP2C9, S-mephenytoin 4"-hydroxylation by CYP2C19, bufuralol 1"-hydroxylation by CYP2D6, and testosterone 6beta-hydroxylation by CYP3A4.	bufuralol	213-222	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
10647906-4	1999	Methylenedioxyphenyl compounds which possess a bulky structure such as 1,4-benzothiazine showed substantial inhibition of S-warfarin 7-hydroxylation catalysed by CYP2C9, S-mephenytoin 4"-hydroxylation by CYP2C19, bufuralol 1"-hydroxylation by CYP2D6, and testosterone 6beta-hydroxylation by CYP3A4.	Testosterone	255-267	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
10627170-0	1999	CYP2C9 is a principal low-affinity phenacetin O-deethylase: fluvoxamine is not a specific CYP1A2 inhibitor.	Fluvoxamine	60-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10586395-1	1999	The objective of this randomized, double-blind, two-period crossover study was to investigate whether concomitant steady-state lansoprazole influences the pharmacokinetics of CYP2C9 substrates using single intravenously dosed phenytoin as a model substrate.	Lansoprazole	127-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	175-181
10630892-5	1999	When the same formats of CYP2C9 were incubated with the anabolic steroids, no 6beta-hydroxyl metabolites were formed.	Steroids	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
10449188-6	1999	Based on microsome studies and the incubations with human hepatocytes and engineered cells, we estimated that in vivo CYP2C9 would be exclusively responsible for the 4" hydroxylation of diclofenac (&gt;99.5%) as well as 5-hydroxydiclofenac (&gt;97%).	Diclofenac	186-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
10597902-1	1999	Cetirizine, terfenadine, loratadine, astemizole and mizolastine were compared for their ability to inhibit marker activities for CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4 and for some glucuronidation isoenzymes in human liver microsomes.	Cetirizine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
10597902-1	1999	Cetirizine, terfenadine, loratadine, astemizole and mizolastine were compared for their ability to inhibit marker activities for CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4 and for some glucuronidation isoenzymes in human liver microsomes.	Terfenadine	12-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
10597902-1	1999	Cetirizine, terfenadine, loratadine, astemizole and mizolastine were compared for their ability to inhibit marker activities for CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4 and for some glucuronidation isoenzymes in human liver microsomes.	Loratadine	25-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
10597902-1	1999	Cetirizine, terfenadine, loratadine, astemizole and mizolastine were compared for their ability to inhibit marker activities for CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4 and for some glucuronidation isoenzymes in human liver microsomes.	Astemizole	37-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
10597902-1	1999	Cetirizine, terfenadine, loratadine, astemizole and mizolastine were compared for their ability to inhibit marker activities for CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4 and for some glucuronidation isoenzymes in human liver microsomes.	mizolastine	52-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
10597902-4	1999	Furthermore, loratadine activated the CYP2C9-catalyzed tolbutamide hydroxylation (ca.	Loratadine	13-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
10597902-4	1999	Furthermore, loratadine activated the CYP2C9-catalyzed tolbutamide hydroxylation (ca.	Tolbutamide	55-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
10597902-6	1999	Mizolastine appeared to be a relatively weak and unspecific inhibitor of CYP2E1, CYP2C9, CYP2D6 and CYP3A4 (IC50Ss in the 100 micromolar range).	mizolastine	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
10562462-0	1999	Rapid detection of CYP2C9*3 alleles by real-time fluorescence PCR based on SYBR Green.	sybr green	75-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
10562462-1	1999	CYP2C9 catalyzes the metabolism of important drugs such as phenytoin, S-warfarin, tolbutamide, losartan, and nonsteroidal anti-inflammatory drugs.	Phenytoin	59-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10562462-1	1999	CYP2C9 catalyzes the metabolism of important drugs such as phenytoin, S-warfarin, tolbutamide, losartan, and nonsteroidal anti-inflammatory drugs.	Warfarin	70-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10562462-1	1999	CYP2C9 catalyzes the metabolism of important drugs such as phenytoin, S-warfarin, tolbutamide, losartan, and nonsteroidal anti-inflammatory drugs.	Tolbutamide	82-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10562462-1	1999	CYP2C9 catalyzes the metabolism of important drugs such as phenytoin, S-warfarin, tolbutamide, losartan, and nonsteroidal anti-inflammatory drugs.	Losartan	95-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10584064-6	1999	The CYP2C9 model was then used to characterize explicit enzyme complexes with three structurally and chemically diverse substrates: (S)-naproxen, phenytoin, and progesterone.	Naproxen	132-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
10584064-6	1999	The CYP2C9 model was then used to characterize explicit enzyme complexes with three structurally and chemically diverse substrates: (S)-naproxen, phenytoin, and progesterone.	Phenytoin	146-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
10584064-6	1999	The CYP2C9 model was then used to characterize explicit enzyme complexes with three structurally and chemically diverse substrates: (S)-naproxen, phenytoin, and progesterone.	Progesterone	161-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
10870095-6	1999	In vitro inhibition of CYP2C9 by zafirlukast is consistent with clinical studies showing impaired clearance of S-warfarin and enhanced anti-thrombotic effects, although the in vitro IC(50) value is higher than the usual range of clinically relevant plasma concentrations.	zafirlukast	33-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
10870095-6	1999	In vitro inhibition of CYP2C9 by zafirlukast is consistent with clinical studies showing impaired clearance of S-warfarin and enhanced anti-thrombotic effects, although the in vitro IC(50) value is higher than the usual range of clinically relevant plasma concentrations.	Sulfur	111-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
10870095-6	1999	In vitro inhibition of CYP2C9 by zafirlukast is consistent with clinical studies showing impaired clearance of S-warfarin and enhanced anti-thrombotic effects, although the in vitro IC(50) value is higher than the usual range of clinically relevant plasma concentrations.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
10870095-7	1999	Zafirlukast deserves further clinical study as an inhibitor of other CYP2C9 substrates such as nonsteroidal anti-inflammatory agents, tolbutamide, phenytoin and mestranol.	zafirlukast	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
10449188-6	1999	Based on microsome studies and the incubations with human hepatocytes and engineered cells, we estimated that in vivo CYP2C9 would be exclusively responsible for the 4" hydroxylation of diclofenac (&gt;99.5%) as well as 5-hydroxydiclofenac (&gt;97%).	5-hydroxydiclofenac	220-239	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
10510155-6	1999	Omeprazole (a CYP2C19 substrate) at high concentrations and sulphaphenazole (a selective inhibitor of CYP2C9) substantially inhibited N-demethylsertraline formation.	Sulfaphenazole	60-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
10510154-0	1999	Frequency of cytochrome P450 CYP2C9 variants in a Turkish population and functional relevance for phenytoin.	Phenytoin	98-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
10449188-7	1999	CYP2C9 was exclusively responsible for the formation of 3"-hydroxydiclofenac.	3'-Hydroxydiclofenac	56-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10510154-7	1999	Mean phenytoin serum concentrations at 12 h after dosage were 4.16 mg l-1 (95% CI 3.86-4.46) in carriers of the genotype CYP2C9*1/1, 5.52 mg l-1 (4.66-6.39) in CYP2C9*1/2, and 5.65 mg l-1 (4.86-6.43) in CYP2C9*1/3.	Phenytoin	5-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
10510154-7	1999	Mean phenytoin serum concentrations at 12 h after dosage were 4.16 mg l-1 (95% CI 3.86-4.46) in carriers of the genotype CYP2C9*1/1, 5.52 mg l-1 (4.66-6.39) in CYP2C9*1/2, and 5.65 mg l-1 (4.86-6.43) in CYP2C9*1/3.	Phenytoin	5-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
10510154-7	1999	Mean phenytoin serum concentrations at 12 h after dosage were 4.16 mg l-1 (95% CI 3.86-4.46) in carriers of the genotype CYP2C9*1/1, 5.52 mg l-1 (4.66-6.39) in CYP2C9*1/2, and 5.65 mg l-1 (4.86-6.43) in CYP2C9*1/3.	Phenytoin	5-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
10510154-13	1999	The 12 h serum concentrations after a single phenytoin dose may be used for routine phenotyping of CYP2C9 mediated metabolic clearance and the p-HPPH/P ratios may be even more sensitive indicators of CYP2C9 activity.	Phenytoin	45-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
10510155-6	1999	Omeprazole (a CYP2C19 substrate) at high concentrations and sulphaphenazole (a selective inhibitor of CYP2C9) substantially inhibited N-demethylsertraline formation.	desmethylsertraline	134-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
10510155-10	1999	CONCLUSIONS: The polymorphic enzyme CYP2C19 catalyses the high-affinity N-demethylation of sertraline, while CYP2C9 is one of the low-affinity components of this metabolic pathway.	Nitrogen	2-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
10510155-10	1999	CONCLUSIONS: The polymorphic enzyme CYP2C19 catalyses the high-affinity N-demethylation of sertraline, while CYP2C9 is one of the low-affinity components of this metabolic pathway.	Sertraline	91-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
10460808-5	1999	Ketoconazole (CYP3A inhibitor) inhibited approximately 40% of the generation of both metabolites, sulfaphenazole (CYP2C inhibitor) inhibited the formation of ND-Z, whereas alpha-naphtoflavone (CYP1A), quinidine (CYP2D6), and chlorzoxazone (CYP2E1) did not affect zopiclone metabolism.	Sulfaphenazole	98-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-119
10510156-7	1999	There was some evidence for CYP2C9 playing a minor role in the metabolism of rosiglitazone.	Rosiglitazone	77-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
10510156-8	1999	Sulphaphenazole caused limited inhibition (&lt;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.	Sulfaphenazole	0-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
10510156-8	1999	Sulphaphenazole caused limited inhibition (&lt;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 9	Homo sapiens	138-144
10510156-8	1999	Sulphaphenazole caused limited inhibition (&lt;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.	Nitrogen	147-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
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 9	Homo sapiens	163-169
10460803-6	1999	N-demethylation is primarily mediated by CYP2C9, CYP2C8, and CYP1A2; dihydrodiol formation by CYP2C9 and CYP1A2; deamination by CYP3A4; and side chain oxidation equally by CYP1A2, CYP2C8, CYP2C9, and CYP2C19.	Nitrogen	0-1	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
10460803-6	1999	N-demethylation is primarily mediated by CYP2C9, CYP2C8, and CYP1A2; dihydrodiol formation by CYP2C9 and CYP1A2; deamination by CYP3A4; and side chain oxidation equally by CYP1A2, CYP2C8, CYP2C9, and CYP2C19.	Nitrogen	0-1	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
10510154-13	1999	The 12 h serum concentrations after a single phenytoin dose may be used for routine phenotyping of CYP2C9 mediated metabolic clearance and the p-HPPH/P ratios may be even more sensitive indicators of CYP2C9 activity.	p-hpph	143-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	200-206
10460803-6	1999	N-demethylation is primarily mediated by CYP2C9, CYP2C8, and CYP1A2; dihydrodiol formation by CYP2C9 and CYP1A2; deamination by CYP3A4; and side chain oxidation equally by CYP1A2, CYP2C8, CYP2C9, and CYP2C19.	Nitrogen	0-1	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
10460808-7	1999	Recombinant CYP2C8 had the highest enzymatic activity toward zopiclone metabolism into both its metabolites, followed by CYP2C9 and 3A4.	zopiclone	61-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
10460803-6	1999	N-demethylation is primarily mediated by CYP2C9, CYP2C8, and CYP1A2; dihydrodiol formation by CYP2C9 and CYP1A2; deamination by CYP3A4; and side chain oxidation equally by CYP1A2, CYP2C8, CYP2C9, and CYP2C19.	trans-1,2-dihydro-1,2-naphthalenediol	69-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
10460803-6	1999	N-demethylation is primarily mediated by CYP2C9, CYP2C8, and CYP1A2; dihydrodiol formation by CYP2C9 and CYP1A2; deamination by CYP3A4; and side chain oxidation equally by CYP1A2, CYP2C8, CYP2C9, and CYP2C19.	trans-1,2-dihydro-1,2-naphthalenediol	69-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
10417492-9	1999	4"-Hydroxymephenytoin formation was inhibited significantly by omeprazole, diethyldithiocarbamate, proguanil, furafylline, diazepam, troleandomycin, and sulphaphenazole (CYP2C9).	4-hydroxymephenytoin	0-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-176
10503815-5	1999	CYP2C9 is saturated by therapeutic doses of phenytoin, and at steady state both enzymes are probably operant in most people.	Phenytoin	44-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10548450-10	1999	Among the CYP inhibitors examined (alpha-naphthoflavone, sulphaphenazole, omeprazole, quinidine and troleandomycin), sulphaphenazole (a CYP2C9 inhibitor) showed the most potent inhibitory effect on the 5-hydroxylation of S-MTPPA by human liver microsomes.	Troleandomycin	100-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
10548450-10	1999	Among the CYP inhibitors examined (alpha-naphthoflavone, sulphaphenazole, omeprazole, quinidine and troleandomycin), sulphaphenazole (a CYP2C9 inhibitor) showed the most potent inhibitory effect on the 5-hydroxylation of S-MTPPA by human liver microsomes.	Sulfaphenazole	117-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
10548450-12	1999	When incubated with microsomes containing cDNA-expressed CYP isozymes, S-MTPPA was substantially oxidized to MA6 only by CYP2C9.	2-(4-(3-methyl-2-thienyl)phenyl)propionic acid	71-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
10473927-4	1999	Although the mechanism of the interaction is unclear, it has been postulated that 5-FU interferes with the synthesis of hepatic cytochrome P-450 2C9.	Fluorouracil	82-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-148
10417492-9	1999	4"-Hydroxymephenytoin formation was inhibited significantly by omeprazole, diethyldithiocarbamate, proguanil, furafylline, diazepam, troleandomycin, and sulphaphenazole (CYP2C9).	Sulfaphenazole	153-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-176
10383922-6	1999	Azelastine, desmethylazelastine, and 6-hydroxyazelastine competitively inhibited CYP2C9 activity (Ki = 13.	azelastine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
10383917-5	1999	At the substrate concentration of 20 microM, which approximated the apparent KM value, sulfaphenazole (CYP2C9 inhibitor) and triazolam (CYP3A substrate) reduced the N-demethylation activities by 20 to 35% in human liver microsomes, whereas the inhibition induced by mephenytoin (CYP2C19 substrate) or quinidine (CYP2D6 inhibitor) was marginal.	Sulfaphenazole	87-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
10463513-7	1999	Celecoxib is metabolized in the liver by the cytochrome P-450 isozyme CYP2C9, and thus serious drug interactions are possible.	Celecoxib	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
10383922-6	1999	Azelastine, desmethylazelastine, and 6-hydroxyazelastine competitively inhibited CYP2C9 activity (Ki = 13.	desmethylazelastine	12-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
10383929-8	1999	Furthermore, allicin formation by human liver microsomes was correlated with p-nitrophenol hydroxylase activity, a marker of CYP2E1, and tolbutamide hydroxylase activity, a marker of CYP2C9.	allicin	13-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	183-189
10383917-5	1999	At the substrate concentration of 20 microM, which approximated the apparent KM value, sulfaphenazole (CYP2C9 inhibitor) and triazolam (CYP3A substrate) reduced the N-demethylation activities by 20 to 35% in human liver microsomes, whereas the inhibition induced by mephenytoin (CYP2C19 substrate) or quinidine (CYP2D6 inhibitor) was marginal.	Triazolam	125-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
10383917-5	1999	At the substrate concentration of 20 microM, which approximated the apparent KM value, sulfaphenazole (CYP2C9 inhibitor) and triazolam (CYP3A substrate) reduced the N-demethylation activities by 20 to 35% in human liver microsomes, whereas the inhibition induced by mephenytoin (CYP2C19 substrate) or quinidine (CYP2D6 inhibitor) was marginal.	Mephenytoin	266-277	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
10383917-5	1999	At the substrate concentration of 20 microM, which approximated the apparent KM value, sulfaphenazole (CYP2C9 inhibitor) and triazolam (CYP3A substrate) reduced the N-demethylation activities by 20 to 35% in human liver microsomes, whereas the inhibition induced by mephenytoin (CYP2C19 substrate) or quinidine (CYP2D6 inhibitor) was marginal.	Quinidine	301-310	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
10383922-6	1999	Azelastine, desmethylazelastine, and 6-hydroxyazelastine competitively inhibited CYP2C9 activity (Ki = 13.	6-hydroxyazelastine	37-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
10383917-8	1999	In particular, CYP2C19, CYP2B6, CYP2C9-Arg, CYP2D6-Val, and CYP3A4 all showed relatively high activity.	Arginine	39-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
10383922-14	1999	The inhibition of CYP2C9, CYP2C19, and CYP3A4 activity by azelastine and its two metabolites might be clinically insignificant.	azelastine	58-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
10383917-10	1999	The results suggest that at least five isoforms of CYP (CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP3A4) are involved in the sertraline N-demethylation in human liver microsomes and that the contribution of any individual isoform does not exceed 40% of overall metabolism.	sertraline n	117-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
10413320-1	1999	CYP2C9 is mainly responsible for the metabolic clearance of phenytoin and (S)-warfarin.	Phenytoin	60-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10413320-1	1999	CYP2C9 is mainly responsible for the metabolic clearance of phenytoin and (S)-warfarin.	Warfarin	74-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10413320-2	1999	We have shown previously that mutations in the CYP2C9 gene are associated with diminished metabolism of (S)-warfarin, and so we have now studied the metabolism of phenytoin to its primary inactive metabolite, (S)-pHPPH, by these mutant enzymes.	Warfarin	104-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
10413320-2	1999	We have shown previously that mutations in the CYP2C9 gene are associated with diminished metabolism of (S)-warfarin, and so we have now studied the metabolism of phenytoin to its primary inactive metabolite, (S)-pHPPH, by these mutant enzymes.	Phenytoin	163-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
10413320-2	1999	We have shown previously that mutations in the CYP2C9 gene are associated with diminished metabolism of (S)-warfarin, and so we have now studied the metabolism of phenytoin to its primary inactive metabolite, (S)-pHPPH, by these mutant enzymes.	(s)-phpph	209-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
10413320-4	1999	The data demonstrate that the CYP2C9*3 gene product retains only 4-6% of the metabolic efficiency of the wild-type protein, CYP2C9*1, towards phenytoin and (S)-warfarin.	Phenytoin	142-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
10413320-4	1999	The data demonstrate that the CYP2C9*3 gene product retains only 4-6% of the metabolic efficiency of the wild-type protein, CYP2C9*1, towards phenytoin and (S)-warfarin.	Warfarin	156-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
10381752-2	1999	The predominant P-450 enzyme involved in meloxicam metabolism is CYP 2C9, with a minor contribution of CYP 3A4.	Meloxicam	41-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-72
10381752-6	1999	Using expressed cytochrome P-450 enzymes and selective chemical inhibitors of CYP 2C9 and CYP 3A4, it was found that quinidine markedly increased the rate of CYP 3A4-mediated meloxicam hydroxylation but was virtually without effect on CYP 2C9.	Quinidine	117-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-85
10381752-6	1999	Using expressed cytochrome P-450 enzymes and selective chemical inhibitors of CYP 2C9 and CYP 3A4, it was found that quinidine markedly increased the rate of CYP 3A4-mediated meloxicam hydroxylation but was virtually without effect on CYP 2C9.	Quinidine	117-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	235-242
10381752-6	1999	Using expressed cytochrome P-450 enzymes and selective chemical inhibitors of CYP 2C9 and CYP 3A4, it was found that quinidine markedly increased the rate of CYP 3A4-mediated meloxicam hydroxylation but was virtually without effect on CYP 2C9.	Meloxicam	175-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-85
10422890-4	1999	In addition, clozapine may inhibit the activity of CYP2C9 and CYP2C19, and induce CYP1A, CYP2B and CYP3A.	Clozapine	13-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
10357778-4	1999	DNA from normal tissue was also evaluated for polymorphisms in cytochrome P450 2C9 (CYP2C9) at two sites, codons 144 (Arg/Cys) and 359 (Ile/Leu), for glutathione S-transferase P1 (GSTP1) at codon 105 and for NAD(P)H:quinone oxidoreductase (NQO1) at codon 187 (Pro/Ser).	Arginine	118-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-82
10357778-4	1999	DNA from normal tissue was also evaluated for polymorphisms in cytochrome P450 2C9 (CYP2C9) at two sites, codons 144 (Arg/Cys) and 359 (Ile/Leu), for glutathione S-transferase P1 (GSTP1) at codon 105 and for NAD(P)H:quinone oxidoreductase (NQO1) at codon 187 (Pro/Ser).	Arginine	118-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
10357778-4	1999	DNA from normal tissue was also evaluated for polymorphisms in cytochrome P450 2C9 (CYP2C9) at two sites, codons 144 (Arg/Cys) and 359 (Ile/Leu), for glutathione S-transferase P1 (GSTP1) at codon 105 and for NAD(P)H:quinone oxidoreductase (NQO1) at codon 187 (Pro/Ser).	nad(p)h	208-215	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
10348802-4	1999	This investigation determined single-dose disulfiram effects on human CYP 2C9, 2C19, 2D6, and 3A4 activities in vivo.	Disulfiram	42-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-77
10348802-8	1999	CYP2C9, 2C19, 2D6, and 3A4 activities were determined from the tolbutamide metabolic ratio, 4"-hydroxymephenytoin excretion, and dextromethorphan/dextrorphan ratios in urine and midazolam systemic clearance, respectively.	Tolbutamide	63-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10348802-8	1999	CYP2C9, 2C19, 2D6, and 3A4 activities were determined from the tolbutamide metabolic ratio, 4"-hydroxymephenytoin excretion, and dextromethorphan/dextrorphan ratios in urine and midazolam systemic clearance, respectively.	4-hydroxymephenytoin	92-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10348802-8	1999	CYP2C9, 2C19, 2D6, and 3A4 activities were determined from the tolbutamide metabolic ratio, 4"-hydroxymephenytoin excretion, and dextromethorphan/dextrorphan ratios in urine and midazolam systemic clearance, respectively.	Dextromethorphan	129-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10348802-8	1999	CYP2C9, 2C19, 2D6, and 3A4 activities were determined from the tolbutamide metabolic ratio, 4"-hydroxymephenytoin excretion, and dextromethorphan/dextrorphan ratios in urine and midazolam systemic clearance, respectively.	Dextrorphan	146-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10348802-8	1999	CYP2C9, 2C19, 2D6, and 3A4 activities were determined from the tolbutamide metabolic ratio, 4"-hydroxymephenytoin excretion, and dextromethorphan/dextrorphan ratios in urine and midazolam systemic clearance, respectively.	Midazolam	178-187	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
10230773-0	1999	Human CYP2C-mediated stereoselective phenytoin hydroxylation in Japanese: difference in chiral preference of CYP2C9 and CYP2C19.	Phenytoin	37-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
10230773-7	1999	These results, in addition to inhibition experiments with anti-human CYP2C antibody, indicate that phenytoin hydroxylation is mainly catalyzed by CYP2C9.	Phenytoin	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
10230773-8	1999	Furthermore, CYP2C19 showed limited contribution to phenytoin 4"-hydroxylation with a different chiral preference from CYP2C9.	phenytoin 4"	52-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
10357778-4	1999	DNA from normal tissue was also evaluated for polymorphisms in cytochrome P450 2C9 (CYP2C9) at two sites, codons 144 (Arg/Cys) and 359 (Ile/Leu), for glutathione S-transferase P1 (GSTP1) at codon 105 and for NAD(P)H:quinone oxidoreductase (NQO1) at codon 187 (Pro/Ser).	Serine	264-267	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
10418968-11	1999	Furafylline, sulfaphenazole, quinidine, and ketoconazole were found to be specific inhibitors of CYP1A2, CYP2C9, CYP2D6, and CYP3A4, respectively.	furafylline	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
10418968-11	1999	Furafylline, sulfaphenazole, quinidine, and ketoconazole were found to be specific inhibitors of CYP1A2, CYP2C9, CYP2D6, and CYP3A4, respectively.	Sulfaphenazole	13-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
10418968-11	1999	Furafylline, sulfaphenazole, quinidine, and ketoconazole were found to be specific inhibitors of CYP1A2, CYP2C9, CYP2D6, and CYP3A4, respectively.	Quinidine	29-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
10418968-11	1999	Furafylline, sulfaphenazole, quinidine, and ketoconazole were found to be specific inhibitors of CYP1A2, CYP2C9, CYP2D6, and CYP3A4, respectively.	Ketoconazole	44-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
10418968-12	1999	Tranylcypromine and diethyldithiocarbamate were found to be less specific, with inhibitory effects towards several CYP isoforms, including CYP2A6, CYP2C9, CYP2C19, and CYP2E1.	Tranylcypromine	0-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
10418968-12	1999	Tranylcypromine and diethyldithiocarbamate were found to be less specific, with inhibitory effects towards several CYP isoforms, including CYP2A6, CYP2C9, CYP2C19, and CYP2E1.	Ditiocarb	20-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	147-153
10192828-6	1999	Studies using expressed cytochromes showed that ODV was formed by CYP2C9, -2C19, and -2D6.	Desvenlafaxine Succinate	48-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
10192828-12	1999	Studies using expressed cytochromes showed that NDV was formed by CYP2C9, -2C19, and -3A4.	N-desmethylvenlafaxine	48-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
10233205-11	1999	CONCLUSIONS: The N-demethylation of methadone in human liver microsomes is not markedly stereoselective, and is mediated mainly by CYP3A4 with the possible involvement of CYP2C9 and CYP2C19.	Methadone	36-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
10233205-8	1999	Sulphaphenazole (CYP2C9) also significantly inhibited (P&lt;0.05) EDDP formation (range 14-25%).	Sulfaphenazole	0-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
10079071-0	1999	Enzymatic determinants of the substrate specificity of CYP2C9: role of B"-C loop residues in providing the pi-stacking anchor site for warfarin binding.	Warfarin	135-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
10233205-8	1999	Sulphaphenazole (CYP2C9) also significantly inhibited (P&lt;0.05) EDDP formation (range 14-25%).	2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine	66-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
10197301-0	1999	The effects of fluvastatin, a CYP2C9 inhibitor, on losartan pharmacokinetics in healthy volunteers.	Fluvastatin	15-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
10197301-1	1999	Losartan is an angiotensin II receptor antagonist that is metabolized by CYP2C9 and CYP3A4 to a more potent antihypertensive metabolite, E3174.	Losartan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
10197301-1	1999	Losartan is an angiotensin II receptor antagonist that is metabolized by CYP2C9 and CYP3A4 to a more potent antihypertensive metabolite, E3174.	losartan carboxylic acid	137-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
10197301-8	1999	Inhibition of losartan metabolism appears to require both CYP2C9 and CYP3A4 inhibition.	Losartan	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
10375008-6	1999	In comparison with ketoconazole, itraconazole and fluconazole, D0870 was the most potent inhibitor of CYP2C9 activity.	Fluconazole	50-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
10375008-6	1999	In comparison with ketoconazole, itraconazole and fluconazole, D0870 was the most potent inhibitor of CYP2C9 activity.	ICI 195739	63-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
10079071-1	1999	Previous modeling efforts have suggested that coumarin ligand binding to CYP2C9 is dictated by electrostatic and pi-stacking interactions with complementary amino acids of the protein.	coumarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
10079071-10	1999	Finally, the F114L mutant effected a greater than 100-fold increase in the Ki for inhibition of CYP2C9 activity by sulfaphenazole.	Sulfaphenazole	115-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
10079071-11	1999	These data support a role for B"-C helix loop residues F114 and V113 in the hydrophobic binding of warfarin to CYP2C9, and are consistent with pi-stacking to F114 for certain aromatic ligands.	Warfarin	99-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
10073515-0	1999	Association of polymorphisms in the cytochrome P450 CYP2C9 with warfarin dose requirement and risk of bleeding complications.	Warfarin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
10064574-3	1999	Several enzymes, but mainly CYP2C9, catalyzed fluvastatin metabolism.	Fluvastatin	46-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
10064574-4	1999	Only CYP2C9 inhibitors such as sulfaphenazole inhibited the formation of both 6-hydroxy- and N-deisopropyl-fluvastatin.	Sulfaphenazole	31-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	5-11
10064574-4	1999	Only CYP2C9 inhibitors such as sulfaphenazole inhibited the formation of both 6-hydroxy- and N-deisopropyl-fluvastatin.	6-hydroxy- and n-deisopropyl-fluvastatin	78-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	5-11
10064574-5	1999	5-Hydroxy-fluvastatin formation was reduced by compounds that are inhibitors of CYP2C9, CYP3A, or CYP2C8.	5-hydroxy-fluvastatin	0-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
10064574-6	1999	Fluvastatin in turn inhibited CYP2C9-catalyzed tolbutamide and diclofenac hydroxylation with Ki values of 0.3 and 0.5 microM, respectively.	Fluvastatin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
10064574-6	1999	Fluvastatin in turn inhibited CYP2C9-catalyzed tolbutamide and diclofenac hydroxylation with Ki values of 0.3 and 0.5 microM, respectively.	Tolbutamide	47-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
10064574-6	1999	Fluvastatin in turn inhibited CYP2C9-catalyzed tolbutamide and diclofenac hydroxylation with Ki values of 0.3 and 0.5 microM, respectively.	Diclofenac	63-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
10064574-8	1999	All three fluvastatin metabolites were also formed by recombinant CYP2C9, whereas CYP1A1, CYP2C8, CYP2D6, and CYP3A4 produced only 5-hydroxy-fluvastatin.	Fluvastatin	10-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
10064574-12	1999	This data indicates that several human cytochrome P-450 enzymes metabolize fluvastatin with CYP2C9 contributing 50-80%.	Fluvastatin	75-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
9925971-5	1999	For formation of M2, both a rabbit CYP3A polyclonal antibody (110 microliter/mg microsomal protein) and ketoconazole (2 micromol/l), a CYP3A inhibitor, showed about 50% inhibitory effects; other specific inhibitors of CYP1A2, CYP2B6, CYP2C9, CYP2C19, CYP2D6 and CYP2E1 showed no significant effects.	Ketoconazole	104-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	234-240
10073515-1	1999	BACKGROUND: The cytochrome P450 CYP2C9 is responsible for the metabolism of S-warfarin.	Warfarin	76-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
10073515-4	1999	We have studied the effect of CYP2C9 polymorphism on the in-vivo warfarin dose requirement.	Warfarin	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
10073515-8	1999	FINDINGS: The odds ratio for individuals with a low warfarin dose requirement having one or more CYP2C9 variant alleles compared with the normal population was 6.21 (95% CI 2.48-15.6).	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
10073515-10	1999	INTERPRETATION: We have shown that there is a strong association between CYP2C9 variant alleles and low warfarin dose requirement.	Warfarin	104-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
10073515-11	1999	CYP2C9 genotyping may identify a subgroup of patients who have difficulty at induction of warfarin therapy and are potentially at a higher risk of bleeding complications.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
9929518-13	1999	Enzyme kinetics suggest that nifedipine is a noncompetitive-type inhibitor of CYP2C9-mediated catalytic activities.	Nifedipine	29-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
10027801-4	1999	Cytochrome P450 2C9, which catalyzes the major route of oxidative metabolism of diclofenac to produce 4"-hydroxydiclofenac, did not appear to be responsible for the formation of the protein adducts, because sulfaphenazole, an inhibitor of this enzyme, did not affect protein adduct formation.	Diclofenac	80-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
10027801-4	1999	Cytochrome P450 2C9, which catalyzes the major route of oxidative metabolism of diclofenac to produce 4"-hydroxydiclofenac, did not appear to be responsible for the formation of the protein adducts, because sulfaphenazole, an inhibitor of this enzyme, did not affect protein adduct formation.	4'-hydroxydiclofenac	102-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
10190649-2	1999	Despite the widespread use of tolbutamide in Asian populations, the pharmacokinetics of tolbutamide, a CYP2C9 substrate, have not been described in ethnic Chinese.	Tolbutamide	88-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
9929510-3	1999	Methanol did not substantially inhibit (&lt;/=10%) any of the activities at 0.3%, but did inhibit CYP1A1, CYP2B6, CYP2C9, and CYP2D6 by 12 to 26% at 1%.	Methanol	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
9929518-14	1999	Finally, only microsomes containing recombinant human liver CYP2C9 were capable of oxidizing irbesartan.	Irbesartan	93-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
9929510-10	1999	Acetonitrile also increased CYP2C9 activity by 10 to 15% above control values at 1 to 3% solvent.	acetonitrile	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
9929518-7	1999	769) with tolbutamide (CYP2C9 substrate) 4-methyl-hydroxylation.	Tolbutamide	10-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
9929518-15	1999	These results provide evidence that CYP2C9 plays a major role in irbesartan oxidation.	Irbesartan	65-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
9929518-8	1999	Oxidation of irbesartan was markedly inhibited by sulfaphenazole (CYP2C9 inhibitor), but not by any of several other CYP inhibitors.	Irbesartan	13-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
9929518-8	1999	Oxidation of irbesartan was markedly inhibited by sulfaphenazole (CYP2C9 inhibitor), but not by any of several other CYP inhibitors.	Sulfaphenazole	50-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
10192756-0	1999	Inhibition of CYP2C9 by selective serotonin reuptake inhibitors: in vitro studies with tolbutamide and (S)-warfarin using human liver microsomes.	Warfarin	103-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
9929518-9	1999	In the same manner, both tolbutamide and warfarin (CYP2C9 substrates), were competitive-type inhibitors of irbesartan oxidation with Ki values of 500 and 30 microM, respectively.	Tolbutamide	25-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
9929518-9	1999	In the same manner, both tolbutamide and warfarin (CYP2C9 substrates), were competitive-type inhibitors of irbesartan oxidation with Ki values of 500 and 30 microM, respectively.	Warfarin	41-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
9929518-9	1999	In the same manner, both tolbutamide and warfarin (CYP2C9 substrates), were competitive-type inhibitors of irbesartan oxidation with Ki values of 500 and 30 microM, respectively.	Irbesartan	107-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
10192756-1	1999	OBJECTIVE: To investigate the in vitro potential of selective serotonin reuptake inhibitors (SSRIs) to inhibit two CYP2C9-catalysed reactions, tolbutamide 4-methylhydroxylation and (S)-warfarin 7-hydroxylation.	Tolbutamide	143-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
10192756-10	1999	This is consistent with in vivo data indicating that amongst the SSRIs, fluvoxamine has the greatest potential for inhibiting CYP2C9-mediated drug metabolism.	Fluvoxamine	72-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
10208645-7	1999	An additional blood sample was obtained from this individual to determine if he possessed any of the known CYP2C9 or CYP2C19 allelic variants that would account for his poor clearance of the CYP2C9 substrates (phenytoin and glipizide) compared with the CYP3A4 (nifedipine) and CYP2D6 (chlorpheniramine) substrates.	Nifedipine	261-271	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
10048600-3	1999	In the present study, in vitro metabolism of risperidone (100 microM) was investigated using the recombinant human cytochrome P450 (CYP) enzymes CYP1A1, CYP1A2, CYP2C8, CYP2C9-arg144, CYP2C9-cys144, CYP2C19, CYP2D6, CYP3A4 and CYP3A5 supplemented with an NADPH-generating system.	Risperidone	45-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
10048600-3	1999	In the present study, in vitro metabolism of risperidone (100 microM) was investigated using the recombinant human cytochrome P450 (CYP) enzymes CYP1A1, CYP1A2, CYP2C8, CYP2C9-arg144, CYP2C9-cys144, CYP2C19, CYP2D6, CYP3A4 and CYP3A5 supplemented with an NADPH-generating system.	Risperidone	45-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	184-190
10208645-7	1999	An additional blood sample was obtained from this individual to determine if he possessed any of the known CYP2C9 or CYP2C19 allelic variants that would account for his poor clearance of the CYP2C9 substrates (phenytoin and glipizide) compared with the CYP3A4 (nifedipine) and CYP2D6 (chlorpheniramine) substrates.	Chlorpheniramine	285-301	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
9920790-1	1999	Cytochrome P450 2C9 (CYP2C9) catalysis the metabolism of important drugs such as phenytoin, S-warfarin, tolbutamide, losartan, torasemide, and nonsteroidal anti-inflammatory drugs.	Phenytoin	81-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
9920790-1	1999	Cytochrome P450 2C9 (CYP2C9) catalysis the metabolism of important drugs such as phenytoin, S-warfarin, tolbutamide, losartan, torasemide, and nonsteroidal anti-inflammatory drugs.	Phenytoin	81-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
9920790-1	1999	Cytochrome P450 2C9 (CYP2C9) catalysis the metabolism of important drugs such as phenytoin, S-warfarin, tolbutamide, losartan, torasemide, and nonsteroidal anti-inflammatory drugs.	Warfarin	92-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
9920790-1	1999	Cytochrome P450 2C9 (CYP2C9) catalysis the metabolism of important drugs such as phenytoin, S-warfarin, tolbutamide, losartan, torasemide, and nonsteroidal anti-inflammatory drugs.	Warfarin	92-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
9920790-1	1999	Cytochrome P450 2C9 (CYP2C9) catalysis the metabolism of important drugs such as phenytoin, S-warfarin, tolbutamide, losartan, torasemide, and nonsteroidal anti-inflammatory drugs.	Tolbutamide	104-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
9920790-1	1999	Cytochrome P450 2C9 (CYP2C9) catalysis the metabolism of important drugs such as phenytoin, S-warfarin, tolbutamide, losartan, torasemide, and nonsteroidal anti-inflammatory drugs.	Tolbutamide	104-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
9920790-1	1999	Cytochrome P450 2C9 (CYP2C9) catalysis the metabolism of important drugs such as phenytoin, S-warfarin, tolbutamide, losartan, torasemide, and nonsteroidal anti-inflammatory drugs.	Losartan	117-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
9920790-1	1999	Cytochrome P450 2C9 (CYP2C9) catalysis the metabolism of important drugs such as phenytoin, S-warfarin, tolbutamide, losartan, torasemide, and nonsteroidal anti-inflammatory drugs.	Losartan	117-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
9920790-1	1999	Cytochrome P450 2C9 (CYP2C9) catalysis the metabolism of important drugs such as phenytoin, S-warfarin, tolbutamide, losartan, torasemide, and nonsteroidal anti-inflammatory drugs.	Torsemide	127-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
9920790-1	1999	Cytochrome P450 2C9 (CYP2C9) catalysis the metabolism of important drugs such as phenytoin, S-warfarin, tolbutamide, losartan, torasemide, and nonsteroidal anti-inflammatory drugs.	Torsemide	127-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
9860067-0	1998	The effects of genetic polymorphisms of CYP2C9 and CYP2C19 on phenytoin metabolism in Japanese adult patients with epilepsy: studies in stereoselective hydroxylation and population pharmacokinetics.	Phenytoin	62-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
10574228-5	1999	Ginsenoside Rd produced weak inhibitory activity against the surrogate substrates for CYP3A4 and CYP2D6 and even weaker inhibitory activity against the surrogate substrates for CYP2C19 and CYP2C9.	Ginsenosides	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	189-195
10574228-7	1999	Ginsenoside Rc produced an increase in the activity of CYP2C9 (70% at 200 uM) and ginsenoside Rf produced an increase in the activity of CYP3A4 (54% at 200 uM).	ginsenoside Rc	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
10078840-6	1999	Furafylline, sulphaphenazole, omeprazole, quinidine and ketoconazole were identified as specific markers for the respective CYP1A2 (IC50 = 6 microM), CYP2C9 (0.7 microM), CYP2C19 (6 microM), CYP2D6 (0.02 microM) and CYP3A4 (0.2 microM) inhibition screens.	Ketoconazole	56-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
10208642-0	1999	The effect of genetic polymorphisms in CYP2C9 on sulphamethoxazole N-hydroxylation.	sulphamethoxazole n	49-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
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
10208642-1	1999	Sulphamethoxazole undergoes CYP2C9-mediated bioactivation to a hydroxylamine.	Hydroxylamine	63-76	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
10208645-0	1999	Pharmacokinetics of chlorpheniramine, phenytoin, glipizide and nifedipine in an individual homozygous for the CYP2C9*3 allele.	Chlorpheniramine	20-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
10208645-0	1999	Pharmacokinetics of chlorpheniramine, phenytoin, glipizide and nifedipine in an individual homozygous for the CYP2C9*3 allele.	Nifedipine	63-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
10208645-4	1999	A male Caucasian who participated in six bioavailability studies in our laboratory over a period of several years showed extremely low clearance of two drugs: phenytoin and glipizide (both substrates of CYP2C9), but not for nifedipine (a CYP3A4 substrate) and chlorpheniramine (a CYP2D6 substrate).	Phenytoin	159-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	203-209
10208645-4	1999	A male Caucasian who participated in six bioavailability studies in our laboratory over a period of several years showed extremely low clearance of two drugs: phenytoin and glipizide (both substrates of CYP2C9), but not for nifedipine (a CYP3A4 substrate) and chlorpheniramine (a CYP2D6 substrate).	Glipizide	173-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	203-209
10208645-4	1999	A male Caucasian who participated in six bioavailability studies in our laboratory over a period of several years showed extremely low clearance of two drugs: phenytoin and glipizide (both substrates of CYP2C9), but not for nifedipine (a CYP3A4 substrate) and chlorpheniramine (a CYP2D6 substrate).	Chlorpheniramine	260-276	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	203-209
10208645-7	1999	An additional blood sample was obtained from this individual to determine if he possessed any of the known CYP2C9 or CYP2C19 allelic variants that would account for his poor clearance of the CYP2C9 substrates (phenytoin and glipizide) compared with the CYP3A4 (nifedipine) and CYP2D6 (chlorpheniramine) substrates.	Phenytoin	210-219	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
10208645-7	1999	An additional blood sample was obtained from this individual to determine if he possessed any of the known CYP2C9 or CYP2C19 allelic variants that would account for his poor clearance of the CYP2C9 substrates (phenytoin and glipizide) compared with the CYP3A4 (nifedipine) and CYP2D6 (chlorpheniramine) substrates.	Phenytoin	210-219	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
10208645-7	1999	An additional blood sample was obtained from this individual to determine if he possessed any of the known CYP2C9 or CYP2C19 allelic variants that would account for his poor clearance of the CYP2C9 substrates (phenytoin and glipizide) compared with the CYP3A4 (nifedipine) and CYP2D6 (chlorpheniramine) substrates.	Glipizide	224-233	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
10078840-6	1999	Furafylline, sulphaphenazole, omeprazole, quinidine and ketoconazole were identified as specific markers for the respective CYP1A2 (IC50 = 6 microM), CYP2C9 (0.7 microM), CYP2C19 (6 microM), CYP2D6 (0.02 microM) and CYP3A4 (0.2 microM) inhibition screens.	furafylline	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
9866708-3	1998	CYP2C9 converted arachidonic and linoleic acids to epoxides/diols and monohydroxy fatty acids.	arachidonic	17-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
9866708-3	1998	CYP2C9 converted arachidonic and linoleic acids to epoxides/diols and monohydroxy fatty acids.	Linoleic Acids	33-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
9866708-3	1998	CYP2C9 converted arachidonic and linoleic acids to epoxides/diols and monohydroxy fatty acids.	Epoxy Compounds	51-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
9866708-3	1998	CYP2C9 converted arachidonic and linoleic acids to epoxides/diols and monohydroxy fatty acids.	diols	60-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
9866708-3	1998	CYP2C9 converted arachidonic and linoleic acids to epoxides/diols and monohydroxy fatty acids.	monohydroxy fatty acids	70-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
9866708-5	1998	Incubation of CYP2C9 under oxygen-18 gas showed that all HETEs had incorporated oxygen-18 to the same degree.	Oxygen	27-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
9866708-5	1998	Incubation of CYP2C9 under oxygen-18 gas showed that all HETEs had incorporated oxygen-18 to the same degree.	Oxygen	80-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
9866708-6	1998	Chiral HPLC showed that CYP2C9 formed 15R-HETE (72% of the R enantiomer), 13S-HETE (90%), and 11R-HETE (57%).	15R-HETE	38-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
9866708-6	1998	Chiral HPLC showed that CYP2C9 formed 15R-HETE (72% of the R enantiomer), 13S-HETE (90%), and 11R-HETE (57%).	13-hydroxyeicosatetraenoic acid	74-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
9860067-1	1998	PURPOSE: The aim of this study was to clarify the effects of genetic polymorphisms of cytochrome P450 (CYP) 2C9 and 2C19 on the metabolism of phenytoin (PHT).	Phenytoin	142-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-120
9860067-1	1998	PURPOSE: The aim of this study was to clarify the effects of genetic polymorphisms of cytochrome P450 (CYP) 2C9 and 2C19 on the metabolism of phenytoin (PHT).	Phenytoin	153-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-120
9866708-6	1998	Chiral HPLC showed that CYP2C9 formed 15R-HETE (72% of the R enantiomer), 13S-HETE (90%), and 11R-HETE (57%).	11-hydroxy-5,8,12,14-eicosatetraenoic acid	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
9864282-15	1998	We conclude that CYP2C9 and possibly CYP2C19 and important isoforms catalysing the initial hydroxylation of desogestrel.	Desogestrel	108-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
9916601-9	1998	Sildenafil is cleared predominantly by the hepatic microsomal isoenzymes CYP3A4 (major route) and CYP2C9 (minor route).	Sildenafil Citrate	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
9864282-5	1998	Desogestrel was metabolised by microsomes from lymphoblasts containing cDNA-expressed CYP2C9 and CYP2C19 to 3alpha-hydroxydesogestrel with small amounts of 3beta-hydroxydesogestrel also being observed.	Desogestrel	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
9864282-9	1998	Sulfaphenazole potently inhibited 3alpha-hydroxydesogestrel formation by CYP2C9 microsomes with a Ki value of 0.91 microM.	Sulfaphenazole	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
9864282-9	1998	Sulfaphenazole potently inhibited 3alpha-hydroxydesogestrel formation by CYP2C9 microsomes with a Ki value of 0.91 microM.	3alpha-Hydroxydesogestrel	34-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
9864282-11	1998	Sulfaphenazole partially inhibited 3alpha-hydroxydesogestrel and 3-ketodesogestrel formation in human liver microsomes indicating a possible in vivo role for CYP2C9.	Sulfaphenazole	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
9840430-3	1998	In vitro metabolism of clozapine was investigated using human CYP1A1, CYP1A2, CYP2C8, CYP2E1, CYP2C9-arg144, CYP2C9-cys144, CYP2C19, CYP2D6, CYP3A4, CYP3A5 and FMO3 supplemented with an NADPH generating system.	Clozapine	23-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
9840430-3	1998	In vitro metabolism of clozapine was investigated using human CYP1A1, CYP1A2, CYP2C8, CYP2E1, CYP2C9-arg144, CYP2C9-cys144, CYP2C19, CYP2D6, CYP3A4, CYP3A5 and FMO3 supplemented with an NADPH generating system.	Clozapine	23-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
9763401-7	1998	Ketoconazole (2.0 microM), a CYP3A-selective inhibitor, inhibited the hydroxylation of both compounds by 53-67%, and sulfaphenazole (CYP2C9-selective) decreased activity by 10-20%.	Sulfaphenazole	117-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
9735164-0	1998	Identification of residues 286 and 289 as critical for conferring substrate specificity of human CYP2C9 for diclofenac and ibuprofen.	Diclofenac	108-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
9812178-16	1998	Since ritonavir is also an inducer of several metabolising enzymes [CYP1A4, glucuronosyl transferase (GT), and possibly CYP2C9 and CYP2C19], the magnitude of drug interactions is difficult to predict, particularly for drugs that are metabolised by multiple enzymes or have low intrinsic clearance by CYP3A.	Ritonavir	6-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
9825828-0	1998	Comparisons between in-vitro and in-vivo metabolism of (S)-warfarin: catalytic activities of cDNA-expressed CYP2C9, its Leu359 variant and their mixture versus unbound clearance in patients with the corresponding CYP2C9 genotypes.	Warfarin	55-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
9825828-0	1998	Comparisons between in-vitro and in-vivo metabolism of (S)-warfarin: catalytic activities of cDNA-expressed CYP2C9, its Leu359 variant and their mixture versus unbound clearance in patients with the corresponding CYP2C9 genotypes.	Warfarin	55-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	213-219
9825828-5	1998	Consequently, there was a significant correlation (r = 0.99, P &lt; 0.05) between the in-vitro Cl(int) for (S)-warfarin 7-hydroxylation and the in-vivo Cl(po,u) for (S)-warfarin in relation to the CYP2C9*3 polymorphism.	Warfarin	107-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
9825828-6	1998	In conclusion, the in-vitro model for human CYP2C9*3 polymorphism using recombinant cytochrome P450 proteins would serve as a useful means for predicting changes in in-vivo kinetics for (S)-warfarin and possibly other CYP2C9 substrates in relation to CYP2C9*3 polymorphism.	Warfarin	186-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
9825830-5	1998	Haloperidol and CPHP formation rates in the nine liver preparations were significantly correlated with dextromethorphan N-demethylase activity (a marker of CYP3A4 activity), but not with the CYP2D6, CYP1A2 and CYP2C9 activity.	Haloperidol	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	210-216
9825830-5	1998	Haloperidol and CPHP formation rates in the nine liver preparations were significantly correlated with dextromethorphan N-demethylase activity (a marker of CYP3A4 activity), but not with the CYP2D6, CYP1A2 and CYP2C9 activity.	4-(4'-chlorophenyl)-4-piperidinol	16-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	210-216
9735164-0	1998	Identification of residues 286 and 289 as critical for conferring substrate specificity of human CYP2C9 for diclofenac and ibuprofen.	Ibuprofen	123-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
9735164-1	1998	Specificity of human CYP2C9 for two substrates, diclofenac and ibuprofen, was studied using chimeras and site-directed mutants of CYP2C9 and the highly related CYP2C19 expressed in Escherichia coli.	Diclofenac	48-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
9804052-5	1998	In the treatment of transplant patients, from a drug interaction perspective, pravastatin, which is not significantly metabolized by CYP enzymes, and fluvastatin, presumably a CYP2C9 substrate, compare favorably with the other statins for which the major metabolic pathways are catalyzed by CYP3A.	Fluvastatin	150-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
9735164-1	1998	Specificity of human CYP2C9 for two substrates, diclofenac and ibuprofen, was studied using chimeras and site-directed mutants of CYP2C9 and the highly related CYP2C19 expressed in Escherichia coli.	Ibuprofen	63-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
9735164-1	1998	Specificity of human CYP2C9 for two substrates, diclofenac and ibuprofen, was studied using chimeras and site-directed mutants of CYP2C9 and the highly related CYP2C19 expressed in Escherichia coli.	Ibuprofen	63-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
9735164-4	1998	The regiospecificity of this construct for metabolism of ibuprofen differed from that of CYP2C9 by favoring 2-hydroxylation over 3-hydroxylation.	Ibuprofen	57-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
9735164-5	1998	A CYP2C9 construct containing residues 228-340 of CYP2C19 lacked both diclofenac and ibuprofen hydroxylase activities.	Diclofenac	70-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	2-8
9735164-6	1998	When residues 228-282 (containing SRS 3) of CYP2C9 were replaced by those of CYP2C19, the chimera retained appreciable activity for diclofenac and ibuprofen, and tolbutamide activity was inhibited by a specific CYP2C9 inhibitor, sulfaphenazole.	Diclofenac	132-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
9735164-6	1998	When residues 228-282 (containing SRS 3) of CYP2C9 were replaced by those of CYP2C19, the chimera retained appreciable activity for diclofenac and ibuprofen, and tolbutamide activity was inhibited by a specific CYP2C9 inhibitor, sulfaphenazole.	Ibuprofen	147-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
9735164-6	1998	When residues 228-282 (containing SRS 3) of CYP2C9 were replaced by those of CYP2C19, the chimera retained appreciable activity for diclofenac and ibuprofen, and tolbutamide activity was inhibited by a specific CYP2C9 inhibitor, sulfaphenazole.	Tolbutamide	162-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
9735164-6	1998	When residues 228-282 (containing SRS 3) of CYP2C9 were replaced by those of CYP2C19, the chimera retained appreciable activity for diclofenac and ibuprofen, and tolbutamide activity was inhibited by a specific CYP2C9 inhibitor, sulfaphenazole.	Sulfaphenazole	229-243	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
9735164-13	1998	Therefore residues 286 and 289 of CYP2C9 are important in conferring specificity for diclofenac and ibuprofen.	Diclofenac	85-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
9735164-13	1998	Therefore residues 286 and 289 of CYP2C9 are important in conferring specificity for diclofenac and ibuprofen.	Ibuprofen	100-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
9733665-7	1998	Co-incubation of liver microsomes with methoxychlor and various P450 isoform-selective inhibitors suggested involvement of several P450s in mono-O-demethylation, including CYP1A2, CYP2A6, CYP2C9, and CYP2C19.	Methoxychlor	39-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	188-194
9811160-0	1998	Multiple human cytochromes contribute to biotransformation of dextromethorphan in-vitro: role of CYP2C9, CYP2C19, CYP2D6, and CYP3A.	Dextromethorphan	62-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
9764927-3	1998	Propofol produced inhibition of CYP1A2 (phenacetin O-deethylation), CYP2C9 (tolbutamide 4"-hydroxylation), CYP2D6 (dextromethorphan O-demethylation) and CYP3A4 (testosterone 6beta-hydroxylation) activities with IC50 = 40, 49, 213 and 32 microM respectively.	Propofol	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
9811160-4	1998	Dextrorphan was formed from dextromethorphan by microsomes from cDNA-transfected lymphoblastoid cells expressing CYP2C9, -2C19, and -2D6 but not by those expressing CYP1A2, -2E1 or -3A4.	Dextrorphan	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
9811160-8	1998	3-Methoxymorphinan was formed by microsomes from cDNA-transfected lymphoblastoid cells expressing CYP2C9, -2C19, -2D6, and -3A4, but not by those expressing CYP1A2 or -2E1.	3-methoxymorphinan	0-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
9811160-11	1998	After adjustment for relative abundance, CYP3A4 was identified as the dominant enzyme mediating 3-methoxymorphinan formation from dextromethorphan, although CYP2C9 and -2C19 were estimated to contribute to 3-methoxymorphinan formation, particularly at low substrate concentrations.	3-methoxymorphinan	206-224	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
9698292-0	1998	Human N-demethylation of (S)-mephenytoin by cytochrome P450s 2C9 and 2B6.	Mephenytoin	25-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-72
9698292-5	1998	Of the recombinant P450 isoforms tested, only CYP2B6 and CYP2C9 formed nirvanol from (S)-MP.	ethylphenylhydantoin	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
9867310-3	1998	The main probe drugs include caffeine and theophylline, whose metabolism is catalysed by CYP1A2, tolbutamide, phenytoin and ibuprofen, catalysed by CYP2C9, amitriptyline and nortriptyline, catalysed by CYP2C19, acetaminophen, catalysed by CYP2E1 and lidocaine, midazolam and terfenadine, catalysed by 3A3/4.	Ibuprofen	124-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
9867310-3	1998	The main probe drugs include caffeine and theophylline, whose metabolism is catalysed by CYP1A2, tolbutamide, phenytoin and ibuprofen, catalysed by CYP2C9, amitriptyline and nortriptyline, catalysed by CYP2C19, acetaminophen, catalysed by CYP2E1 and lidocaine, midazolam and terfenadine, catalysed by 3A3/4.	Nortriptyline	174-187	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
9867310-3	1998	The main probe drugs include caffeine and theophylline, whose metabolism is catalysed by CYP1A2, tolbutamide, phenytoin and ibuprofen, catalysed by CYP2C9, amitriptyline and nortriptyline, catalysed by CYP2C19, acetaminophen, catalysed by CYP2E1 and lidocaine, midazolam and terfenadine, catalysed by 3A3/4.	Caffeine	29-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
9867310-3	1998	The main probe drugs include caffeine and theophylline, whose metabolism is catalysed by CYP1A2, tolbutamide, phenytoin and ibuprofen, catalysed by CYP2C9, amitriptyline and nortriptyline, catalysed by CYP2C19, acetaminophen, catalysed by CYP2E1 and lidocaine, midazolam and terfenadine, catalysed by 3A3/4.	Acetaminophen	211-224	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
9867310-3	1998	The main probe drugs include caffeine and theophylline, whose metabolism is catalysed by CYP1A2, tolbutamide, phenytoin and ibuprofen, catalysed by CYP2C9, amitriptyline and nortriptyline, catalysed by CYP2C19, acetaminophen, catalysed by CYP2E1 and lidocaine, midazolam and terfenadine, catalysed by 3A3/4.	Theophylline	42-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
9867310-3	1998	The main probe drugs include caffeine and theophylline, whose metabolism is catalysed by CYP1A2, tolbutamide, phenytoin and ibuprofen, catalysed by CYP2C9, amitriptyline and nortriptyline, catalysed by CYP2C19, acetaminophen, catalysed by CYP2E1 and lidocaine, midazolam and terfenadine, catalysed by 3A3/4.	Lidocaine	250-259	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
9867310-3	1998	The main probe drugs include caffeine and theophylline, whose metabolism is catalysed by CYP1A2, tolbutamide, phenytoin and ibuprofen, catalysed by CYP2C9, amitriptyline and nortriptyline, catalysed by CYP2C19, acetaminophen, catalysed by CYP2E1 and lidocaine, midazolam and terfenadine, catalysed by 3A3/4.	Midazolam	261-270	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
9867310-3	1998	The main probe drugs include caffeine and theophylline, whose metabolism is catalysed by CYP1A2, tolbutamide, phenytoin and ibuprofen, catalysed by CYP2C9, amitriptyline and nortriptyline, catalysed by CYP2C19, acetaminophen, catalysed by CYP2E1 and lidocaine, midazolam and terfenadine, catalysed by 3A3/4.	Terfenadine	275-286	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
9698079-0	1998	Comparative studies on the catalytic roles of cytochrome P450 2C9 and its Cys- and Leu-variants in the oxidation of warfarin, flurbiprofen, and diclofenac by human liver microsomes.	Warfarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-65
9698079-0	1998	Comparative studies on the catalytic roles of cytochrome P450 2C9 and its Cys- and Leu-variants in the oxidation of warfarin, flurbiprofen, and diclofenac by human liver microsomes.	Flurbiprofen	126-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-65
9698079-0	1998	Comparative studies on the catalytic roles of cytochrome P450 2C9 and its Cys- and Leu-variants in the oxidation of warfarin, flurbiprofen, and diclofenac by human liver microsomes.	Diclofenac	144-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-65
9698079-7	1998	Activities for the oxidation of these CYP2C9 substrates in humans with heterozygous Leu359 allele is likely to be dependent on the levels of expression of each of the wild- and Leu-variants in the livers.	Leucine	84-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
9698079-8	1998	However, one of the humans with a heterozygous Leu allele was found to have very low activities towards the oxidation of CYP2C9 substrates.	Leucine	47-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
9578596-0	1998	Characterization of CYP2C19 and CYP2C9 from human liver: respective roles in microsomal tolbutamide, S-mephenytoin, and omeprazole hydroxylations.	Tolbutamide	88-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
9755458-7	1998	Recently, an allelic variant of CYP2C9 that causes substitution of Leu359 for Ile359 has been shown to be associated with the decreased metabolic clearance of various therapeutic agents including warfarin, tolbutamide and phenytoin.	Warfarin	196-204	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
9755458-7	1998	Recently, an allelic variant of CYP2C9 that causes substitution of Leu359 for Ile359 has been shown to be associated with the decreased metabolic clearance of various therapeutic agents including warfarin, tolbutamide and phenytoin.	Tolbutamide	206-217	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
9755458-7	1998	Recently, an allelic variant of CYP2C9 that causes substitution of Leu359 for Ile359 has been shown to be associated with the decreased metabolic clearance of various therapeutic agents including warfarin, tolbutamide and phenytoin.	Phenytoin	222-231	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
9663807-3	1998	CYP2C9 activity in vivo is inducible by rifampicin.	Rifampin	40-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
9663807-4	1998	Evidence suggests that CYP2C9 substrates may also be induced variably by carbamazepine, ethanol and phenobarbitone.	Carbamazepine	73-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
9663807-4	1998	Evidence suggests that CYP2C9 substrates may also be induced variably by carbamazepine, ethanol and phenobarbitone.	Ethanol	88-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
9663807-4	1998	Evidence suggests that CYP2C9 substrates may also be induced variably by carbamazepine, ethanol and phenobarbitone.	Phenobarbital	100-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
9663807-7	1998	Polymorphisms in the coding region of the CYP2C9 gene produce variants at amino acid residues 144 (Arg144Cys) and 359 (Ile359Leu) of the CYP2C9 protein.	ile359leu	119-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
9663807-7	1998	Polymorphisms in the coding region of the CYP2C9 gene produce variants at amino acid residues 144 (Arg144Cys) and 359 (Ile359Leu) of the CYP2C9 protein.	ile359leu	119-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
9616194-5	1998	Trazodone (100 microM) was then incubated with microsomes from cells expressing human CYP1A1, CYP1A2, CYP2C8, CYP2C9arg, CYP2C9cys, CYP2C19, CYP2D6, or CYP3A4.	Trazodone	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
9616194-5	1998	Trazodone (100 microM) was then incubated with microsomes from cells expressing human CYP1A1, CYP1A2, CYP2C8, CYP2C9arg, CYP2C9cys, CYP2C19, CYP2D6, or CYP3A4.	Trazodone	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
9578596-3	1998	To that end, we purified CYP2C19, CYP2C9, and CYP2C8 from human liver samples using conventional chromatographic techniques and examined their capacity to oxidize S-mephenytoin, omeprazole, and tolbutamide.	Mephenytoin	163-176	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
9578596-3	1998	To that end, we purified CYP2C19, CYP2C9, and CYP2C8 from human liver samples using conventional chromatographic techniques and examined their capacity to oxidize S-mephenytoin, omeprazole, and tolbutamide.	Tolbutamide	194-205	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
9578596-6	1998	The kinetic parameters of CYP2C19-mediated tolbutamide hydroxylation (Km = 650 microM, Vmax = 3.71 min-1) somewhat resembled those of the CYP2C9-catalyzed reaction (Km = 178-407 microM, Vmax = 2.95-7.08 min-1).	Tolbutamide	43-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
9578596-0	1998	Characterization of CYP2C19 and CYP2C9 from human liver: respective roles in microsomal tolbutamide, S-mephenytoin, and omeprazole hydroxylations.	Mephenytoin	101-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
9578596-11	1998	A significant relationship was likewise observed between microsomal tolbutamide hydroxylation and CYP2C9 content (r = 0.664; P &lt; 0.02) but not with CYP2C19 content (r = 0.393; P = 0.184).	Tolbutamide	68-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
9578596-0	1998	Characterization of CYP2C19 and CYP2C9 from human liver: respective roles in microsomal tolbutamide, S-mephenytoin, and omeprazole hydroxylations.	Omeprazole	120-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
9630825-0	1998	Metabolism of warfarin enantiomers in Japanese patients with heart disease having different CYP2C9 and CYP2C19 genotypes.	Warfarin	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
9630825-1	1998	OBJECTIVE: To determine whether genetic polymorphism of cytochrome P450 (CYP) 2C9 affects the in vivo metabolism of warfarin enantiomers.	Warfarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-81
9630825-11	1998	CONCLUSION: Heterozygotes for CYP2C9 I1e359/Leu allele have reduced in vivo metabolism of (S)-warfarin but not (R)-warfarin.	Leucine	44-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
9630825-11	1998	CONCLUSION: Heterozygotes for CYP2C9 I1e359/Leu allele have reduced in vivo metabolism of (S)-warfarin but not (R)-warfarin.	Warfarin	90-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
9630825-12	1998	Because (S)-warfarin has a greater anticoagulant potency than its (R)-congener, the genetic polymorphism of CYP2C9 may partly account for the large interpatient variability in therapeutic dosages of warfarin.	Warfarin	8-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
9630825-12	1998	Because (S)-warfarin has a greater anticoagulant potency than its (R)-congener, the genetic polymorphism of CYP2C9 may partly account for the large interpatient variability in therapeutic dosages of warfarin.	Warfarin	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
9521735-3	1998	Sigmoidal kinetic characteristics were observed for carbamazepine metabolism by CYP3A4 and naphthalene metabolism by CYPs 2B6, 2C8, 2C9, and 3A5 as well as dapsone metabolism by CYP2C9.	Carbamazepine	52-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	178-184
9531525-7	1998	Ketoconazole (5 microM), a selective CYP3A inhibitor, produced up to 75% inhibition, whereas other CYP-specific inhibitors, i.e. quinidine (CYP2D6), 7,8-benzoflavone (CYP1A2), and sulfaphenazole (CYP2C9), showed no significant effects.	Ketoconazole	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
9531513-7	1998	Microsomes from cells overexpressing CYP2D6 formed 5-HM, whereas N-dealkylated tolterodine was formed by microsomes expressing CYP2C9, -2C19, and -3A4.	Tolterodine Tartrate	79-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-133
9531513-8	1998	The Km for formation of N-dealkylated tolterodine by CYP3A4 was similar to that obtained in human liver microsomes and higher for CYP2C9 and -2C19.	Nitrogen	24-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-146
9531513-8	1998	The Km for formation of N-dealkylated tolterodine by CYP3A4 was similar to that obtained in human liver microsomes and higher for CYP2C9 and -2C19.	Tolterodine Tartrate	38-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-146
9615477-1	1998	The 4"-hydroxylated metabolite of diclofenac was produced by biocatalysis for probing specific human drug-metabolising enzymes (CYP2C9).	Diclofenac	34-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
9530332-5	1998	Deleted chromatin at the distal breakpoint includes the cytochrome P450IIC (CYP2C) gene cluster, thought to be involved in steroid hormone metabolism and therefore of possible significance to the growth rate of this androgen-dependent cell line.	Steroids	123-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-81
9584328-7	1998	CYP1A1/2-, CYP2A6-, CYP2C9- and CYP2E1-associated activities were inhibited less potently or not at all by oxybutynin when compared with reference inhibitors.	oxybutynin	107-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
9521735-3	1998	Sigmoidal kinetic characteristics were observed for carbamazepine metabolism by CYP3A4 and naphthalene metabolism by CYPs 2B6, 2C8, 2C9, and 3A5 as well as dapsone metabolism by CYP2C9.	Dapsone	156-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	178-184
9521735-4	1998	Naphthalene metabolism by CYP3A4 and naproxen metabolism by CYP2C9 demonstrated nonhyperbolic enzyme kinetics suggestive of a low Km, low Vmax component for the first substrate molecule and a high Km, high Vmax component for the second substrate molecule.	naphthalene	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
9521735-4	1998	Naphthalene metabolism by CYP3A4 and naproxen metabolism by CYP2C9 demonstrated nonhyperbolic enzyme kinetics suggestive of a low Km, low Vmax component for the first substrate molecule and a high Km, high Vmax component for the second substrate molecule.	Naproxen	37-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
9521735-5	1998	7, 8-Benzoflavone activation of phenanthrene metabolism by CYP3A4 and dapsone activation of flurbiprofen and naproxen metabolism by CYP2C9 were also observed.	alpha-naphthoflavone	0-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
9521735-5	1998	7, 8-Benzoflavone activation of phenanthrene metabolism by CYP3A4 and dapsone activation of flurbiprofen and naproxen metabolism by CYP2C9 were also observed.	phenanthrene	32-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
9521735-5	1998	7, 8-Benzoflavone activation of phenanthrene metabolism by CYP3A4 and dapsone activation of flurbiprofen and naproxen metabolism by CYP2C9 were also observed.	Dapsone	70-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
9521735-5	1998	7, 8-Benzoflavone activation of phenanthrene metabolism by CYP3A4 and dapsone activation of flurbiprofen and naproxen metabolism by CYP2C9 were also observed.	Flurbiprofen	92-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
9521735-5	1998	7, 8-Benzoflavone activation of phenanthrene metabolism by CYP3A4 and dapsone activation of flurbiprofen and naproxen metabolism by CYP2C9 were also observed.	Naproxen	109-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
9534880-0	1998	Hepatic cytochrome P450 CYP2C activity in psoriasis: studies using proguanil as a probe compound.	Proguanil	67-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-29
9586947-8	1998	Upon reconstitution, human liver b5 plus NADH:b5 reductase and CYP2C9 plus NADPH:P450 reductase were both effective catalysts of AZT reduction, which was also supported when CYP2A6 or CYP2E1 was substituted for CYP2C9.	NAD	41-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	211-217
9586947-8	1998	Upon reconstitution, human liver b5 plus NADH:b5 reductase and CYP2C9 plus NADPH:P450 reductase were both effective catalysts of AZT reduction, which was also supported when CYP2A6 or CYP2E1 was substituted for CYP2C9.	Zidovudine	129-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
9586947-8	1998	Upon reconstitution, human liver b5 plus NADH:b5 reductase and CYP2C9 plus NADPH:P450 reductase were both effective catalysts of AZT reduction, which was also supported when CYP2A6 or CYP2E1 was substituted for CYP2C9.	Zidovudine	129-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	211-217
9534880-3	1998	We used proguanil as a probe to study CYP2C activity, and by implication retinol metabolism, in psoriasis.	Proguanil	8-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-43
9542475-1	1998	BACKGROUND: Losartan is metabolized by CYP2C9 and CYP3A4 to an active metabolite, E3174, which has greater antihypertensive activity than the parent compound.	Losartan	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
9549640-4	1998	Ritonavir had high inhibition potency against cytochrome P450-2C9 (tolbutamide hydroxylation), -2C19 (S-mephenytoin hydroxylation), and -2D6 (dextromethorphan O-demethylation and desipramine hydroxylation), while the other protease inhibitors had one or more orders of magnitude lower inhibitory activity against these reactions.	Ritonavir	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-65
9542475-1	1998	BACKGROUND: Losartan is metabolized by CYP2C9 and CYP3A4 to an active metabolite, E3174, which has greater antihypertensive activity than the parent compound.	losartan carboxylic acid	82-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
9542475-13	1998	Further studies are needed to define the contribution of other isozymes, particularly CYP2C9, to the pharmacokinetics of losartan and E3174.	Losartan	121-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
9542475-13	1998	Further studies are needed to define the contribution of other isozymes, particularly CYP2C9, to the pharmacokinetics of losartan and E3174.	losartan carboxylic acid	134-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
9549641-7	1998	The CYP 1A2 inhibitor alpha-naphthoflavone and the CYP 2C9 inhibitor sulfaphenazole produced much less inhibition of amitriptyline N-demethylation at both substrate concentrations.	Sulfaphenazole	69-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-58
9492390-0	1998	Cytochrome P450 2C9 catalyzes indomethacin O-demethylation in human liver microsomes.	Indomethacin	30-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
9492390-6	1998	When the capacity for indomethacin O-demethylation in microsomes of B lymphoblastoid cells expressing human CYPs was investigated at an indomethacin concentration of 5 microM, cDNA-expressed CYP2C9 exhibited 6-fold greater activity than did CYP2C19.	Indomethacin	22-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
9492390-6	1998	When the capacity for indomethacin O-demethylation in microsomes of B lymphoblastoid cells expressing human CYPs was investigated at an indomethacin concentration of 5 microM, cDNA-expressed CYP2C9 exhibited 6-fold greater activity than did CYP2C19.	Indomethacin	136-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
9492390-9	1998	Considering the 16-fold higher intrinsic clearance of CYP2C9, compared with that of CYP2C19, and these expression levels in human livers, the contribution of CYP2C19 to indomethacin O-demethylation was considered to be negligible.	Indomethacin	169-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
9492390-10	1998	Indomethacin appears to be O-demethylated exclusively by CYP2C9 in humans.	Indomethacin	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
9491822-5	1998	RESULTS: Furafylline was a potent, selective inhibitor of phenacetin O-deethylation (CYP1A2-mediated) in human liver microsomes (IC50 = 0.48 microM), but inhibited both phenacetin O-deethylation and tolbutamide 4-hydroxylation (CYP2C9-mediated) at equimolar concentrations in rat liver microsomes (IC50 = 20.8 and 24.0 microM respectively).	furafylline	9-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	228-234
9551703-1	1998	OBJECTIVE: Losartan is metabolised to its active metabolite E-3174 by CYP2C9 and CYP3A4 in vitro.	Losartan	11-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
9551703-1	1998	OBJECTIVE: Losartan is metabolised to its active metabolite E-3174 by CYP2C9 and CYP3A4 in vitro.	losartan carboxylic acid	60-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
9551703-2	1998	Itraconazole is an inhibitor of CYP3A4, whereas fluconazole affects CYP2C9 more than CYP3A4.	Fluconazole	48-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
9551703-13	1998	This implicates that, in man, CYP2C9 is a major enzyme for the formation of E-3174 from losartan.	losartan carboxylic acid	76-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
9551703-13	1998	This implicates that, in man, CYP2C9 is a major enzyme for the formation of E-3174 from losartan.	Losartan	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
9435160-3	1998	CYP1A2, CYP2C8, CYP2C9, CYP2C19 and CYP3A4 converted [14C]linoleic acid to 14C-labeled 11-hydroxyoctadecadienoic acid (11-HODE), whereas [14C]arachidonic acid was oxygenated by CYP1A2 and CYP3A4 to 14C-labeled 13-hydroxyeicosatrienoic acid (13-HETE), 10-HETE and 7-HETE as determined by HPLC.	Carbon-14	75-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
9522436-5	1998	Humans with the Cys allele CYP2C9 variant, which was detected in 22% of Caucasians, were found to have similar catalytic rates to those of the wild-type in the oxidations of tolbutamide and racemic warfarin, whereas humans with the Leu allele, which was detected in 8% Japanese and 7% Caucasian samples, had lower catalytic rates than those of other two groups.	Cysteine	16-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
9522436-5	1998	Humans with the Cys allele CYP2C9 variant, which was detected in 22% of Caucasians, were found to have similar catalytic rates to those of the wild-type in the oxidations of tolbutamide and racemic warfarin, whereas humans with the Leu allele, which was detected in 8% Japanese and 7% Caucasian samples, had lower catalytic rates than those of other two groups.	Tolbutamide	174-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
9522436-5	1998	Humans with the Cys allele CYP2C9 variant, which was detected in 22% of Caucasians, were found to have similar catalytic rates to those of the wild-type in the oxidations of tolbutamide and racemic warfarin, whereas humans with the Leu allele, which was detected in 8% Japanese and 7% Caucasian samples, had lower catalytic rates than those of other two groups.	Warfarin	198-206	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
9522436-5	1998	Humans with the Cys allele CYP2C9 variant, which was detected in 22% of Caucasians, were found to have similar catalytic rates to those of the wild-type in the oxidations of tolbutamide and racemic warfarin, whereas humans with the Leu allele, which was detected in 8% Japanese and 7% Caucasian samples, had lower catalytic rates than those of other two groups.	Leucine	232-235	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
9522436-9	1998	Both human liver microsomes and recombinant CYP2C9 catalysed 7-hydroxylation of S-warfarin more extensively than those of R-warfarin.	Warfarin	80-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
9522436-11	1998	Anti-CYP2C9 antibodies and sulphaphenazole inhibited the 6- and 7-hydroxylation of S-warfarin, but not R-warfarin, by &gt; 90% and the methyl hydroxylation of tolbutamide by about 50%.	Warfarin	83-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	5-11
9522436-11	1998	Anti-CYP2C9 antibodies and sulphaphenazole inhibited the 6- and 7-hydroxylation of S-warfarin, but not R-warfarin, by &gt; 90% and the methyl hydroxylation of tolbutamide by about 50%.	Tolbutamide	159-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	5-11
9522436-13	1998	These results suggest that humans with Leu allele of CYP2C9 have lower Vmax"s for S-warfarin 7-hydroxylation and tolbutamide methyl hydroxylation than those with wild-type and Cys allele CYP2C9, although the K(m)"s are not very different in liver microsomes of these three groups of humans.	Leucine	39-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
9522436-13	1998	These results suggest that humans with Leu allele of CYP2C9 have lower Vmax"s for S-warfarin 7-hydroxylation and tolbutamide methyl hydroxylation than those with wild-type and Cys allele CYP2C9, although the K(m)"s are not very different in liver microsomes of these three groups of humans.	Leucine	39-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	187-193
9522436-13	1998	These results suggest that humans with Leu allele of CYP2C9 have lower Vmax"s for S-warfarin 7-hydroxylation and tolbutamide methyl hydroxylation than those with wild-type and Cys allele CYP2C9, although the K(m)"s are not very different in liver microsomes of these three groups of humans.	Warfarin	82-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
9522436-13	1998	These results suggest that humans with Leu allele of CYP2C9 have lower Vmax"s for S-warfarin 7-hydroxylation and tolbutamide methyl hydroxylation than those with wild-type and Cys allele CYP2C9, although the K(m)"s are not very different in liver microsomes of these three groups of humans.	Warfarin	82-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	187-193
9522436-13	1998	These results suggest that humans with Leu allele of CYP2C9 have lower Vmax"s for S-warfarin 7-hydroxylation and tolbutamide methyl hydroxylation than those with wild-type and Cys allele CYP2C9, although the K(m)"s are not very different in liver microsomes of these three groups of humans.	Tolbutamide	113-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
9522436-13	1998	These results suggest that humans with Leu allele of CYP2C9 have lower Vmax"s for S-warfarin 7-hydroxylation and tolbutamide methyl hydroxylation than those with wild-type and Cys allele CYP2C9, although the K(m)"s are not very different in liver microsomes of these three groups of humans.	Cysteine	176-179	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
9522436-14	1998	R-warfarin hydroxylation may be catalysed by P450 enzymes other than CYP2C9 in man.	Warfarin	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
9435160-3	1998	CYP1A2, CYP2C8, CYP2C9, CYP2C19 and CYP3A4 converted [14C]linoleic acid to 14C-labeled 11-hydroxyoctadecadienoic acid (11-HODE), whereas [14C]arachidonic acid was oxygenated by CYP1A2 and CYP3A4 to 14C-labeled 13-hydroxyeicosatrienoic acid (13-HETE), 10-HETE and 7-HETE as determined by HPLC.	Carbon-14	54-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
9435160-3	1998	CYP1A2, CYP2C8, CYP2C9, CYP2C19 and CYP3A4 converted [14C]linoleic acid to 14C-labeled 11-hydroxyoctadecadienoic acid (11-HODE), whereas [14C]arachidonic acid was oxygenated by CYP1A2 and CYP3A4 to 14C-labeled 13-hydroxyeicosatrienoic acid (13-HETE), 10-HETE and 7-HETE as determined by HPLC.	Linoleic Acid	58-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
9435160-3	1998	CYP1A2, CYP2C8, CYP2C9, CYP2C19 and CYP3A4 converted [14C]linoleic acid to 14C-labeled 11-hydroxyoctadecadienoic acid (11-HODE), whereas [14C]arachidonic acid was oxygenated by CYP1A2 and CYP3A4 to 14C-labeled 13-hydroxyeicosatrienoic acid (13-HETE), 10-HETE and 7-HETE as determined by HPLC.	Carbon-14	54-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
9435160-3	1998	CYP1A2, CYP2C8, CYP2C9, CYP2C19 and CYP3A4 converted [14C]linoleic acid to 14C-labeled 11-hydroxyoctadecadienoic acid (11-HODE), whereas [14C]arachidonic acid was oxygenated by CYP1A2 and CYP3A4 to 14C-labeled 13-hydroxyeicosatrienoic acid (13-HETE), 10-HETE and 7-HETE as determined by HPLC.	11-hydroxyoctadecadienoic acid	87-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
9435160-3	1998	CYP1A2, CYP2C8, CYP2C9, CYP2C19 and CYP3A4 converted [14C]linoleic acid to 14C-labeled 11-hydroxyoctadecadienoic acid (11-HODE), whereas [14C]arachidonic acid was oxygenated by CYP1A2 and CYP3A4 to 14C-labeled 13-hydroxyeicosatrienoic acid (13-HETE), 10-HETE and 7-HETE as determined by HPLC.	11-hydroxy-9,12-octadecadienoic acid	119-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
9435160-3	1998	CYP1A2, CYP2C8, CYP2C9, CYP2C19 and CYP3A4 converted [14C]linoleic acid to 14C-labeled 11-hydroxyoctadecadienoic acid (11-HODE), whereas [14C]arachidonic acid was oxygenated by CYP1A2 and CYP3A4 to 14C-labeled 13-hydroxyeicosatrienoic acid (13-HETE), 10-HETE and 7-HETE as determined by HPLC.	Arachidonic Acid	142-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
9435160-3	1998	CYP1A2, CYP2C8, CYP2C9, CYP2C19 and CYP3A4 converted [14C]linoleic acid to 14C-labeled 11-hydroxyoctadecadienoic acid (11-HODE), whereas [14C]arachidonic acid was oxygenated by CYP1A2 and CYP3A4 to 14C-labeled 13-hydroxyeicosatrienoic acid (13-HETE), 10-HETE and 7-HETE as determined by HPLC.	Carbon-14	75-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
9435160-3	1998	CYP1A2, CYP2C8, CYP2C9, CYP2C19 and CYP3A4 converted [14C]linoleic acid to 14C-labeled 11-hydroxyoctadecadienoic acid (11-HODE), whereas [14C]arachidonic acid was oxygenated by CYP1A2 and CYP3A4 to 14C-labeled 13-hydroxyeicosatrienoic acid (13-HETE), 10-HETE and 7-HETE as determined by HPLC.	13-hydroxyeicosatrienoic acid	210-239	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
9435160-3	1998	CYP1A2, CYP2C8, CYP2C9, CYP2C19 and CYP3A4 converted [14C]linoleic acid to 14C-labeled 11-hydroxyoctadecadienoic acid (11-HODE), whereas [14C]arachidonic acid was oxygenated by CYP1A2 and CYP3A4 to 14C-labeled 13-hydroxyeicosatrienoic acid (13-HETE), 10-HETE and 7-HETE as determined by HPLC.	13-Hete	241-248	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
9435160-3	1998	CYP1A2, CYP2C8, CYP2C9, CYP2C19 and CYP3A4 converted [14C]linoleic acid to 14C-labeled 11-hydroxyoctadecadienoic acid (11-HODE), whereas [14C]arachidonic acid was oxygenated by CYP1A2 and CYP3A4 to 14C-labeled 13-hydroxyeicosatrienoic acid (13-HETE), 10-HETE and 7-HETE as determined by HPLC.	10-hydroxyeicosatetraenoic acid	251-258	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
9435160-3	1998	CYP1A2, CYP2C8, CYP2C9, CYP2C19 and CYP3A4 converted [14C]linoleic acid to 14C-labeled 11-hydroxyoctadecadienoic acid (11-HODE), whereas [14C]arachidonic acid was oxygenated by CYP1A2 and CYP3A4 to 14C-labeled 13-hydroxyeicosatrienoic acid (13-HETE), 10-HETE and 7-HETE as determined by HPLC.	7-hydroxyeicosatetraenoic acid	263-269	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
9435160-5	1998	CYP2C9 appeared to form 12R-HETE and 13-HETE, whereas CYP2C8 formed 13-HETE, 11-HETE and 15-HETE as main monohydroxy metabolites.	13-Hete	37-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
9435160-5	1998	CYP2C9 appeared to form 12R-HETE and 13-HETE, whereas CYP2C8 formed 13-HETE, 11-HETE and 15-HETE as main monohydroxy metabolites.	Hydroxyeicosatetraenoic Acids	27-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
9416970-4	1997	Anti-CYP2C9 antibodies inhibited completely the 7-hydroxylation of S-warfarin, but not R-warfarin, catalyzed by human liver microsomes, while anti-CYP1A2 inhibited R-warfarin 7-hydroxylation by about 70%.	Warfarin	67-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	5-11
9493314-8	1998	CYP2C9 and, to a much lesser extent, CYP3A4 were found to convert ME to M7.	Meloxicam	66-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
9416970-7	1997	These results suggest that R- and S-warfarin enantiomers are catalyzed principally by CYP1A2 and CYP2C9, respectively, in human liver microsomes, and that the pharmacokinetic properties of S-warfarin may be altered by R-warfarin in vivo when racemic warfarin is administered clinically to humans.	Warfarin	36-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
14577221-0	1998	Determination of CYP2C9-catalyzed diclofenac 4"-hydroxylation by high-performance liquid chromatography.	diclofenac 4"	34-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
9416970-5	1997	Interestingly, the racemic warfarin 7-hydroxylation activities (turnover numbers of 1.6 +/- 1.0 pmol/min/mg protein in 35 human samples) were found to be low compared with the S-warfarin 7-hydroxylation activities (4.1 +/- 2.5 pmol/min/mg protein), indicating that R-warfarin may have affected the CYP2C9-dependent S-warfarin 7-hydroxylation activities when racemic warfarin was used as a substrate.	Warfarin	27-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	298-304
9416970-7	1997	These results suggest that R- and S-warfarin enantiomers are catalyzed principally by CYP1A2 and CYP2C9, respectively, in human liver microsomes, and that the pharmacokinetic properties of S-warfarin may be altered by R-warfarin in vivo when racemic warfarin is administered clinically to humans.	Warfarin	34-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
9416970-7	1997	These results suggest that R- and S-warfarin enantiomers are catalyzed principally by CYP1A2 and CYP2C9, respectively, in human liver microsomes, and that the pharmacokinetic properties of S-warfarin may be altered by R-warfarin in vivo when racemic warfarin is administered clinically to humans.	Warfarin	218-228	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
9431831-7	1997	Ketoconazole, an inhibitor of CYP3A4, inhibited competitively CPHP formation (Ki=0.1 microM), whereas sulphaphenazole (CYP2C9), furafylline (CYP1A2) and quinidine (CYP2D6) gave only little inhibition (IC50 &gt; 100 microM).	Sulfaphenazole	102-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
9431831-11	1997	HAL inhibited dextromethorphan O-demethylase (CYP2D6) with IC50 values between 2.7 and 8.5 microM, but not (IC50 &gt; 100 microM) dextromethorphan N-demethylase (CYP3A4), phenacetin O-deethylase (CYP1A2) or tolbutamide hydroxylase (CYP2C9).	Haloperidol	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	232-238
9384467-6	1997	Thus, assuming comparable molar concentrations at the site of inhibition, fluvoxamine can be expected to have the highest probability of interfering with the metabolism of CYP2C9 substrates.	Fluvoxamine	74-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
9429229-3	1997	Similarly, the hydroxylation of tolbutamide, a marker for CYP2C9 was undetected in fetal liver microsomes and rose in the first month after birth.	Tolbutamide	32-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
9429229-4	1997	In adult liver preparations, the hydroxylation of diazepam correlated well with the CYP3 A content of microsomes (r = 0.858, p &lt; 0.01) and with the 6 beta hydroxylation of testosterone (r = 0.830, p &lt; 0.005), whereas demethylation was related to the bulk of CYP2C proteins (r = 0.865, p &lt; 0.005).	Diazepam	50-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	264-269
9429229-7	1997	In newborns, barbiturates and to a lesser extent steroids, acted as inducers of CYP2C isoforms and increased tolbutamide hydroxylation, diazepam demethylation and diazepam hydroxylation by 2 to 10-fold.	Barbiturates	13-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-85
9429229-7	1997	In newborns, barbiturates and to a lesser extent steroids, acted as inducers of CYP2C isoforms and increased tolbutamide hydroxylation, diazepam demethylation and diazepam hydroxylation by 2 to 10-fold.	Steroids	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-85
9526963-0	1997	Warfarin analog inhibition of human CYP2C9-catalyzed S-warfarin 7-hydroxylation.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
9526963-0	1997	Warfarin analog inhibition of human CYP2C9-catalyzed S-warfarin 7-hydroxylation.	Warfarin	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
9526963-1	1997	Human metabolism of the S-warfarin enantiomer is catalyzed primarily by cytochrome P4502C9 (CYP2C9), which, because of the enzyme"s broad drug substrate specificity, leads to drug-S-warfarin interactions.	Warfarin	26-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
9526963-1	1997	Human metabolism of the S-warfarin enantiomer is catalyzed primarily by cytochrome P4502C9 (CYP2C9), which, because of the enzyme"s broad drug substrate specificity, leads to drug-S-warfarin interactions.	Warfarin	182-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
9526963-2	1997	Several warfarin analogs have been synthesized and used to determine whether they exhibit diminished interactions with CYP2C9.	Warfarin	8-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
9526963-3	1997	The kinetics of the warfarin analogs" inhibition of human liver microsomal CYP2C9 catalyzed metabolism of S-warfarin to S-7-hydroxywarfarin have been investigated.	Warfarin	20-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
9526963-3	1997	The kinetics of the warfarin analogs" inhibition of human liver microsomal CYP2C9 catalyzed metabolism of S-warfarin to S-7-hydroxywarfarin have been investigated.	Warfarin	106-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
9526963-3	1997	The kinetics of the warfarin analogs" inhibition of human liver microsomal CYP2C9 catalyzed metabolism of S-warfarin to S-7-hydroxywarfarin have been investigated.	7-hydroxywarfarin	120-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
9526963-6	1997	The fluorine substituted warfarins and the S-warfarin alcohol apparently bind with high affinity to CYP2C9.	Fluorine	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
9526963-6	1997	The fluorine substituted warfarins and the S-warfarin alcohol apparently bind with high affinity to CYP2C9.	Warfarin	25-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
9526963-6	1997	The fluorine substituted warfarins and the S-warfarin alcohol apparently bind with high affinity to CYP2C9.	Sulfur	43-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
9526963-6	1997	The fluorine substituted warfarins and the S-warfarin alcohol apparently bind with high affinity to CYP2C9.	6-hydroxywarfarin	45-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
9526963-8	1997	The R-warfarin alcohol did not inhibit CYP2C9 catalyzed metabolism of S-warfarin and is less likely than warfarin to participate in CYP2C9 associated warfarin-drug interactions.	r-warfarin alcohol	4-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
9526963-8	1997	The R-warfarin alcohol did not inhibit CYP2C9 catalyzed metabolism of S-warfarin and is less likely than warfarin to participate in CYP2C9 associated warfarin-drug interactions.	Warfarin	6-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
9384467-7	1997	S-fluoxetine is on average a 5 fold weaker CYP2C9 inhibitor than either R-fluoxetine or the racemic mixture.	Fluoxetine	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
9353388-0	1997	Human CYP2C9 and CYP2A6 mediate formation of the hepatotoxin 4-ene-valproic acid.	2-propyl-4-pentenoic acid	61-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
9390115-5	1997	The influence of ticlopidine on CYP2C9, the other cytochrome P450 isoform that metabolizes phenytoin, is relatively weak, with a calculated Ki of 38.8 +/- 27 mumol/L.	Ticlopidine	17-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
9390115-5	1997	The influence of ticlopidine on CYP2C9, the other cytochrome P450 isoform that metabolizes phenytoin, is relatively weak, with a calculated Ki of 38.8 +/- 27 mumol/L.	Phenytoin	91-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
9353355-5	1997	Omeprazole 5-hydroxylation by liver microsomes of a human sample that contained relatively high levels of CYP3A4 and low levels of CYP2C19 were inhibited very significantly by ketoconazole and anti-CYP3A4 antibodies, although a human sample having high in CYP2C19 and low in CYP3A4 was found to be sensitive toward fluvoxamine and anti-CYP2C9 antibodies.	Omeprazole	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	336-342
9353355-5	1997	Omeprazole 5-hydroxylation by liver microsomes of a human sample that contained relatively high levels of CYP3A4 and low levels of CYP2C19 were inhibited very significantly by ketoconazole and anti-CYP3A4 antibodies, although a human sample having high in CYP2C19 and low in CYP3A4 was found to be sensitive toward fluvoxamine and anti-CYP2C9 antibodies.	Ketoconazole	176-188	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	336-342
9335524-1	1997	Purified recombinant human liver cytochrome P450 2C9 was produced, from expression of the corresponding cDNA in yeast, in quantities large enough for UV-visible and 1H NMR experiments.	Hydrogen	165-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-52
9335524-4	1997	On the contrary, sulfaphenazole led to a low-spin (S = 1/2) CYP 2C9 complex upon binding of its NH2 group to CYP 2C9 iron.	Sulfaphenazole	17-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-67
9335524-4	1997	On the contrary, sulfaphenazole led to a low-spin (S = 1/2) CYP 2C9 complex upon binding of its NH2 group to CYP 2C9 iron.	Sulfaphenazole	17-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-116
9335524-4	1997	On the contrary, sulfaphenazole led to a low-spin (S = 1/2) CYP 2C9 complex upon binding of its NH2 group to CYP 2C9 iron.	Iron	117-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-67
9335524-4	1997	On the contrary, sulfaphenazole led to a low-spin (S = 1/2) CYP 2C9 complex upon binding of its NH2 group to CYP 2C9 iron.	Iron	117-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-116
9335524-5	1997	Interactions of the five substrates with the enzyme were studied by paramagnetic relaxation effects of CYP 2C9-iron(III) on the 1H NMR spectrum of each substrate.	Iron	111-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-110
9335524-5	1997	Interactions of the five substrates with the enzyme were studied by paramagnetic relaxation effects of CYP 2C9-iron(III) on the 1H NMR spectrum of each substrate.	Hydrogen	128-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-110
9335524-7	1997	Finally, a model for substrate positioning in the CYP 2C9 active site was constructed by molecular modeling studies under the constraint of the iron-proton distances.	Iron	144-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-57
9335524-9	1997	Sulfaphenazole was easily included in that model; its very high affinity for CYP 2C9 is due to a third structural feature, the presence of its NH2 function which binds to CYP 2C9 iron.	Sulfaphenazole	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-84
9335524-9	1997	Sulfaphenazole was easily included in that model; its very high affinity for CYP 2C9 is due to a third structural feature, the presence of its NH2 function which binds to CYP 2C9 iron.	Sulfaphenazole	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-178
9335524-9	1997	Sulfaphenazole was easily included in that model; its very high affinity for CYP 2C9 is due to a third structural feature, the presence of its NH2 function which binds to CYP 2C9 iron.	Iron	179-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-84
9335524-9	1997	Sulfaphenazole was easily included in that model; its very high affinity for CYP 2C9 is due to a third structural feature, the presence of its NH2 function which binds to CYP 2C9 iron.	Iron	179-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-178
9328296-3	1997	These steroid chemicals also inhibited CYP2C9-dependent S-warfarin 7-hydroxylation activities though lesser extents seen with those in CYP2C19 enzyme.	Steroids	6-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
9328296-3	1997	These steroid chemicals also inhibited CYP2C9-dependent S-warfarin 7-hydroxylation activities though lesser extents seen with those in CYP2C19 enzyme.	Warfarin	58-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
9328296-4	1997	Progesterone was found to be a competitive inhibitor of CYP2C19 and CYP2C9 in human liver microsomes.	Progesterone	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
9328296-6	1997	CYP2C9 also had progesterone 21-hydroxylation activities, although the activities were lower than those catalyzed by CYP2C19.	Progesterone	16-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
9328296-9	1997	Immunoinhibition experiments suggested that anti-CYP2C9 (which inhibits both CYP2C9 and CYP2C19 catalytic activities) suppressed the progesterone 21-hydroxylation activities catalyzed by liver microsomes of humans and monkeys and that anti-CYP2C11 inhibited the progesterone 21-hydroxylation activities catalyzed by liver microsomes of male rats.	Progesterone	133-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
9328296-9	1997	Immunoinhibition experiments suggested that anti-CYP2C9 (which inhibits both CYP2C9 and CYP2C19 catalytic activities) suppressed the progesterone 21-hydroxylation activities catalyzed by liver microsomes of humans and monkeys and that anti-CYP2C11 inhibited the progesterone 21-hydroxylation activities catalyzed by liver microsomes of male rats.	Progesterone	133-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
9328296-9	1997	Immunoinhibition experiments suggested that anti-CYP2C9 (which inhibits both CYP2C9 and CYP2C19 catalytic activities) suppressed the progesterone 21-hydroxylation activities catalyzed by liver microsomes of humans and monkeys and that anti-CYP2C11 inhibited the progesterone 21-hydroxylation activities catalyzed by liver microsomes of male rats.	Progesterone	262-274	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
9328296-9	1997	Immunoinhibition experiments suggested that anti-CYP2C9 (which inhibits both CYP2C9 and CYP2C19 catalytic activities) suppressed the progesterone 21-hydroxylation activities catalyzed by liver microsomes of humans and monkeys and that anti-CYP2C11 inhibited the progesterone 21-hydroxylation activities catalyzed by liver microsomes of male rats.	Progesterone	262-274	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
9328296-11	1997	Androstenedione formation catalyzed by liver microsomes of humans and monkeys and of male rats was suppressed by anti-CYP2C9 and anti-CYP2C11, respectively.	Androstenedione	0-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
9328296-13	1997	CYP2C9 may have some, but lesser extent than those by CYP2C19, of the catalytic roles for the metabolism of progesterone and testosterone by human liver microsomes.	Progesterone	108-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
9328296-13	1997	CYP2C9 may have some, but lesser extent than those by CYP2C19, of the catalytic roles for the metabolism of progesterone and testosterone by human liver microsomes.	Testosterone	125-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
9352571-0	1997	Genetic association between sensitivity to warfarin and expression of CYP2C9*3.	Warfarin	43-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
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.	4-hydroxycyclophosphamide	194-197	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
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
9352571-1	1997	Cytochrome P4502C9 (CYP2C9) is largely responsible for terminating the anticoagulant effect of racemic warfarin via hydroxylation of the pharmacologically more potent S-enantiomer to inactive metabolites.	Warfarin	103-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-18
9352571-1	1997	Cytochrome P4502C9 (CYP2C9) is largely responsible for terminating the anticoagulant effect of racemic warfarin via hydroxylation of the pharmacologically more potent S-enantiomer to inactive metabolites.	Warfarin	103-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
9352571-9	1997	Therefore, expression of CYP2C9*3 is associated with diminished clearance of S-warfarin and a dangerously exacerbated therapeutic response to normal doses of the racemic drug.	Sulfur	77-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
9352571-9	1997	Therefore, expression of CYP2C9*3 is associated with diminished clearance of S-warfarin and a dangerously exacerbated therapeutic response to normal doses of the racemic drug.	Warfarin	79-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
9298519-8	1997	Cytochrome P450-2C9 appears to be the principal human cytochrome mediating fluoxetine N-demethylation.	Fluoxetine	75-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
9333104-1	1997	OBJECTIVE: To examine the genetic polymorphism of CYP2C9 and CYP2C19 and its effect on the pharmacokinetics of phenytoin among 44 Japanese patients with epilepsy.	Phenytoin	111-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
9278209-11	1997	Saquinavir was the least potent CYP3A4 inhibitor (K(i) = 2.99 +/- 0.87 microM) and produced some inhibition of CYP2C9 (approximately 50% at 50 microM).	Saquinavir	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
9278209-1	1997	AIMS: To compare the inhibitory potential of the HIV protease inhibitors saquinavir, ritonavir and indinavir against CYP1A2, CYP2C9, CYP2E1 and CYP3A4 catalysed metabolic reactions in human liver microsomes in vitro.	Saquinavir	73-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
9278209-1	1997	AIMS: To compare the inhibitory potential of the HIV protease inhibitors saquinavir, ritonavir and indinavir against CYP1A2, CYP2C9, CYP2E1 and CYP3A4 catalysed metabolic reactions in human liver microsomes in vitro.	Ritonavir	85-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
9278209-1	1997	AIMS: To compare the inhibitory potential of the HIV protease inhibitors saquinavir, ritonavir and indinavir against CYP1A2, CYP2C9, CYP2E1 and CYP3A4 catalysed metabolic reactions in human liver microsomes in vitro.	Indinavir	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
9205822-0	1997	Venlafaxine: in vitro inhibition of CYP2D6 dependent imipramine and desipramine metabolism; comparative studies with selected SSRIs, and effects on human hepatic CYP3A4, CYP2C9 and CYP1A2.	Venlafaxine Hydrochloride	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-176
9224780-6	1997	Both drugs were competitive inhibitors of CYP2C9-catalyzed conversion of tolbutamide to 4-hydroxytolbutamide (K(i) = 40.1 +/- 14.8 microM for omeprazole, K(i) = 52.1 +/- 1.4 microM for lansoprazole) and were noncompetitive inhibitors of CYP3A-catalyzed conversion of dextromethorphan to 3-methoxymorphinan (K(i) = 84.4 +/- 4.0 microM for omeprazole, K(i) = 170.4 +/- 7.1 microM for lansoprazole).	Tolbutamide	73-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
9224780-6	1997	Both drugs were competitive inhibitors of CYP2C9-catalyzed conversion of tolbutamide to 4-hydroxytolbutamide (K(i) = 40.1 +/- 14.8 microM for omeprazole, K(i) = 52.1 +/- 1.4 microM for lansoprazole) and were noncompetitive inhibitors of CYP3A-catalyzed conversion of dextromethorphan to 3-methoxymorphinan (K(i) = 84.4 +/- 4.0 microM for omeprazole, K(i) = 170.4 +/- 7.1 microM for lansoprazole).	4'-hydroxytolbutamide	88-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
9224780-6	1997	Both drugs were competitive inhibitors of CYP2C9-catalyzed conversion of tolbutamide to 4-hydroxytolbutamide (K(i) = 40.1 +/- 14.8 microM for omeprazole, K(i) = 52.1 +/- 1.4 microM for lansoprazole) and were noncompetitive inhibitors of CYP3A-catalyzed conversion of dextromethorphan to 3-methoxymorphinan (K(i) = 84.4 +/- 4.0 microM for omeprazole, K(i) = 170.4 +/- 7.1 microM for lansoprazole).	Omeprazole	142-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
9224780-6	1997	Both drugs were competitive inhibitors of CYP2C9-catalyzed conversion of tolbutamide to 4-hydroxytolbutamide (K(i) = 40.1 +/- 14.8 microM for omeprazole, K(i) = 52.1 +/- 1.4 microM for lansoprazole) and were noncompetitive inhibitors of CYP3A-catalyzed conversion of dextromethorphan to 3-methoxymorphinan (K(i) = 84.4 +/- 4.0 microM for omeprazole, K(i) = 170.4 +/- 7.1 microM for lansoprazole).	Lansoprazole	185-197	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
9224780-6	1997	Both drugs were competitive inhibitors of CYP2C9-catalyzed conversion of tolbutamide to 4-hydroxytolbutamide (K(i) = 40.1 +/- 14.8 microM for omeprazole, K(i) = 52.1 +/- 1.4 microM for lansoprazole) and were noncompetitive inhibitors of CYP3A-catalyzed conversion of dextromethorphan to 3-methoxymorphinan (K(i) = 84.4 +/- 4.0 microM for omeprazole, K(i) = 170.4 +/- 7.1 microM for lansoprazole).	Dextromethorphan	267-283	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
9296349-5	1997	cDNA-expressed CYP2C9 (Arg 144 and Cys 144) favored S-2- and S-3-hydroxyibuprofen formation, but CYP2C8 favored R-2-hydroxyibuprofen formation.	Arginine	23-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
9296349-5	1997	cDNA-expressed CYP2C9 (Arg 144 and Cys 144) favored S-2- and S-3-hydroxyibuprofen formation, but CYP2C8 favored R-2-hydroxyibuprofen formation.	Cysteine	35-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
9296349-5	1997	cDNA-expressed CYP2C9 (Arg 144 and Cys 144) favored S-2- and S-3-hydroxyibuprofen formation, but CYP2C8 favored R-2-hydroxyibuprofen formation.	s-2- and s-3-hydroxyibuprofen	52-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
9296349-10	1997	The relative levels of both CYP2C8 and CYP2C9 and the expression of the corresponding variants may influence the disposition of ibuprofen in vivo.	Ibuprofen	128-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
9224780-6	1997	Both drugs were competitive inhibitors of CYP2C9-catalyzed conversion of tolbutamide to 4-hydroxytolbutamide (K(i) = 40.1 +/- 14.8 microM for omeprazole, K(i) = 52.1 +/- 1.4 microM for lansoprazole) and were noncompetitive inhibitors of CYP3A-catalyzed conversion of dextromethorphan to 3-methoxymorphinan (K(i) = 84.4 +/- 4.0 microM for omeprazole, K(i) = 170.4 +/- 7.1 microM for lansoprazole).	3-methoxymorphinan	287-305	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
9224780-6	1997	Both drugs were competitive inhibitors of CYP2C9-catalyzed conversion of tolbutamide to 4-hydroxytolbutamide (K(i) = 40.1 +/- 14.8 microM for omeprazole, K(i) = 52.1 +/- 1.4 microM for lansoprazole) and were noncompetitive inhibitors of CYP3A-catalyzed conversion of dextromethorphan to 3-methoxymorphinan (K(i) = 84.4 +/- 4.0 microM for omeprazole, K(i) = 170.4 +/- 7.1 microM for lansoprazole).	Omeprazole	338-348	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
9224780-6	1997	Both drugs were competitive inhibitors of CYP2C9-catalyzed conversion of tolbutamide to 4-hydroxytolbutamide (K(i) = 40.1 +/- 14.8 microM for omeprazole, K(i) = 52.1 +/- 1.4 microM for lansoprazole) and were noncompetitive inhibitors of CYP3A-catalyzed conversion of dextromethorphan to 3-methoxymorphinan (K(i) = 84.4 +/- 4.0 microM for omeprazole, K(i) = 170.4 +/- 7.1 microM for lansoprazole).	Lansoprazole	382-394	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
9223567-7	1997	CYP3A4 in lymphoblastoid cell microsomes catalyzed DTZ N-demethylation but CYP2C8 and CYP2C9 were also active (approximately 20% and 10% of the activity supported by CYP3A4); seven other CYPs produced little or no N-desmethyl DTZ from DTZ.	N-monodemethyldiltiazem	214-229	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
9186495-2	1997	CYP2C10 required cytochrome b5 (b5) for optimal rates of tolbutamide and S-warfarin oxidations and b5 could be replaced by apo-b5; apo-b5 and b5 effects on the reconstituted systems have already been reported in systems containing CYP3A4 for the oxidation of testosterone and nifedipine and for the rapid reduction of CYP3A4 by NADPH-P450 reductase (H. Yamazaki et al., 1996, J. Biol.	Tolbutamide	57-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-7
9186495-2	1997	CYP2C10 required cytochrome b5 (b5) for optimal rates of tolbutamide and S-warfarin oxidations and b5 could be replaced by apo-b5; apo-b5 and b5 effects on the reconstituted systems have already been reported in systems containing CYP3A4 for the oxidation of testosterone and nifedipine and for the rapid reduction of CYP3A4 by NADPH-P450 reductase (H. Yamazaki et al., 1996, J. Biol.	Warfarin	75-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-7
9186495-2	1997	CYP2C10 required cytochrome b5 (b5) for optimal rates of tolbutamide and S-warfarin oxidations and b5 could be replaced by apo-b5; apo-b5 and b5 effects on the reconstituted systems have already been reported in systems containing CYP3A4 for the oxidation of testosterone and nifedipine and for the rapid reduction of CYP3A4 by NADPH-P450 reductase (H. Yamazaki et al., 1996, J. Biol.	Testosterone	259-271	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-7
9186495-2	1997	CYP2C10 required cytochrome b5 (b5) for optimal rates of tolbutamide and S-warfarin oxidations and b5 could be replaced by apo-b5; apo-b5 and b5 effects on the reconstituted systems have already been reported in systems containing CYP3A4 for the oxidation of testosterone and nifedipine and for the rapid reduction of CYP3A4 by NADPH-P450 reductase (H. Yamazaki et al., 1996, J. Biol.	Nifedipine	276-286	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-7
9186495-8	1997	Interestingly, we found that testosterone 6 beta-hydroxylation by CYP3A4 was stimulated by CYP1A2 (and also by a modified form in which the first 36 residues of the native human protein were removed) and CYP1A1 as well as by b5, and such stimulations were not seen when other P450 proteins (e.g., CYP2C10, 2D6, or 2E1) were added to the reconstituted systems.	Testosterone	29-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	297-304
9205822-6	1997	Venlafaxine"s IC50 values for CYP3A4, CYP1A2 CYP2C9 were determined based on inhibition of probe substrate activities (testosterone 6 beta-hydroxylation, ethoxyresorufin O-dealkylase and tolbutamide 4-hydroxylation, respectively).	Venlafaxine Hydrochloride	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
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 9	Homo sapiens	307-313
9241660-6	1997	The rates of (S)-warfarin 7-hydroxylation by CYP2C9 and the R144C variant also exhibited differential dependence on salt concentration which further supported a difference in interaction with OR.	Warfarin	13-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
9157990-4	1997	These inductions were associated with corresponding increases in immunoreactive CYP2B6, CYP2C8, CYP2C9, and CYP3A4, all previously shown to catalyze oxazaphosphorine activation.	oxazaphosphorine	149-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
9241660-6	1997	The rates of (S)-warfarin 7-hydroxylation by CYP2C9 and the R144C variant also exhibited differential dependence on salt concentration which further supported a difference in interaction with OR.	Salts	116-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
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
9241661-0	1997	Identification of the polymorphically expressed CYP2C19 and the wild-type CYP2C9-ILE359 allele as low-Km catalysts of cyclophosphamide and ifosfamide activation.	Ifosfamide	139-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
9241661-3	1997	Recombinant CYP2C8, CYP2C19, two allelic variants of CYP2C18, and six variants of CYP2C9 expressed in a yeast cDNA expression system were each enzymatically active, as judged by the ability of the isolated microsomes to catalyse 7-ethoxycoumarin O-deethylation after reconstitution with purified NADPH-cytochrome P450 reductase and cytochrome b5.	3-ethoxychromen-2-one	231-245	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
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 &lt; CYP2C18 &lt; CYP2C9 &lt; 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 &lt; CYP2C18 &lt; CYP2C9 &lt; CYP2C8.	Cyclophosphamide	5-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
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 &lt; CYP2C18 &lt; CYP2C9 &lt; CYP2C8.	Ifosfamide	135-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
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.	Tolbutamide	105-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
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
9241661-7	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.	Ifosfamide	272-282	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
9241661-8	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.	Ifosfamide	158-168	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
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 9	Homo sapiens	31-37
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
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.	Ifosfamide	116-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
9089421-3	1997	Incubation of a fixed concentration of mestranol (3 mumol/L) with varying concentrations of CYP inhibitors revealed strong inhibition of ethinyl estradiol formation by sulfaphenazole, a specific CYP2C9 inhibitor, with an average inhibitor concentration at one half of Emax (IC50) of 3.6 mumol/L (range, 1.8-8.3 mumol/L) and an average maximal inhibitory capacity (Emax) of 75% (range, 60-91%).	Mestranol	39-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
9089421-8	1997	Strong inhibition of ethinyl estradiol formation by sulfaphenazole suggests a major contribution of CYP2C9 to this reaction.	Ethinyl Estradiol	21-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
9115051-14	1997	Clearances of the two NSAIDs were significantly correlated, suggesting that a common P450 isozyme (most likely CYP2C9, in that piroxicam is a known substrate of this isozyme) may be at least partly involved in the oxidative metabolism of these NSAIDs.	Piroxicam	127-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
9170147-0	1997	Relationship between CYP2C9 and 2C19 genotypes and tolbutamide methyl hydroxylation and S-mephenytoin 4"-hydroxylation activities in livers of Japanese and Caucasian populations.	Tolbutamide	51-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
9170147-10	1997	Good correlations were found between levels of CYP2C9 and activities of tolbutamide methyl hydroxylation (r = 0.77) and between levels of CYP2C19 and activities of S-mephenytoin 4"-hydroxylation (r = 0.86) in liver microsomes of the human samples examined.	Tolbutamide	72-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
9170147-11	1997	Tolbutamide methyl hydroxylation activities were lower in human samples with the Leu359 allele of CYP2C9 than those with the Cys144 allele and wild-type (Arg144-Ile359); the former type showed slightly higher K(m) values.	Tolbutamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
9172960-6	1997	In human liver microsomes, orphenadrine strongly decreased the marker activities of CYP2B6, CYP2D6, as well as CYP2C9; and partially decreased the marker activities of CYP1A2, CYP2A6, CYP3A4, and CYP2C19.	Orphenadrine	27-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
9172960-7	1997	In the competitive inhibition protocol, methimazole had no effect on the marker activities of CYP2E1 and CYP2A6; slightly decreased CYP2D6 marker activity; partially decreased the marker activities of CYP2C19, CYP2C9, and CYP2B6; and dramatically decreased CYP3A4 marker activity.	Methimazole	40-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	210-216
9089421-8	1997	Strong inhibition of ethinyl estradiol formation by sulfaphenazole suggests a major contribution of CYP2C9 to this reaction.	Sulfaphenazole	52-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
9089421-3	1997	Incubation of a fixed concentration of mestranol (3 mumol/L) with varying concentrations of CYP inhibitors revealed strong inhibition of ethinyl estradiol formation by sulfaphenazole, a specific CYP2C9 inhibitor, with an average inhibitor concentration at one half of Emax (IC50) of 3.6 mumol/L (range, 1.8-8.3 mumol/L) and an average maximal inhibitory capacity (Emax) of 75% (range, 60-91%).	Ethinyl Estradiol	137-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
9089421-3	1997	Incubation of a fixed concentration of mestranol (3 mumol/L) with varying concentrations of CYP inhibitors revealed strong inhibition of ethinyl estradiol formation by sulfaphenazole, a specific CYP2C9 inhibitor, with an average inhibitor concentration at one half of Emax (IC50) of 3.6 mumol/L (range, 1.8-8.3 mumol/L) and an average maximal inhibitory capacity (Emax) of 75% (range, 60-91%).	Sulfaphenazole	168-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
9089421-5	1997	alpha-Naphthoflavone (a CYP1A1/2 inhibitor only at concentrations &lt; 2 mumol/L and a CYP2C9 inhibitor at higher concentrations) had a weak inhibitory effect on ethinyl estradiol formation (&lt; 20% decrease in mestranol demethylation activity).	alpha-naphthoflavone	0-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
9089421-5	1997	alpha-Naphthoflavone (a CYP1A1/2 inhibitor only at concentrations &lt; 2 mumol/L and a CYP2C9 inhibitor at higher concentrations) had a weak inhibitory effect on ethinyl estradiol formation (&lt; 20% decrease in mestranol demethylation activity).	Ethinyl Estradiol	162-179	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
9131945-5	1997	A further decrease in activity was associated with the addition of the CYP2C9 inhibitor sulphaphenazole such that the residual kinetics were best described by a single Michaelis-Menten function.	Sulfaphenazole	88-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
9131945-9	1997	Microsomes from yeast cells expressing CYP2D6 and from human lymphoblastoid cells expressing CYP3A4 or CYP2C9-Arg N-demethylated AMI, but those from cells expressing CYPs 1A2 and 2C19 did not.	Arginine	110-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
9131945-9	1997	Microsomes from yeast cells expressing CYP2D6 and from human lymphoblastoid cells expressing CYP3A4 or CYP2C9-Arg N-demethylated AMI, but those from cells expressing CYPs 1A2 and 2C19 did not.	Nitrogen	114-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
9131945-9	1997	Microsomes from yeast cells expressing CYP2D6 and from human lymphoblastoid cells expressing CYP3A4 or CYP2C9-Arg N-demethylated AMI, but those from cells expressing CYPs 1A2 and 2C19 did not.	Amitriptyline	129-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
9068931-22	1997	Fluoxetine substantially inhibits CYP2D6 and probably CYP2C9/10, moderately inhibits CYP2C19 and mildly inhibits CYP3A3/4.	Fluoxetine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
9029042-6	1997	At a substrate concentration of 10 microM, diazepam N-demethylation in a panel of human liver microsomes was inhibited 42 +/- 12% (mean +/- SD, N = 6) by a polyclonal anti-CYP2C antibody.	Diazepam	43-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-177
9023313-12	1997	Testosterone 6beta-hydroxylation (mediated by CYP3A4), 7-ethylresorufin O-deethylation (CYP1A2) and tolbutamide methyl hydroxylation (CYP2C9/10), but not aniline 4-hydroxylation (CYP2E1), were inhibited effectively by parathion.	Testosterone	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
9023313-12	1997	Testosterone 6beta-hydroxylation (mediated by CYP3A4), 7-ethylresorufin O-deethylation (CYP1A2) and tolbutamide methyl hydroxylation (CYP2C9/10), but not aniline 4-hydroxylation (CYP2E1), were inhibited effectively by parathion.	aniline	154-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
9023313-12	1997	Testosterone 6beta-hydroxylation (mediated by CYP3A4), 7-ethylresorufin O-deethylation (CYP1A2) and tolbutamide methyl hydroxylation (CYP2C9/10), but not aniline 4-hydroxylation (CYP2E1), were inhibited effectively by parathion.	Parathion	218-227	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
9037249-6	1997	Inhibition of activity by quinidine (1 microM), sulphaphenazole (20 microM) and ketoconazole (2 microM), selective inhibitors of CYPs 2D6, 2C9 and 3A4, respectively, was 0-80%, 0-80% and 12-57%.	Quinidine	26-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-142
9037249-6	1997	Inhibition of activity by quinidine (1 microM), sulphaphenazole (20 microM) and ketoconazole (2 microM), selective inhibitors of CYPs 2D6, 2C9 and 3A4, respectively, was 0-80%, 0-80% and 12-57%.	Sulfaphenazole	48-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-142
9037249-6	1997	Inhibition of activity by quinidine (1 microM), sulphaphenazole (20 microM) and ketoconazole (2 microM), selective inhibitors of CYPs 2D6, 2C9 and 3A4, respectively, was 0-80%, 0-80% and 12-57%.	Ketoconazole	80-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-142
8960070-7	1997	The formation rates of both colchicine metabolites were correlated significantly with nifedipine oxidase activity, a marker of CYP3A4 activity (r = 0.96, P &lt; 0.001), but not with the metabolic markers of CYP2A6, CYP2C19, CYP2C9, CYP2D6, and CYP2E1 activities.	Colchicine	28-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	224-230
9068933-5	1997	This suggests that the change in tolbutamide clearance may be due to a slight inhibition of the cytochrome P450 (CYP) isoenzyme CYP2C9/10 when sertraline was administered in its maximum recommended dosage.	Tolbutamide	33-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
9068933-5	1997	This suggests that the change in tolbutamide clearance may be due to a slight inhibition of the cytochrome P450 (CYP) isoenzyme CYP2C9/10 when sertraline was administered in its maximum recommended dosage.	Sertraline	143-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
9068934-8	1997	The metabolism of warfarin is principally mediated by the cytochrome P450 (CYP) isoenzyme CYP2C9/10.	Warfarin	18-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Arginine	151-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-120
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Arginine	151-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Cysteine	155-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-120
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Cysteine	155-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Tyrosine	173-176	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-120
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Tyrosine	173-176	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Cysteine	177-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-120
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Cysteine	177-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Isoleucine	195-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-120
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Isoleucine	195-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Leucine	199-202	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-120
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Leucine	199-202	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Glycine	220-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-120
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Glycine	220-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Aspartic Acid	224-227	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-120
9110362-1	1997	Single nucleotide substitutions are known to result in a different amino acid at one of four sites in cytochrome P4502C9 (CYP2C9) namely: residue 144: Arg/Cys; residue 358: Tyr/Cys; residue 359: Ile/Leu and residue 417: Gly/Asp.	Aspartic Acid	224-227	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
9010637-5	1997	The inducers of CYP3A and/or CYP2C9 (e.g. rifampicin and phenytoin) are likely to alter the disposition of seratrodast.	Rifampin	42-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
9010637-5	1997	The inducers of CYP3A and/or CYP2C9 (e.g. rifampicin and phenytoin) are likely to alter the disposition of seratrodast.	Phenytoin	57-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
9021169-1	1996	The metabolism of isoprene was investigated with microsomes derived from cell lines expressing human CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2D6, CYP2E1, or CYP3A4.	isoprene	18-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
8973193-0	1996	Interaction of sulfaphenazole derivatives with human liver cytochromes P450 2C: molecular origin of the specific inhibitory effects of sulfaphenazole on CYP 2C9 and consequences for the substrate binding site topology of CYP 2C9.	Sulfaphenazole	15-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-160
8973193-0	1996	Interaction of sulfaphenazole derivatives with human liver cytochromes P450 2C: molecular origin of the specific inhibitory effects of sulfaphenazole on CYP 2C9 and consequences for the substrate binding site topology of CYP 2C9.	Sulfaphenazole	15-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	221-228
8973193-0	1996	Interaction of sulfaphenazole derivatives with human liver cytochromes P450 2C: molecular origin of the specific inhibitory effects of sulfaphenazole on CYP 2C9 and consequences for the substrate binding site topology of CYP 2C9.	Sulfaphenazole	135-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-160
8973193-3	1996	From difference visible spectroscopy experiments using microsomes of yeast expressing various human P450s, 1 selectively interacts only with CYP 2C9 with the appearance of a peak at 429 nm as expected for the formation of a P450 Fe(III)-nitrogenous ligand complex (Ks = 0.4 +/- 0.1 microM).	ferric sulfate	229-236	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-148
8973193-3	1996	From difference visible spectroscopy experiments using microsomes of yeast expressing various human P450s, 1 selectively interacts only with CYP 2C9 with the appearance of a peak at 429 nm as expected for the formation of a P450 Fe(III)-nitrogenous ligand complex (Ks = 0.4 +/- 0.1 microM).	Potassium	265-267	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-148
8973193-4	1996	Comparative studies of the spectral interaction and inhibitory effects of twelve compounds related to 1 with CYP 2C9 showed that the aniline function of 1 is responsible for the formation of the iron-nitrogen bond of the 429 nm-absorbing complex and is necessary for the inhibitory effects of 1.	aniline	133-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-116
8973193-4	1996	Comparative studies of the spectral interaction and inhibitory effects of twelve compounds related to 1 with CYP 2C9 showed that the aniline function of 1 is responsible for the formation of the iron-nitrogen bond of the 429 nm-absorbing complex and is necessary for the inhibitory effects of 1.	Iron	195-199	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-116
8973193-4	1996	Comparative studies of the spectral interaction and inhibitory effects of twelve compounds related to 1 with CYP 2C9 showed that the aniline function of 1 is responsible for the formation of the iron-nitrogen bond of the 429 nm-absorbing complex and is necessary for the inhibitory effects of 1.	Nitrogen	200-208	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-116
8973193-6	1996	A model for the binding of 1 in the CYP 2C9 active site is proposed; that takes into account three major interactions that should be at the origin of the high-affinity and specific inhibitory effects of 1 toward CYP 2C9: (i) the binding of its nitrogen atom to CYP 2C9 iron, (ii) an ionic interaction of its SO2N- anionic site with a cationic residue of CYP 2C9, and (iii) an interaction of its N-phenyl group with an hydrophobic part of the protein active site.	Nitrogen	244-252	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-43
8973193-6	1996	A model for the binding of 1 in the CYP 2C9 active site is proposed; that takes into account three major interactions that should be at the origin of the high-affinity and specific inhibitory effects of 1 toward CYP 2C9: (i) the binding of its nitrogen atom to CYP 2C9 iron, (ii) an ionic interaction of its SO2N- anionic site with a cationic residue of CYP 2C9, and (iii) an interaction of its N-phenyl group with an hydrophobic part of the protein active site.	Nitrogen	244-252	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-219
8973193-6	1996	A model for the binding of 1 in the CYP 2C9 active site is proposed; that takes into account three major interactions that should be at the origin of the high-affinity and specific inhibitory effects of 1 toward CYP 2C9: (i) the binding of its nitrogen atom to CYP 2C9 iron, (ii) an ionic interaction of its SO2N- anionic site with a cationic residue of CYP 2C9, and (iii) an interaction of its N-phenyl group with an hydrophobic part of the protein active site.	Nitrogen	244-252	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-219
8973193-6	1996	A model for the binding of 1 in the CYP 2C9 active site is proposed; that takes into account three major interactions that should be at the origin of the high-affinity and specific inhibitory effects of 1 toward CYP 2C9: (i) the binding of its nitrogen atom to CYP 2C9 iron, (ii) an ionic interaction of its SO2N- anionic site with a cationic residue of CYP 2C9, and (iii) an interaction of its N-phenyl group with an hydrophobic part of the protein active site.	Nitrogen	244-252	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-219
8973193-6	1996	A model for the binding of 1 in the CYP 2C9 active site is proposed; that takes into account three major interactions that should be at the origin of the high-affinity and specific inhibitory effects of 1 toward CYP 2C9: (i) the binding of its nitrogen atom to CYP 2C9 iron, (ii) an ionic interaction of its SO2N- anionic site with a cationic residue of CYP 2C9, and (iii) an interaction of its N-phenyl group with an hydrophobic part of the protein active site.	Iron	269-273	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-43
8973193-6	1996	A model for the binding of 1 in the CYP 2C9 active site is proposed; that takes into account three major interactions that should be at the origin of the high-affinity and specific inhibitory effects of 1 toward CYP 2C9: (i) the binding of its nitrogen atom to CYP 2C9 iron, (ii) an ionic interaction of its SO2N- anionic site with a cationic residue of CYP 2C9, and (iii) an interaction of its N-phenyl group with an hydrophobic part of the protein active site.	Iron	269-273	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-219
8973193-6	1996	A model for the binding of 1 in the CYP 2C9 active site is proposed; that takes into account three major interactions that should be at the origin of the high-affinity and specific inhibitory effects of 1 toward CYP 2C9: (i) the binding of its nitrogen atom to CYP 2C9 iron, (ii) an ionic interaction of its SO2N- anionic site with a cationic residue of CYP 2C9, and (iii) an interaction of its N-phenyl group with an hydrophobic part of the protein active site.	Iron	269-273	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-219
8973193-6	1996	A model for the binding of 1 in the CYP 2C9 active site is proposed; that takes into account three major interactions that should be at the origin of the high-affinity and specific inhibitory effects of 1 toward CYP 2C9: (i) the binding of its nitrogen atom to CYP 2C9 iron, (ii) an ionic interaction of its SO2N- anionic site with a cationic residue of CYP 2C9, and (iii) an interaction of its N-phenyl group with an hydrophobic part of the protein active site.	Iron	269-273	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-219
8973193-6	1996	A model for the binding of 1 in the CYP 2C9 active site is proposed; that takes into account three major interactions that should be at the origin of the high-affinity and specific inhibitory effects of 1 toward CYP 2C9: (i) the binding of its nitrogen atom to CYP 2C9 iron, (ii) an ionic interaction of its SO2N- anionic site with a cationic residue of CYP 2C9, and (iii) an interaction of its N-phenyl group with an hydrophobic part of the protein active site.	so2n	308-312	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-43
8973193-6	1996	A model for the binding of 1 in the CYP 2C9 active site is proposed; that takes into account three major interactions that should be at the origin of the high-affinity and specific inhibitory effects of 1 toward CYP 2C9: (i) the binding of its nitrogen atom to CYP 2C9 iron, (ii) an ionic interaction of its SO2N- anionic site with a cationic residue of CYP 2C9, and (iii) an interaction of its N-phenyl group with an hydrophobic part of the protein active site.	so2n	308-312	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-219
8973193-6	1996	A model for the binding of 1 in the CYP 2C9 active site is proposed; that takes into account three major interactions that should be at the origin of the high-affinity and specific inhibitory effects of 1 toward CYP 2C9: (i) the binding of its nitrogen atom to CYP 2C9 iron, (ii) an ionic interaction of its SO2N- anionic site with a cationic residue of CYP 2C9, and (iii) an interaction of its N-phenyl group with an hydrophobic part of the protein active site.	so2n	308-312	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-219
8973193-6	1996	A model for the binding of 1 in the CYP 2C9 active site is proposed; that takes into account three major interactions that should be at the origin of the high-affinity and specific inhibitory effects of 1 toward CYP 2C9: (i) the binding of its nitrogen atom to CYP 2C9 iron, (ii) an ionic interaction of its SO2N- anionic site with a cationic residue of CYP 2C9, and (iii) an interaction of its N-phenyl group with an hydrophobic part of the protein active site.	so2n	308-312	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-219
8944768-8	1996	Mechanism-based inactivation of cytochrome P-450 during tienilic acid oxidation was observed in the case of CYP 2C9 but was not detectable with CYP 2C18 and CYP 2C8.	Ticrynafen	56-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-115
9004453-3	1996	A retroviral vector construct, containing a human CYP2C10 cDNA, was transfected in V79-NH Chinese hamster lung cells by calcium phosphate co-precipitation.	calcium phosphate	120-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-57
9004453-6	1996	Enzymatic activity of CYP2C10 was detected by 4-methylhydroxylation of tolbutamide.	Tolbutamide	71-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-29
9032002-6	1996	Fluoxetine is a substantial inhibitor of CYP2D6, has mild effects on CYP3A3/4, and may also have effects on CYP2C9/10 and CYP2C19.	Fluoxetine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
8944768-2	1996	Oxidation of tienilic acid by human cytochromes P-450 (CYP) 2C9, 2C18, 2C8 and 2C19 was studied using recombinant enzymes expressed in yeast.	Ticrynafen	13-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-63
8944768-9	1996	Tienilic acid thus appears to be a mechanism-based inhibitor specific for CYP 2C9 in human liver.	Ticrynafen	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-81
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 9	Homo sapiens	0-7
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 9	Homo sapiens	30-36
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 9	Homo sapiens	177-184
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 9	Homo sapiens	177-184
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 9	Homo sapiens	177-184
8937439-3	1996	The major oxidative pathway in flurbiprofen metabolism is to a 4"-hydroxy metabolite, and recently we demonstrated that cytochrome P450 2C9 and its R144C variant were involved in this process (Tracy et al., Biochem Pharmacol 49: 1269-1275, 1995).	Flurbiprofen	31-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-139
8937439-5	1996	In evaluating flurbiprofen as a potential probe for cytochrome P450 2C9, it is important to assess the involvement of additional P450s in this process.	Flurbiprofen	14-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-71
8946475-1	1996	Cytochrome P450 CYP2C9 metabolizes a wide variety of clinically important drugs, including phenytoin, tolbutamide, warfarin and a large number of non-steroidal anti-inflammatory drugs.	Phenytoin	91-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
8946475-1	1996	Cytochrome P450 CYP2C9 metabolizes a wide variety of clinically important drugs, including phenytoin, tolbutamide, warfarin and a large number of non-steroidal anti-inflammatory drugs.	Tolbutamide	102-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
8946475-1	1996	Cytochrome P450 CYP2C9 metabolizes a wide variety of clinically important drugs, including phenytoin, tolbutamide, warfarin and a large number of non-steroidal anti-inflammatory drugs.	Warfarin	115-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
8823314-2	1996	Patients with tienilic acid hepatitis exhibit autoantibodies that recognize unalkylated cytochrome P450 2C9 in humans but recognize 2C11 in rats.	Ticrynafen	14-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-107
9131488-10	1996	Differences in rates of production of hydroxylamine metabolites of the drugs by cytochrome P450 (CYP2C9), myeloperoxidase, and thyroid, roxidase, along with an inherited abnormality in detoxification of the hydroxylamines are critically important in determining individual differences in adverse reaction risk.	Hydroxylamine	38-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
9131488-10	1996	Differences in rates of production of hydroxylamine metabolites of the drugs by cytochrome P450 (CYP2C9), myeloperoxidase, and thyroid, roxidase, along with an inherited abnormality in detoxification of the hydroxylamines are critically important in determining individual differences in adverse reaction risk.	Hydroxylamines	207-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
8809086-1	1996	The purpose of the present studies was to define the role of the I359L allelic variant of CYP2C9 in the metabolism of the low therapeutic index anticoagulant warfarin, by performing in vitro kinetic studies with the two enantiomers of the drug.	Warfarin	158-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
8886601-8	1996	Furthermore, rates of norfentanyl production by 10 individual human liver samples were highly correlated (r2 = 0.876, F = 56.46 p &lt; 0.001) with immunochemically determined levels of CYP3A4 present in the samples but not with levels of CYP2C8, CYP2C9, CYP2C19, or CYP2E1.	norfentanyl	22-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	246-252
8873220-0	1996	The role of the CYP2C9-Leu359 allelic variant in the tolbutamide polymorphism.	Tolbutamide	53-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
8687505-8	1996	The precocious expression of CYP2C in SIDS could result in a higher production of epoxyeicosatrienoic acids in the neonate, believed to act as relaxant of pulmonary smooth muscles.	epoxyeicosatrienoic acids	82-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-34
8700140-2	1996	Cytochrome P4502C9(CYP2C9), involved in the metabolism of tienilic acid, was shown to be a target for tienilic acid-reactive metabolites and for autoantibodies.	Ticrynafen	58-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
8700140-2	1996	Cytochrome P4502C9(CYP2C9), involved in the metabolism of tienilic acid, was shown to be a target for tienilic acid-reactive metabolites and for autoantibodies.	Ticrynafen	102-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
8886617-1	1996	The effect of branch pathways on the observed intramolecular isotope effect and deuterium retention associated with 6- and 7-hydroxylation of selectively monodeuterated (R)- and (S)-warfarin with cytochrome P450 (CYP) 2C9 and CYP1A2 were studied.	Deuterium	80-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-221
8886617-1	1996	The effect of branch pathways on the observed intramolecular isotope effect and deuterium retention associated with 6- and 7-hydroxylation of selectively monodeuterated (R)- and (S)-warfarin with cytochrome P450 (CYP) 2C9 and CYP1A2 were studied.	(r)- and (s)-warfarin	169-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-221
8886617-2	1996	cDNA-expressed CYP2C9 was incubated with enantiomerically pure (S)-7d1- and (S)-6d1-warfarin, and expressed CYP1A2 was incubated with enantiomerically pure (R)-7d1- and (R)-6d1-warfarin.	Sulfur	63-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
8886617-2	1996	cDNA-expressed CYP2C9 was incubated with enantiomerically pure (S)-7d1- and (S)-6d1-warfarin, and expressed CYP1A2 was incubated with enantiomerically pure (R)-7d1- and (R)-6d1-warfarin.	1,5-anhydro-2-deoxy-d-arabino-hexitol	67-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
8886617-2	1996	cDNA-expressed CYP2C9 was incubated with enantiomerically pure (S)-7d1- and (S)-6d1-warfarin, and expressed CYP1A2 was incubated with enantiomerically pure (R)-7d1- and (R)-6d1-warfarin.	(s)-6d1-warfarin	76-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
8886617-2	1996	cDNA-expressed CYP2C9 was incubated with enantiomerically pure (S)-7d1- and (S)-6d1-warfarin, and expressed CYP1A2 was incubated with enantiomerically pure (R)-7d1- and (R)-6d1-warfarin.	(r)-7d1	156-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
8886617-2	1996	cDNA-expressed CYP2C9 was incubated with enantiomerically pure (S)-7d1- and (S)-6d1-warfarin, and expressed CYP1A2 was incubated with enantiomerically pure (R)-7d1- and (R)-6d1-warfarin.	(r)-6d1	169-176	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
8886617-2	1996	cDNA-expressed CYP2C9 was incubated with enantiomerically pure (S)-7d1- and (S)-6d1-warfarin, and expressed CYP1A2 was incubated with enantiomerically pure (R)-7d1- and (R)-6d1-warfarin.	Warfarin	84-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
8886617-5	1996	Deuterium isotope effects of 1.17 and 1.23 accompanied formation of 7-hydroxywarfarin from (S)-7d1-warfarin by CYP2C9 and from (R)-7d1-warfarin by CYP1A2, respectively.	Deuterium	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
8886617-5	1996	Deuterium isotope effects of 1.17 and 1.23 accompanied formation of 7-hydroxywarfarin from (S)-7d1-warfarin by CYP2C9 and from (R)-7d1-warfarin by CYP1A2, respectively.	7-hydroxywarfarin	68-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
8886617-5	1996	Deuterium isotope effects of 1.17 and 1.23 accompanied formation of 7-hydroxywarfarin from (S)-7d1-warfarin by CYP2C9 and from (R)-7d1-warfarin by CYP1A2, respectively.	(s)-7d1	91-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
8886617-5	1996	Deuterium isotope effects of 1.17 and 1.23 accompanied formation of 7-hydroxywarfarin from (S)-7d1-warfarin by CYP2C9 and from (R)-7d1-warfarin by CYP1A2, respectively.	Warfarin	77-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
8886617-5	1996	Deuterium isotope effects of 1.17 and 1.23 accompanied formation of 7-hydroxywarfarin from (S)-7d1-warfarin by CYP2C9 and from (R)-7d1-warfarin by CYP1A2, respectively.	Warfarin	99-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
8874828-1	1996	We examined the effect of CYP2C9/19 polymorphisms on the pharmacokinetics of phenytoin in 17 Japanese patients with epilepsy.	Phenytoin	77-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
8873220-11	1996	Studies in a recombinant yeast expression system showed that the Leu359 variant had the highest Km and the lowest Vmac for hydroxylation of tolbutamide of all the CYP2C9 allelic variants.	vmac	114-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-169
8873220-11	1996	Studies in a recombinant yeast expression system showed that the Leu359 variant had the highest Km and the lowest Vmac for hydroxylation of tolbutamide of all the CYP2C9 allelic variants.	Tolbutamide	140-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-169
8873220-13	1996	The present data suggest that the incidence of the Leu359 allelic variant of CYP2C9 may account for the occurrence of poor metabolizers of tolbutamide.	Tolbutamide	139-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
8681486-10	1996	LKM-2 antibodies (anti-CYP2C) caused a 75% to 100% inhibition of norantipyrine and a 58% to 80% inhibition of 3-hydroxymethylantipyrine formation.	Edaravone	65-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-28
8681455-3	1996	In particular, the CYP102-derived structures of CYP3A4, CYP2D6 and CYP2C9 are able to rationalize the routes of tamoxifen metabolism reported in human subjects.	Tamoxifen	112-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
8799527-11	1996	Sulphaphenazole (SPA), a CYP2C9 inhibitor, decreased the rate of NT formation in a concentration dependent manner, whereas a polyclonal rat liver CYP2C11 antibody, inhibitory for S-mephenytoin 4"-hydroxylation in humans, had no important effect on this reaction.	Sulfaphenazole	0-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
8799527-11	1996	Sulphaphenazole (SPA), a CYP2C9 inhibitor, decreased the rate of NT formation in a concentration dependent manner, whereas a polyclonal rat liver CYP2C11 antibody, inhibitory for S-mephenytoin 4"-hydroxylation in humans, had no important effect on this reaction.	Sulfaphenazole	17-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
8681486-10	1996	LKM-2 antibodies (anti-CYP2C) caused a 75% to 100% inhibition of norantipyrine and a 58% to 80% inhibition of 3-hydroxymethylantipyrine formation.	3-hydroxymethylantipyrine	110-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-28
8681486-17	1996	The CYP2C subfamily contains the predominant enzymes for norantipyrine formation, and CYP1A2 is also involved.	Edaravone	57-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-9
8681486-18	1996	Formation of 3-hydroxymethylantipyrine is mediated by CYP1A2 and CYP2C9.	3-hydroxymethylantipyrine	13-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
8905247-8	1996	We propose that the following vicious circle may be involved in this interaction: induction by phenytoin of hepatic enzymes involved in the metabolism of T4 and T3, decreased serum free T4 levels causing decreased activity of hepatic NADPH cytochrome P-450 reductase, a resultant decrease in hepatic P-450 IIC9 catalyzed hydroxylation of phenytoin, increased serum phenytoin concentrations and further induction of T4 and T3 hepatic metabolism.	Phenytoin	95-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	300-310
8793607-3	1996	Diclofenac is widely used in the treatment of rheumatic diseases and is mainly metabolized in the liver by CYP2C9.	Diclofenac	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
8627562-10	1996	The cDNA expressed enzymes CYP2C8, CYP2C9 and CYP2C19 catalyzed varying rates of lansoprazole 5-hydroxylation at a substrate concentration of 50 microM, but only CYPC19 catalyzed this reaction at 1 microM.	Lansoprazole	81-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
8866821-1	1996	A preliminary report implicated cytochrome P450 (CYP) 2C9 in the human liver microsomal O-demethylation of S-naproxen, suggesting that this pathway may be suitable for investigation of human hepatic CYP2C9 in vitro.	Naproxen	107-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-57
8866821-1	1996	A preliminary report implicated cytochrome P450 (CYP) 2C9 in the human liver microsomal O-demethylation of S-naproxen, suggesting that this pathway may be suitable for investigation of human hepatic CYP2C9 in vitro.	Naproxen	107-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	199-205
8866821-2	1996	Kinetic and inhibitor studies with human liver microsomes and confirmatory investigations with cDNA-expressed enzymes were undertaken here to define the role of CYP2C9 and other isoforms in the O-demethylation of R- and S-naproxen.	r- and s-naproxen	213-230	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
8866821-7	1996	cDNA-expressed CYP2C9 and CYP1A2 were both shown to O-demethylate R- and S-naproxen.	o-demethylate r- and s-naproxen	52-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
8866821-9	1996	The data demonstrate that CYP2C9 and CYP1A2 together account for the majority of human liver R- and S-naproxen O-demethylation, precluding the use of either R- or S-naproxen as a CYP isoform-specific substrate in vitro and in vivo.	r- and s-naproxen	93-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
8801060-13	1996	In contrast, amiodarone (IC50, 25 microM) and flecainide (49 microM) inhibited CYP2C9 and quinidine (0.26 microM), and flecainide (0.44 microM) inhibited CYP2D6.	Amiodarone	13-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
8801060-13	1996	In contrast, amiodarone (IC50, 25 microM) and flecainide (49 microM) inhibited CYP2C9 and quinidine (0.26 microM), and flecainide (0.44 microM) inhibited CYP2D6.	Flecainide	46-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
8861733-3	1996	Diclofenac is widely used in the treatment of rheumatic diseases and is mainly metabolized in the liver by CYP2C9.	Diclofenac	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
8866916-0	1996	In vitro interaction of the antipsychotic agent olanzapine with human cytochromes P450 CYP2C9, CYP2C19, CYP2D6 and CYP3A.	Olanzapine	48-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
8866916-2	1996	The ability of olanzapine to inhibit the metabolism of marker catalytic activities for the cytochromes P450 CYP3A, CYP2D6, CYP2C9, and CYP2C19 was examined.	Olanzapine	15-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
8866916-7	1996	Tolbutamide metabolism to 4-hydroxy tolbutamide, form selective for CYP2C9, was competitively inhibited by clozapine and phenytoin (Ki of 31 microM and 17 microM, respectively).	Tolbutamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
8866916-7	1996	Tolbutamide metabolism to 4-hydroxy tolbutamide, form selective for CYP2C9, was competitively inhibited by clozapine and phenytoin (Ki of 31 microM and 17 microM, respectively).	4'-hydroxytolbutamide	26-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
8866916-7	1996	Tolbutamide metabolism to 4-hydroxy tolbutamide, form selective for CYP2C9, was competitively inhibited by clozapine and phenytoin (Ki of 31 microM and 17 microM, respectively).	Clozapine	107-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
8866916-7	1996	Tolbutamide metabolism to 4-hydroxy tolbutamide, form selective for CYP2C9, was competitively inhibited by clozapine and phenytoin (Ki of 31 microM and 17 microM, respectively).	Phenytoin	121-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
8866916-12	1996	The calculated percent inhibition by olanzapine of substrates metabolized by CYP3A, CYP2D6, CYP2C9, and CYP2C19 was modeled assuming a total plasma concentration in the therapeutic range (0.2 microM).	Olanzapine	37-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
8742240-4	1996	There are now a number of substrates reported that have routes of metabolism ascribed specifically to cytochrome P4502C9 (CYP2C9), the isoform mainly responsible for tolbutamide hydroxylation.	Tolbutamide	166-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-120
8742240-4	1996	There are now a number of substrates reported that have routes of metabolism ascribed specifically to cytochrome P4502C9 (CYP2C9), the isoform mainly responsible for tolbutamide hydroxylation.	Tolbutamide	166-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
8742240-6	1996	The substrate specificity has been rationalized in terms of a hydrogen bond donor/acceptor model and, by use of molecular modeling, an active site template model for CYP2C9 has been generated.	Hydrogen	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	166-172
8542584-8	1996	We have demonstrated that the mutation frequency of ochratoxin A was increased dependent upon concentration in NIH/3T3 cell lines, stably expressing human CYP1A1, CYP1A2, CYP2C10, and CYP3A4.	ochratoxin A	52-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-178
8825200-12	1996	It is concluded that the O-demethylation of naproxen (&lt; or = 0.4 mM) is catalyzed by CYP2C subfamily members (CYP2C9/10) and CYP1A2 in human liver microsomes.	Naproxen	44-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-93
8825200-12	1996	It is concluded that the O-demethylation of naproxen (&lt; or = 0.4 mM) is catalyzed by CYP2C subfamily members (CYP2C9/10) and CYP1A2 in human liver microsomes.	Naproxen	44-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-122
8613951-6	1996	Ritonavir was also found to be an inhibitor of the reactions mediated by CYP2D6 (IC50 = 2.5 microM) and CYP2C9/10 (IC50 = 8.0 microM).	Ritonavir	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
8613951-7	1996	The results of this study indicate the potential for in vivo inhibition of the metabolism by ritonavir of drugs that are CYP3A, CYP2D6 and, to a lesser extent, CYP2C9/10 substrates.	Ritonavir	93-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
8822040-2	1996	Recently, it has been shown that phenytoin and tolbutamide are metabolised by CYP2C9/10 whereas mephenytoin is metabolised by CYP2C19.	Phenytoin	33-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
8822040-2	1996	Recently, it has been shown that phenytoin and tolbutamide are metabolised by CYP2C9/10 whereas mephenytoin is metabolised by CYP2C19.	Tolbutamide	47-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
8737761-2	1996	METHODS: Affinity was determined as the inhibitory potency for prototype reactions for 3 major drug metabolising enzymes: diclofenac 4"-hydroxylation (CYP2C9), dextromethorphan O-demethylation (CYP2D6), and midazolam 1"-hydroxylation (CYP3A4).	Diclofenac	122-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	151-157
8857077-4	1996	The apparent affinity of lornoxicam was high for CYP2C9, but negligible for CYP3A4 and CYP2D6.	lornoxicam	25-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
8737761-4	1996	Racemic and (+)- and (-)-fluvastatin showed moderate affinity (estimated Ki &gt; 50 micromol.1(-1)) for CYP2D6 and CYP3A4, whereas their affinity for CYP2C9 was high (estimated Ki &lt; 1 micromol.1(-1)).	(+)- and (-)-fluvastatin	12-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
8737761-6	1996	CONCLUSION: Fluvastatin selectively inhibits a major drug metabolising enzyme (CYP2C9), the (+)-isomer (pharmacologically more active) showing 4-5 fold higher affinity.	Fluvastatin	12-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
8737761-7	1996	As already reported for lovastatin and simvastatin, in vivo drug interactions by inhibition of liver oxidation of CYP2C9 substrates (e.g. hypoglyceamic sulphonylureas and oral anticoagulants) may be expected.	Lovastatin	24-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
8737761-7	1996	As already reported for lovastatin and simvastatin, in vivo drug interactions by inhibition of liver oxidation of CYP2C9 substrates (e.g. hypoglyceamic sulphonylureas and oral anticoagulants) may be expected.	Simvastatin	39-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
8857077-0	1996	Role of human liver microsomal CYP2C9 in the biotransformation of lornoxicam.	lornoxicam	66-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
8857077-2	1996	The reaction kinetics were characterised, the affinity of lornoxicam for three major human drug metabolising cytochrome P-450 isozymes (CYP2C9, CYP2D6 and CYP3A4) was determined, and inhibition of the reaction by known substrates (diclofenac, ibuprofen, mefenamic acid, phenytoin, tolbutamide and warfarin) and the prototype inhibitor (sulphaphenazole) of CYP2C9 was investigated.	lornoxicam	58-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
8857077-2	1996	The reaction kinetics were characterised, the affinity of lornoxicam for three major human drug metabolising cytochrome P-450 isozymes (CYP2C9, CYP2D6 and CYP3A4) was determined, and inhibition of the reaction by known substrates (diclofenac, ibuprofen, mefenamic acid, phenytoin, tolbutamide and warfarin) and the prototype inhibitor (sulphaphenazole) of CYP2C9 was investigated.	lornoxicam	58-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	356-362
8857077-5	1996	Inhibition of lornoxicam 5"-hydroxylation by CYP2C9 substrates and sulphaphenazole competitively and completely inhibited lornoxicam 5"-hydroxylation (Ki = 0.31 mu mol center dot l-1 as well as lornoxicam clearance (Ki = 0.33 mu mol center dot l-1), partial metabolic clearance (fm) = 0.95).	lornoxicam	14-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
8857077-5	1996	Inhibition of lornoxicam 5"-hydroxylation by CYP2C9 substrates and sulphaphenazole competitively and completely inhibited lornoxicam 5"-hydroxylation (Ki = 0.31 mu mol center dot l-1 as well as lornoxicam clearance (Ki = 0.33 mu mol center dot l-1), partial metabolic clearance (fm) = 0.95).	lornoxicam	122-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
8857077-5	1996	Inhibition of lornoxicam 5"-hydroxylation by CYP2C9 substrates and sulphaphenazole competitively and completely inhibited lornoxicam 5"-hydroxylation (Ki = 0.31 mu mol center dot l-1 as well as lornoxicam clearance (Ki = 0.33 mu mol center dot l-1), partial metabolic clearance (fm) = 0.95).	lornoxicam	122-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
8857077-6	1996	CONCLUSION: 5"-Hydroxylation appears to be the only cytochrome P-450 catalysed metabolic reaction of lornoxicam by human liver microsomes and this major in vivo biotransformation pathway is catalysed virtually exclusively by CYP2C9.	lornoxicam	101-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	225-231
8750925-8	1995	Anti-LKM2 (anti-liver/kidney microsome) autoantibodies (which inhibit CYP2C9 and 2C19) and sulfaphenazole (a specific CYP2C9 inhibitor) reduced the maximum rate of formation of D-703 by 81.5 +/- 4.5% and 45%, that of D-702 by 52.7 +/- 7.5% and 72.5%, respectively.	D 703	177-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
8698676-1	1996	The article focuses on the effects of the serotonin selective reuptake inhibitors (SSRIs) on specific drug metabolizing isoenzymes: CYP2D6, CYP3A3/4, CYP1A2, CYP2C9, and CYP2C19.	Serotonin	42-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
8703658-9	1995	Studies with low molecular weight inhibitors illustrate the importance of CYP2C9 and CYP3A in dapsone N-hydroxylation.	Dapsone	94-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
8750925-8	1995	Anti-LKM2 (anti-liver/kidney microsome) autoantibodies (which inhibit CYP2C9 and 2C19) and sulfaphenazole (a specific CYP2C9 inhibitor) reduced the maximum rate of formation of D-703 by 81.5 +/- 4.5% and 45%, that of D-702 by 52.7 +/- 7.5% and 72.5%, respectively.	Sulfaphenazole	91-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
8747411-0	1995	Genetic polymorphism of CYP2C9 and its effect on warfarin maintenance dose requirement in patients undergoing anticoagulation therapy.	Warfarin	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
8654205-5	1995	The turnover rates (min-1) of DETC-Me sulfoxidation by the cDNA-expressed cytochrome P450 enzymes ranked as follows: CYP3A4 &gt; CYP2A6 = CYP2C9 &gt; CYP1A2 &gt; CYP2B6 = CYP2E1 &gt; CYP1A1 &gt; CYP2D6.	detc-me	30-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
7586933-0	1995	In vivo inhibition profile of cytochrome P450TB (CYP2C9) by (+/-)-fluvastatin.	Fluvastatin	60-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
7586933-1	1995	BACKGROUND: (+/-)-Fluvastatin is a synthetic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor that selectively and competitively inhibits P450TB (CYP2C9) in vitro.	Fluvastatin	12-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	165-171
8587855-3	1995	This review summarizes information to date regarding the inhibitory potency of fluoxetine, fluvoxamine, paroxetine, sertraline, nefazodone, and venlafaxine on five isoenzyme systems: CYP2D6, CYP3A3/4, CYP1A2, CYP2C9, and CYP2C19.	Fluoxetine	79-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	209-215
8587855-3	1995	This review summarizes information to date regarding the inhibitory potency of fluoxetine, fluvoxamine, paroxetine, sertraline, nefazodone, and venlafaxine on five isoenzyme systems: CYP2D6, CYP3A3/4, CYP1A2, CYP2C9, and CYP2C19.	Sertraline	116-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	209-215
8587855-3	1995	This review summarizes information to date regarding the inhibitory potency of fluoxetine, fluvoxamine, paroxetine, sertraline, nefazodone, and venlafaxine on five isoenzyme systems: CYP2D6, CYP3A3/4, CYP1A2, CYP2C9, and CYP2C19.	nefazodone	128-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	209-215
8587855-3	1995	This review summarizes information to date regarding the inhibitory potency of fluoxetine, fluvoxamine, paroxetine, sertraline, nefazodone, and venlafaxine on five isoenzyme systems: CYP2D6, CYP3A3/4, CYP1A2, CYP2C9, and CYP2C19.	Venlafaxine Hydrochloride	144-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	209-215
8654202-5	1995	In addition, the respective omega-OH finasteride and omega-oic acid finasteride metabolites were generated only by microsomes containing recombinant CYP3A4, but not the other isozymes (CYP1A1, CYP2B6, CYP2C8, CYP2C9, CYP2D6, and CYP2E1).	omega-oh finasteride	28-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	209-215
7574697-10	1995	Compared to Cyp 2C8, arachidonic acid epoxidation by Cyp 2C10 was less regio- and stereo-selective and generated mixtures of 8(S), 9(R)-, 11(S), 12(R)-, and 14(R), 15(S)-epoxyeicosatrienoic acids (with optical purities of 66, 69, 63%, respectively).	Arachidonic Acid	21-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-61
8654202-5	1995	In addition, the respective omega-OH finasteride and omega-oic acid finasteride metabolites were generated only by microsomes containing recombinant CYP3A4, but not the other isozymes (CYP1A1, CYP2B6, CYP2C8, CYP2C9, CYP2D6, and CYP2E1).	omega-oic acid finasteride	53-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	209-215
8654206-3	1995	Results suggested that whereas the metabolism of zileuton and Abbott-66193 were mediated by the same CYP forms, the CYP forms responsible for hydroxylation (CYP1A2 and CYP2C9/10) were distinct from those involved in sulfoxidation (CYP3A &gt; CYP2C9/10).	zileuton	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	242-248
8654206-6	1995	On the other hand, hydroxylation of the two compounds (zileuton, Km = 0.34 +/- 0.25 mM, Vmax = 17.8 +/- 5.58 pmol/min/mg; Abbott-66193,Km = 0.39 +/- 0.14 mM, Vmax = 1061 +/- 220 pmol/min/mg) was significantly correlated with 7-ethoxyresorufin O-deethylase (CYP1A2; r=0.652-0.762; p&lt;0.01, N=11) and tolbutamide methyl hydroxylase (CYP2C9/10; r=0.863-0.935; p&lt;0.01, N=10) activity in human liver microsome, and was inhibited (26-51%) by well-known CYP1A2 inhibitors (furafylline and alpha-naphthoflavone).	zileuton	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	333-339
8654206-8	1995	Abbott-66193 was a better substrate for CYP2C9/10, when compared with zileuton: 1) the effect of sulfaphenazole on hydroxylation in human liver microsomes was more pronounced for Abbott-66193 than zileuton (56% vs. 9% inhibition); and 2) the rate of Abbott-66193 hydroxylation by purified CYP2C9 was almost 30-fold greater than that of zilueton.	Sulfaphenazole	97-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
7574697-10	1995	Compared to Cyp 2C8, arachidonic acid epoxidation by Cyp 2C10 was less regio- and stereo-selective and generated mixtures of 8(S), 9(R)-, 11(S), 12(R)-, and 14(R), 15(S)-epoxyeicosatrienoic acids (with optical purities of 66, 69, 63%, respectively).	Sulfur	126-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-61
7574697-10	1995	Compared to Cyp 2C8, arachidonic acid epoxidation by Cyp 2C10 was less regio- and stereo-selective and generated mixtures of 8(S), 9(R)-, 11(S), 12(R)-, and 14(R), 15(S)-epoxyeicosatrienoic acids (with optical purities of 66, 69, 63%, respectively).	(r)	132-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-61
7574697-10	1995	Compared to Cyp 2C8, arachidonic acid epoxidation by Cyp 2C10 was less regio- and stereo-selective and generated mixtures of 8(S), 9(R)-, 11(S), 12(R)-, and 14(R), 15(S)-epoxyeicosatrienoic acids (with optical purities of 66, 69, 63%, respectively).	(s)-epoxyeicosatrienoic acids	166-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-61
7614688-7	1995	Treatment of cynomolgus monkeys with rifampicin induced hepatic cytochromes P450 related to human CYP3A4 and CYP2C9/10 without inducing CYP1A1 or CYP1A2.	Rifampin	37-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
7654690-0	1995	The substrate binding site of human liver cytochrome P450 2C9: an approach using designed tienilic acid derivatives and molecular modeling.	Ticrynafen	90-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-61
7654690-2	1995	The ability of 10 2-aroylthiophenes related to tienilic acid to act as substrates for CYP2C9 was studied.	2-aroylthiophenes	18-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
7654690-2	1995	The ability of 10 2-aroylthiophenes related to tienilic acid to act as substrates for CYP2C9 was studied.	Ticrynafen	47-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
7654690-8	1995	In fact, the four new substrates of CYP2C9 described in this study, a carboxylic acid, phenol, and tetrazole derivative, each of which is related to tienilic acid, and the antiinflammatory drug, suprofen (with Km between 12 and 130 microM and kcat between 0.2 and 1.3 min-1), as well as almost all CYP2C9 substrates reported in the literature, exhibit a pKa below 7 (except phenytoin whose pKa is 8.1).	Carboxylic Acids	70-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
7654690-8	1995	In fact, the four new substrates of CYP2C9 described in this study, a carboxylic acid, phenol, and tetrazole derivative, each of which is related to tienilic acid, and the antiinflammatory drug, suprofen (with Km between 12 and 130 microM and kcat between 0.2 and 1.3 min-1), as well as almost all CYP2C9 substrates reported in the literature, exhibit a pKa below 7 (except phenytoin whose pKa is 8.1).	Carboxylic Acids	70-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	298-304
7654690-8	1995	In fact, the four new substrates of CYP2C9 described in this study, a carboxylic acid, phenol, and tetrazole derivative, each of which is related to tienilic acid, and the antiinflammatory drug, suprofen (with Km between 12 and 130 microM and kcat between 0.2 and 1.3 min-1), as well as almost all CYP2C9 substrates reported in the literature, exhibit a pKa below 7 (except phenytoin whose pKa is 8.1).	Phenol	87-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
7654690-8	1995	In fact, the four new substrates of CYP2C9 described in this study, a carboxylic acid, phenol, and tetrazole derivative, each of which is related to tienilic acid, and the antiinflammatory drug, suprofen (with Km between 12 and 130 microM and kcat between 0.2 and 1.3 min-1), as well as almost all CYP2C9 substrates reported in the literature, exhibit a pKa below 7 (except phenytoin whose pKa is 8.1).	1H-tetrazole	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
7654690-8	1995	In fact, the four new substrates of CYP2C9 described in this study, a carboxylic acid, phenol, and tetrazole derivative, each of which is related to tienilic acid, and the antiinflammatory drug, suprofen (with Km between 12 and 130 microM and kcat between 0.2 and 1.3 min-1), as well as almost all CYP2C9 substrates reported in the literature, exhibit a pKa below 7 (except phenytoin whose pKa is 8.1).	1H-tetrazole	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	298-304
7654690-8	1995	In fact, the four new substrates of CYP2C9 described in this study, a carboxylic acid, phenol, and tetrazole derivative, each of which is related to tienilic acid, and the antiinflammatory drug, suprofen (with Km between 12 and 130 microM and kcat between 0.2 and 1.3 min-1), as well as almost all CYP2C9 substrates reported in the literature, exhibit a pKa below 7 (except phenytoin whose pKa is 8.1).	Ticrynafen	149-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
7654690-8	1995	In fact, the four new substrates of CYP2C9 described in this study, a carboxylic acid, phenol, and tetrazole derivative, each of which is related to tienilic acid, and the antiinflammatory drug, suprofen (with Km between 12 and 130 microM and kcat between 0.2 and 1.3 min-1), as well as almost all CYP2C9 substrates reported in the literature, exhibit a pKa below 7 (except phenytoin whose pKa is 8.1).	Suprofen	195-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
7654690-8	1995	In fact, the four new substrates of CYP2C9 described in this study, a carboxylic acid, phenol, and tetrazole derivative, each of which is related to tienilic acid, and the antiinflammatory drug, suprofen (with Km between 12 and 130 microM and kcat between 0.2 and 1.3 min-1), as well as almost all CYP2C9 substrates reported in the literature, exhibit a pKa below 7 (except phenytoin whose pKa is 8.1).	Suprofen	195-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	298-304
7654690-8	1995	In fact, the four new substrates of CYP2C9 described in this study, a carboxylic acid, phenol, and tetrazole derivative, each of which is related to tienilic acid, and the antiinflammatory drug, suprofen (with Km between 12 and 130 microM and kcat between 0.2 and 1.3 min-1), as well as almost all CYP2C9 substrates reported in the literature, exhibit a pKa below 7 (except phenytoin whose pKa is 8.1).	Phenytoin	374-383	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
7654690-10	1995	By using molecular modeling techniques, 12 CYP2C9 substrates were superimposed with respect to their hydroxylation site and fitted onto templates, which were rigid molecules such as (S)-warfarin and phenytoin.	Warfarin	182-194	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
7654690-10	1995	By using molecular modeling techniques, 12 CYP2C9 substrates were superimposed with respect to their hydroxylation site and fitted onto templates, which were rigid molecules such as (S)-warfarin and phenytoin.	Phenytoin	199-208	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
8535411-0	1995	Involvement of CYP2C in the metabolism of cannabinoids by human hepatic microsomes from an old woman.	Cannabinoids	42-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-20
7614688-12	1995	Since cytochromes P4503A and/or P4502C are constitutively expressed in cynomolgus monkey hepatic microsomes, and upon induction with rifampicin are associated with an increased metabolic activation of IQ but not MeIQx, it appears that CYP3A and/or CYP2C are the isoform(s) showing the selective substrate specificity in the metabolic activation of IQ over MeIQx.	Rifampin	133-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	248-253
7625847-0	1995	Arachidonic acid metabolism by human cytochrome P450s 2C8, 2C9, 2E1, and 1A2: regioselective oxygenation and evidence for a role for CYP2C enzymes in arachidonic acid epoxygenation in human liver microsomes.	Arachidonic Acid	0-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-138
7625847-0	1995	Arachidonic acid metabolism by human cytochrome P450s 2C8, 2C9, 2E1, and 1A2: regioselective oxygenation and evidence for a role for CYP2C enzymes in arachidonic acid epoxygenation in human liver microsomes.	Arachidonic Acid	150-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-138
7625847-17	1995	The CYP2C inhibitor sulfaphenazole depressed human liver microsomal epoxygenase activity by 50% at 50 microM, while alpha-naphthoflavone inhibited arachidonic acid epoxygenase activity by 27% at 2 microM and by 32% at 10 microM.	Sulfaphenazole	20-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-9
7625847-18	1995	Collectively, these findings suggest that human liver microsomal arachidonic acid metabolism is catalyzed principally by CYP2C enzymes.	Arachidonic Acid	65-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-126
7614688-16	1995	Furthermore, the poor metabolic activation of MeIQx by CYP3A and CYP2C, coupled with low constitutive levels of CYP1A isozymes, provide a metabolic explanation for the low hepatocarcinogenic potency of MeIQx in cynomolgus monkeys.	2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline	46-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-70
7614688-16	1995	Furthermore, the poor metabolic activation of MeIQx by CYP3A and CYP2C, coupled with low constitutive levels of CYP1A isozymes, provide a metabolic explanation for the low hepatocarcinogenic potency of MeIQx in cynomolgus monkeys.	2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline	202-207	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-70
7794915-6	1995	Gel shift analysis demonstrated that nuclear proteins from HepG2 cells had a high binding affinity for a 20-bp oligonucleotide containing the HPF-1 site of CYP2C9.	Oligonucleotides	111-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
7763308-0	1995	Role of cytochrome P450 2C9 and an allelic variant in the 4"-hydroxylation of (R)- and (S)-flurbiprofen.	(r)- and (s)-flurbiprofen	78-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-27
7741772-1	1995	58C80 [2-(4-t-butylcyclohexyl)-3-hydroxy-1,4-naphthoquinone] is an experimental naphthoquinone antimalarial drug which undergoes extensive alkyl hydroxylation to a single t-butylhydroxy metabolite in man in vivo and also in human liver microsomes, where this is catalysed primarily by a 54 kDa CYP2C9 form of cytochrome P450, P450hB20-27.	Bupravaquone	7-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	294-300
7741772-1	1995	58C80 [2-(4-t-butylcyclohexyl)-3-hydroxy-1,4-naphthoquinone] is an experimental naphthoquinone antimalarial drug which undergoes extensive alkyl hydroxylation to a single t-butylhydroxy metabolite in man in vivo and also in human liver microsomes, where this is catalysed primarily by a 54 kDa CYP2C9 form of cytochrome P450, P450hB20-27.	Naphthoquinones	45-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	294-300
7736913-8	1995	Inhibitors of CYP3A4/5 (gestodene and ketoconazole) and CYP2C9/10 (sulfaphenazole) attenuated the oxidation of both substrates.	Sulfaphenazole	67-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
7891318-0	1995	Human hepatic cytochrome P450 2C9 catalyzes the rate-limiting pathway of torsemide metabolism.	Torsemide	73-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-33
7891318-5	1995	The microsomal reaction was almost completely abolished by the specific CYP2C9 inhibitor sulfaphenazole and was inhibited competitively by the alternative CYP2C9 substrate tolbutamide.	Sulfaphenazole	89-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
7891318-5	1995	The microsomal reaction was almost completely abolished by the specific CYP2C9 inhibitor sulfaphenazole and was inhibited competitively by the alternative CYP2C9 substrate tolbutamide.	Sulfaphenazole	89-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
7891318-5	1995	The microsomal reaction was almost completely abolished by the specific CYP2C9 inhibitor sulfaphenazole and was inhibited competitively by the alternative CYP2C9 substrate tolbutamide.	Tolbutamide	172-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
7891318-5	1995	The microsomal reaction was almost completely abolished by the specific CYP2C9 inhibitor sulfaphenazole and was inhibited competitively by the alternative CYP2C9 substrate tolbutamide.	Tolbutamide	172-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
7891318-6	1995	Torsemide tolyl methylhydroxylase activity in microsomes from 16 human livers correlated significantly (rs = .81-.88) with tolbutamide and phenytoin hydroxylation, both CYP2C9-mediated reactions.	Torsemide	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
7891318-7	1995	Complementary DNA-expressed CYP2C9 catalyzed torsemide tolyl methylhydroxylation with an apparent Km (23 microM) similar to that observed for human liver microsomes and the IC50 values for sulfaphenazole inhibition of the reaction were essentially identical for the two enzyme sources.	Torsemide	45-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
7891318-7	1995	Complementary DNA-expressed CYP2C9 catalyzed torsemide tolyl methylhydroxylation with an apparent Km (23 microM) similar to that observed for human liver microsomes and the IC50 values for sulfaphenazole inhibition of the reaction were essentially identical for the two enzyme sources.	Sulfaphenazole	189-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
7891318-8	1995	Taken together, these data demonstrate that human hepatic torsemide tolyl methylhydroxylation is catalyzed predominantly, if not solely, by CYP2C9.	Torsemide	58-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
7628308-7	1995	In a panel of human microsomes, SMX-HA formation correlated with tolbutamide hydroxylase activity (r = 0.75; p = 0.01); CYP2C9 content (r = 0.79; p &lt; 0.01) and was inhibited 70% by 500 microM tolbutamide and 90% by 100 microM sulfaphenazole.	sulfamethoxazole hydroxylamine	32-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
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
7736913-9	1995	It was then demonstrated that microsomes containing either recombinant human liver CYP2C9 or CYP3A4 were capable of oxidizing both losartan and the aldehyde E3179 to the carboxylic acid E3174.	Losartan	131-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
7736913-9	1995	It was then demonstrated that microsomes containing either recombinant human liver CYP2C9 or CYP3A4 were capable of oxidizing both losartan and the aldehyde E3179 to the carboxylic acid E3174.	Aldehydes	148-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
7736913-9	1995	It was then demonstrated that microsomes containing either recombinant human liver CYP2C9 or CYP3A4 were capable of oxidizing both losartan and the aldehyde E3179 to the carboxylic acid E3174.	Carboxylic Acids	170-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
7736913-10	1995	Subsequently, it was shown that rabbit anti-CYP2C9 and anti-CYP3A3/4 inhibited the oxidation of losartan to E3174 in incubations with human liver microsomes.	Losartan	96-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
7736913-10	1995	Subsequently, it was shown that rabbit anti-CYP2C9 and anti-CYP3A3/4 inhibited the oxidation of losartan to E3174 in incubations with human liver microsomes.	losartan carboxylic acid	108-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
7720520-5	1995	The probes sulfaphenazole (CYP2C9) and quinidine (CYP2D6) selectively inhibited tolbutamide methylhydroxylation and bufuralol 1"-hydroxylation, respectively.	Sulfaphenazole	11-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
7773301-4	1995	The T416--&gt;C mutation in exon 3 of CYP2C9 (Cys144--&gt;Arg) creates an Ava II site.	Arginine	58-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
7773301-13	1995	The G1236--&gt;A mutation in exon 8 of CYP2C9 (Gly417--&gt;Asp) creates a Hph I site.	Aspartic Acid	59-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
7720520-5	1995	The probes sulfaphenazole (CYP2C9) and quinidine (CYP2D6) selectively inhibited tolbutamide methylhydroxylation and bufuralol 1"-hydroxylation, respectively.	Tolbutamide	80-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
7720520-5	1995	The probes sulfaphenazole (CYP2C9) and quinidine (CYP2D6) selectively inhibited tolbutamide methylhydroxylation and bufuralol 1"-hydroxylation, respectively.	bufuralol	116-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
8203907-8	1994	Overall, these results establish that (a) TAO is a selective inhibitor of the human CYP3A subfamily; (b) ANF potently inhibits CYP2C8 and CYP2C9, in addition to CYPs 1A1 and 1A2; and (c) DDC cannot be employed as a diagnostic inhibitory probe for CYP2E1.	Troleandomycin	42-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
7704034-4	1994	CYP2C9 is important in the metabolism certain of therapeutically used drugs including the anticoagulant drug warfarin and a number of nonsteroidal antiinflammatory drugs.	Warfarin	109-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
7704038-5	1994	An antibody raised against CYP2C9 (anti-human CYP2C) strongly inhibited diazepam N-demethylation in EM liver microsomes at a low substrate concentration (20 microM).	Diazepam	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
7704038-5	1994	An antibody raised against CYP2C9 (anti-human CYP2C) strongly inhibited diazepam N-demethylation in EM liver microsomes at a low substrate concentration (20 microM).	Diazepam	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-32
7981013-11	1994	Studies with a series of CYP isoform selective inhibitors and with an inhibitory anti-CYP2C antibody indicated that temazepam formation was carried out mainly by CYP3A isoforms, whereas the formation of N-desmethyldiazepam was mediated by both CYP3A isoforms and S-mephenytoin hydroxylase.	Temazepam	116-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-91
7981013-11	1994	Studies with a series of CYP isoform selective inhibitors and with an inhibitory anti-CYP2C antibody indicated that temazepam formation was carried out mainly by CYP3A isoforms, whereas the formation of N-desmethyldiazepam was mediated by both CYP3A isoforms and S-mephenytoin hydroxylase.	Nordazepam	203-222	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-91
8375128-1	1993	V. In vivo CYP2C9 activity as probed by (S)-warfarin is not enhanced in cystic fibrosis.	Warfarin	40-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
7903909-8	1994	Conversely, the formation of metabolite M5 remained unaffected by antibodies against CYP3A and by CYP3A substrates but was sensitive to diazepam inhibition, a preferential substrate of CYP2C.	Diazepam	136-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	185-190
8148870-0	1993	Cytochrome P450 mediated metabolism of diazepam in human and rat: involvement of human CYP2C in N-demethylation in the substrate concentration-dependent manner.	Diazepam	39-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-92
8148870-0	1993	Cytochrome P450 mediated metabolism of diazepam in human and rat: involvement of human CYP2C in N-demethylation in the substrate concentration-dependent manner.	Nitrogen	96-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-92
8148870-5	1993	Inhibitions of the N-demethylation by anti-CYP2C antibody and S-mephenytoin also depended on the substrate concentration and was detectable only at a low substrate concentration.	Nitrogen	19-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-48
8216369-0	1993	Cytochrome P450 2C9 is responsible for hydroxylation of the naphthoquinone antimalarial drug 58C80 in human liver.	Naphthoquinones	60-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
8004131-0	1994	Impaired (S)-warfarin metabolism catalysed by the R144C allelic variant of CYP2C9.	Warfarin	13-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
8286335-0	1994	Thiophene derivatives as new mechanism-based inhibitors of cytochromes P-450: inactivation of yeast-expressed human liver cytochrome P-450 2C9 by tienilic acid.	Thiophenes	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-142
8286335-0	1994	Thiophene derivatives as new mechanism-based inhibitors of cytochromes P-450: inactivation of yeast-expressed human liver cytochrome P-450 2C9 by tienilic acid.	Ticrynafen	146-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-142
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 9	Homo sapiens	138-144
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 9	Homo sapiens	36-42
8518837-6	1993	Furthermore, CYP2C9 produced by cDNA expression in yeasts, catalysed tolbutamide hydroxylation at rates similar to the rapid metabolizer group at both the 0.1 mM and 2.4 mM concentrations.	Tolbutamide	69-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
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 9	Homo sapiens	87-93
8518837-8	1993	Clear correlations were observed between the rate of microsomal tolbutamide hydroxylation at 0.1 mM and CYP2C9 protein content or the rate of S-mephenytoin 4"-hydroxylation in human liver.	Tolbutamide	64-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
8518837-9	1993	These results indicate that considerable portions of microsomal tolbutamide hydroxylation are catalysed by CYP2C9 or the closely related form in the rapid metabolizers.	Tolbutamide	64-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
2200675-5	1990	Phenobarbital and rifampicin increased P-450 IIC8/9/10 mRNA transcripts and the corresponding protein, while 3-methylcholanthrene was ineffective.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-54
8454228-2	1993	Debrisoquine/sparteine and mephenytoin polymorphisms are now known to be derived from defects in the human liver of specific forms of microsomal CYP (P450 or previously termed cytochrome P-450), CYP2D6 and CYP2C9 (2C18), respectively.	Debrisoquin	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	206-212
8454228-2	1993	Debrisoquine/sparteine and mephenytoin polymorphisms are now known to be derived from defects in the human liver of specific forms of microsomal CYP (P450 or previously termed cytochrome P-450), CYP2D6 and CYP2C9 (2C18), respectively.	Sparteine	13-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	206-212
8454228-2	1993	Debrisoquine/sparteine and mephenytoin polymorphisms are now known to be derived from defects in the human liver of specific forms of microsomal CYP (P450 or previously termed cytochrome P-450), CYP2D6 and CYP2C9 (2C18), respectively.	Mephenytoin	27-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	206-212
1445376-5	1992	The expressed enzymes showed tolbutamide hydroxylase activities, and these activities were inhibited by antibodies against P-450-HM2, a probable CYP2C9.	p-450-hm2	123-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
8070855-4	1993	Of the 10 human P450 forms studied, CYP2B6 was the most effective in forming of styrene glycol, followed by CYP1A2, CYP2E1 and CYP2C8; the human P450s CYP3A3, CYP3A4 and CYP3A5 also catalysed metabolism, but were much less active; and CYP2A6, CYP2C9 and CYP2D6 had little detectable activity.	styrene glycol	80-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	243-249
8417277-0	1993	Cytochrome P450TB (CYP2C): a major monooxygenase catalyzing diclofenac 4"-hydroxylation in human liver.	Diclofenac	60-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-24
8417277-2	1993	Inhibition studies were performed with tolbutamide and sulfaphenazole (respectively the prototype substrate and a selective inhibitor of cytochrome P450TB--CYP2C subfamily), and with phenytoin and (+/-)-warfarin, other proposed substrates of P450TB.	Sulfaphenazole	55-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-161
8417277-2	1993	Inhibition studies were performed with tolbutamide and sulfaphenazole (respectively the prototype substrate and a selective inhibitor of cytochrome P450TB--CYP2C subfamily), and with phenytoin and (+/-)-warfarin, other proposed substrates of P450TB.	Terbium	152-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-161
8417277-6	1993	Diclofenac 4"-hydroxylation is predominantly catalyzed by a cytochrome P450 isozyme of the CYP2C subfamily, most likely CYP2C9.	Diclofenac	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-96
8417277-6	1993	Diclofenac 4"-hydroxylation is predominantly catalyzed by a cytochrome P450 isozyme of the CYP2C subfamily, most likely CYP2C9.	Diclofenac	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
1917894-0	1991	Cytochrome P-450 human-2 (P-450IIC9) in mephenytoin hydroxylation polymorphism in human livers: differences in substrate and stereoselectivities among microheterogeneous P-450IIC species expressed in yeasts.	Mephenytoin	40-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-35
2200675-5	1990	Phenobarbital and rifampicin increased P-450 IIC8/9/10 mRNA transcripts and the corresponding protein, while 3-methylcholanthrene was ineffective.	Rifampin	18-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-54
20702214-3	1990	Phenobarbital and rifampicin were found to increase the levels of P-450 IIC8, 9, 10 mRNA and protein while troleandomycin and 3-methylcholanthrene were ineffective.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-79
20702214-3	1990	Phenobarbital and rifampicin were found to increase the levels of P-450 IIC8, 9, 10 mRNA and protein while troleandomycin and 3-methylcholanthrene were ineffective.	Rifampin	18-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-79
33822485-2	2021	Ivosidenib is an inducer of the CYP2B6, CYP2C8, CYP2C9, and CYP3A4 and an inhibitor of P-glycoprotein (P-gp), organic anion transporting polypeptide-1B1/1B3 (OATP1B1/1B3), and organic anion transporter-3 (OAT3) in vitro.	ivosidenib	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
33822485-7	2021	The model was also used to predict the DDIs of ivosidenib with CYP2B6, CYP2C8, CYP2C9, P-gp, OATP1B1/1B3, and OAT3 substrates.	ivosidenib	47-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
33802239-6	2021	We found that lignans with one or two methylenedioxyphenyl groups inhibited CYP2B6, CYP2C8, CYP2C9, CYP2C19, and CYP2E1 activities in a time- and concentration-dependent like their CYP3A inhibition.	Lignans	14-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
33811620-0	2021	Influence of CYP2C9, VKORC1, and CYP4F2 polymorphisms on the pharmacodynamic parameters of warfarin: a cross-sectional study.	Warfarin	91-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
33811620-9	2021	Groups" II and III CYP2C9 and VKORC1 genotypes were observed with reduced stable warfarin dose, increased WSI, higher log-INR variability, and increased bleeding risk.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
33811620-10	2021	The presence of *2 or *3 allele in CYP2C9 was observed with reduced stable warfarin doses akin to the presence of T alleles in VKORC1; however, the doses increased with T alleles in CYP4F2.	Warfarin	75-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
33811620-12	2021	Evaluating CYP2C9, VKORC1, and CYP4F2 genetic polymorphisms prior to warfarin initiation is likely to optimize therapeutic response.	Warfarin	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
33814360-8	2021	Voriconazole is metabolized and is a strong inhibitor of cytochrome (CYP)3A4, CYP2C9/10 and CYP2C19.	Voriconazole	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
33802239-10	2021	This suggests that the time-dependent inhibition of gomisin A against CYP2C8, CYP2C9, and CYP3A4 is due to the production of carbene reactive metabolite.	schizandrol B	52-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
33802239-10	2021	This suggests that the time-dependent inhibition of gomisin A against CYP2C8, CYP2C9, and CYP3A4 is due to the production of carbene reactive metabolite.	carbene	125-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
33588415-3	2020	We investigated the effect of sEH inhibitor (TPPU) on the expression of villin, CYP2C8, CYP2C9, CYP2J2, and sEH in undifferentiated and in vitro differentiated HT-29 and Caco2 cell lines.	TPPU	45-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
33780197-2	2020	The most important factor predicting daily warfarin dose is individual genotype, polymorphisms of genes CYP2C9 (warfarin metabolism) and VKORC1 (sensitivity for warfarin).	Warfarin	43-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
33780197-2	2020	The most important factor predicting daily warfarin dose is individual genotype, polymorphisms of genes CYP2C9 (warfarin metabolism) and VKORC1 (sensitivity for warfarin).	Warfarin	112-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
33780197-2	2020	The most important factor predicting daily warfarin dose is individual genotype, polymorphisms of genes CYP2C9 (warfarin metabolism) and VKORC1 (sensitivity for warfarin).	Warfarin	112-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
25385663-1	2015	Genotypes for cytochrome P450 (CYP) 2C9 and vitamin K epoxide reductase complex 1 (VKORC1) contribute significantly to the inter-patient variability in warfarin dose requirements.	Warfarin	152-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-39
28371488-10	2018	This study is vital to clinical usage of warfarin not only because of the pharmacokinetic parameters of the 2 pharmaceutical dosage forms of warfarin but also to obtain data on the prevalence of CYP2C9 and VKORC1 genes and their influence on the concentration of warfarin.	Warfarin	41-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
29368402-3	2018	The parameters for cytochrome P450 (CYP) 3A and CYP2C9 induction by rifampicin were similarly optimized using clinical DDI data with midazolam and tolbutamide as probe substrates, respectively.	Rifampin	68-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
9686881-0	1998	Chiral phase analysis of warfarin enantiomers in patient plasma in relation to CYP2C9 genotype.	Warfarin	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
24002148-10	2013	Efinaconazole is a CYP inhibitor like other azole antifungals, and its lowest ki is 91 ng/mL for CYP2C9, a &gt;130-fold higher concentration than the mean steady state Cmax observed in patients.	efinaconazole	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
24002148-10	2013	Efinaconazole is a CYP inhibitor like other azole antifungals, and its lowest ki is 91 ng/mL for CYP2C9, a &gt;130-fold higher concentration than the mean steady state Cmax observed in patients.	Azoles	8-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
9686881-7	1998	Two warfarin patients homozygous for the mutant CYP2C9*2 and CYP2C9*3 alleles exhibited elevated S/R ratios relative to the mean for individuals homozygous for the wild-type CYP2C9*1 allele.	Warfarin	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
9686881-7	1998	Two warfarin patients homozygous for the mutant CYP2C9*2 and CYP2C9*3 alleles exhibited elevated S/R ratios relative to the mean for individuals homozygous for the wild-type CYP2C9*1 allele.	Warfarin	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
9686881-7	1998	Two warfarin patients homozygous for the mutant CYP2C9*2 and CYP2C9*3 alleles exhibited elevated S/R ratios relative to the mean for individuals homozygous for the wild-type CYP2C9*1 allele.	Warfarin	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
9686881-8	1998	This method is suitable for population studies aimed at establishing the effect of polymorphic expression of CYP2C9 alleles on S-warfarin elimination in humans.	Warfarin	129-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
34078115-6	2022	IL-6 inhibitors (sirukumab, tocilizumab, sarilumab) significantly enhance metabolism via CYP2C9 (s-warfarin), CYP2C19 (omeprazole), and CYP3A4 (simvastatin, midazolam) and reduce metabolism via CYP1A2 (caffeine).	Warfarin	99-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
17646282-4	2007	Incubating (R)-tofisopam with recombinant cytochrome P450 (P450) or with human liver microsomes and isoform-selective P450 chemical inhibitors indicated that M3 was primarily catalyzed by CYP2C9.	tofisopam	11-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	188-194
34671112-5	2022	Seventy-three percent had normal functioning SLCO1B1 transporter, 4% carried the HLA-B*58:01 risk variant, and 35% carried VKORC1 and CYP2C9 variants that increased warfarin sensitivity.	Warfarin	165-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
34656068-1	2022	Sulfonylureas (SUs) are predominantly metabolized by cytochrome p450 2C9 (CYP2C9) and cytochrome p450 2C19 (CYP2C19) enzymes.	Sulfonylurea Compounds	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-72
34656068-1	2022	Sulfonylureas (SUs) are predominantly metabolized by cytochrome p450 2C9 (CYP2C9) and cytochrome p450 2C19 (CYP2C19) enzymes.	Sulfonylurea Compounds	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
34656068-1	2022	Sulfonylureas (SUs) are predominantly metabolized by cytochrome p450 2C9 (CYP2C9) and cytochrome p450 2C19 (CYP2C19) enzymes.	Sulfonylurea Compounds	15-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-72
34656068-1	2022	Sulfonylureas (SUs) are predominantly metabolized by cytochrome p450 2C9 (CYP2C9) and cytochrome p450 2C19 (CYP2C19) enzymes.	Sulfonylurea Compounds	15-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
34656068-2	2022	CYP2C9 polymorphisms are associated with greater treatment response and hypoglycemic risk in SU users.	Sulfonylurea Compounds	93-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
34453556-1	2022	PURPOSE: The purpose of this paper is to study the correlation between demographic and clinical factors and warfarin dose of patients in Chinese Han population taking warfarin and study gene polymorphisms impact of related gene loci (CYP2C9*3, VKORC1-1639G > A) on warfarin doses, to establish a model to predict initial standard dose and maintenance dose based on CYP2C9*3, VKORC1-1639G > A genotype.	Warfarin	108-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	234-240
34920277-2	2022	We investigated the role of SNPs in CYP2C9, CYP2C19, CYP2D6, UGT2B15, and UGT1A7 genes in the biotransformation of phthalates (DEHP, DEP, DiBP, DnBP, BBzP, DiNP, DidP) and DINCH by determining their urine metabolites.	phthalic acid	115-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
34920277-6	2022	The most pronounced was the influence of CYP2C9*2 and *3 on the reduced DEHP biotransformation, with lower levels of metabolites and their ratios in men and women.	Diethylhexyl Phthalate	72-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
34920277-10	2022	Our observations confirm the effect of CYP2C9*2 and *3 SNPs towards reduced DEHP biotransformation.	Diethylhexyl Phthalate	76-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
34453556-1	2022	PURPOSE: The purpose of this paper is to study the correlation between demographic and clinical factors and warfarin dose of patients in Chinese Han population taking warfarin and study gene polymorphisms impact of related gene loci (CYP2C9*3, VKORC1-1639G > A) on warfarin doses, to establish a model to predict initial standard dose and maintenance dose based on CYP2C9*3, VKORC1-1639G > A genotype.	Warfarin	108-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	365-371
34453556-1	2022	PURPOSE: The purpose of this paper is to study the correlation between demographic and clinical factors and warfarin dose of patients in Chinese Han population taking warfarin and study gene polymorphisms impact of related gene loci (CYP2C9*3, VKORC1-1639G > A) on warfarin doses, to establish a model to predict initial standard dose and maintenance dose based on CYP2C9*3, VKORC1-1639G > A genotype.	Warfarin	265-273	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	234-240
34453556-4	2022	RESULTS: The initial dose of warfarin (mg/day) was calculated as (1.346 + 0.350 x (VKORC1-1639G > A) - 0.273 x (CYP2C9*3) + 0.245 x (body surface area) - 0.003 x (age) - 0.036 x (amine-iodine) + 0.021 x (sex))2.	Warfarin	29-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
34453556-6	2022	The maintenance dose of warfarin (mg/day) was calculated as (1.336 + 0.299 x (VKORC1-1639G > A) + 0.480 x (body surface area) - 0.214 x (CYP2C9*3) - 0.074 x (amine-iodine) - 0.003 x (age) - 0.077 x (statins) - 0.002 x (height))2.	Warfarin	24-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
34872459-11	2021	Patients with tuberculosis with older age and genetic polymorphism of CYP3A4, CYP2C9, and CYP2C19 who received long-term rifampicin treatment were more likely to have antituberculosis drug-induced liver injury.	Rifampin	121-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
34780725-4	2022	We also confirmed dabrafenib as a CYP2C8, CYP2C9, CYP3A4, and CYP3A5 inhibitor.	dabrafenib	18-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
34865639-3	2021	METHODS: Preclinical evaluation of strasseriolides A-D was performed by MTT-based cytotoxicity assay in THLE-2 (CRL-2706) liver cells, cardiotoxicity screening using the FluxOR  potassium assay in hERG expressed HEK cells, LC-MS-based analysis of drug-drug interaction involving CYP3A4, CYP2D6 and CYP2C9 isoforms inhibition and metabolic stability assays in human liver microsomes.	strasseriolides	35-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	298-304
34748821-0	2021	CYP2C9 and 3A4 play opposing roles in bioactivation and detoxification of diphenylamine NSAIDs.	Diphenylamine	74-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
34748821-8	2021	When considering hepatic CYP abundance, CYP2C9 almost exclusively accounted for diphenylamine NSAID bioactivations, whereas CYP3A4 provided a critical counterbalance favoring their overall detoxification.	Diphenylamine	80-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
34896433-5	2022	In addition, alisertib was characterized as a low- to moderate-affinity inhibitor of recombinant CYP3A4, CYP2C8, CYP2C9, CYP2C19, and CYP2D6 isoenzymes, but without potential clinical relevance.	MLN 8237	13-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
34952963-0	2022	Effects of CYP2C9*3 and *13 alleles on the pharmacokinetics and pharmacodynamics of glipizide in healthy Korean subjects.	Glipizide	84-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
34952963-3	2022	In this study, we investigated the effects of CYP2C9*3 and *13 variant alleles on the pharmacokinetics and pharmacodynamics of glipizide.	Glipizide	127-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
34952963-7	2022	The results represented that CYP2C9*3 and *13 alleles significantly affected the pharmacokinetics of glipizide.	Glipizide	101-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
34952963-8	2022	In subjects with CYP2C9*1/*3 and CYP2C9*1/*13 genotypes, the mean AUC0-  were increased by 44.8% and 58.2%, respectively (both P < 0.001), compared to those of subjects with CYP2C9*1/*1 genotype, while effects of glipizide on plasma glucose and insulin levels were not significantly different between CYP2C9 genotype groups.	Glipizide	213-222	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
34952963-8	2022	In subjects with CYP2C9*1/*3 and CYP2C9*1/*13 genotypes, the mean AUC0-  were increased by 44.8% and 58.2%, respectively (both P < 0.001), compared to those of subjects with CYP2C9*1/*1 genotype, while effects of glipizide on plasma glucose and insulin levels were not significantly different between CYP2C9 genotype groups.	Glucose	233-240	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
34952963-9	2022	In conclusion, individuals carrying the defective CYP2C9*3 and CYP2C9*13 alleles have markedly elevated plasma concentrations of glipizide compared with CYP2C9*1/*1 wild-type.	Glipizide	129-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
34952963-9	2022	In conclusion, individuals carrying the defective CYP2C9*3 and CYP2C9*13 alleles have markedly elevated plasma concentrations of glipizide compared with CYP2C9*1/*1 wild-type.	Glipizide	129-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
34807366-2	2021	Cytochrome P450 (CYP) 2C9 and CYP3A4 are major and minor enzymes involved in the metabolism of meloxicam.	Meloxicam	95-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-25
34807366-3	2021	Impaired enzyme activity of CYP2C9 variants increases the plasma exposures of meloxicam and the risk of adverse events.	Meloxicam	78-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
34807366-12	2021	This study is expected to contribute to reducing the risk of adverse events of meloxicam through optimization of meloxicam dosing in different CYP2C9 genotypes.	Meloxicam	79-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
34817825-0	2021	Physiologically based pharmacokinetic modeling of candesartan related to CYP2C9 genetic polymorphism in adult and pediatric patients.	candesartan	50-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
34817825-3	2021	Candesartan is metabolized by cytochrome P450 2C9 (CYP2C9) enzyme or uridine diphosphate glucurinosyltransferase 1A3, or excreted in an unchanged form through urine, biliary tract and feces.	candesartan	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-49
34817825-3	2021	Candesartan is metabolized by cytochrome P450 2C9 (CYP2C9) enzyme or uridine diphosphate glucurinosyltransferase 1A3, or excreted in an unchanged form through urine, biliary tract and feces.	candesartan	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
34505930-12	2021	CONCLUSION: Ruxolitinib exposure is increased in GvHD patients in comparison to myelofibrosis patients due to reduced clearance and comedication with CYP3A4 or CYP2C9 inhibitors.	ruxolitinib	12-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
33915070-8	2021	For the inhibition of CYP2C9 and 2E1, pogostone acted as a competitive inhibitor with the Ki value of 6.46 and 7.67 muM and was not affected by the incubation time.	Pogostone	38-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-36
34493602-8	2021	These data suggest that cannabinoids and major THC metabolites are able to inhibit the activities of multiple CYP enzymes, and basic static modelling of these data suggest the possibility of pharmacokinetic interactions between these cannabinoids and xenobiotics extensively metabolized by CYP2B6, CYP2C9 and CYP2D6.	Cannabinoids	24-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	298-304
34493602-8	2021	These data suggest that cannabinoids and major THC metabolites are able to inhibit the activities of multiple CYP enzymes, and basic static modelling of these data suggest the possibility of pharmacokinetic interactions between these cannabinoids and xenobiotics extensively metabolized by CYP2B6, CYP2C9 and CYP2D6.	Dronabinol	47-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	298-304
34493602-8	2021	These data suggest that cannabinoids and major THC metabolites are able to inhibit the activities of multiple CYP enzymes, and basic static modelling of these data suggest the possibility of pharmacokinetic interactions between these cannabinoids and xenobiotics extensively metabolized by CYP2B6, CYP2C9 and CYP2D6.	Cannabinoids	234-246	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	298-304
34493602-9	2021	Significance Statement Major cannabinoids and their metabolites found in the plasma of cannabis users inhibit several CYP enzymes, including CYP2B6, CYP2C9, and CYP2D6.	Cannabinoids	29-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
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
34382722-2	2021	Genetic variation in CYP2C9 and VKORC1 has been the traditional focus in evaluating warfarin dose variability, with little focus on other genes.	Warfarin	84-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
34382722-3	2021	OBJECTIVE: We set out to evaluate 27 single nucleotide polymorphisms (SNPs) in the CYP2C cluster loci and 8 genes (VKORC1, ABCB1, CYP2C9, CYP2C19, CYP2C8, CYP1A2, CYP3A4, and CYP3A5) involved in pharmacokinetics of warfarin.	Warfarin	215-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
34382722-6	2021	RESULTS: Among black Africans, the SNPs CYP2C rs12777823G>A, CYP2C9 c.449G>A (*8), CYP2C9 c.1003C>T (*11) and CYP2C8 c.805A>T (*2) were significantly associated with warfarin maintenance dose.	Warfarin	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
34382722-6	2021	RESULTS: Among black Africans, the SNPs CYP2C rs12777823G>A, CYP2C9 c.449G>A (*8), CYP2C9 c.1003C>T (*11) and CYP2C8 c.805A>T (*2) were significantly associated with warfarin maintenance dose.	Warfarin	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
34382722-8	2021	The presence of CYP2C8*2 and CYP3A5*6 alleles was associated with increased mean warfarin maintenance dose, whereas CYP2C9*8 allele was associated with reduced warfarin maintenance dose.	Warfarin	160-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
34729928-11	2022	The genetic variants within VKORC1 rs9934438 and CYP2C9 rs4086116 explained 39% and 27% of the variability in the weekly warfarin dose requirement in the Qatari and Egyptians, respectively.	Warfarin	121-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
34727989-12	2021	CONCLUSIONS: Based on the clinical course and literature review, we believe that hypoglycemia in the present case was due to a drug interaction, caused by inhibition of CYP2C9 by bucolome and competitive inhibition of CYP2C9 by warfarin, which affected the pharmacokinetics of glimepiride.	Warfarin	228-236	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
34727989-12	2021	CONCLUSIONS: Based on the clinical course and literature review, we believe that hypoglycemia in the present case was due to a drug interaction, caused by inhibition of CYP2C9 by bucolome and competitive inhibition of CYP2C9 by warfarin, which affected the pharmacokinetics of glimepiride.	glimepiride	277-288	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
34727989-12	2021	CONCLUSIONS: Based on the clinical course and literature review, we believe that hypoglycemia in the present case was due to a drug interaction, caused by inhibition of CYP2C9 by bucolome and competitive inhibition of CYP2C9 by warfarin, which affected the pharmacokinetics of glimepiride.	glimepiride	277-288	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
34729928-13	2022	It confirms the importance of VKORC1 and CYP2C9 variants in warfarin dose variability among patients from the MENA region.	Warfarin	60-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
34721047-11	2021	In contrast, ticagrelor-O-glucuronide weakly inhibited CYP2B6, CYP2C9 and CYP2C19 activity with apparent IC50 values of 45.0, 20.0 and 18.8 muM, respectively.	ticagrelor-o-glucuronide	13-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
34357562-5	2021	The reduced function alleles CYP2C9*2 and CYP2C9*3, and VKORC1 rs9923231 (c.-1639G>A) are associated with increased sensitivity to warfarin and a low dose requirement to prevent bleeding episodes, whereas CYP4F2 rs2108622 (p.Val433Met) carriers have higher dose requirements (warfarin resistance).	Warfarin	131-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
34357562-5	2021	The reduced function alleles CYP2C9*2 and CYP2C9*3, and VKORC1 rs9923231 (c.-1639G>A) are associated with increased sensitivity to warfarin and a low dose requirement to prevent bleeding episodes, whereas CYP4F2 rs2108622 (p.Val433Met) carriers have higher dose requirements (warfarin resistance).	Warfarin	131-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
34357562-5	2021	The reduced function alleles CYP2C9*2 and CYP2C9*3, and VKORC1 rs9923231 (c.-1639G>A) are associated with increased sensitivity to warfarin and a low dose requirement to prevent bleeding episodes, whereas CYP4F2 rs2108622 (p.Val433Met) carriers have higher dose requirements (warfarin resistance).	Warfarin	276-284	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
34693729-2	2021	Nala PGx Core  is a multi-gene qPCR-based panel of 20 allele variants, comprising 18 SNPs and two CYP2D6 copy number markers across four pharmacogenes - CYP2C9, CYP2C19, CYP2D6 and SLCO1B1.	N-acetylleucinamide	0-4	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
34498315-2	2021	METHODS: A MassARRAY approach was used to detect single nucleotide polymorphism (SNP) loci in the URAT1 and CYP2C9 genes (16 and 2 loci, respectively) in 111 patients with hypertension and hyperuricemia taking losartan and in 121 healthy controls.	Losartan	210-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
34330718-11	2021	Significance Statement This study demonstrates that both CYP2C19 and CYP2C9 are involved in CBD metabolism to the active metabolite 7-OH-CBD, and CYP3A4 is a major contributor to CBD metabolism through pathways other than 7-hydroxylation.	7-Hydroxycannabidiol	132-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
34330718-12	2021	7-OH-CBD formation was associated with human liver microsomal CYP2C19 activity, but not CYP2C19 genotype, and CYP2C9 was found to contribute significantly to 7-OH-CBD generation.	7-Hydroxycannabidiol	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
34330718-12	2021	7-OH-CBD formation was associated with human liver microsomal CYP2C19 activity, but not CYP2C19 genotype, and CYP2C9 was found to contribute significantly to 7-OH-CBD generation.	7-Hydroxycannabidiol	158-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
34330718-6	2021	The results from reaction phenotyping experiments with recombinant CYP enzymes and CYP-selective chemical inhibitors indicated that both CYP2C19 and CYP2C9 are capable of CBD metabolism to 7-OH-CBD.	Cannabidiol	171-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
34330718-6	2021	The results from reaction phenotyping experiments with recombinant CYP enzymes and CYP-selective chemical inhibitors indicated that both CYP2C19 and CYP2C9 are capable of CBD metabolism to 7-OH-CBD.	7-Hydroxycannabidiol	189-197	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
34330718-9	2021	In a subset of single-donor human liver microsomes with moderate to low CYP2C19 activity, CYP2C9 inhibition significantly reduced 7-OH-CBD formation, suggesting that CYP2C9 may play a greater role in CBD 7-hydroxylation than previously thought.	7-Hydroxycannabidiol	130-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
34330718-9	2021	In a subset of single-donor human liver microsomes with moderate to low CYP2C19 activity, CYP2C9 inhibition significantly reduced 7-OH-CBD formation, suggesting that CYP2C9 may play a greater role in CBD 7-hydroxylation than previously thought.	7-Hydroxycannabidiol	130-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	166-172
34330718-9	2021	In a subset of single-donor human liver microsomes with moderate to low CYP2C19 activity, CYP2C9 inhibition significantly reduced 7-OH-CBD formation, suggesting that CYP2C9 may play a greater role in CBD 7-hydroxylation than previously thought.	Cannabidiol	200-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
34330718-9	2021	In a subset of single-donor human liver microsomes with moderate to low CYP2C19 activity, CYP2C9 inhibition significantly reduced 7-OH-CBD formation, suggesting that CYP2C9 may play a greater role in CBD 7-hydroxylation than previously thought.	Cannabidiol	200-203	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	166-172
34330718-10	2021	Collectively, these data indicate that both CYP2C19 and CYP2C9 are important contributors in CBD metabolism to the active metabolite 7-OH-CBD.	Cannabidiol	93-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
34330718-10	2021	Collectively, these data indicate that both CYP2C19 and CYP2C9 are important contributors in CBD metabolism to the active metabolite 7-OH-CBD.	7-Hydroxycannabidiol	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
34330718-11	2021	Significance Statement This study demonstrates that both CYP2C19 and CYP2C9 are involved in CBD metabolism to the active metabolite 7-OH-CBD, and CYP3A4 is a major contributor to CBD metabolism through pathways other than 7-hydroxylation.	Cannabidiol	92-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
34429480-1	2021	CYP2C9, one of the most abundant hepatic cytochrome P450 enzymes, is involved in metabolism of 15-20% of clinically important drugs (warfarin, sulfonylureas, phenytoin, non-steroid anti-inflammatory drugs).	Warfarin	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
34106453-1	2021	BACKGROUND: Several studies optimized the warfarin dose based on CYP2C9*2, CYP2C9*3, VKORC1 -1639 G > A, CYP4F2 V433M.	Warfarin	42-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
34106453-1	2021	BACKGROUND: Several studies optimized the warfarin dose based on CYP2C9*2, CYP2C9*3, VKORC1 -1639 G > A, CYP4F2 V433M.	Warfarin	42-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
34680932-1	2021	The genotypes of vitamin K epoxide reductase complex 1 (VKORC1) and cytochrome P450 2C9 (CYP2C9) can influence therapeutic warfarin doses.	Warfarin	123-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-87
34680932-1	2021	The genotypes of vitamin K epoxide reductase complex 1 (VKORC1) and cytochrome P450 2C9 (CYP2C9) can influence therapeutic warfarin doses.	Warfarin	123-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
34900803-0	2021	A pharmacogenetic pilot study of CYP2C9 common genetic variant and sulfonylureas therapeutic response in type 2 diabetes mellitus patients.	Sulfonylurea Compounds	67-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
34900803-2	2021	Sulfonylureas (SFUs) are the most widely used among the oral antidiabetic drugs that are highly metabolized by cytochrome P450 family 2 subfamily C member 9 (CYP2C9).	Sulfonylurea Compounds	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-156
34900803-2	2021	Sulfonylureas (SFUs) are the most widely used among the oral antidiabetic drugs that are highly metabolized by cytochrome P450 family 2 subfamily C member 9 (CYP2C9).	Sulfonylurea Compounds	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
34900803-2	2021	Sulfonylureas (SFUs) are the most widely used among the oral antidiabetic drugs that are highly metabolized by cytochrome P450 family 2 subfamily C member 9 (CYP2C9).	Sulfonylurea Compounds	15-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-156
34900803-2	2021	Sulfonylureas (SFUs) are the most widely used among the oral antidiabetic drugs that are highly metabolized by cytochrome P450 family 2 subfamily C member 9 (CYP2C9).	Sulfonylurea Compounds	15-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
34314704-2	2021	In particular, the anti-coagulant warfarin is prescribed to over 15 million people annually and polymorphisms in CYP2C9 can affect individual drug response and lead to an increased risk of hemorrhage.	Warfarin	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
34273250-0	2021	Prediction of the drug-drug interaction potential of the alpha-acid glycoprotein bound, CYP3A4/CYP2C9 metabolized oncology drug, erdafitinib.	erdafitinib	129-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
34273250-2	2021	Erdafitinib binds preferentially to alpha1-acid glycoprotein (AGP), and is primarily metabolized by cytochrome P450 (CYP) 2C9 and 3A4.	erdafitinib	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-125
34273250-3	2021	This article describes a physiologically based pharmacokinetic (PBPK) model for erdafitinib to assess the drug-drug interaction (DDI) potential of CYP3A4 and CYP2C9 inhibitors, and CYP3A4/CYP2C9 inducers on erdafitinib PK in cancer patients exhibiting higher AGP levels and in population with different CYP2C9 genotypes.	erdafitinib	80-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
34273250-3	2021	This article describes a physiologically based pharmacokinetic (PBPK) model for erdafitinib to assess the drug-drug interaction (DDI) potential of CYP3A4 and CYP2C9 inhibitors, and CYP3A4/CYP2C9 inducers on erdafitinib PK in cancer patients exhibiting higher AGP levels and in population with different CYP2C9 genotypes.	erdafitinib	80-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	188-194
34273250-3	2021	This article describes a physiologically based pharmacokinetic (PBPK) model for erdafitinib to assess the drug-drug interaction (DDI) potential of CYP3A4 and CYP2C9 inhibitors, and CYP3A4/CYP2C9 inducers on erdafitinib PK in cancer patients exhibiting higher AGP levels and in population with different CYP2C9 genotypes.	erdafitinib	80-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	303-309
34273250-3	2021	This article describes a physiologically based pharmacokinetic (PBPK) model for erdafitinib to assess the drug-drug interaction (DDI) potential of CYP3A4 and CYP2C9 inhibitors, and CYP3A4/CYP2C9 inducers on erdafitinib PK in cancer patients exhibiting higher AGP levels and in population with different CYP2C9 genotypes.	erdafitinib	207-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	188-194
34273250-6	2021	Erdafitinib clearance in the PBPK model consisted of multiple pathways (CYP2C9/3A4, renal, intestinal; additional hepatic clearance), making the compound less susceptible to DDIs.	erdafitinib	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-82
34273250-7	2021	In poor metabolizing CYP2C9 populations carrying the CYP2C9*3/*3 genotype, simulations shown clinically relevant increase in erdafitinib plasma concentrations.	erdafitinib	125-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
34273250-7	2021	In poor metabolizing CYP2C9 populations carrying the CYP2C9*3/*3 genotype, simulations shown clinically relevant increase in erdafitinib plasma concentrations.	erdafitinib	125-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
34664206-5	2021	The processes implemented to describe the rosuvastatin pharmacokinetics and DDIs are active uptake by OATP2B1, OATP1B1/OATP1B3 and OAT3, active efflux by BCRP and Pgp, metabolism by CYP2C9 and passive glomerular filtration.	Rosuvastatin Calcium	42-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	182-188
34638547-5	2021	The X-ray crystal structure of CYP2C9*8, which represents an amino acid variation from arginine to histidine at position 150 (R150H), was solved in complex with losartan.	Losartan	161-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
34638547-6	2021	The overall conformation of the CYP2C9*8-losartan complex was similar to the previously solved complex with wild type (WT) protein, but it differs in the occupancy of losartan.	8-losartan	39-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
34638547-6	2021	The overall conformation of the CYP2C9*8-losartan complex was similar to the previously solved complex with wild type (WT) protein, but it differs in the occupancy of losartan.	Losartan	167-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
34638547-10	2021	Interestingly, the CYP2C9*8 interaction with losartan was not as weak as the CYP2C9*3 variant, which showed up to three-fold weaker average dissociation constant compared to the WT.	Losartan	45-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
34638547-11	2021	Taken together, the structural and solution characterization yields insights into the similarities and differences of losartan binding to CYP2C9 variants and provides a useful framework for probing the role of amino acid substitution and substrate dependent activity.	Losartan	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
34575495-2	2021	Resveratrol enantiomers showed stereoselective inhibition of CYP2C9, CYP3A, and UGT1A1.	Resveratrol	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
34109627-2	2021	Genetic variation within the CYP2C9 gene locus impacts the metabolism or bioactivation of many clinically important drugs including NSAIDs, phenytoin, anti-diabetic agents and angiotensin receptor blocker.	Phenytoin	140-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
34109627-3	2021	Variable CYP2C9 activity is of particular importance regarding efficacy and safety of warfarin and siponimod as indicated in their package inserts.	Warfarin	86-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
34109627-3	2021	Variable CYP2C9 activity is of particular importance regarding efficacy and safety of warfarin and siponimod as indicated in their package inserts.	siponimod	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
34429480-1	2021	CYP2C9, one of the most abundant hepatic cytochrome P450 enzymes, is involved in metabolism of 15-20% of clinically important drugs (warfarin, sulfonylureas, phenytoin, non-steroid anti-inflammatory drugs).	Sulfonylurea Compounds	143-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
34429480-1	2021	CYP2C9, one of the most abundant hepatic cytochrome P450 enzymes, is involved in metabolism of 15-20% of clinically important drugs (warfarin, sulfonylureas, phenytoin, non-steroid anti-inflammatory drugs).	Phenytoin	158-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
34429480-1	2021	CYP2C9, one of the most abundant hepatic cytochrome P450 enzymes, is involved in metabolism of 15-20% of clinically important drugs (warfarin, sulfonylureas, phenytoin, non-steroid anti-inflammatory drugs).	Steroids	173-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
34429480-4	2021	The presence of CYP2C9*3 allele was associated with CYP2C9 functional impairment, and CYP2C9*2 influenced tolbutamide 4"-hydroxylase activity only in subjects with two polymorphic alleles, whereas the contribution of CYP2C8*3 was not confirmed.	Tolbutamide	106-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
34429480-5	2021	In addition to CYP2C9 genetic polymorphisms, non-genetic factors (co-medication with CYP2C9-specific inhibitors/inducers and non-specific factors including amoxicillin + clavulanic acid therapy or chronic alcohol consumption) contributed to the prediction of hepatic CYP2C9 activity; however, a CYP2C9 genotype-phenotype mismatch still existed in 32.6% of the subjects.	Amoxicillin-Potassium Clavulanate Combination	156-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	267-273
34429480-5	2021	In addition to CYP2C9 genetic polymorphisms, non-genetic factors (co-medication with CYP2C9-specific inhibitors/inducers and non-specific factors including amoxicillin + clavulanic acid therapy or chronic alcohol consumption) contributed to the prediction of hepatic CYP2C9 activity; however, a CYP2C9 genotype-phenotype mismatch still existed in 32.6% of the subjects.	Alcohols	205-212	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	267-273
34194474-11	2021	The CYP2C9 alleles, * 2 (rs1799853C>T) and * 3 (rs1057910A>C) that are predictive of low enzyme activity were more common in subjects who experienced hypoglycemia after treatment with sulfonylureas.	Sulfonylurea Compounds	184-197	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
34242938-7	2021	The final PBPK/PD model of warfarin enantiomers was verified and validated by different dosing regimens, ethnicities and genetic polymorphisms, and used to perform DDI simulations between warfarin racemate and sorafenib among general populations and sub-populations with various CYP2C9 and VKORC1 genotypes.	Warfarin	27-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	279-285
34242938-7	2021	The final PBPK/PD model of warfarin enantiomers was verified and validated by different dosing regimens, ethnicities and genetic polymorphisms, and used to perform DDI simulations between warfarin racemate and sorafenib among general populations and sub-populations with various CYP2C9 and VKORC1 genotypes.	Sorafenib	210-219	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	279-285
34074714-4	2021	The IC50 for inhibition of CYP2C8, CYP2C9, and CYP3A4/5 for verinurad was {greater than or equal to}14.5 microM, and Iu,max/IC50 was <0.02 at the anticipated therapeutic Cmax and therefore was not considered a DDI risk.	verinurad	60-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
34246203-4	2021	The aims of the present study are to assess the possible association of CYP2D6 and CYP2C9 polymorphisms with the efficacy and safety of tramadol and ketorolac in postoperative pain.	Tramadol	136-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
34246203-4	2021	The aims of the present study are to assess the possible association of CYP2D6 and CYP2C9 polymorphisms with the efficacy and safety of tramadol and ketorolac in postoperative pain.	Ketorolac	149-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
34246203-15	2021	CONCLUSIONS: CYP2D6 and CYP2C9 can predict analgesic effectiveness of tramadol and ketorolac.	Tramadol	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
34246203-15	2021	CONCLUSIONS: CYP2D6 and CYP2C9 can predict analgesic effectiveness of tramadol and ketorolac.	Ketorolac	83-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
34246203-16	2021	CYP2C9 can predict the risk of gastrointestinal bleeding, including those hidden to ketorolac.	Ketorolac	84-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
34304363-0	2021	Physiologically based pharmacokinetic (PBPK) modeling for prediction of celecoxib pharmacokinetics according to CYP2C9 genetic polymorphism.	Celecoxib	72-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
34304363-3	2021	Many studies reported that CYP2C9 genetic polymorphism has significant effects on the pharmacokinetics of celecoxib and the occurrence of adverse drug reactions.	Celecoxib	106-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
34304363-4	2021	The aim of this study was to develop a physiologically based pharmacokinetic (PBPK) model of celecoxib according to CYP2C9 genetic polymorphism for personalized pharmacotherapy.	Celecoxib	93-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
34304363-6	2021	Based on the conducted pharmacokinetic study and a previous pharmacokinetic study involving subjects with CYP2C9*1/*13 and CYP2C9*3/*3 genotype, PBPK model for celecoxib was developed.	Celecoxib	160-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
34304363-6	2021	Based on the conducted pharmacokinetic study and a previous pharmacokinetic study involving subjects with CYP2C9*1/*13 and CYP2C9*3/*3 genotype, PBPK model for celecoxib was developed.	Celecoxib	160-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
34304363-9	2021	As a result, the developed PBPK model of celecoxib successfully described the pharmacokinetics of each CYP2C9 genotype group and its predicted values were within the acceptance criterion.	Celecoxib	41-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
34304363-11	2021	This study demonstrates the possibility of determining the appropriate dosage of celecoxib for each individual through the PBPK modeling with CYP2C9 genomic information.	Celecoxib	81-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
34143391-5	2021	Lenabasum is a CYP substrate, and the model predicted lenabasum clearance of 51% by CYP2C9, 37% by CYP2C8, and 12% by CYP3A4.	lenabasum	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
34143391-5	2021	Lenabasum is a CYP substrate, and the model predicted lenabasum clearance of 51% by CYP2C9, 37% by CYP2C8, and 12% by CYP3A4.	lenabasum	54-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
34060344-0	2021	A meta-analysis of effects of CYP2C9 and CYP2C19 polymorphisms on phenytoin pharmacokinetic parameters.	Phenytoin	66-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
34060344-1	2021	Aim: Phenytoin is metabolized through CYP2C9 and CYP2C19.	Phenytoin	5-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
34060344-8	2021	Conclusion: The dosage regimen for patients in the CYP2C9IM group to achieve phenytoin therapeutic levels was 2.1-3.4 mg/kg/day.	Phenytoin	77-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
34210056-0	2021	Influence of CYP2C9 Genetic Polymorphisms on the Pharmacokinetics of Losartan and Its Active Metabolite E-3174: A Systematic Review and Meta-Analysis.	Losartan	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
34210056-0	2021	Influence of CYP2C9 Genetic Polymorphisms on the Pharmacokinetics of Losartan and Its Active Metabolite E-3174: A Systematic Review and Meta-Analysis.	losartan carboxylic acid	104-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
34210056-1	2021	This study aimed to investigate the influence of CYP2C9 genetic polymorphisms on the pharmacokinetics of losartan and its active metabolite, E-3174, through a systematic review and meta-analysis.	Losartan	105-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
34210056-5	2021	We found that healthy volunteers with CYP2C9*2 or *3 carriers had higher area under the curve (AUC0- ) of losartan (mean difference (MD) 0.17 mug h/mL; 95% confidence intervals (CI): 0.04, 0.29) and lower AUC0-  of E-3174 (MD -0.35 mug h/mL; 95% CI: -0.62, -0.08) than those with CYP2C9*1/*1.	Losartan	106-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
34210056-7	2021	For half-life, subjects with CYP2C9*2 or *3 carriers had longer half-lives of losartan and E-3174 than those with CYP2C9*1/*1 (MD 0.47 h; 95% CI: 0.32, 0.61 and MD 0.68 h; 95% CI: 0.44, 0.92, respectively).	Losartan	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
34210056-7	2021	For half-life, subjects with CYP2C9*2 or *3 carriers had longer half-lives of losartan and E-3174 than those with CYP2C9*1/*1 (MD 0.47 h; 95% CI: 0.32, 0.61 and MD 0.68 h; 95% CI: 0.44, 0.92, respectively).	losartan carboxylic acid	91-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
34210056-8	2021	This meta-analysis suggests that the pharmacokinetics of losartan and E-3174 are associated with the CYP2C9 polymorphisms.	Losartan	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
34210056-8	2021	This meta-analysis suggests that the pharmacokinetics of losartan and E-3174 are associated with the CYP2C9 polymorphisms.	losartan carboxylic acid	70-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
34082641-5	2021	The inhibition of CYP2C9 and 2D was not affected by the incubation time but was found to be competitive with the Ki values of 6.7 and 6.6 muM, respectively.The inhibitory effect of 4-O-galloylalbiflorin on the activity of CYP3A, 2C9, and 2D implying the potential drug-drug interaction between 4-O-galloylalbiflorin and the drugs metabolized by these CYP450s.	4-O-galloylalbiflorin	181-202	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
34082641-5	2021	The inhibition of CYP2C9 and 2D was not affected by the incubation time but was found to be competitive with the Ki values of 6.7 and 6.6 muM, respectively.The inhibitory effect of 4-O-galloylalbiflorin on the activity of CYP3A, 2C9, and 2D implying the potential drug-drug interaction between 4-O-galloylalbiflorin and the drugs metabolized by these CYP450s.	4-O-galloylalbiflorin	294-315	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
34228652-0	2021	Impact of VKORC1, CYP2C9, and CYP4F2 Polymorphisms on Optimal Warfarin Dose: Does Ethnicity Matters?	Warfarin	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
34181150-11	2021	CYP2C9-mediated metabolism was inhibited by nearly all the cannabinoids with estimated Ki values of 0.2-3.2 muM.	Cannabinoids	59-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
34181150-14	2021	CYP2C9-mediated metabolism was inhibited by cannabinoids at clinically relevant concentrations.	Cannabinoids	44-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
34104863-8	2021	The combination of azithromycin intake, a known inhibitor of CYP2C9, with the presence of CYP2C9*2 and -1639G>A VKORC1, two variants associated with warfarin hypersensitivity, have likely contributed to explain the warfarin overdose and the difficulty to reverse warfarin effect in this patient.	Warfarin	215-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
34104863-8	2021	The combination of azithromycin intake, a known inhibitor of CYP2C9, with the presence of CYP2C9*2 and -1639G>A VKORC1, two variants associated with warfarin hypersensitivity, have likely contributed to explain the warfarin overdose and the difficulty to reverse warfarin effect in this patient.	Azithromycin	19-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
34104863-8	2021	The combination of azithromycin intake, a known inhibitor of CYP2C9, with the presence of CYP2C9*2 and -1639G>A VKORC1, two variants associated with warfarin hypersensitivity, have likely contributed to explain the warfarin overdose and the difficulty to reverse warfarin effect in this patient.	Azithromycin	19-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
34116570-11	2021	Herbacetin inhibited CYP3A4, CYP2B6, CYP2C9, and CYP2E1 in a mixed manner, but non-competitively blocked CYP2D6.	herbacetin	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
34104863-8	2021	The combination of azithromycin intake, a known inhibitor of CYP2C9, with the presence of CYP2C9*2 and -1639G>A VKORC1, two variants associated with warfarin hypersensitivity, have likely contributed to explain the warfarin overdose and the difficulty to reverse warfarin effect in this patient.	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
34104863-8	2021	The combination of azithromycin intake, a known inhibitor of CYP2C9, with the presence of CYP2C9*2 and -1639G>A VKORC1, two variants associated with warfarin hypersensitivity, have likely contributed to explain the warfarin overdose and the difficulty to reverse warfarin effect in this patient.	Warfarin	263-271	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
34092821-4	2021	Objective: The objective of this study was to investigate the effect of polymorphisms of the CYP3A4, CYP2C9, CYP3A5, ABCB1, CYP2C19, SCL6A4, and 5-HTR2A genes on the concentration/dose indicator of mirtazapine and on the CYP3A expression level obtained by measuring the miR-27b plasma concentration levels in patients suffering from a recurrent depressive disorder.	Mirtazapine	198-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
34199712-10	2021	CYP3A4 and CYP2C9 were also responsible for the metabolism of tamoxifen.	Tamoxifen	62-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
34199712-11	2021	CYP2C9 especially impacted the hydroxylation to 4-OHtam, and this involved the OATP1B1 (SLCO1B1) transporter.	4-ohtam	48-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
34104133-2	2021	Objectives: To identify occurrence of polymorphisms of the CYP2C9 and VKORC1 genes in patients taking warfarin and relate these profiles to their medication dosages and the Time in Therapeutic Range (TTR).	Warfarin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
34471061-4	2021	On comparing the results of ES with those of estradiol (E2), it was found that CYP2C8 was about 2.5 times higher and CYP2C9 was about 3 times higher, and ES was more likely to be a substrate for the 2-hydroxylation reaction by both CYPs.	estradiol 17-sulfate	28-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
34164480-0	2021	The association of adjusted plasma valproic acid concentration with CYP2C9 gene polymorphism in patients with epilepsy: a systematic review and meta-analysis.	Valproic Acid	35-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
34164480-2	2021	Although there is increasing evidence to suggest that CYP2C9 gene polymorphisms are associated with interindividual variability of VPA metabolism, the results are debatable.	Valproic Acid	131-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
34164480-3	2021	Therefore, in the present study, we conducted a meta-analysis to evaluate the correlation between CYP2C9 gene polymorphisms and adjusted plasma VPA concentration.	Valproic Acid	144-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
34164480-6	2021	We calculated 95% confidence intervals (CIs) and mean differences (MDs) to assess the strength of the relationship of CYP2C9 gene polymorphisms with adjusted plasma VPA concentration.	Valproic Acid	165-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
34164480-8	2021	The pooled analysis showed that the CYP2C9 A1075C (AA vs. AC) polymorphism was related to the adjusted plasma concentration of VPA (P=0.02, I2= 82%).	Valproic Acid	127-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
34164480-12	2021	A reduced VPA dosage may be recommendable for children, particularly Asian children, who are CYP2C9 A1075C AC carriers.	Valproic Acid	10-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
34164480-13	2021	Further studies could provide high-quality evidence to confirm the correlation between VPA pharmacokinetics and CYP2C9 A1075C polymorphisms.	Valproic Acid	87-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
34471061-4	2021	On comparing the results of ES with those of estradiol (E2), it was found that CYP2C8 was about 2.5 times higher and CYP2C9 was about 3 times higher, and ES was more likely to be a substrate for the 2-hydroxylation reaction by both CYPs.	Estradiol	45-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
34471061-4	2021	On comparing the results of ES with those of estradiol (E2), it was found that CYP2C8 was about 2.5 times higher and CYP2C9 was about 3 times higher, and ES was more likely to be a substrate for the 2-hydroxylation reaction by both CYPs.	Estradiol	56-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
34272716-6	2021	Molecular docking studies further confirmed that (S)-warfarin and diclofenac preferentially bind in different regions of the CYP2C9 active site, with (S)-warfarin occupying a distal "warfarin-binding pocket" and diclofenac occupying a binding site close to the active heme moiety.	Diclofenac	212-222	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
34272716-0	2021	Case Study 9: Probe-Dependent Binding Explains Lack of CYP2C9 Inactivation by 1-Aminobenzotriazole (ABT).	1-aminobenzotriazole	78-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
34272716-6	2021	Molecular docking studies further confirmed that (S)-warfarin and diclofenac preferentially bind in different regions of the CYP2C9 active site, with (S)-warfarin occupying a distal "warfarin-binding pocket" and diclofenac occupying a binding site close to the active heme moiety.	Heme	268-272	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
34272716-0	2021	Case Study 9: Probe-Dependent Binding Explains Lack of CYP2C9 Inactivation by 1-Aminobenzotriazole (ABT).	1-aminobenzotriazole	100-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
34272716-7	2021	ABT preferentially binds in the distal warfarin-binding pocket, supporting that diclofenac is minimally deterred from access to the CYP2C9 active site in the presence of ABT, thus resulting in minimal inactivation.	Diclofenac	80-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
34272716-3	2021	In evaluating a time-saving assay using diclofenac as the CYP2C9 probe substrate, a discrepancy was observed in which minimal inhibition was detected using diclofenac whereas using (S)-warfarin resulted in potent inhibition, supporting the presence of dual-binding sites in the relatively large CYP2C9 active site cavity.These observations provided further insights into explaining the reported ineffective inactivation of CYP2C9 for the pan-CYP inactivator 1-aminobenzotriazole (ABT).	Diclofenac	40-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
34272716-3	2021	In evaluating a time-saving assay using diclofenac as the CYP2C9 probe substrate, a discrepancy was observed in which minimal inhibition was detected using diclofenac whereas using (S)-warfarin resulted in potent inhibition, supporting the presence of dual-binding sites in the relatively large CYP2C9 active site cavity.These observations provided further insights into explaining the reported ineffective inactivation of CYP2C9 for the pan-CYP inactivator 1-aminobenzotriazole (ABT).	Diclofenac	40-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	295-301
34272716-7	2021	ABT preferentially binds in the distal warfarin-binding pocket, supporting that diclofenac is minimally deterred from access to the CYP2C9 active site in the presence of ABT, thus resulting in minimal inactivation.	1-aminobenzotriazole	170-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
34272716-3	2021	In evaluating a time-saving assay using diclofenac as the CYP2C9 probe substrate, a discrepancy was observed in which minimal inhibition was detected using diclofenac whereas using (S)-warfarin resulted in potent inhibition, supporting the presence of dual-binding sites in the relatively large CYP2C9 active site cavity.These observations provided further insights into explaining the reported ineffective inactivation of CYP2C9 for the pan-CYP inactivator 1-aminobenzotriazole (ABT).	Diclofenac	156-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	295-301
34272716-8	2021	Simultaneously docking of (S)-warfarin and ABT revealed that (S)-warfarin outcompetes ABT for the distal binding site and results in the binding of ABT to the CYP2C9 active site, supporting the observations of potent inactivation of CYP2C9 when (S)-warfarin is the probe substrate.These results highlight that probe selection is crucial when evaluating CYP inhibition potential, and it is recommended that multiple probes be utilized for CYP2C9, similar to the approach routinely employed for CYP3A4.	Warfarin	61-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
34272716-3	2021	In evaluating a time-saving assay using diclofenac as the CYP2C9 probe substrate, a discrepancy was observed in which minimal inhibition was detected using diclofenac whereas using (S)-warfarin resulted in potent inhibition, supporting the presence of dual-binding sites in the relatively large CYP2C9 active site cavity.These observations provided further insights into explaining the reported ineffective inactivation of CYP2C9 for the pan-CYP inactivator 1-aminobenzotriazole (ABT).	Warfarin	181-193	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	295-301
34272716-8	2021	Simultaneously docking of (S)-warfarin and ABT revealed that (S)-warfarin outcompetes ABT for the distal binding site and results in the binding of ABT to the CYP2C9 active site, supporting the observations of potent inactivation of CYP2C9 when (S)-warfarin is the probe substrate.These results highlight that probe selection is crucial when evaluating CYP inhibition potential, and it is recommended that multiple probes be utilized for CYP2C9, similar to the approach routinely employed for CYP3A4.	1-aminobenzotriazole	148-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
34272716-3	2021	In evaluating a time-saving assay using diclofenac as the CYP2C9 probe substrate, a discrepancy was observed in which minimal inhibition was detected using diclofenac whereas using (S)-warfarin resulted in potent inhibition, supporting the presence of dual-binding sites in the relatively large CYP2C9 active site cavity.These observations provided further insights into explaining the reported ineffective inactivation of CYP2C9 for the pan-CYP inactivator 1-aminobenzotriazole (ABT).	1-aminobenzotriazole	458-478	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
34272716-8	2021	Simultaneously docking of (S)-warfarin and ABT revealed that (S)-warfarin outcompetes ABT for the distal binding site and results in the binding of ABT to the CYP2C9 active site, supporting the observations of potent inactivation of CYP2C9 when (S)-warfarin is the probe substrate.These results highlight that probe selection is crucial when evaluating CYP inhibition potential, and it is recommended that multiple probes be utilized for CYP2C9, similar to the approach routinely employed for CYP3A4.	Warfarin	245-257	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	233-239
34272716-3	2021	In evaluating a time-saving assay using diclofenac as the CYP2C9 probe substrate, a discrepancy was observed in which minimal inhibition was detected using diclofenac whereas using (S)-warfarin resulted in potent inhibition, supporting the presence of dual-binding sites in the relatively large CYP2C9 active site cavity.These observations provided further insights into explaining the reported ineffective inactivation of CYP2C9 for the pan-CYP inactivator 1-aminobenzotriazole (ABT).	1-aminobenzotriazole	458-478	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	295-301
34272716-3	2021	In evaluating a time-saving assay using diclofenac as the CYP2C9 probe substrate, a discrepancy was observed in which minimal inhibition was detected using diclofenac whereas using (S)-warfarin resulted in potent inhibition, supporting the presence of dual-binding sites in the relatively large CYP2C9 active site cavity.These observations provided further insights into explaining the reported ineffective inactivation of CYP2C9 for the pan-CYP inactivator 1-aminobenzotriazole (ABT).	1-aminobenzotriazole	458-478	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	423-429
34272716-3	2021	In evaluating a time-saving assay using diclofenac as the CYP2C9 probe substrate, a discrepancy was observed in which minimal inhibition was detected using diclofenac whereas using (S)-warfarin resulted in potent inhibition, supporting the presence of dual-binding sites in the relatively large CYP2C9 active site cavity.These observations provided further insights into explaining the reported ineffective inactivation of CYP2C9 for the pan-CYP inactivator 1-aminobenzotriazole (ABT).	1-aminobenzotriazole	480-483	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
34272716-3	2021	In evaluating a time-saving assay using diclofenac as the CYP2C9 probe substrate, a discrepancy was observed in which minimal inhibition was detected using diclofenac whereas using (S)-warfarin resulted in potent inhibition, supporting the presence of dual-binding sites in the relatively large CYP2C9 active site cavity.These observations provided further insights into explaining the reported ineffective inactivation of CYP2C9 for the pan-CYP inactivator 1-aminobenzotriazole (ABT).	1-aminobenzotriazole	480-483	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	295-301
34272716-3	2021	In evaluating a time-saving assay using diclofenac as the CYP2C9 probe substrate, a discrepancy was observed in which minimal inhibition was detected using diclofenac whereas using (S)-warfarin resulted in potent inhibition, supporting the presence of dual-binding sites in the relatively large CYP2C9 active site cavity.These observations provided further insights into explaining the reported ineffective inactivation of CYP2C9 for the pan-CYP inactivator 1-aminobenzotriazole (ABT).	1-aminobenzotriazole	480-483	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	423-429
34272716-4	2021	Mechanistic reversible and time-dependent inhibition experiments revealed that the ineffective CYP2C9 inactivation by ABT was also probe-dependent, with utilization of (S)-warfarin as the probe substrate resulting in more potent CYP2C9 inhibition by ABT compared to diclofenac.	1-aminobenzotriazole	118-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
34272716-4	2021	Mechanistic reversible and time-dependent inhibition experiments revealed that the ineffective CYP2C9 inactivation by ABT was also probe-dependent, with utilization of (S)-warfarin as the probe substrate resulting in more potent CYP2C9 inhibition by ABT compared to diclofenac.	1-aminobenzotriazole	118-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	229-235
34272716-4	2021	Mechanistic reversible and time-dependent inhibition experiments revealed that the ineffective CYP2C9 inactivation by ABT was also probe-dependent, with utilization of (S)-warfarin as the probe substrate resulting in more potent CYP2C9 inhibition by ABT compared to diclofenac.	Warfarin	168-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
34272716-4	2021	Mechanistic reversible and time-dependent inhibition experiments revealed that the ineffective CYP2C9 inactivation by ABT was also probe-dependent, with utilization of (S)-warfarin as the probe substrate resulting in more potent CYP2C9 inhibition by ABT compared to diclofenac.	Warfarin	168-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	229-235
34272716-4	2021	Mechanistic reversible and time-dependent inhibition experiments revealed that the ineffective CYP2C9 inactivation by ABT was also probe-dependent, with utilization of (S)-warfarin as the probe substrate resulting in more potent CYP2C9 inhibition by ABT compared to diclofenac.	1-aminobenzotriazole	250-253	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
34272716-4	2021	Mechanistic reversible and time-dependent inhibition experiments revealed that the ineffective CYP2C9 inactivation by ABT was also probe-dependent, with utilization of (S)-warfarin as the probe substrate resulting in more potent CYP2C9 inhibition by ABT compared to diclofenac.	1-aminobenzotriazole	250-253	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	229-235
34272716-4	2021	Mechanistic reversible and time-dependent inhibition experiments revealed that the ineffective CYP2C9 inactivation by ABT was also probe-dependent, with utilization of (S)-warfarin as the probe substrate resulting in more potent CYP2C9 inhibition by ABT compared to diclofenac.	Diclofenac	266-276	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
34272716-5	2021	Addition of (S)-warfarin to the reversible and time-dependent inhibition experiments between ABT and diclofenac resulted in an attenuation of the inhibitory effects of ABT on CYP2C9-mediated diclofenac metabolism.	Warfarin	12-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	175-181
34272716-5	2021	Addition of (S)-warfarin to the reversible and time-dependent inhibition experiments between ABT and diclofenac resulted in an attenuation of the inhibitory effects of ABT on CYP2C9-mediated diclofenac metabolism.	1-aminobenzotriazole	93-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	175-181
34272716-5	2021	Addition of (S)-warfarin to the reversible and time-dependent inhibition experiments between ABT and diclofenac resulted in an attenuation of the inhibitory effects of ABT on CYP2C9-mediated diclofenac metabolism.	Diclofenac	101-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	175-181
34272716-5	2021	Addition of (S)-warfarin to the reversible and time-dependent inhibition experiments between ABT and diclofenac resulted in an attenuation of the inhibitory effects of ABT on CYP2C9-mediated diclofenac metabolism.	1-aminobenzotriazole	168-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	175-181
34272716-5	2021	Addition of (S)-warfarin to the reversible and time-dependent inhibition experiments between ABT and diclofenac resulted in an attenuation of the inhibitory effects of ABT on CYP2C9-mediated diclofenac metabolism.	Diclofenac	191-201	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	175-181
34802403-0	2021	Influence of CYP2C9 Polymorphisms on Plasma Concentration of Warfarin and 7-Hydroxy Warfarin in South Indian Patients.	Warfarin	61-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
34802403-1	2021	BACKGROUND: Warfarin is primarily metabolized by cytochrome P450 2C9 (CYP2C9), which is encoded by the CYP2C9 gene.	Warfarin	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-68
34802403-1	2021	BACKGROUND: Warfarin is primarily metabolized by cytochrome P450 2C9 (CYP2C9), which is encoded by the CYP2C9 gene.	Warfarin	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
34802403-1	2021	BACKGROUND: Warfarin is primarily metabolized by cytochrome P450 2C9 (CYP2C9), which is encoded by the CYP2C9 gene.	Warfarin	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
34802403-2	2021	CYP2C9*2 and CYP2C9*3 variants significantly influence warfarin metabolism and subsequently the required dose of warfarin.	Warfarin	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
34802403-2	2021	CYP2C9*2 and CYP2C9*3 variants significantly influence warfarin metabolism and subsequently the required dose of warfarin.	Warfarin	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
34802403-2	2021	CYP2C9*2 and CYP2C9*3 variants significantly influence warfarin metabolism and subsequently the required dose of warfarin.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
34802403-2	2021	CYP2C9*2 and CYP2C9*3 variants significantly influence warfarin metabolism and subsequently the required dose of warfarin.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
34272716-6	2021	Molecular docking studies further confirmed that (S)-warfarin and diclofenac preferentially bind in different regions of the CYP2C9 active site, with (S)-warfarin occupying a distal "warfarin-binding pocket" and diclofenac occupying a binding site close to the active heme moiety.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
34272716-9	2021	Further, utilization of ABT as a pan-inhibitor of CYP activity for investigational compounds, both in vitro and in vivo, should be accompanied with the understanding that residual CYP-mediated oxidative metabolism could potentially be observed for CYP2C9 substrates and should not necessarily be attributed to non-P450-mediated metabolism.	1-aminobenzotriazole	24-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	248-254
34272716-6	2021	Molecular docking studies further confirmed that (S)-warfarin and diclofenac preferentially bind in different regions of the CYP2C9 active site, with (S)-warfarin occupying a distal "warfarin-binding pocket" and diclofenac occupying a binding site close to the active heme moiety.	Diclofenac	66-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
34272716-6	2021	Molecular docking studies further confirmed that (S)-warfarin and diclofenac preferentially bind in different regions of the CYP2C9 active site, with (S)-warfarin occupying a distal "warfarin-binding pocket" and diclofenac occupying a binding site close to the active heme moiety.	Warfarin	154-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
34802403-3	2021	OBJECTIVE: The current retrospective study was aimed to determine the influence of CYP2C9 variants on warfarin metabolic ratio (MR, warfarin/7-hydroxy warfarin) and warfarin maintenance therapy in 210 patients (mean age 44.6+-11.6 (SD) years; male to female ratio 81:129).	Warfarin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
34802403-3	2021	OBJECTIVE: The current retrospective study was aimed to determine the influence of CYP2C9 variants on warfarin metabolic ratio (MR, warfarin/7-hydroxy warfarin) and warfarin maintenance therapy in 210 patients (mean age 44.6+-11.6 (SD) years; male to female ratio 81:129).	Warfarin	132-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
34802403-3	2021	OBJECTIVE: The current retrospective study was aimed to determine the influence of CYP2C9 variants on warfarin metabolic ratio (MR, warfarin/7-hydroxy warfarin) and warfarin maintenance therapy in 210 patients (mean age 44.6+-11.6 (SD) years; male to female ratio 81:129).	7-hydroxywarfarin	141-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
34802403-9	2021	Patients carrying other CYP2C9 variants required 39% lower warfarin maintenance dose (3.3+-1.2 mg) than CYP2C9*1*1 carrier (4.9+-1.8 mg), (p<0.0001).	Warfarin	59-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
34802403-12	2021	CONCLUSION: The present study results provide, insights on effect of CYP2C9 genetic polymorphisms on inter-individual variability in warfarin metabolism and emphasizes utility of phenotyping in a setting of genotype-guided dosing of warfarin in the South Indian population.	Warfarin	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
34272716-6	2021	Molecular docking studies further confirmed that (S)-warfarin and diclofenac preferentially bind in different regions of the CYP2C9 active site, with (S)-warfarin occupying a distal "warfarin-binding pocket" and diclofenac occupying a binding site close to the active heme moiety.	Warfarin	183-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
34900058-6	2021	Results: Ifosfamide levels increased according to the genotype, and patients with the variant rs1799853 in CYP2C9 genotype CC had lower levels of ifosfamide (median = 1.8 mumol/l, Q25 0.9-Q75 4.6) compared with patients with genotype TT + CT (median = 2.8 mumol/l, Q25 1.9-Q75 5.1), p < 0.001.	Ifosfamide	146-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
34900058-9	2021	Conclusions: Polymorphisms in CYP2C9 and CYP3A4 genes are associated with high levels of ifosfamide.	Ifosfamide	89-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
35370222-1	2022	We encountered cases in which the anticoagulant effects of warfarin (CYP2C9 substrate) were reversibly attenuated by the concomitant administration of rifampicin or bosentan, which are potent pregnane X receptor (PXR) ligands.	Warfarin	59-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
35370222-1	2022	We encountered cases in which the anticoagulant effects of warfarin (CYP2C9 substrate) were reversibly attenuated by the concomitant administration of rifampicin or bosentan, which are potent pregnane X receptor (PXR) ligands.	Rifampin	151-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
35370222-1	2022	We encountered cases in which the anticoagulant effects of warfarin (CYP2C9 substrate) were reversibly attenuated by the concomitant administration of rifampicin or bosentan, which are potent pregnane X receptor (PXR) ligands.	Bosentan	165-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
35168147-5	2022	Flurbiprofen/naproxen and piroxicam are located in the active site and the primary binding site of CYP2C9, respectively.	Piroxicam	26-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
35370140-3	2022	To populate a THC/11-OH-THC PBPK model, we previously characterized the depletion clearance of THC (by CYP2C9) and 11-OH-THC (by UGT, CYP3A, and CYP2C9) in adult human liver microsomes.	Dronabinol	14-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
35370140-3	2022	To populate a THC/11-OH-THC PBPK model, we previously characterized the depletion clearance of THC (by CYP2C9) and 11-OH-THC (by UGT, CYP3A, and CYP2C9) in adult human liver microsomes.	Dronabinol	14-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
35370140-3	2022	To populate a THC/11-OH-THC PBPK model, we previously characterized the depletion clearance of THC (by CYP2C9) and 11-OH-THC (by UGT, CYP3A, and CYP2C9) in adult human liver microsomes.	11-Hydroxytetrahydrocannabinol	18-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
35370140-3	2022	To populate a THC/11-OH-THC PBPK model, we previously characterized the depletion clearance of THC (by CYP2C9) and 11-OH-THC (by UGT, CYP3A, and CYP2C9) in adult human liver microsomes.	11-Hydroxytetrahydrocannabinol	18-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
35168147-1	2022	Some non-steroidal anti-inflammatory drugs (NSAIDs) exhibit atypical kinetic behavior when binding together with dapsone in CYP2C9.	Dapsone	113-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
35168147-3	2022	Here, molecular docking and molecular dynamics (MD) simulations are performed to explore the cooperative binding of dapsone and three NSAIDs in CYP2C9.	Dapsone	116-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
35370140-3	2022	To populate a THC/11-OH-THC PBPK model, we previously characterized the depletion clearance of THC (by CYP2C9) and 11-OH-THC (by UGT, CYP3A, and CYP2C9) in adult human liver microsomes.	Dronabinol	95-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
35168147-5	2022	Flurbiprofen/naproxen and piroxicam are located in the active site and the primary binding site of CYP2C9, respectively.	Flurbiprofen	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
35599347-5	2022	FFA and nFFA were direct in vitro inhibitors of CYP2D6 (IC50 , 4.7 and 16 microM, respectively) but did not substantially inhibit CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, or CYP3A4/5.	Fenfluramine	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
35168147-5	2022	Flurbiprofen/naproxen and piroxicam are located in the active site and the primary binding site of CYP2C9, respectively.	Naproxen	13-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
35061161-2	2022	The herbal hepatoprotective medicine, silybin A inhibits cytochrome P450 (CYP) 2C9 and 3A4 enzymes, thus, may interact with the drugs that are substrates of CYP2C9 and 3A4, such as losartan.	Silybin	38-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-90
35061161-2	2022	The herbal hepatoprotective medicine, silybin A inhibits cytochrome P450 (CYP) 2C9 and 3A4 enzymes, thus, may interact with the drugs that are substrates of CYP2C9 and 3A4, such as losartan.	Silybin	38-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
35061161-2	2022	The herbal hepatoprotective medicine, silybin A inhibits cytochrome P450 (CYP) 2C9 and 3A4 enzymes, thus, may interact with the drugs that are substrates of CYP2C9 and 3A4, such as losartan.	Losartan	181-189	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-90
35061161-2	2022	The herbal hepatoprotective medicine, silybin A inhibits cytochrome P450 (CYP) 2C9 and 3A4 enzymes, thus, may interact with the drugs that are substrates of CYP2C9 and 3A4, such as losartan.	Losartan	181-189	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
35061161-4	2022	This study aimed to assess silybin A-losartan interaction in different CYP2C9 genotypes using physiological-based pharmacokinetic (PBPK) model approach.	Silybin	27-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
35061161-4	2022	This study aimed to assess silybin A-losartan interaction in different CYP2C9 genotypes using physiological-based pharmacokinetic (PBPK) model approach.	Losartan	37-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
35061161-10	2022	In CYP 2C9*1/*1 genotype, AUC and Cmax of losartan were increased 1.16 and 1.37 folds, respectively falling in a range stipulated for negligible interaction.	Losartan	42-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	3-10
35061161-11	2022	Increase in AUC and Cmax by 0.873 and 0.294 folds, respectively in CYP2C9*1/*3 after co-administration of silybin A exhibited a minor interaction with losartan.	Silybin	106-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
35061161-11	2022	Increase in AUC and Cmax by 0.873 and 0.294 folds, respectively in CYP2C9*1/*3 after co-administration of silybin A exhibited a minor interaction with losartan.	Losartan	151-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
35061161-12	2022	However, in individuals with CYP2C9*1/*2 genotype, the losartan"s AUC and Cmax were decreased by 0.01 folds, manifesting a moderate interaction.	Losartan	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
35061161-13	2022	Hence, in CYP2C9*1/*1 and CYP2C9*1/*3 genotypes, silybin A is a weak CYP inhibitor for losartan while in CYP2C9*1/*2 genotype, the co-administration of silybin consequents into a moderate pharmacokinetic interaction with losartan.	Losartan	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
35370140-3	2022	To populate a THC/11-OH-THC PBPK model, we previously characterized the depletion clearance of THC (by CYP2C9) and 11-OH-THC (by UGT, CYP3A, and CYP2C9) in adult human liver microsomes.	Dronabinol	95-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
35370140-3	2022	To populate a THC/11-OH-THC PBPK model, we previously characterized the depletion clearance of THC (by CYP2C9) and 11-OH-THC (by UGT, CYP3A, and CYP2C9) in adult human liver microsomes.	11-Hydroxytetrahydrocannabinol	115-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
35081606-0	2022	Effects of CYP2C19, CYP2C9 and CYP3A4 gene polymorphisms on plasma voriconazole levels in Chinese pediatric patients.	Voriconazole	67-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
35081606-2	2022	Previous studies suggested that voriconazole was extensively metabolized by CYP450 enzyme system, including CYP2C19, CYP2C9 and CYP3A4, which contributed to the individual variability of the pharmacokinetic process of voriconazole.	Voriconazole	32-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
35081606-2	2022	Previous studies suggested that voriconazole was extensively metabolized by CYP450 enzyme system, including CYP2C19, CYP2C9 and CYP3A4, which contributed to the individual variability of the pharmacokinetic process of voriconazole.	Voriconazole	218-230	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
35081606-3	2022	This study aimed to investigate the effects of CYP2C19, CYP2C9 and CYP3A4 gene polymorphisms on plasma voriconazole concentrations in Chinese pediatric patients.	Voriconazole	103-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
35599347-5	2022	FFA and nFFA were direct in vitro inhibitors of CYP2D6 (IC50 , 4.7 and 16 microM, respectively) but did not substantially inhibit CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, or CYP3A4/5.	Norfenfluramine	8-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
35583123-0	2022	Methysticin Acts as a Mechanism-Based Inactivator of Cytochrome P450 2C9.	methysticin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-72
35622425-4	2022	DDI for warfarin mainly involve moderate to strong inhibitors/inducers of cytochrome P450 (CYP) 2C9, which is responsible for the elimination of the more potent S-isomer of warfarin.	Warfarin	8-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-99
35622425-4	2022	DDI for warfarin mainly involve moderate to strong inhibitors/inducers of cytochrome P450 (CYP) 2C9, which is responsible for the elimination of the more potent S-isomer of warfarin.	Warfarin	173-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-99
35583123-12	2022	Both ortho-quinone and carbene intermediates appeared to be involved in the inactivation of CYP2C9 induced by methysticin.	2-benzoquinone	5-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
35590072-6	2022	For PharmGKB level 1A variants, CYP2C9 status for phenytoin prescription was the only relevant information.	Phenytoin	50-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
35583123-3	2022	Methysticin exhibited time-, concentration-, and NADPH-dependent inhibition on CYP2C9 using diclofenac as a probe substrate.	methysticin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
35583123-12	2022	Both ortho-quinone and carbene intermediates appeared to be involved in the inactivation of CYP2C9 induced by methysticin.	carbene	23-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
35583123-3	2022	Methysticin exhibited time-, concentration-, and NADPH-dependent inhibition on CYP2C9 using diclofenac as a probe substrate.	NADP	49-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
35583123-12	2022	Both ortho-quinone and carbene intermediates appeared to be involved in the inactivation of CYP2C9 induced by methysticin.	methysticin	110-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
35583123-3	2022	Methysticin exhibited time-, concentration-, and NADPH-dependent inhibition on CYP2C9 using diclofenac as a probe substrate.	Diclofenac	92-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
35583123-4	2022	Approximately 85% of CYP2C9 activity was inhibited by methysticin at 50 muM after a 30 min preincubation with human liver microsomes in the presence of NADPH.	methysticin	54-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
35583123-4	2022	Approximately 85% of CYP2C9 activity was inhibited by methysticin at 50 muM after a 30 min preincubation with human liver microsomes in the presence of NADPH.	NADP	152-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
35583123-6	2022	Sulfaphenazole (competitive inhibitor of CYP2C9) displayed a significant protective effect on methysticin-induced CYP2C9 inactivation.	Sulfaphenazole	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
35583123-6	2022	Sulfaphenazole (competitive inhibitor of CYP2C9) displayed a significant protective effect on methysticin-induced CYP2C9 inactivation.	Sulfaphenazole	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
35583123-6	2022	Sulfaphenazole (competitive inhibitor of CYP2C9) displayed a significant protective effect on methysticin-induced CYP2C9 inactivation.	methysticin	94-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
35583123-6	2022	Sulfaphenazole (competitive inhibitor of CYP2C9) displayed a significant protective effect on methysticin-induced CYP2C9 inactivation.	methysticin	94-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
35583123-8	2022	A carbene intermediate was postulated to be involved in methysticin-induced CYP2C9 inactivation as K3Fe(CN)6 recovered 14.96% of CYP2C9 activity.	carbene	2-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
35583123-8	2022	A carbene intermediate was postulated to be involved in methysticin-induced CYP2C9 inactivation as K3Fe(CN)6 recovered 14.96% of CYP2C9 activity.	carbene	2-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
35583123-8	2022	A carbene intermediate was postulated to be involved in methysticin-induced CYP2C9 inactivation as K3Fe(CN)6 recovered 14.96% of CYP2C9 activity.	methysticin	56-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
35583123-8	2022	A carbene intermediate was postulated to be involved in methysticin-induced CYP2C9 inactivation as K3Fe(CN)6 recovered 14.96% of CYP2C9 activity.	methysticin	56-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
35583123-8	2022	A carbene intermediate was postulated to be involved in methysticin-induced CYP2C9 inactivation as K3Fe(CN)6 recovered 14.96% of CYP2C9 activity.	k3fe	99-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
35583123-8	2022	A carbene intermediate was postulated to be involved in methysticin-induced CYP2C9 inactivation as K3Fe(CN)6 recovered 14.96% of CYP2C9 activity.	k3fe	99-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
35583123-9	2022	A methysticin-derived ortho-quinone intermediate dependent on NADPH was trapped by GSH, and this intermediate was believed to be involved in CYP2C9 inactivation.	methysticin	2-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
35583123-9	2022	A methysticin-derived ortho-quinone intermediate dependent on NADPH was trapped by GSH, and this intermediate was believed to be involved in CYP2C9 inactivation.	derived ortho-quinone	14-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
35583123-9	2022	A methysticin-derived ortho-quinone intermediate dependent on NADPH was trapped by GSH, and this intermediate was believed to be involved in CYP2C9 inactivation.	NADP	62-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
35583123-9	2022	A methysticin-derived ortho-quinone intermediate dependent on NADPH was trapped by GSH, and this intermediate was believed to be involved in CYP2C9 inactivation.	Glutathione	83-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
35583123-11	2022	Taken together, the present work demonstrated that methysticin was a mechanism-based inactivator of CYP2C9.	methysticin	51-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
35629204-10	2022	These data might be relevant for implementation in the diverse clinical guidelines for the pharmacogenetic analysis of the CYP2C9 gene before treatment with different drugs, such as non-steroidal anti-inflammatory drugs, warfarin, phenytoin and statins.	Warfarin	221-229	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
35629204-10	2022	These data might be relevant for implementation in the diverse clinical guidelines for the pharmacogenetic analysis of the CYP2C9 gene before treatment with different drugs, such as non-steroidal anti-inflammatory drugs, warfarin, phenytoin and statins.	Phenytoin	231-240	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
35620290-14	2022	The dosage regimen, body mass index, CYP2C9 genetic polymorphism and fluconazole combination may had influences on siponimod pharmacokinetics.	siponimod	115-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
35545255-6	2022	In human hepatocytes (n=3), 13cisRA, atRA and 4-oxo-13cisRA decreased OATP1B1, CYP1A2, CYP2C9, and CYP2D6 mRNA and increased CYP2B6 and CYP3A4 mRNA in a concentration-dependent manner.	13cisra	28-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
35545255-6	2022	In human hepatocytes (n=3), 13cisRA, atRA and 4-oxo-13cisRA decreased OATP1B1, CYP1A2, CYP2C9, and CYP2D6 mRNA and increased CYP2B6 and CYP3A4 mRNA in a concentration-dependent manner.	Tretinoin	37-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
35545255-6	2022	In human hepatocytes (n=3), 13cisRA, atRA and 4-oxo-13cisRA decreased OATP1B1, CYP1A2, CYP2C9, and CYP2D6 mRNA and increased CYP2B6 and CYP3A4 mRNA in a concentration-dependent manner.	4-oxo-13cisra	46-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
35289081-7	2022	As a result, the marginal plasma exposure changes of typical CYP3A and CYP2C9 substrates were less than the bioequivalence threshold, indicating that anlotinib has a very low potential of causing clinically meaningful DDI through the inhibition of several major CYP enzymes.	anlotinib	150-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
35246464-5	2022	The current study also demonstrated that selective inhibition sufficient for fm calculation was achieved by inhibitors of CYP1A2 (20 microM furafylline), CYP2C8 (40 microM montelukast), CYP2C9 (40 microM sulfaphenazole), CYP2C19 (3 microM (-)N-3-benzyl-phenobarbital) and CYP2D6 (5 microM quinidine).	Sulfaphenazole	204-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	186-192
35246464-5	2022	The current study also demonstrated that selective inhibition sufficient for fm calculation was achieved by inhibitors of CYP1A2 (20 microM furafylline), CYP2C8 (40 microM montelukast), CYP2C9 (40 microM sulfaphenazole), CYP2C19 (3 microM (-)N-3-benzyl-phenobarbital) and CYP2D6 (5 microM quinidine).	N-3-benzylphenobarbital	242-266	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	186-192
35246464-5	2022	The current study also demonstrated that selective inhibition sufficient for fm calculation was achieved by inhibitors of CYP1A2 (20 microM furafylline), CYP2C8 (40 microM montelukast), CYP2C9 (40 microM sulfaphenazole), CYP2C19 (3 microM (-)N-3-benzyl-phenobarbital) and CYP2D6 (5 microM quinidine).	Quinidine	289-298	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	186-192
35426132-0	2022	The Impact of CYP2C9*11 Genetic Polymorphism on the Pharmacokinetics of Phenytoin and (S)-Warfarin.	Phenytoin	72-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
35138605-11	2022	After combined treatment of HepG2 cells with warfarin + PNS, CYP1A2 expression was upregulated (P  < 0.05) and CYP3A4 was downregulated (P  < 0.05) but there was no effect on CYP2C9.	Warfarin	45-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	175-181
35439929-1	2022	OBJECTIVE: To explore the role of genetic testing of VKORC1 and CYP2C9 in determining the dosage of warfarin after aortic valve replacement.	Warfarin	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
35247543-9	2022	CONCLUSIONS: Observed inhibition of metabolic enzymes indicated that remibrutinib is a weak inhibitor of CYP3A4 and CYP2C9 and is not a clinically relevant inhibitor of uptake and efflux transporters, except for intestinal P-glycoprotein and breast cancer resistance protein inhibition.	Remibrutinib	69-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
35380455-4	2022	The most studied gene-drug pairs were clopidogrel and warfarin associated with cytochrome p450 and vitamin K epoxide reductase complex subunit 1 genes (CYP2C19, CYP2C9 and VKORC1), classified as critically low quality.	Clopidogrel	38-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
35380455-4	2022	The most studied gene-drug pairs were clopidogrel and warfarin associated with cytochrome p450 and vitamin K epoxide reductase complex subunit 1 genes (CYP2C19, CYP2C9 and VKORC1), classified as critically low quality.	Warfarin	54-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
35426132-0	2022	The Impact of CYP2C9*11 Genetic Polymorphism on the Pharmacokinetics of Phenytoin and (S)-Warfarin.	Warfarin	86-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
35426132-5	2022	The objective of the current study was to characterize the in-vivo activity of CYP2C9 among carriers of CYP2C9*11, one of the "African" alleles and the fourth most common CYP2C9 variant allele among Caucasians by using two prototype substrates, phenytoin and (S)-warfarin.	Phenytoin	245-254	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
35426132-5	2022	The objective of the current study was to characterize the in-vivo activity of CYP2C9 among carriers of CYP2C9*11, one of the "African" alleles and the fourth most common CYP2C9 variant allele among Caucasians by using two prototype substrates, phenytoin and (S)-warfarin.	Warfarin	259-271	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
35426132-11	2022	Among patients of African ancestry CYP2C9*11 genetic analysis should be considered prior to prescribing of narrow therapeutic window drugs such as phenytoin, warfarin, NSAIDs or siponimod.	Phenytoin	147-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
35426132-11	2022	Among patients of African ancestry CYP2C9*11 genetic analysis should be considered prior to prescribing of narrow therapeutic window drugs such as phenytoin, warfarin, NSAIDs or siponimod.	Warfarin	158-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
35426132-11	2022	Among patients of African ancestry CYP2C9*11 genetic analysis should be considered prior to prescribing of narrow therapeutic window drugs such as phenytoin, warfarin, NSAIDs or siponimod.	siponimod	178-187	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
35456605-0	2022	Population Pharmacokinetic (Pop-PK) Analysis of Torsemide in Healthy Korean Males Considering CYP2C9 and OATP1B1 Genetic Polymorphisms.	Torsemide	48-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
35365981-0	2022	Association of VKORC1 and CYP2C9 single-nucleotide polymorphisms with warfarin dose adjustment in Saudi patients.	Warfarin	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
35365981-2	2022	Previous reports have suggested that polymorphisms in VKORC1 and CYP2C9 genes could influence warfarin therapy.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
35365981-8	2022	Similarly, there was a significant reduction in warfarin daily maintenance dose among CYP2C9*1/*3 and CYP2C9*1/*2 groups compared to CYP2C9*1/*1.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
35365981-8	2022	Similarly, there was a significant reduction in warfarin daily maintenance dose among CYP2C9*1/*3 and CYP2C9*1/*2 groups compared to CYP2C9*1/*1.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
35365981-10	2022	CONCLUSIONS: Similar to other populations, the VKORC1 and CYP2C9 gene polymorphisms are significantly associated with warfarin dosage in Saudi patients.	Warfarin	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
35365981-11	2022	The presence of at least one copy of the mutant alleles for VKORC1 -1173C>T, CYP2C9*2, and CYP2C9*3 is associated with a significant reduction in warfarin maintenance dose.	Warfarin	146-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
35365981-11	2022	The presence of at least one copy of the mutant alleles for VKORC1 -1173C>T, CYP2C9*2, and CYP2C9*3 is associated with a significant reduction in warfarin maintenance dose.	Warfarin	146-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
35108398-0	2022	Warfarin Dosing in Patients with CYP2C9*5 Variant Alleles.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
35108398-2	2022	The cytochrome P450 2C9*5 (CYP2C9*5) allele is found almost exclusively in populations of African ancestry, and in-vitro studies suggest CYP2C9*5 is associated with reduced clearance of warfarin.	Warfarin	186-194	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
35108398-2	2022	The cytochrome P450 2C9*5 (CYP2C9*5) allele is found almost exclusively in populations of African ancestry, and in-vitro studies suggest CYP2C9*5 is associated with reduced clearance of warfarin.	Warfarin	186-194	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
35108398-4	2022	In this multi-centered study of 2298 patients (49% female, 35% Black) taking warfarin, we quantified the association between the CYP2C9*5 allele and warfarin requirements.	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
35108398-6	2022	Without taking CYP2C9*5 into account, pharmacogenetic algorithms that include other SNPs overestimated the warfarin dose by 30% (95% CI (19%-40%), p<0.001), an average of 1.87 mg/d (SD 1.64) in heterozygotes (p < 0.001).	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
35108398-9	2022	Patients carrying CYP2C9*5 require a clinically relevant reduction in warfarin dose.	Warfarin	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
35115300-8	2022	Oral (130 mg) or inhaled (75 mg) THC was predicted to precipitate interactions with drugs predominately metabolized by CYP2C9 (diclofenac, 6.6 or 2.3, respectively) >3A (midazolam, 1.8) >1A2 (theophylline, 1.4).	Dronabinol	33-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
35115300-8	2022	Oral (130 mg) or inhaled (75 mg) THC was predicted to precipitate interactions with drugs predominately metabolized by CYP2C9 (diclofenac, 6.6 or 2.3, respectively) >3A (midazolam, 1.8) >1A2 (theophylline, 1.4).	Diclofenac	127-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
35115300-8	2022	Oral (130 mg) or inhaled (75 mg) THC was predicted to precipitate interactions with drugs predominately metabolized by CYP2C9 (diclofenac, 6.6 or 2.3, respectively) >3A (midazolam, 1.8) >1A2 (theophylline, 1.4).	Theophylline	192-204	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
35456605-9	2022	According to the genetic polymorphisms of OATP1B1 and CYP2C9, significant associations were found in the V/F, CL/F, and CL2/F of torsemide.	Torsemide	129-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
35456605-11	2022	Considering that torsemide is a substrate for CYP2C9 and OATP1B1, it was important to search for genetic polymorphisms in CYP2C9 and OATP1B1 as covariates to explain the PK diversity of torsemide between individuals.	Torsemide	17-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
35456605-11	2022	Considering that torsemide is a substrate for CYP2C9 and OATP1B1, it was important to search for genetic polymorphisms in CYP2C9 and OATP1B1 as covariates to explain the PK diversity of torsemide between individuals.	Torsemide	17-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
35456605-14	2022	These results suggested that the phenotypes of CYP2C9 and OATP1B1 produced significant differences in torsemide PKs.	Torsemide	102-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
35456605-15	2022	Considering that CYP2C9 and OATP1B1 phenotypes as covariates affected different PK parameters of torsemide, it could be inferred that torsemide"s cell membrane permeation process by OATP1B1 and the metabolic process by CYP2C9 could independently affect each other in vivo without interplay.	Torsemide	97-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
35456605-15	2022	Considering that CYP2C9 and OATP1B1 phenotypes as covariates affected different PK parameters of torsemide, it could be inferred that torsemide"s cell membrane permeation process by OATP1B1 and the metabolic process by CYP2C9 could independently affect each other in vivo without interplay.	Torsemide	97-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	219-225
35456605-15	2022	Considering that CYP2C9 and OATP1B1 phenotypes as covariates affected different PK parameters of torsemide, it could be inferred that torsemide"s cell membrane permeation process by OATP1B1 and the metabolic process by CYP2C9 could independently affect each other in vivo without interplay.	Torsemide	134-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
35456605-15	2022	Considering that CYP2C9 and OATP1B1 phenotypes as covariates affected different PK parameters of torsemide, it could be inferred that torsemide"s cell membrane permeation process by OATP1B1 and the metabolic process by CYP2C9 could independently affect each other in vivo without interplay.	Torsemide	134-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	219-225
35401180-6	2022	Compared with the control group, the expression of P-glycoprotein (P-gp), CYP1A2, CYP2C9, CYP3A4, and nuclear receptor, PXR, were altered in the amoxicillin -treated groups.	Amoxicillin	145-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
35345577-0	2022	Association of AGTR1 A1166C and CYP2C9*3 Gene Polymorphisms with the Antihypertensive Effect of Valsartan.	Valsartan	96-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
35345577-2	2022	The present study aimed to investigate whether the antihypertensive effect of the ARB drug valsartan was associated with angiotensin II type 1 receptor (AGTR1) gene polymorphism (A1166 C) and cytochrome P450 enzyme 2C9 (CYP2C9) gene polymorphism (CYP2C9*3).	Valsartan	91-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	192-218
35345577-2	2022	The present study aimed to investigate whether the antihypertensive effect of the ARB drug valsartan was associated with angiotensin II type 1 receptor (AGTR1) gene polymorphism (A1166 C) and cytochrome P450 enzyme 2C9 (CYP2C9) gene polymorphism (CYP2C9*3).	Valsartan	91-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	247-253
35345577-2	2022	The present study aimed to investigate whether the antihypertensive effect of the ARB drug valsartan was associated with angiotensin II type 1 receptor (AGTR1) gene polymorphism (A1166 C) and cytochrome P450 enzyme 2C9 (CYP2C9) gene polymorphism (CYP2C9*3).	Valsartan	91-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	220-226
35062050-13	2022	In the NAFLD model, Omeprazole maintained an expected induction of CYP1A1, however Phenytoin and Rifampicin showed elevated induction of CYP2B6 and CYP2C9 compared to healthy cultures.	Phenytoin	83-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
35293300-9	2022	ZY12201 Ki values were 0.38, 0.25, 0.07, 0.01, 0.06, 0.02, 7.13, 0.03 and 0.003 muM for CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4/5 (substrate: testosterone) and CYP3A4/5 (substrate: midazolam), respectively.	zy12201	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
35293300-10	2022	Time-dependant CYP inhibition potential of ZY12201 was assessed against CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4/5 and no apparent IC50 shift was observed.	zy12201	43-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
35293300-14	2022	ZY12201 is a non-time-dependent inhibitor of CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4/5.	zy12201	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
35202038-0	2022	Association between CYP2C9, VKORC1, VDR, and APOE genotypes on warfarin maintenance and response during initial anticoagulation for Chinese patients with heart valve replacement.	Warfarin	63-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
35335853-4	2022	The Michaelis-Menten kinetics of voriconazole N-oxide (NO) formation, the major circulating metabolite, by CYP2C19, CYP2C9 and CYP3A4, was determined in incubations of human recombinant CYP enzymes and liver and intestine microsomes.	Voriconazole N-Oxide	33-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
35062050-13	2022	In the NAFLD model, Omeprazole maintained an expected induction of CYP1A1, however Phenytoin and Rifampicin showed elevated induction of CYP2B6 and CYP2C9 compared to healthy cultures.	Rifampin	97-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
35342886-8	2022	CYP2C9-reduced metabolism genotypes were associated with losartan response and uncontrolled hypertension (odds ratio (OR), 5.2; 95% CI, 1.9 to 14.7).	Losartan	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
35078445-12	2022	In vitro, we further confirmed that curcumin significantly downregulated the expression of AURKA, CDK1, and TOP2A genes, while significantly upregulated the expression of CYP2B6, CYP2C9, and CYP3A4 genes.	Curcumin	36-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	179-185
35078445-13	2022	CONCLUSIONS: Our results provided a novel panel of AURKA, CDK1, TOP2A, CYP2C9, and CYP3A4 candidate genes for curcumin related chemotherapy of hepatocellular carcinoma.	Curcumin	110-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
35000550-3	2021	In vitro, CC-90001 glucuronidation was catalyzed by UGT1A9, UGT1A4, and UGT1A1, while oxidative metabolism was primarily mediated by CYP3A4/5 with minor contributions from CYP1A2, CYP2C9, CYP2B6, and CYP2D6.2.	CC-90001	10-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	180-186
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 9	Homo sapiens	28-34
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 9	Homo sapiens	121-127
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 9	Homo sapiens	121-127
35000550-4	2021	CC-90001 in vitro inhibits CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, and CYP3A4 <= 55% at 100 muM, and the inhibition was negligible at <=30 muM.	CC-90001	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
2827463-0	1988	Human cytochrome P-450 PB-1: a multigene family involved in mephenytoin and steroid oxidations that maps to chromosome 10.	Mephenytoin	60-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-27
35169023-1	2022	BACKGROUND: The aim of this study was to investigate the effect of CYB2B6 (c.516G>T, rs3745274), CYP2C9 (c.1075A>C, rs1057910) and UGT1A9 (c.98T>C, rs72551330) polymorphisms on the pharmacokinetics of single-drug propofol in adult patients undergoing intravenous sedation.	Propofol	213-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
2827463-0	1988	Human cytochrome P-450 PB-1: a multigene family involved in mephenytoin and steroid oxidations that maps to chromosome 10.	Steroids	76-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-27
33346393-0	2021	A network meta-analysis of CYP2C9, CYP2C9 with VKORC1 and CYP2C9 with VKORC1 and CYP4F2 genotype-based warfarin dosing strategies compared to traditional.	Warfarin	103-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
33336382-7	2021	In addition, metamizole weakly induced CYP2C9 (decrease in the flurbiprofen AUC by 22%) and moderately CYP2C19 (decrease in the omeprazole AUC by 66%) but did not alter CYP2D6 activity.	Dipyrone	13-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
33336382-7	2021	In addition, metamizole weakly induced CYP2C9 (decrease in the flurbiprofen AUC by 22%) and moderately CYP2C19 (decrease in the omeprazole AUC by 66%) but did not alter CYP2D6 activity.	Flurbiprofen	63-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
33346393-0	2021	A network meta-analysis of CYP2C9, CYP2C9 with VKORC1 and CYP2C9 with VKORC1 and CYP4F2 genotype-based warfarin dosing strategies compared to traditional.	Warfarin	103-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
33346393-7	2021	CYP2C9-based warfarin dosing was associated with a shorter time to first therapeutic INR (WMD: -2.73, 95% CI: -3.41, -2.05) and stable INR/warfarin dose (WMD: -8.1, 95% CI: -12.54, -3.66).	Warfarin	13-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
33346393-7	2021	CYP2C9-based warfarin dosing was associated with a shorter time to first therapeutic INR (WMD: -2.73, 95% CI: -3.41, -2.05) and stable INR/warfarin dose (WMD: -8.1, 95% CI: -12.54, -3.66).	Warfarin	139-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
33346393-8	2021	CYP2C9 and VKORC1 were observed with a shorter time to first therapeutic INR (WMD: -1.92, 95% CI: -3.23, -0.61) and stable INR/warfarin dose (WMD: -4.6, 95% CI: -6.87, -2.34) along with a longer TTR (%) (WMD: 3.91, 95% CI: 1.18, 6.63).	Warfarin	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
33346393-11	2021	WHAT IS NEW AND CONCLUSION: The present evidence is supportive of personalizing warfarin dose based only on CYP2C9 and VKORC1 genotypes compared to traditional strategies.	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
33961833-3	2021	Our data indicated that miconazole potently inhibited phenytoin hydroxylation in both pooled HLMs and recombinant cytochrome P450 2C9 (CYP2C9) with the Ki values of 125 +-7 nM and 30 +- 2 nM, respectively.	Miconazole	24-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-133
33955686-0	2021	Effect of GLPG1205, a GPR84 Modulator, on CYP2C9, CYP2C19, and CYP1A2 Enzymes: In Vitro and Phase 1 Studies.	GLPG1205	10-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
33652071-8	2021	These findings indicate that CYP3A5, CYP3A4, CYP2C8 and CYP2C9 play a major role in the transformation of carfentanil to M1 (norcarfentanil), M11, M13 and M15 through N-dealkylation of piperidine ring, hydroxylation of phenethyl group and ketone formation on phenethyl linker by human liver micrsomes.	carfentanil	106-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
33652071-8	2021	These findings indicate that CYP3A5, CYP3A4, CYP2C8 and CYP2C9 play a major role in the transformation of carfentanil to M1 (norcarfentanil), M11, M13 and M15 through N-dealkylation of piperidine ring, hydroxylation of phenethyl group and ketone formation on phenethyl linker by human liver micrsomes.	Norcarfentanil	125-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
33652071-8	2021	These findings indicate that CYP3A5, CYP3A4, CYP2C8 and CYP2C9 play a major role in the transformation of carfentanil to M1 (norcarfentanil), M11, M13 and M15 through N-dealkylation of piperidine ring, hydroxylation of phenethyl group and ketone formation on phenethyl linker by human liver micrsomes.	Piperidines	185-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
33652071-8	2021	These findings indicate that CYP3A5, CYP3A4, CYP2C8 and CYP2C9 play a major role in the transformation of carfentanil to M1 (norcarfentanil), M11, M13 and M15 through N-dealkylation of piperidine ring, hydroxylation of phenethyl group and ketone formation on phenethyl linker by human liver micrsomes.	2-phenylethyl acetate	219-228	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
33652071-8	2021	These findings indicate that CYP3A5, CYP3A4, CYP2C8 and CYP2C9 play a major role in the transformation of carfentanil to M1 (norcarfentanil), M11, M13 and M15 through N-dealkylation of piperidine ring, hydroxylation of phenethyl group and ketone formation on phenethyl linker by human liver micrsomes.	Ketones	239-245	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
33652071-8	2021	These findings indicate that CYP3A5, CYP3A4, CYP2C8 and CYP2C9 play a major role in the transformation of carfentanil to M1 (norcarfentanil), M11, M13 and M15 through N-dealkylation of piperidine ring, hydroxylation of phenethyl group and ketone formation on phenethyl linker by human liver micrsomes.	2-phenylethyl acetate	259-268	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
33955686-3	2021	In vitro experiments indicated weak inhibition of CYP1A2 and moderate but reversible inhibition of CYP2C9 and CYP2C19 by GLPG1205.	GLPG1205	121-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
33961833-3	2021	Our data indicated that miconazole potently inhibited phenytoin hydroxylation in both pooled HLMs and recombinant cytochrome P450 2C9 (CYP2C9) with the Ki values of 125 +-7 nM and 30 +- 2 nM, respectively.	Miconazole	24-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-141
33961833-3	2021	Our data indicated that miconazole potently inhibited phenytoin hydroxylation in both pooled HLMs and recombinant cytochrome P450 2C9 (CYP2C9) with the Ki values of 125 +-7 nM and 30 +- 2 nM, respectively.	Phenytoin	54-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-133
33961833-3	2021	Our data indicated that miconazole potently inhibited phenytoin hydroxylation in both pooled HLMs and recombinant cytochrome P450 2C9 (CYP2C9) with the Ki values of 125 +-7 nM and 30 +- 2 nM, respectively.	Phenytoin	54-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-141
33632714-3	2021	M1L is present at a minor allele frequency of 6.3% in Yup"ik Alaska Native people and, thus, can contribute to the risk of an adverse drug response from narrow therapeutic index CYP2C9 substrates, such as (S)-warfarin.	Warfarin	205-217	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	178-184
33958549-6	2021	Our results showed that 13 SNPs on 6 genes (CYP2C9, VKORC1, ABCB1, PROC, EPHX1 and SETD1A) were associated with the individual stable warfarin dose.	Warfarin	134-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
33958549-9	2021	We discovered that, genetic variants in CYP2C9, VKORC1, ABCB1, PROC, EPHX1 and SETD1A may affect the stable warfarin dose requirement in Han Chinese patients with valvular disease.	Warfarin	108-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
33632714-9	2021	Here, we validated (S)-naproxen as a CYP2C9 probe substrate to characterize the in vivo functional activity of the CYP2C9 Leu1 variant.	Naproxen	19-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
33632714-5	2021	We first confirmed the selectivity of (S)-naproxen O-demethylation by CYP2C9 using activity phenotyped human liver microsomes and selective CYP inhibitors, then developed and validated a novel LC/MS method for simultaneous quantification of (S)-naproxen, (S)-O-desmethyl naproxen, and naproxen acyl glucuronide in human urine.	Naproxen	38-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
33632714-9	2021	Here, we validated (S)-naproxen as a CYP2C9 probe substrate to characterize the in vivo functional activity of the CYP2C9 Leu1 variant.	Naproxen	19-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
33610566-8	2021	Moreover, isobavachalcone demonstrated broad-spectrum inhibitory effects against CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, UGT1A1, UGT1A9, UGT2B7 with IC50 values of 1.08-9.78 muM.	isobavachalcone	10-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
33509019-0	2021	Effect of CYP2C9 genetic polymorphism and breviscapine on losartan pharmacokinetics in healthy subjects.	Losartan	58-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
33509019-7	2021	Individuals with genotype CYP2C9*1/*3 showed a significant increase in AUC (0-36) (2335 +- 851.8 ng h ml-1 vs. 1927 +- 949.5 ng h ml-1, p < 0.05) and AUC (0- ) (2363 +- 875.6 ng h ml-1 vs. 1966 +- 966.1 ng h ml-1, p < 0.05) of E-3174 after breviscapine treatment compared to the placebo group.	breviscapine	240-252	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
33509019-9	2021	The activity of CYP2C9 enzyme to losartan metabolism was more significant in subjects with CYP2C9*1/*3 than those with CYP2C9*1/*1 genotype.	Losartan	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
33509019-9	2021	The activity of CYP2C9 enzyme to losartan metabolism was more significant in subjects with CYP2C9*1/*3 than those with CYP2C9*1/*1 genotype.	Losartan	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
33509019-9	2021	The activity of CYP2C9 enzyme to losartan metabolism was more significant in subjects with CYP2C9*1/*3 than those with CYP2C9*1/*1 genotype.	Losartan	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
33840516-0	2021	Association Between the CYP2C9 Genotype and Hypoglycemia Among Patients With Type 2 Diabetes Receiving Sulfonylurea Treatment: A Meta-analysis.	Sulfonylurea Compounds	103-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
33663326-2	2021	To determine the drug-drug interaction risk for cytochrome P450, and SLC and ABC transporters, brexpiprazole and its metabolite, DM-3411 were assessed in this in vitro investigation.Brexpiprazole exhibited weak inhibitory effects (IC50 >13 mumol/L) on CYP2C9, CYP2C19, CYP2D6 and CYP3A4 activities, but had moderate inhibitor activity on CYP2B6 (IC50 8.19 mumol/L).	brexpiprazole	182-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	252-258
33890704-6	2021	Treatment with metamizole, a CAR-dependent inducer of CYP2B6, CYP2C9, CYP2C19 and CYP3A4, accentuated the effect of deglucuronidation on AUC and MR.	Dipyrone	15-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
33859491-0	2021	CYP2C9*3/*3 Gene Expression Affects the Total and Free Concentrations of Valproic Acid in Pediatric Patients with Epilepsy.	Valproic Acid	73-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
33859491-7	2021	VPA"s daily doses and free drug concentrations were significantly lower in the CYP2C9 *3/*3 genotype group versus the CYP2C9 *1/*3 and CYP2C9 *1/*1 groups (P<0.05).	Valproic Acid	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
33859491-7	2021	VPA"s daily doses and free drug concentrations were significantly lower in the CYP2C9 *3/*3 genotype group versus the CYP2C9 *1/*3 and CYP2C9 *1/*1 groups (P<0.05).	Valproic Acid	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
33859491-7	2021	VPA"s daily doses and free drug concentrations were significantly lower in the CYP2C9 *3/*3 genotype group versus the CYP2C9 *1/*3 and CYP2C9 *1/*1 groups (P<0.05).	Valproic Acid	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
33859491-11	2021	Additionally, CYP2C9 *3/*3 expression affects VPA metabolism.	Valproic Acid	46-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
33840516-2	2021	Because impaired catalytic function is likely to affect sulfonylurea metabolism, it is predictable that CYP2C9 loss-of-function alleles may increase the risk of sulfonylurea-induced hypoglycemia.	Sulfonylurea Compounds	56-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
33840516-2	2021	Because impaired catalytic function is likely to affect sulfonylurea metabolism, it is predictable that CYP2C9 loss-of-function alleles may increase the risk of sulfonylurea-induced hypoglycemia.	Sulfonylurea Compounds	161-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
33840516-3	2021	This systematic review and meta-analysis aimed to assess the association between CYP2C9 genotype and hypoglycemia among patients with type 2 diabetes mellitus (T2DM) receiving sulfonylurea.	Sulfonylurea Compounds	176-188	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
33840516-4	2021	METHODS: We searched for studies on the association between CYP2C9 genotype and sulfonylurea-induced hypoglycemia among patients with T2DM, published through August 7, 2020, using PubMed, Web of Science, and EMBASE.	Sulfonylurea Compounds	80-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
33840516-7	2021	The CYP2C9 variant alleles were associated with an increase in sulfonylurea-induced hypoglycemia compared with wild-type homozygote (OR = 1.24; 95% CI, 1.03-1.48).	Sulfonylurea Compounds	63-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
33840516-9	2021	IMPLICATIONS: On the basis of these results, CYP2C9 genotyping may be useful for predicting the risk of hypoglycemia during sulfonylurea treatment for T2DM.	Sulfonylurea Compounds	124-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
28520374-0	2012	Phenytoin Therapy and HLA-B*15:02 and CYP2C9 Genotypes Phenytoin is an antiseizure medication used for the prevention of focal seizures and generalized tonic-clonic convulsions (1).	Phenytoin	55-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
28520374-4	2012	CYP2C9 is one of the main enzymes involved in the metabolism of phenytoin, and variant CYP2C9 alleles are known to influence phenytoin drug levels.	Phenytoin	64-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
28520374-4	2012	CYP2C9 is one of the main enzymes involved in the metabolism of phenytoin, and variant CYP2C9 alleles are known to influence phenytoin drug levels.	Phenytoin	64-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
28520374-4	2012	CYP2C9 is one of the main enzymes involved in the metabolism of phenytoin, and variant CYP2C9 alleles are known to influence phenytoin drug levels.	Phenytoin	125-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
28520374-4	2012	CYP2C9 is one of the main enzymes involved in the metabolism of phenytoin, and variant CYP2C9 alleles are known to influence phenytoin drug levels.	Phenytoin	125-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
28520374-12	2012	The label also mentions that variant CYP2C9 alleles may contribute to unusually high levels of phenytoin (1).	Phenytoin	95-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
33421896-3	2021	The redox properties of the immobilised proteins were investigated by cyclic voltammetry and electrocatalysis was measured in presence of the largely used anticoagulant drug S-warfarin, marker substrate for CYP2C9.	Warfarin	174-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	207-213
33421896-4	2021	Immobilisation of the CYP2C9-FLD, CYP2C9*2-FLD and CYP2C9*3-FLD on DDAB modified glassy carbon electrodes showed well defined redox couples on the oxygen-free cyclic voltammograms and mid-point potentials of all enzymes were calculated.	didodecyldimethylammonium	67-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
33421896-4	2021	Immobilisation of the CYP2C9-FLD, CYP2C9*2-FLD and CYP2C9*3-FLD on DDAB modified glassy carbon electrodes showed well defined redox couples on the oxygen-free cyclic voltammograms and mid-point potentials of all enzymes were calculated.	didodecyldimethylammonium	67-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
33421896-4	2021	Immobilisation of the CYP2C9-FLD, CYP2C9*2-FLD and CYP2C9*3-FLD on DDAB modified glassy carbon electrodes showed well defined redox couples on the oxygen-free cyclic voltammograms and mid-point potentials of all enzymes were calculated.	didodecyldimethylammonium	67-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
33421896-4	2021	Immobilisation of the CYP2C9-FLD, CYP2C9*2-FLD and CYP2C9*3-FLD on DDAB modified glassy carbon electrodes showed well defined redox couples on the oxygen-free cyclic voltammograms and mid-point potentials of all enzymes were calculated.	Carbon	88-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
33421896-4	2021	Immobilisation of the CYP2C9-FLD, CYP2C9*2-FLD and CYP2C9*3-FLD on DDAB modified glassy carbon electrodes showed well defined redox couples on the oxygen-free cyclic voltammograms and mid-point potentials of all enzymes were calculated.	Carbon	88-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
33421896-4	2021	Immobilisation of the CYP2C9-FLD, CYP2C9*2-FLD and CYP2C9*3-FLD on DDAB modified glassy carbon electrodes showed well defined redox couples on the oxygen-free cyclic voltammograms and mid-point potentials of all enzymes were calculated.	Carbon	88-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
33421896-4	2021	Immobilisation of the CYP2C9-FLD, CYP2C9*2-FLD and CYP2C9*3-FLD on DDAB modified glassy carbon electrodes showed well defined redox couples on the oxygen-free cyclic voltammograms and mid-point potentials of all enzymes were calculated.	Oxygen	147-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
33421896-4	2021	Immobilisation of the CYP2C9-FLD, CYP2C9*2-FLD and CYP2C9*3-FLD on DDAB modified glassy carbon electrodes showed well defined redox couples on the oxygen-free cyclic voltammograms and mid-point potentials of all enzymes were calculated.	Oxygen	147-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
33450066-5	2021	KEY RESULTS: Using microsomes containing recombinant CYPs expressed in human vascular tissues, we show that nitrite is released from NTG and PETN with CYP2C9 and CYP2C8 being most efficient.	Nitrites	108-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	151-157
33421896-4	2021	Immobilisation of the CYP2C9-FLD, CYP2C9*2-FLD and CYP2C9*3-FLD on DDAB modified glassy carbon electrodes showed well defined redox couples on the oxygen-free cyclic voltammograms and mid-point potentials of all enzymes were calculated.	Oxygen	147-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
33675325-7	2021	For all patients, pharmacogenetic diagnostic for the genes CYP2C9, CYP2C19 and NAT2, which are involved in metamizole metabolism and degradation of toxic metabolites, was initiated.	Dipyrone	107-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
33394101-2	2021	The study investigated the drug-drug interaction (DDI) potential of ceritinib when coadministered with midazolam and warfarin as probe substrates for CYP3A and CYP2C9 activity, respectively.	ceritinib	68-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
33394101-11	2021	CONCLUSION: Ceritinib is a strong CYP3A inhibitor and a weak CYP2C9 inhibitor.	ceritinib	12-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
33849700-0	2021	The inhibition of CYP1A2, CYP2C9, and CYP2D6 by pterostilbene in human liver microsomes.	pterostilbene	48-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
33849700-1	2021	This study used human liver microsomes to assess pterostilbene"s effect on the metabolic activity of cytochrome P450 (CYP) 1A2, CYP2C9, and CYP2D6.	pterostilbene	49-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
33849700-4	2021	In this study, pterostilbene inhibited CYP1A2, CYP2C9, and CYP2D6"s metabolic activities in vitro.	pterostilbene	15-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
33849700-5	2021	CYP2C9"s activity was most significantly inhibited by pterostilbene; its IC50 value was 0.12+-0.04 muM.	pterostilbene	54-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
33849700-7	2021	The finding that suggests that pterostilbene has the potential to interact with CYP2C9 substrates in vivo.	pterostilbene	31-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
33731883-4	2021	Genetic polymorphisms of CYP2C9, the main enzyme involved in the metabolism of sulfonylureas, have been associated with the risk of severe hypoglycaemia, particularly in poor metabolizers carrying CYP2C9 *3/*3 genotype, and especially in the case of patients treated with glimepiride.	Sulfonylurea Compounds	79-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
33731883-4	2021	Genetic polymorphisms of CYP2C9, the main enzyme involved in the metabolism of sulfonylureas, have been associated with the risk of severe hypoglycaemia, particularly in poor metabolizers carrying CYP2C9 *3/*3 genotype, and especially in the case of patients treated with glimepiride.	Sulfonylurea Compounds	79-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
33731883-4	2021	Genetic polymorphisms of CYP2C9, the main enzyme involved in the metabolism of sulfonylureas, have been associated with the risk of severe hypoglycaemia, particularly in poor metabolizers carrying CYP2C9 *3/*3 genotype, and especially in the case of patients treated with glimepiride.	glimepiride	272-283	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
33731883-4	2021	Genetic polymorphisms of CYP2C9, the main enzyme involved in the metabolism of sulfonylureas, have been associated with the risk of severe hypoglycaemia, particularly in poor metabolizers carrying CYP2C9 *3/*3 genotype, and especially in the case of patients treated with glimepiride.	glimepiride	272-283	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
33731883-5	2021	The objectives of the present study were to evaluate the potential clinical and economic outcomes of using CYP2C9 genotype data to guide the management of SU regimen in patients initiating glimepiride therapy, and to identify factors affecting the cost-effectiveness of this treatment scheme.	glimepiride	189-200	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
33731883-9	2021	In conclusion, the potential cost of CYP2C9 genotype-guided dosing for glimepiride therapy is relatively high, and associated with modest improvements with respect to the number of hypoglycaemia avoided, as compared with standard dosing.	glimepiride	71-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
33243500-3	2021	The results indicated that Mo or/and Cd induced CYP1A1, CYP1B1, CYP2C9, CYP3A8 and CYP4B1 mRNA levels, decreased superoxide dismutase (SOD), catalase (CAT) activities and glutathione peroxidase (GSH-Px) content, and increased malondialdehyde (MDA) and hydrogen peroxide (H2O2) contents.	Cadmium	37-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
33556367-8	2021	In contrast, the binding of both SOR and SNO to active site residues in the closely related human CYP2C9 enzyme was similar, as were the IC50s determined against CYP2C9-mediated losartan oxidation.	Sorafenib	33-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
33556367-8	2021	In contrast, the binding of both SOR and SNO to active site residues in the closely related human CYP2C9 enzyme was similar, as were the IC50s determined against CYP2C9-mediated losartan oxidation.	Losartan	178-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
33754183-0	2021	S-warfarin limited sampling strategy with a population pharmacokinetic approach to estimate exposure and cytochrome P450 (CYP) 2C9 activity in healthy adults.	Warfarin	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-130
33754183-1	2021	PURPOSE: S-warfarin is used to phenotype cytochrome P450 (CYP) 2C9 activity.	Warfarin	9-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-66
33754183-11	2021	During CYP2C9 induction, S-warfarin LSMs had unacceptable %MPE, %MAE, and %RMSE.	Warfarin	25-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	7-13
33754183-12	2021	CONCLUSIONS: Phenotyping studies with S-warfarin in healthy subjects can utilize a single- and/or a 2-timepoint LSM with a population PK approach to estimate constitutive CYP2C9 activity.	Warfarin	38-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
33740842-2	2021	Cannabinoids are subjected to a significant first-pass metabolism in the liver involving the cytochrome P450 enzymes (CYP) 2C9, CYP2C19 and CYP3A4 [2];.	Cannabinoids	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-126
33727862-1	2021	Purpose: To assess the association between VKORC1 and CYP2C9 variants and the incidence of adverse drug reactions in warfarin-treated patients in a real-world setting.	Warfarin	117-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
33675325-14	2021	In conclusion, metamizole-induced agranulocytosis most likely was a consequence of the underlying genetical predisposition, that is, polymorphisms in the genes NAT2, CYP2C9 and CYP2C19.	Dipyrone	15-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	166-172
32736411-1	2021	AIMS: We evaluated the potential effect of sonidegib at an oral dose of 800 mg once daily (QD) on the pharmacokinetics (PK) of the probe drugs warfarin (CYP2C9) and bupropion (CYP2B6).	sonidegib	43-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
33191909-1	2021	OBJECTIVE: We attempted to examine the applicability of a population pharmacokinetic-pharmacodynamic (PK-PD) model describing the metabolic interaction between warfarin and sorafenib due to CYP2C9 inhibition and to predict the plasma concentrations of sorafenib and S-warfarin, the international normalized ratio (INR), and the optimal maintenance dose of warfarin in the presence of sorafenib in vivo.	Warfarin	160-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
33278335-1	2021	VKORC1 and CYP2C9 genotypes explain less variability in warfarin dose requirements in African Americans (AAs) compared to Europeans.	Warfarin	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
33278335-2	2021	Variants in BCKDK and GATA-4 gene regions, purported to regulate VKORC1 and CYP2C9 expression, have been shown to play an important role in warfarin dose requirements in Europeans and Asians, respectively.	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
33191909-1	2021	OBJECTIVE: We attempted to examine the applicability of a population pharmacokinetic-pharmacodynamic (PK-PD) model describing the metabolic interaction between warfarin and sorafenib due to CYP2C9 inhibition and to predict the plasma concentrations of sorafenib and S-warfarin, the international normalized ratio (INR), and the optimal maintenance dose of warfarin in the presence of sorafenib in vivo.	Sorafenib	173-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
32918831-2	2021	In vitro data showed pexidartinib"s potential to inhibit and induce cytochrome P450 (CYP) 3A, inhibit CYP2C9, CYP2C19 and P-glycoprotein (P-gp).	pexidartinib	21-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
32918831-3	2021	Herein, 2 open-label, single-sequence, crossover studies evaluated the drug-drug interaction potential of pexidartinib on CYP enzymes (CYP2C9, CYP2C19, and CYP3A) and P-gp.	pexidartinib	106-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-141
32918831-11	2021	These results indicate that pexidartinib is a moderate inducer of CYP3A and a weak inhibitor of CYP2C9 and does not significantly affect CYP2C19-mediated metabolism or P-gp transport.	pexidartinib	28-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
33253783-5	2021	Scaling of relative P450 efficiencies based on average liver concentration revealed that CYP2C8 dominates the sudoxicam bioactivation pathway and CYP2C9 dominates meloxicam detoxification.	Meloxicam	163-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
33600055-4	2021	In this study, we systematically evaluated the effects of protein crystal structural models, scoring functions, heme forms, conserved active site water molecule, and protein flexibility on SOMs prediction of CYP2C9 substrates.	Heme	112-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	208-214
33600055-4	2021	In this study, we systematically evaluated the effects of protein crystal structural models, scoring functions, heme forms, conserved active site water molecule, and protein flexibility on SOMs prediction of CYP2C9 substrates.	Water	146-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	208-214
33341662-0	2021	Effects of acid and lactone forms of statins on S-warfarin 7-hydroxylation catalyzed by human liver microsomes and recombinant CYP2C9 variants (CYP2C9.1 and CYP2C9.3).	Warfarin	48-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-133
33747646-4	2021	These medications inhibit two vital enzymes of cytochrome P-450, CYP2C9 and CYP3A4, potentiating the effects of ATRA on calcium metabolism.	Tretinoin	112-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
33747646-4	2021	These medications inhibit two vital enzymes of cytochrome P-450, CYP2C9 and CYP3A4, potentiating the effects of ATRA on calcium metabolism.	Calcium	120-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
33540768-1	2021	Cytochrome P450 2C9 (CYP2C9) is an important drug-metabolizing enzyme that contributes to the metabolism of approximately 15% of clinically used drugs, including warfarin, which is known for its narrow therapeutic window.	Warfarin	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
33540768-1	2021	Cytochrome P450 2C9 (CYP2C9) is an important drug-metabolizing enzyme that contributes to the metabolism of approximately 15% of clinically used drugs, including warfarin, which is known for its narrow therapeutic window.	Warfarin	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
33540768-4	2021	These CYP2C9 variants were heterologously expressed in 293FT cells, and the kinetic parameters (Km, kcat, Vmax, catalytic efficiency, and CLint) of (S)-warfarin 7-hydroxylation and tolbutamide 4-hydroxylation were estimated.	Warfarin	148-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
33540768-6	2021	A strong correlation was found in catalytic efficiencies between (S)-warfarin 7-hydroxylation and tolbutamide 4-hydroxylation among all studied CYP2C9 variants.	Warfarin	65-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
33540768-6	2021	A strong correlation was found in catalytic efficiencies between (S)-warfarin 7-hydroxylation and tolbutamide 4-hydroxylation among all studied CYP2C9 variants.	Tolbutamide	98-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
33540768-8	2021	Our findings could clarify a part of discrepancies among genotype-phenotype associations based on the novel CYP2C9 rare allelic variants and could, therefore, improve personalized medicine, including the selection of the appropriate warfarin dose.	Warfarin	233-241	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
33341662-1	2021	The inhibition of CYP2C9-mediated warfarin metabolism by acid or lactone forms of statin converted in the body and effects of CYP2C9 genetic variants on their inhibition are not fully understood.	Warfarin	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
33341662-1	2021	The inhibition of CYP2C9-mediated warfarin metabolism by acid or lactone forms of statin converted in the body and effects of CYP2C9 genetic variants on their inhibition are not fully understood.	Lactones	65-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
33341662-7	2021	These results indicated that lactone forms of statins other than fluvastatin showed more potent inhibition of CYP2C9-catalyzed S-warfarin 7-hydroxylation than the corresponding acid forms.	Lactones	29-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
33341662-7	2021	These results indicated that lactone forms of statins other than fluvastatin showed more potent inhibition of CYP2C9-catalyzed S-warfarin 7-hydroxylation than the corresponding acid forms.	Fluvastatin	65-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
33341662-7	2021	These results indicated that lactone forms of statins other than fluvastatin showed more potent inhibition of CYP2C9-catalyzed S-warfarin 7-hydroxylation than the corresponding acid forms.	Warfarin	127-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
33341662-8	2021	Furthermore, our results indicated that Ile359Leu substitution in CYP2C9 affected the inhibitory potencies of statins.	ile359leu	40-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
33259822-5	2021	The formation of MFA-quinoneimine by recombinant CYP1A2 and CYP2C9 was significantly decreased by the addition of human liver cytosol, and the extent of the decrease in the metabolite formed by CYP1A2 was larger than that by CYP2C9.	mfa-quinoneimine	17-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
32779747-1	2021	Phenytoin is an antiepileptic drug with a narrow therapeutic index and large inter-patient pharmacokinetic variability, partly due to genetic variation in CYP2C9.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
32779747-3	2021	We summarize evidence from the published literature supporting these associations and provide therapeutic recommendations for the use of phenytoin based on CYP2C9 and/or HLA-B genotypes (updates on cpicpgx.org).	Phenytoin	137-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
32869328-4	2021	A clinical study in healthy subjects (n = 27) evaluated the inhibition of CYP3A4, CYP2C8, and CYP2C9 in vivo by administering single doses of probe CYP substrates (midazolam, pioglitazone, and tolbutamide) alone and in combination with relacorilant (350 mg).	Midazolam	164-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
32869328-4	2021	A clinical study in healthy subjects (n = 27) evaluated the inhibition of CYP3A4, CYP2C8, and CYP2C9 in vivo by administering single doses of probe CYP substrates (midazolam, pioglitazone, and tolbutamide) alone and in combination with relacorilant (350 mg).	Tolbutamide	193-204	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
33039464-11	2021	LoT positively predicts genomic predisposition (CYP2C9*2) for Bosentan-induced cholestasis.	Bosentan	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
33259822-5	2021	The formation of MFA-quinoneimine by recombinant CYP1A2 and CYP2C9 was significantly decreased by the addition of human liver cytosol, and the extent of the decrease in the metabolite formed by CYP1A2 was larger than that by CYP2C9.	mfa-quinoneimine	17-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	225-231
28520369-0	2012	Celecoxib Therapy and CYP2C9 Genotype Celecoxib is a nonsteroidal anti-inflammatory drug (NSAID) that is used in the management of osteoarthritis, rheumatoid arthritis, menstrual symptoms, and acute pain.	Celecoxib	38-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
28520369-3	2012	The CYP2C9 gene encodes an enzyme involved in the metabolism of many drugs, and is one of the main enzymes that metabolizes and inactivates celecoxib.	Celecoxib	140-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
33542643-2	2021	Due to rifampin"s strong induction of CYP2C9, most cases could not attain the target international normalized ratio (INR) despite warfarin dose escalation.	Rifampin	7-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
28520369-6	2012	The FDA-approved drug label for celecoxib states: "patients who are known or suspected to be poor CYP2C9 metabolizers based on genotype or previous history/experience with other CYP2C9 substrates (such as warfarin, phenytoin) should be administered celecoxib with caution.	Celecoxib	32-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
33542643-8	2021	The analysis revealed that the subject carries CYP2C9*3*3 and VKORC1-1639 (GA) mutations, classifying her as a slow metabolizer and, hence, highly warfarin-sensitive.	Warfarin	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
28520369-6	2012	The FDA-approved drug label for celecoxib states: "patients who are known or suspected to be poor CYP2C9 metabolizers based on genotype or previous history/experience with other CYP2C9 substrates (such as warfarin, phenytoin) should be administered celecoxib with caution.	Celecoxib	32-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	178-184
33093187-6	2021	Mitragynine was tested against CYP2C9 (diclofenac 4"-hydroxylation), CYP2D6 (dextromethorphan O-demethylation), and CYP3A (midazolam 1"-hydroxylation) activities in human liver microsomes (HLMs) and CYP3A activity in human intestinal microsomes (HIMs).	mitragynine	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
33498694-10	2021	Additionally, we describe that fluoxetine is a CYP2C9 substrate and a mechanism-based inhibitor of CYP2C19.	Fluoxetine	31-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
33378980-5	2021	Polymorphisms in CYP2C9, SLC22A1, ABCB1, ABCC2, and APOC3 were related to olanzapine pharmacokinetic variability.	Olanzapine	74-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
32860733-4	2021	In the U.S. cohort, VKORC1 and CYP2C9 variants were associated with lower warfarin dose (beta=-0.29, p<2.0x10-16 ; beta=-0.21, p=4.7x10-7 , respectively) whereas CYP4F2 and NQO1 variants were associated with higher dose (beta=0.10, p=2x10-4 ; beta=0.10, p=0.01, respectively).	Warfarin	74-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
32860733-7	2021	We confirmed the association of variants in VKORC1, CYP2C9, and CYP4F2 with warfarin dose in Latinos from U.S. and Brazil.	Warfarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
33309749-5	2021	Furthermore, in contrast to imidazole derivative C38, the tert-butylimidazole derivative 20 is a poor inhibitor of CYP3A4, CYP2D6 and CYP2C9.	tert-butylimidazole	58-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
33321412-5	2021	Knipholone was also the most effective in increasing the expression of CYP3A4 (8.47 +- 2.5 fold) and CYP2C9 (2.64 +- 0.3 fold) at 10 microM.	knipholone	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
33321412-7	2021	In a CYP inhibition assay, the methanolic extract as well as the anthraquinones strongly inhibited the catalytic activity of CYP2C9 while, inhibition of CYP3A4 was weak.	Anthraquinones	65-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
32813611-0	2021	Main contribution of UGT1A1 and CYP2C9 in the metabolism of UR-1102, a novel agent for the treatment of gout.	UR-1102	60-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
31709648-0	2020	The presence of two reduced function variants in CYP2C9 influences the acute response to glipizide.	Glipizide	89-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
33341937-0	2021	Hypoglycemia and glycemic control with glyburide in women with gestational diabetes and genetic variants of cytochrome P450 2C9 and/or OATP1B3.	Glyburide	39-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-127
33341937-1	2021	Glyburide is mainly metabolized by the cytochrome P450 2C9 (CYP2C9) enzyme and enters the liver via the transporter OATP1B3.	Glyburide	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-58
33341937-1	2021	Glyburide is mainly metabolized by the cytochrome P450 2C9 (CYP2C9) enzyme and enters the liver via the transporter OATP1B3.	Glyburide	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
33341937-2	2021	The variants OATP1B3*4 (699 G>A; rs7311358) and CYP2C9*2 and *3 are known to have a significant influence on the hepatic uptake and metabolism of glyburide, with lower clearance than in the wild type.	Glyburide	146-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
33341937-7	2021	In conclusion, the no function variants CYP2C9*3 and OATP1B3*4 are associated with a higher risk of hypoglycemia and a lower dose of glyburide in women with gestational diabetes treated with glyburide, which is consistent with the pharmacokinetic roles of both CYP2C9 and OATP1B3.	Glyburide	133-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
33341937-7	2021	In conclusion, the no function variants CYP2C9*3 and OATP1B3*4 are associated with a higher risk of hypoglycemia and a lower dose of glyburide in women with gestational diabetes treated with glyburide, which is consistent with the pharmacokinetic roles of both CYP2C9 and OATP1B3.	Glyburide	133-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	261-267
33341937-7	2021	In conclusion, the no function variants CYP2C9*3 and OATP1B3*4 are associated with a higher risk of hypoglycemia and a lower dose of glyburide in women with gestational diabetes treated with glyburide, which is consistent with the pharmacokinetic roles of both CYP2C9 and OATP1B3.	Glyburide	191-200	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
31709648-8	2020	CONCLUSIONS: Carriers of two reduced function alleles in CYP2C9 may experience an increased insulin response to glipizide and be predisposed to a higher risk of hypoglycaemia, although no effect of genotype was seen in glucose-based measurements.	Glipizide	112-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
31709648-8	2020	CONCLUSIONS: Carriers of two reduced function alleles in CYP2C9 may experience an increased insulin response to glipizide and be predisposed to a higher risk of hypoglycaemia, although no effect of genotype was seen in glucose-based measurements.	Glucose	219-226	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
31709648-9	2020	Further studies are needed to clarify the utility of CYP2C9 genotyping to guide sulfonylurea treatment.	Sulfonylurea Compounds	80-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
32279279-5	2020	Moreover, iloperidone attenuated the activity of CYP1A2 (Ki = 45 and 31 microM in microsomes and supersomes) and CYP2C19 via a mixed mechanism (Ki = 6.5 and 32 microM in microsomes and supersomes) but did not affect CYP2C9.	iloperidone	10-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	216-222
32648321-12	2020	CONCLUSIONS: CYP1A1 and CYP2C9, UGT1A1, UGT1A7, UGT1A8 and UGT1A9, and MRP4 all played important roles in the metabolism and disposition of bavachin.	bavachin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
33635755-14	2020	CBD is hydroxylated to 7-OH-CBD and 7-COOH-CBD by cytochrome P450 enzymes CYP3A4 and CYP2C9 in the liver and is excreted mainly in feces and less in urine.	Cannabidiol	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
33635755-14	2020	CBD is hydroxylated to 7-OH-CBD and 7-COOH-CBD by cytochrome P450 enzymes CYP3A4 and CYP2C9 in the liver and is excreted mainly in feces and less in urine.	7-Hydroxycannabidiol	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
33635755-14	2020	CBD is hydroxylated to 7-OH-CBD and 7-COOH-CBD by cytochrome P450 enzymes CYP3A4 and CYP2C9 in the liver and is excreted mainly in feces and less in urine.	7-cooh-cbd	36-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
31319733-8	2020	DISCUSSION: The elevation in INR can be explained by the inhibition of CYP2C9 by cannabis use causing decreased metabolism of warfarin.	Warfarin	126-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
32223485-3	2020	In addition, the enzyme kinetic parameters were calculated.Results: The results showed that the activity of CYP3A4, CYP2E1 and CYP2C9 was inhibited by CEP, with IC50 values of 16.29, 25.62 and 24.57 muM, respectively, but other CYP isoforms were not affected.	cepharanthine	151-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-133
32279279-6	2020	Lurasidone moderately inhibited CYP1A2 (Ki = 12.6 and 15.5 microM in microsomes and supersomes), CYP2C9 (Ki = 18 and 3.5 microM in microsomes and supersomes) and CYP2C19 via a mixed mechanism (Ki = 18 and 18.4 microM in microsomes and supersomes), and CYP3A4 via a competitive mechanism (Ki = 29.4 and 9.1 microM in microsomes and supersomes).	Lurasidone Hydrochloride	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
33350885-0	2020	Effect of CYP2C9 *11/*11 genotype on initial and long-term warfarin dose requirement and therapeutic response.	Warfarin	59-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
32279279-9	2020	The obtained results indicate that metabolic/pharmacokinetic interactions with iloperidone (involving mainly CYP3A4 and CYP2D6) and possibly with lurasidone (involving CYP1A2, CYP2C9 or CYP2C19) may occur during combined therapy.	Lurasidone Hydrochloride	146-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
32504053-3	2020	In a retrospective case-control study in European American patients with T2DM, we examined the potential association between CYP2C9 reduced-function variants and sulfonylurea-related hypoglycemia.	Sulfonylurea Compounds	162-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
33350885-4	2020	This case report sheds further light on the clinical impact of CYP2C9 *11/*11 on warfarin dose requirements, short- and long-term treatment response and practical considerations for warfarin management in suspected carriers of rare variant CYP2C9 alleles.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
33350885-4	2020	This case report sheds further light on the clinical impact of CYP2C9 *11/*11 on warfarin dose requirements, short- and long-term treatment response and practical considerations for warfarin management in suspected carriers of rare variant CYP2C9 alleles.	Warfarin	182-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	240-246
33262574-2	2020	Methods: The recombinant cytochrome P450 alleles protein of CYP2C9 and CYP3A4 expressed in insect baculovirus expression system were reacted with 10-500 microM sildenafil for 30 minutes at 37 C, and the reaction was terminated by cooling to -80 C immediately.	Sildenafil Citrate	160-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
33180507-6	2020	Additionally, (S)-18 exhibits no apparent inhibitory effect on CYP isoforms except for a moderate effect on CYP2C9.	(s)-18	14-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
33262574-0	2020	Functional Measurement of CYP2C9 and CYP3A4 Allelic Polymorphism on Sildenafil Metabolism.	Sildenafil Citrate	68-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
33262574-9	2020	Conclusion: These findings were the first evaluation of all these infrequent CYP2C9 and CYP3A4 alleles for sildenafil metabolism; when treating people who carry these CYP2C9 and CYP3A4 variants, there should be more focus on the relation of dose intensity, side effects and therapeutic efficacy when administering sildenafil.	Sildenafil Citrate	107-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
33262574-9	2020	Conclusion: These findings were the first evaluation of all these infrequent CYP2C9 and CYP3A4 alleles for sildenafil metabolism; when treating people who carry these CYP2C9 and CYP3A4 variants, there should be more focus on the relation of dose intensity, side effects and therapeutic efficacy when administering sildenafil.	Sildenafil Citrate	107-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
33262574-9	2020	Conclusion: These findings were the first evaluation of all these infrequent CYP2C9 and CYP3A4 alleles for sildenafil metabolism; when treating people who carry these CYP2C9 and CYP3A4 variants, there should be more focus on the relation of dose intensity, side effects and therapeutic efficacy when administering sildenafil.	Sildenafil Citrate	314-324	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
33262574-9	2020	Conclusion: These findings were the first evaluation of all these infrequent CYP2C9 and CYP3A4 alleles for sildenafil metabolism; when treating people who carry these CYP2C9 and CYP3A4 variants, there should be more focus on the relation of dose intensity, side effects and therapeutic efficacy when administering sildenafil.	Sildenafil Citrate	314-324	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
33262574-10	2020	The study will provide fundamental data on effect of CYP2C9 and CYP3A4 allelic variation on sildenafil metabolism for further clinical research.	Sildenafil Citrate	92-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
33240461-1	2020	CYP2C9 gene encodes an enzyme involved in the metabolism of a wide variety of drugs which include celecoxib.	Celecoxib	98-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
33330279-7	2020	We also analyzed the influence of exogenous factors on the level of 25(OH)D in children of the three study regions, as well as the relationship of the level of 25(OH)D with variants CYP2C9 * 2 (c.430C>T; R144C), CYP2C9 * 3 (c,1075A>C; I359L), CYP2D6 * 4 (1846G>A), CYP3A4 * 3 (c.1334T>C), and CYP3A4 * 1B (c.-392C>T) and rs731236, rs2228570 and rs1544410 in the VDR gene.	25(oh)d	160-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	182-188
33330279-14	2020	Conclusion: Exogenous factors (time of year, place of residence, and prophylactic administration of cholecalciferol), as well as endogenous factors (age and sex), play a determining role in the development of vitamin D deficiency and insufficiency; in contrast to genetic factors-polymorphic variants of the genes of xenobiotic phase 1 enzymes (CYP2C9, CYP2C19, CYP2D6, and CYP3A4) and the VDR gene-which do not play such role.	Vitamin D	209-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	345-351
33181661-5	2020	Therefore, it is recommended to detect the genotype of CYP2C9 in patients and evaluate the interaction between the 2 drugs to adjust the warfarin dose.	Warfarin	137-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
33147873-0	2020	Physiologically Based Pharmacokinetic/Pharmacodynamic Modeling to Predict the Impact of CYP2C9 Genetic Polymorphisms, Co-Medication and Formulation on the Pharmacokinetics and Pharmacodynamics of Flurbiprofen.	Flurbiprofen	196-208	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
33147873-3	2020	Flurbiprofen has absolute bioavailability of ~95% and linear pharmacokinetics in the dose range of 50-300 mg. Its absorption is considered variable and complex, often associated with double peak phenomena, and its pharmacokinetics are characterized by high inter-subject variability, mainly due to its metabolism by the polymorphic CYP2C9 (fmCYP2C9 >= 0.71).	Flurbiprofen	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	332-338
32583677-1	2020	Aim: Our aim was to examine the effect of CYP2C9 and VKORC1 polymorphisms on warfarin dose requirements in Turkish patients.	Warfarin	77-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
32583677-3	2020	Results: Patients with CYP2C9 *1/*1 and VKORC1 -1639 GG and GA genotypes required higher warfarin doses in comparison to wild type VKORC1 genotype.	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
32583677-4	2020	Patients with CYP2C9 *1/*3 and VKORC1 -1639 GG genotypes simultaneously, required the lowest dose of warfarin (4.64 mg/day).	Warfarin	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
32583677-5	2020	Patients with CYP2C9 *1/*1 and VKORC1 9041 AA genotype were found to require higher warfarin doses.	Warfarin	84-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
32583677-6	2020	Conclusion: Our results provide additional evidence to support the hypothesis that CYP2C9 *2, *3, VKORC1 9041 G > A polymorphisms explain considerable proportion of inter-individual variability in warfarin dose requirement.	Warfarin	197-205	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
32712703-8	2020	In addition, this study showed significantly higher values in the ratio of Delta9-THC/Delta9-THC-COOH for the carriers of the CYP2C9 variants CYP2C9*2 and CYP2C9*3 compared with the carriers of the corresponding wild-type alleles.	Dronabinol	82-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
32712703-8	2020	In addition, this study showed significantly higher values in the ratio of Delta9-THC/Delta9-THC-COOH for the carriers of the CYP2C9 variants CYP2C9*2 and CYP2C9*3 compared with the carriers of the corresponding wild-type alleles.	Dronabinol	82-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
32712703-8	2020	In addition, this study showed significantly higher values in the ratio of Delta9-THC/Delta9-THC-COOH for the carriers of the CYP2C9 variants CYP2C9*2 and CYP2C9*3 compared with the carriers of the corresponding wild-type alleles.	Dronabinol	82-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
32712703-8	2020	In addition, this study showed significantly higher values in the ratio of Delta9-THC/Delta9-THC-COOH for the carriers of the CYP2C9 variants CYP2C9*2 and CYP2C9*3 compared with the carriers of the corresponding wild-type alleles.	Dronabinol	93-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
32712703-8	2020	In addition, this study showed significantly higher values in the ratio of Delta9-THC/Delta9-THC-COOH for the carriers of the CYP2C9 variants CYP2C9*2 and CYP2C9*3 compared with the carriers of the corresponding wild-type alleles.	Dronabinol	93-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
32712703-8	2020	In addition, this study showed significantly higher values in the ratio of Delta9-THC/Delta9-THC-COOH for the carriers of the CYP2C9 variants CYP2C9*2 and CYP2C9*3 compared with the carriers of the corresponding wild-type alleles.	Dronabinol	93-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
32712703-8	2020	In addition, this study showed significantly higher values in the ratio of Delta9-THC/Delta9-THC-COOH for the carriers of the CYP2C9 variants CYP2C9*2 and CYP2C9*3 compared with the carriers of the corresponding wild-type alleles.	Carbonic Acid	97-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
32712703-8	2020	In addition, this study showed significantly higher values in the ratio of Delta9-THC/Delta9-THC-COOH for the carriers of the CYP2C9 variants CYP2C9*2 and CYP2C9*3 compared with the carriers of the corresponding wild-type alleles.	Carbonic Acid	97-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
32712703-8	2020	In addition, this study showed significantly higher values in the ratio of Delta9-THC/Delta9-THC-COOH for the carriers of the CYP2C9 variants CYP2C9*2 and CYP2C9*3 compared with the carriers of the corresponding wild-type alleles.	Carbonic Acid	97-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
32712703-9	2020	Therefore, an impact of variations of the CYP2C9 gene on the interpretation of cannabinoid plasma concentrations in DUID cases should be considered.	Cannabinoids	79-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
33138123-4	2020	AB-PINACA reversibly inhibited the metabolic activities of CYP2C8 (Ki, 16.9 microM), CYP2C9 (Ki, 6.7 microM), and CYP2C19 (Ki, 16.1 microM) and the transport activity of OAT3 (Ki, 8.3 microM).	N-(1-amino-3-methyl-1-oxobutan-2-yl)-1-pentyl-1H-indazole-3-carboxamide	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
32882369-11	2020	Systemic 0.1 % terbinafine treatment in the Chip2 increased RHS expression of EGFR, increased apoptotic cells in the liver, downregulated liver albumin expression and upregulated CYP2C9 significantly (p < 0.05), acting as an effective hepatotoxic terbinafine control.	Terbinafine	15-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	179-185
32712703-7	2020	We recognized significantly lower Delta9-THC-COOH concentrations for CYP2C9*3 (p = 0.001) and a trend of lower Delta9-THC-COOH concentrations for CYP2C9*2 which did not reach statistical significance (p = 0.068).	Carbonic Acid	45-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
32712703-7	2020	We recognized significantly lower Delta9-THC-COOH concentrations for CYP2C9*3 (p = 0.001) and a trend of lower Delta9-THC-COOH concentrations for CYP2C9*2 which did not reach statistical significance (p = 0.068).	delta9	34-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
32938720-0	2020	Structure of Cytochrome P450 2C9*2 in Complex with Losartan: Insights into the Effect of Genetic Polymorphism.	Losartan	51-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-32
32938720-4	2020	The crystal structure of CYP2C9*2 in complex with an antihypertensive drug losartan was solved using X-ray crystallography at 3.1-A resolution.	Losartan	75-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
32938720-5	2020	The Arg144Cys variation in the *2 complex disrupts the hydrogen-bonding interactions that were observed between the side chain of arginine and neighboring residues in the losartan complex of CYP2C9 and the wild-type (WT) ligand-free structure.	arg144cys	4-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
32938720-5	2020	The Arg144Cys variation in the *2 complex disrupts the hydrogen-bonding interactions that were observed between the side chain of arginine and neighboring residues in the losartan complex of CYP2C9 and the wild-type (WT) ligand-free structure.	Hydrogen	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
32938720-5	2020	The Arg144Cys variation in the *2 complex disrupts the hydrogen-bonding interactions that were observed between the side chain of arginine and neighboring residues in the losartan complex of CYP2C9 and the wild-type (WT) ligand-free structure.	Arginine	130-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
32938720-5	2020	The Arg144Cys variation in the *2 complex disrupts the hydrogen-bonding interactions that were observed between the side chain of arginine and neighboring residues in the losartan complex of CYP2C9 and the wild-type (WT) ligand-free structure.	Losartan	171-179	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
32938720-7	2020	The new structure revealed distinct interactions of losartan in the compact active site of CYP2C9*2 and differed in occupancy at the other binding sites previously identified in the WT-losartan complex.	Losartan	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
32938720-8	2020	Furthermore, the binding studies in solution using losartan illustrated lower activity of the CYP2C9*2 compared with the WT.	Losartan	51-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
32938720-9	2020	Together, the findings yield valuable insights into the decreased hydroxylation activity of losartan in patients carrying CYP2C9*2 allele and provide a useful framework to investigate the effect of a single-nucleotide polymorphism that leads to altered metabolism of diverse drug substrates.	Losartan	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
32938720-11	2020	How the CYP2C9*2 variant induces altered drug metabolism is poorly understood given that the Arg144Cys variation is located far away from the active site.	arg144cys	93-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
32763815-14	2020	Isozymes of CYP1A2, CYP2C9, UGT1A1, UGT1A6, UGT1A9, UGT2B7 and UGT2B15 were involved in phase I and phase II metabolism of osalmid.	osalmide	123-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
32661014-6	2020	Our observations revealed that chrysin conjugates are strong inhibitors of certain biotransformation enzymes (e.g., CYP2C9) and transporters (e.g., OATP1B1, OATP1B3, OATP2B1, and BCRP) examined.	chrysin	31-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
32628284-7	2020	Simultaneously, PXR-RXRalpha would activate the expression of CYP2C9; metabolic kinetics of ursolic acid in CYP metabolizing enzyme lysate of Caco2 cells and Caco2-PXR-RXR cells was studied and it was found that the Km values were 81.99 +- 44.32 and 60.05 +- 29.62 microg/ml, and Vmax values were 3.77 +- 0.86 and 3.41 +- 0.96 microg   ml-1    min-1 , respectively.	ursolic acid	92-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
33071782-0	2020	Comparison of CYP2C9 Activity in Ethiopian and Non-Ethiopian Jews Using Phenytoin as a Probe.	Phenytoin	72-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
33071782-2	2020	The objective of the study was to compare CYP2C9 activity by using Phenytoin Metabolic Ratio (PMR) between Ethiopian and non-Ethiopian Jews.	Phenytoin	67-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
32968106-4	2020	We studied modulation by microsomal membrane-bound and soluble cyt b5 of the hydroxylation of salicylic acid to gentisic acid and ROS release by CYP2C9 activity in human liver microsomes (HLMs) and by CYP2C9 baculosomes.	Reactive Oxygen Species	130-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
32968106-5	2020	CYP2C9 accounts for nearly 75% of salicylic acid hydroxylation in HLMs at concentrations reached after usual aspirin doses.	Salicylic Acid	34-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
32968106-5	2020	CYP2C9 accounts for nearly 75% of salicylic acid hydroxylation in HLMs at concentrations reached after usual aspirin doses.	Aspirin	109-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
32968106-6	2020	The anti-cyt b5 antibody SC9513 largely inhibits the rate of salicylic acid hydroxylation by CYP2C9 in HLMs and CYP2C9 baculosomes, increasing the KM approximately threefold.	sc9513	25-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
32968106-6	2020	The anti-cyt b5 antibody SC9513 largely inhibits the rate of salicylic acid hydroxylation by CYP2C9 in HLMs and CYP2C9 baculosomes, increasing the KM approximately threefold.	sc9513	25-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
32968106-6	2020	The anti-cyt b5 antibody SC9513 largely inhibits the rate of salicylic acid hydroxylation by CYP2C9 in HLMs and CYP2C9 baculosomes, increasing the KM approximately threefold.	Salicylic Acid	61-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
33005200-4	2020	100 muM of kurarinone strongly inhibited more than 90% of UGT1A1, UGT1A6, CYP1A2, and CYP2C9.	kurarinone	11-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
32863324-0	2020	Phenotypic analysis of human CYP2C9 polymorphisms using fluorine-substituted tolbutamide.	Fluorine	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
32863324-0	2020	Phenotypic analysis of human CYP2C9 polymorphisms using fluorine-substituted tolbutamide.	Tolbutamide	77-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
32863324-1	2020	To investigate the effect of fluorine substitution on tolbutamide (TB) hydroxylation catalyzed by CYP2C9, the hydroxylation of TB and its fluorinated derivative 3"-fluoro-tolbutamide (3"-F-TB) by recombinant human CYP2C9*1, CYP2C9*2, and CYP2C9*3 was analyzed.	Fluorine	29-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
32863324-1	2020	To investigate the effect of fluorine substitution on tolbutamide (TB) hydroxylation catalyzed by CYP2C9, the hydroxylation of TB and its fluorinated derivative 3"-fluoro-tolbutamide (3"-F-TB) by recombinant human CYP2C9*1, CYP2C9*2, and CYP2C9*3 was analyzed.	Tolbutamide	54-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
32863324-1	2020	To investigate the effect of fluorine substitution on tolbutamide (TB) hydroxylation catalyzed by CYP2C9, the hydroxylation of TB and its fluorinated derivative 3"-fluoro-tolbutamide (3"-F-TB) by recombinant human CYP2C9*1, CYP2C9*2, and CYP2C9*3 was analyzed.	Tolbutamide	67-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
32591416-10	2020	SIGNIFICANCE STATEMENT: Robust kinetic parameters were determined for the reversible and time-dependent inhibition of CYP2C9, CYP2D6 and CYP3A4/5 activities in HLMs by major component isoquinoline alkaloids contained in the botanical natural product (NP) goldenseal.	isoquinoline	184-196	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
32863324-1	2020	To investigate the effect of fluorine substitution on tolbutamide (TB) hydroxylation catalyzed by CYP2C9, the hydroxylation of TB and its fluorinated derivative 3"-fluoro-tolbutamide (3"-F-TB) by recombinant human CYP2C9*1, CYP2C9*2, and CYP2C9*3 was analyzed.	Tolbutamide	127-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
32863324-1	2020	To investigate the effect of fluorine substitution on tolbutamide (TB) hydroxylation catalyzed by CYP2C9, the hydroxylation of TB and its fluorinated derivative 3"-fluoro-tolbutamide (3"-F-TB) by recombinant human CYP2C9*1, CYP2C9*2, and CYP2C9*3 was analyzed.	3"-f-tb	184-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
32661920-1	2020	Zolpidem, a widely prescribed hypnotic agent, is extensively metabolized by cytochrome P450 (CYP) 3A4, and CYP2C9, CYP1A2 and CYP2D6 are also involved in the metabolism of zolpidem.	Zolpidem	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
32661920-1	2020	Zolpidem, a widely prescribed hypnotic agent, is extensively metabolized by cytochrome P450 (CYP) 3A4, and CYP2C9, CYP1A2 and CYP2D6 are also involved in the metabolism of zolpidem.	Zolpidem	172-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
32628284-8	2020	However, in human CYP metabolizing recombinase, we found that both CYP2C9 and CYP34A were involved in the metabolism of ursolic acid.	ursolic acid	120-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
32729746-4	2020	Fluvastatin is metabolized by CYP2C9, whereas pravastatin, rosuvastatin, and pitavastatin are unaffected by inhibition by either CYP.	Fluvastatin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
32338345-7	2020	CONCLUSIONS: Co-administration of apalutamide with CYP3A4, CYP2C19, CYP2C9, P-gp, BCRP or OATP1B1 substrates may cause loss of activity for these medications.	apalutamide	34-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
32216088-0	2020	Associations of CYP2C9 and CYP2C19 pharmacogenetic variation with phenytoin-induced cutaneous adverse drug reactions.	Phenytoin	66-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
32216088-1	2020	The role of CYP2C9 and CYP2C19 genetic variation in risk for phenytoin-induced cutaneous adverse drug events is not well understood independently of the HLA-B*15:02 risk allele.	Phenytoin	61-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
32216088-9	2020	Genetic variation reducing CYP2C9 metabolic activity may increase risk for phenytoin-induced cutaneous adverse events in the absence of the HLA-B*15:02 risk allele.	Phenytoin	75-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
32270628-0	2020	Impact of CYP2C9-Interacting Drugs on Warfarin Pharmacogenomics.	Warfarin	38-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
32270628-4	2020	Study participants predicted to be sensitive responders to warfarin based on CYP2C9 and VKORC1 genotypes, had significantly greater international normalized ratio (INR) variability over time.	Warfarin	59-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
32773350-0	2020	CYP2 C9 polymorphism among patients with oral squamous cell carcinoma and its role in altering the metabolism of benzo[a]pyrene.	Benzo(a)pyrene	113-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-7
33967488-0	2020	How genetic variation was analyzed in phenytoin-induced gingival enlargement using single-nucleotide polymorphism of candidate gene CYP2C9?	Phenytoin	38-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
33967488-12	2020	However, larger scale genome-wide study has to be carried out to confirm one of the etiopathogenesis as mutation of the CYP2C9 gene, in phenytoin-induced gingival overgrowth.	Phenytoin	136-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
32893731-0	2020	Effects of rare CYP2C9 alleles on stable warfarin doses in Chinese Han patients with atrial fibrillation.	Warfarin	41-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
32893731-2	2020	Here, the role of rare CYP2C9 alleles on warfarin doses in Chinese Han patients was investigated.	Warfarin	41-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
32893731-7	2020	Inclusion of the rare CYP2C9 alleles in the prediction model added an extra 3.7% warfarin dose predictive power.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
32893731-8	2020	Conclusion: CYP2C9*13, *16 and *60 was associated with lower stable warfarin doses in Chinese patients.	Warfarin	68-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
32893731-9	2020	The algorithm including rare CYP2C9 alleles tends to more accurately predict stable warfarin doses.	Warfarin	84-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
32583524-8	2020	We found that orbitazine was metabolized by CYP3A4, CYP2C9 and CYP2D6 in a human liver microsomes incubation system.	orbitazine	14-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
32773350-2	2020	We also investigated the interaction between CYP2 C9 wild type and the polymorphic variants with benzo[a]pyrene by using molecular docking analysis.	Benzo(a)pyrene	97-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-52
32773350-5	2020	Molecular docking was then carried out to determine the interaction of CYP2 C9*1, CYP2 C9*2, and CYP2 C9*3 with benzo[a]pyrene.	Benzo(a)pyrene	112-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-78
32773350-5	2020	Molecular docking was then carried out to determine the interaction of CYP2 C9*1, CYP2 C9*2, and CYP2 C9*3 with benzo[a]pyrene.	Benzo(a)pyrene	112-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-89
32773350-5	2020	Molecular docking was then carried out to determine the interaction of CYP2 C9*1, CYP2 C9*2, and CYP2 C9*3 with benzo[a]pyrene.	Benzo(a)pyrene	112-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-89
32773350-8	2020	The docking analysis showed benzo[a]pyrene to bind specifically to the altered single nucleotide catalytic site in the polymorphic CYP2 C9*3 enzyme.	Benzo(a)pyrene	28-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-138
32773350-10	2020	The modified docking of CYP2 C9*3 with benzo[a]pyrene signifies altered metabolism in vivo.	Benzo(a)pyrene	39-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-31
32129697-5	2020	Rucaparib reversibly inhibited CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3As (IC50, 3.55, 12.9, 5.42, 41.6, and 17.2-22.9 microM [2 substrates], respectively), but not CYP2B6 or CYP2C8 (>190 microM).	rucaparib	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
32385545-0	2020	Influence of CYP2C9 and CYP2A6 on plasma concentrations of valproic acid: a meta-analysis.	Valproic Acid	59-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
33194861-3	2020	Numerous genes have been implicated in warfarin pharmacogenetics, with genes encoding CYP2C9 and VKORC1 shown to be the most important determinants of drug dosage requirements.	Warfarin	39-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
33194861-6	2020	LEARNING POINTS: Genetic warfarin resistance is rare and mainly associated with two genes encoding CYP2C9 and VKORC1.In addition to dietary counselling and drug compliance, options in warfarin-resistant patients include increasing the warfarin dose, which carries a risk of bleeding complications, or switching to novel oral anticoagulants, which increases the risk of prosthetic valve thrombosis.We replaced a metallic valve with a bioprosthetic valve, which is the first time this has been documented in a patient with warfarin resistance.	Warfarin	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
33194861-6	2020	LEARNING POINTS: Genetic warfarin resistance is rare and mainly associated with two genes encoding CYP2C9 and VKORC1.In addition to dietary counselling and drug compliance, options in warfarin-resistant patients include increasing the warfarin dose, which carries a risk of bleeding complications, or switching to novel oral anticoagulants, which increases the risk of prosthetic valve thrombosis.We replaced a metallic valve with a bioprosthetic valve, which is the first time this has been documented in a patient with warfarin resistance.	Warfarin	184-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
33194861-6	2020	LEARNING POINTS: Genetic warfarin resistance is rare and mainly associated with two genes encoding CYP2C9 and VKORC1.In addition to dietary counselling and drug compliance, options in warfarin-resistant patients include increasing the warfarin dose, which carries a risk of bleeding complications, or switching to novel oral anticoagulants, which increases the risk of prosthetic valve thrombosis.We replaced a metallic valve with a bioprosthetic valve, which is the first time this has been documented in a patient with warfarin resistance.	Warfarin	184-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
33194861-6	2020	LEARNING POINTS: Genetic warfarin resistance is rare and mainly associated with two genes encoding CYP2C9 and VKORC1.In addition to dietary counselling and drug compliance, options in warfarin-resistant patients include increasing the warfarin dose, which carries a risk of bleeding complications, or switching to novel oral anticoagulants, which increases the risk of prosthetic valve thrombosis.We replaced a metallic valve with a bioprosthetic valve, which is the first time this has been documented in a patient with warfarin resistance.	Warfarin	184-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
32601017-0	2020	Inhibitory effects of sesamin on CYP2C9-dependent 7-hydroxylation of S-warfarin.	sesamin	22-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
32601017-0	2020	Inhibitory effects of sesamin on CYP2C9-dependent 7-hydroxylation of S-warfarin.	Warfarin	69-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
32601017-2	2020	This finding suggests that sesamin predominantly binds to CYP2C9 at another site for which it has a higher affinity than its affinity for the active site, thereby inhibiting the activity of CYP2C9 non-competitively.	sesamin	27-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
32601017-2	2020	This finding suggests that sesamin predominantly binds to CYP2C9 at another site for which it has a higher affinity than its affinity for the active site, thereby inhibiting the activity of CYP2C9 non-competitively.	sesamin	27-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
32601017-4	2020	In addition, the recombinant CYP2C9-dependent 7-hydroxylation activity of S-warfarin was competitively inhibited by sesamin with a Ki value of 13.1 muM.	Warfarin	74-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
32601017-4	2020	In addition, the recombinant CYP2C9-dependent 7-hydroxylation activity of S-warfarin was competitively inhibited by sesamin with a Ki value of 13.1 muM.	sesamin	116-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
32601017-5	2020	These results are consistent with the fact that sesamin is a good substrate of CYP2C9, and its activity follows Michaelis-Menten kinetics.	sesamin	48-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
32868386-0	2020	Impact of CYP2C19 and CYP2C9 gene polymorphisms on sodium valproate plasma concentration in patients with epilepsy.	Valproic Acid	51-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
32868386-1	2020	BACKGROUND: Valproic acid (VPA) is a broad spectrum anticonvulsant drug, which could be partially metabolised by cytochrome P450 (CYP) 2C9 and 2C19 enzymes.	Valproic Acid	12-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-147
32868386-1	2020	BACKGROUND: Valproic acid (VPA) is a broad spectrum anticonvulsant drug, which could be partially metabolised by cytochrome P450 (CYP) 2C9 and 2C19 enzymes.	Valproic Acid	27-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-147
32868386-2	2020	This study was designed to investigate the relationship between CYP2C19 and CYP2C9 gene polymorphisms and the plasma concentrations of VPA in subjects with epilepsy.	Valproic Acid	135-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
32868386-10	2020	RESULTS: The genetic frequencies of CYP2C19*2, CYP2C19*3 and CYP2C9*13 were 33.1%, 3.0% and 5.4%, respectively, among patients with epilepsy from Yunnan province, China who used VPA therapy.	Valproic Acid	178-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
32531309-2	2020	The dose of warfarin varies significantly within populations, and the dose is closely related to the genetic polymorphisms of the CYP2C9 and VKORC1 genes.	Warfarin	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
32531309-3	2020	In this study, a new CYP2C9 nonsynonymous mutation (8576C > T) was detected after the genetic screening of 162 patients took warfarin.	Warfarin	125-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
32809952-4	2020	The k e of warfarin given a cytochrome P450 2C9 (CYP2C9) genotype ranged from 0.0189 to 0.0075 h-1.	Warfarin	11-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-47
32809952-4	2020	The k e of warfarin given a cytochrome P450 2C9 (CYP2C9) genotype ranged from 0.0189 to 0.0075 h-1.	Warfarin	11-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
32125665-4	2020	RESULTS: Finerenone caused direct inhibitory effects on CYP activities in vitro in the rank order CYP2C8, CYP1A1 > CYP3A4 > CYP2C9 and CYP2C19, but not on other major CYP isoforms.	finerenone	9-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
32125665-6	2020	The major metabolites of finerenone demonstrated minor reversible inhibition of CYP1A1, CYP2C9 and CYP3A4 with no hint of time-dependent inhibition of any CYP isoform.	finerenone	25-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
32385545-2	2020	Specifically, CYP2C9 and CYP2A6 are the main enzymes responsible for VPA metabolism.	Valproic Acid	69-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
32510242-2	2020	Genetic polymorphisms in the metabolism of phenytoin, particularly CYP2C9, are strongly associated with increased plasma concentrations and can result in toxicity.	Phenytoin	43-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
32385545-3	2020	However, the correlation between plasma VPA concentrations and CYP2C9 and CYP2A6 gene variations is uncertain.	Valproic Acid	40-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
32510242-4	2020	Recent pharmacogenomic studies show genetic polymorphisms in CYP2C9, as well as HLA alleles, are significantly associated with phenytoin-related SCAR.	Phenytoin	127-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
32510242-5	2020	AREAS COVERED: Updated pharmacogenomic information of CYP2C9 variants and HLA alleles involved in phenytoin-associated cutaneous adverse drug reactions (cADRs) are discussed in this article.	Phenytoin	98-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
32385545-4	2020	This meta-analysis aimed to investigate the relationship between CYP2C9 and CYP2A6 variants and plasma concentrations of VPA.	Valproic Acid	121-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
32510242-6	2020	EXPERT OPINION: CYP2C9*3 has been identified as the most significant genetic variant associated with increased phenytoin concentrations and adverse events.	Phenytoin	111-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
32385545-10	2020	We found that CYP2C9*3 was associated with standardized plasma VPA concentration; *3 allele carriers had a 0.70-mug/mL higher concentration per mg/kg than non-carriers (95% CI 0.25, 1.15; P = 0.002).	Valproic Acid	63-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
32510242-7	2020	Recent pharmacogenomic findings reveal that CYP2C9*3 and HLA alleles, i.e. HLA-B*15:02, HLA-B*13:01, and HLA-B*51:01, are important genetic variants in the occurrence of phenytoin-induced cADRs or SCAR.	Phenytoin	170-179	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
32385545-12	2020	CONCLUSION: This meta-analysis demonstrated that CYP2C9*3 and CYP2A6*4 genetic variants affect plasma VPA concentrations.	Valproic Acid	102-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
32238050-1	2020	Osthol, a pharmacologically active ingredient in various traditional Chinese medicines, is predominantly metabolized by CYP2C9.	osthol	0-6	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
32423989-1	2020	CYP2C9 is a major form of human liver cytochrome P450 that is responsible for the oxidative metabolism of several widely used low therapeutic index drugs, including (S)-warfarin and phenytoin.	Warfarin	169-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
32423989-1	2020	CYP2C9 is a major form of human liver cytochrome P450 that is responsible for the oxidative metabolism of several widely used low therapeutic index drugs, including (S)-warfarin and phenytoin.	Phenytoin	182-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
32423989-7	2020	Steady-state kinetic analyses revealed that the relative catalytic efficiency ratios of (S)-warfarin metabolism by the P279T and N218I variants were 87% and 24%, respectively, of wildtype CYP2C9 protein.	Warfarin	88-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	188-194
32294527-1	2020	Epoxyeicosatrienoic acids (EETs) are synthetized from arachidonic acid by the action of members of the CYP2C and CYP2J subfamilies of cytochrome P450 (CYPs).	epoxyeicosatrienoic acids	0-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-108
32294527-1	2020	Epoxyeicosatrienoic acids (EETs) are synthetized from arachidonic acid by the action of members of the CYP2C and CYP2J subfamilies of cytochrome P450 (CYPs).	eets	27-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-108
32294527-1	2020	Epoxyeicosatrienoic acids (EETs) are synthetized from arachidonic acid by the action of members of the CYP2C and CYP2J subfamilies of cytochrome P450 (CYPs).	Arachidonic Acid	54-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-108
32238050-0	2020	Osthole inhibited the activity of CYP2C9 in human liver microsomes and influenced indomethacin pharmacokinetics in rats.	osthol	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
32700644-0	2020	Prediction of the impact of CYP2C9 and VKORC1 genotypes on warfarin-sorafenib interactions in whites and Asians.	Warfarin	59-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
32700644-0	2020	Prediction of the impact of CYP2C9 and VKORC1 genotypes on warfarin-sorafenib interactions in whites and Asians.	Sorafenib	68-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
32700644-1	2020	Aim: To predict the impact of the different CYP2C9 and VKORC1 genotypes on warfarin-sorafenib interactions in whites and Asians.	Warfarin	75-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
32700644-1	2020	Aim: To predict the impact of the different CYP2C9 and VKORC1 genotypes on warfarin-sorafenib interactions in whites and Asians.	Sorafenib	84-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
32238050-4	2020	Interestingly, we found that osthole inhibits the activity of CYP2C11 in a non-competitive manner in RLMs, while inhibits CYP2C9 activity in a competitive manner in pooled HLMs.	osthol	29-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
32700644-3	2020	Results: INRs were predicted to be 2.0-2.1- versus 1.8-1.9-times higher in the presence of sorafenib in the CYP2C9 (*1/*1 vs *1/*3) groups than those for warfarin alone in both whites and Asians.	Sorafenib	91-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
32238050-5	2020	Then, the effects of CYP2C9*1/*2/*3 allele on the pharmacokinetics of osthole were identified.	osthol	70-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	osthol	174-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	osthol	174-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	osthol	174-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	osthol	174-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	osthol	174-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	Indomethacin	225-237	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	Indomethacin	225-237	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	Indomethacin	225-237	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	Indomethacin	225-237	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	Indomethacin	225-237	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	osthol	271-278	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	osthol	271-278	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	osthol	271-278	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	osthol	271-278	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
32238050-6	2020	In human CYP2C9 isoform, the Ki value of 21.93 muM (CYP2C9*1), 18.10 muM (CYP2C9*2), 13.12 muM (CYP2C9*3) indicate that there are individual differences in the inhibition of osthole on CYP2C9 activity.We investigated how the indomethacin pharmacokinetics was affected by osthole in SD rat.	osthol	271-278	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
32765265-6	2020	The effect of genetic polymorphisms known to influence dose response of warfarin (CYP2C9, VKORC1) were implemented into the model by modifying warfarin clearance (CYP2C9 *1: 0.2 L/h; *2: 0.14 L/h, *3: 0.04 L/h) and the concentration of available vitamin K (VKORC1 GA: -22% from normal vitamin K concentration; AA: -44% from normal vitamin K concentration).	Warfarin	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
32754031-9	2020	By means of stepwise multiple regression analysis, we established a new elder warfarin dosing algorithm (R2=0.3714) containing height, creatinine, amiodarone usage, CYP2C9 (*1*2 or *1*3), and VKORC1 (GA or GG) genotypes.	Warfarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	165-171
32754031-12	2020	Polymorphism of CYP2C9 and VKORC1 obviously affected warfarin stable dose of the elder Han-Chinese.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
32765265-6	2020	The effect of genetic polymorphisms known to influence dose response of warfarin (CYP2C9, VKORC1) were implemented into the model by modifying warfarin clearance (CYP2C9 *1: 0.2 L/h; *2: 0.14 L/h, *3: 0.04 L/h) and the concentration of available vitamin K (VKORC1 GA: -22% from normal vitamin K concentration; AA: -44% from normal vitamin K concentration).	Warfarin	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-169
32765265-6	2020	The effect of genetic polymorphisms known to influence dose response of warfarin (CYP2C9, VKORC1) were implemented into the model by modifying warfarin clearance (CYP2C9 *1: 0.2 L/h; *2: 0.14 L/h, *3: 0.04 L/h) and the concentration of available vitamin K (VKORC1 GA: -22% from normal vitamin K concentration; AA: -44% from normal vitamin K concentration).	Warfarin	143-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
32765265-6	2020	The effect of genetic polymorphisms known to influence dose response of warfarin (CYP2C9, VKORC1) were implemented into the model by modifying warfarin clearance (CYP2C9 *1: 0.2 L/h; *2: 0.14 L/h, *3: 0.04 L/h) and the concentration of available vitamin K (VKORC1 GA: -22% from normal vitamin K concentration; AA: -44% from normal vitamin K concentration).	Warfarin	143-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-169
33680011-0	2020	The Contribution of VKORC1 and CYP2C9 Genetic Polymorphisms and Patients" Demographic Characteristics with Warfarin Maintenance Doses: A Suggested Warfarin Dosing Algorithm.	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
32276000-4	2020	The CYP2C9 genomic region holding important warfarin drug-metabolizing SNPs was sequenced from 159 individuals belong from five major ethnic groups of Pakistani population.	Warfarin	44-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
32276000-9	2020	Several SNPs, including the previously reported warfarin associated variants, i.e. rs2860905, rs1799853 (CYP2C9*2) and rs72558189 (CYP2C9*14) were detected in these population groups with diverse frequencies.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
32276000-12	2020	The pharmacogeneticsassessment of the CYP2C9 genetic variations identified in current study may important to test against the warfarin efficacy for different ethnicity of Pakistani population.	Warfarin	126-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
33680011-0	2020	The Contribution of VKORC1 and CYP2C9 Genetic Polymorphisms and Patients" Demographic Characteristics with Warfarin Maintenance Doses: A Suggested Warfarin Dosing Algorithm.	Warfarin	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
33680011-6	2020	The patients who carried the A allele at position -1639 VKORC1 and the variants CYP2C9 *2 and *3 required a significantly lower daily mean warfarin dosage (P = 0.001).	Warfarin	139-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
33680011-8	2020	This study showed that in the heart valve replacement patients considering VKORC1 and CYP2C9 polymorphisms beside demographic characteristics such as age will be helpful in pre-treatment dosing of warfarin which in turn reduces the complications associated with inappropriate warfarin dosing.	Warfarin	197-205	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
32380173-7	2020	The warfarin sensitivity allele recommendations in this report incorporate the previous CYP2C9 allele recommendations and additional genes and alleles that are specific to warfarin sensitivity testing.	Warfarin	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
33680011-8	2020	This study showed that in the heart valve replacement patients considering VKORC1 and CYP2C9 polymorphisms beside demographic characteristics such as age will be helpful in pre-treatment dosing of warfarin which in turn reduces the complications associated with inappropriate warfarin dosing.	Warfarin	276-284	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
33612460-0	2020	Pharmacogenetics of sulfonylurea: Presence of CYP2C9*2, CYP2C9*3 and a novel allele, CYP2C9*61, in Type 2 diabetes patients under sulfonylurea therapy.	Sulfonylurea Compounds	20-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
32586526-0	2020	Variants in ADRB1 and CYP2C9: Association with Response to Atenolol and Losartan in Marfan Syndrome.	Atenolol	59-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
32586526-0	2020	Variants in ADRB1 and CYP2C9: Association with Response to Atenolol and Losartan in Marfan Syndrome.	Losartan	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
32586526-2	2020	STUDY DESIGN: In a subset of 250 white, non-Hispanic participants with Marfan syndrome in a prior randomized trial of atenolol vs losartan, the common variants rs1801252 and rs1801253 in ADRB1 and rs1799853 and rs1057910 in CYP2C9 were analyzed.	Atenolol	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	224-230
33612460-0	2020	Pharmacogenetics of sulfonylurea: Presence of CYP2C9*2, CYP2C9*3 and a novel allele, CYP2C9*61, in Type 2 diabetes patients under sulfonylurea therapy.	Sulfonylurea Compounds	20-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
33583789-6	2020	Furthermore, we demonstrated that Paeoniflorin and Amygdalin had obvious inhibiting effects on CYP2C9 and CYP2E1.	peoniflorin	34-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
33612460-0	2020	Pharmacogenetics of sulfonylurea: Presence of CYP2C9*2, CYP2C9*3 and a novel allele, CYP2C9*61, in Type 2 diabetes patients under sulfonylurea therapy.	Sulfonylurea Compounds	20-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
33583789-6	2020	Furthermore, we demonstrated that Paeoniflorin and Amygdalin had obvious inhibiting effects on CYP2C9 and CYP2E1.	Amygdalin	51-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
33612460-1	2020	CYP2C9 is an important member of the cytochrome P450 gene family involved in the metabolism of 15% of the drugs including an oral antidiabetic agent sulfonylurea.	Sulfonylurea Compounds	149-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
33612460-2	2020	This study aims to investigate the frequency of CYP2C9*2 and CYP2C9*3 alleles of the gene in the sulfonylurea treated diabetic subjects in Pakistan.	Sulfonylurea Compounds	97-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
33612460-2	2020	This study aims to investigate the frequency of CYP2C9*2 and CYP2C9*3 alleles of the gene in the sulfonylurea treated diabetic subjects in Pakistan.	Sulfonylurea Compounds	97-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
32238418-5	2020	Here, we investigated the ability of the major human drug-metabolizing P450s, namely CYP3A4, CYP2C9, CYP2C19, CYP2D6 and CYP1A2, to use different OSs: H2O2; tert-butyl hydroperoxide (tert-BuOOH); CuOOH; (diacetoxyiodo)benzene (BAIB); and bis(trifluoroacetoxy)iodobenzene (F-BAIB).	tert-Butylhydroperoxide	157-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
32575674-0	2020	rs622342 in SLC22A1, CYP2C9*2 and CYP2C9*3 and Glycemic Response in Individuals with Type 2 Diabetes Mellitus Receiving Metformin/Sulfonylurea Combination Therapy: 6-Month Follow-Up Study.	Metformin	120-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
32575674-0	2020	rs622342 in SLC22A1, CYP2C9*2 and CYP2C9*3 and Glycemic Response in Individuals with Type 2 Diabetes Mellitus Receiving Metformin/Sulfonylurea Combination Therapy: 6-Month Follow-Up Study.	Sulfonylurea Compounds	130-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
32575674-11	2020	CONCLUSION: The combination of metformin/sulfonylurea therapy led to the maximum glycemic control in individuals with T2DM carrying AA or AC genotypes in SLC22A1 and *1*3 in CYP2C9.	Metformin	31-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	174-180
32575674-11	2020	CONCLUSION: The combination of metformin/sulfonylurea therapy led to the maximum glycemic control in individuals with T2DM carrying AA or AC genotypes in SLC22A1 and *1*3 in CYP2C9.	Sulfonylurea Compounds	41-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	174-180
32606720-0	2020	The Effect of CYP2C9 Genotype Variants in Type 2 Diabetes on the Pharmacological Effectiveness of Sulfonylureas, Diabetic Retinopathy, and Nephropathy.	Sulfonylurea Compounds	98-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
32279544-3	2020	The aim of this study was to determine whether the presence of certain allelic variants in genes CYP2B6, CYP2C9, CYP3A4 and CYP3A5 increases the risk of toxicity in Mexican children with solid tumours treated with ifosfamide.Objective: The aim of this study was to determine whether the presence of certain allelic variants of genes CYP2B6, CYP2C9, CYP3A4 and CYP3A5 increases the risk of toxicity in children with solid tumours treated with ifosfamide.Materials and methods: A total of 131 DNA samples were genotyped by real-time polymerase chain reaction (RT-PCR) using TaqMan probes.	Ifosfamide	214-224	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
32279544-3	2020	The aim of this study was to determine whether the presence of certain allelic variants in genes CYP2B6, CYP2C9, CYP3A4 and CYP3A5 increases the risk of toxicity in Mexican children with solid tumours treated with ifosfamide.Objective: The aim of this study was to determine whether the presence of certain allelic variants of genes CYP2B6, CYP2C9, CYP3A4 and CYP3A5 increases the risk of toxicity in children with solid tumours treated with ifosfamide.Materials and methods: A total of 131 DNA samples were genotyped by real-time polymerase chain reaction (RT-PCR) using TaqMan probes.	Ifosfamide	214-224	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	341-347
32238418-5	2020	Here, we investigated the ability of the major human drug-metabolizing P450s, namely CYP3A4, CYP2C9, CYP2C19, CYP2D6 and CYP1A2, to use different OSs: H2O2; tert-butyl hydroperoxide (tert-BuOOH); CuOOH; (diacetoxyiodo)benzene (BAIB); and bis(trifluoroacetoxy)iodobenzene (F-BAIB).	OSS	146-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
32238418-5	2020	Here, we investigated the ability of the major human drug-metabolizing P450s, namely CYP3A4, CYP2C9, CYP2C19, CYP2D6 and CYP1A2, to use different OSs: H2O2; tert-butyl hydroperoxide (tert-BuOOH); CuOOH; (diacetoxyiodo)benzene (BAIB); and bis(trifluoroacetoxy)iodobenzene (F-BAIB).	Hydrogen Peroxide	151-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
32606720-10	2020	The findings also showed that the plasma level of sulfonylureas (i.e., glibenclamide and gliclazide) was the highest in the patients with the CYP2C9*3 allele.	Sulfonylurea Compounds	50-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
32606720-10	2020	The findings also showed that the plasma level of sulfonylureas (i.e., glibenclamide and gliclazide) was the highest in the patients with the CYP2C9*3 allele.	Glyburide	71-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
32606720-10	2020	The findings also showed that the plasma level of sulfonylureas (i.e., glibenclamide and gliclazide) was the highest in the patients with the CYP2C9*3 allele.	Gliclazide	89-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
32527038-8	2020	There was a trend for an association of phenprocoumon-risk profiles (low VKORC1 or CYP2C9 activity) with phenprocoumon-suspecting ADRs (p = 0.052).	Phenprocoumon	40-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
32527038-8	2020	There was a trend for an association of phenprocoumon-risk profiles (low VKORC1 or CYP2C9 activity) with phenprocoumon-suspecting ADRs (p = 0.052).	Phenprocoumon	105-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
32279544-3	2020	The aim of this study was to determine whether the presence of certain allelic variants in genes CYP2B6, CYP2C9, CYP3A4 and CYP3A5 increases the risk of toxicity in Mexican children with solid tumours treated with ifosfamide.Objective: The aim of this study was to determine whether the presence of certain allelic variants of genes CYP2B6, CYP2C9, CYP3A4 and CYP3A5 increases the risk of toxicity in children with solid tumours treated with ifosfamide.Materials and methods: A total of 131 DNA samples were genotyped by real-time polymerase chain reaction (RT-PCR) using TaqMan probes.	Ifosfamide	442-452	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
32193358-7	2020	A competitive inhibition between PZQ enantiomers for CYP2C9, 2C19, 3A4 and 3A5 was revealed.	Praziquantel	33-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
32238418-5	2020	Here, we investigated the ability of the major human drug-metabolizing P450s, namely CYP3A4, CYP2C9, CYP2C19, CYP2D6 and CYP1A2, to use different OSs: H2O2; tert-butyl hydroperoxide (tert-BuOOH); CuOOH; (diacetoxyiodo)benzene (BAIB); and bis(trifluoroacetoxy)iodobenzene (F-BAIB).	tert-Butylhydroperoxide	183-193	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
32238418-5	2020	Here, we investigated the ability of the major human drug-metabolizing P450s, namely CYP3A4, CYP2C9, CYP2C19, CYP2D6 and CYP1A2, to use different OSs: H2O2; tert-butyl hydroperoxide (tert-BuOOH); CuOOH; (diacetoxyiodo)benzene (BAIB); and bis(trifluoroacetoxy)iodobenzene (F-BAIB).	cuooh	196-201	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
32238418-5	2020	Here, we investigated the ability of the major human drug-metabolizing P450s, namely CYP3A4, CYP2C9, CYP2C19, CYP2D6 and CYP1A2, to use different OSs: H2O2; tert-butyl hydroperoxide (tert-BuOOH); CuOOH; (diacetoxyiodo)benzene (BAIB); and bis(trifluoroacetoxy)iodobenzene (F-BAIB).	phenyliodosodiacetate	203-225	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
32238418-5	2020	Here, we investigated the ability of the major human drug-metabolizing P450s, namely CYP3A4, CYP2C9, CYP2C19, CYP2D6 and CYP1A2, to use different OSs: H2O2; tert-butyl hydroperoxide (tert-BuOOH); CuOOH; (diacetoxyiodo)benzene (BAIB); and bis(trifluoroacetoxy)iodobenzene (F-BAIB).	3-aminoisobutyric acid	227-231	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
32238418-5	2020	Here, we investigated the ability of the major human drug-metabolizing P450s, namely CYP3A4, CYP2C9, CYP2C19, CYP2D6 and CYP1A2, to use different OSs: H2O2; tert-butyl hydroperoxide (tert-BuOOH); CuOOH; (diacetoxyiodo)benzene (BAIB); and bis(trifluoroacetoxy)iodobenzene (F-BAIB).	(bis(trifluoroacetoxy)iodo)benzene	238-270	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
32238418-5	2020	Here, we investigated the ability of the major human drug-metabolizing P450s, namely CYP3A4, CYP2C9, CYP2C19, CYP2D6 and CYP1A2, to use different OSs: H2O2; tert-butyl hydroperoxide (tert-BuOOH); CuOOH; (diacetoxyiodo)benzene (BAIB); and bis(trifluoroacetoxy)iodobenzene (F-BAIB).	3-aminoisobutyric acid	273-278	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
32453717-0	2020	CYP2C9, a Metabolic CYP450s Enzyme, Plays Critical Roles in Activating Ellagic Acid in Human Intestinal Epithelial Cells.	Ellagic Acid	71-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
32453717-9	2020	EA treatment at different concentrations (10 mug/mL and 50 mug/mL) remarkably decreased cell viability of HIEC cells expressing CYP2C9 compared to the untreated control (p<0.01), in a concentration-dependent and time-dependent manner.	Ellagic Acid	0-2	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
32453717-10	2020	Expression of CYP2C9 significantly increased the apoptosis rate of HIEC cells treated with EA compared to that in HIEC cells without any CYP450s expression (p<0.01).	Ellagic Acid	91-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
32453717-11	2020	The clearance rate of EA in CYP2B6-expressing (p<0.05) and CYP2C9-expressing (p<0.001) HIEC cell models was remarkably reduced after 120 min.	Ellagic Acid	22-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
32453717-12	2020	CONCLUSIONS Ellagic acid was effectively activated by CYP2C9 in HIEC cells and caused cytotoxicity and apoptosis of HIEC cells.	Ellagic Acid	12-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
32453717-13	2020	Therefore, CYP2C9 is main metabolic enzyme of EA when compared to other CYP450 HIEC cell models.	Ellagic Acid	46-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
32457604-10	2020	Conclusions: Decreased function alleles of CYP2C9 were highly predictive of vestibular-cerebellar ADRs to phenytoin in our study (p = 0.001).	Phenytoin	106-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
32546963-2	2020	The in vitro inhibition studies suggested that apatinib exerted potent inhibition on CYP3A4 and CYP2C9.	apatinib	47-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
32546963-12	2020	Owing to the risk of pharmacokinetic drug-drug interactions based on CYP3A4/CYP2C9 inhibition by apatinib, caution is advised in the concurrent use of apatinib with either CYP2C9 or CYP3A4 substrates.	apatinib	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
32457621-2	2020	We aimed to investigate frequency and concordance on CYP2D6, CYP2C19, and CYP2C9 (CYP2D6/2C19/2C9)-mediated potential DDIs at the Lifelines cohort and linked data from the pharmacy database IADB.nl.	Didanosine	118-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
32457621-2	2020	We aimed to investigate frequency and concordance on CYP2D6, CYP2C19, and CYP2C9 (CYP2D6/2C19/2C9)-mediated potential DDIs at the Lifelines cohort and linked data from the pharmacy database IADB.nl.	Didanosine	118-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-97
32406758-3	2020	CYP2C9 is one of the most abundant CYP enzymes and responsible for the metabolism of over 15% clinical drugs, including oral sulfonylurea hypoglycemics, nonsteroidal anti-inflammatory agents, selective cyclooxygenase-2 inhibitors, antiepileptics, angiotensin II receptor inhibitors and anticoagulants.	Sulfonylurea Compounds	125-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30277905-7	2020	Edoxaban is superior to warfarin in patients with increased risk of bleeding with warfarin because of variants in CYP2C9 and VKORC1 genes.	edoxaban	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
30277905-7	2020	Edoxaban is superior to warfarin in patients with increased risk of bleeding with warfarin because of variants in CYP2C9 and VKORC1 genes.	Warfarin	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
31646624-0	2020	HLA-B*51:01 and CYP2C9*3 are risk factors for phenytoin-induced eruption in the Japanese population: analysis of data from the Biobank Japan Project.	Phenytoin	46-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
31646624-1	2020	CYP2C9*3 and HLA-B alleles are reportedly associated with phenytoin-induced eruption in some East Asian populations; however, this finding is not readily applicable to the Japanese population.	Phenytoin	58-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
31646624-5	2020	CYP2C9*3 carrier status was significantly associated with phenytoin-induced eruption (P = 0.0022, odds ratio 7.05, 95% confidence interval 2.44-20.4).	Phenytoin	58-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
31646624-8	2020	CYP2C9*3 and HLA-B*51:01 allele carrier statuses are significantly associated with phenytoin-induced eruption; thus, checking this carrier status before prescription would decrease it in clinical practice.	Phenytoin	83-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
32406758-4	2020	Diclofenac (4"-hydroxylase) and tolbutamide (methylhydroxylation) are widely used as probe substrates for CYP2C9.	Diclofenac	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
32406758-4	2020	Diclofenac (4"-hydroxylase) and tolbutamide (methylhydroxylation) are widely used as probe substrates for CYP2C9.	Tolbutamide	32-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
32274641-5	2020	This is an observational nested case-control study that was conducted on a cohort of Qatari patients treated with warfarin with previously identified genotype for the CYP2C9, VKORC1, and CYP2F4.	Warfarin	114-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
31938857-0	2020	Phenytoin intoxication associated with omeprazole administration in a child with defective CYP2C9.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
31938857-0	2020	Phenytoin intoxication associated with omeprazole administration in a child with defective CYP2C9.	Omeprazole	39-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
31938857-2	2020	Phenytoin is a commonly used drug, and its metabolism is mediated by a specific cytochrome-P450 isoform, CYP2C9, which is encoded by a polymorphic gene.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
31938857-4	2020	Here we describe a case of phenytoin intoxication in a child with defective CYP2C9, after omeprazole administration.	Phenytoin	27-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
31938857-4	2020	Here we describe a case of phenytoin intoxication in a child with defective CYP2C9, after omeprazole administration.	Omeprazole	90-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
31848875-3	2020	In a recent study in patients awaiting surgery, following warfarin cessation the INR declined slower over time in those with two CYP2C9 variant alleles, increasing age, weight and number of comorbidities and that INR decline was faster in those with higher maintenance INR value.	Warfarin	58-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
31724188-7	2020	Several case reports show cannabis may inhibit the metabolism of warfarin because of CYP2C9 interactions, resulting in increased plasma concentrations, increased international normalized ratio , and risk of bleeding.	Warfarin	65-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
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
32290339-0	2020	Strong and Selective Inhibitory Effects of the Biflavonoid Selamariscina A against CYP2C8 and CYP2C9 Enzyme Activities in Human Liver Microsomes.	Biflavonoids	47-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
32290339-0	2020	Strong and Selective Inhibitory Effects of the Biflavonoid Selamariscina A against CYP2C8 and CYP2C9 Enzyme Activities in Human Liver Microsomes.	selamariscina a	59-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
32290339-7	2020	Returning to the P450 activities, selamariscina A inhibited CYP2C9-mediated diclofenac hydroxylation and tolbutamide hydroxylation with respective Ki values of 0.032 and 0.065 muM in a competitive and noncompetitive manner.	Diclofenac	76-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
32290339-10	2020	This information might be useful in predicting herb-drug interaction potential between biflavonoids and co-administered drugs mainly metabolized by CYP2C8 and CYP2C9.	Biflavonoids	87-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
32272615-0	2020	Lack of Correlation between In Vitro and In Vivo Studies on the Inhibitory Effects of (-)-Sophoranone on CYP2C9 is Attributable to Low Oral Absorption and Extensive Plasma Protein Binding of (-)-Sophoranone.	sophoranone	88-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
32272615-3	2020	Of the nine tested CYPs, it exerted the strongest inhibitory effect on CYP2C9-mediated tolbutamide 4-hydroxylation with the lowest IC50 (Ki) value of 0.966 +- 0.149 muM (0.503 +- 0.0383 muM), in a competitive manner.	Tolbutamide	87-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
32272615-4	2020	Additionally, it strongly inhibited other CYP2C9-catalyzed diclofenac 4"-hydroxylation and losartan oxidation activities.	Diclofenac	59-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
32272615-4	2020	Additionally, it strongly inhibited other CYP2C9-catalyzed diclofenac 4"-hydroxylation and losartan oxidation activities.	Losartan	91-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
32802593-3	2020	Fluvoxamine inhibits many cytochrome P450 enzyme (CYP) including CYP2C9, which metabolizes azilsartan.	Fluvoxamine	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
32802593-3	2020	Fluvoxamine inhibits many cytochrome P450 enzyme (CYP) including CYP2C9, which metabolizes azilsartan.	azilsartan	91-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
32219822-11	2020	CONCLUSION: The polymorphisms of CYP2C9, VKORC1 and CYP4F2 genes can influence the stable dose of warfarin in Shandong population.	Warfarin	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
32094096-7	2020	Interestingly, CYP2C9, CYP2C19, and CYP3A5 extensive metabolizers tended to be associated with lower cyclosporine C/D ratio when combined with voriconazole, but the results were not statistically significant.	cyclosporine c	101-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
32094096-7	2020	Interestingly, CYP2C9, CYP2C19, and CYP3A5 extensive metabolizers tended to be associated with lower cyclosporine C/D ratio when combined with voriconazole, but the results were not statistically significant.	Voriconazole	143-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
31673144-7	2020	Patients with CYP2C9 *1/*2, *1/*3, *2/*2, *2/*3, or *3/*3 required a lower warfarin maintenance dose compared with patients with CYP2C9 *1/*1 (SMD = -0.610, 95% CI: -0.802 to -0.419, I2 = 0%).	Warfarin	75-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
31653973-1	2020	The objective of this study is to estimate the prevalence of VKORC1, CYP2C9, and CYP4F2 genetic variants and their contribution to warfarin dose variability in Qataris.	Warfarin	131-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
31653973-6	2020	Carriers of at least one CYP2C9 decreased function allele (*2 or *3) required lower median (IQR) warfarin doses compared to noncarriers [24.5 (14.5) mg/week vs. 35 (21) mg/week, p < 0.001].	Warfarin	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
31653973-11	2020	This study concluded that VKORC1 (-1639G>A), CYP2C9*2 & *3 are the most significant predictors of warfarin dose along with HTN, HF and smoking.	Warfarin	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
31673144-11	2020	Our meta-analysis provides evidence that CYP2C9 and VKORC1 variant statuses affect warfarin maintenance dose in children, but not CYP4F2.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
32155912-5	2020	Therefore, in this in vitro study, we investigated the interactions of 24 microbial flavonoid metabolites with human serum albumin and cytochrome P450 (CYP2C9, 2C19, and 3A4) enzymes.	Flavonoids	84-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	152-158
32155912-8	2020	All CYP isoforms examined were significantly inhibited by O-desmethylangolensin; nevertheless, only its effect on CYP2C9 seems to be relevant.	O-desmethylangolensin	58-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
32071341-0	2020	Genome-Wide Association Study of VKORC1 and CYP2C9 on acenocoumarol dose, stroke recurrence and intracranial haemorrhage in Spain.	Acenocoumarol	54-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
32106262-7	2020	During maintenance of human iPS-HLCs, ALB and urea producing abilities and CYP2C9, CYP2C19, and CYP3A4 activities were the highest when using HCM.	hcm	142-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
32106262-11	2020	However, the CYP2C9, CYP2C19, and CYP3A4 activities were the highest when using HCM and WEM.	hcm	80-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
32071341-9	2020	In conclusion, variants in VKORC1 and CYP2C9 are associated with acenocoumarol maintenance dose, stroke recurrence and ICH in a Spanish cohort.	Acenocoumarol	65-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
31591509-6	2020	Most studies (78%) examined warfarin-CYP2C9/VKORC1 or clopidogrel-CYP2C19.	Warfarin	28-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
31591509-11	2020	Supportive evidence exists for clopidogrel-CYP2C19 and warfarin-CYP2C9/VKORC1, but evidence is limited in other drug-gene combinations.	Warfarin	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
32050158-5	2020	Therefore, the aim of this study was to develop, validate and optimize a simplified assay for the probe drugs caffeine (metabolized by CYP1A2), omeprazole (CYP2C19), losartan (CYP2C9), dextromethorphan (CYP2D6), midazolam (CYP3A4) and their respective enzyme-specific metabolites in small volumes (100 muL) of human plasma, that addresses the issues noted.	Caffeine	110-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
32050158-5	2020	Therefore, the aim of this study was to develop, validate and optimize a simplified assay for the probe drugs caffeine (metabolized by CYP1A2), omeprazole (CYP2C19), losartan (CYP2C9), dextromethorphan (CYP2D6), midazolam (CYP3A4) and their respective enzyme-specific metabolites in small volumes (100 muL) of human plasma, that addresses the issues noted.	Dextromethorphan	185-201	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
32050158-5	2020	Therefore, the aim of this study was to develop, validate and optimize a simplified assay for the probe drugs caffeine (metabolized by CYP1A2), omeprazole (CYP2C19), losartan (CYP2C9), dextromethorphan (CYP2D6), midazolam (CYP3A4) and their respective enzyme-specific metabolites in small volumes (100 muL) of human plasma, that addresses the issues noted.	Midazolam	212-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
32071341-2	2020	Variants in CYP2C9 and VKORC1 have been associated with acenocoumarol maintenance dose.	Acenocoumarol	56-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
32071341-3	2020	We analysed whether any of the 49 polymorphisms in CYP2C9 and VKORC1 previously associated with acenocoumarol maintenance dose in a Genome-Wide Association study (GWAs) in Dutch population are associated with stroke recurrence, intracranial haemorrhage (ICH) and acenocoumarol maintenance dose in a Spanish population.	Acenocoumarol	96-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
31854189-0	2020	Different roles of human cytochrome P450 2C9 and 3A enzymes in diclofenac 4"- and 5-hydroxylations mediated by metabolically inactivated human hepatocytes in previously transplanted chimeric mice.	Diclofenac	63-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-44
31875297-0	2020	Author"s Response to: "Letter to the Editor in Response to: "Effect of Polymorphisms in CYP2C9 and CYP2C19 on the Disposition, Safety and Metabolism of Progesterone Administrated Orally or Vaginally"".	Progesterone	152-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
31973625-1	2020	The role of mirSNPs in the 3"UTR of VKORC1, CYP2C9 and CYP4F2 genes that could influence warfarin dose variability via a discrete miRNA-mediated mechanism remains unexplained.	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
33758819-3	2020	Warfarin sodium is an oral anticoagulant that is primarily metabolized by cytochrome P450 2C9 (CYP2C9).	Warfarin	0-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-93
33758819-3	2020	Warfarin sodium is an oral anticoagulant that is primarily metabolized by cytochrome P450 2C9 (CYP2C9).	Warfarin	0-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
31744669-2	2020	A sensitive, specific, and fast ultra-high performance liquid chromatography/tandem mass spectrometry (UHPLC-MS/MS) method was developed and validated for determination of caffeine (probe of CYP1A2), tolbutamide (probe of CYP2C9), dextromethorphan (probe of CYP2D6), and alprazolam (probe of CYP3A4/5) in human serum.	Caffeine	172-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	222-228
31875298-0	2020	Letter to the Editor in Response to "Effect of Polymorphisms in CYP2C9 and CYP2C19 on the Disposition, Safety and Metabolism of Progesterone Administrated Orally or Vaginally".	Progesterone	128-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
31785970-0	2020	Cytochrome P450 2C9 polymorphism: Effect of amino acid substitutions on protein flexibility in the presence of tamoxifen.	Tamoxifen	111-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
31657866-6	2020	RESULTS: Experiments with human liver microsomes and primary human hepatocytes in 3D co-culture confirmed that flurbiprofen is a suitable CYP2C9 substrate.	Flurbiprofen	111-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
31785970-1	2020	Tamoxifen is a prodrug and cytochrome P450 2C9 (CYP2C9) has a significant role in the formation of a therapeutically more potent metabolite (4-hydroxytamoxifen) than tamoxifen.	Tamoxifen	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-46
31679131-6	2020	Etravirine exhibits the potential for bi-directional drug-drug interactions with other antiretrovirals and concomitant medications through its interactions with cytochrome P450 (CYP) isozymes: CYP3A4, CYP2C9, and CYP2C19.	etravirine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	201-207
31785970-1	2020	Tamoxifen is a prodrug and cytochrome P450 2C9 (CYP2C9) has a significant role in the formation of a therapeutically more potent metabolite (4-hydroxytamoxifen) than tamoxifen.	Tamoxifen	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
31785970-1	2020	Tamoxifen is a prodrug and cytochrome P450 2C9 (CYP2C9) has a significant role in the formation of a therapeutically more potent metabolite (4-hydroxytamoxifen) than tamoxifen.	afimoxifene	141-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-46
31785970-1	2020	Tamoxifen is a prodrug and cytochrome P450 2C9 (CYP2C9) has a significant role in the formation of a therapeutically more potent metabolite (4-hydroxytamoxifen) than tamoxifen.	afimoxifene	141-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
31785970-1	2020	Tamoxifen is a prodrug and cytochrome P450 2C9 (CYP2C9) has a significant role in the formation of a therapeutically more potent metabolite (4-hydroxytamoxifen) than tamoxifen.	Tamoxifen	150-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-46
31785970-1	2020	Tamoxifen is a prodrug and cytochrome P450 2C9 (CYP2C9) has a significant role in the formation of a therapeutically more potent metabolite (4-hydroxytamoxifen) than tamoxifen.	Tamoxifen	150-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
31785970-5	2020	Therefore, in order to understand the genotype-phenotype association, it is aimed to study the interatomic interactions of amino acid substitutions in CYP2C9 variants in the presence of tamoxifen.	Tamoxifen	186-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	151-157
31785970-6	2020	Computational structural biology approach was adopted to study the effect of amino acid substitutions of polymorphic variants of CYP2C9 R144C (*2), I359 L (*3), D360E (*5), R150H (*8), R335W (*11) and L90 P (*13) on the flexibility of the enzyme in the presence of tamoxifen.	Tamoxifen	265-274	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
31785970-10	2020	Further, the effect of amino acid substitutions CYP2C9 variants on the protein flexibility in the presence of tamoxifen in 4-hydroxy orientation was evaluated by molecular dynamics (MD) simulations.	Tamoxifen	110-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
31785970-14	2020	Thus, the interatomic interaction study of CYP2C9 variants in the presence of tamoxifen predicts the plausible effect of the investigated variants on the therapeutic outcome of tamoxifen.	Tamoxifen	78-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
31785970-14	2020	Thus, the interatomic interaction study of CYP2C9 variants in the presence of tamoxifen predicts the plausible effect of the investigated variants on the therapeutic outcome of tamoxifen.	Tamoxifen	177-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
31673875-12	2020	CONCLUSION: Coadministration of fluconazole or itraconazole or other moderate/strong CYP2C9 or CYP3A4 inhibitors may increase exposure to erdafitinib in healthy adults and thus may warrant erdafitinib dose reduction or use of alternative concomitant medications with no or minimal CYP2C9 or CYP3A4 inhibition potential.	Itraconazole	47-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	281-287
31673875-12	2020	CONCLUSION: Coadministration of fluconazole or itraconazole or other moderate/strong CYP2C9 or CYP3A4 inhibitors may increase exposure to erdafitinib in healthy adults and thus may warrant erdafitinib dose reduction or use of alternative concomitant medications with no or minimal CYP2C9 or CYP3A4 inhibition potential.	erdafitinib	138-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
31673875-1	2020	BACKGROUND AND OBJECTIVES: Erdafitinib, an oral selective pan-fibroblast growth factor receptor (FGFR) kinase inhibitor, is primarily metabolized by cytochrome P450 (CYP) 2C9 and 3A4.	erdafitinib	27-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-174
31673875-2	2020	The aim of this phase 1 study was to assess the pharmacokinetics and safety of erdafitinib in healthy participants when coadministered with fluconazole (moderate CYP2C9 and CYP3A inhibitor), and itraconazole (a strong CYP3A4 and P-glycoprotein inhibitor).	erdafitinib	79-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
31673875-12	2020	CONCLUSION: Coadministration of fluconazole or itraconazole or other moderate/strong CYP2C9 or CYP3A4 inhibitors may increase exposure to erdafitinib in healthy adults and thus may warrant erdafitinib dose reduction or use of alternative concomitant medications with no or minimal CYP2C9 or CYP3A4 inhibition potential.	erdafitinib	138-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	281-287
31673875-12	2020	CONCLUSION: Coadministration of fluconazole or itraconazole or other moderate/strong CYP2C9 or CYP3A4 inhibitors may increase exposure to erdafitinib in healthy adults and thus may warrant erdafitinib dose reduction or use of alternative concomitant medications with no or minimal CYP2C9 or CYP3A4 inhibition potential.	Fluconazole	32-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	281-287
31673875-12	2020	CONCLUSION: Coadministration of fluconazole or itraconazole or other moderate/strong CYP2C9 or CYP3A4 inhibitors may increase exposure to erdafitinib in healthy adults and thus may warrant erdafitinib dose reduction or use of alternative concomitant medications with no or minimal CYP2C9 or CYP3A4 inhibition potential.	erdafitinib	189-200	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
31720756-0	2020	Non-genetic factors and polymorphisms in genes CYP2C9 and VKORC1: predictive algorithms for TTR in Brazilian patients on warfarin.	Warfarin	121-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
32047440-0	2019	Phenprocoumon Dose Requirements, Dose Stability and Time in Therapeutic Range in Elderly Patients With CYP2C9 and VKORC1 Polymorphisms.	Phenprocoumon	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
31395958-0	2020	Algorithm for predicting low maintenance doses of warfarin using age and polymorphisms in genes CYP2C9 and VKORC1 in Brazilian subjects.	Warfarin	50-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
32024122-6	2020	Reactions selective for flavin-containing monooxygenases (FMOs), CYP1B1, CYP2C9, CYP2J2, and CYP3A4 all show significant rates in human lung microsomal incubations, but all activities are higher when rat lung microsomes are used.	Flavins	24-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
32433020-11	2020	Distinct expression of UGT1A1, CYP2B6, CYP2C9, CYP3A4, and CYP7A1 genes explains the ability to clear toxins and bilirubin as observed in normal hepatocytes.	Bilirubin	113-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
32047440-1	2019	Background: Dose requirements of vitamin K antagonists are associated with CYP2C9 and VKORC1, but, compared to warfarin, less data is available about phenprocoumon.	Vitamin K	33-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
32047440-3	2019	Methods: Aim was to scrutinize phenprocoumon dose requirements, dose stability and anticoagulation quality in association to CYP2C9 and VKORC1 in a natural cohort of elderly primary care patients.	Phenprocoumon	31-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
31941150-2	2020	Herein, a new bergamottin containing a nitroxide moiety (SL-bergamottin, SL-BM, 10) was synthesized; chemically characterized, evaluated as a potential inhibitor of the CYP2C19, CYP3A4, and CYP2C9 enzymes; and compared to BM and known inhibitors such as ketoconazole (KET) (3A4), warfarin (WAR) (2C9), and ticlopidine (TIC) (2C19).	bergamottin	14-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
31815452-5	2020	It was determined that UGT2B7 converts bromfenac to BI, and that while CYP2C8, CYP2C9 and CYP2C19 catalyze the hydroxylation of bromfenac, only CYP2C9 forms thioether adducts when incubated with NAC or GSH as trapping agents.	bromfenac	128-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
31815452-5	2020	It was determined that UGT2B7 converts bromfenac to BI, and that while CYP2C8, CYP2C9 and CYP2C19 catalyze the hydroxylation of bromfenac, only CYP2C9 forms thioether adducts when incubated with NAC or GSH as trapping agents.	Sulfides	157-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
31815452-5	2020	It was determined that UGT2B7 converts bromfenac to BI, and that while CYP2C8, CYP2C9 and CYP2C19 catalyze the hydroxylation of bromfenac, only CYP2C9 forms thioether adducts when incubated with NAC or GSH as trapping agents.	Glutathione	202-205	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
32021384-0	2020	The Effect of UGT1A9, CYP2B6 and CYP2C9 Genes Polymorphism on Propofol Pharmacokinetics in Children.	Propofol	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
32021384-1	2020	Purpose: This study was conducted to determine the effect of UGT1A9 98T>C, CYP2B6 516G>T and CYP2C9 430C>T genetic polymorphisms on the pharmacokinetics of propofol in children of different sexes and ages who undergone total intravenous anesthesia (TIVA) and deep sedation during diagnostic and therapeutic procedures.	Propofol	156-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
32021384-9	2020	Conclusion: Further investigations of UGT1A9, CYP2B6 and CYP2C9 and other genes that participate in propofol metabolism as well as detailed analyses of the general conditions, administered therapies and associated diseases could explain the large interindividual variability of propofol metabolism in children.	Propofol	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
32038232-1	2019	The cytochrome P450 2C9 and vitamin K epoxide reductase complex subunit 1 genotypes are associated with anticoagulation control and the clinical events in warfarin therapy.	Warfarin	155-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-23
31941150-2	2020	Herein, a new bergamottin containing a nitroxide moiety (SL-bergamottin, SL-BM, 10) was synthesized; chemically characterized, evaluated as a potential inhibitor of the CYP2C19, CYP3A4, and CYP2C9 enzymes; and compared to BM and known inhibitors such as ketoconazole (KET) (3A4), warfarin (WAR) (2C9), and ticlopidine (TIC) (2C19).	sl-bergamottin	57-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
32407272-1	2020	BACKGROUND: Metoclopramide is metabolized by various cytochrome P450 (CYP) enzymes such as CYP3A4, CYP1A2, CYP2D6, CYP2C9, and CYP2C19.	Metoclopramide	12-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
31854268-4	2020	Conclusion: VKORC1 rs9923231, CYP2C9*3 rs1057910, ApoE rs7412, age, BMI and concomitant amiodarone play an important role in stable dose variation of warfarin in elderly Shanghai Han Chinese patients, whereas ABCB1 rs1045642 is not a significant genetic factor.	Amiodarone	88-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
32228310-6	2020	CYP2C9*3 polymorphisms were associated with time to therapeutic range for acenocoumarol in Chilean patients, and the CYP4F2 TT genotype, MDR1 A allele, CYP1A2 A allele, and CYP3A4T allele are promising variants that merit further analysis.	Acenocoumarol	74-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
31378969-6	2020	Upadacitinib 30 mg once daily (a dose that is twice the optimal dose in rheumatoid arthritis based on phase 3 results) has a limited effect on CYP3A activity (26% decrease in exposure of midazolam, a sensitive CYP3A substrate) and no relevant effects on CYP1A2, CYP2C9, CYP2C19, or CYP2D6 activity in vivo.	upadacitinib	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	262-268
31648049-11	2020	CYP2C9 and CYP2C19 were the two CYP isozymes that produced 3"-hydroxylnalbuphine and 4"-hydroxylnalbuphine.	AN 3	59-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
31648049-11	2020	CYP2C9 and CYP2C19 were the two CYP isozymes that produced 3"-hydroxylnalbuphine and 4"-hydroxylnalbuphine.	BE 4-4-4-4	85-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
31889870-1	2020	Warfarin doses are greatly affected by polymorphism altering cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) gene.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-80
33132262-2	2020	We developed a novel hypouricemic agent because benzbromarone, a commercially available uricosuric agent, has several problems, such as drug-induced liver injury or drug-drug interaction caused by CYP2C9 inhibition.	Benzbromarone	48-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
31889870-1	2020	Warfarin doses are greatly affected by polymorphism altering cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) gene.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
31889870-11	2020	Both genotypes (CYP2C9 and VKORC1) require different dosing of warfarin than non-carriers in order to minimize the risk of warfarin overdosing and avoidance of the drug-related problems (DRPs).	Warfarin	63-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
31889870-11	2020	Both genotypes (CYP2C9 and VKORC1) require different dosing of warfarin than non-carriers in order to minimize the risk of warfarin overdosing and avoidance of the drug-related problems (DRPs).	Warfarin	123-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
31820397-1	2019	Zolpidem is extensively metabolized by CYP3A4, CYP2C9 and CYP1A2.	zolpidem	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
31835701-0	2019	Influence of Selected Carbon Nanostructures on the CYP2C9 Enzyme of the P450 Cytochrome.	Carbon	22-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
31835701-5	2019	The objective of this study was to evaluate the influence of three carbon nanostructures on the activity and expression at the mRNA and protein levels of CYP2C9 isoenzyme from the CYP2C subfamily: Diamond nanoparticles, graphite nanoparticles, and graphene oxide platelets.	Carbon	67-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
31835701-5	2019	The objective of this study was to evaluate the influence of three carbon nanostructures on the activity and expression at the mRNA and protein levels of CYP2C9 isoenzyme from the CYP2C subfamily: Diamond nanoparticles, graphite nanoparticles, and graphene oxide platelets.	Diamond	197-204	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
31835701-5	2019	The objective of this study was to evaluate the influence of three carbon nanostructures on the activity and expression at the mRNA and protein levels of CYP2C9 isoenzyme from the CYP2C subfamily: Diamond nanoparticles, graphite nanoparticles, and graphene oxide platelets.	Graphite	220-228	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
31835701-5	2019	The objective of this study was to evaluate the influence of three carbon nanostructures on the activity and expression at the mRNA and protein levels of CYP2C9 isoenzyme from the CYP2C subfamily: Diamond nanoparticles, graphite nanoparticles, and graphene oxide platelets.	Graphite	248-262	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
31835701-7	2019	A microsome model was used to assess the influence of the three-carbon nanostructures on the activity of the CYP2C9 isoenzyme.	Carbon	64-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
32186616-2	2019	Its dosage is related to the genetic characteristics of CYP2C9 enzymatic activity, which metabolizes losartan to its active form E-3174, responsible for the antihypertensive effect.	Losartan	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
31605674-6	2019	The findings confirmed that CYP3A4 was a major contributor (at least 30% total metabolism) to all three of the possible N-dealkylation pathways; however, CYP2C9, and not CYP2C19, played a critical role in terbinafine metabolism and even exceeded CYP3A4 contributions for terbinafine N-demethylation.	Nitrogen	120-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
31605674-6	2019	The findings confirmed that CYP3A4 was a major contributor (at least 30% total metabolism) to all three of the possible N-dealkylation pathways; however, CYP2C9, and not CYP2C19, played a critical role in terbinafine metabolism and even exceeded CYP3A4 contributions for terbinafine N-demethylation.	terbinafine	205-216	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
31605674-6	2019	The findings confirmed that CYP3A4 was a major contributor (at least 30% total metabolism) to all three of the possible N-dealkylation pathways; however, CYP2C9, and not CYP2C19, played a critical role in terbinafine metabolism and even exceeded CYP3A4 contributions for terbinafine N-demethylation.	terbinafine	271-282	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
31605674-6	2019	The findings confirmed that CYP3A4 was a major contributor (at least 30% total metabolism) to all three of the possible N-dealkylation pathways; however, CYP2C9, and not CYP2C19, played a critical role in terbinafine metabolism and even exceeded CYP3A4 contributions for terbinafine N-demethylation.	Nitrogen	283-284	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
31605674-11	2019	Taken together, the significance of CYP2C9 and 3A4 and to a lesser extent, CYP2C19, in terbinafine metabolism is consistent with reported drug interactions.	terbinafine	87-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
31468576-0	2019	Drug interactions between warfarin and lenvatinib in a patient with the CYP2C9*1/*3 and VKORC1-1639G/A genotype.	Warfarin	26-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
31468576-0	2019	Drug interactions between warfarin and lenvatinib in a patient with the CYP2C9*1/*3 and VKORC1-1639G/A genotype.	lenvatinib	39-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
31468576-2	2019	(S)-Warfarin is metabolized to (S)-7-hydroxywarfarin by CYP2C9 and (S)-4"-hydroxywarfarin by CYP2C8.	Warfarin	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
31468576-2	2019	(S)-Warfarin is metabolized to (S)-7-hydroxywarfarin by CYP2C9 and (S)-4"-hydroxywarfarin by CYP2C8.	7-hydroxywarfarin	31-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
31468576-3	2019	Here, we report drug interactions between warfarin and lenvatinib in a patient with CYP2C9*1/*3.	Warfarin	42-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
31468576-3	2019	Here, we report drug interactions between warfarin and lenvatinib in a patient with CYP2C9*1/*3.	lenvatinib	55-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
31468576-8	2019	WHAT IS NEW AND CONCLUSION: Lenvatinib-dependent (S)-warfarin inhibition could involve CYP2C9 and CYP2C8.	lenvatinib	28-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
31468576-8	2019	WHAT IS NEW AND CONCLUSION: Lenvatinib-dependent (S)-warfarin inhibition could involve CYP2C9 and CYP2C8.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
31274208-0	2019	Prolonged Pharmacokinetic Interaction Between Capecitabine and a CYP2C9 Substrate, Celecoxib.	Capecitabine	46-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
31274208-0	2019	Prolonged Pharmacokinetic Interaction Between Capecitabine and a CYP2C9 Substrate, Celecoxib.	Celecoxib	83-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
31274208-1	2019	This study investigated the time course and magnitude of the pharmacokinetic interaction between capecitabine and the cytochrome P450 (CYP) 2C9 substrate celecoxib, with implications for coadministration of fluoropyrimidines with CYP2C9 substrates such as warfarin.	Capecitabine	97-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-143
31274208-1	2019	This study investigated the time course and magnitude of the pharmacokinetic interaction between capecitabine and the cytochrome P450 (CYP) 2C9 substrate celecoxib, with implications for coadministration of fluoropyrimidines with CYP2C9 substrates such as warfarin.	Capecitabine	97-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	230-236
31274208-1	2019	This study investigated the time course and magnitude of the pharmacokinetic interaction between capecitabine and the cytochrome P450 (CYP) 2C9 substrate celecoxib, with implications for coadministration of fluoropyrimidines with CYP2C9 substrates such as warfarin.	Celecoxib	154-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-143
31274208-1	2019	This study investigated the time course and magnitude of the pharmacokinetic interaction between capecitabine and the cytochrome P450 (CYP) 2C9 substrate celecoxib, with implications for coadministration of fluoropyrimidines with CYP2C9 substrates such as warfarin.	Celecoxib	154-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	230-236
31274208-1	2019	This study investigated the time course and magnitude of the pharmacokinetic interaction between capecitabine and the cytochrome P450 (CYP) 2C9 substrate celecoxib, with implications for coadministration of fluoropyrimidines with CYP2C9 substrates such as warfarin.	Warfarin	256-264	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-143
31274208-7	2019	Close monitoring should be undertaken when administering fluoropyrimidines with CYP2C9 substrates with narrow therapeutic indexes while also weighing the benefits and risks for individual patients.	fluoropyrimidines	57-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
32186616-2	2019	Its dosage is related to the genetic characteristics of CYP2C9 enzymatic activity, which metabolizes losartan to its active form E-3174, responsible for the antihypertensive effect.	losartan carboxylic acid	129-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
32186616-10	2019	A non-significant tendency to need a larger dose of losartan was observed with the CYP2C9 * 3 allele, with an odds ratio (OR) of 1.46 (95% confidence intervals (CI) 0.01-18.64).	Losartan	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
32186616-13	2019	The presence of CYP2C9*3 is associated with the need for higher doses of losartan, possibly due to a decrease in the conversion of losartan to E-3174.	Losartan	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
32186616-13	2019	The presence of CYP2C9*3 is associated with the need for higher doses of losartan, possibly due to a decrease in the conversion of losartan to E-3174.	Losartan	131-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
32186616-13	2019	The presence of CYP2C9*3 is associated with the need for higher doses of losartan, possibly due to a decrease in the conversion of losartan to E-3174.	losartan carboxylic acid	143-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
31420941-2	2019	We previously constructed a physiologically-based pharmacokinetic (PBPK) model of rifampicin accounting for the components for the induction of cytochrome P450 (CYP) 3A/CYP2C9 and the inhibition of organic anion transporting polypeptide 1B (OATP1B).	Rifampin	82-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
31199498-1	2019	We predicted the drug-drug interaction (DDI) potential of siponimod in presence of cytochrome P450 (CYP)2C9/CYP3A4 inhibitors/inducers in subjects with different CYP2C9 genotypes by physiologically-based pharmacokinetic (PK) modeling.	siponimod	58-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-107
31199498-1	2019	We predicted the drug-drug interaction (DDI) potential of siponimod in presence of cytochrome P450 (CYP)2C9/CYP3A4 inhibitors/inducers in subjects with different CYP2C9 genotypes by physiologically-based pharmacokinetic (PK) modeling.	siponimod	58-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
31392364-0	2019	Siponimod pharmacokinetics, safety, and tolerability in combination with the potent CYP3A4 inhibitor itraconazole in healthy subjects with different CYP2C9 genotypes.	siponimod	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
31318064-7	2019	These interesting results steered to enumerate the possible role of IS01957 towards diclofenac pharmacokinetics through a panel of mechanistic investigations: (a) BCRP dependent ATPase activity was markedly interfered by IS01957; (b) IS01957 increased the intestinal permeability of diclofenac in the single pass in-situ perfusion model; (c) IS01957 inhibited the CYP2C9 catalyzed diclofenac 4-hydroxylation in human liver microsomes.	is01957	68-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	364-370
31318064-7	2019	These interesting results steered to enumerate the possible role of IS01957 towards diclofenac pharmacokinetics through a panel of mechanistic investigations: (a) BCRP dependent ATPase activity was markedly interfered by IS01957; (b) IS01957 increased the intestinal permeability of diclofenac in the single pass in-situ perfusion model; (c) IS01957 inhibited the CYP2C9 catalyzed diclofenac 4-hydroxylation in human liver microsomes.	Diclofenac	84-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	364-370
31392364-1	2019	PURPOSE: To evaluate the PK and safety of siponimod, a substrate of CYP2C9/3A4, in the presence or absence of a CYP3A4 inhibitor, itraconazole.	siponimod	42-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
31640208-7	2019	About 30 genes implicated in the metabolism coumarins derivatives were identified, the most important being CYP2C9 and VKORC, each with several polymorphisms.	coumarin	44-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
31064211-7	2019	In patients with wild-type genotypes for VKORC1, CYP2C9*2, CYP2C9*3, and CYP4F2, the highest warfarin requirement was found in Caucasians, lower in Hispanics, and lowest in Asians.	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
31064211-7	2019	In patients with wild-type genotypes for VKORC1, CYP2C9*2, CYP2C9*3, and CYP4F2, the highest warfarin requirement was found in Caucasians, lower in Hispanics, and lowest in Asians.	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
31064211-10	2019	CYP2C9 variants were associated with lower ADW doses; frequencies of CYP2C9*2 and CYP2C9*3 mutations were higher in Caucasians than in Hispanics but rare to none in Asians.	ADW 742	43-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
31676845-7	2019	We also demonstrated that matured Huh7s can be used for drug induction studies, where CYP3A4, CYP1A2, CYP2C9, and CYP2C19 inductions were achieved following rifampicin treatment.	Rifampin	157-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
31731555-4	2019	Furthermore, the inhibitory effects of DHF on cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) and xanthine oxidase (XO) enzymes were also tested using in vitro models.	6,7-dihydroxyflavone	39-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
31515991-3	2019	Auriculasin inhibited UGT1A6, UGT1A8, UGT1A10, UGT2B7, CYP2C9, and CYP3A4 strongly at a concentration of 100 muM.	auriculasin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
31515991-6	2019	In addition, CYP2D6, CYP2C9, CYP2C19, and CYP2C8 were the major CYP isoforms involved in the metabolism of auriculasin.	auriculasin	107-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
31276316-7	2019	Unexpectedly, several mutants showed significantly improved activity towards CYP2C9 (mutant 1-014) and/or CYP2A6 (mutants 1-014, 1-015, 1-053 and 1-077) using NADPH, even though the mutations were introduced at locations remote from the putative CPR-P450 interaction face.	NADP	159-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
30557096-7	2019	The results indicated that catalpol could inhibit the activity of CYP3A4, CYP2E1 and CYP2C9, with IC50 values of 14.27, 22.4 and 14.69 muM, respectively, but those other CYP isoforms were not affected.	catalpol	27-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
31616008-3	2019	Mechanistically, we also found a gender-specific correlation of the CYP2C9rs1799853T/T genotype with serum vitamin D3 levels (P = 0.00085) and a modest effect on IL1beta levels after stimulation of PBMCs or blood with LPS and PHA (P = 0.0057 and P = 0.0058).	Cholecalciferol	107-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
31176252-9	2019	Furthermore, reaction phenotyping studies revealed that, despite the low hepatic clearance in the first pass metabolism of TEB, multiple human CYP450 isoforms were involved in TEB metabolism when TEBOH enantiomers were generated, mainly CYP3A4 and CYP2C9, which makes TEB accumulation in the human body more difficult due to multiple metabolic pathways.	tebuconazole	123-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	248-254
31324935-1	2019	PURPOSE: Ruxolitinib is metabolized by cytochrome P450 (CYP)3A4 and CYP2C9.	ruxolitinib	9-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
31482508-0	2019	Effect of Polymorphisms in CYP2C9 and CYP2C19 on the Disposition, Safety and Metabolism of Progesterone Administrated Orally or Vaginally.	Progesterone	91-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
31482508-6	2019	CONCLUSION: This is the first study that reports variability in progesterone disposition according to the CYP2C19 and CYP2C9 phenotype.	Progesterone	64-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
31114948-2	2019	Cytochrome P450 (CYP) 2C9, the primary enzyme responsible for THC metabolism, has two single nucleotide polymorphisms-Arg144Cys (*2) and Ile359Leu (*3).	Dronabinol	62-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-25
31399508-8	2019	These results strongly support a high propensity for rhinacanthin-C as a perpetrator of clinical herb-drug interaction via inhibiting various influx and efflux drug transporters (i.e., P-gp, BCRP, OATP1B1, and OATP1B3) and CYP isoforms (i.e., CYP2C8, CYP2C9, and CYP2C19).	rhinacanthin-C	53-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	251-257
31058419-2	2019	Amlodipine is mainly metabolized by cytochrome P450 (CYP) 3A4, whereas losartan is metabolized by CYP2C9 and CYP3A4.	Losartan	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
30825074-4	2019	METHODS: This study was performed to investigate the inhibitory effects of myricetin on human CYP3A4, CYP2B6, CYP2C9, CYP2D6 and rat CYP3A2, CYP2B1, CYP2C11, CYP2D1 through the cocktail approach using ultra-performance liquid chromatography tandem mass spectrometry.	myricetin	75-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
31114948-6	2019	We therefore sought to characterize the pharmacokinetics of THC and its major metabolites 11-hydroxy-delta-9-tetrahydrocannabinol (THC-OH) and 11-nor-9-carboxy-delta-9-tetrahydrocannabinol (THC-COOH) in healthy volunteers with known CYP2C9 status by non-compartmental analysis (NCA), compartmental modeling (CM) and minimal physiologically based pharmacokinetic (mPBPK) modeling.	Dronabinol	60-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	233-239
31114948-11	2019	THC hepatic clearance is dependent on the CYP2C9 genetic variant in the population.	Dronabinol	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
31114948-14	2019	THC-OH is also a high extraction ratio drug, but its hepatic clearance is significantly impacted by the hepatic diffusional barrier that impedes its access to hepatic CYP2C9.	thc-oh	0-6	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
31114948-15	2019	THC-COOH is glucuronidated and renally cleared; subjects homozygous for CYP2C9*3 have reduced exposure to this metabolite as a result of the polymorphism reducing THC production, the hepatic diffusional barrier impeding egress from the hepatocyte, and increased renal clearance.	Dronabinol	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
31114948-15	2019	THC-COOH is glucuronidated and renally cleared; subjects homozygous for CYP2C9*3 have reduced exposure to this metabolite as a result of the polymorphism reducing THC production, the hepatic diffusional barrier impeding egress from the hepatocyte, and increased renal clearance.	Carbonic Acid	4-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
31114948-15	2019	THC-COOH is glucuronidated and renally cleared; subjects homozygous for CYP2C9*3 have reduced exposure to this metabolite as a result of the polymorphism reducing THC production, the hepatic diffusional barrier impeding egress from the hepatocyte, and increased renal clearance.	Dronabinol	163-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
31114948-16	2019	CONCLUSION: It has recently been reported that the terminal metabolite THC-COOH is active, implying the exposure difference in individuals homozygous for CYP2C9*3 may become therapeutically relevant.	Dronabinol	71-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
31114948-16	2019	CONCLUSION: It has recently been reported that the terminal metabolite THC-COOH is active, implying the exposure difference in individuals homozygous for CYP2C9*3 may become therapeutically relevant.	Carbonic Acid	75-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
31186542-5	2019	In addition to selected SNPs, VKORC1 g.6399C&gt;T, and CYP2C9 c.1075A&gt;C, which were known to have significant effects on warfarin stable doses, were also included in the study.	Warfarin	124-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
31421085-6	2019	KEY FINDINGS: At 100 muM, licoricidin strongly inhibited CYP2C9, CYP2C19, CYP3A4, UGT1A3, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT2B4, UGT2B7, UGT2B15, and UGT2B17.	licoricidin	26-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
33061049-2	2019	CYP2C9 is a hepatic drug-metabolizing enzyme in the CYP450 superfamily and is the primary metabolizing enzyme of warfarin.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
31461080-0	2019	Assessing the clinical impact of CYP2C9 pharmacogenetic variation on phenytoin prescribing practice and patient response in an integrated health system.	Phenytoin	69-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
33061049-8	2019	Majority of the patients, the 83 in warfarin group and the 40 in acenocoumarol group, had a wild CYP2C9 diplotype.	Acenocoumarol	65-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
29676195-8	2019	Enzyme kinetic studies showed that sophocarpine is not only a noncompetitive inhibitor of CYP3A4 but also a competitive inhibitor of CYP2C9, with Ki values of 6.74 and 9.19 muM, respectively.	sophocarpine	35-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
31461080-1	2019	OBJECTIVE: To assess the impact of CYP2C9 variation on phenytoin patient response and clinician prescribing practice where genotype was unknown during treatment.	Phenytoin	55-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
31461080-3	2019	We used laboratory test results, medication dispensing records, and medical notes to identify associations of CYP2C9 genotype with phenytoin blood concentration, neurologic side effects, and medication dispensing patterns reflecting clinician prescribing practice and patient response.	Phenytoin	131-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
31461080-6	2019	Decreased function CYP2C9 genotypes were associated with medication dispensing patterns indicating dose decrease, use of alternative anticonvulsants, and worse adherence, although these associations varied by treatment indication for phenytoin.	Phenytoin	234-243	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
31206740-5	2019	We also describe an additional case of phenytoin DRESS (RegiSCAR DRESS score 7) in an Aboriginal Australian that was associated with HLA-B*56:02 and with CYP2C9*1/*3 genotype.	Phenytoin	39-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
31492893-5	2019	Based on combined polymorphisms in CYP2C9 and VKORC1, we established a clinical classification for warfarin sensitivity.	Warfarin	99-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
31259734-0	2019	AKR1D1*36 C>T (rs1872930) allelic variant is associated with variability of the CYP2C9 genotype predicted pharmacokinetics of ibuprofen enantiomers - a pilot study in healthy volunteers.	Ibuprofen	126-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
31259734-1	2019	The relative contribution of CYP2C9 allelic variants to the pharmacokinetics (PK) of ibuprofen (IBP) enantiomers has been studied extensively, but the potential clinical benefit of pharmacogenetically guided IBP treatment is not evident yet.	Ibuprofen	85-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
31487853-5	2019	We describe herein the modeling and simulation of CYP 2C9 and CYP 2C19 in a phospholipid bilayer.	Phospholipids	76-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-57
30989645-3	2019	CYP2C9*3 associated with significantly increased area under the plasma concentration-time curve (AUC) of both 3R,5S-fluvastatin and 3S,5R-fluvastatin (by 67% and 94% per variant allele copy, P = 3.77 x 10-9 and P = 3.19 x 10-12 ).	3r,5s-fluvastatin	110-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30989645-3	2019	CYP2C9*3 associated with significantly increased area under the plasma concentration-time curve (AUC) of both 3R,5S-fluvastatin and 3S,5R-fluvastatin (by 67% and 94% per variant allele copy, P = 3.77 x 10-9 and P = 3.19 x 10-12 ).	3s,5r-fluvastatin	132-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30989645-5	2019	A candidate gene analysis suggested that CYP2C9*2 also affects the AUC of both fluvastatin enantiomers and that SLCO2B1 single-nucleotide variations may affect the AUC of 3S,5R-fluvastatin.	Fluvastatin	79-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
30989645-7	2019	Genotyping of both CYP2C9 and SLCO1B1 may be useful in predicting fluvastatin efficacy and myotoxicity.	Fluvastatin	66-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
31336317-2	2019	GFZ may affect the metabolism of various drugs, including statins, by inhibiting the sinusoidal influx transporter OATP1B1 and also CYP2C9 and CYP2C8 enzymes.	Gemfibrozil	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
31453773-0	2019	Low-frequency variants at the CYP2C9 locus among Puerto Rican patients on warfarin: in silico predictions of functionality and conservation.	Warfarin	74-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
31075510-7	2019	A separate recommendation on warfarin PGx testing is being developed to include recommendations on CYP2C9 alleles and additional warfarin sensitivity-associated genes and alleles.	Warfarin	29-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
31447576-0	2019	Polymorphisms of CYP2C9*2, CYP2C9*3 and VKORC1 genes related to time in therapeutic range in patients with atrial fibrillation using warfarin.	Warfarin	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
31447576-0	2019	Polymorphisms of CYP2C9*2, CYP2C9*3 and VKORC1 genes related to time in therapeutic range in patients with atrial fibrillation using warfarin.	Warfarin	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
31447576-11	2019	Conclusion: The genotypes of the CYP2C9*3 (AA) and VKORC1 -1639 (GG) genes were associated with the worst quality of anticoagulation control (TTR) in patients with AF using warfarin in the northeast of Brazil.	Warfarin	173-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
31433338-6	2019	FINDINGS: After comparing the in vitro inhibition parameters to physiologically achievable cannabinoid concentrations, it was concluded that CYP2C9, CYP1A1/2, and CYP1B1 are likely to be inhibited by all 3 major cannabinoids Delta-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN).	Cannabinoids	91-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
31433338-6	2019	FINDINGS: After comparing the in vitro inhibition parameters to physiologically achievable cannabinoid concentrations, it was concluded that CYP2C9, CYP1A1/2, and CYP1B1 are likely to be inhibited by all 3 major cannabinoids Delta-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN).	delta-tetrahydrocannabinol	225-251	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
31433338-6	2019	FINDINGS: After comparing the in vitro inhibition parameters to physiologically achievable cannabinoid concentrations, it was concluded that CYP2C9, CYP1A1/2, and CYP1B1 are likely to be inhibited by all 3 major cannabinoids Delta-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN).	Dronabinol	253-256	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
31433338-6	2019	FINDINGS: After comparing the in vitro inhibition parameters to physiologically achievable cannabinoid concentrations, it was concluded that CYP2C9, CYP1A1/2, and CYP1B1 are likely to be inhibited by all 3 major cannabinoids Delta-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN).	Cannabidiol	259-270	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
31433338-6	2019	FINDINGS: After comparing the in vitro inhibition parameters to physiologically achievable cannabinoid concentrations, it was concluded that CYP2C9, CYP1A1/2, and CYP1B1 are likely to be inhibited by all 3 major cannabinoids Delta-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN).	Cannabidiol	272-275	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
31433338-6	2019	FINDINGS: After comparing the in vitro inhibition parameters to physiologically achievable cannabinoid concentrations, it was concluded that CYP2C9, CYP1A1/2, and CYP1B1 are likely to be inhibited by all 3 major cannabinoids Delta-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN).	Cannabinol	241-251	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
31433338-6	2019	FINDINGS: After comparing the in vitro inhibition parameters to physiologically achievable cannabinoid concentrations, it was concluded that CYP2C9, CYP1A1/2, and CYP1B1 are likely to be inhibited by all 3 major cannabinoids Delta-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN).	Cannabinol	294-297	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
31433338-9	2019	Delta-Tetrahydrocannabinol also activates CYP2C9 and induces CYP1A1.	delta-tetrahydrocannabinol	0-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
31163215-3	2019	All tested coumarins except a C4 phenyl derivative (11) showed higher inhibitory activities for CYP2A6 over the other CYP isoforms, including CYP1A2, CYP2D6, CYP2E1, CYP3A4, CYP2C8, and CYP2C9.	Coumarins	11-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	186-192
31486736-0	2019	CYP2C9*2 is associated with indomethacin treatment failure for patent ductus arteriosus.	Indomethacin	28-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
31453773-3	2019	Results: CYP2C9*5,*8,*9,*11,*12,*21 and a novel *61 induce conformational changes that affect the binding site of S-warfarin.	Warfarin	114-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
31486736-5	2019	Conclusion: Age, surfactant use, and CYP2C9*2 influence indomethacin treatment outcome in preterm infants with PDA.	Indomethacin	56-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
31453773-5	2019	Conclusion: The unfavorable distance of S-warfarin from heme group, and low-binding interactions due to these CYP2C9 variants, suggest major complications during warfarin therapy.	Warfarin	162-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
30675694-3	2019	METHODS: A PBPK model of hyperforin accounting for the induction of cytochrome P450 (CYP) 3A, CYP2C9 and CYP2C19 was developed in the Simcyp  Simulator (version 17) and verified using published, clinically observed pharmacokinetic data.	hyperforin	25-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
31068367-5	2019	To describe the pharmacokinetic interaction profile of alectinib in a complete fashion, its possible inhibitory properties toward clinically relevant P450 enzymes (i.e., CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP3A4, or CYP3A5) were evaluated using human P450-expressing insect microsomes, revealing alectinib as a poor interactor.	alectinib	55-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	194-200
30852642-1	2019	PURPOSE: Large inter-individual differences in warfarin maintenance dose are mostly due to the effect of genetic polymorphisms in multiple genes, including vitamin K epoxide reductase complex 1 (VKORC1), cytochromes P450 2C9 (CYP2C9), and cytochrome P450 4F2 (CYP4F2).	Warfarin	47-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	204-224
30852642-1	2019	PURPOSE: Large inter-individual differences in warfarin maintenance dose are mostly due to the effect of genetic polymorphisms in multiple genes, including vitamin K epoxide reductase complex 1 (VKORC1), cytochromes P450 2C9 (CYP2C9), and cytochrome P450 4F2 (CYP4F2).	Warfarin	47-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	226-232
30675694-8	2019	CONCLUSION: In the current study, a PBPK model for hyperforin was successfully developed, with a predictive capability for the interactions of SJW with different CYP3A, CYP2C9 and CYP2C19 substrates.	hyperforin	51-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
30758919-2	2019	In vitro, lesinurad was shown to be a weak inhibitor of cytochrome P450 (CYP)2C9 and a weak inducer of CYP3A4.	lesinurad	10-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-80
31048453-7	2019	CYP2C9 pathway was the major pathway for depletion of THC (fm = 0.91, Km,u = 3 nM) and formation of 11-OH-THC.	Dronabinol	54-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
31048453-7	2019	CYP2C9 pathway was the major pathway for depletion of THC (fm = 0.91, Km,u = 3 nM) and formation of 11-OH-THC.	11-Hydroxytetrahydrocannabinol	100-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
31608877-0	2019	Relationship of S/R warfarin ratio with CYP2C9 genotypes in Pakistani population.	Warfarin	20-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
31048453-9	2019	11-OH-THC was depleted by UGTs (fm = 0.67 and Km,u = 39 nM), CYP3A4 (fm = 0.18, Km,u = 824 nM), and CYP2C9 (fm = 0.15, Km,u = 33 nM).	11-Hydroxytetrahydrocannabinol	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
29945531-1	2019	BACKGROUND: Voriconazole is extensively metabolized by the CYP450 isoenzymes 2C19 and 3A4 and to a lesser extent by CYP2C9; therefore, any medication that affects this pathway can alter its plasma concentration.	Voriconazole	12-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
31608877-3	2019	This study was carried out to determine the effect of CYP2C9*2 and CYP2C9*3 polymorphisms on S/R warfarin ratio.	Warfarin	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
31608877-3	2019	This study was carried out to determine the effect of CYP2C9*2 and CYP2C9*3 polymorphisms on S/R warfarin ratio.	Warfarin	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
31608877-7	2019	The concentration of S-warfarin was significantly different among CYP2C9 genotypes (p =0.018) whereas there was no effect on R-warfarin (p =0.134).	Warfarin	21-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
31608877-8	2019	There was statistically significant effect of different CYP2C9 genotypes on S/R warfarin ratio (p=0.000).	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
31608877-9	2019	It is concluded that CYP2C9 polymorphisms influence CYP2C9 enzymatic activity in turn affecting S-warfari levels but not R-warfarin, thus leading to different S/R warfarin enantiomers ratio among different CYP2C9 genotypes.	s-warfari	96-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
31608877-9	2019	It is concluded that CYP2C9 polymorphisms influence CYP2C9 enzymatic activity in turn affecting S-warfari levels but not R-warfarin, thus leading to different S/R warfarin enantiomers ratio among different CYP2C9 genotypes.	s-warfari	96-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
31608877-9	2019	It is concluded that CYP2C9 polymorphisms influence CYP2C9 enzymatic activity in turn affecting S-warfari levels but not R-warfarin, thus leading to different S/R warfarin enantiomers ratio among different CYP2C9 genotypes.	s-warfari	96-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
30506689-0	2019	Effect of CYP4F2, VKORC1, and CYP2C9 in Influencing Coumarin Dose: A Single-Patient Data Meta-Analysis in More Than 15,000 Individuals.	coumarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
31239454-8	2019	Furthermore, the results indicate that coumarin (CYP2A), midazolam (CYP3A), tolbutamide (CYP2C), and dextromethorphan (CYP2D) are as selective for porcine as for human CYP450.	Tolbutamide	76-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-94
30306496-0	2019	Effect of 95% Ethanol Khat Extract and Cathinone on in vitro Human Recombinant Cytochrome P450 (CYP) 2C9, CYP2D6, and CYP3A4 Activity.	cathinone	39-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-104
30992242-2	2019	Activities of CYP2C9, CYP2C19, and CYP3A4 were determined by using the prototypical substrates tolbutamide, omeprazole and midazolam, respectively.	Midazolam	123-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
30992242-2	2019	Activities of CYP2C9, CYP2C19, and CYP3A4 were determined by using the prototypical substrates tolbutamide, omeprazole and midazolam, respectively.	Tolbutamide	95-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
30992242-2	2019	Activities of CYP2C9, CYP2C19, and CYP3A4 were determined by using the prototypical substrates tolbutamide, omeprazole and midazolam, respectively.	Omeprazole	108-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
30306496-4	2019	This study aimed to reveal the inhibitory potencies of khat ethanol extract (KEE) and its major active ingredient (cathinone) on human cytochrome P450 (CYP) 2C9, CYP2D6, and CYP3A4 enzymes activities, which are collectively responsible for metabolizing 70-80% clinically used drugs.	Ethanol	60-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-160
30306496-4	2019	This study aimed to reveal the inhibitory potencies of khat ethanol extract (KEE) and its major active ingredient (cathinone) on human cytochrome P450 (CYP) 2C9, CYP2D6, and CYP3A4 enzymes activities, which are collectively responsible for metabolizing 70-80% clinically used drugs.	cathinone	115-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-160
30955332-4	2019	The MeOH extract exhibited significant inhibition of the major human CYP450 isozymes (CYP3A4, CYP1A2, CYP2D6, CYP2C9, and CYP2C19).	Methanol	4-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
30991128-11	2019	Overall, the present investigation suggested that myclobutanil moderately inhibits CYP2D6 and CYP2C9 in vitro and strongly inhibits CYP3A and CYP2C19 in vitro.	systhane	50-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
30525241-0	2019	Association between polymorphisms of VKORC1 and CYP2C9 genes with warfarin maintenance dose in a group of warfarin users in Birjand city, Iran.	Warfarin	66-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
30525241-0	2019	Association between polymorphisms of VKORC1 and CYP2C9 genes with warfarin maintenance dose in a group of warfarin users in Birjand city, Iran.	Warfarin	106-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
30525241-3	2019	The aim of the present study was to evaluate the frequency of CYP2C9 and VKORC1 gene polymorphisms and their association with warfarin maintenance dose in a sample of cardiovascular patients in Birjand, South-Khorasan province of Iran.	Warfarin	126-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
31145690-0	2019	Drug-drug interaction (DDI) assessments of ruxolitinib, a dual substrate of CYP3A4 and CYP2C9, using a verified physiologically based pharmacokinetic (PBPK) model to support regulatory submissions.	ruxolitinib	43-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
31145690-1	2019	Ruxolitinib is mainly metabolized by cytochrome P450 (CYP) enzymes CYP3A4 and CYP2C9 followed by minor contributions of other hepatic CYP enzymes in vitro.	ruxolitinib	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
31145690-2	2019	A physiologically based pharmacokinetic (PBPK) model was established to evaluate the changes in the ruxolitinib systemic exposures with co-administration of CYP3A4 and CYP2C9 perpetrators.	ruxolitinib	100-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
31145690-3	2019	The fractions metabolized in the liver via oxidation by CYP enzymes (fm,CYP3A4 = 0.75, fm,CYP2C9 = 0.19, and fm,CYPothers = 0.06) for an initial ruxolitinib model based on in vitro data were optimized (0.43, 0.56, and 0.01, respectively) using the observed exposure changes of ruxolitinib (10 mg) with co-administered ketoconazole (200 mg).	ruxolitinib	145-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
31145690-9	2019	Furthermore, an AUC increase of ruxolitinib in the absence or presence of the dual CYP3A4 and CYP2C9 inhibitor fluconazole (100-400 mg) was prospectively estimated to be 1.94- to 4.31-fold.	ruxolitinib	32-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
31145690-9	2019	Furthermore, an AUC increase of ruxolitinib in the absence or presence of the dual CYP3A4 and CYP2C9 inhibitor fluconazole (100-400 mg) was prospectively estimated to be 1.94- to 4.31-fold.	Fluconazole	111-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
31145690-11	2019	A ruxolitinib PBPK model with optimized fm,CYP3A4 and fm,CYP2C9 was established to evaluate victim DDI risks.	ruxolitinib	2-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
31145690-12	2019	The previous minimal PBPK model was supported by the FDA for the dose reduction strategy, halving the dose with the concomitant use of strong CYP3A4 inhibitors and dual inhibitors on CYP2C9 and CYP3A4, such as fluconazole at &lt;=200 mg. Fluconazole simulation results were used as supportive evidence in discussions with the FDA and EMA about ruxolitinib dose adjustment when co-administering perpetrator drugs.	Fluconazole	210-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	183-189
31086662-0	2019	Frequency of CYP2C9 (*2, *3 and IVS8-109A&gt;T) allelic variants, and their clinical implications, among Mexican patients with diabetes mellitus type 2 undergoing treatment with glibenclamide and metformin.	Glyburide	178-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
31086662-0	2019	Frequency of CYP2C9 (*2, *3 and IVS8-109A&gt;T) allelic variants, and their clinical implications, among Mexican patients with diabetes mellitus type 2 undergoing treatment with glibenclamide and metformin.	Metformin	196-205	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
31086662-1	2019	The majority of Mexican patients with diabetes mellitus type 2 (DMT2) (67.9-85.0%) are prescribed sulphonylureas (SUs), which are metabolized by cytochrome P450 2C9 (abbreviated as CYP2C9).	Sulfonylurea Compounds	114-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-164
31086662-1	2019	The majority of Mexican patients with diabetes mellitus type 2 (DMT2) (67.9-85.0%) are prescribed sulphonylureas (SUs), which are metabolized by cytochrome P450 2C9 (abbreviated as CYP2C9).	Sulfonylurea Compounds	114-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
30730615-6	2019	Overall, ASP8477 was a weak inhibitor for CYP3A4 and CYP2C9, a moderate to strong inhibitor for CYP2C19, and a weak to strong inhibitor for CYP2D6, with doses from 20 to 100 mg.	pyridin-3-yl 4-(phenylcarbamoyl)piperidine-1-carboxylate	9-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
30821933-0	2019	VKORC1 and Novel CYP2C9 Variation Predict Warfarin Response in Alaska Native and American Indian People.	Warfarin	42-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
31037455-8	2019	CYP2C9 *1/*3, VKORC1 AA, concomitant amiodarone, and nonheart valve replacement reduced the warfarin Km by 30.4%, 74.3%, 34.5%, and 39.4%, respectively.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30770140-1	2019	BACKGROUND: Amiodarone, which inhibits CYP2C9 and P-glycoprotein, is commonly prescribed with non-vitamin K antagonist oral anticoagulants (NOACs) and polypharmacy in high-risk atrial fibrillation (AF) patients.	Amiodarone	12-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
30589990-2	2019	Warfarin was the most extensively studied drug in a PGx context: a genomewide association study targeting warfarin stable dose identified significant signals in VKORC1 and CYP2C9, several PGx dosing algorithms were developed based on these and other genes, and the implications of population admixture on extrapolation of dosing recommendations in the CPIC guidelines were examined.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
30589990-2	2019	Warfarin was the most extensively studied drug in a PGx context: a genomewide association study targeting warfarin stable dose identified significant signals in VKORC1 and CYP2C9, several PGx dosing algorithms were developed based on these and other genes, and the implications of population admixture on extrapolation of dosing recommendations in the CPIC guidelines were examined.	Warfarin	106-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
29779438-3	2019	Other CYP enzymes contributing to the metabolism of one or more of the three pyrethroids were CYP1A2, CYP2C8, CYP2C9*1, CYP2D6*1, CYP3A4 and CYP3A5.	Pyrethrins	77-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
31061616-0	2019	Effects of CYP2C9 and VKORC1 polymorphisms on warfarin sensitivity and responsiveness during the stabilization phase of therapy.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
31061616-1	2019	The main objective of this study is to assess the effects of CYP2C9 and VKORC1 polymorphisms on warfarin sensitivity and responsiveness in a Jordanian population during the stabilization phase of treatment.	Warfarin	96-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
31061616-6	2019	Carriers of the CYP2C9 polymorphisms rs1057910 and rs4086116 had an increased risk of warfarin sensitivity compared to subjects with no or only one polymorphism.	Warfarin	86-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
31061616-9	2019	The presence of any of CYP2C9 or VKORC1 polymorphisms is associated with sensitivity to warfarin during the stabilization period.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
30903874-9	2019	Furthermore, single nucleotide polymorphisms (SNPs) in CYP2C9, VKORC1, and MIR133 genes can help physicians to predict individual warfarin dose requirement.	Warfarin	130-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
31531081-7	2019	Statistically significant association between clinically optimized warfarin dose and indication for the treatment, age, and warfarin sensitivity determined by VKORC1, CYP2C9 gene polymorphisms were confirmed.	Warfarin	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
30520061-8	2019	The LC-MS/MS data showed DHI intensively inhibit CYP2A6 activity and the intensity of inhibition was followed by CYP2C8, CYP3A4, CYP2C19, CYP2B6, CYP2D6, CYP1A2, CYP2E1 and CYP2C9 in vitro.	dehydrosoyasaponin I	25-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	173-179
31531081-7	2019	Statistically significant association between clinically optimized warfarin dose and indication for the treatment, age, and warfarin sensitivity determined by VKORC1, CYP2C9 gene polymorphisms were confirmed.	Warfarin	124-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
29298995-1	2019	Warfarin is primarily metabolized by cytochrome 2C9, encoded by gene CYP2C9.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
30983536-0	2019	Extremely low therapeutic doses of acenocoumarol in a patient with CYP2C9*3/*3 and VKORC1-1639A/A genotype.	Acenocoumarol	35-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
30983536-4	2019	We present the first reported case of a patient with the compounded genotype CYP2C9*3*3 and VKORC1-1639A/A under treatment with acenocoumarol, and review of other reported cases with analogous genotypic profiles but under treatment with warfarin.	Acenocoumarol	128-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
30983536-4	2019	We present the first reported case of a patient with the compounded genotype CYP2C9*3*3 and VKORC1-1639A/A under treatment with acenocoumarol, and review of other reported cases with analogous genotypic profiles but under treatment with warfarin.	Warfarin	237-245	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
30789308-0	2019	Polymorphisms in CYP1A2, CYP2C9 and ABCB1 affect agomelatine pharmacokinetics.	agomelatine	49-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
30712247-0	2019	Interpretation of the effect of CYP2C9, VKORC1 and CYP4F2 variants on warfarin dosing adjustment in Turkey.	Warfarin	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
30521883-4	2019	Increased expression of CYP2C epoxygenases, together with increased levels of their arachidonic acid-derived products, is often observed in tumors and tumor-associated vasculature, making these enzymes an ideal target for anti-cancer therapies.	Arachidonic Acid	84-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-29
30562214-0	2019	Individuals with CYP2C8 and CYP2C9 reduced metabolism haplotypes self-adjusted ibuprofen dose in the Coriell Personalized Medicine Collaborative.	Ibuprofen	79-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
30562214-1	2019	OBJECTIVES: The objectives of this study were to determine whether differences in CYP2C8 and CYP2C9 haplotype influence the dose of ibuprofen self-administered by individuals, and to examine the potential relationship between CYP2C8 and CYP2C9 reduced metabolism haplotypes and adverse events.	Ibuprofen	132-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
30562214-2	2019	PARTICIPANTS AND METHODS: We investigated relationships between genetic variations in CYP2C8 and CYP2C9 and ibuprofen use, dose, and side effects (reported by questionnaire) in 445 participants from the Coriell Personalized Medicine Collaborative.	Ibuprofen	108-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
30562214-3	2019	RESULTS: Carriers of reduced metabolism haplotypes for CYP2C8 (*2, *3, *4) and CYP2C9 (*2, *3) were significantly (P=0.0171) more likely than those lacking these variants to take less than the recommended dose of ibuprofen, after controlling for sex, age, race, and cohort.	Ibuprofen	213-222	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
30562214-6	2019	CONCLUSION: These results suggest a subset of individuals with genetic variation in CYP2C8 and CYP2C9 recognize that they obtain adequate drug efficacy with lower ibuprofen doses, or take lower doses due to prior side effects.	Ibuprofen	163-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
29298995-2	2019	Here, we investigated whether variants in nuclear receptor genes which regulate the expression of CYP2C9 are associated with warfarin response.	Warfarin	125-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
30962704-0	2019	Impact of a variable number tandem repeat in the CYP2C9 promoter on warfarin sensitivity and responsiveness in Jordanians with cardiovascular disease.	Warfarin	68-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
30962704-1	2019	Purpose: The purpose of this study was to investigate the influence of CYP/CYP450 2C9 (CYP2C9) promoter variable number tandem repeat (p-VNTR) polymorphism on susceptibility to cardiovascular disease and on warfarin sensitivity and responsiveness, in Jordanians with cardiovascular disease during initiation and stabilization phases of therapy.	Warfarin	207-215	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
30962704-3	2019	PCR-based methods were performed to analyze the effects of CYP2C9 p-VNTR polymorphism on warfarin metabolism.	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
30690186-9	2019	Atipamezole has more effective inhibition to CYP2C9 mediated diclofenac hydroxylation in human and animal liver microsomes with IC50 values of 1.50-5.20 muM than that of ABT at 74.7-460 muM.	atipamezole	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
30690186-9	2019	Atipamezole has more effective inhibition to CYP2C9 mediated diclofenac hydroxylation in human and animal liver microsomes with IC50 values of 1.50-5.20 muM than that of ABT at 74.7-460 muM.	Diclofenac	61-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
30690186-9	2019	Atipamezole has more effective inhibition to CYP2C9 mediated diclofenac hydroxylation in human and animal liver microsomes with IC50 values of 1.50-5.20 muM than that of ABT at 74.7-460 muM.	1-aminobenzotriazole	170-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
30617764-11	2019	CONCLUSION: The presence of mutations in VKORC1 or CYP2C9 is associated with increased risk of bleeding in patients with BCS on warfarin.	Warfarin	128-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
30088221-0	2019	Effect of Fluconazole Coadministration and CYP2C9 Genetic Polymorphism on Siponimod Pharmacokinetics in Healthy Subjects.	siponimod	74-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
30617764-0	2019	Mutations in CYP2C9 and/or VKORC1 haplotype are associated with higher bleeding complications in patients with Budd-Chiari syndrome on warfarin.	Warfarin	135-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
30088221-1	2019	OBJECTIVES: The aim of this study was to assess the pharmacokinetics (PK) and safety/tolerability of siponimod in healthy subjects when coadministered with (1) the moderate cytochrome P450 (CYP) 2C9 and CYP3A inhibitor fluconazole (Study A), and (2) with three different CYP2C9 genotype variants (Study B).	siponimod	101-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	173-198
30088221-1	2019	OBJECTIVES: The aim of this study was to assess the pharmacokinetics (PK) and safety/tolerability of siponimod in healthy subjects when coadministered with (1) the moderate cytochrome P450 (CYP) 2C9 and CYP3A inhibitor fluconazole (Study A), and (2) with three different CYP2C9 genotype variants (Study B).	siponimod	101-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	271-277
30088221-6	2019	In Study B, the AUCs of siponimod were approximately two to fourfold greater in subjects with the CYP2C9*2/*3 and CYP2C9*3/*3 genotypes, with a minor increase in Cmax versus the CYP2C9*1/*1 genotype.	siponimod	24-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
30088221-6	2019	In Study B, the AUCs of siponimod were approximately two to fourfold greater in subjects with the CYP2C9*2/*3 and CYP2C9*3/*3 genotypes, with a minor increase in Cmax versus the CYP2C9*1/*1 genotype.	siponimod	24-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
30088221-6	2019	In Study B, the AUCs of siponimod were approximately two to fourfold greater in subjects with the CYP2C9*2/*3 and CYP2C9*3/*3 genotypes, with a minor increase in Cmax versus the CYP2C9*1/*1 genotype.	siponimod	24-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
30088221-9	2019	CONCLUSIONS: Changes in siponimod PK, when coadministered with fluconazole at steady-state and in subjects with different CYP2C9 genotypes, indicate that the reduced CYP2C9 enzymatic activity does not affect the absorption phase of siponimod but prolongs the elimination phase.	siponimod	24-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
30088221-9	2019	CONCLUSIONS: Changes in siponimod PK, when coadministered with fluconazole at steady-state and in subjects with different CYP2C9 genotypes, indicate that the reduced CYP2C9 enzymatic activity does not affect the absorption phase of siponimod but prolongs the elimination phase.	siponimod	24-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	166-172
30088221-9	2019	CONCLUSIONS: Changes in siponimod PK, when coadministered with fluconazole at steady-state and in subjects with different CYP2C9 genotypes, indicate that the reduced CYP2C9 enzymatic activity does not affect the absorption phase of siponimod but prolongs the elimination phase.	Fluconazole	63-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	166-172
30088221-10	2019	These results confirm the relevance of CYP2C9 activity on siponimod metabolism in humans.	siponimod	58-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
30617764-2	2019	Vitamin K epoxide reductase complex 1 (VKORC1) and CYP2C9 are involved in the metabolism of warfarin.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
30823561-5	2019	The metabolism of 25B-NBF was catalyzed by CYP1A1, CYP1A2, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2J2, CYP3A4, and UGT2B7 enzymes.	SSW3KY7SWW	18-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
30883300-4	2019	The difference in patients" pharmacodynamic responses to warfarin has been attributed to genetic variation in warfarin metabolism and molecular targets (e.g., CYP2C9 and VKORC1) and host-environment interactions.	Warfarin	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
30883300-4	2019	The difference in patients" pharmacodynamic responses to warfarin has been attributed to genetic variation in warfarin metabolism and molecular targets (e.g., CYP2C9 and VKORC1) and host-environment interactions.	Warfarin	110-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
30883300-12	2019	CYP2C9*5, *8, *9, and *11, and VKORC1 Asp36Tyr genetic variants explained warfarin variability in Africans better, compared to CYP2C9*2 and *3.	Warfarin	74-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30443705-0	2019	Non randomized study on the potential of nitisinone to inhibit cytochrome P450 2C9, 2D6, 2E1 and the organic anion transporters OAT1 and OAT3 in healthy volunteers.	nitisinone	41-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-82
30443705-1	2019	PURPOSE: Nitisinone inhibits the cytochrome P450 (CYP) subfamilies CYP2C9, CYP2D6, and CYP2E1 and the organic anion transporter (OAT) isoforms OAT1 and OAT3 in vitro.	nitisinone	9-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
30443705-11	2019	Nitisinone was a moderate inhibitor of CYP2C9, and treatment may therefore result in increased plasma concentrations of comedications metabolized primarily via this enzyme.	nitisinone	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
30472588-2	2019	In this study, we used a cocktail of bupropion, losartan and dapsone for in vivo phenotyping of CYP2B6, CYP2C9 and N-acetyltransferase-2 (NAT2) in plasma.	Dapsone	61-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
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 9	Homo sapiens	132-138
30472588-2	2019	In this study, we used a cocktail of bupropion, losartan and dapsone for in vivo phenotyping of CYP2B6, CYP2C9 and N-acetyltransferase-2 (NAT2) in plasma.	Bupropion	37-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
30472588-14	2019	CONCLUSIONS: This study advocates the use of a cocktail of bupropion, losartan and dapsone for in vivo phenotyping of CYP2B6, CYP2C9 and NAT2, which is important in determining therapeutic dose levels of anti-HIV and anti-TB drugs in HIV/AIDS-TB coinfections.	Bupropion	59-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
30472588-14	2019	CONCLUSIONS: This study advocates the use of a cocktail of bupropion, losartan and dapsone for in vivo phenotyping of CYP2B6, CYP2C9 and NAT2, which is important in determining therapeutic dose levels of anti-HIV and anti-TB drugs in HIV/AIDS-TB coinfections.	Losartan	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
30472588-14	2019	CONCLUSIONS: This study advocates the use of a cocktail of bupropion, losartan and dapsone for in vivo phenotyping of CYP2B6, CYP2C9 and NAT2, which is important in determining therapeutic dose levels of anti-HIV and anti-TB drugs in HIV/AIDS-TB coinfections.	Dapsone	83-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
30270535-0	2019	HLA Alleles and CYP2C9*3 as Predictors of Phenytoin Hypersensitivity in East Asians.	Phenytoin	42-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
30466000-6	2019	Moreover, RA weakly inhibited CYP2C9 and 2E1 activities with IC50 values of 39.6 and 61.0 muM, respectively, while moderately inhibiting UGT1A1, 1A6, and 2B7 with IC50 values of 9.24, 19.1, and 23.4 muM, respectively.	rosmarinic acid	10-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
30447161-6	2019	CONCLUSIONS AND IMPLICATIONS: The combined results show that the 5"-hydroxylation of flucloxacillin is primarily catalysed by CYP3A4, CYP3A7 and CYP2C9.	Floxacillin	85-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
30270535-2	2019	In addition to cytochrome P450 (CYP)2C9*3, we found that HLA-B*13:01, HLA-B*15:02, and HLA-B*51:01 were significantly associated with phenytoin hypersensitivity with distinct phenotypic specificities.	Phenytoin	134-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-39
30270535-3	2019	Strikingly, we showed an increase in predictive sensitivity of concurrently testing CYP2C9*3/HLA-B*13:01/HLA-B*15:02/HLA-B*51:01 from 30.5-71.9% for selecting the individuals with the risk of developing phenytoin-SCAR in Taiwanese cohorts, accompanied by a specificity of 77.7% (combined sensitivity, 64.7%; specificity, 71.9% for three Asian populations).	Phenytoin	203-212	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
30270535-5	2019	In conclusion, combining the assessment of risk alleles of HLA and CYP2C9 potentiated the usefulness of predictive genetic tests to prevent phenytoin hypersensitivity in Asians.	Phenytoin	140-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
30121860-0	2019	Height, VKORC1 1173, and CYP2C9 Genotypes Determine Warfarin Dose for Pediatric Patients with Kawasaki Disease in Southwest China.	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
30159654-0	2019	Effect of CYP2C9 Polymorphisms on the Pharmacokinetics of Indomethacin During Pregnancy.	Indomethacin	58-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
30159654-1	2019	BACKGROUND AND OBJECTIVE: Cytochrome P450 (CYP) 2C9 catalyzes the biotransformation of indomethacin to its inactive metabolite O-desmethylindomethacin (DMI).	Indomethacin	87-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-51
30159654-1	2019	BACKGROUND AND OBJECTIVE: Cytochrome P450 (CYP) 2C9 catalyzes the biotransformation of indomethacin to its inactive metabolite O-desmethylindomethacin (DMI).	5-hydroxyindomethacin	127-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-51
30159654-1	2019	BACKGROUND AND OBJECTIVE: Cytochrome P450 (CYP) 2C9 catalyzes the biotransformation of indomethacin to its inactive metabolite O-desmethylindomethacin (DMI).	5-hydroxyindomethacin	152-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-51
30159654-2	2019	The aim of this work was to determine the effect of CYP2C9 polymorphisms on indomethacin metabolism in pregnant women.	Indomethacin	76-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
30159654-10	2019	CONCLUSION: Although our results are limited by sample size and are not statistically significant, these data suggest that certain genetic polymorphisms of CYP2C9 may lead to an increased metabolic ratio and an increase in the clearance of indomethacin.	Indomethacin	240-252	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
30159654-11	2019	More data are needed to assess the impact of CYP2C9 genotype on the effectiveness of indomethacin as a tocolytic agent.	Indomethacin	85-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
30678826-9	2019	Interestingly, several metabolites including the 4-hydroxyl form of CPA (4-OH-CPA) and phosphamide mustard were detected in the CYP2B6, CYP2C19, and CYP3A4 expression systems, but not in the CYP2C9 and CYP2D6 system.	4-hydroxyl	49-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
30678826-9	2019	Interestingly, several metabolites including the 4-hydroxyl form of CPA (4-OH-CPA) and phosphamide mustard were detected in the CYP2B6, CYP2C19, and CYP3A4 expression systems, but not in the CYP2C9 and CYP2D6 system.	Dimethoate	87-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	191-197
30678826-13	2019	Additionally, CPA metabolites like 4-OH-CPA and phosphamide mustard produced by human CYP2B6, CYP2C9, CYP2C19, and CYP3A4 are suggested to be major determinants of micronucleus induction by CPA.	Dimethoate	48-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
29375004-5	2019	Contributions of CYP3A4 and CYP2C9 to metabolism of deoxypodophyllotoxin and nateglinide were also predicted.	deoxypodophyllotoxin	52-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
29375004-8	2019	Predicted contributions of CYP3A4 and CYP2C9 to nateglinide metabolism were 8.18-37.84% and 36.08-94.04%, separately.	Nateglinide	48-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
29382249-6	2019	Methoxsalen is a direct inhibitor and inhibited the activities (&gt;90%) of all enzymes at a concentration of 300 microM except for CYP2C9.	Methoxsalen	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
29382249-9	2019	ABT is a potent TDI of several P450 except for CYP2C19 (47%) and CYP2C9 (27%).	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
30326170-1	2019	Delta-9-tetrahydrocannabinol (THC), the main psychoactive cannabinoid in cannabis, may inhibit the cytochrome P450 enzyme CYP2C9.	Dronabinol	0-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
30326170-1	2019	Delta-9-tetrahydrocannabinol (THC), the main psychoactive cannabinoid in cannabis, may inhibit the cytochrome P450 enzyme CYP2C9.	Dronabinol	30-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
30326170-1	2019	Delta-9-tetrahydrocannabinol (THC), the main psychoactive cannabinoid in cannabis, may inhibit the cytochrome P450 enzyme CYP2C9.	Cannabinoids	58-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
30326170-6	2019	The in vitro study indicated that THC inhibits the CYP2C9-mediated metabolism of warfarin.	Dronabinol	34-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
30326170-6	2019	The in vitro study indicated that THC inhibits the CYP2C9-mediated metabolism of warfarin.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
30336288-11	2019	Identification of orthologous human CYP2C9 and CYP3A4 enzyme families in vultures will be an important further step in explaining the differences in the metabolic pathway(s) of meloxicam and diclofenac for the species.	Meloxicam	177-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
30336288-11	2019	Identification of orthologous human CYP2C9 and CYP3A4 enzyme families in vultures will be an important further step in explaining the differences in the metabolic pathway(s) of meloxicam and diclofenac for the species.	Diclofenac	191-201	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
29119932-0	2019	Relevance of CYP2C9 Function in Valproate Therapy.	Valproic Acid	32-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
29119932-4	2019	METHODS: CYP2C9 mediated oxidation of valproate, which is the minor metabolic pathway in adults, appears to become the principal route in children.	Valproic Acid	38-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
29119932-5	2019	Genetic and non-genetic variations in CYP2C9 activity can result in significant inter- and intra-individual differences in valproate pharmacokinetics and valproate induced adverse reactions.	Valproic Acid	123-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
29119932-5	2019	Genetic and non-genetic variations in CYP2C9 activity can result in significant inter- and intra-individual differences in valproate pharmacokinetics and valproate induced adverse reactions.	Valproic Acid	154-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
29119932-6	2019	RESULTS: The loss-of-function alleles, CYP2C9*2 or CYP2C9*3, display significant reduction in valproate metabolism in children; furthermore, low CYP2C9 expression in patients with CYP2C9*1/*1 genotype also leads to a decrease in valproate metabolizing capacity.	Valproic Acid	94-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
29119932-6	2019	RESULTS: The loss-of-function alleles, CYP2C9*2 or CYP2C9*3, display significant reduction in valproate metabolism in children; furthermore, low CYP2C9 expression in patients with CYP2C9*1/*1 genotype also leads to a decrease in valproate metabolizing capacity.	Valproic Acid	94-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
29119932-6	2019	RESULTS: The loss-of-function alleles, CYP2C9*2 or CYP2C9*3, display significant reduction in valproate metabolism in children; furthermore, low CYP2C9 expression in patients with CYP2C9*1/*1 genotype also leads to a decrease in valproate metabolizing capacity.	Valproic Acid	94-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
29119932-6	2019	RESULTS: The loss-of-function alleles, CYP2C9*2 or CYP2C9*3, display significant reduction in valproate metabolism in children; furthermore, low CYP2C9 expression in patients with CYP2C9*1/*1 genotype also leads to a decrease in valproate metabolizing capacity.	Valproic Acid	94-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
29119932-6	2019	RESULTS: The loss-of-function alleles, CYP2C9*2 or CYP2C9*3, display significant reduction in valproate metabolism in children; furthermore, low CYP2C9 expression in patients with CYP2C9*1/*1 genotype also leads to a decrease in valproate metabolizing capacity.	Valproic Acid	229-238	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
29119932-6	2019	RESULTS: The loss-of-function alleles, CYP2C9*2 or CYP2C9*3, display significant reduction in valproate metabolism in children; furthermore, low CYP2C9 expression in patients with CYP2C9*1/*1 genotype also leads to a decrease in valproate metabolizing capacity.	Valproic Acid	229-238	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
29119932-6	2019	RESULTS: The loss-of-function alleles, CYP2C9*2 or CYP2C9*3, display significant reduction in valproate metabolism in children; furthermore, low CYP2C9 expression in patients with CYP2C9*1/*1 genotype also leads to a decrease in valproate metabolizing capacity.	Valproic Acid	229-238	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
29119932-6	2019	RESULTS: The loss-of-function alleles, CYP2C9*2 or CYP2C9*3, display significant reduction in valproate metabolism in children; furthermore, low CYP2C9 expression in patients with CYP2C9*1/*1 genotype also leads to a decrease in valproate metabolizing capacity.	Valproic Acid	229-238	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
29119932-8	2019	CONCLUSION: Novel strategy for valproate therapy adjusted to CYP2C9-status (CYP2C9 genotype and CYP2C9 expression) is strongly recommended in childhood.	Valproic Acid	31-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
29119932-8	2019	CONCLUSION: Novel strategy for valproate therapy adjusted to CYP2C9-status (CYP2C9 genotype and CYP2C9 expression) is strongly recommended in childhood.	Valproic Acid	31-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
29119932-8	2019	CONCLUSION: Novel strategy for valproate therapy adjusted to CYP2C9-status (CYP2C9 genotype and CYP2C9 expression) is strongly recommended in childhood.	Valproic Acid	31-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
29119932-9	2019	The early knowledge of pediatric patients" CYP2C9-status facilitates the optimization of valproate dosing which contributes to the avoidance of misdosing induced adverse reactions, such as abnormal blood levels of ammonia and alkaline phosphatase, and improves the safety of children"s anticonvulsant therapy.	Valproic Acid	89-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
30566377-2	2019	The rs12777823G&gt;A single-nucleotide polymorphism (SNP) in the CYP2C gene cluster has been shown to influence optimal warfarin doses in African Americans.	Warfarin	120-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-70
30566377-11	2019	Given ongoing worldwide efforts to identify clinically relevant human genetic variation impacting on optimal warfarin dose selection, the African ancestry-specific genetic variant in the CYP2C cluster and others warrant further research and consideration in development of future warfarin dosing algorithms for precision medicine guidelines.	Warfarin	109-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	187-192
30566377-11	2019	Given ongoing worldwide efforts to identify clinically relevant human genetic variation impacting on optimal warfarin dose selection, the African ancestry-specific genetic variant in the CYP2C cluster and others warrant further research and consideration in development of future warfarin dosing algorithms for precision medicine guidelines.	Warfarin	280-288	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	187-192
30584236-2	2018	This study purposed to investigate the effect of OATP1B3 and CYP2C9 genetic polymorphisms on the transport and metabolism of glibenclamide and glipizide in human.	Glyburide	125-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
30518301-0	2019	CYP2C9*61, a rare missense variant identified in a Puerto Rican patient with low warfarin dose requirements.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30518301-3	2019	This case report describes a rare missense variant at exon 9 of CYP2C9 (rs202201137; c.1370A>G transition; p.Asn457Ser) found in a Puerto Rican patient with low warfarin dose requirements (3 mg/day).	Warfarin	161-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
30518301-4	2019	The haplotype characterized by two amino acid changes, Asn457Ser and Arg144Cys (rs1799853; c.430C>T), has been designated CYP2C9*61 by the Pharmacogene Variation Consortium.	asn457ser	55-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
30584236-0	2018	OATP1B3 (699G&gt;A) and CYP2C9*2, *3 significantly influenced the transport and metabolism of glibenclamide and glipizide.	Glyburide	94-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
29297772-6	2019	CC-223 was metabolized by CYP2C9 and CYP3A, while metabolism of M1 was mediated by CYP2C8 and CYP3A.	CC-223	0-6	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
30584236-2	2018	This study purposed to investigate the effect of OATP1B3 and CYP2C9 genetic polymorphisms on the transport and metabolism of glibenclamide and glipizide in human.	Glipizide	143-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
30584236-0	2018	OATP1B3 (699G&gt;A) and CYP2C9*2, *3 significantly influenced the transport and metabolism of glibenclamide and glipizide.	Glipizide	112-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
30584236-3	2018	An LC-MS method was used to determine the uptake of glibenclamide and glipizide in OATP1B3, OATP1B3 (344T &gt; G) and OATP1B3 (699G &gt; A)-HEK293T cells and their metabolism in CYP2C9*1, *2 and *3 recombinase system.	Glyburide	52-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	178-184
30584236-6	2018	Glibenclamide can be metabolized in CYP2C9*1, *2 and *3 recombinase system with the Vmax values of 1.58 +- 0.71, 0.69 +- 0.25, and 0.41 +- 0.13 nmol/min/mg protein, while glipizide was metabolized with Vmax of 8.82 +- 2.78, 5.99 +- 1.95, and 2.87 +- 1.03 nmol/min/mg protein, respectively.	Glyburide	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
30584236-6	2018	Glibenclamide can be metabolized in CYP2C9*1, *2 and *3 recombinase system with the Vmax values of 1.58 +- 0.71, 0.69 +- 0.25, and 0.41 +- 0.13 nmol/min/mg protein, while glipizide was metabolized with Vmax of 8.82 +- 2.78, 5.99 +- 1.95, and 2.87 +- 1.03 nmol/min/mg protein, respectively.	Glipizide	171-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
30584236-7	2018	The internal clearance of glibenclamide and glipizide in CYP2C9*2 and *3 was markedly reduced compared to that in CYP2C9*1.	Glyburide	26-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
30584236-7	2018	The internal clearance of glibenclamide and glipizide in CYP2C9*2 and *3 was markedly reduced compared to that in CYP2C9*1.	Glyburide	26-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
30584236-7	2018	The internal clearance of glibenclamide and glipizide in CYP2C9*2 and *3 was markedly reduced compared to that in CYP2C9*1.	Glipizide	44-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
30584236-8	2018	These results collectively demonstrate that OATP1B3 (699G &gt; A) and CYP2C9*2 and *3 have a significant influence on the transport and metabolism of glibenclamide and glipizide.	Glyburide	150-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
30584236-8	2018	These results collectively demonstrate that OATP1B3 (699G &gt; A) and CYP2C9*2 and *3 have a significant influence on the transport and metabolism of glibenclamide and glipizide.	Glipizide	168-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
29569712-1	2018	Rifampin demonstrated dose-dependent relative induction between cytochrome P (CYP)3A and P-glycoprotein (P-gp), organic anion transporting polypeptides (OATPs), or CYP2C9; P-gp, OATP, and CYP2C9 induction was one drug-drug interaction (DDI) category lower than that observed for CYP3A across a wide range of pregnane X receptor (PXR) agonism.	Rifampin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	164-170
30412386-8	2018	Kinetic analyses using recombinant proteins revealed that CYP2C9 variants (A82V and H344R) showed substantially lower  Ks values than the wild type, although CYP1A1 variant (V382I) showed kinetic parameters similar to the wild type.	Potassium	119-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
30105453-0	2018	Siponimod pharmacokinetics, safety, and tolerability in combination with rifampin, a CYP2C9/3A4 inducer, in healthy subjects.	siponimod	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
29744741-6	2018	Furthermore, 1 microM naltrexone hydrochloride inhibited CYP3A4 enzyme activity, the most by 37.9% followed by CYP2C9 (36.5%) and CYP2D6 (31.8%).	Naltrexone	22-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
29744741-7	2018	The CYP2C9 and CYP2D6 metabolic activities were greatly affected by naltrexone hydrochloride, which even at the lowest concentration of naltrexone hydrochloride (0.01 microM) significantly decreased the metabolic activity by 34.9 and 16.0%, respectively.	Naltrexone	68-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
29744741-7	2018	The CYP2C9 and CYP2D6 metabolic activities were greatly affected by naltrexone hydrochloride, which even at the lowest concentration of naltrexone hydrochloride (0.01 microM) significantly decreased the metabolic activity by 34.9 and 16.0%, respectively.	Naltrexone	136-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
29744741-9	2018	CONCLUSION: These outcomes advocate that there is a great possibility of drug interactions resulting from the concurrent administration of naltrexone hydrochloride with actives that are metabolized by these CYP enzymes, particularly CYP2C9 and CYP2D6.	Naltrexone	139-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	233-239
30105453-1	2018	PURPOSE: To assess the potential pharmacokinetic (PK) interactions between siponimod and rifampin, a strong CYP3A4/moderate CYP2C9 inducer, in healthy subjects.	siponimod	75-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
30105453-1	2018	PURPOSE: To assess the potential pharmacokinetic (PK) interactions between siponimod and rifampin, a strong CYP3A4/moderate CYP2C9 inducer, in healthy subjects.	Rifampin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
30105453-14	2018	CONCLUSIONS: The study findings suggest that in the presence of rifampin, a strong CYP3A4/moderate CYP2C9 inducer, siponimod showed significant decrease in Cmax,ss (45%) and AUCtau,ss (57%) in healthy subjects.	Rifampin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
29569712-1	2018	Rifampin demonstrated dose-dependent relative induction between cytochrome P (CYP)3A and P-glycoprotein (P-gp), organic anion transporting polypeptides (OATPs), or CYP2C9; P-gp, OATP, and CYP2C9 induction was one drug-drug interaction (DDI) category lower than that observed for CYP3A across a wide range of pregnane X receptor (PXR) agonism.	Rifampin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	188-194
29633238-0	2018	Drinking Ethanol Has Few Acute Effects on CYP2C9, CYP2C19, NAT2, and P-Glycoprotein Activities but Somewhat Inhibits CYP1A2, CYP2D6, and Intestinal CYP3A: So What?	Ethanol	9-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
29905956-0	2018	Population Pharmacokinetic/Pharmacodynamic Analyses of Avatrombopag in Patients With Chronic Liver Disease and Optimal Dose Adjustment Guide With Concomitantly Administered CYP3A and CYP2C9 Inhibitors.	avatrombopag	55-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	183-189
30595245-0	2018	Association between genetic polymorphisms of CYP2C9 and VKORC1 and safety and efficacy of warfarin: Results of a 5 years audit.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
30595245-1	2018	OBJECTIVE: Genetic polymorphisms of CYP2C9 and VKORC1 play major role in pharmacokinetics and pharmacodynamics of warfarin, respectively.	Warfarin	114-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
30179260-7	2018	Additionally, nilotinib is a competitive inhibitor of CYP3A4/5, CYP2C8, CYP2C9, CYP2D6, and uridine diphosphate glucuronosyltransferase 1A1.	nilotinib	14-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
29802808-0	2018	CYP2C9*3 gene variant contributes independently to glycaemic control in patients with type 2 diabetes treated with glibenclamide.	Glyburide	115-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30142539-0	2018	Interactions of casticin, ipriflavone, and resveratrol with serum albumin and their inhibitory effects on CYP2C9 and CYP3A4 enzymes.	casticin	16-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
29802808-2	2018	In this cross-sectional study, the aim was to explore the association of genetic variants in CYP2C9, ABCC8, KCNJ11 and TCF7L2 with good glycaemic control in Mexican type 2 diabetes (T2D) treated with glibenclamide.	Glyburide	200-213	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
29802808-11	2018	WHAT IS NEW AND CONCLUSION: The findings suggest that CYP2C9*3 genetic variant independently contributes to good glycaemic control of patients with type 2 diabetes treated with glibenclamide.	Glyburide	177-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
30205091-2	2018	Methadone undergoes N-demethylation by multiple cytochrome P450 (CYP) enzymes including CYP3A4, CYP2B6, CYP2C19, CYP2D6, CYP2C9, and CYP2C8.	Methadone	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
30205091-2	2018	Methadone undergoes N-demethylation by multiple cytochrome P450 (CYP) enzymes including CYP3A4, CYP2B6, CYP2C19, CYP2D6, CYP2C9, and CYP2C8.	Nitrogen	20-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
30363031-1	2018	OBJECTIVE: The aim of this study was to determine the impact of the SLCO1B1, apolipoprotein E (ApoE), and CYP2C9 genotypes on the lipid-lowering efficacy of fluvastatin.	Fluvastatin	157-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
30486437-0	2018	Impact of CYP2C9 and VKORC1 Polymorphisms on Warfarin Sensitivity and Responsiveness in Jordanian Cardiovascular Patients during the Initiation Therapy.	Warfarin	45-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
30486437-4	2018	This study confirmed a genetic association of the CYP2C9*3 and VKORC1 rs10871454, rs8050894, rs9934438, and rs17708472 SNPs with warfarin sensitivity.	Warfarin	129-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
30486437-5	2018	This study also found an association between CYP2C9 and VKORC1 genetic haplotype blocks and warfarin sensitivity.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
30486437-6	2018	The initial warfarin dose was significantly related to the CYP2C9*3 polymorphism and the four VKORC1 SNPs (p &lt; 0.001).	Warfarin	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
30486437-7	2018	There were significant associations between rs4086116 SNP and TAT haplotype within CYP2C9 gene and rs17708472 SNP and CCGG haplotype within VKORC1 gene and warfarin responsiveness.	Warfarin	156-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
30363031-0	2018	The association between the SLCO1B1, apolipoprotein E, and CYP2C9 genes and lipid response to fluvastatin: a meta-analysis.	Fluvastatin	94-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
30452466-9	2018	Among loci which have extraordinary MAFs in Roma population two have strong proof of clinical importance: rs1799853 (CYP2C9) for warfarin dosage, and rs12248560 (CYP2C19) for clopidogrel dosage, efficacy and toxicity.	Warfarin	129-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
30452466-9	2018	Among loci which have extraordinary MAFs in Roma population two have strong proof of clinical importance: rs1799853 (CYP2C9) for warfarin dosage, and rs12248560 (CYP2C19) for clopidogrel dosage, efficacy and toxicity.	Clopidogrel	175-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
30142539-8	2018	Our results suggest that high intake of CAS and RES may interfere with the albumin-binding of Site II ligands as well as the metabolism of drugs by CYP2C9 and/or CYP3A4 enzymes, while large doses of IPR may affect the CYP3A4-catalyzed biotransformation of some drugs.	casticin	40-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
30142539-8	2018	Our results suggest that high intake of CAS and RES may interfere with the albumin-binding of Site II ligands as well as the metabolism of drugs by CYP2C9 and/or CYP3A4 enzymes, while large doses of IPR may affect the CYP3A4-catalyzed biotransformation of some drugs.	Resveratrol	48-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
30142539-6	2018	Furthermore, the effects of CAS, IPR, and RES on CYP2C9 and CYP3A4 enzymes were examined, employing diclofenac and testosterone as substrates, respectively.	Resveratrol	42-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
30142539-7	2018	Our main observations are the following: (1) Polyphenols formed stable complexes with albumin (K = 104-105 L/mol); (2) CAS and RES slightly displaced naproxen from human albumin, while albumin-binding of warfarin was not affected; (3) CAS and RES significantly inhibited CYP2C9, with CAS being as potent as the positive control warfarin; (4) each polyphenol significantly inhibited CYP3A4, with RES being stronger and CAS slightly weaker than the known inhibitor naringenin.	Polyphenols	45-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	271-277
30362120-5	2018	Inhibition studies with chemical inhibitors and antibodies suggested that arachidonic acid, the substrate of CYP2J2, and CYP2J2-specific antibody effectively inhibited the formation of SYL-927-M in HLMs whereas no significant inhibition was observed with the inhibitors for CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1 and CYP3A4, demonstrating that CYP2J2 was primarily responsible for the formation of SYL-927-M.	Arachidonic Acid	74-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	290-296
30142539-7	2018	Our main observations are the following: (1) Polyphenols formed stable complexes with albumin (K = 104-105 L/mol); (2) CAS and RES slightly displaced naproxen from human albumin, while albumin-binding of warfarin was not affected; (3) CAS and RES significantly inhibited CYP2C9, with CAS being as potent as the positive control warfarin; (4) each polyphenol significantly inhibited CYP3A4, with RES being stronger and CAS slightly weaker than the known inhibitor naringenin.	casticin	119-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	271-277
30138636-6	2018	On CYP2C9, apatinb exhibited the noncompetitive inhibition (Ki = 0.71 muM) while it inhibited CYP2C11 uncompetitively (Ki = 3.30 muM).	apatinb	11-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	3-9
30345882-4	2018	Observational studies have demonstrated the significant impact of single nucleotide polymorphisms in CYP2C9 and VKORC1 on warfarin dose in patients of European ancestry and African-Americans.	Warfarin	122-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
30321703-5	2018	RESULTS: S-warfarin clearance was significantly lower in patients with either CYP2C9 single (*2 or *3) or double (*2*2 or *2*3) variant alleles compared to those with wild-type genotype (P &lt; 0.001).	Warfarin	11-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
30321703-6	2018	Regression analysis revealed that patient age (P = 0.037) and CYP2C9 *2*2 &amp; *2*3 genotype (P = 0.005), but not VKORC1 genotype, significantly affected the time taken for the resumption of normal coagulation (INR value declining to &lt;=1.5).	Adenosine Monophosphate	75-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
30099291-0	2018	Effects of dibutyl phthalate and di(2-ethylhexyl) phthalate with their metabolites on CYP2C9*1 and CYP2C19*1 activities in vitro.	Dibutyl Phthalate	11-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
30321703-7	2018	CONCLUSIONS: The inter-individual variability in the time needed for normal coagulation to resume following warfarin withdrawal is influenced, in the main, by variance in S-warfarin clearance, which in turn is affected by CYP2C9 polymorphism and age.	Warfarin	108-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	222-228
30321703-7	2018	CONCLUSIONS: The inter-individual variability in the time needed for normal coagulation to resume following warfarin withdrawal is influenced, in the main, by variance in S-warfarin clearance, which in turn is affected by CYP2C9 polymorphism and age.	Warfarin	173-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	222-228
30321703-8	2018	Cost-effectiveness of pharmacogenetics-based algorithms incorporating CYP2C9 genotype and patient age could be increased if used not only to guide dosing decisions but also estimation of the correct length of time needed for individual patients to stop taking warfarin prior to surgery.	Warfarin	260-268	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
30099291-0	2018	Effects of dibutyl phthalate and di(2-ethylhexyl) phthalate with their metabolites on CYP2C9*1 and CYP2C19*1 activities in vitro.	Diethylhexyl Phthalate	33-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
30099291-1	2018	The aim of this article is to assess the effect of phthalates on the activities of CYP2C9 and CYP2C19 in vitro.	phthalic acid	51-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
30099291-4	2018	The results showed dibutyl phthalate (DBP) significantly inhibited CYP2C9*1 with an activity inhibition rate of 67.3% and half-maximal inhibitory concentration (IC50) of 29.63 mumol L-1, but its metabolite monobutyl phthalate (MBP) had no significant effect.	Dibutyl Phthalate	19-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
30099291-4	2018	The results showed dibutyl phthalate (DBP) significantly inhibited CYP2C9*1 with an activity inhibition rate of 67.3% and half-maximal inhibitory concentration (IC50) of 29.63 mumol L-1, but its metabolite monobutyl phthalate (MBP) had no significant effect.	Dibutyl Phthalate	38-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
30099291-8	2018	Further investigation showed MEHP was a competitive inhibitor of CYP2C9*1 (Ki = 7.063 mumol L-1), and DBP was a competitive inhibitor of CYP2C19*1 (Ki = 7.013 mumol L-1) against their substrates, both phthalates were non-competitive inhibitors of the cofactor NADPH.	mono-(2-ethylhexyl)phthalate	29-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
30099291-9	2018	Our results suggested that DBP, DEHP, and their metabolites exhibited significant inhibitory effects toward either CYP2C9*1 or CYP2C19*1.	Diethylhexyl Phthalate	32-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
30356105-6	2018	Similarly, South Asians had a significantly higher frequency of CYP2C9*3 (12% SDS, 13% GIH, 11% SAS) vs. 7% in Europeans (pgenotype = <1.0E-05) and "T" allele of CYP4F2 (36%) SDS, (43%) GIH, 40% (SAS) vs. (29%) in Europeans (pgenotype = <1.0E-05); both associated with a higher risk of bleeding with warfarin.	sds	78-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
30339708-3	2018	Remarkable efforts have been made to develop the machine learning based warfarin dosing algorithms incorporating clinical factors and genetic variants such as polymorphisms in CYP2C9 and VKORC1.	Warfarin	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
30410385-3	2018	CYP2C9 and VKORC1 gene polymorphisms affect warfarin metabolism and dosage.	Warfarin	44-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30410385-8	2018	Results: Median weekly prescribed warfarin dosage was significantly lower in patients having the VKORC1-1639 AA genotype and poor CYP2C9*2/*2,*2/*3 metabolizers than their wild-type counterparts.	Warfarin	34-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
29994939-3	2018	The recent pharmacogenetics studies revealed an association of the organic cation transporter 1 (OCT1) and ATP-binding cassette C3 (ABCC3) polymorphisms with morphine-related adverse effects, an effect of polymorphisms in cytochrome P450 gene CYP2D6 on the analgesic efficacy of tramadol and no effect of CYP2C8 and CYP2C9 variants on efficacy of piroxicam.	Morphine	158-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	316-322
30010032-7	2018	Conversely, the inhibitory ratios of 3,4-DCPB (16 mug/mL, 59 muM) on the activities of CYP2C9, CYP2C19, CYP1A2 and CYP2D6 were 97.6%, 59.0%, 53.5% and 36.5%, respectively.	3,4-dichlorophenyl-propenoyl-sec-butylamine	37-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
30010032-10	2018	3,4-DCPB inhibited the activities of CYP2C9, CYP2C19, CYP1A2 and CYP2D6, rather than that CYP2E1 and CYP3A4 enzymes, suggesting that the different effects of 3,4-DCPB on the CYP450 enzymes might influence metabolic drug-drug interaction in antiepileptics therapy.	3,4-dichlorophenyl-propenoyl-sec-butylamine	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
30010032-10	2018	3,4-DCPB inhibited the activities of CYP2C9, CYP2C19, CYP1A2 and CYP2D6, rather than that CYP2E1 and CYP3A4 enzymes, suggesting that the different effects of 3,4-DCPB on the CYP450 enzymes might influence metabolic drug-drug interaction in antiepileptics therapy.	3,4-dichlorophenyl-propenoyl-sec-butylamine	158-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
29958892-4	2018	RESULTS: In this case we present a patient with multifactorial vitamin K deficiency (due to nutritional defects and multiple genetic mutations in VKOR and CYP2C9) that was exacerbated by antibiotic and warfarin therapy during her hospital admission.	Warfarin	202-210	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
30319126-7	2018	Moreover, enzalutamide may require dose adjustment for other drugs since it is a potent inductor of CYP3A4 and a moderate inductor of CYP2C9 y el CYP2C19.	enzalutamide	10-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
30219715-4	2018	In individual HLMs with variable CYP2D6 activities, a significant correlation was observed between celecoxib hydroxylation and CYP2D6-selective dextromethorphan O-demethylation when CYP2C9 and CYP3A4 activities were suppressed (r = 0.97, P &lt; 0.0001).	Celecoxib	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	182-188
30219715-4	2018	In individual HLMs with variable CYP2D6 activities, a significant correlation was observed between celecoxib hydroxylation and CYP2D6-selective dextromethorphan O-demethylation when CYP2C9 and CYP3A4 activities were suppressed (r = 0.97, P &lt; 0.0001).	Dextromethorphan	144-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	182-188
30219715-8	2018	Using HLMs from individual donors, the relative contribution of CYP2D6 to celecoxib metabolism was found to be highly variable and dependent on CYP2C9 genotypes, ranging from no contribution in extensive metabolizers with CYP2C9*1*1 genotype to approximately 30% in slow metabolizers with allelic variants CYP2C9*1*3 and CYP2C9*3*3.	Celecoxib	74-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
30219715-9	2018	These results demonstrate that celecoxib may become a potential victim of CYP2D6-associated drug-drug interactions, particularly in individuals with reduced CYP2C9 activity.	Celecoxib	31-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
30219715-0	2018	Celecoxib is a substrate of CYP2D6: Impact on celecoxib metabolism in individuals with CYP2C9*3 variants.	Celecoxib	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
30219715-0	2018	Celecoxib is a substrate of CYP2D6: Impact on celecoxib metabolism in individuals with CYP2C9*3 variants.	Celecoxib	46-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
30219715-3	2018	In human liver microsomes (HLMs), a concentration-dependent inhibition of celecoxib hydroxylation by quinidine was observed after CYP2C9 and CYP3A4 were inhibited.	Celecoxib	74-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
30219715-3	2018	In human liver microsomes (HLMs), a concentration-dependent inhibition of celecoxib hydroxylation by quinidine was observed after CYP2C9 and CYP3A4 were inhibited.	Quinidine	101-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
30283820-0	2018	DRESS after IV phenytoin associated with cytochrome P450 CYP2C9*3 homozygosity.	Phenytoin	15-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
30098040-0	2018	Metabolism of steroids by cytochrome P450 2C9 variants.	Steroids	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-45
30178440-0	2018	The influences of CYP2C9*1/*3 genotype on the pharmacokinetics of zolpidem.	Zolpidem	66-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
29916837-7	2018	To explain the association between demographic, clinical and genotype data (VKORC1, CYP2C9 and CYP4F2) and the mean weekly dose of acenocoumarol, we performed a multiple linear regression model.	Acenocoumarol	131-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
30012669-0	2018	The Cytochrome P450 Slow Metabolizers CYP2C9*2 and CYP2C9*3 Directly Regulate Tumorigenesis via Reduced Epoxyeicosatrienoic Acid Production.	epoxyeicosatrienoic acid	104-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
30012669-0	2018	The Cytochrome P450 Slow Metabolizers CYP2C9*2 and CYP2C9*3 Directly Regulate Tumorigenesis via Reduced Epoxyeicosatrienoic Acid Production.	epoxyeicosatrienoic acid	104-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
30012669-1	2018	Increased expression of cytochrome P450 CYP2C9, together with elevated levels of its products epoxyeicosatrienoic acids (EET), is associated with aggressiveness in cancer.	epoxyeicosatrienoic acids	94-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
30012669-1	2018	Increased expression of cytochrome P450 CYP2C9, together with elevated levels of its products epoxyeicosatrienoic acids (EET), is associated with aggressiveness in cancer.	EET	121-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
30012669-3	2018	Although genetic differences in CYP2C9-dependent oxidation of arachidonic acid (AA) have been reported, the roles of CYP2C9*2 and CYP2C9*3 in EET biosynthesis and their relevance to disease are unknown.	Arachidonic Acid	62-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
30012669-5	2018	When injected into mice, NSCLC cells expressing CYP2C9*2 and CYP2C9*3 produced lower levels of EETs and developed fewer, smaller, and less vascularized tumors than cells expressing CYP2C9*1.	eets	95-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
30012669-5	2018	When injected into mice, NSCLC cells expressing CYP2C9*2 and CYP2C9*3 produced lower levels of EETs and developed fewer, smaller, and less vascularized tumors than cells expressing CYP2C9*1.	eets	95-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
30012669-5	2018	When injected into mice, NSCLC cells expressing CYP2C9*2 and CYP2C9*3 produced lower levels of EETs and developed fewer, smaller, and less vascularized tumors than cells expressing CYP2C9*1.	eets	95-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
30012669-7	2018	Purified CYP2C9*2 and CYP2C9*3 exhibited attenuated catalytic efficiency in producing EETs, primarily due to impaired reduction of these two variants by NADPH-P450 reductase.	eets	86-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
30012669-7	2018	Purified CYP2C9*2 and CYP2C9*3 exhibited attenuated catalytic efficiency in producing EETs, primarily due to impaired reduction of these two variants by NADPH-P450 reductase.	eets	86-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
28992765-6	2018	The major isoforms of CYP involved in the metabolism of warfarin sodium are CYP1A2 (for the R-warfarin) and CYP2C9 (for the S-warfarin).	Warfarin	56-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
28992765-6	2018	The major isoforms of CYP involved in the metabolism of warfarin sodium are CYP1A2 (for the R-warfarin) and CYP2C9 (for the S-warfarin).	Warfarin	92-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
28992765-6	2018	The major isoforms of CYP involved in the metabolism of warfarin sodium are CYP1A2 (for the R-warfarin) and CYP2C9 (for the S-warfarin).	Sulfur	124-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
28992765-6	2018	The major isoforms of CYP involved in the metabolism of warfarin sodium are CYP1A2 (for the R-warfarin) and CYP2C9 (for the S-warfarin).	Warfarin	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
28992765-7	2018	The probes for testing CYP1A2 are phenacetin and caffeine while for CYP2C9 tolbutamide.	Tolbutamide	75-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
29756176-0	2018	Response: Similar effect of quercetin on CYP2E1 and CYP2C9 activities in humans?	Quercetin	28-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
29770840-0	2018	Similar effect of quercetin on CYP2E1 and CYP2C9 activities in humans?	Quercetin	18-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
30178440-1	2018	Zolpidem is predominantly metabolized by CYP3A4, and to a lesser extent by CYP2C9, CYP1A2, CYP2D6 and CYP2C19.	Zolpidem	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
30178440-2	2018	The aim of this study was to identify the effects of CYP2C9*3 allele on the pharmacokinetics of zolpidem.	Zolpidem	96-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
30178440-5	2018	In addition, since zolpidem is metabolized at a high rate by CYP3A4, the effect of CYP2C9*3 allele on the pharmacokinetics of zolpidem was also observed in the condition where CYP3A4 was sufficiently inhibited by the steady-state concentration of clarithromycin, a potent CYP3A4 inhibitor.	Zolpidem	19-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
30098040-5	2018	CYP2C9.2, CYP2C9.3, CYP2C9.4, CYP2C9.16, CYP2C9.28, CYP2C9.48 and CYP2C9.52 had higher testosterone 6beta-hydroxylation than CYP2C9.1.	testosterone 6beta	87-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30178440-5	2018	In addition, since zolpidem is metabolized at a high rate by CYP3A4, the effect of CYP2C9*3 allele on the pharmacokinetics of zolpidem was also observed in the condition where CYP3A4 was sufficiently inhibited by the steady-state concentration of clarithromycin, a potent CYP3A4 inhibitor.	Zolpidem	126-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
30178440-5	2018	In addition, since zolpidem is metabolized at a high rate by CYP3A4, the effect of CYP2C9*3 allele on the pharmacokinetics of zolpidem was also observed in the condition where CYP3A4 was sufficiently inhibited by the steady-state concentration of clarithromycin, a potent CYP3A4 inhibitor.	Clarithromycin	247-261	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
30098040-5	2018	CYP2C9.2, CYP2C9.3, CYP2C9.4, CYP2C9.16, CYP2C9.28, CYP2C9.48 and CYP2C9.52 had higher testosterone 6beta-hydroxylation than CYP2C9.1.	testosterone 6beta	87-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
30098040-5	2018	CYP2C9.2, CYP2C9.3, CYP2C9.4, CYP2C9.16, CYP2C9.28, CYP2C9.48 and CYP2C9.52 had higher testosterone 6beta-hydroxylation than CYP2C9.1.	testosterone 6beta	87-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
30098040-5	2018	CYP2C9.2, CYP2C9.3, CYP2C9.4, CYP2C9.16, CYP2C9.28, CYP2C9.48 and CYP2C9.52 had higher testosterone 6beta-hydroxylation than CYP2C9.1.	testosterone 6beta	87-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
30098040-5	2018	CYP2C9.2, CYP2C9.3, CYP2C9.4, CYP2C9.16, CYP2C9.28, CYP2C9.48 and CYP2C9.52 had higher testosterone 6beta-hydroxylation than CYP2C9.1.	testosterone 6beta	87-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
30098040-5	2018	CYP2C9.2, CYP2C9.3, CYP2C9.4, CYP2C9.16, CYP2C9.28, CYP2C9.48 and CYP2C9.52 had higher testosterone 6beta-hydroxylation than CYP2C9.1.	testosterone 6beta	87-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
30098040-5	2018	CYP2C9.2, CYP2C9.3, CYP2C9.4, CYP2C9.16, CYP2C9.28, CYP2C9.48 and CYP2C9.52 had higher testosterone 6beta-hydroxylation than CYP2C9.1.	testosterone 6beta	87-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
29859403-3	2018	Azoles" affinities toward human cytochrome P450 isoforms involved in xenobiotic metabolism (CYP3A4, CYP2C9 and CYP2D6) as well as fungal CYP51 were estimated with a ligand-protein docking model based on the ChemScore scoring function.	Azoles	0-6	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
30098040-5	2018	CYP2C9.2, CYP2C9.3, CYP2C9.4, CYP2C9.16, CYP2C9.28, CYP2C9.48 and CYP2C9.52 had higher testosterone 6beta-hydroxylation than CYP2C9.1.	testosterone 6beta	87-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
30098040-6	2018	CYP2C9.4 showed higher progesterone 6beta-hydroxylation activity than CYP2C9.1.	Progesterone	23-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30098040-7	2018	CYP2C9.28 and CYP2C9.48 showed higher progesterone 11alpha-hydroxylation activity than CYP2C9.1.	Progesterone	38-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30098040-7	2018	CYP2C9.28 and CYP2C9.48 showed higher progesterone 11alpha-hydroxylation activity than CYP2C9.1.	Progesterone	38-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
30098040-7	2018	CYP2C9.28 and CYP2C9.48 showed higher progesterone 11alpha-hydroxylation activity than CYP2C9.1.	Progesterone	38-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
30098040-9	2018	CYP2C9.2, CYP2C9.3, CYP2C9.16 and CYP2C9.30 had higher estrone 16alpha-hydroxylation activity than CYP2C9.1.	Estrone	55-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30098040-9	2018	CYP2C9.2, CYP2C9.3, CYP2C9.16 and CYP2C9.30 had higher estrone 16alpha-hydroxylation activity than CYP2C9.1.	Estrone	55-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
30117082-1	2018	Zolpidem is indicated for the short-term treatment of insomnia and it is predominantly metabolized by CYP3A4, and to a lesser extent by CYP2C19, CYP1A2, and CYP2C9.	Zolpidem	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
30098040-9	2018	CYP2C9.2, CYP2C9.3, CYP2C9.16 and CYP2C9.30 had higher estrone 16alpha-hydroxylation activity than CYP2C9.1.	Estrone	55-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
30098040-9	2018	CYP2C9.2, CYP2C9.3, CYP2C9.16 and CYP2C9.30 had higher estrone 16alpha-hydroxylation activity than CYP2C9.1.	Estrone	55-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
30098040-9	2018	CYP2C9.2, CYP2C9.3, CYP2C9.16 and CYP2C9.30 had higher estrone 16alpha-hydroxylation activity than CYP2C9.1.	Estrone	55-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
30098040-10	2018	CYP2C9.3 had higher estrone 11alpha-hydroxylation activity than CYP2C9.1.	Estrone	20-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
29741099-8	2018	There are suggestions that genotyping the CYP2C9 and VKORC1 genes is useful for determining a more appropriate initial dose and thereby increasing the effectiveness and safety of warfarin.	Warfarin	179-187	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
29578591-5	2018	Danshensu and rosmarinic acid inhibited CYP2E1 and CYP2C9 with IC50 values of 36.63 and 75.76 mum, and 34.42 and 76.89 mum, respectively.	3,4-dihydroxyphenyllactic acid	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
29578591-5	2018	Danshensu and rosmarinic acid inhibited CYP2E1 and CYP2C9 with IC50 values of 36.63 and 75.76 mum, and 34.42 and 76.89 mum, respectively.	rosmarinic acid	14-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
29578591-6	2018	Salvianolic acid A and B inhibited CYP2D6, CYP2E1 and CYP2C9 with IC50 values of 33.79, 21.64 and 31.94 mum, and 45.47, 13.52 and 24.15 mum, respectively.	salvianolic acid A	0-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
29578591-6	2018	Salvianolic acid A and B inhibited CYP2D6, CYP2E1 and CYP2C9 with IC50 values of 33.79, 21.64 and 31.94 mum, and 45.47, 13.52 and 24.15 mum, respectively.	Boron	23-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
29885857-3	2018	Gentisic acid (GA) is a minor catabolite of aspirin; yet humans carrying CYP2C9-variants incapable to catabolize aspirin to GA do not benefit from aspirin in prevention against colonic adenoma.	2,5-dihydroxybenzoic acid	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
29885857-3	2018	Gentisic acid (GA) is a minor catabolite of aspirin; yet humans carrying CYP2C9-variants incapable to catabolize aspirin to GA do not benefit from aspirin in prevention against colonic adenoma.	Aspirin	113-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
29885857-3	2018	Gentisic acid (GA) is a minor catabolite of aspirin; yet humans carrying CYP2C9-variants incapable to catabolize aspirin to GA do not benefit from aspirin in prevention against colonic adenoma.	2,5-dihydroxybenzoic acid	124-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
29885857-3	2018	Gentisic acid (GA) is a minor catabolite of aspirin; yet humans carrying CYP2C9-variants incapable to catabolize aspirin to GA do not benefit from aspirin in prevention against colonic adenoma.	Aspirin	113-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
29578591-4	2018	The results showed that DHI inhibited CYP2C19, CYP2D6, CYP3A4, CYP2E1 and CYP2C9 with IC50 values of 1.26, 1.42, 1.63, 1.10 and 1.67% (v/v), respectively.	dehydrosoyasaponin I	24-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
30017171-2	2018	Co-administration with other medications can affect the cytochrome P450 (CYP) 2C9 enzyme function; thus, imrecoxib metabolism can be affected.	Imrecoxib	105-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-81
30017171-3	2018	The purpose of this research was to evaluate the effects of fluconazole, which is known to inhibit CYP2C9, on imrecoxib"s pharmacokinetic (PK) parameters.	Fluconazole	60-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
30017171-3	2018	The purpose of this research was to evaluate the effects of fluconazole, which is known to inhibit CYP2C9, on imrecoxib"s pharmacokinetic (PK) parameters.	Imrecoxib	110-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
30017171-14	2018	Hence, it is necessary to adjust the imrecoxib dose when it is concurrently used with other CYP2C9 inhibitors.	Imrecoxib	37-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
30415235-5	2018	CYP2C9 and VKORC1 polymorphisms are essential determinants in the genotype-guided dosing of warfarin and may distinguish patients who would benefit from switching to direct oral anticoagulants (DOACs).	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30415235-5	2018	CYP2C9 and VKORC1 polymorphisms are essential determinants in the genotype-guided dosing of warfarin and may distinguish patients who would benefit from switching to direct oral anticoagulants (DOACs).	doacs	194-199	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30065771-8	2018	It was indicated that low warfarin dose requirements are strongly associated with the presence of CYP2C9 and VKORC1-1639 variant alleles.	Warfarin	26-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
29621561-0	2018	Different inhibitory effects of azole-containing drugs and pesticides on CYP2C9 polymorphic forms: An in vitro study.	Azoles	32-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
29621561-4	2018	Due to the similarities in CYP organization throughout species, azoles can interact not only with the target fungal CYP51 substrate-binding site but can also modulate the catalytic activity of human cytochrome P450s, including CYP2C9, causing severe adverse effects.	Azoles	64-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	227-233
29621561-5	2018	In the present study the potency of azole-containing drugs and pesticides to inhibit recombinant wild-type CYP2C9*1 and the allelic variants CYP2C9*2 and CYP2C9*3 was evaluated.	Azoles	36-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
29621561-5	2018	In the present study the potency of azole-containing drugs and pesticides to inhibit recombinant wild-type CYP2C9*1 and the allelic variants CYP2C9*2 and CYP2C9*3 was evaluated.	Azoles	36-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
29621561-5	2018	In the present study the potency of azole-containing drugs and pesticides to inhibit recombinant wild-type CYP2C9*1 and the allelic variants CYP2C9*2 and CYP2C9*3 was evaluated.	Azoles	36-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
29621561-7	2018	Moreover, addition of cytochrome b5 resulted in a decrease of CYP2C9*3 activity to diclofenac in a concentration-dependent manner.	Diclofenac	83-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
29621561-8	2018	Increasing the knowledge of how azoles influence polymorphic variants of CYP2C9 could help individualize drug treatment, leading to optimization of the selection of drugs and doses for individuals based on genetic information.	Azoles	32-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
30065771-1	2018	Polymorphism in the genes encoding CYP2C9 enzyme and VKORC1 reductase significantly influence warfarin dose requirement since patients with CYP2C9*2, CYP2C9*3 and VKORC1 mutant alleles require lower warfarin maintenance doses.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
30065771-1	2018	Polymorphism in the genes encoding CYP2C9 enzyme and VKORC1 reductase significantly influence warfarin dose requirement since patients with CYP2C9*2, CYP2C9*3 and VKORC1 mutant alleles require lower warfarin maintenance doses.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
30065771-1	2018	Polymorphism in the genes encoding CYP2C9 enzyme and VKORC1 reductase significantly influence warfarin dose requirement since patients with CYP2C9*2, CYP2C9*3 and VKORC1 mutant alleles require lower warfarin maintenance doses.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
30065771-1	2018	Polymorphism in the genes encoding CYP2C9 enzyme and VKORC1 reductase significantly influence warfarin dose requirement since patients with CYP2C9*2, CYP2C9*3 and VKORC1 mutant alleles require lower warfarin maintenance doses.	Warfarin	199-207	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
30065771-1	2018	Polymorphism in the genes encoding CYP2C9 enzyme and VKORC1 reductase significantly influence warfarin dose requirement since patients with CYP2C9*2, CYP2C9*3 and VKORC1 mutant alleles require lower warfarin maintenance doses.	Warfarin	199-207	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
30065771-1	2018	Polymorphism in the genes encoding CYP2C9 enzyme and VKORC1 reductase significantly influence warfarin dose requirement since patients with CYP2C9*2, CYP2C9*3 and VKORC1 mutant alleles require lower warfarin maintenance doses.	Warfarin	199-207	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
30030468-0	2018	CYP2C9 and OATP1B1 genetic polymorphisms affect the metabolism and transport of glimepiride and gliclazide.	glimepiride	80-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30030468-6	2018	The clearance of glimepiride and gliclazide in CYP2C9*2 and *3 was significantly reduced compared to the wild-type.	glimepiride	17-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
30030468-0	2018	CYP2C9 and OATP1B1 genetic polymorphisms affect the metabolism and transport of glimepiride and gliclazide.	Gliclazide	96-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30030468-6	2018	The clearance of glimepiride and gliclazide in CYP2C9*2 and *3 was significantly reduced compared to the wild-type.	Gliclazide	33-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
30030468-2	2018	The aim of this study was to assess the effect of CYP2C9 and OATP1B1 genetic polymorphisms on the metabolism and transport of glimepiride and gliclazide.	glimepiride	126-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
30030468-7	2018	These findings collectively indicate that OATP1B1*5 and *15 and CYP2C9*2 and *3 have a significant effect on the transport and metabolism of glimepiride and gliclazide.	glimepiride	141-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
30030468-2	2018	The aim of this study was to assess the effect of CYP2C9 and OATP1B1 genetic polymorphisms on the metabolism and transport of glimepiride and gliclazide.	Gliclazide	142-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
30030468-7	2018	These findings collectively indicate that OATP1B1*5 and *15 and CYP2C9*2 and *3 have a significant effect on the transport and metabolism of glimepiride and gliclazide.	Gliclazide	157-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
30030468-5	2018	Glimepiride in the presence of CYP2C9*1, *2 and *3 recombinase had Vmax values of 21.58 +- 7.78, 15.69 +- 5.59, and 9.17 +- 3.03 nmol/min/mg protein, while gliclazide had Vmax values of 15.73 +- 3.11, 10.53 +- 4.06, and 6.21 +- 2.94 nmol/min/mg protein, respectively.	glimepiride	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
30030468-5	2018	Glimepiride in the presence of CYP2C9*1, *2 and *3 recombinase had Vmax values of 21.58 +- 7.78, 15.69 +- 5.59, and 9.17 +- 3.03 nmol/min/mg protein, while gliclazide had Vmax values of 15.73 +- 3.11, 10.53 +- 4.06, and 6.21 +- 2.94 nmol/min/mg protein, respectively.	Gliclazide	156-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
29781049-1	2018	PURPOSE: This study aimed to investigate relationships between times in therapeutic range (TTR) or warfarin sensitivity indexes (WSI) and VKORC1-1639G&gt;A and CYP2C9 polymorphisms in patients with left ventricular assist devices (LVAD).	Warfarin	99-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
30034221-0	2018	Does celecoxib inhibit agomelatine metabolism via CYP2C9 or CYP1A2?	Celecoxib	5-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
29377603-11	2018	The changes in the mean of the Cmax and AUCtau of celecoxib were greater in intermediate metabolizers of cytochrome 2C9 (CYP2C9) than in normal metabolizers.	Celecoxib	50-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
29794812-1	2018	: Mutations in the genes encoding vitamin K epoxide reductase complex subunit 1 (VKORC1) and cytochrome P450 2C9 (CYP2C9) largely contribute to the inter-individual variations in vitamin K antagonists (VKAs) dose requirements.	Vitamin K	34-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
29628024-0	2018	The association between CYP2C9/2C19 polymorphisms and phenytoin maintenance doses in Asian epileptic patients: A systematic review and meta-analysis : .	Phenytoin	54-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
29628024-5	2018	RevMan 5.2.3 software was used to analyze the relationship between CYP2C9/2C19 polymorphisms and PHT maintenance doses.	Phenytoin	97-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
29628024-9	2018	Patients with heterozygous CYP2C9 or both heterozygous CYP2C9 and CYP2C19 showed a trend but not a statistically-significant decrease of PHT dose, but dosage adjustment was recommended.	Phenytoin	137-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
29628024-9	2018	Patients with heterozygous CYP2C9 or both heterozygous CYP2C9 and CYP2C19 showed a trend but not a statistically-significant decrease of PHT dose, but dosage adjustment was recommended.	Phenytoin	137-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
29628024-10	2018	CONCLUSION: The meta-analysis indicates that CYP2C9 and CYP2C19 polymorphisms are associated with lower PHT maintenance dosage in Asian epileptic patients.	Phenytoin	104-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
29789925-0	2018	Associations of polymorphisms of CYP2D6 and CYP2C9 with early onset severe pre-eclampsia and response to labetalol therapy.	Labetalol	105-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
29789925-3	2018	The aim of this study was to evaluate the associations of polymorphisms of cytochrome P450, family 2, subfamily D, polypeptide 6 (CYP2D6) and cytochrome P450, family 2, subfamily C, polypeptide 9 (CYP2C9) with PPE and the relationship among CYP2D6, CYP2C9 polymorphisms and response to labetalol therapy.	Labetalol	286-295	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-195
29989011-7	2018	However, at 10 microM TQ, CYP2C9 enzyme activity was maximally inhibited by 69.69%, followed by CYP3A4 (23.59%) &gt; CYP1A2 (23.51%) &gt; CYP2D6 (11.42%).	thymoquinone	22-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
29578577-2	2018	Posaconazole (POS), a substrate of glucuronosyltransferase and P-glycoprotein, and voriconazole (VRC), a substrate of CYP2C9/19, are commonly administered to transplant recipients.	Voriconazole	83-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
29578577-2	2018	Posaconazole (POS), a substrate of glucuronosyltransferase and P-glycoprotein, and voriconazole (VRC), a substrate of CYP2C9/19, are commonly administered to transplant recipients.	Voriconazole	97-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
29578577-13	2018	These results suggest that letermovir may be a perpetrator of CYP2C9/19-mediated drug-drug interactions.	letermovir	27-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
29989011-1	2018	The aim of the present study was to investigate the potential effect of thymoquinone (TQ) on the metabolic activity of four major drug metabolizing enzymes in human liver microsomes, namely cytochrome P450 (CYP) 1A2, CYP2C9, CYP2D6 and CYP3A4.	thymoquinone	72-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	217-223
29989011-1	2018	The aim of the present study was to investigate the potential effect of thymoquinone (TQ) on the metabolic activity of four major drug metabolizing enzymes in human liver microsomes, namely cytochrome P450 (CYP) 1A2, CYP2C9, CYP2D6 and CYP3A4.	thymoquinone	86-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	217-223
29989011-2	2018	The inhibition of CYP enzymatic activities by TQ was evaluated by incubating typical substrates (phenacetin for CYP1A2, tolbutamide for CYP2C9, dextromethorphan for CYP2D6, and testosterone for CYP3A4) with human liver microsomes and NADPH in the absence or presence of TQ (1, 10 and 100 microM).	thymoquinone	46-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
29778033-3	2018	Polymorphisms in the vitamin K expoxide reductase 1 (VKORC1) and cytochrome P4502C9 (CYP2C9) genes have been reported to influence the warfarin dose.	Warfarin	135-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
29778033-4	2018	We investigated the effects of the VKORC1 and CYP2C9 genotypes on the warfarin dose in pediatric patients with giant CAAs after KD.	Warfarin	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
29778033-11	2018	Three patients with CYP2C9*1/*3 had a lower warfarin dose than did those with the wild CYP2C9*1/*1 genotype, but the difference did not reach significance (p &gt; 0.05).	Warfarin	44-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
29119333-5	2018	METHODS: A PBPK model was optimized in SimCYP  for tolbutamide as a CYP2C9 substrate, based on published in vitro and clinical data.	Tolbutamide	51-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
29620050-13	2018	Based on early reported human pharmacokinetics, drug interaction indices were 0.16 for CYP3A4 and 0.02 for CYP2C9, suggesting that anlotinib had a low propensity to precipitate drug interactions on these enzymes.	anlotinib	131-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
29119333-0	2018	Physiologically Based Pharmacokinetic Modelling of Cytochrome P450 2C9-Related Tolbutamide Drug Interactions with Sulfaphenazole and Tasisulam.	Tolbutamide	79-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-70
28737453-16	2018	Selexipag is an inhibitor of CYP2C8 and CYP2C9 and induces CYP3A4 and CYP2C9 in vitro.	selexipag	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
28737453-16	2018	Selexipag is an inhibitor of CYP2C8 and CYP2C9 and induces CYP3A4 and CYP2C9 in vitro.	selexipag	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
28520347-0	2012	Warfarin Therapy and the Genotypes CYP2C9 and VKORC1 Warfarin is an anticoagulant that acts by reducing the activity of vitamin K-dependent clotting factors.	Vitamin K	120-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
28520347-3	2012	A patient"s CYP2C9 and VKORC1 genotype can be used to help determine the optimal starting dose of warfarin.	Warfarin	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
28520347-4	2012	The CYP2C9 gene encodes one of the main enzymes involved in the metabolism of warfarin.	Warfarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
28520347-5	2012	Several variant CYP2C9 alleles are associated with reduced enzyme activity and lower clearance rates of warfarin.	Warfarin	104-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
28520347-6	2012	Patients who carry at least one copy of such a variant allele (such as CYP2C9*2 and CYP2C9*3) have reduced metabolism leading to higher warfarin concentrations.	Warfarin	136-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
28520347-6	2012	Patients who carry at least one copy of such a variant allele (such as CYP2C9*2 and CYP2C9*3) have reduced metabolism leading to higher warfarin concentrations.	Warfarin	136-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
28520347-7	2012	On average, they require a lower daily warfarin dose than patients who are homozygous for the wild-type CYP2C9*1 allele.	Warfarin	39-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
28520347-10	2012	The FDA-approved warfarin drug label provides a dosing table based on CYP2C9 and VKORC1 genotypes (Table 1).	Warfarin	17-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
29710546-0	2018	Pharmacokinetic interaction of diosmetin and silibinin with other drugs: Inhibition of CYP2C9-mediated biotransformation and displacement from serum albumin.	diosmetin	31-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
29710546-0	2018	Pharmacokinetic interaction of diosmetin and silibinin with other drugs: Inhibition of CYP2C9-mediated biotransformation and displacement from serum albumin.	Silybin	45-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
29710546-5	2018	In this study, the inhibitory action of DIO and SIL on CYP2C9-catalyzed metabolism of diclofenac to 4"-hydroxydiclofenac was examined, using warfarin as a positive control.	diosmetin	40-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
29710546-5	2018	In this study, the inhibitory action of DIO and SIL on CYP2C9-catalyzed metabolism of diclofenac to 4"-hydroxydiclofenac was examined, using warfarin as a positive control.	Diclofenac	86-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
29710546-5	2018	In this study, the inhibitory action of DIO and SIL on CYP2C9-catalyzed metabolism of diclofenac to 4"-hydroxydiclofenac was examined, using warfarin as a positive control.	4'-hydroxydiclofenac	100-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
29710546-5	2018	In this study, the inhibitory action of DIO and SIL on CYP2C9-catalyzed metabolism of diclofenac to 4"-hydroxydiclofenac was examined, using warfarin as a positive control.	Warfarin	141-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
29710546-7	2018	It is demonstrated that DIO and SIL are potent inhibitors of CYP2C9 enzyme and are able to displace the Site I ligand warfarin from human serum albumin.	diosmetin	24-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
29710546-7	2018	It is demonstrated that DIO and SIL are potent inhibitors of CYP2C9 enzyme and are able to displace the Site I ligand warfarin from human serum albumin.	Silybin	32-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
29710546-7	2018	It is demonstrated that DIO and SIL are potent inhibitors of CYP2C9 enzyme and are able to displace the Site I ligand warfarin from human serum albumin.	Warfarin	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
29119333-0	2018	Physiologically Based Pharmacokinetic Modelling of Cytochrome P450 2C9-Related Tolbutamide Drug Interactions with Sulfaphenazole and Tasisulam.	Sulfaphenazole	114-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-70
29119333-0	2018	Physiologically Based Pharmacokinetic Modelling of Cytochrome P450 2C9-Related Tolbutamide Drug Interactions with Sulfaphenazole and Tasisulam.	N-((5-bromo-2-thienyl)sulfonyl)-2,4-dichlorobenzamide	133-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-70
29119333-11	2018	CONCLUSIONS: This optimized tolbutamide PBPK model was verified with two strong CYP2C9 inhibitors and can be applied to the prediction of CYP2C9 interactions for novel inhibitors.	Tolbutamide	28-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
29119333-2	2018	Previously published physiologically based pharmacokinetic (PBPK) models of tolbutamide are based on an assumption that its metabolic clearance is exclusively through CYP2C9; however, many studies indicate that CYP2C9 metabolism is only responsible for 80-90% of the total clearance.	Tolbutamide	76-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
29119333-11	2018	CONCLUSIONS: This optimized tolbutamide PBPK model was verified with two strong CYP2C9 inhibitors and can be applied to the prediction of CYP2C9 interactions for novel inhibitors.	Tolbutamide	28-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
29119333-2	2018	Previously published physiologically based pharmacokinetic (PBPK) models of tolbutamide are based on an assumption that its metabolic clearance is exclusively through CYP2C9; however, many studies indicate that CYP2C9 metabolism is only responsible for 80-90% of the total clearance.	Tolbutamide	76-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	211-217
29746595-2	2018	The allelic variant CYP2C9*30 (A477T) is associated to diminished response to the antihypertensive effects of the prodrug losartan and affected metabolism of other drugs.	Losartan	122-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
29119333-4	2018	This paper describes the development and verification of SimCYP -based PBPK models that accurately describe the human pharmacokinetics of tolbutamide when dosed alone or in combination with the CYP2C9 inhibitors sulfaphenazole and tasisulam.	Tolbutamide	138-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	194-200
29274302-0	2018	Association of CYP2C9*3 with phenytoin-induced Stevens-Johnson syndrome and toxic epidermal necrolysis: A systematic review and meta-analysis.	Phenytoin	29-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
29274302-3	2018	The aim of this meta-analysis was to evaluate the association between CYP2C9*3 and PHT-induced SJS/TEN.	Phenytoin	83-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
29274302-5	2018	Studies exploring the relationship between CYP2C9*3 and PHT-induced SJS and TEN were included.	Phenytoin	56-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
29274302-10	2018	WHAT IS NEW AND CONCLUSION: A significant association between CYP2C9*3 and PHT-induced SJS/TEN was identified, especially in a Thai population.	Phenytoin	75-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
29274302-11	2018	CYP2C9*3 is thus a credible predictive genetic marker of PHT-induced SJS/TEN.	Phenytoin	57-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
29530595-6	2018	Here, pulsed and continuous wave (CW) EPR demonstrate that water-bridged complexes are remarkably common among a range of nitrogenous drugs or drug fragments that bind to CYP3A4 or CYP2C9.	Water	59-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
29880089-1	2018	In chronic kidney disease (CKD) patients, the ratio of warfarin enantiomers is changed and becomes unstable due to a reduction of cytochrome P450 (CYP) 2C9 activity of, which contributes to the development of hemorrhagic complications.	Warfarin	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-155
29538081-8	2018	RECENT FINDINGS: DAH has been associated with the presence of variant alleles in vitamin K epoxide reductase complex 1, cytochrome P450 (CYP)2C9 and CYP2C19 genes.	dah	17-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-144
29475833-1	2018	Bosentan is a substrate of hepatic uptake transporter organic anion-transporting polypeptides (OATPs), and undergoes extensive hepatic metabolism by cytochrome P450 (P450), namely, CYP3A4 and CYP2C9.	Bosentan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	192-198
29368187-1	2018	PURPOSE: The objective of this study is to assess the effects of green tea and its major catechin component, (-)-epigallocatechin gallate (EGCG), on CYP2C9-mediated substrate metabolism in vitro, and the pharmacokinetics of fluvastatin in healthy volunteers.	Catechin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
28401802-12	2018	This study found that routine medication with warfarin provides significantly different levels of anticoagulant control between patients with wild-type genotypes and patients with heterozygous polymorphism genotypes of VKORC1 rs9923231 or CYP2C9 rs1057910.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	239-245
28401802-13	2018	Patients with heterozygous polymorphism genotypes of VKORC1 or CYP2C9 require genotype-directed therapy with warfarin to increase efficacy and safety in anticoagulant treatment.	Warfarin	109-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
28401802-1	2018	Differences in warfarin maintenance dosages based on the presence of polymorphisms in VKORC1, CYP2C9, CYP4F2, and ORM1 can be determined through dosage adjustment according to routine guidelines.	Warfarin	15-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
29368187-1	2018	PURPOSE: The objective of this study is to assess the effects of green tea and its major catechin component, (-)-epigallocatechin gallate (EGCG), on CYP2C9-mediated substrate metabolism in vitro, and the pharmacokinetics of fluvastatin in healthy volunteers.	epigallocatechin gallate	109-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
29368187-1	2018	PURPOSE: The objective of this study is to assess the effects of green tea and its major catechin component, (-)-epigallocatechin gallate (EGCG), on CYP2C9-mediated substrate metabolism in vitro, and the pharmacokinetics of fluvastatin in healthy volunteers.	epigallocatechin gallate	139-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
29368187-2	2018	METHODS: The metabolism of diclofenac and fluvastatin in human recombinant CYP2C9 was investigated in the presence of EGCG.	Diclofenac	27-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
29368187-2	2018	METHODS: The metabolism of diclofenac and fluvastatin in human recombinant CYP2C9 was investigated in the presence of EGCG.	Fluvastatin	42-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
29368187-2	2018	METHODS: The metabolism of diclofenac and fluvastatin in human recombinant CYP2C9 was investigated in the presence of EGCG.	epigallocatechin gallate	118-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
29368187-9	2018	CONCLUSIONS: Although in vitro studies indicated that EGCG and brewed green tea produce significant inhibitory effects on CYP2C9 activity, the concomitant administration of green tea and fluvastatin in healthy volunteers did not influence the pharmacokinetics of fluvastatin.	epigallocatechin gallate	54-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
29596975-4	2018	CYP2C9, CYP3A4, and CYP3A5 were involved in the formation of FMS S-oxide, which was further metabolized to BR-A-557 by CYP3A4/5.	Oxides	65-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
29596975-5	2018	CYP2C9 played an exclusive role in n-butyl hydroxylation.	Nitrogen	15-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
29596975-9	2018	In addition, simultaneous determination of the FMS metabolites may be used to evaluate CYP2C9 and CYP3A4/5 activity.	fimasartan	47-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
29522717-0	2018	Altered metabolism of synthetic cannabinoid JWH-018 by human cytochrome P450 2C9 and variants.	1-pentyl-3-(1-naphthoyl)indole	44-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-80
29724296-2	2018	METHOD: A total of 22 patients who required an extreme warfarin dosage from VKORC1 -1639AA &amp; CYP2C9*1*1 genotype group were enrolled in this study.	Warfarin	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
29522717-3	2018	The major enzyme involved in the metabolism of JWH-018 is CYP2C9, a highly polymorphic enzyme found largely in the intestines and liver, with *1 being designated as the wild type, and *2 and *3 as the two most common variants.	(4-methyl-1-naphthyl)-(1-pentylindol-3-yl)methanone	47-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
29522717-6	2018	Here, in vitro enzyme kinetic assays performed with human recombinant CYP2C9 variants (*1, *2, and *3) revealed that oxidative metabolism by CYP2C9*3 resulted in significantly less formation of (omega)-OH and (omega-1)-OH metabolites.	(omega)-oh	194-204	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
29522717-6	2018	Here, in vitro enzyme kinetic assays performed with human recombinant CYP2C9 variants (*1, *2, and *3) revealed that oxidative metabolism by CYP2C9*3 resulted in significantly less formation of (omega)-OH and (omega-1)-OH metabolites.	(omega)-oh	194-204	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
29522717-6	2018	Here, in vitro enzyme kinetic assays performed with human recombinant CYP2C9 variants (*1, *2, and *3) revealed that oxidative metabolism by CYP2C9*3 resulted in significantly less formation of (omega)-OH and (omega-1)-OH metabolites.	(omega-1)-oh	209-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
29522717-6	2018	Here, in vitro enzyme kinetic assays performed with human recombinant CYP2C9 variants (*1, *2, and *3) revealed that oxidative metabolism by CYP2C9*3 resulted in significantly less formation of (omega)-OH and (omega-1)-OH metabolites.	(omega-1)-oh	209-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
29522717-7	2018	Surprisingly, CYP2C9*2 was roughly 3.6-fold more efficient as the CYP2C9*1 enzyme based on Vmax/Km, increasing the rate of JWH-018 metabolism and allowed for a much more rapid elimination.	(4-methyl-1-naphthyl)-(1-pentylindol-3-yl)methanone	123-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
29522717-7	2018	Surprisingly, CYP2C9*2 was roughly 3.6-fold more efficient as the CYP2C9*1 enzyme based on Vmax/Km, increasing the rate of JWH-018 metabolism and allowed for a much more rapid elimination.	(4-methyl-1-naphthyl)-(1-pentylindol-3-yl)methanone	123-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
29622878-0	2018	The Influence of CYP2C9 and VKORC1 Gene Polymorphisms on the Response to Warfarin in Egyptians.	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
29488228-4	2018	Utilizing valsartan hydroxylase assay as probe, all forms of glucosamine and chondroitin exhibited IC50 values beyond 1000 muM, indicating very weak potential in inhibiting CYP2C9.	Glucosamine	61-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	173-179
29488228-4	2018	Utilizing valsartan hydroxylase assay as probe, all forms of glucosamine and chondroitin exhibited IC50 values beyond 1000 muM, indicating very weak potential in inhibiting CYP2C9.	Chondroitin	77-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	173-179
29273968-3	2018	SimCYP, a physiologically based PK model, was developed and used to predict the effects of fluconazole and CYP2C9 genetic polymorphism on siponimod metabolism.	siponimod	138-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
29273968-5	2018	RESULTS: Correlation analysis suggested that CYP2C9 is the main enzyme responsible for siponimod metabolism in humans.	siponimod	87-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
29273968-6	2018	Compared with the CYP2C9*1/*1 genotype, HLM incubations from CYP2C9*3/*3 and CYP2C9*2/*2 donors showed ~ 10- and 3-fold decrease in siponimod metabolism, respectively.	siponimod	132-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
29273968-6	2018	Compared with the CYP2C9*1/*1 genotype, HLM incubations from CYP2C9*3/*3 and CYP2C9*2/*2 donors showed ~ 10- and 3-fold decrease in siponimod metabolism, respectively.	siponimod	132-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
29273968-7	2018	Simulations of enzyme contribution predicted that in the CYP2C9*1/*1 genotype, CYP2C9 is predominantly responsible for siponimod metabolism (~ 81%), whereas in the CYP2C9*3/*3 genotype, its contribution is reduced to 11%.	siponimod	119-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
29273968-7	2018	Simulations of enzyme contribution predicted that in the CYP2C9*1/*1 genotype, CYP2C9 is predominantly responsible for siponimod metabolism (~ 81%), whereas in the CYP2C9*3/*3 genotype, its contribution is reduced to 11%.	siponimod	119-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
29273968-7	2018	Simulations of enzyme contribution predicted that in the CYP2C9*1/*1 genotype, CYP2C9 is predominantly responsible for siponimod metabolism (~ 81%), whereas in the CYP2C9*3/*3 genotype, its contribution is reduced to 11%.	siponimod	119-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
29273968-8	2018	The predicted exposure increase of siponimod with fluconazole 200 mg was 2.0-2.4-fold for CYP2C9*1/*1 genotype.	siponimod	35-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
29622878-3	2018	Cytochrome P-450 2C9 is the principle enzyme that terminates the anticoagulant effect of warfarin by catalyzing the conversion of the pharmacologically more potent S-enantiomer to its inactive metabolites.	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-20
29273968-8	2018	The predicted exposure increase of siponimod with fluconazole 200 mg was 2.0-2.4-fold for CYP2C9*1/*1 genotype.	Fluconazole	50-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
29273968-12	2018	In silico simulation predicted a significant reduction in siponimod clearance in the CYP2C9*2/*2 and CYP2C9*3/*3 genotypes based on the in vitro metabolism data; the predicted exposure was close (within 30%) to the observed results for the CYP2C9*2/*3 and CYP2C9*3/*3 genotypes.	siponimod	58-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
29622878-6	2018	The current study aimed to investigate the pharmacogenetic effect of CYP2C9 and VKORC1 gene polymorphisms on the patients response to warfarin.	Warfarin	134-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
29273968-12	2018	In silico simulation predicted a significant reduction in siponimod clearance in the CYP2C9*2/*2 and CYP2C9*3/*3 genotypes based on the in vitro metabolism data; the predicted exposure was close (within 30%) to the observed results for the CYP2C9*2/*3 and CYP2C9*3/*3 genotypes.	siponimod	58-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
29622878-19	2018	Data from our study suggest that together with clinical factors, VKORC1 and CYP2C9 polymorphisms are important contributors to warfarin dosing and may help predict adverse effects in Egyptian patients.	Warfarin	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
29273968-12	2018	In silico simulation predicted a significant reduction in siponimod clearance in the CYP2C9*2/*2 and CYP2C9*3/*3 genotypes based on the in vitro metabolism data; the predicted exposure was close (within 30%) to the observed results for the CYP2C9*2/*3 and CYP2C9*3/*3 genotypes.	siponimod	58-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
29273968-12	2018	In silico simulation predicted a significant reduction in siponimod clearance in the CYP2C9*2/*2 and CYP2C9*3/*3 genotypes based on the in vitro metabolism data; the predicted exposure was close (within 30%) to the observed results for the CYP2C9*2/*3 and CYP2C9*3/*3 genotypes.	siponimod	58-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
29623958-0	2018	Correction to: The Influence of CYP2C9 and VKORC1 Gene Polymorphisms on the Response to Warfarin in Egyptians.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
29563776-4	2018	In an in vitro study, celecoxib with a series of concentrations was added to an incubation mixture containing recombinant human CYP2C9, human or rat liver microsomes to determine the half-maximal inhibitory concentration on the metabolism of agomelatine.	Celecoxib	22-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
29636628-0	2018	CYP2C9 polymorphisms in epilepsy: influence on phenytoin treatment.	Phenytoin	47-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
29636628-3	2018	Genetic polymorphism of CYP2C9 may reduce the metabolism of PHT by 25-50% in patients with variants *2 and *3 compared to those with wild-type variant *1.	Phenytoin	60-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
29636628-7	2018	The presence of HLA-B*15:02 and CYP2C9 *2 or *3 in the same patient increases the risk of Stevens-Johnson syndrome and toxic epidermal necrolysis; hence, PHT should not be prescribed in these patients.	Phenytoin	154-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
29636628-8	2018	In patients with CYP2C9 *1/*2 or *1/*3 alleles (intermediate metabolizers), the usual PHT maintenance dose (5-10 mg/kg/day) must be reduced by 25%, and in those with CYP2C9 *2/*2, *2/*3 or *3/*3 alleles (poor metabolizers), the dose must be reduced by 50%.	Phenytoin	86-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
29636628-10	2018	In this paper, we aim to review the influence of CYP2C9 polymorphism on the metabolization of PHT and the clinical implications of poor metabolization in the treatment of epilepsies.	Phenytoin	94-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
29563776-5	2018	Moreover, a mechanism study was performed to determine the inhibitory effect of celecoxib on CYP2C9.	Celecoxib	80-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
29433307-2	2018	Cytochrome P450 2C9 ( CYP2C9) genotype-guided warfarin dosing is recommended in the clinic, given the more potent S-warfarin is primarily metabolized by CYP2C9.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
29563776-7	2018	In addition, celecoxib inhibited the metabolism of agomelatine in the in vitro studies, which was determined to be by a competitive mechanism on CYP2C9.	Celecoxib	13-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
29563776-7	2018	In addition, celecoxib inhibited the metabolism of agomelatine in the in vitro studies, which was determined to be by a competitive mechanism on CYP2C9.	agomelatine	51-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
29433307-2	2018	Cytochrome P450 2C9 ( CYP2C9) genotype-guided warfarin dosing is recommended in the clinic, given the more potent S-warfarin is primarily metabolized by CYP2C9.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
29433307-2	2018	Cytochrome P450 2C9 ( CYP2C9) genotype-guided warfarin dosing is recommended in the clinic, given the more potent S-warfarin is primarily metabolized by CYP2C9.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
29433307-2	2018	Cytochrome P450 2C9 ( CYP2C9) genotype-guided warfarin dosing is recommended in the clinic, given the more potent S-warfarin is primarily metabolized by CYP2C9.	Warfarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
29433307-2	2018	Cytochrome P450 2C9 ( CYP2C9) genotype-guided warfarin dosing is recommended in the clinic, given the more potent S-warfarin is primarily metabolized by CYP2C9.	Warfarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
29433307-2	2018	Cytochrome P450 2C9 ( CYP2C9) genotype-guided warfarin dosing is recommended in the clinic, given the more potent S-warfarin is primarily metabolized by CYP2C9.	Warfarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
29433307-3	2018	However, only about 20-30% of interpatient variability in S-warfarin clearance is associated with CYP2C9 genotype.	Warfarin	60-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
29105855-0	2018	Dicloxacillin induces CYP2C19, CYP2C9 and CYP3A4 in vivo and in vitro.	Dicloxacillin	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
27879469-11	2018	Although Cytochrome P450 2C9 (CYP2C9) and VKORC1 polymorphisms together attributed only 3.8% variability in warfarin dose but it was statistically significant ( p value = .004).	Warfarin	108-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-28
29353070-2	2018	Cytochrome P450 2C9 (CYP2C9) plays the key role in transformation of coumarin and thus, influences determination of warfarin dosage.	coumarin	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
29353070-2	2018	Cytochrome P450 2C9 (CYP2C9) plays the key role in transformation of coumarin and thus, influences determination of warfarin dosage.	coumarin	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
29353070-2	2018	Cytochrome P450 2C9 (CYP2C9) plays the key role in transformation of coumarin and thus, influences determination of warfarin dosage.	Warfarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
29353070-2	2018	Cytochrome P450 2C9 (CYP2C9) plays the key role in transformation of coumarin and thus, influences determination of warfarin dosage.	Warfarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
29353070-3	2018	A number of factors including dietary compounds such as sesamin, caffeic acid and ferulic acids can regulate the activity of CYP2C9.	sesamin	56-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
29353070-3	2018	A number of factors including dietary compounds such as sesamin, caffeic acid and ferulic acids can regulate the activity of CYP2C9.	caffeic acid	65-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
29353070-3	2018	A number of factors including dietary compounds such as sesamin, caffeic acid and ferulic acids can regulate the activity of CYP2C9.	ferulic acid	82-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
29353070-4	2018	The present study tested the hypothesis that sesamin, episesamin, caffeic acid and ferulic acid decreases the rate of warfarin 7-hydroxylation via inhibition of hepatic CYP2C9.	sesamin	45-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
29353070-4	2018	The present study tested the hypothesis that sesamin, episesamin, caffeic acid and ferulic acid decreases the rate of warfarin 7-hydroxylation via inhibition of hepatic CYP2C9.	sesamin	54-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
27879469-11	2018	Although Cytochrome P450 2C9 (CYP2C9) and VKORC1 polymorphisms together attributed only 3.8% variability in warfarin dose but it was statistically significant ( p value = .004).	Warfarin	108-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
29353070-4	2018	The present study tested the hypothesis that sesamin, episesamin, caffeic acid and ferulic acid decreases the rate of warfarin 7-hydroxylation via inhibition of hepatic CYP2C9.	caffeic acid	66-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
28049362-5	2018	Five variables, that is, VKORC1-1639 G&gt;A, CYP2C9*2, CYP2C9*3, age, and diet, were found to be significantly associated with warfarin response in univariate analysis.	Warfarin	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
29353070-4	2018	The present study tested the hypothesis that sesamin, episesamin, caffeic acid and ferulic acid decreases the rate of warfarin 7-hydroxylation via inhibition of hepatic CYP2C9.	ferulic acid	83-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
28049362-5	2018	Five variables, that is, VKORC1-1639 G&gt;A, CYP2C9*2, CYP2C9*3, age, and diet, were found to be significantly associated with warfarin response in univariate analysis.	Warfarin	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
29404794-3	2018	RESULTS: Investigated steroids usually reveal a high gastrointestinal absorption and a good oral bioavailability, may inhibit someof the human cytochromes involved in the metabolism of xenobiotics (CYP2C9 being the most affected) and reflect a good capacity for skin penetration.	Steroids	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	198-204
29326367-0	2018	Organic Anion Transporter 2 Mediates Hepatic Uptake of Tolbutamide, a CYP2C9 Probe Drug.	Tolbutamide	55-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
29326367-1	2018	Tolbutamide is primarily metabolized by CYP2C9, and, thus, is frequently applied as a clinical probe substrate for CYP2C9 activity.	Tolbutamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
29326367-1	2018	Tolbutamide is primarily metabolized by CYP2C9, and, thus, is frequently applied as a clinical probe substrate for CYP2C9 activity.	Tolbutamide	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
29326367-9	2018	In contrast to the rapid equilibrium (CYP2C9-only) model, the permeability-limited (OAT2-CYP2C9 interplay) model better described the plasma concentration-time profiles of tolbutamide.	Tolbutamide	172-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
29326367-10	2018	Additionally, the latter well described tolbutamide pharmacokinetics in carriers of CYP2C9 genetic variants and quantitatively rationalized its known drug-drug interactions.	Tolbutamide	40-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
29568565-1	2018	Aim: To evaluate applicability of CYP2C9*2, *3 and VKORC1-1639G &gt; A based algorithm to predict warfarin stable dose (WSD) in a group of Palestinian patients.	Warfarin	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
29305929-5	2018	The production of 11-hydroxylauric acid was mediated by CYP2E1, CYP2C9, CYP2B6, CYP1A2, CYP3A4, and CYP4A11.	11-hydroxydodecanoic acid	18-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
29168292-0	2018	Evaluation of the effect of quercetin treatment on CYP2C9 enzyme activity of diclofenac in healthy human volunteers.	Quercetin	28-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
29168292-0	2018	Evaluation of the effect of quercetin treatment on CYP2C9 enzyme activity of diclofenac in healthy human volunteers.	Diclofenac	77-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
29168292-9	2018	The results suggest that quercetin might have inhibited CYP2C9-mediated metabolism of DIC.	Quercetin	25-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
29314710-8	2018	Second, enzyme kinetic studies showed that the initial metabolic steps were formed by cytochrome P450 isoforms (CYP) CYP1A2, CYP2B6, CYP2C9, CYP2C19, CYP2D6, and CYP3A4 resulting in pyrrolidine, thiophene or alkyl hydroxy metabolites depending on the length of the alkyl chain.	pyrrolidine	182-193	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
29314710-8	2018	Second, enzyme kinetic studies showed that the initial metabolic steps were formed by cytochrome P450 isoforms (CYP) CYP1A2, CYP2B6, CYP2C9, CYP2C19, CYP2D6, and CYP3A4 resulting in pyrrolidine, thiophene or alkyl hydroxy metabolites depending on the length of the alkyl chain.	Thiophenes	195-204	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
30135636-10	2018	CYP2C9 is a major enzyme responsible for the metabolism of phenytoin.	Phenytoin	59-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
28656666-1	2018	Data on the association of CYP2C9 genetic polymorphisms with sulfonylurea (SU)-induced hypoglycaemia (SH) are inconsistent.	Sulfonylurea Compounds	61-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
29542427-9	2018	Meanwhile, all individual biomarkers showed no, less or moderate inhibitory effect towards all the tested CYP450 except for curcumin that showed inhibition of CYP2C8 (91%), CYP2C9 (81%) and CYP2C19 (72%) at 10microM.	Curcumin	124-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	173-179
29542427-10	2018	CONCLUSION: Curcumin was found to be an active constituent that might contribute to the inhibition of SynacinnTM against CYP2C8, CYP2C9 and CYP2C19.	Curcumin	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
29760340-5	2018	The age and SNPs in VKORC1 and CYP2C9 were significantly associated with the weekly acenocoumarol dose requirement (p = 0.023, p = 0.0001 and p = 0.001 respectively).	Acenocoumarol	84-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
29760340-7	2018	Non-parametric analysis confirmed the accumulate effect of variant alleles at VKORC1 -1639 G&gt;A, VKORC1 1173 C&gt;T and CYP2C9 SNPs on the acenocoumarol dose requirement.	Acenocoumarol	141-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
29760340-9	2018	The multiple linear regression analysis showed that mutation in VKORC1 -1639, VKORC1 1173 SNPs, or in CYP2C9 haplotype reduces the mean acenocoumarol weekly dose to 25.4%, 23.4% and 6.2%, respectively.	Acenocoumarol	136-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
30117405-8	2018	CYP2C9 was inhibited by triclabendazole, triclabendazole sulfoxide, triclabendazole sulfone, montelukast, montelukast sulfoxide and montelukast sulfone with IC50 of 1.17 microM, 1.95 microM, 0.69 microM, 1.34 microM, 3.61 microM and 2.15 microM, respectively.	Triclabendazole	24-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30117405-8	2018	CYP2C9 was inhibited by triclabendazole, triclabendazole sulfoxide, triclabendazole sulfone, montelukast, montelukast sulfoxide and montelukast sulfone with IC50 of 1.17 microM, 1.95 microM, 0.69 microM, 1.34 microM, 3.61 microM and 2.15 microM, respectively.	triclabendazole sulfoxide	41-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30117405-8	2018	CYP2C9 was inhibited by triclabendazole, triclabendazole sulfoxide, triclabendazole sulfone, montelukast, montelukast sulfoxide and montelukast sulfone with IC50 of 1.17 microM, 1.95 microM, 0.69 microM, 1.34 microM, 3.61 microM and 2.15 microM, respectively.	Triclabendazole sulfone	68-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30117405-8	2018	CYP2C9 was inhibited by triclabendazole, triclabendazole sulfoxide, triclabendazole sulfone, montelukast, montelukast sulfoxide and montelukast sulfone with IC50 of 1.17 microM, 1.95 microM, 0.69 microM, 1.34 microM, 3.61 microM and 2.15 microM, respectively.	montelukast	93-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30117405-8	2018	CYP2C9 was inhibited by triclabendazole, triclabendazole sulfoxide, triclabendazole sulfone, montelukast, montelukast sulfoxide and montelukast sulfone with IC50 of 1.17 microM, 1.95 microM, 0.69 microM, 1.34 microM, 3.61 microM and 2.15 microM, respectively.	Montelukast sulfoxide	106-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
30117405-8	2018	CYP2C9 was inhibited by triclabendazole, triclabendazole sulfoxide, triclabendazole sulfone, montelukast, montelukast sulfoxide and montelukast sulfone with IC50 of 1.17 microM, 1.95 microM, 0.69 microM, 1.34 microM, 3.61 microM and 2.15 microM, respectively.	Montelukast Sulfone	132-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
28656666-1	2018	Data on the association of CYP2C9 genetic polymorphisms with sulfonylurea (SU)-induced hypoglycaemia (SH) are inconsistent.	Sulfonylurea Compounds	75-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
28656666-6	2018	The number of CYP2C9 deficient alleles was associated with nearly three-fold higher odds of hypoglycaemia (OR, 2.81; 95% CI, 1.30-6.09; P = .009) and better response to SU treatment (beta, -0.218; SE, 0.074; P = .003) only in patients carrying the POR*1/*1 genotype.	Sulfonylurea Compounds	169-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
28656666-7	2018	Our results indicate that interaction between CYP2C9 and POR genes may be an important determinant of efficacy and severe adverse effects of SU treatment.	Sulfonylurea Compounds	141-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
27958378-4	2018	In ancestry-specific meta-analyses, eight novel pharmacogenomic loci met the threshold for genome-wide significance (P&lt;5 x 10-8), and a pharmacokinetic variant in CYP2C9 (rs1057910) that has been associated with sulfonylurea-related treatment effects and other adverse drug reactions in previous studies was replicated.	Sulfonylurea Compounds	215-227	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	166-172
29182754-1	2017	Many lines of evidence suggest that warfarin dosing variability is significantly associated with cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) variant alleles.	Warfarin	36-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-116
29283396-6	2017	Warfarin is the most well studied CYP2C9 substrate; recent work on use of dosing algorithms that include CYP2C9 genotype to improve patient safety during initiation of warfarin dosing are reviewed and prospects for their clinical implementation considered.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
29283396-6	2017	Warfarin is the most well studied CYP2C9 substrate; recent work on use of dosing algorithms that include CYP2C9 genotype to improve patient safety during initiation of warfarin dosing are reviewed and prospects for their clinical implementation considered.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
29283396-6	2017	Warfarin is the most well studied CYP2C9 substrate; recent work on use of dosing algorithms that include CYP2C9 genotype to improve patient safety during initiation of warfarin dosing are reviewed and prospects for their clinical implementation considered.	Warfarin	168-176	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
29252193-1	2017	BACKGROUND: We have earlier developed a pharmacogenomic algorithm for acenocoumarol dose prediction in Greek patients that included CYP2C9/VKORC1 genetic information.	Acenocoumarol	70-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
29393278-5	2018	In general, ordonin has induced effects on the major member of CYP450s mRNA and protein expression, as well as on the enzyme activity in human HepaRG cells, especially on CYP3A4 and CYP2C9.	ordonin	12-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	182-188
29503429-5	2018	Whereas sesamin metabolism is mainly mediated by CYP2C9 in human liver, sesamin causes a mechanism-based inhibition (MBI) of CYP2C9.	sesamin	72-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
29503429-6	2018	However, we found that the metabolite-intermediate complex between CYP2C9 and sesamin was unstable, and the effects of sesamin appeared to be minimal.	sesamin	78-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
29252193-7	2017	For CYP4F2, significant effects were found on patients" ability to reach stable dose and on acenocoumarol dose requirements when CYP2C9/VKORC1 sub-phenotypes were analyzed.	Acenocoumarol	92-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
29252193-9	2017	Additionally, in CYP2C9 intermediate metabolizers (IMs), after adjusting for age, weight, and VKORC1 genotypes, CYP4F2 genotypes were significantly associated with acenocoumarol stable dose (beta: 0.07; 95% CI: 0.006-0.134; p=0.033).	Acenocoumarol	164-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
29182754-1	2017	Many lines of evidence suggest that warfarin dosing variability is significantly associated with cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) variant alleles.	Warfarin	36-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
29182754-5	2017	We also found that patients with CYP2C9 *1 and VKORC1 -1639G alleles required the highest dosages of warfarin, while the carriers of CYP2C9 variant *2 and *3 alleles and VKORC1 -1639A required less warfarin.	Warfarin	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
29182754-5	2017	We also found that patients with CYP2C9 *1 and VKORC1 -1639G alleles required the highest dosages of warfarin, while the carriers of CYP2C9 variant *2 and *3 alleles and VKORC1 -1639A required less warfarin.	Warfarin	198-206	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
29182754-5	2017	We also found that patients with CYP2C9 *1 and VKORC1 -1639G alleles required the highest dosages of warfarin, while the carriers of CYP2C9 variant *2 and *3 alleles and VKORC1 -1639A required less warfarin.	Warfarin	198-206	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
29182754-6	2017	Univariate regression analysis showed that age and presence of CYP2C9 *2 allele significantly influenced the daily warfarin dose requirement.	Warfarin	115-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
29182754-7	2017	Our findings provide additional evidence to support the hypothesis that CYP2C9*2 (430C/T), *3 (1075A/C) and VKORC1 (-1639G/A) polymorphisms explain a considerable proportion of interindividual variability in warfarin dose.	Warfarin	208-216	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
29148818-0	2017	Dissociation Constants of Cytochrome P450 2C9/Cytochrome P450 Reductase Complexes in a Lipid Bilayer Membrane Depend on NADPH: A Single-Protein Tracking Study.	NADP	120-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-45
29148818-7	2017	An Arrhenius analysis of diffusion constants was also carried out, demonstrating that the reduced forms of CPR and CYP2C9 interact differently with the biomimetic ER and may, in addition to protein conformational changes, contribute to the observed NADPH-dependent shift in Kd.	NADP	249-254	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
28686288-2	2017	This study describes the differential distribution of amino acid substitution variants of CYP2C8 (*2-I269F &amp; *3-R139K) and CYP2C9 (*2-C144R &amp; *3-L359A) genes in 234 type 2 diabetes mellitus (T2DM) patients and 218 healthy controls from Andhra Pradesh, South India.	Adenosine Monophosphate	145-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-133
29137842-8	2017	Extensive metabolism of cetrozole and TMD-322 was observed in the CYP2C19 expression system among the test CYP isoforms (CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4).	cetrozole	24-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
29055218-0	2017	CYP2C9 and VKORC1 in therapeutic dosing and safety of acenocoumarol treatment: implication for clinical practice in Hungary.	Acenocoumarol	54-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
29055218-1	2017	The purpose of this work was to investigate the contribution of CYP2C9 and VKORC1 to acenocoumarol (AC) dose variability, bleeding events in Hungary.	Acenocoumarol	85-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
29055218-1	2017	The purpose of this work was to investigate the contribution of CYP2C9 and VKORC1 to acenocoumarol (AC) dose variability, bleeding events in Hungary.	Acenocoumarol	100-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
29100760-2	2017	Human CYP2C9 exhibits extensive genetic polymorphism and numbers of clinic studies have demonstrated that CYP2C9 genetic polymorphism has a significant influence on the pharmacokinetics of benzbromarone.	Benzbromarone	189-202	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
29024493-5	2017	Simulations using PK/PD models showed that CYP2C9 genotype is the factor that affects the PDs of meloxicam.	3-{1-[3-(Dimethylamino)propyl]-2-Methyl-1h-Indol-3-Yl}-4-(2-Methyl-1h-Indol-3-Yl)-1h-Pyrrole-2,5-Dione	90-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
29024493-5	2017	Simulations using PK/PD models showed that CYP2C9 genotype is the factor that affects the PDs of meloxicam.	Meloxicam	97-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
29100760-2	2017	Human CYP2C9 exhibits extensive genetic polymorphism and numbers of clinic studies have demonstrated that CYP2C9 genetic polymorphism has a significant influence on the pharmacokinetics of benzbromarone.	Benzbromarone	189-202	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
29100760-0	2017	Comparative study on the interaction between 3 CYP2C9 allelic isoforms and benzbromarone by using LC-MS/MS method.	Benzbromarone	75-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
29100760-1	2017	Benzbromarone is a uricosuric drug metabolized predominantly by cytochrome P450 2C9 from in vitro findings.	Benzbromarone	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-83
29100760-3	2017	But in vitro study on the interaction between CYP2C9 allelic isoforms and benzbromarone was rare.	Benzbromarone	74-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
29100760-4	2017	Here, an LC-MS/MS method was established and validated to determine the concentration of benzbromarone in different CYP2C9 enzyme incubation systems for the drug-enzyme interaction study.	Benzbromarone	89-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
29100760-6	2017	Based on this method, the interaction between 3 CYP2C9 allelic isoforms and benzbromarone was researched by kinetics parameters (Km, Vmax, Clint).	Benzbromarone	76-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
29100760-7	2017	As a result, CYP2C9*1 displayed the highest metabolic activity towards benzbromarone, CYP2C9*2 showed a little lower catalytic activity than CYP2C9*1 (relative clearance/*1=85.86%), CYP2C9*3 showed the lowest catalytic activity (relative clearance/*1=21.57%).	Benzbromarone	71-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
29100760-7	2017	As a result, CYP2C9*1 displayed the highest metabolic activity towards benzbromarone, CYP2C9*2 showed a little lower catalytic activity than CYP2C9*1 (relative clearance/*1=85.86%), CYP2C9*3 showed the lowest catalytic activity (relative clearance/*1=21.57%).	Benzbromarone	71-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
29100760-7	2017	As a result, CYP2C9*1 displayed the highest metabolic activity towards benzbromarone, CYP2C9*2 showed a little lower catalytic activity than CYP2C9*1 (relative clearance/*1=85.86%), CYP2C9*3 showed the lowest catalytic activity (relative clearance/*1=21.57%).	Benzbromarone	71-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
29100760-7	2017	As a result, CYP2C9*1 displayed the highest metabolic activity towards benzbromarone, CYP2C9*2 showed a little lower catalytic activity than CYP2C9*1 (relative clearance/*1=85.86%), CYP2C9*3 showed the lowest catalytic activity (relative clearance/*1=21.57%).	Benzbromarone	71-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
29100760-8	2017	The result illustrated that various CYP2C9 allelic isoforms showed different enzymatic activities towards benzbromarone, which could offer effective consultation for personalized administration in clinic.	Benzbromarone	106-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
27937048-3	2017	Polymorphisms of CYP3A4, CYP3A5, CYP2C9 and non-genetic factors such as age, gender, body mass index (BMI), transaminase levels, concomitant medications might also affect voriconazole initial steady serum trough concentration (VICmin) in haematological patients, but the effects were not clear.	Voriconazole	171-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
28962866-5	2017	KEY FINDINGS: The in vitro metabolic enzyme of DCO was CYP3A4 (mediated the formation of metabolites M1-M5), CYP2C9 (mediated the formation of metabolites M1-M3, M6 and M8) and CYP2D6 (mediated the formation of metabolite M3) in HLM.	3,3-DICHLORO-2-PHOSPHONOMETHYL-ACRYLIC ACID	47-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
32095470-8	2017	Two SNPs (rs11165069 from ABCA4 (p=0.00002); rs17847036 from CYP2C9 (p=0.000001)) showed significant associations with talniflumate C max.	talniflumate	119-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
28522373-1	2017	Carvedilol, a drug available as a racemic mixture, is metabolised into hydroxyphenylcarvedilol (OHC) by CYP2D6 and O-desmethylcarvedilol (DMC) by CYP2C9 followed by conjugation to glucuronides.	Carvedilol	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
27414183-7	2017	The sulfate conjugation by SULT2A1 also contributed to the metabolism of TAK-438 to form TAK-438 N-sulfate, and CYP2C9 mediated the formation of M-IV-Sul from TAK-438 N-sulfate.	tak-438 n-sulfate	159-176	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
28522373-1	2017	Carvedilol, a drug available as a racemic mixture, is metabolised into hydroxyphenylcarvedilol (OHC) by CYP2D6 and O-desmethylcarvedilol (DMC) by CYP2C9 followed by conjugation to glucuronides.	hydroxyphenylcarvedilol	71-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
28522373-1	2017	Carvedilol, a drug available as a racemic mixture, is metabolised into hydroxyphenylcarvedilol (OHC) by CYP2D6 and O-desmethylcarvedilol (DMC) by CYP2C9 followed by conjugation to glucuronides.	ohc	96-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
28522373-1	2017	Carvedilol, a drug available as a racemic mixture, is metabolised into hydroxyphenylcarvedilol (OHC) by CYP2D6 and O-desmethylcarvedilol (DMC) by CYP2C9 followed by conjugation to glucuronides.	desmethylcarvedilol	138-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
28522373-7	2017	Even though data are limited, it appears that despite inhibition of CYP2C9 due to long-term glibenclamide administration to T2DM patients, overall no differences are observed in the total clearance of carvedilol when compared to healthy subjects (43.1 vs. 45.9L/h for (S)-(-)-carvedilol and 29.0 vs. 33.1L/h for (R)-(+)-carvedilol).	Glyburide	92-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
28522373-8	2017	These results provide evidence of a compensatory mechanism for the inhibition of CYP2C9, with higher contribution of CYP2D6 activity to the elimination of carvedilol.	Carvedilol	155-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
28689179-8	2017	CONCLUSION: In this study, CYP2C9 and VKORC1 genotypes identified patients with VTE at increased bleeding risk with warfarin.	Warfarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
28941798-6	2017	The aim of this study was to investigate the potential inhibition of shikonin against CYP1A2, CYP2B1/6, CYP2C9/11, CYP2D1/6, CYP2E1 and CYP3A2/4 activities in human and rat liver microsomes through cocktail approach in vitro.	shikonin	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
28941798-8	2017	In human liver microsomes, shikonin was not only a mixed inhibitor of CYP1A2, CYP2B6, CYP2C9, CYP2D6 and CYP3A4, but also a competitive inhibitor of CYP2E1, with Ki values no more than 7.72muM.	shikonin	27-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
29099769-8	2017	R-AML was also a significantly more potent inhibitor of CYP2C9 (Ki 12.11 microM/S-AML 21.45 microM) and CYP2C19 (Ki 5.97 microM/S-AML 7.22 muM.	Amlodipine	0-5	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
29076107-10	2017	CONCLUSION: These findings confirm that amenamevir (as a cytochrome P450 3A4 substrate) can interact with ketoconazole or rifampicin, and (as a cytochrome P450 3A4 inducer) can interact with midazolam; however, no interaction between amenamevir and (S)-warfarin was observed, indicating that amenamevir is not an inducer of cytochrome P450 2C9.	ASP2151	40-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	324-343
28758225-0	2017	Metabolism of 7-ethoxycoumarin, flavanone and steroids by cytochrome P450 2C9 variants.	7-ethoxycoumarin	14-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-77
28758225-0	2017	Metabolism of 7-ethoxycoumarin, flavanone and steroids by cytochrome P450 2C9 variants.	flavanone	32-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-77
28758225-0	2017	Metabolism of 7-ethoxycoumarin, flavanone and steroids by cytochrome P450 2C9 variants.	Steroids	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-77
28758225-7	2017	All the CYP2C9 variants showed lower flavanone 6-hydroxylation activities than CYP2C9.1 (the wild-type).	flavanone	37-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
28758225-8	2017	CYP2C9.38 showed higher activities in testosterone 6beta-hydroxylation, progesterone 6beta-/16alpha-hydroxylation, estrone 11alpha-hydroxylation and estradiol 6alpha-hydroxylation than CYP2C9.1.	Testosterone	38-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
28758225-8	2017	CYP2C9.38 showed higher activities in testosterone 6beta-hydroxylation, progesterone 6beta-/16alpha-hydroxylation, estrone 11alpha-hydroxylation and estradiol 6alpha-hydroxylation than CYP2C9.1.	Progesterone	72-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
28758225-8	2017	CYP2C9.38 showed higher activities in testosterone 6beta-hydroxylation, progesterone 6beta-/16alpha-hydroxylation, estrone 11alpha-hydroxylation and estradiol 6alpha-hydroxylation than CYP2C9.1.	Estrone	115-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
28758225-8	2017	CYP2C9.38 showed higher activities in testosterone 6beta-hydroxylation, progesterone 6beta-/16alpha-hydroxylation, estrone 11alpha-hydroxylation and estradiol 6alpha-hydroxylation than CYP2C9.1.	Estradiol	149-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
28758225-11	2017	These results indicate that the substrate specificity of CYP2C9.9 and CYP2C9.10 was not changed, but CYP2C9.8, CYP2C9.12 and CYP2C9.40 showed different substrate specificity toward steroids compared with CYP2C9.1; and especially CYP2C9.38 displayed diverse substrate specificities towards 7-ethoxycoumarin and steroids.	Steroids	181-189	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
28887089-6	2017	In addition, the inhibitory activities of steviol and stevioside towards the major cytochrome P450 enzymes CYP3A4, CYP2C9, CYP2D6, CYP1A2 and CYP2B6 were evaluated in vitro.	steviol	42-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
28887089-6	2017	In addition, the inhibitory activities of steviol and stevioside towards the major cytochrome P450 enzymes CYP3A4, CYP2C9, CYP2D6, CYP1A2 and CYP2B6 were evaluated in vitro.	stevioside	54-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
28887089-8	2017	A weak inhibition of CYP3A4 and CYP2C9 with steviol was also found.	steviol	44-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
28893623-2	2017	Abiraterone is known to inhibit several drug metabolizing cytochrome P450 enzymes including CYP1A2, CYP2D6, CYP2C8, CYP2C9, CYP2C19, CYP3A4 and CYP3A5, but its effects on steroid metabolizing P450 enzymes are not clear.	abiraterone	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
28834238-0	2017	Long-term outcomes of elderly patients with CYP2C9 and VKORC1 variants treated with vitamin K antagonists.	Vitamin K	84-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
28933798-1	2017	Chronic kidney disease (CKD) complicates warfarin anticoagulation partially through its effect on CYP2C9 activity.	Warfarin	41-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
28933798-12	2017	CKD increased the effect of CYP2C9 genetic variation on (S)-warfarin and (R,S)-warfarin metabolism.	Warfarin	56-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
28933798-12	2017	CKD increased the effect of CYP2C9 genetic variation on (S)-warfarin and (R,S)-warfarin metabolism.	(r,s)-warfarin	73-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
29023392-9	2017	All curcuminoids exhibited multiple pharmacological effects in vitro, including potent antioxidant activity as well as inhibition of CYP2C9, CYP3A4 and lipoxygenase activity without affecting the release of TNF-alpha.	curcuminoids	4-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
28609430-0	2017	Polymorphisms in CYP2C9 are associated with response to indomethacin among neonates with patent ductus arteriosus.	Indomethacin	56-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
28609430-4	2017	This study investigated the association between single-nucleotide polymorphisms (SNPs) in CYP2C9 and the closure of PDA in response to indomethacin.MethodsSix SNPs in CYP2C9 were analyzed for association with indomethacin response.	single-nucleotide	48-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
28609430-4	2017	This study investigated the association between single-nucleotide polymorphisms (SNPs) in CYP2C9 and the closure of PDA in response to indomethacin.MethodsSix SNPs in CYP2C9 were analyzed for association with indomethacin response.	Indomethacin	135-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
28609430-4	2017	This study investigated the association between single-nucleotide polymorphisms (SNPs) in CYP2C9 and the closure of PDA in response to indomethacin.MethodsSix SNPs in CYP2C9 were analyzed for association with indomethacin response.	methodssix	148-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
28609430-4	2017	This study investigated the association between single-nucleotide polymorphisms (SNPs) in CYP2C9 and the closure of PDA in response to indomethacin.MethodsSix SNPs in CYP2C9 were analyzed for association with indomethacin response.	methodssix	148-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
28609430-4	2017	This study investigated the association between single-nucleotide polymorphisms (SNPs) in CYP2C9 and the closure of PDA in response to indomethacin.MethodsSix SNPs in CYP2C9 were analyzed for association with indomethacin response.	Indomethacin	209-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
28609430-7	2017	Among indomethacin responders, the G allele of rs2153628 and the T allele of rs1799853 were overtransmitted from the parents to their child (OR: 2.667, 95% CI: 1.374, 5.177 and OR: 2.375, 95% CI: 1.040, 5.425, respectively), consistent with the case-control analysis.ConclusionWe identified an association between two SNPs in CYP2C9, rs2153628 and rs1799853, and indomethacin response for the treatment of PDA.	Indomethacin	6-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	326-332
28877533-7	2017	CONCLUSION: Our results further support a minor contribution of CYP2C9 genetic variability toward steady-state endoxifen concentrations.	4-hydroxy-N-desmethyltamoxifen	111-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
28972767-3	2017	Here we report the crystal structures of human CYP2C9 and its polymorphic variants, *3 (I359L) and *30 (A477T), with an antihypertensive drug losartan.	Losartan	142-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
28723731-8	2017	An increase in mean methadone C/D ratios was also seen for homozygous carriers of CYP3A5*3 and heterozygous carriers of CYP2C9*2 or *3 and CYP2C19*2 or *3.	Methadone	20-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
28374982-0	2017	Angiotensin II Receptor Blockers Inhibit the Generation of Epoxyeicosatrienoic Acid from Arachidonic Acid in Recombinant CYP2C9, CYP2J2 and Human Liver Microsomes.	epoxyeicosatrienoic acid	59-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
28374982-0	2017	Angiotensin II Receptor Blockers Inhibit the Generation of Epoxyeicosatrienoic Acid from Arachidonic Acid in Recombinant CYP2C9, CYP2J2 and Human Liver Microsomes.	Arachidonic Acid	89-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
28374982-1	2017	Cytochrome P450 (CYP) 2C9, CYP2C8 and CYP2J2 enzymes, which metabolize arachidonic acid (AA) to epoxyeicosatrienoic acids, have cardioprotective effects including anti-inflammation and vasodilation.	Arachidonic Acid	71-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-25
28374982-1	2017	Cytochrome P450 (CYP) 2C9, CYP2C8 and CYP2J2 enzymes, which metabolize arachidonic acid (AA) to epoxyeicosatrienoic acids, have cardioprotective effects including anti-inflammation and vasodilation.	epoxyeicosatrienoic acids	96-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-25
27313202-0	2017	Frequency of Common CYP2C9 Polymorphisms and Their Impact on Warfarin Dose Requirement in Pakistani Population.	Warfarin	61-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
27313202-1	2017	Polymorphisms in cytochrome P450 (CYP) 2C9 (CYP2C9) gene result in interindividual variability in warfarin dose requirement.	Warfarin	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-42
27313202-1	2017	Polymorphisms in cytochrome P450 (CYP) 2C9 (CYP2C9) gene result in interindividual variability in warfarin dose requirement.	Warfarin	98-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
27313202-3	2017	This study was carried out in Pakistani population to evaluate the contribution of common CYP2C9 polymorphisms to warfarin therapy.	Warfarin	114-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
27335128-0	2017	Influence of VKORC1 and CYP2C9 Polymorphisms on Daily Acenocoumarol Dose Requirement in South Indian Patients With Mechanical Heart Valves.	Acenocoumarol	54-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
27335128-3	2017	Our aim was to investigate the influence of polymorphisms of VKORC1 and CYP2C9 genes on the mean daily dose requirement of acenocoumarol.	Acenocoumarol	123-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
27335128-9	2017	Patients with a wild type of both VKORC1 (-1639GG and 1173CC) and CYP2C9 gene variants required higher acenocoumarol dose compared to those with mutant genotype ( P = 0.023 and P = 0.008 respectively).	Acenocoumarol	103-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
27335128-11	2017	CONCLUSION: Presence of a mutant allele of VKORC1 (-1639A &amp; 1173T) and CYP2C9 genes increased the odds of requiring a lower mean dosage of acenocoumarol.	Acenocoumarol	143-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
28284562-0	2017	The VKORC1 and CYP2C9 genotypes significantly effect Vitamin K antagonist dosing only in patients over the age of 20years.	Vitamin K	53-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
28934153-9	2017	Selaginellin and selaginellin M also showed medium inhibitory potential against CYP2C9, CYP2J2, UGT1A1, and UGT1A3 (1 muM &lt; IC50 &lt; 5 muM).	selaginellin S	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
28934153-9	2017	Selaginellin and selaginellin M also showed medium inhibitory potential against CYP2C9, CYP2J2, UGT1A1, and UGT1A3 (1 muM &lt; IC50 &lt; 5 muM).	selaginellin M	17-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
28198005-2	2017	Evidence from the published literature is presented for CYP2C9, VKORC1, CYP4F2, and rs12777823 genotype-guided warfarin dosing to achieve a target international normalized ratio of 2-3 when clinical genotype results are available.	Warfarin	111-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
28748348-9	2017	While CYP2C9*2 and *3 variants significantly reduced phenytoin metabolism, the impacts of CYP2C19*2 and *3 variants were unclear.	Phenytoin	53-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
28927781-0	2017	Function of 38 variants CYP2C9 polymorphism on ketamine metabolism in vitro.	Ketamine	47-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
28435143-5	2017	In this study, we estimated the coefficient of variation (CV) for the intrinsic hepatic clearance of tolbutamide by CYP2C9 for each CYP2C9 genotype using previously reported area under the blood concentration curve (AUC) and oral clearance (CLoral) values in a Monte Carlo simulation with a dispersion model.	Tolbutamide	101-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
28435143-5	2017	In this study, we estimated the coefficient of variation (CV) for the intrinsic hepatic clearance of tolbutamide by CYP2C9 for each CYP2C9 genotype using previously reported area under the blood concentration curve (AUC) and oral clearance (CLoral) values in a Monte Carlo simulation with a dispersion model.	Tolbutamide	101-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
28435143-6	2017	The CVs for tolbutamide CLint,h,CYP2C9 were estimated to be 18.1%, 23.9%, 25.4%, 22.3%, 13.0%, and 19.8% for CYP2C9*1/*1, *1/*2, *1/*3, *2/*2, *2/*3, and *3/*3, respectively.	Tolbutamide	12-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
28639119-1	2017	PURPOSE: In vitro data showed that selexipag and its active metabolite (ACT-333679) have an inductive effect on CYP3A4, CYP2B6, and CYP2C9 at concentrations approximately 100-fold higher than the maximum plasma concentration (C max) measured under steady-state conditions.	selexipag	35-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
28872889-13	2017	The genotype distributions of the CYP2C9*3, CYP2D6*10, and CYP3A5*3 genetic polymorphisms were associated with the warfarin maintenance dose.	Warfarin	115-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
28872889-15	2017	Moreover, CYP2C9*3, CYP2D6*10, and CYP3A5*3 are associated with the warfarin maintenance dose.	Warfarin	68-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
28927781-5	2017	RESULT: Catalytic activity of thirty-eight CYP2C9 alleles on ketamine metabolism to norketamine was surveyed.	Ketamine	61-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
28927781-5	2017	RESULT: Catalytic activity of thirty-eight CYP2C9 alleles on ketamine metabolism to norketamine was surveyed.	norketamine	84-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
28820457-0	2017	Role of CYP2C9, CYP2C19 and EPHX Polymorphism in the Pharmacokinetic of Phenytoin: A Study on Uruguayan Caucasian Subjects.	Phenytoin	72-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
29156869-4	2017	A warfarin dosing algorithm was developed based on age, height, CYP2C9, VKORC1, and GGCX genotype.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
29181084-2	2017	Patients &amp; methods: Test results for three common cardiovascular drug-gene tests (warfarin-CYP2C9-VKORC1, clopidogrel-CYP2C19 and simvastatin-SLCO1B1) of 208 patients in the Ohio State University-Coriell Personalized Medicine Collaborative were examined to determine the incidence of potentially actionable test results.	Warfarin	86-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
28841884-18	2017	UGT1A6/CYP2C9 polymorphisms have influence on VPA metabolism.	Valproic Acid	46-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	7-13
28820457-1	2017	Phenytoin (PHT) oxidative route leads to its main metabolite p-hydroxyphenytoin (p-HPPH), by means of CYP2C9 and CYP2C19.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
28820457-1	2017	Phenytoin (PHT) oxidative route leads to its main metabolite p-hydroxyphenytoin (p-HPPH), by means of CYP2C9 and CYP2C19.	Phenytoin	11-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
28820457-1	2017	Phenytoin (PHT) oxidative route leads to its main metabolite p-hydroxyphenytoin (p-HPPH), by means of CYP2C9 and CYP2C19.	hydroxyphenytoin	61-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
28820457-1	2017	Phenytoin (PHT) oxidative route leads to its main metabolite p-hydroxyphenytoin (p-HPPH), by means of CYP2C9 and CYP2C19.	p-hpph	81-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
28429387-2	2017	Polymorphisms in the VKORC1, CYP2C9 and CYP4F2 genes have been verified to correlate with warfarin stable dosage (WSD).	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
28550460-6	2017	Similarly, the patients with CYP2C9*3 variant allele required significantly lower warfarin SWDs than those with homozygous wild-type (p = 0.006).	Warfarin	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
29156869-7	2017	A warfarin dosing algorithm showed that age, height, CYP2C9, VKORC1, and GGCX genotype were the best variables for estimating warfarin dose (R2 = 41.2%).	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
28273397-0	2017	Associations of CYP2C9 and CYP2A6 Polymorphisms with the Concentrations of Valproate and its Hepatotoxin Metabolites and Valproate-Induced Hepatotoxicity.	Valproic Acid	75-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
28273397-0	2017	Associations of CYP2C9 and CYP2A6 Polymorphisms with the Concentrations of Valproate and its Hepatotoxin Metabolites and Valproate-Induced Hepatotoxicity.	Valproic Acid	121-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
27853934-8	2017	RESULTS: N-oxides of clozapine (CYP2B6/2C19) and voriconazole (CYP2C9/3A4) showed CYP inhibition &gt;=50%.	n-oxides	9-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
27853934-8	2017	RESULTS: N-oxides of clozapine (CYP2B6/2C19) and voriconazole (CYP2C9/3A4) showed CYP inhibition &gt;=50%.	Clozapine	21-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
27853934-8	2017	RESULTS: N-oxides of clozapine (CYP2B6/2C19) and voriconazole (CYP2C9/3A4) showed CYP inhibition &gt;=50%.	Voriconazole	49-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
28608988-0	2017	Dosing algorithms for vitamin K antagonists across VKORC1 and CYP2C9 genotypes: comment.	Vitamin K	22-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
28604475-10	2017	RESULTS: First, the concomitant use of carbapenems (beta" = -0.422) and UGT1A6 (552 AA   AC) (beta" = -0.249) had a significant negative correlation with the weight-adjusted VPA serum concentration (C:W ratio), whereas CYP2C9 (1075 AA   AC) (beta" = 0.186) and gender (female compared with male) (beta" = 0.322) showed a positive correlation with VPA serum C:W ratio.	Carbapenems	39-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	219-225
28638342-7	2017	The CYP2C9 variant rs2860905, which was found in all the major haplotypes occurring in the Puerto Rican population, showed stronger association with warfarin sensitivity (&lt;4 mg/day) than common variants CYP2C9*2 and CYP2C9*3.	Warfarin	149-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
28805981-3	2017	Another aim was to examine the in vitro influence of ethanol on the CYP2C9 activity.	Ethanol	53-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
28805981-4	2017	Human CYP2C9 (wild type) isolated from a baculovirus-infected cell system was incubated with 0.8 mumol/L losartan for 20 min.	Losartan	105-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
28805981-7	2017	Formation of the CYP2C9-produced losartan metabolite EXP-3174 was determined by validated LC-MS/MS methodology.	Losartan	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
28805981-15	2017	The presence of ethanol inhibited CYP2C9 activity in a concentration-dependent manner.	Ethanol	16-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
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.	Busulfan	156-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
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
28685643-0	2017	Clinical effect of CYP2C9*5/*6 genotype on a patient"s warfarin dose requirement.	Warfarin	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
28685643-1	2017	We describe a 38-year-old African-American female treated with warfarin for acute bilateral pulmonary emboli who is a carrier of two rare CYP2C9 variant alleles, *5 and *6, along with VKORC1 -1639GG and CYP4F2 433Val/Val genotypes.	Warfarin	63-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
28685643-3	2017	This case sheds further light on the cumulative clinical impact of the CYP2C9 variant alleles, *5 and *6, on warfarin dose requirements and practical considerations for warfarin genotyping in a racially and ethnically diverse population.	Warfarin	109-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
28685643-3	2017	This case sheds further light on the cumulative clinical impact of the CYP2C9 variant alleles, *5 and *6, on warfarin dose requirements and practical considerations for warfarin genotyping in a racially and ethnically diverse population.	Warfarin	169-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
28740425-0	2017	Efficacy of piroxicam for postoperative pain after lower third molar surgery associated with CYP2C8*3 and CYP2C9.	Piroxicam	12-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
28740425-2	2017	The aim of this study was to evaluate the possible association of polymorphisms in the CYP2C8*3 and CYP2C9 genes with the clinical efficacy of oral piroxicam (20 mg daily for 4 days) after lower third molar surgeries with regard to postoperative pain, swelling, trismus, adverse reactions, need for rescue medication and the volunteer"s overall satisfaction.	Piroxicam	148-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
28283499-6	2017	CYP2B6 and to an even lesser extent CYP2C9 were also observed to catalyze NGMN metabolism.	ngmn	74-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
28370504-0	2017	CYP1A1m1 and CYP2C9*2 and *3 polymorphism and risk to develop ARV-associated hepatotoxicity and its severity.	omega-N-Allylarginine	62-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
28370504-8	2017	CYP2C9*31075AC genotype among alcohol users was likely to be associated with development of ARV-associated hepatotoxicity (OR = 1.67, p = 0.38).	Alcohols	30-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
28370504-8	2017	CYP2C9*31075AC genotype among alcohol users was likely to be associated with development of ARV-associated hepatotoxicity (OR = 1.67, p = 0.38).	omega-N-Allylarginine	92-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
28370504-11	2017	CYP1A1m1 3801TC, 3801CC, and CYP2C9*3 1075AC genotypes among combined alcohol + nevirapine users increased the risk of development of ARV-associated hepatotoxicity (OR = 1.41, p = 0.53; OR = 1.49, p = 0.83; OR = 1.78, p = 0.35).	Alcohols	70-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
28370504-11	2017	CYP1A1m1 3801TC, 3801CC, and CYP2C9*3 1075AC genotypes among combined alcohol + nevirapine users increased the risk of development of ARV-associated hepatotoxicity (OR = 1.41, p = 0.53; OR = 1.49, p = 0.83; OR = 1.78, p = 0.35).	Nevirapine	80-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
28370504-11	2017	CYP1A1m1 3801TC, 3801CC, and CYP2C9*3 1075AC genotypes among combined alcohol + nevirapine users increased the risk of development of ARV-associated hepatotoxicity (OR = 1.41, p = 0.53; OR = 1.49, p = 0.83; OR = 1.78, p = 0.35).	omega-N-Allylarginine	134-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
28370504-13	2017	CYP2C9*31075AC genotype with combined alcohol and nevirapine usage indicated a risk for development of ARV-associated hepatotoxicity.	Alcohols	38-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
28370504-13	2017	CYP2C9*31075AC genotype with combined alcohol and nevirapine usage indicated a risk for development of ARV-associated hepatotoxicity.	Nevirapine	50-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
28484907-4	2017	MAM-2201 potently inhibited CYP2C9-catalyzed diclofenac 4"-hydroxylation, CYP3A4-catalyzed midazolam 1"-hydroxylation, and UGT1A3-catalyzed chenodeoxycholic acid 24-acyl-glucuronidation, with K i values of 5.6, 5.4 and 5.0 microM, respectively.	Diclofenac	45-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
28114735-2	2017	Carvedilol is mainly metabolized by glucuronidation, by CYP2D6 to hydroxyphenylcarvedilol (OHC), and by CYP2C9 to O-desmethylcarvedilol (DMC).	Carvedilol	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
28262345-1	2017	OBJECTIVES: The aim of this study was to evaluate the associations between polymorphisms of VKORC1, CYP2C9, CYP4F2, NR3C1 and VDR genes and stable warfarin doses in Korean patients with mechanical heart valves.	Warfarin	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
28262345-9	2017	CONCLUSIONS: This study showed that stable warfarin dose is associated with VDR SNPs along with VKORC1, CYP2C9, and CYP4F2 SNPs.	Warfarin	43-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
28114735-2	2017	Carvedilol is mainly metabolized by glucuronidation, by CYP2D6 to hydroxyphenylcarvedilol (OHC), and by CYP2C9 to O-desmethylcarvedilol (DMC).	desmethylcarvedilol	114-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
28114735-2	2017	Carvedilol is mainly metabolized by glucuronidation, by CYP2D6 to hydroxyphenylcarvedilol (OHC), and by CYP2C9 to O-desmethylcarvedilol (DMC).	desmethylcarvedilol	137-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
28626479-1	2017	The genetic factors are determinants in required dosage changes of warfarin among which are polymorphisms of CYP2C9 and VKORC1 genes.	Warfarin	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
28412319-2	2017	We hypothesized that genetic factors related to warfarin metabolism (CYP2C9) and activity (VKORC1) would show stronger associations than modifiable factors with the quality of anticoagulation control and risks for thromboembolism and hemorrhage.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
28284082-1	2017	Cytochrome P450 (CYP) 2C9 and CYP2C19 genetic mutant could influence the plasma concentration of glipizide in human subjects, which refers to glipizide safety and adverse effects in clinic practice.	Glipizide	97-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-25
28284082-1	2017	Cytochrome P450 (CYP) 2C9 and CYP2C19 genetic mutant could influence the plasma concentration of glipizide in human subjects, which refers to glipizide safety and adverse effects in clinic practice.	Glipizide	142-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-25
27665573-0	2017	Evaluation of Concomitant Antiretrovirals and CYP2C9/CYP2C19 Polymorphisms on the Pharmacokinetics of Etravirine.	etravirine	102-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
27665573-2	2017	Etravirine is primarily metabolized by cytochrome P450 (CYP) 2C9, CYP2C19, and CYP3A.	etravirine	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-64
28032893-2	2017	Utilizing data from a diverse population of 257 patients who received VKORC1 and CYP2C9 genotype-guided warfarin dosing, we aimed to examine genotype-associated differences in anticoagulation endpoints and derive a novel pharmacogenetic nomogram to more optimally dose warfarin.	Warfarin	104-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
27665573-3	2017	This analysis determined the impact of concomitant antiretrovirals and CYP2C9/CYP2C19 phenotype on the pharmacokinetics of etravirine.	etravirine	123-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
27665573-10	2017	CL/F increased non-linearly with body weight and creatinine clearance (CLCR), and also varied based on CYP2C9/CYP2C19 phenotype.	Fluorine	3-4	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
27665573-11	2017	CONCLUSIONS: In this analysis, body weight, CLCR, and CYP2C9/CYP2C19 phenotype were found to describe some of the variability in CL/F.	Fluorine	132-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
28315807-0	2017	Association of CYP2C9, CYP2A6, ACSM2A, and CPT1A gene polymorphisms with adverse effects of valproic acid in Chinese patients with epilepsy.	Valproic Acid	92-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
28315807-5	2017	RESULTS: CYP2C9 mutations had a significant impact on 4-ene-VPA concentration, in patients with wild-type CYP2C9 (CYP2C9*1), which has a greater capacity for VPA metabolism than the mutant type (CYP2C9*3), liver dysfunction was substantially higher.	4-ene	54-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
28315807-5	2017	RESULTS: CYP2C9 mutations had a significant impact on 4-ene-VPA concentration, in patients with wild-type CYP2C9 (CYP2C9*1), which has a greater capacity for VPA metabolism than the mutant type (CYP2C9*3), liver dysfunction was substantially higher.	4-ene	54-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
28173639-5	2017	In primary human hepatocytes, CYP2C9 and CYP3A4 gene expression and activities decreased upon treatment with 20 muM bosentan+200 muM rifampin.	Bosentan	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
28173639-5	2017	In primary human hepatocytes, CYP2C9 and CYP3A4 gene expression and activities decreased upon treatment with 20 muM bosentan+200 muM rifampin.	Rifampin	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
28315807-1	2017	OBJECTIVE: To explore the influence of CYP2C9, CYP2A6, ACSM2A, CPT1A gene polymorphisms on valproic acid (VPA) and its role in metabolism-related liver dysfunction in order to guide the clinical safety and rational use of VPA.	Valproic Acid	91-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
28315807-5	2017	RESULTS: CYP2C9 mutations had a significant impact on 4-ene-VPA concentration, in patients with wild-type CYP2C9 (CYP2C9*1), which has a greater capacity for VPA metabolism than the mutant type (CYP2C9*3), liver dysfunction was substantially higher.	4-ene	54-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
28315807-5	2017	RESULTS: CYP2C9 mutations had a significant impact on 4-ene-VPA concentration, in patients with wild-type CYP2C9 (CYP2C9*1), which has a greater capacity for VPA metabolism than the mutant type (CYP2C9*3), liver dysfunction was substantially higher.	4-ene	54-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
28315807-1	2017	OBJECTIVE: To explore the influence of CYP2C9, CYP2A6, ACSM2A, CPT1A gene polymorphisms on valproic acid (VPA) and its role in metabolism-related liver dysfunction in order to guide the clinical safety and rational use of VPA.	Valproic Acid	106-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
28157069-0	2017	Delayed de-induction of CYP2C9 compared to CYP3A after discontinuation of rifampicin: Report of two cases : .	Rifampin	74-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
28157069-3	2017	To clarify the time courses of deinduction of CYP2C9 and -CYP3A activities after rifampicin withdrawal, we monitored these enzyme activities in 2 patients over time after discontinuing rifampicin.	Rifampin	81-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
28157069-3	2017	To clarify the time courses of deinduction of CYP2C9 and -CYP3A activities after rifampicin withdrawal, we monitored these enzyme activities in 2 patients over time after discontinuing rifampicin.	Rifampin	185-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
28157069-7	2017	We monitored CYP2C9 and CYP3A activities over their clinical courses by measuring the metabolic clearance of S-warfarin to S-7-hydroxywarfarin and that of cortisol to 6beta-hydroxycortisol, respectively.	Warfarin	109-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
28157069-7	2017	We monitored CYP2C9 and CYP3A activities over their clinical courses by measuring the metabolic clearance of S-warfarin to S-7-hydroxywarfarin and that of cortisol to 6beta-hydroxycortisol, respectively.	Hydrocortisone	155-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
28157069-7	2017	We monitored CYP2C9 and CYP3A activities over their clinical courses by measuring the metabolic clearance of S-warfarin to S-7-hydroxywarfarin and that of cortisol to 6beta-hydroxycortisol, respectively.	6 beta-hydroxycortisol	167-188	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
27826892-0	2017	The effect of UGT1A9, CYP2B6 and CYP2C9 genes polymorphism on individual differences in propofol pharmacokinetics among Polish patients undergoing general anaesthesia.	Propofol	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
28468305-5	2017	Dimethyllirioresinol weakly inhibited CYP2C19 and CYP2C8 with IC50 values of 55.1 and 85.0 muM, respectively, without inhibition of CYP1A2, CYP2A6, CYP2B6, CYP2C9, CYP2D6, and CYP3A4 activities at 100 muM.	dimethyllirioresinol	0-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
27826892-4	2017	The aim of our study was to verify the impact of genetic changes c.516G&gt;T in the CYP2B6, c.98T&gt;C in the UGT1A9 and c.1075A&gt;C in the CYP2C9 genes on the individual propofol pharmacokinetic profile in the Polish patients undergoing general anaesthesia.	Propofol	172-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
28073118-9	2017	The main human cytochrome P450 isoforms involved in Artepillin C metabolism had been identified, and the results suggest a majority contribution of CYP2E1 and CYP2C9 in the formation of the two metabolites.	artepillin C	52-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	159-165
28073119-4	2017	The apparent Ki value for CYP2C9 was 50.60 microM and those for CYP3A4/5 were 48.71 microM and 31.25 microM using two different probe substrates, nifedipine and midazolam, respectively.	Nifedipine	146-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
28073119-4	2017	The apparent Ki value for CYP2C9 was 50.60 microM and those for CYP3A4/5 were 48.71 microM and 31.25 microM using two different probe substrates, nifedipine and midazolam, respectively.	Midazolam	161-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
28520385-3	2012	Prasugrel is metabolized to its active metabolite primarily by CYP3A5 and CYP2B6, and to a lesser extent by CYP2C9 and CYP2C19.	Prasugrel Hydrochloride	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
28484392-0	2017	"Late" Withdrawal Syndrome after Carbamazepine In Utero Exposure in a CYP2C9 Slow Metabolizer Newborn.	Carbamazepine	33-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
28484392-5	2017	The infant genotype analysis showed two low activity CYP2C9 allelic variants (*2/*3 heterozygote) predicting a CYP2C9 slow metabolizer phenotype which could explain reduced carbamazepine elimination and a late and long-lasting withdrawal symptoms observed 3 days after birth.	Carbamazepine	173-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
28484392-5	2017	The infant genotype analysis showed two low activity CYP2C9 allelic variants (*2/*3 heterozygote) predicting a CYP2C9 slow metabolizer phenotype which could explain reduced carbamazepine elimination and a late and long-lasting withdrawal symptoms observed 3 days after birth.	Carbamazepine	173-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
28274629-4	2017	6-Paradol showed concentration-dependent inhibitory effects on CYP1A2, CYP2B6, CYP2C8, CYP2C9, and CYP2C19 isozymes, with IC50 values ranging from 3.8 to 21.4microM in recombinant CYP isozymes.	6-paradol	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
27763679-9	2017	CYP2C9 *1/*3 genotype had reduced clearance for S-warfarin, but increased clearance for R-warfarin.	Sulfur	48-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27763679-9	2017	CYP2C9 *1/*3 genotype had reduced clearance for S-warfarin, but increased clearance for R-warfarin.	Warfarin	50-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27763679-9	2017	CYP2C9 *1/*3 genotype had reduced clearance for S-warfarin, but increased clearance for R-warfarin.	Warfarin	88-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
28099407-2	2017	We investigated whether the variant genotypes of cytochrome P450 2C8 (CYP2C8), CYP2C9, CYP3A5 and transporter ABCB1 influence the pharmacokinetic phenotype of the substrate pioglitazone in Chinese individuals.	Pioglitazone	173-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
28135601-8	2017	On the other hand, tested flavonoids showed no or weaker inhibition of CYP2C9 compared to warfarin, making it very unlikely that quercetin or its metabolites can significantly inhibit the CYP2C9-mediated inactivation of warfarin.	Warfarin	220-228	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	188-194
28135054-7	2017	Pharmacogenomics-guided warfarin dosing algorithms that include the well-established VKORC1 and CYP2C9 polymorphisms explain only a small proportion of inter-individual variability in African Americans (AAs).	Warfarin	24-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
28135054-11	2017	Inclusion of rs4889606 genotypes, along with CYP2C9 alleles, rs9923231 genotypes and clinical variables, explained 31% of the inter-patient variability in warfarin dose requirement.	Warfarin	155-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
28135601-0	2017	Interaction of quercetin and its metabolites with warfarin: Displacement of warfarin from serum albumin and inhibition of CYP2C9 enzyme.	Quercetin	15-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
28135601-0	2017	Interaction of quercetin and its metabolites with warfarin: Displacement of warfarin from serum albumin and inhibition of CYP2C9 enzyme.	Warfarin	50-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
28135601-5	2017	Furthermore, the inhibitory effects of these flavonoids on CYP2C9 enzyme were tested because the metabolic elimination of warfarin is catalysed principally by this enzyme.	Flavonoids	45-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
28179134-3	2017	The results demonstrate that most of the unsaturated fatty acids showed marked inhibition towards CYP2C8 mediated amodiaquine N-deethylation followed by inhibition of CYP2C9 and CYP2B6 mediated activities.	Fatty Acids, Unsaturated	41-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
30455562-0	2017	Warfarin maintenance dose associated with genetic polymorphisms of CYP2C9.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
30455562-1	2017	BACKGROUND: Cytochrome P450 2C9 (CYP2C9) gene polymorphisms alters the required warfarin dose in patients, due to pharmacogenetic events.	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-31
30455562-1	2017	BACKGROUND: Cytochrome P450 2C9 (CYP2C9) gene polymorphisms alters the required warfarin dose in patients, due to pharmacogenetic events.	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
30455562-9	2017	CONCLUSIONS: Due to the relatively high frequency of CYP2C9 polymorphisms in the study population, the clinicians should become aware of these results to reduce the risk of hemorrhage when prescribing warfarin.	Warfarin	201-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
28129313-2	2017	Some SSRIs are potent CYP2C9 inhibitors that may increase warfarin plasma concentrations and the risk of bleeding.	Warfarin	58-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
28129313-3	2017	We aimed to examine the effect of the putative CYP2C9-mediated warfarin-SSRI interaction on clinical outcomes.	Warfarin	63-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
28129313-10	2017	CONCLUSIONS: Patients concomitantly treated with warfarin and SSRIs that are potent CYP2C9 inhibitors had comparable rates of bleeding events, ischemic or thromboembolic events, and mortality as did patients cotreated with warfarin and other SSRIs, although small but potentially meaningful effects on bleeding cannot be completely excluded.	Warfarin	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
28099407-7	2017	Unexpectedly, the pioglitazone AUC0-48 in CYP2C9*3 carriers was lower (50.8%), whereas the AUC0-48 ratios of metabolites M-III/pioglitazone and M-IV/pioglitazone increased to 134.3 and 155.8%, respectively, compared with the wild-type CYP2C9*1/*1 homozygous.	Pioglitazone	18-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
27312150-5	2017	The most potent inhibitors were genistein and daidzein inhibiting noncompetitively the CYP2C9 with Ki of 35.95 +- 6.96 and 60.56 +- 3.53 mumol/l and CYP3A4 (inhibited by genistein with Ki of 23.25 +- 5.85 mumol/l also by a noncompetitive mechanism).	Genistein	32-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
27312150-5	2017	The most potent inhibitors were genistein and daidzein inhibiting noncompetitively the CYP2C9 with Ki of 35.95 +- 6.96 and 60.56 +- 3.53 mumol/l and CYP3A4 (inhibited by genistein with Ki of 23.25 +- 5.85 mumol/l also by a noncompetitive mechanism).	daidzein	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
27312150-5	2017	The most potent inhibitors were genistein and daidzein inhibiting noncompetitively the CYP2C9 with Ki of 35.95 +- 6.96 and 60.56 +- 3.53 mumol/l and CYP3A4 (inhibited by genistein with Ki of 23.25 +- 5.85 mumol/l also by a noncompetitive mechanism).	Genistein	170-179	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
27312150-8	2017	Genistein and daidzein inhibit noncompetitively CYP3A4 and CYP2C9.	Genistein	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
27312150-8	2017	Genistein and daidzein inhibit noncompetitively CYP3A4 and CYP2C9.	daidzein	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
27864660-4	2017	A single 200-mg oral dose of celecoxib was given to 52 Korean subjects with different CYP2C9 genotypes: CYP2C9EM (n = 26; CYP2C9*1/*1), CYP2C9IM (n = 24; CYP2C9*1/*3 and *1/*13), and CYP2C9PM (n = 2; CYP2C9*3/*3).	Celecoxib	29-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
28287454-6	2017	These in vitro results indicate that AM-2201 needs to be examined for potential pharmacokinetic drug interactions in vivo due to its potent inhibition of CYP2C8, CYP2C9, CYP3A4, UGT1A3, and UGT2B7 enzyme activities.	1-(5-fluoropentyl)-3-(1-naphthoyl)indole	37-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
27864660-0	2017	Effects of CYP2C9 genetic polymorphisms on the pharmacokinetics of celecoxib and its carboxylic acid metabolite.	Celecoxib	67-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
27864660-2	2017	The predominant hepatic metabolism of celecoxib to celecoxib carboxylic acid (CCA) is mediated mainly by CYP2C9.	Celecoxib	38-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
28408837-0	2017	Polymorphisms of VKORC1 and CYP2C9 are associated with warfarin sensitivity in Chinese population.	Warfarin	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
28408837-3	2017	The present study was designed to clarify the real biological significance of the polymorphisms of VKORC1 and cytochrome P450 2C9 (CYP2C9) in warfarin metabolism.	Warfarin	142-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-129
28408837-3	2017	The present study was designed to clarify the real biological significance of the polymorphisms of VKORC1 and cytochrome P450 2C9 (CYP2C9) in warfarin metabolism.	Warfarin	142-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
28408837-8	2017	VKORC1 1173CT, 1542GC, 2255CT, 3730CT carriers and CYP2C9 exon 4 -65GC carriers had significantly higher warfarin daily dosage than others (3.2+-0.6 vs 3.1+-1.1 vs 2.6+-0.8 mg/day).	Warfarin	105-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
28083852-0	2017	DNA sensors to assess the effect of VKORC1 and CYP2C9 gene polymorphisms on warfarin dose requirement in Chinese patients with atrial fibrillation.	Warfarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
28083852-1	2017	The optimal dose of warfarin depends on polymorphisms in the VKORC1 (the vitamin K epoxide reductase complex subunit (1) and CYP2C9 (cytochrome P450 2C9) genes.	Warfarin	20-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
28083852-1	2017	The optimal dose of warfarin depends on polymorphisms in the VKORC1 (the vitamin K epoxide reductase complex subunit (1) and CYP2C9 (cytochrome P450 2C9) genes.	Warfarin	20-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-152
27864660-4	2017	A single 200-mg oral dose of celecoxib was given to 52 Korean subjects with different CYP2C9 genotypes: CYP2C9EM (n = 26; CYP2C9*1/*1), CYP2C9IM (n = 24; CYP2C9*1/*3 and *1/*13), and CYP2C9PM (n = 2; CYP2C9*3/*3).	Celecoxib	29-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
27864660-2	2017	The predominant hepatic metabolism of celecoxib to celecoxib carboxylic acid (CCA) is mediated mainly by CYP2C9.	SC-62807	51-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
27864660-2	2017	The predominant hepatic metabolism of celecoxib to celecoxib carboxylic acid (CCA) is mediated mainly by CYP2C9.	1-methylcyclohexanecarboxylic acid	78-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
27864660-3	2017	We investigated the effects of the major CYP2C9 genetic variants in Asian populations, CYP2C9*3 and CYP2C9*13, on the pharmacokinetics of celecoxib and its carboxylic acid metabolite in healthy Korean subjects.	Celecoxib	138-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
27864660-3	2017	We investigated the effects of the major CYP2C9 genetic variants in Asian populations, CYP2C9*3 and CYP2C9*13, on the pharmacokinetics of celecoxib and its carboxylic acid metabolite in healthy Korean subjects.	Celecoxib	138-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
27864660-3	2017	We investigated the effects of the major CYP2C9 genetic variants in Asian populations, CYP2C9*3 and CYP2C9*13, on the pharmacokinetics of celecoxib and its carboxylic acid metabolite in healthy Korean subjects.	Celecoxib	138-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
27864660-4	2017	A single 200-mg oral dose of celecoxib was given to 52 Korean subjects with different CYP2C9 genotypes: CYP2C9EM (n = 26; CYP2C9*1/*1), CYP2C9IM (n = 24; CYP2C9*1/*3 and *1/*13), and CYP2C9PM (n = 2; CYP2C9*3/*3).	Celecoxib	29-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
27864660-4	2017	A single 200-mg oral dose of celecoxib was given to 52 Korean subjects with different CYP2C9 genotypes: CYP2C9EM (n = 26; CYP2C9*1/*1), CYP2C9IM (n = 24; CYP2C9*1/*3 and *1/*13), and CYP2C9PM (n = 2; CYP2C9*3/*3).	Celecoxib	29-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
27864660-6	2017	The mean area under the plasma concentration-time curve (AUC0- ) of celecoxib was increased 1.63-fold (P &lt; 0.001), and the apparent oral clearance (CL/F) of celecoxib was decreased by 39.6% in the CYP2C9IM genotype group compared with that of CYP2C9EM (P &lt; 0.001).	Celecoxib	160-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	200-206
27864660-7	2017	The overall pharmacokinetic parameters for celecoxib in CYP2C9*1/*13 subjects were similar to those in CYP2C9*1/*3 subjects.	Celecoxib	43-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
27864660-8	2017	Two subjects with CYP2C9PM genotype both showed markedly higher AUC0- , prolonged half-life, and lower CL/F for celecoxib than did subjects with CYP2C9EM and IM genotypes.	Celecoxib	112-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
27864660-8	2017	Two subjects with CYP2C9PM genotype both showed markedly higher AUC0- , prolonged half-life, and lower CL/F for celecoxib than did subjects with CYP2C9EM and IM genotypes.	Celecoxib	112-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
27864660-9	2017	CYP2C9*3 and CYP2C9*13 variant alleles significantly affected the plasma concentration of celecoxib.	Celecoxib	90-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27864660-9	2017	CYP2C9*3 and CYP2C9*13 variant alleles significantly affected the plasma concentration of celecoxib.	Celecoxib	90-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
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 9	Homo sapiens	24-30
27718269-11	2017	High expression of CYP3A4, CYP2C8, CYP2C9, and CYP2D6 may be risk factors for hepatotoxicity caused by AQ-therapy.	Amodiaquine	103-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
28074333-8	2017	CONCLUSION: The results suggest that other cytochrome P450 enzymes, including CYP2C9, CYP3A4, and CEP2E1, in addition to CYP28, also play an important role in the metabolism of rosiglitazone.	Rosiglitazone	177-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
28063245-0	2017	Dosing algorithms for vitamin K antagonists across VKORC1 and CYP2C9 genotypes.	Vitamin K	22-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
27273787-0	2017	Upregulation of human CYP2C9 expression by Bisphenol A via estrogen receptor alpha (ERalpha) and Med25.	bisphenol A	43-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
27273787-5	2017	We further identify the mechanism of BPA upregulation of CYP2C9 expression.	bisphenol A	37-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
27273787-8	2017	Our findings suggest that BPA exposure has a potential risk for adverse health effects in human liver metabolism by upregulation of CYP2C9 expression.	bisphenol A	26-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
28063245-13	2017	Conclusions EU-PACT genetic-guided dose initiation algorithms for acenocoumarol and phenprocoumon could have predicted the dose overcautiously in the VKORC1 AA-CYP2C9*1*1 subgroup.	Acenocoumarol	66-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
27539372-0	2017	CYP2C9 Genotype-Dependent Warfarin Pharmacokinetics: Impact of CYP2C9 Genotype on R- and S-Warfarin and Their Oxidative Metabolites.	Warfarin	26-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27539372-0	2017	CYP2C9 Genotype-Dependent Warfarin Pharmacokinetics: Impact of CYP2C9 Genotype on R- and S-Warfarin and Their Oxidative Metabolites.	Warfarin	26-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
27539372-0	2017	CYP2C9 Genotype-Dependent Warfarin Pharmacokinetics: Impact of CYP2C9 Genotype on R- and S-Warfarin and Their Oxidative Metabolites.	Warfarin	91-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27539372-0	2017	CYP2C9 Genotype-Dependent Warfarin Pharmacokinetics: Impact of CYP2C9 Genotype on R- and S-Warfarin and Their Oxidative Metabolites.	Warfarin	91-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
27539372-1	2017	Multiple factors can impact warfarin therapy, including genetic variations in the drug-metabolizing enzyme cytochrome P450 2C9 (CYP2C9).	Warfarin	28-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-126
27539372-1	2017	Multiple factors can impact warfarin therapy, including genetic variations in the drug-metabolizing enzyme cytochrome P450 2C9 (CYP2C9).	Warfarin	28-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
27539372-3	2017	Genetic variations in CYP2C9, the primary enzyme governing the metabolic clearance of the more potent S-enantiomer of the racemic anticoagulant warfarin, may impact warfarin-drug interactions.	Warfarin	144-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
27539372-3	2017	Genetic variations in CYP2C9, the primary enzyme governing the metabolic clearance of the more potent S-enantiomer of the racemic anticoagulant warfarin, may impact warfarin-drug interactions.	Warfarin	165-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
27539372-5	2017	Plasma clearance of S-warfarin, but not R-warfarin, decreased multiexponentially and in a CYP2C9 gene-dependent manner: 56%, 70%, and 75% for CYP2C9*1/*3, CYP2C9*2/*3, and CYP2C9*3/*3 genotypes, respectively, compared with CYP2C9*1/*1, resulting in pronounced differences in the S:R ratio that identified warfarin-sensitive genotypes.	Warfarin	20-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
27539372-5	2017	Plasma clearance of S-warfarin, but not R-warfarin, decreased multiexponentially and in a CYP2C9 gene-dependent manner: 56%, 70%, and 75% for CYP2C9*1/*3, CYP2C9*2/*3, and CYP2C9*3/*3 genotypes, respectively, compared with CYP2C9*1/*1, resulting in pronounced differences in the S:R ratio that identified warfarin-sensitive genotypes.	Warfarin	20-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
27539372-5	2017	Plasma clearance of S-warfarin, but not R-warfarin, decreased multiexponentially and in a CYP2C9 gene-dependent manner: 56%, 70%, and 75% for CYP2C9*1/*3, CYP2C9*2/*3, and CYP2C9*3/*3 genotypes, respectively, compared with CYP2C9*1/*1, resulting in pronounced differences in the S:R ratio that identified warfarin-sensitive genotypes.	Warfarin	20-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
27539372-5	2017	Plasma clearance of S-warfarin, but not R-warfarin, decreased multiexponentially and in a CYP2C9 gene-dependent manner: 56%, 70%, and 75% for CYP2C9*1/*3, CYP2C9*2/*3, and CYP2C9*3/*3 genotypes, respectively, compared with CYP2C9*1/*1, resulting in pronounced differences in the S:R ratio that identified warfarin-sensitive genotypes.	Warfarin	20-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
27539372-5	2017	Plasma clearance of S-warfarin, but not R-warfarin, decreased multiexponentially and in a CYP2C9 gene-dependent manner: 56%, 70%, and 75% for CYP2C9*1/*3, CYP2C9*2/*3, and CYP2C9*3/*3 genotypes, respectively, compared with CYP2C9*1/*1, resulting in pronounced differences in the S:R ratio that identified warfarin-sensitive genotypes.	Warfarin	20-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
27539372-5	2017	Plasma clearance of S-warfarin, but not R-warfarin, decreased multiexponentially and in a CYP2C9 gene-dependent manner: 56%, 70%, and 75% for CYP2C9*1/*3, CYP2C9*2/*3, and CYP2C9*3/*3 genotypes, respectively, compared with CYP2C9*1/*1, resulting in pronounced differences in the S:R ratio that identified warfarin-sensitive genotypes.	Warfarin	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
27539372-5	2017	Plasma clearance of S-warfarin, but not R-warfarin, decreased multiexponentially and in a CYP2C9 gene-dependent manner: 56%, 70%, and 75% for CYP2C9*1/*3, CYP2C9*2/*3, and CYP2C9*3/*3 genotypes, respectively, compared with CYP2C9*1/*1, resulting in pronounced differences in the S:R ratio that identified warfarin-sensitive genotypes.	Warfarin	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
27539372-5	2017	Plasma clearance of S-warfarin, but not R-warfarin, decreased multiexponentially and in a CYP2C9 gene-dependent manner: 56%, 70%, and 75% for CYP2C9*1/*3, CYP2C9*2/*3, and CYP2C9*3/*3 genotypes, respectively, compared with CYP2C9*1/*1, resulting in pronounced differences in the S:R ratio that identified warfarin-sensitive genotypes.	Warfarin	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
27539372-5	2017	Plasma clearance of S-warfarin, but not R-warfarin, decreased multiexponentially and in a CYP2C9 gene-dependent manner: 56%, 70%, and 75% for CYP2C9*1/*3, CYP2C9*2/*3, and CYP2C9*3/*3 genotypes, respectively, compared with CYP2C9*1/*1, resulting in pronounced differences in the S:R ratio that identified warfarin-sensitive genotypes.	Warfarin	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
27539372-5	2017	Plasma clearance of S-warfarin, but not R-warfarin, decreased multiexponentially and in a CYP2C9 gene-dependent manner: 56%, 70%, and 75% for CYP2C9*1/*3, CYP2C9*2/*3, and CYP2C9*3/*3 genotypes, respectively, compared with CYP2C9*1/*1, resulting in pronounced differences in the S:R ratio that identified warfarin-sensitive genotypes.	Warfarin	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	142-148
27539372-6	2017	CYP2C9 was the primary P450 enzyme contributing to S-warfarin metabolism and a minor contributor to R-warfarin metabolism.	Sulfur	51-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27539372-6	2017	CYP2C9 was the primary P450 enzyme contributing to S-warfarin metabolism and a minor contributor to R-warfarin metabolism.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27539372-6	2017	CYP2C9 was the primary P450 enzyme contributing to S-warfarin metabolism and a minor contributor to R-warfarin metabolism.	Warfarin	100-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27539372-7	2017	In the presence of a defective CYP2C9 allele, switching of warfarin metabolism to other oxidative pathways and P450 enzymes for the metabolic elimination of S-warfarin was not observed.	Warfarin	59-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
27539372-7	2017	In the presence of a defective CYP2C9 allele, switching of warfarin metabolism to other oxidative pathways and P450 enzymes for the metabolic elimination of S-warfarin was not observed.	Warfarin	159-167	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
27539372-9	2017	Understanding the impact of CYP2C9 genetics on warfarin pharmacokinetics lays the foundation for future genotype-dependent warfarin-drug interaction studies.	Warfarin	47-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
27539372-9	2017	Understanding the impact of CYP2C9 genetics on warfarin pharmacokinetics lays the foundation for future genotype-dependent warfarin-drug interaction studies.	Warfarin	123-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
28224948-10	2017	Patients, however, homozygous for CYP2C9 *1,*3, and VKORC1 required less than 5 mg/day of warfarin to maintain the INR within the therapeutic range.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
28649054-0	2017	Effect of VKORC1 and CYP2C9 polymorphisms on warfarin dose requirement in Bangladeshi population.	Warfarin	45-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
28649054-2	2017	Large inter-individuals variability due to age, gender, diet, concurrent drug interactions and variations in CYP2C9 and VKORC1 genes make the management of warfarin therapy challenging and yet no study has been conducted on the Bangladeshi population.	Warfarin	156-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
28649054-3	2017	The aim of the study was to identify the role of VKORC1 and CYP2C9 polymorphisms in Bangladeshi population in dose requirement of warfarin.	Warfarin	130-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
28649054-8	2017	The results of this study indicate that comparatively higher daily maintenance doses of warfarin were required to achieve the target INR for patients carrying both GG genotype of VKORC1rs9923231 and wild type variant of CYP2C9*3 whereas minimum dose were required for patient having AA genotype of VKORC1rs9923231 and *3/*3 variant of CYP2C9.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	220-226
28649054-8	2017	The results of this study indicate that comparatively higher daily maintenance doses of warfarin were required to achieve the target INR for patients carrying both GG genotype of VKORC1rs9923231 and wild type variant of CYP2C9*3 whereas minimum dose were required for patient having AA genotype of VKORC1rs9923231 and *3/*3 variant of CYP2C9.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	335-341
27934636-7	2017	Only using the RAF derived from testosterone for CYP3A4 produced the expected CYP2C9 contribution of 72%-87% and 47%-69% for metabolism of losartan and meloxicam, respectively.	Meloxicam	152-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
27934636-4	2017	The RAF value for CYP3A4 or CYP2C9 derived from a particular P450-selective probe reaction was applied to calculate RAF-scaled CLint for other probe reactions of the same P450 isoform in a crossover manner and compared with the measured HLM CLint When RAF derived from midazolam or nifedipine was used for CYP3A4, the ICR for testosterone 6beta-hydroxylation was 31 and 25, respectively, suggesting significantly diverse interactions of CYP3A4 probes with the testing systems.	Midazolam	269-278	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
27661060-1	2017	AIM: To assess the effect of Cytochrome P450 2C9 (CYP2C9) gene polymorphism on pediatric warfarin maintenance dosage requirement.	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-48
27661060-1	2017	AIM: To assess the effect of Cytochrome P450 2C9 (CYP2C9) gene polymorphism on pediatric warfarin maintenance dosage requirement.	Warfarin	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
27661060-5	2017	Review Manager version 5.2.3 software was used to analyze the relationship between CYP2C9 polymorphisms and warfarin maintenance doses in pediatric patients.	Warfarin	108-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
27661060-7	2017	RESULTS: Maintenance warfarin doses in patients with CYP2C9 *1/*2 genotype, CYP2C9 *1/*3 genotype, and CYP2C9 variant carriers which contain at least one variant allele (*2 or *3) were from 15% to 41% lower than doses in patients with the wild-type allele (CYP2C9 *1/*1): All differences were significant with P-values &lt;.05.	Warfarin	21-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
27661060-9	2017	CONCLUSIONS: We found that CYP2C9 gene polymorphism (referring to the presence of *1/*2, *1/*3, and variant genotypes in the population in addition to the wild type) was significantly associated with decreased warfarin maintenance dose requirements.	Warfarin	210-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
28131653-7	2017	We also found that the 6-hydroxylation of 1"-hydroxy BBR is mainly catalyzed by CYP2C9 and that several CYPs and/or non-enzymatic reaction are involved in the formation of GSH adducts from 1",6-dihydroxy BBR.	1'-hydroxybenzbromarone	42-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
27934636-4	2017	The RAF value for CYP3A4 or CYP2C9 derived from a particular P450-selective probe reaction was applied to calculate RAF-scaled CLint for other probe reactions of the same P450 isoform in a crossover manner and compared with the measured HLM CLint When RAF derived from midazolam or nifedipine was used for CYP3A4, the ICR for testosterone 6beta-hydroxylation was 31 and 25, respectively, suggesting significantly diverse interactions of CYP3A4 probes with the testing systems.	Nifedipine	282-292	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
27934636-4	2017	The RAF value for CYP3A4 or CYP2C9 derived from a particular P450-selective probe reaction was applied to calculate RAF-scaled CLint for other probe reactions of the same P450 isoform in a crossover manner and compared with the measured HLM CLint When RAF derived from midazolam or nifedipine was used for CYP3A4, the ICR for testosterone 6beta-hydroxylation was 31 and 25, respectively, suggesting significantly diverse interactions of CYP3A4 probes with the testing systems.	testosterone 6beta	326-344	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
27934636-6	2017	In addition, these RAF values were applied to losartan and meloxicam, whose metabolism is mostly CYP2C9 mediated.	Losartan	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
27934636-6	2017	In addition, these RAF values were applied to losartan and meloxicam, whose metabolism is mostly CYP2C9 mediated.	Meloxicam	59-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
27934636-7	2017	Only using the RAF derived from testosterone for CYP3A4 produced the expected CYP2C9 contribution of 72%-87% and 47%-69% for metabolism of losartan and meloxicam, respectively.	Testosterone	32-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
27934636-7	2017	Only using the RAF derived from testosterone for CYP3A4 produced the expected CYP2C9 contribution of 72%-87% and 47%-69% for metabolism of losartan and meloxicam, respectively.	Losartan	139-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
27117036-0	2017	Warfarin dose requirements with different genotypes of CYP2C9 and VKORC1 for patients with atrial fibrillation and valve replacement.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
27117036-1	2017	AIMS: To investigate whether genetic variants of CYP2C9 and VKORC1 have different effects on the dose of warfarin in 180 Han Chinese patients who were recruited from the Fu Wai Hospital.	Warfarin	105-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
27117036-3	2017	METHODS: DNA was isolated and genotyped using a Warfarin dosage Prediction Kit for single nucleotide polymorphisms (SNPs) of CYP2C9 and VKORC1.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
27117036-4	2017	RESULTS: The VKORC1 and CYP2C9*3 polymorphisms are significantly associated with warfarin maintenance dosages.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
27117036-8	2017	The mean warfarin daily dose requirements in the genotypes of VKORC1 and CYP2C9 were not dependent on the medical indication(s) present.	Warfarin	9-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
27117036-9	2017	CONCLUSIONS: Genetic variants of CYP2C9, VKORC1, and age are significant determinants of the maintenance dose of warfarin.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
27878474-0	2017	Quantitative Assessment of CYP2C9 Genetic Polymorphisms Effect on the Oral Clearance of S-Warfarin in Healthy Subjects.	Warfarin	88-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
27878474-1	2017	BACKGROUND: Genetic polymorphisms in CYP2C9 account for 10-20% of the variability in warfarin dose requirement.	Warfarin	85-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
27878474-2	2017	As such CYP2C9 genetic polymorphisms are commonly included in algorithms aimed to optimize warfarin therapy as a way to account for variability in warfarin responsiveness that is due to altered pharmacokinetics.	Warfarin	91-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
27878474-2	2017	As such CYP2C9 genetic polymorphisms are commonly included in algorithms aimed to optimize warfarin therapy as a way to account for variability in warfarin responsiveness that is due to altered pharmacokinetics.	Warfarin	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
27878474-9	2017	CONCLUSIONS: The current study provides an estimate concerning the effect of CYP2C9 polymorphisms on S-warfarin pharmacokinetics among healthy subjects.	Warfarin	103-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
27052193-12	2017	The results suggest that the altered pharmacokinetics of DIC might be attributed to PIP mediated inhibition of CYP2C9 enzyme, which indicates the clinically significant interaction present between DIC and PIP.	piperine	84-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
28867723-0	2017	The Inhibitory Effect of Telmisartan on the Metabolism of Arachidonic Acid by CYP2C9 and CYP2C8: An in Vitro Study.	Telmisartan	25-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
27990512-5	2017	A multiplex allele-specific PCR reaction was used to generate products corresponding to 3 genetic variants associated with warfarin sensitivity [CYP2C9 *2, CYP2C9 *3, and VKORC1 (1173C&gt;T)] and an internal control product.	Warfarin	123-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
27990512-5	2017	A multiplex allele-specific PCR reaction was used to generate products corresponding to 3 genetic variants associated with warfarin sensitivity [CYP2C9 *2, CYP2C9 *3, and VKORC1 (1173C&gt;T)] and an internal control product.	Warfarin	123-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
28867723-0	2017	The Inhibitory Effect of Telmisartan on the Metabolism of Arachidonic Acid by CYP2C9 and CYP2C8: An in Vitro Study.	Arachidonic Acid	58-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
28867723-7	2017	Dixon and Lineweaver-Burk plots indicated that telmisartan is a mixed inhibitor of both CYP2C9 and CYP2C8; telmisartan did not show a time-dependent inhibition toward these CYP enzymes.	Telmisartan	47-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
28867723-4	2017	We recently demonstrated that telmisartan, one of angiotensin II receptor blockers, inhibits AA metabolism by CYP enzymes, including CYP2C8, CYP2C9, and CYP2J2.	Telmisartan	30-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
28867723-8	2017	Based on the CRs, both CYP2C9 and CYP2C8 are the key enzymes in the metabolism of AA in the human liver.	Chromium	13-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
28674251-0	2017	Co-administration of Fluvastatin and CYP3A4 and CYP2C8 Inhibitors May Increase the Exposure to Fluvastatin in Carriers of CYP2C9 Genetic Variants.	Fluvastatin	21-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
28867723-5	2017	We conducted studies of AA metabolism using recombinant CYP enzymes to estimate the inhibition constant and the type of inhibition by telmisartan of CYP2C9 and CYP2C8.	Telmisartan	134-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
28674251-0	2017	Co-administration of Fluvastatin and CYP3A4 and CYP2C8 Inhibitors May Increase the Exposure to Fluvastatin in Carriers of CYP2C9 Genetic Variants.	Fluvastatin	95-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
27925230-3	2017	Genetic polymorphisms for cytochrome CYP2C9 and VKORC1 explain some of the variability, especially in warfarin and acenocoumarol responses.	Warfarin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
28674251-1	2017	Fluvastatin, which is one of the hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors (statins), is primarily metabolized by CYP2C9 and to a lesser extent by CYP3A4 and CYP2C8.	Fluvastatin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
28674251-4	2017	Since CYP2C9 is a polymorphic enzyme, we investigated the effect of DDI via CYP2C9, CYP3A4, and CYP2C8 on fluvastatin pharmacokinetics by using a validated prediction method in relation to CYP2C9 variants.	Fluvastatin	106-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	6-12
28674251-4	2017	Since CYP2C9 is a polymorphic enzyme, we investigated the effect of DDI via CYP2C9, CYP3A4, and CYP2C8 on fluvastatin pharmacokinetics by using a validated prediction method in relation to CYP2C9 variants.	Fluvastatin	106-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
28674251-4	2017	Since CYP2C9 is a polymorphic enzyme, we investigated the effect of DDI via CYP2C9, CYP3A4, and CYP2C8 on fluvastatin pharmacokinetics by using a validated prediction method in relation to CYP2C9 variants.	Fluvastatin	106-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
28674251-5	2017	The predicted increases in the area under the concentration-time curve (AUC) ratios of fluvastatin in carriers with CYP2C9*1/*2, CYP2C9*1/*3, CYP2C9*2/*2, CYP2C9*2/*3, and CYP2C9*3/*3 versus that found in carriers with CYP2C9*1/*1 were 1.16, 1.35, 1.37, 1.65, and 2.06, respectively.	Fluvastatin	87-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	116-122
28674251-5	2017	The predicted increases in the area under the concentration-time curve (AUC) ratios of fluvastatin in carriers with CYP2C9*1/*2, CYP2C9*1/*3, CYP2C9*2/*2, CYP2C9*2/*3, and CYP2C9*3/*3 versus that found in carriers with CYP2C9*1/*1 were 1.16, 1.35, 1.37, 1.65, and 2.06, respectively.	Fluvastatin	87-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
28674251-5	2017	The predicted increases in the area under the concentration-time curve (AUC) ratios of fluvastatin in carriers with CYP2C9*1/*2, CYP2C9*1/*3, CYP2C9*2/*2, CYP2C9*2/*3, and CYP2C9*3/*3 versus that found in carriers with CYP2C9*1/*1 were 1.16, 1.35, 1.37, 1.65, and 2.06, respectively.	Fluvastatin	87-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
28674251-5	2017	The predicted increases in the area under the concentration-time curve (AUC) ratios of fluvastatin in carriers with CYP2C9*1/*2, CYP2C9*1/*3, CYP2C9*2/*2, CYP2C9*2/*3, and CYP2C9*3/*3 versus that found in carriers with CYP2C9*1/*1 were 1.16, 1.35, 1.37, 1.65, and 2.06, respectively.	Fluvastatin	87-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
28674251-5	2017	The predicted increases in the area under the concentration-time curve (AUC) ratios of fluvastatin in carriers with CYP2C9*1/*2, CYP2C9*1/*3, CYP2C9*2/*2, CYP2C9*2/*3, and CYP2C9*3/*3 versus that found in carriers with CYP2C9*1/*1 were 1.16, 1.35, 1.37, 1.65, and 2.06, respectively.	Fluvastatin	87-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
28674251-5	2017	The predicted increases in the area under the concentration-time curve (AUC) ratios of fluvastatin in carriers with CYP2C9*1/*2, CYP2C9*1/*3, CYP2C9*2/*2, CYP2C9*2/*3, and CYP2C9*3/*3 versus that found in carriers with CYP2C9*1/*1 were 1.16, 1.35, 1.37, 1.65, and 2.06, respectively.	Fluvastatin	87-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
28674251-6	2017	Our in silico model predicted that administration of fluvastatin in conjunction with the potent inhibitors that completely inhibited CYP3A4 and CYP2C8 in carriers with the CYP2C9*3/*3 variant would cause a 3.23- and 2.60-fold increase in the AUC ratios, respectively, when compared to that for the carriers with the CYP2C9*1/*1 taking fluvastatin alone.	Fluvastatin	53-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
28674251-6	2017	Our in silico model predicted that administration of fluvastatin in conjunction with the potent inhibitors that completely inhibited CYP3A4 and CYP2C8 in carriers with the CYP2C9*3/*3 variant would cause a 3.23- and 2.60-fold increase in the AUC ratios, respectively, when compared to that for the carriers with the CYP2C9*1/*1 taking fluvastatin alone.	Fluvastatin	53-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	316-322
28674251-6	2017	Our in silico model predicted that administration of fluvastatin in conjunction with the potent inhibitors that completely inhibited CYP3A4 and CYP2C8 in carriers with the CYP2C9*3/*3 variant would cause a 3.23- and 2.60-fold increase in the AUC ratios, respectively, when compared to that for the carriers with the CYP2C9*1/*1 taking fluvastatin alone.	Fluvastatin	335-346	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	172-178
27925230-3	2017	Genetic polymorphisms for cytochrome CYP2C9 and VKORC1 explain some of the variability, especially in warfarin and acenocoumarol responses.	Acenocoumarol	115-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
29472822-6	2017	This case report addresses the influence of CYP2C9 genetic polymorphism (a single nucleotide polymorphism) on phenytoin drug metabolism, thereby causing DRESS syndrome.	Phenytoin	110-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
28867752-3	2017	Single nucleotide polymorphisms (SNPs) in CYP2C9 and VKORC1 play a role in the pharmacokinetics and dynamics of warfarin and acenocoumarol and they determine the efficacy of treatment by controlling drug clearance in treated individuals.	Warfarin	112-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
28867752-3	2017	Single nucleotide polymorphisms (SNPs) in CYP2C9 and VKORC1 play a role in the pharmacokinetics and dynamics of warfarin and acenocoumarol and they determine the efficacy of treatment by controlling drug clearance in treated individuals.	Acenocoumarol	125-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
28867752-0	2017	Genotyping of CYP2C9 and VKORC1 polymorphisms predicts south Indian patients with deep vein thrombosis as fast metabolizers of warfarin/acenocoumarin.	Warfarin	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
28867752-8	2017	None of the patients tested positive for poor drug metabolizing genotypes of the CYP2C9 gene and only 1.6% of the south Indian population was sensitive to warfarin treatment.	Warfarin	155-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
28867752-0	2017	Genotyping of CYP2C9 and VKORC1 polymorphisms predicts south Indian patients with deep vein thrombosis as fast metabolizers of warfarin/acenocoumarin.	Acenocoumarol	136-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
27638959-7	2016	CYP2C9-humanized mice have similar bile acid metabolites as the Cyp2c-null mice, indicating that human CYP2C9 does not oxidize CDCA and UDCA, thus explaining the species differences in production of MCA.	Bile Acids and Salts	35-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27889507-0	2017	CYP2C9 Genotypes Modify Benzodiazepine-Related Fall Risk: Original Results From Three Studies With Meta-Analysis.	Benzodiazepines	24-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27889507-1	2017	OBJECTIVE: To investigate whether the CYP2C9*2 and *3 variants modify benzodiazepine-related fall risk.	Benzodiazepines	70-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
27889507-13	2017	CYP2C9*2 or *3 allele variants modified benzodiazepine-related fall risk.	Benzodiazepines	40-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27889507-14	2017	Compared to nonusers, those carrying a CYP2C9*2 or *3 allele and using benzodiazepines had a 45% increased fall risk (HR, 1.45 95% CI, 1.21; 1.73), whereas CYP2C9*1 homozygotes using benzodiazepines had no increased fall risk (HR, 1.14; 95% CI, 0.90; 1.45).	Benzodiazepines	183-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
27889507-15	2017	Within benzodiazepine users, having a CYP2C9*2 or *3 allele was associated with an increased fall risk (HR, 1.35; 95% CI, 1.06; 1.72).	Benzodiazepines	7-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
27889507-17	2017	CONCLUSIONS: CYP2C9*2 and *3 allele variants modify benzodiazepine-related fall risk.	Benzodiazepines	52-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
27889507-20	2017	However, because the exact role of CYP2C9 in benzodiazepine metabolism is still unclear, additional research is warranted.	Benzodiazepines	45-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
26454199-3	2017	Warfarin"s more potent enantiomer is primarily metabolized by cytochrome P450 2C9 and has a narrow therapeutic window.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-81
27743182-11	2017	Our study suggests that polymorphic variants of VKORC1 and CYP2C9 affect warfarin dose independently, whereas CYP2C19 did not contribute to warfarin therapy.	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
28079798-8	2017	In the dosing algorithm we developed, we confirmed the strongest effects of VKORC1, CYP2C9 on warfarin dosing.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
27967328-4	2017	RESULTS: CYP2C9 and VKORC1 genotypes, age and weight affected acenocoumarol dose and predicted 53.9% of its variability.	Acenocoumarol	62-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
27992547-2	2016	Pharmacogenomics studies have shown that variants in CYP2C9 and VKORC1 genes are strongly and consistently associated with warfarin dose variability.	Warfarin	123-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
27992547-10	2016	Variants in the VKORC1 and CYP2C9 were the most significant predictors of warfarin dose in all populations.	Warfarin	74-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
27992547-12	2016	CONCLUSION: Variants of VKORC1 and CYP2C9 are the strongest predictors of warfarin dose variability among the different populations from MENA.	Warfarin	74-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
28302415-13	2017	Patients with CYP2C9 *1/*3 genotype were thrice more likely to have toxic plasma concentrations of phenytoin as compared to those with wild-type genotype (*1/*1) (Adjusted odds ratio - 3.36; 95% C.I.	Phenytoin	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
27743182-6	2017	Patient with VKORC1-1639 G &gt; A, CYP2C9*2 and CYP2C9*3 genetic variants need significant lower warfarin dose than patient with wild type allele of VKORC1 1639 G or CYP2C9*1.	Warfarin	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
27743182-6	2017	Patient with VKORC1-1639 G &gt; A, CYP2C9*2 and CYP2C9*3 genetic variants need significant lower warfarin dose than patient with wild type allele of VKORC1 1639 G or CYP2C9*1.	Warfarin	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
27743182-6	2017	Patient with VKORC1-1639 G &gt; A, CYP2C9*2 and CYP2C9*3 genetic variants need significant lower warfarin dose than patient with wild type allele of VKORC1 1639 G or CYP2C9*1.	Warfarin	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
29457079-14	2017	When warfarin and methadone are used together, we have to consider their interaction by comparing the competitive inhibition of CYP2C9 to the induction of CYP3A4 by methadone, because CYP3A4 metabolize various drugs including oxycodone.	Warfarin	5-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
29457079-14	2017	When warfarin and methadone are used together, we have to consider their interaction by comparing the competitive inhibition of CYP2C9 to the induction of CYP3A4 by methadone, because CYP3A4 metabolize various drugs including oxycodone.	Methadone	18-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
29457079-14	2017	When warfarin and methadone are used together, we have to consider their interaction by comparing the competitive inhibition of CYP2C9 to the induction of CYP3A4 by methadone, because CYP3A4 metabolize various drugs including oxycodone.	Oxycodone	226-235	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
26644206-11	2017	Our study provided another kind of evidence that VKORC1 rs7294, CYP2C9 rs1057910, CYP4F2 rs2108622 and ORM1 rs17650 affected the action of warfarin in different styles.	Warfarin	139-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
27839691-2	2016	Aceclofenac is converted to 4"-hydroxyaceclofenac and diclofenac via CYP2C9-mediated hydroxylation and hydrolysis, respectively.	aceclofenac	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
27839691-2	2016	Aceclofenac is converted to 4"-hydroxyaceclofenac and diclofenac via CYP2C9-mediated hydroxylation and hydrolysis, respectively.	4'-hydroxyaceclofenac	28-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
27839691-2	2016	Aceclofenac is converted to 4"-hydroxyaceclofenac and diclofenac via CYP2C9-mediated hydroxylation and hydrolysis, respectively.	Diclofenac	54-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
27839691-3	2016	CYP2C9 also mediates the hydroxylation of diclofenac to yield 4"-hydroxydiclofenac and the hydrolysis of 4"-hydroxyaceclofenac to 4"-hydroxydiclofenac.	Diclofenac	42-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27839691-3	2016	CYP2C9 also mediates the hydroxylation of diclofenac to yield 4"-hydroxydiclofenac and the hydrolysis of 4"-hydroxyaceclofenac to 4"-hydroxydiclofenac.	4'-hydroxydiclofenac	62-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27839691-3	2016	CYP2C9 also mediates the hydroxylation of diclofenac to yield 4"-hydroxydiclofenac and the hydrolysis of 4"-hydroxyaceclofenac to 4"-hydroxydiclofenac.	4'-hydroxyaceclofenac	105-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27839691-3	2016	CYP2C9 also mediates the hydroxylation of diclofenac to yield 4"-hydroxydiclofenac and the hydrolysis of 4"-hydroxyaceclofenac to 4"-hydroxydiclofenac.	4'-hydroxydiclofenac	130-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27885968-1	2016	AIM: To evaluate a possible role of CYP2C9 genotyping for sulfonylureas (SUs) prescription in Russia.	Sulfonylurea Compounds	73-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
27198207-0	2016	Multigene and Drug Interaction Approach for Tamoxifen Metabolite Patterns Reveals Possible Involvement of CYP2C9, CYP2C19, and ABCB1.	Tamoxifen	44-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
27198207-9	2016	Lower concentrations of endoxifen and endoxifen/4-hydroxytamoxifen ratios were seen with impaired CYP2C9 (P = .05 and P = .03, respectively) if patients had the same CYP2D6 phenotype and were not taking a CYP2D6 or CYP2C19 inhibitor.	4-hydroxy-N-desmethyltamoxifen	24-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
27198207-9	2016	Lower concentrations of endoxifen and endoxifen/4-hydroxytamoxifen ratios were seen with impaired CYP2C9 (P = .05 and P = .03, respectively) if patients had the same CYP2D6 phenotype and were not taking a CYP2D6 or CYP2C19 inhibitor.	4-hydroxy-N-desmethyltamoxifen	38-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
27198207-9	2016	Lower concentrations of endoxifen and endoxifen/4-hydroxytamoxifen ratios were seen with impaired CYP2C9 (P = .05 and P = .03, respectively) if patients had the same CYP2D6 phenotype and were not taking a CYP2D6 or CYP2C19 inhibitor.	hydroxytamoxifen	48-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
27198207-13	2016	Thus, impairment in CYP2C9, CYP2C19, or ABCB1 contributes to a lower steady-state endoxifen concentration at the dose studied.	4-hydroxy-N-desmethyltamoxifen	82-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
27885968-0	2016	Possible approaches to CYP2C9-guided prescription of sulfonylureas in Russia.	Sulfonylurea Compounds	53-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
27885968-2	2016	MATERIALS &amp; METHODS: We have collected the current data on correlation between SUs pharmacodynamics and CYP2C9 polymorphisms.	Adenosine Monophosphate	11-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
27885968-1	2016	AIM: To evaluate a possible role of CYP2C9 genotyping for sulfonylureas (SUs) prescription in Russia.	Sulfonylurea Compounds	58-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
27885968-2	2016	MATERIALS &amp; METHODS: We have collected the current data on correlation between SUs pharmacodynamics and CYP2C9 polymorphisms.	Sulfonylurea Compounds	83-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
27885968-6	2016	CONCLUSION: Considering the received data and the existed knowledge on CYP2C9 influence on SUs pharmacokinetics and pharmacodynamics, we propose a possible approach to CYP2C9-guided SUs prescription for Russians.	Sulfonylurea Compounds	91-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
27885968-6	2016	CONCLUSION: Considering the received data and the existed knowledge on CYP2C9 influence on SUs pharmacokinetics and pharmacodynamics, we propose a possible approach to CYP2C9-guided SUs prescription for Russians.	Sulfonylurea Compounds	91-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
27885968-6	2016	CONCLUSION: Considering the received data and the existed knowledge on CYP2C9 influence on SUs pharmacokinetics and pharmacodynamics, we propose a possible approach to CYP2C9-guided SUs prescription for Russians.	Sulfonylurea Compounds	182-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
27885968-6	2016	CONCLUSION: Considering the received data and the existed knowledge on CYP2C9 influence on SUs pharmacokinetics and pharmacodynamics, we propose a possible approach to CYP2C9-guided SUs prescription for Russians.	Sulfonylurea Compounds	182-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
25719441-2	2016	Omeprazole is an acid suppressant and CYP2C9, CYP3A4, and CYP2C19 substrate and inhibitor, as well as inhibitor of transporters (like P-gp).	Omeprazole	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
25830869-5	2016	Increased warfarin sensitivity was associated with increased age; CYP2C9 genotypes 2/3, 1/3, and 3/3; VKORC1 genotypes AA and AG; and amiodarone use.	Warfarin	10-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
25830869-6	2016	Decreased warfarin sensitivity (ie, weekly warfarin dose of &gt;21 mg) was associated with increased height, increased weight, having diabetes mellitus, VKORC1 genotype GG, and CYP2C9 genotype 1/1.	Warfarin	10-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	177-183
25830869-6	2016	Decreased warfarin sensitivity (ie, weekly warfarin dose of &gt;21 mg) was associated with increased height, increased weight, having diabetes mellitus, VKORC1 genotype GG, and CYP2C9 genotype 1/1.	Warfarin	43-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	177-183
27488389-5	2016	RESULTS: A predictive model of warfarin maintenance dose was established and indicated that age, gender, body surface area, aspirin use, CYP2C9*3, CYP4F2 rs2108622, VKORC1 -1639C&gt;T, and POR*37 831-35C&gt;T accounted for 42.4 % of dose variance in patients undergoing anticoagulant treatment.	Warfarin	31-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
27581200-10	2016	CONCLUSION: The SNP C609T within NQO1 and haplotypes of CYP2C9 (1*2 or 1*3) are independently associated to bleeding complications of warfarin at normal INR.	Warfarin	134-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
27561267-8	2016	A variant genotype of CYP2C9 (i.e., *1/*2 and *1/*3) explained also a part of the remaining variability on Gb clearance.	Glyburide	107-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
27393744-0	2016	Implementing Algorithm-Guided Warfarin Dosing in an Ethnically Diverse Patient Population Using Electronic Health Records and Preemptive CYP2C9 and VKORC1 Genetic Testing.	Warfarin	30-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
27632229-3	2016	We genotyped 12 single nucleotide polymorphisms in genes (CYP2C9, VKORC1, CYP4F2, GGCX, EPHX1, CALU) associated with altered warfarin dose requirements and tested their associations with international normalized ratio variability (INRVAR) and percent time in therapeutic range in European-Americans and African-Americans.	Warfarin	125-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
27182616-1	2016	OBJECTIVE: The aim was to investigate the frequency of genetic polymorphisms of cytochrome P4502C9 (CYP2C9) and vitamin K epoxide reductase complex subunit1 (VKORC1) and determine the effect of these polymorphisms on warfarin dose requirements in pediatric patients.	Warfarin	217-225	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-98
27182616-1	2016	OBJECTIVE: The aim was to investigate the frequency of genetic polymorphisms of cytochrome P4502C9 (CYP2C9) and vitamin K epoxide reductase complex subunit1 (VKORC1) and determine the effect of these polymorphisms on warfarin dose requirements in pediatric patients.	Warfarin	217-225	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
27182616-5	2016	The ideal warfarin dose was calculated according to the patient"s age, height, and the presence of CYP2C9*2, CYP2C9*3, and VKORC1 genetic polymorphisms.	Warfarin	10-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
27182616-5	2016	The ideal warfarin dose was calculated according to the patient"s age, height, and the presence of CYP2C9*2, CYP2C9*3, and VKORC1 genetic polymorphisms.	Warfarin	10-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
27258224-0	2016	Effect of CYP2C9 and VKORC1 Gene Variants on Warfarin Response in Patients with Continuous-Flow Left Ventricular Assist Devices.	Warfarin	45-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
30645821-14	2016	Ruxolitinib is mainly metabolised by cytochrome P450 isoenzymes CYP3A4 and CYP2C9, creating a risk of multiple drug interactions.	ruxolitinib	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
26750984-10	2016	Glycyrol decreased CYP2C9-catalyzed diclofenac 4"-hydroxylation activity with IC50 values of 0.67 muM in human recombinant cDNA-expressed CYP2C9.	glycyrol	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
26750984-10	2016	Glycyrol decreased CYP2C9-catalyzed diclofenac 4"-hydroxylation activity with IC50 values of 0.67 muM in human recombinant cDNA-expressed CYP2C9.	glycyrol	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
26750984-10	2016	Glycyrol decreased CYP2C9-catalyzed diclofenac 4"-hydroxylation activity with IC50 values of 0.67 muM in human recombinant cDNA-expressed CYP2C9.	Diclofenac	36-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
27606428-13	2016	The pharmacogenetics studies confirmed that patients carrying the VKORC1 variant-allele required lower warfarin maintenance dosage and that the combination of VKORC1 and CYP2C9 yielded a warfarin responsive index (WRI) inversely related to the number variant alleles.	Warfarin	187-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-176
26750984-7	2016	Glycyrol strongly inhibited CYP1A-mediated phenacetin O-deethylation and CYP2C9-mediated diclofenac 4"-hydroxylation in HLMs, which were the result of competitive inhibition as revealed by a Dixon plot.	glycyrol	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
26750984-7	2016	Glycyrol strongly inhibited CYP1A-mediated phenacetin O-deethylation and CYP2C9-mediated diclofenac 4"-hydroxylation in HLMs, which were the result of competitive inhibition as revealed by a Dixon plot.	Diclofenac	89-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
27474842-3	2016	The aim of this study is to describe the distribution of CYP2C9*2, CYP2C9*3, CYP3A4*22 and CYP3A5*3 defective alleles, according to losartan tolerance in paediatric Marfan patients.	Losartan	132-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
27474842-3	2016	The aim of this study is to describe the distribution of CYP2C9*2, CYP2C9*3, CYP3A4*22 and CYP3A5*3 defective alleles, according to losartan tolerance in paediatric Marfan patients.	Losartan	132-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
27155586-3	2016	The objective of the current study was, in comparison to the standard-therapy method, to investigate the potential of rivaroxaban to improve the treatment of patients with PE, and to reduce hemorrhage in the standard-therapy group through adjusting the dose of warfarin by CYP2C9 and VKORC1 genotypes.	Rivaroxaban	118-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	273-279
27353638-0	2016	Impact of age, gender and CYP2C9/2C19 genotypes on dose-adjusted steady-state serum concentrations of valproic acid-a large-scale study based on naturalistic therapeutic drug monitoring data.	Valproic Acid	102-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
27390048-4	2016	METHODS: We developed the phenytoin-capecitabine interaction model on the assumption that fluorouracil (5-FU) inhibits cytochrome P450 (CYP) 2C9 synthesis in a concentration- dependent manner.	Phenytoin	26-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-144
27390048-4	2016	METHODS: We developed the phenytoin-capecitabine interaction model on the assumption that fluorouracil (5-FU) inhibits cytochrome P450 (CYP) 2C9 synthesis in a concentration- dependent manner.	Capecitabine	36-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-144
27390048-4	2016	METHODS: We developed the phenytoin-capecitabine interaction model on the assumption that fluorouracil (5-FU) inhibits cytochrome P450 (CYP) 2C9 synthesis in a concentration- dependent manner.	Fluorouracil	90-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-144
27390048-4	2016	METHODS: We developed the phenytoin-capecitabine interaction model on the assumption that fluorouracil (5-FU) inhibits cytochrome P450 (CYP) 2C9 synthesis in a concentration- dependent manner.	Fluorouracil	104-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-144
27390048-9	2016	The 50% inhibitory 5-FU concentration for CYP2C9 synthesis and the degradation rate constant of CYP2C9 were estimated to be 0.00310 ng/mL and 0.0768 day-1, respectively.	Fluorouracil	19-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
27390048-9	2016	The 50% inhibitory 5-FU concentration for CYP2C9 synthesis and the degradation rate constant of CYP2C9 were estimated to be 0.00310 ng/mL and 0.0768 day-1, respectively.	Fluorouracil	19-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
27306545-12	2016	The removal of patient covariates, even highly influential covariates such as CYP2C9 genotype for voriconazole, had no clinical impact.	Voriconazole	98-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
27155586-14	2016	Implication of CYP2C9 and VKORC1 genotypes in determining dose of warfarin, however, remains to be further examined in larger cohort studies.	Warfarin	66-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
27485379-0	2016	Commentary on clinical significance of CYP2C9-status-guided valproic acid therapy in children.	Valproic Acid	60-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
27197997-6	2016	Activation of CAR and PXR in cells treated with a high dose of CITCO [6-(4-chlorophenyl)-imidazo(2,1-b)thiazole-5-carbaldehyde] or cotreated with rifampicin and tetracycline resulted in synergistic enhancement of CYP3A4, but not CYP2B6, CYP2C9, or UGT1A1, mRNA expression in HepTR/hCAR/hPXR cells.	6-(4-chlorophenyl)imidazo(2,1-b)(1,3)thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime	63-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	237-243
27197997-6	2016	Activation of CAR and PXR in cells treated with a high dose of CITCO [6-(4-chlorophenyl)-imidazo(2,1-b)thiazole-5-carbaldehyde] or cotreated with rifampicin and tetracycline resulted in synergistic enhancement of CYP3A4, but not CYP2B6, CYP2C9, or UGT1A1, mRNA expression in HepTR/hCAR/hPXR cells.	6-(4-chlorophenyl)-imidazo(2,1-b)thiazole	70-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	237-243
27485380-0	2016	In response: Commentary on clinical significance of CYP2C9-status-guided valproic acid therapy in children.	Valproic Acid	73-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
27191765-1	2016	OBJECTIVE: Genetic polymorphisms of the P450 2C9 enzyme (CYP2C9), CYP2C19 and CYP3A5 gene are known to affect the metabolism of many drugs applied in liver transplant recipients, such as warfarin, voriconazole, and tacrolimus.	Warfarin	187-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
27191765-1	2016	OBJECTIVE: Genetic polymorphisms of the P450 2C9 enzyme (CYP2C9), CYP2C19 and CYP3A5 gene are known to affect the metabolism of many drugs applied in liver transplant recipients, such as warfarin, voriconazole, and tacrolimus.	Voriconazole	197-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
27191765-1	2016	OBJECTIVE: Genetic polymorphisms of the P450 2C9 enzyme (CYP2C9), CYP2C19 and CYP3A5 gene are known to affect the metabolism of many drugs applied in liver transplant recipients, such as warfarin, voriconazole, and tacrolimus.	Tacrolimus	215-225	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
27262824-2	2016	There are some reports of warfarin dose regimens correlating with single nucleotide polymorphisms (SNP) for CYP2C9, VKORC1 and other genes in adults.	Warfarin	26-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
27462768-4	2016	CYP2C9*2 and CYP2C9*3 mediated warfarin sensitivity was observed when vitamin K is in high and low tertiles, respectively.	Vitamin K	70-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
27142473-6	2016	For the vitamin K antagonists, the evidence of the association between variants in VKORC1 and CYP2C9 and the dose is clear.	Vitamin K	8-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
27462768-4	2016	CYP2C9*2 and CYP2C9*3 mediated warfarin sensitivity was observed when vitamin K is in high and low tertiles, respectively.	Warfarin	31-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27398225-1	2016	BACKGROUND: Regorafenib and its metabolites may inhibit the activities of several CYP or UDP-glucuronosyltransferase isoforms, including that of CYP2C9.	regorafenib	12-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
27462768-4	2016	CYP2C9*2 and CYP2C9*3 mediated warfarin sensitivity was observed when vitamin K is in high and low tertiles, respectively.	Warfarin	31-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
27462768-4	2016	CYP2C9*2 and CYP2C9*3 mediated warfarin sensitivity was observed when vitamin K is in high and low tertiles, respectively.	Vitamin K	70-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27161631-5	2016	Furthermore, VT-1129 weakly inhibited human CYP2C9, CYP2C19, and CYP3A4, suggesting a low drug-drug interaction potential.	VT-1129	13-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
27617219-2	2016	Single nucleotide polymorphisms (SNPs) of CYP2C9, CYP4F2, VKORC1 1173 and VKORC1-1639 influence warfarin maintenance dosage.	Warfarin	96-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
27398225-2	2016	Therefore, pharmacological agents that are CYP2C9 substrates may show elevated circulating levels and enhanced drug efficacy when concurrently used with regorafenib.	regorafenib	153-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
27398225-3	2016	Previous studies showed that the area under the plasma concentration-time curve of warfarin, which is the substrate for CYP2C9, increased upon co-administration of regorafenib.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
27398225-3	2016	Previous studies showed that the area under the plasma concentration-time curve of warfarin, which is the substrate for CYP2C9, increased upon co-administration of regorafenib.	regorafenib	164-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
27377818-9	2016	CYP2C9*3 and CYP2C9*13 alleles significantly affected the plasma concentrations of zafirlukast.	zafirlukast	83-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
27377818-9	2016	CYP2C9*3 and CYP2C9*13 alleles significantly affected the plasma concentrations of zafirlukast.	zafirlukast	83-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
27377818-0	2016	Effects of CYP2C9 genetic polymorphisms on the pharmacokinetics of zafirlukast.	zafirlukast	67-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
27302079-5	2016	Here, we have investigated the structural features of CYP2C8, CYP2C9, and CYP2C19 bound with their shared substrate diclofenac to elucidate the underlying molecular mechanism for the substrate regioselectivity of CYP2C subfamily enzymes.	Diclofenac	116-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
27377818-2	2016	Zafirlukast is metabolized mainly by CYP3A4 and CYP2C9.	zafirlukast	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
27377818-4	2016	A single 20-mg oral dose of zafirlukast was given to 23 Korean male subjects divided into two genotype groups according to CYP2C9 genotypes, CYP2C9EM (n = 11; CYP2C9*1/*1) and CYP2C9IM (n = 12; 9 and 3 carriers of CYP2C9*1/*3 and *1/*13, respectively).	zafirlukast	28-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
27377818-6	2016	Compared with the CYP2C9EM group, the Cmax and AUCinf of zafirlukast in the CYP2C9IM group were 1.44- and 1.70-fold higher, respectively (p &lt; 0.01 and p &lt; 0.0001).	zafirlukast	57-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
27377818-6	2016	Compared with the CYP2C9EM group, the Cmax and AUCinf of zafirlukast in the CYP2C9IM group were 1.44- and 1.70-fold higher, respectively (p &lt; 0.01 and p &lt; 0.0001).	zafirlukast	57-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
27377818-7	2016	The CL/F of zafirlukast was 42.8 % lower in the CYP2C9IM group compared with the CYP2C9EM group (p &lt; 0.001).	Fluorine	7-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
27377818-7	2016	The CL/F of zafirlukast was 42.8 % lower in the CYP2C9IM group compared with the CYP2C9EM group (p &lt; 0.001).	zafirlukast	12-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
26581561-5	2016	Taken together with our reported findings of the slow eliminations of amodiaquine and montelukast by monkey CYP2C9, CYP2C19 and CYP2C76, the present results suggest that these at least four chemicals may be good marker substrates for monkey CYP2C8.	Amodiaquine	70-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
26581561-5	2016	Taken together with our reported findings of the slow eliminations of amodiaquine and montelukast by monkey CYP2C9, CYP2C19 and CYP2C76, the present results suggest that these at least four chemicals may be good marker substrates for monkey CYP2C8.	montelukast	86-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
27154258-5	2016	In addition to immune mechanism, metabolism has been found to play a role in the pathogenesis of SCAR, such as recent findings of strong association of CYP2C9*3 with phenytoin-induced SCAR and impaired renal function with allopurinol SCAR.	Phenytoin	166-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	152-158
27154258-5	2016	In addition to immune mechanism, metabolism has been found to play a role in the pathogenesis of SCAR, such as recent findings of strong association of CYP2C9*3 with phenytoin-induced SCAR and impaired renal function with allopurinol SCAR.	Allopurinol	222-233	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	152-158
27163851-0	2016	In vitro metabolism of phenytoin in 36 CYP2C9 variants found in the Chinese population.	Phenytoin	23-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
27163851-3	2016	This study aims to assess the catalytic activities of wild-type (CYP2C9*1) and 36 CYP2C9 allelic variants found in the Chinese population toward phenytoin (PHT) in vitro.	Phenytoin	145-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
27163851-3	2016	This study aims to assess the catalytic activities of wild-type (CYP2C9*1) and 36 CYP2C9 allelic variants found in the Chinese population toward phenytoin (PHT) in vitro.	Phenytoin	156-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
27163851-3	2016	This study aims to assess the catalytic activities of wild-type (CYP2C9*1) and 36 CYP2C9 allelic variants found in the Chinese population toward phenytoin (PHT) in vitro.	Phenytoin	145-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
27163851-3	2016	This study aims to assess the catalytic activities of wild-type (CYP2C9*1) and 36 CYP2C9 allelic variants found in the Chinese population toward phenytoin (PHT) in vitro.	Phenytoin	156-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
27163851-4	2016	Insect microsomes expressing CYP2C9*1 and 36 CYP2C9 variants were incubated with 1-200 muM phenytoin for 30 min at 37  C. Then, these products were extracted and the signal detection was performed by HPLC-MS/MS.	Phenytoin	91-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
27130197-5	2016	The results of the present study show that both formation of 4"-hydroxydiclofenac and it subsequent bioactivation to DF-1",4"-QI is selectively catalyzed by CYP2C9.	4'-hydroxydiclofenac	61-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
27163851-4	2016	Insect microsomes expressing CYP2C9*1 and 36 CYP2C9 variants were incubated with 1-200 muM phenytoin for 30 min at 37  C. Then, these products were extracted and the signal detection was performed by HPLC-MS/MS.	Phenytoin	91-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
27163851-7	2016	The findings suggest that more attention should be paid on subjects carrying these infrequent CYP2C9 alleles when administering phenytoin in clinic.	Phenytoin	128-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
27130197-5	2016	The results of the present study show that both formation of 4"-hydroxydiclofenac and it subsequent bioactivation to DF-1",4"-QI is selectively catalyzed by CYP2C9.	df-1",4"-qi	117-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
27130197-6	2016	However, the two-step bioactivation to DF-2,5-QI appears to be catalyzed with highest activity by two different CYPs: 5-hydroxylation of DF is predominantly catalyzed by CYP3A4, whereas its subsequent bioactivation to DF-2,5-QI is catalyzed with 14-fold higher intrinsic clearance by CYP2C9.	df-2,5-qi	39-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	284-290
27329697-5	2016	In humans, plumbagin was not only a mixed inhibitor of CYP2B6, CYP2C9, CYP2D6, CYP2E1 and CYP3A4, but also a non-competitive inhibitor of CYP1A2, with Ki values no more than 2.16 muM.	plumbagin	11-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
26551762-0	2016	The Role of CYP2C8 and CYP2C9 Genotypes in Losartan-Dependent Inhibition of Paclitaxel Metabolism in Human Liver Microsomes.	Losartan	43-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
27334984-2	2016	In adults, numerous studies confirmed the robust relationship between warfarin maintenance doses and single nucleotide polymorphisms of cytochrome P450 2C9 (CYP2C9), vitamin K epoxide reductase (VKORC1), and cytochrome P450 4F2 (CYP4F2).	Warfarin	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-155
27334984-2	2016	In adults, numerous studies confirmed the robust relationship between warfarin maintenance doses and single nucleotide polymorphisms of cytochrome P450 2C9 (CYP2C9), vitamin K epoxide reductase (VKORC1), and cytochrome P450 4F2 (CYP4F2).	Warfarin	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
27334984-4	2016	The primary objective of the present systematic review and meta-analysis is to assess the effect of genotypes of CYP2C9, VKORC1, and CYP4F2 on warfarin maintenance dose in children.	Warfarin	143-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
27334984-9	2016	DISCUSSION: Our study will provide a comprehensive systematic review and meta-analysis on the potential effects of CYP2C9, VKORC1, or CYP4F2 on the warfarin maintenance dose in children, exploring the feasibility of the development of pharmacogenetic-guided warfarin dosing algorithm for children on oral vitamin K antagonists.	Warfarin	148-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
27296832-1	2016	BACKGROUND: To investigate the associations between atorvastatin-induced liver injury (AILI) and polymorphisms in eight genes possibly involved in the hepatic metabolism (CYP2C9, CYP2C19, CYP3A4, CYP3A5 and UGT1A1) and membrane transport (ABCB1, ABCG2 and SLCO1B1) of atorvastatin, we genotyped 30 AILI and 414 non-AILI patients recruited at BioBank Japan for 15 single nucleotide polymorphisms (SNPs).	Atorvastatin	52-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
26551762-0	2016	The Role of CYP2C8 and CYP2C9 Genotypes in Losartan-Dependent Inhibition of Paclitaxel Metabolism in Human Liver Microsomes.	Paclitaxel	76-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
26551762-1	2016	The aim of the present study was to further investigate a previously identified metabolic interaction between losartan and paclitaxel, which is one of the marker substrates of CYP2C8, by using human liver microsomes (HLMs) from donors with different CYP2C8 and CYP2C9 genotypes.	Losartan	110-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	261-267
26551762-1	2016	The aim of the present study was to further investigate a previously identified metabolic interaction between losartan and paclitaxel, which is one of the marker substrates of CYP2C8, by using human liver microsomes (HLMs) from donors with different CYP2C8 and CYP2C9 genotypes.	Paclitaxel	123-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	261-267
26551762-2	2016	Although CYP2C8 and CYP2C9 exhibit genetic linkage, previous studies have yet to determine whether losartan or its active metabolite, EXP-3174 which is specifically generated by CYP2C9, is responsible for CYP2C8 inhibition.	Losartan	99-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	178-184
26551762-6	2016	HLMs with either CYP2C9*2/*2 or CYP2C9*1/*3 exhibited a lower losartan intrinsic clearance (Vmax /Km ) than other HLMs including those with CYP2C9*1/*1 and CYP2C9*1/*2.	Losartan	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
26551762-6	2016	HLMs with either CYP2C9*2/*2 or CYP2C9*1/*3 exhibited a lower losartan intrinsic clearance (Vmax /Km ) than other HLMs including those with CYP2C9*1/*1 and CYP2C9*1/*2.	Losartan	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
26551762-6	2016	HLMs with either CYP2C9*2/*2 or CYP2C9*1/*3 exhibited a lower losartan intrinsic clearance (Vmax /Km ) than other HLMs including those with CYP2C9*1/*1 and CYP2C9*1/*2.	Losartan	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
26551762-6	2016	HLMs with either CYP2C9*2/*2 or CYP2C9*1/*3 exhibited a lower losartan intrinsic clearance (Vmax /Km ) than other HLMs including those with CYP2C9*1/*1 and CYP2C9*1/*2.	Losartan	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
27511999-8	2016	In turn, VKORC1 c.-1639A, CYP2C9*2 and *3 variants were independently associated with actual warfarin dose (P &lt; 0.0001).	Warfarin	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
26802434-4	2016	The field of pharmacogenetics is now yielding clinically important results, with three examples outlined: sulphonylurea sensitivity in patients with HNF1A maturity-onset diabetes of the young; sulphonylurea sensitivity in patients with Type 2 diabetes with reduced function alleles at CYP2C9, resulting in reduced metabolism of sulphonylureas; and severe metformin intolerance associated with reduced function organic cation transporter 1 (OCT1) variants, exacerbated by drugs that also inhibit OCT1.	Sulfonylurea Compounds	193-206	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	285-291
27511999-10	2016	Possession of CYP2C9*2 and/or CYP2C9*3 allele variants is associated with lower TTR values and warfarin dose variations in AVR patients, the latter affected also by VKORC1 c.-1693G&gt;A polymorphism.	Warfarin	95-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
27511999-10	2016	Possession of CYP2C9*2 and/or CYP2C9*3 allele variants is associated with lower TTR values and warfarin dose variations in AVR patients, the latter affected also by VKORC1 c.-1693G&gt;A polymorphism.	Warfarin	95-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
26122019-4	2016	In multivariate models, CYP2C9 IVS8-109 T was significantly associated with higher PHT plasma concentrations (t(64)=2.27; P=0.03).	Phenytoin	83-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
27214159-1	2016	PURPOSE: Some reports have suggested that bucolome, an inhibitor of cytochrome P450 2C9, is useful for decreasing inter-patient variation in warfarin clearance.	Warfarin	141-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-87
26818625-0	2016	S-Warfarin Limited Sampling Models to Estimate Area Under the Concentration Versus Time Curve for Cytochrome P450 2C9 Baseline Activity and After Induction.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-117
26818625-1	2016	BACKGROUND: Phenotyping cytochrome P450 (CYP) 2C9 activity using S-warfarin has routinely required extensive blood sampling over at least 96 hours after dose to estimate the area under the concentration time curve from zero to infinity (AUC).	Warfarin	65-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-49
26818625-7	2016	RESULTS: Different results were observed for S-warfarin LSMs in estimating CYP2C9 baseline activity, with most studies resulting in unacceptable bias and precision.	Warfarin	47-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
27179628-0	2016	Frequencies of CYP2C9 polymorphisms in North Indian population and their association with drug levels in children on phenytoin monotherapy.	Phenytoin	117-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
27179628-3	2016	METHODS: We studied 89 epileptic children of North Indian population, randomly selected, to see the genotypic and allelic frequency of CYP2C9 and its association with drug levels on phenytoin monotherapy.	Phenytoin	182-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	135-141
27179628-10	2016	CYP2C9*3 allelic group showed significantly higher serum phenytoin levels compared to the wild variants (P = 0.009).	Phenytoin	57-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
26948084-1	2016	Aprepitant is a known inducer of CYP2C9, the main warfarin-metabolizing enzyme.	Warfarin	50-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
26928377-3	2016	This study investigated the associations between the genetic polymorphisms of HLA class I and CYP2C9 and phenytoin-related SCAR in a Thai population.	Phenytoin	105-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
27298492-2	2016	Considering the paucity of data on the polymorphisms of CYP2C9 in Western Indian population, the present study was conducted to evaluate the prevalence of CYP2C9 polymorphisms (*1, *2 and *3) and correlate it with the activity using flurbiprofen (FLB) as a probe drug.	Flurbiprofen	233-245	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
27298492-2	2016	Considering the paucity of data on the polymorphisms of CYP2C9 in Western Indian population, the present study was conducted to evaluate the prevalence of CYP2C9 polymorphisms (*1, *2 and *3) and correlate it with the activity using flurbiprofen (FLB) as a probe drug.	Flurbiprofen	247-250	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
26928377-9	2016	The higher risk of phenytoin-related SJS/TEN was observed in the patients with CYP2C9*3 (odds ratio=4.30, 95% confidence interval=1.41-13.09, P&lt;0.05).	Phenytoin	19-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
26928377-11	2016	The CYP2C9*3 variant was significantly associated with phenytoin-related SJS/TEN, but not DRESS.	Phenytoin	55-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
27128896-3	2016	Aschantin potently inhibited CYP2C8-mediated amodiaquine N-de-ethylation, CYP2C9-mediated diclofenac 4"-hydroxylation, CYP2C19-mediated [S]-mephenytoin 4"-hydroxylation, and CYP3A4-mediated midazolam 1"-hydroxylation, with Ki values of 10.2, 3.7, 5.8, and 12.6 microM, respectively.	aschantin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
26996562-1	2016	PURPOSE: The genes for cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) have been identified as important genetic determinants of warfarin dosing and have been studied.	Warfarin	169-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-42
26996562-1	2016	PURPOSE: The genes for cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) have been identified as important genetic determinants of warfarin dosing and have been studied.	Warfarin	169-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
27128896-3	2016	Aschantin potently inhibited CYP2C8-mediated amodiaquine N-de-ethylation, CYP2C9-mediated diclofenac 4"-hydroxylation, CYP2C19-mediated [S]-mephenytoin 4"-hydroxylation, and CYP3A4-mediated midazolam 1"-hydroxylation, with Ki values of 10.2, 3.7, 5.8, and 12.6 microM, respectively.	Diclofenac	90-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
27518169-7	2016	Among them, CYP2C9 was most strongly inhibited by (-)-catechin-3-O-gallate (CG) (7.60 microM), and CYP1A2 was most strongly inhibited by EGCG (8.93 microM).	catechin gallate	50-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
27199745-0	2016	Functional Characterization of Human CYP2C9 Allelic Variants in COS-7 Cells.	carbonyl sulfide	64-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
27199745-2	2016	To evaluate the functional alternations of CYP2C9(*)2, CYP2C9(*)3, CYP2C9(*)8, CYP2C9(*)11 and CYP2C9(*)31, identified in our previous study in Chinese Han population, allelic variants as well as the wild-type CYP2C9 were transiently expressed in COS-7 cells.	carbonyl sulfide	247-250	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
27073631-0	2016	Clinical application of a new warfarin-dosing regimen based on the CYP2C9 and VKORC1 genotypes in atrial fibrillation patients.	Warfarin	30-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
27073631-1	2016	The polymorphisms of cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex 1 (VKORC1) are important genetic factors for warfarin dose determinations.	Warfarin	135-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-40
27073631-1	2016	The polymorphisms of cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex 1 (VKORC1) are important genetic factors for warfarin dose determinations.	Warfarin	135-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
27073631-2	2016	The present study aimed to investigate the contribution of the CYP2C9 and VKORC1 genotypes to warfarin dose requirement in atrial fibrillation (AF) patients, and to evaluate the clinical application of a warfarin-dosing algorithm.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
27073631-4	2016	A warfarin-dosing algorithm was developed based on age, height, and the CYP2C9 and VKORC1 genotypes of AF patients.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
27073631-5	2016	The results indicated that the mean warfarin daily dose requirement was lower in the CYP2C9*1/*3 genotype compared with those in the homozygous wild-type CYP2C9*1/*1 patients (P&lt;0.05), and was higher in patients with the VKORC1 AG and GG genotypes compared with those with the AA genotype (P&lt;0.05).	Warfarin	36-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
27073631-6	2016	The multivariate regression model showed that age, height, and the CYP2C9 and VKORC1 genotypes were the best variables for estimating warfarin dose (R2=56.4%).	Warfarin	134-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
27073631-11	2016	In conclusion, a new warfarin-dosing algorithm was developed based on the CYP2C9 and VKORC1 genotypes, and it can shorten the time elapse from initiation until warfarin maintenance dose in AF patients with warfarin therapy.	Warfarin	21-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
27073631-11	2016	In conclusion, a new warfarin-dosing algorithm was developed based on the CYP2C9 and VKORC1 genotypes, and it can shorten the time elapse from initiation until warfarin maintenance dose in AF patients with warfarin therapy.	Warfarin	160-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
27073631-11	2016	In conclusion, a new warfarin-dosing algorithm was developed based on the CYP2C9 and VKORC1 genotypes, and it can shorten the time elapse from initiation until warfarin maintenance dose in AF patients with warfarin therapy.	Warfarin	160-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
26878737-4	2016	Genetic variants in CYP2C9 and VKORC1 have been identified and shown to explain some of the variability in warfarin response.	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
27518169-7	2016	Among them, CYP2C9 was most strongly inhibited by (-)-catechin-3-O-gallate (CG) (7.60 microM), and CYP1A2 was most strongly inhibited by EGCG (8.93 microM).	cg	76-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
27518169-7	2016	Among them, CYP2C9 was most strongly inhibited by (-)-catechin-3-O-gallate (CG) (7.60 microM), and CYP1A2 was most strongly inhibited by EGCG (8.93 microM).	epigallocatechin gallate	137-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
27518169-8	2016	Catechin gallate exhibited non-competitive inhibition of CYP2C9, and its Ki value was 9.76 +- 0.47microM.	catechin gallate	0-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
27518169-9	2016	The present study is the first to report the inhibitory effect of CG on CYP2C9.	cg	66-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
27518169-13	2016	The ingestion of beverages containing large amounts of green tea catechins together with drugs that are metabolized by CYP1A2, CYP2C9, and CYP3A4 should be avoided.	Catechin	65-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-133
27055637-8	2016	RESULTS: The stable dose of warfarin was tightly associated with factors like age, height, weight, VKORC1 -1639G&gt;A, CYP2C9(*)3, CYP2C9(*)13 and amiodarone usage.	Warfarin	28-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
26940072-0	2016	Association of Genetic Polymorphisms in the VKORC1 and CYP2C9 Genes with Warfarin Dosage in a Group of Kuwaiti Individuals.	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
26940072-3	2016	Single nucleotide polymorphisms (SNP) in CYP2C9 and VKORC1 have been shown to significantly affect warfarin dosage toleration and this effect varies among different populations.	Warfarin	99-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
26940072-10	2016	CONCLUSIONS: Our data showed that individuals carrying the wild-type allele of CYP2C9 or VKORC1 rs9923231, rs9934438 or rs2884737 are less sensitive than individuals with the variant alleles of these SNPs and therefore required a higher daily maintenance dose of warfarin.	Warfarin	263-271	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
26940072-11	2016	Our study confirms the association between SNPs in CYP2C9 and VKORC1 and warfarin dose tolerance in Kuwaiti patients.	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
27080842-4	2016	The best-known examples are AVK and VKORC1-CYP2C9 or clopidogrel and CYP2C19.	Clopidogrel	53-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
26939024-5	2016	To confirm that the emission is from the heme, we destroyed the heme by titration with cumene hydroperoxide and measured the changes in emission upon titration with compounds known to bind to the distal face of the heme in two human cytochrome P450 enzymes, known as CYP3A4 and CYP2C9.	Heme	41-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	278-284
26927877-3	2016	Carvedilol is metabolized mainly by glucuronidation and, to a lesser extent, by CYP2D6 to hydroxyphenyl carvedilol (OHC) and by CYP2C9 to O-desmethyl carvedilol (DMC).	Carvedilol	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
26927877-3	2016	Carvedilol is metabolized mainly by glucuronidation and, to a lesser extent, by CYP2D6 to hydroxyphenyl carvedilol (OHC) and by CYP2C9 to O-desmethyl carvedilol (DMC).	desmethylcarvedilol	138-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
26927877-3	2016	Carvedilol is metabolized mainly by glucuronidation and, to a lesser extent, by CYP2D6 to hydroxyphenyl carvedilol (OHC) and by CYP2C9 to O-desmethyl carvedilol (DMC).	desmethylcarvedilol	162-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
27055637-8	2016	RESULTS: The stable dose of warfarin was tightly associated with factors like age, height, weight, VKORC1 -1639G&gt;A, CYP2C9(*)3, CYP2C9(*)13 and amiodarone usage.	Warfarin	28-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
27055637-10	2016	The weights of VKORC1 and CYP2C9 for predicting of warfarin dosage were estimated to more than 50%.	Warfarin	51-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
26877175-2	2016	The CYP2C9 was attached to magnetic SiMAG-carboxyl microparticles using the carbodiimide method.	Carbodiimides	76-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
26806573-0	2016	Effects of salvianolic acid B and tanshinone IIA on the pharmacokinetics of losartan in rats by regulating the activities and expression of CYP3A4 and CYP2C9.	Losartan	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	151-157
26877175-5	2016	The on-line kinetic and inhibition studies of CYP2C9"s reaction with diclofenac as a model substrate and sulfaphenazole as a model inhibitor were conducted in order to demonstrate its practical applicability.	Diclofenac	69-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
26877175-5	2016	The on-line kinetic and inhibition studies of CYP2C9"s reaction with diclofenac as a model substrate and sulfaphenazole as a model inhibitor were conducted in order to demonstrate its practical applicability.	Sulfaphenazole	105-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
27622442-0	2016	Prediction of sensitivity to warfarin based on VKORC1 and CYP2C9 polymorphisms in patients from different places in Colombia.	Warfarin	29-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
27622442-9	2016	CONCLUSIONS: These results in a mixed population support the prediction of sensitivity to warfarin based on polymorphisms in VKORC1 and CYP2C9 as a valid approach in Colombian patients.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
27092633-3	2016	This review brings an update about how genetic polymorphisms of CYP2C8 and CYP2C9 enzymes affect the disposition and clinical outcomes of ibuprofen and diclofenac, two of the most common pain relievers.	Ibuprofen	138-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
27092633-3	2016	This review brings an update about how genetic polymorphisms of CYP2C8 and CYP2C9 enzymes affect the disposition and clinical outcomes of ibuprofen and diclofenac, two of the most common pain relievers.	Diclofenac	152-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
27092633-4	2016	The most common side effects associated with the influence of CYP2C8*3 and CYP2C9*2*3 variants on ibuprofen and diclofenac pharmacokinetics are hepatotoxicity and gastrointestinal bleeding.	Ibuprofen	98-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
27092633-4	2016	The most common side effects associated with the influence of CYP2C8*3 and CYP2C9*2*3 variants on ibuprofen and diclofenac pharmacokinetics are hepatotoxicity and gastrointestinal bleeding.	Diclofenac	112-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
24978953-7	2016	Our results suggest that the VKORC1-1639 GG and the wild type CYP2C9*1*1genotypes are associated with the high-dose requirement for warfarin therapy, and that VKORC1-1639 GG is responsible for warfarin resistance and failure in Egyptian patients.	Warfarin	132-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
24978953-0	2016	VKORC1 and CYP2C9 genotypes in Egyptian patients with warfarin resistance.	Warfarin	54-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
24978953-7	2016	Our results suggest that the VKORC1-1639 GG and the wild type CYP2C9*1*1genotypes are associated with the high-dose requirement for warfarin therapy, and that VKORC1-1639 GG is responsible for warfarin resistance and failure in Egyptian patients.	Warfarin	193-201	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
24978953-3	2016	The resistance is associated with polymorphisms of the vitamin K epoxide reductase-oxidase complex (VKORC1) and cytochrome P450-2C9 (CYP2C9) genes, which affect warfarin pharmacodynamics and pharmacokinetics, respectively.	Warfarin	161-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-131
27008632-4	2016	METHODS: We genotyped 5 variants of these genes in a total of 747 diabetic patients enrolled in a trial of glibenclamide (CYP2C9, KCNJ11, TCF7L2, KCNQ1 and CDKN2A/2B gene).	Glyburide	107-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
24978953-3	2016	The resistance is associated with polymorphisms of the vitamin K epoxide reductase-oxidase complex (VKORC1) and cytochrome P450-2C9 (CYP2C9) genes, which affect warfarin pharmacodynamics and pharmacokinetics, respectively.	Warfarin	161-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
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
26267707-2	2016	The dosage of warfarin is strongly affected by genetic variants of CYP2C9 and VKORC1 genes.	Warfarin	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
26886310-0	2016	The Effect of Genetic Polymorphism on the Inhibition of Azole Antifungal Agents Against CYP2C9-Mediated Metabolism.	Azoles	56-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
26886310-1	2016	We investigated the effect of cytochrome P450 (CYP) 2C9 polymorphism on the inhibition of methylhydroxylation activity of tolbutamide, a typical CYP2C9 substrate, by triazole antifungal agents, fluconazole and voriconazole.	Tolbutamide	122-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-55
26886310-1	2016	We investigated the effect of cytochrome P450 (CYP) 2C9 polymorphism on the inhibition of methylhydroxylation activity of tolbutamide, a typical CYP2C9 substrate, by triazole antifungal agents, fluconazole and voriconazole.	Tolbutamide	122-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
26886310-1	2016	We investigated the effect of cytochrome P450 (CYP) 2C9 polymorphism on the inhibition of methylhydroxylation activity of tolbutamide, a typical CYP2C9 substrate, by triazole antifungal agents, fluconazole and voriconazole.	Triazoles	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-55
26886310-1	2016	We investigated the effect of cytochrome P450 (CYP) 2C9 polymorphism on the inhibition of methylhydroxylation activity of tolbutamide, a typical CYP2C9 substrate, by triazole antifungal agents, fluconazole and voriconazole.	Triazoles	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	145-151
26886310-3	2016	These results suggest that more careful administration of azole antifungals to patients with the CYP2C9*2 allele might be required because of the strong inhibitory effects.	Azoles	58-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
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
26719074-2	2016	The purpose of this study was to evaluate the pharmacokinetics and pharmacodynamics of warfarin (as a reference drug metabolized by CYP2C9) in the presence and absence of belinostat.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
26633237-8	2016	The results suggest that the altered pharmacokinetics of DIC might be attributed to RSV mediated inhibition of CYP2C9 enzyme.	Resveratrol	84-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
27180666-4	2016	The response to sulfonylurea derivatives was significantly associated with the variants KCNJ11/ABCC8, TCF7L2 and CYP2C9.	Sulfonylurea Compounds	16-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
27026863-0	2016	Metabolic inhibition of meloxicam by specific CYP2C9 inhibitors in Cunninghamella blakesleeana NCIM 687: in silico and in vitro studies.	Meloxicam	24-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
27026863-4	2016	The in silico studies were further substantiated by in vitro studies, which indicated fenofibrate to be a potent inhibitor of CYP2C9 enzyme followed by sertraline, clopidogrel and fluvoxamine, respectively.	Fenofibrate	86-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
27026863-5	2016	Two-stage fermentation protocol was followed to study metabolism of meloxicam and its inhibition by different CYP2C9 inhibitors.	Meloxicam	68-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
26845774-4	2016	The results showed that CK inhibited the enzyme activities of CYP2C9 and CYP3A4 in the HLMs.	ginsenoside M1	24-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
26845774-8	2016	The results suggested that CK was a substrate and also inhibitors for both CYP2C9 and CYP3A4.	ginsenoside M1	27-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
26845774-9	2016	Patients using CK in combination with therapeutic drugs that are substrates of CYP2C9 and CYP3A4 for different reasons should be careful, although the inhibiting potency of CK is much poorer than that of enzyme-specific inhibitors.	ginsenoside M1	15-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
26658225-5	2016	The EC50 of rifampin for CYP3A4 and CYP2C9 was up to 10-fold lower in HepatoPac than the monocultures.	Rifampin	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
26751406-1	2016	Genotype-based algorithms that include VKORC1 and CYP2C9 genotypes are less predictive of warfarin dose variability in Africans as opposed to Europeans.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
25476996-0	2016	The role of CYP2C9 genetic polymorphism in carvedilol O-desmethylation in vitro.	Carvedilol	43-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
25476996-1	2016	We aimed at investigating the role of CYP2C9 in carvedilol O-desmethylation and identifying the effect of 35 CYP2C9 allelic variants we found in Chinese Han population on the in vitro metabolism of carvedilol.	Carvedilol	198-208	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
25476996-3	2016	Recombinant CYP2C9 microsomes of distinguished genotypes were used to characterize the corresponding enzyme activity toward carvedilol.	Carvedilol	124-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
25476996-5	2016	CYP2C9 plays a certain role in carvedilol metabolism.	Carvedilol	31-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25476996-6	2016	Compared with wild-type CYP2C9*1, the intrinsic clearance (V max/K m) values of all variants toward carvedilol O-desmethylation were significantly altered.	Carvedilol	100-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
26549688-6	2016	RT-PCR analysis showed that PXR SUMOylation in presence of rifampicin also enhances the endogenous expression levels of key PXR-regulated genes like CYP3A4, CYP2C9, MDR1 and UGT1A1.	Rifampin	59-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
26759747-2	2016	Rifampin is a widely used antimicrobial that has major interactions with several medications including warfarin due to its strong P-glycoprotein and liver enzyme inducer activity especially on CYP2C9, CYP3A4, CYP1A2 and CYP2C19.	Rifampin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	193-199
26568290-6	2016	A two-color multiplex allele-specific PCR assay for detecting the warfarin-related single-nucleotide polymorphisms (SNPs) 6853 (-1639G&gt;A) and 6484 (1173C&gt;T) in the VKORC1 gene and the *3 SNP (1075A&gt;C) in the CYP2C9 gene was developed and used for validation studies.	Warfarin	66-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	217-223
26759747-2	2016	Rifampin is a widely used antimicrobial that has major interactions with several medications including warfarin due to its strong P-glycoprotein and liver enzyme inducer activity especially on CYP2C9, CYP3A4, CYP1A2 and CYP2C19.	Warfarin	103-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	193-199
26739746-6	2016	Statistical analyses were performed using Plink and R. RESULTS: VKORC1 and CYP2C9 were the major genetic determinants of warfarin MWD and SMWD, with CYP4F2 having a smaller effect.	Warfarin	121-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
26739746-9	2016	Genotypes for VKORC1 and CYP2C9*3, age, height and weight, as well as other clinical factors such as alcohol consumption, loading dose and concomitant drugs were important for the initial INR response to warfarin.	Warfarin	204-212	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
27174459-6	2016	RESULTS: The final PPK model equations of oral phenytoin were found to be as follows: for patients with CYP2C9 *1/*1, Vmax=22.66.	Phenytoin	47-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
26739746-12	2016	VKORC1 and CYP2C9 genetic polymorphisms are the most important determinants of warfarin dosing, and it is highly unlikely that other common variants of clinical importance influencing warfarin dosage will be found.	Warfarin	79-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
26739746-13	2016	Both VKORC1 and CYP2C9*3 are important determinants of the initial INR response to warfarin.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
25998968-0	2016	Phenytoin toxicity in two-month-old Thai infant with CYP2C9 gene polymorphism--A case report.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
25998968-4	2016	The cytochrome P450 super family plays an important role in phenytoin metabolism, especially CYP2C9 and CYP2C19.	Phenytoin	60-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
25998968-5	2016	In this case report, we profiled a two-month-old Thai infant who developed phenytoin toxicity resulting from CYP2C9 gene polymorphism.	Phenytoin	75-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
26777610-0	2016	Association of Genetic Polymorphisms of CYP2C9 and VKORC1 with Bleeding Following Warfarin: A Case-Control Study.	Warfarin	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
26777610-2	2016	This study aimed to assess the association of CYP2C9 and VKORC1 with the development of bleeding following warfarin.	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
26777610-12	2016	CONCLUSION: A significant association between CYP2C9 (*1,*2,*3) genotype and VKORC1 (1639 G&gt;A) haplotype status has been found with increased bleeding tendency to warfarin.	Warfarin	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
26496779-7	2016	Phenobarbital is metabolized in the liver by CYP2C9 with minor metabolism by CYP2C19 and CYP2E1.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
27216792-6	2016	RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan.	Losartan	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
26502773-6	2016	In hepatocyte toxicity studies, the cell viability of human hepatocytes decreased after exposure to Ro 47-8634, and the observed hepatotoxicity was diminished by pretreatment with tienilic acid (CYP2C9-specific inactivator).	Ticrynafen	180-193	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
27216792-6	2016	RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan.	Valsartan	236-245	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
27216792-6	2016	RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan.	candesartan	247-258	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
27216792-6	2016	RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan.	Irbesartan	260-270	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
27216792-6	2016	RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan.	azilsartan	276-286	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
27216792-6	2016	RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan.	Telmisartan	368-379	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
27216792-6	2016	RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan.	eprosartan	381-391	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
27216792-6	2016	RESULTS: Based on the literatures published, it has been demonstrated that pharmacokinetic interactions of losartan with other agents are mainly via CYP2C9- and CYP3A4-mediated, the role played by CYP enzyme system in the metabolism of valsartan, candesartan, irbesartan, and azilsartan appears modest, and cytochrome P450 system has no influence on the metabolism of telmisartan, eprosartan, olmesartan.	olmesartan	393-403	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
26502773-9	2016	These results suggest that Ro 64-1056 is directly involved in bosentan-induced liver injury partly because CYP2C9 specifically mediates hydroxylation of the t-butyl group of Ro 47-8634.	Bosentan	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
29787666-3	2016	(Argl44Cys) and CYP2C9*3 (Ile359Leu) genes showed that the dominant genotype of CYP2C9*2 was the honiozygous CC carriership and for CYP2C9*3 it was the prevalence of AA genotype, the incidence of which was close and amounted to 80%.	argl44cys	1-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
29787666-3	2016	(Argl44Cys) and CYP2C9*3 (Ile359Leu) genes showed that the dominant genotype of CYP2C9*2 was the honiozygous CC carriership and for CYP2C9*3 it was the prevalence of AA genotype, the incidence of which was close and amounted to 80%.	argl44cys	1-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
27006677-4	2016	To evaluate the effects of vinpocetine on the activity of human CYP3A4, CYP2C9, CYP2C19, CYP2D6, and CYP2E1, human liver microsomes were utilized to incubate with the mixed CYPs probe substrates and the target components.	vinpocetine	27-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
26693855-6	2016	RESULTS: Benzbromarone metabolism resulted in inhibition of CYP3A4 but not CYP2C9 in a time-dependent manner.	Benzbromarone	9-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
27006677-5	2016	The results indicate that vinpocetine exhibited weak inhibitory effect on the CYP2C9, where the IC50 value is 68.96 muM, whereas the IC50 values for CYP3A4, CYP2C19, CYP2D6, and CYP2E1 were all over range of 100 muM, which showed that vinpocetine had no apparent inhibitory effects on these CYPs.	vinpocetine	26-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
27006677-6	2016	In conclusion, the results indicated that drugs metabolized by CYP2C9 coadministrated with vinpocetine may require attention or dose adjustment.	vinpocetine	91-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
26355760-7	2016	Linear regression and ANN models identified several predictors of warfarin dose including age, weight, CYP2C9 genotype *1/*1, VKORC1 genotype, rs12777823 genotype, rs2108622 genotype, congestive heart failure, and amiodarone use.	Warfarin	66-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
27698677-7	2016	CYP1A2, CYP2C9, CYP2D6, CYP2E1, CYP3A4, and CYP2C19 contributed differently to the metabolism of morusin.	morusin	97-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
26870974-1	2016	The aim of the research was to study the frequency of VKROC1 and CYP2C9 genes different alleles for healthy donors and for patients with thrombosis, in two regions of Georgia - in Samegrelo and in Tbilisi and to reveal the interdependence of the studied genes products in the treatment of thrombosis with warfarin.	Warfarin	305-313	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
26870974-3	2016	The protein product of CYP2C9 gene is involved in the metabolism of warfarin.	Warfarin	68-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
28057172-2	2016	METHODS: Aminopyrine N-demethylation and tolbutamide methylhydroxylation by CYP2C8, CYP2C9, and CYP2C19 were determined by the previous reported methods.	Aminopyrine	9-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
26655108-3	2016	These two enantiomers show differences in metabolism by CYPs: S-warfarin undergoes 7 hydroxylation by CYP2C9 and R-warfarin by CYP3A4 to form 10 hydroxy warfarin.	Warfarin	62-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
26655108-12	2016	In addition, we show inhibition of major metabolic pathways of warfarin by sulfaphenazole and ketoconazole which are known specific inhibitors of CYP2C9 and CYP3A4 respectively.	Warfarin	63-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
26655108-12	2016	In addition, we show inhibition of major metabolic pathways of warfarin by sulfaphenazole and ketoconazole which are known specific inhibitors of CYP2C9 and CYP3A4 respectively.	Sulfaphenazole	75-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
26655108-12	2016	In addition, we show inhibition of major metabolic pathways of warfarin by sulfaphenazole and ketoconazole which are known specific inhibitors of CYP2C9 and CYP3A4 respectively.	Ketoconazole	94-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
28057172-2	2016	METHODS: Aminopyrine N-demethylation and tolbutamide methylhydroxylation by CYP2C8, CYP2C9, and CYP2C19 were determined by the previous reported methods.	Tolbutamide	41-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
28057172-6	2016	For tolbutamide methylhydroxylation, the Km and Vmax for CYP2C19 were three and six times higher than the corresponding values for CYP2C9, and the Vmax/Km value for CYP2C19 was twice that for CYP2C9, whereas hydroxylated tolbutamide formed by CYP2C8 was not detected.	Tolbutamide	4-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
28057172-6	2016	For tolbutamide methylhydroxylation, the Km and Vmax for CYP2C19 were three and six times higher than the corresponding values for CYP2C9, and the Vmax/Km value for CYP2C19 was twice that for CYP2C9, whereas hydroxylated tolbutamide formed by CYP2C8 was not detected.	Tolbutamide	4-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	192-198
26569597-4	2016	CYP2C9-based interaction was investigated for both 2-oxo-clopidogrel and glimepiride using HLM and the recombinant CYP2C9 system.	2-oxo-clopidogrel	51-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
26569597-4	2016	CYP2C9-based interaction was investigated for both 2-oxo-clopidogrel and glimepiride using HLM and the recombinant CYP2C9 system.	glimepiride	73-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
26569597-6	2016	For the metabolism of 2-oxo-clopidogrel (the second step of bioactivation), glimepiride demonstrated a relatively strong inhibition against CYP2C9 activity (IC50 12.7 mumol/l).	2-oxo-clopidogrel	22-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
26569597-6	2016	For the metabolism of 2-oxo-clopidogrel (the second step of bioactivation), glimepiride demonstrated a relatively strong inhibition against CYP2C9 activity (IC50 12.7 mumol/l).	glimepiride	76-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
26569597-7	2016	In addition, 2-oxo-clopidogrel displayed a moderate inhibitory effect toward the CYP2C9-mediated metabolism of glimepiride.	2-oxo-clopidogrel	13-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
26569597-7	2016	In addition, 2-oxo-clopidogrel displayed a moderate inhibitory effect toward the CYP2C9-mediated metabolism of glimepiride.	glimepiride	111-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
27287328-3	2016	METHODS: Different concentrations of apigenin were added to a 100 mmol/l Tris-HCl reaction mixture containing 2 pmol/ml recombinant human CYP2C9.1, 0.25 mg/ml human liver microsomes or 0.5 mg/ml rat liver microsomes to determine the half maximal inhibition or a half-maximal inhibitory concentration (IC50) on the metabolism of losartan.	Apigenin	37-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
27287328-5	2016	RESULTS: The results showed that apigenin has the inhibitory effect on the metabolism of losartan in vitro, the IC50 was 7.61, 4.10 and 11.07 mumol/l on recombinant CYP2C9 microsomes, human liver microsomes and rat liver microsomes, respectively.	Apigenin	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	165-171
27287328-5	2016	RESULTS: The results showed that apigenin has the inhibitory effect on the metabolism of losartan in vitro, the IC50 was 7.61, 4.10 and 11.07 mumol/l on recombinant CYP2C9 microsomes, human liver microsomes and rat liver microsomes, respectively.	Losartan	89-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	165-171
27287328-6	2016	Meanwhile, apigenin"s mode of action on human CYP2C9 activity was competitive for the substrate diclofenac.	Diclofenac	96-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
26658169-0	2016	Phenytoin neurotoxicity in a child carrying new STXBP1 and CYP2C9 gene mutations.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
26666467-7	2016	S-warfarin/7-hydroxywarfarin ratio was found to increase in subjects with CYP2C9*2 and CYP2C9*3 justifying the warfarin sensitivity attributed to these variants.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
26666467-7	2016	S-warfarin/7-hydroxywarfarin ratio was found to increase in subjects with CYP2C9*2 and CYP2C9*3 justifying the warfarin sensitivity attributed to these variants.	Warfarin	2-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
26666467-7	2016	S-warfarin/7-hydroxywarfarin ratio was found to increase in subjects with CYP2C9*2 and CYP2C9*3 justifying the warfarin sensitivity attributed to these variants.	7-hydroxywarfarin	11-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
26666467-7	2016	S-warfarin/7-hydroxywarfarin ratio was found to increase in subjects with CYP2C9*2 and CYP2C9*3 justifying the warfarin sensitivity attributed to these variants.	7-hydroxywarfarin	11-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
26666467-7	2016	S-warfarin/7-hydroxywarfarin ratio was found to increase in subjects with CYP2C9*2 and CYP2C9*3 justifying the warfarin sensitivity attributed to these variants.	Warfarin	20-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
26666467-7	2016	S-warfarin/7-hydroxywarfarin ratio was found to increase in subjects with CYP2C9*2 and CYP2C9*3 justifying the warfarin sensitivity attributed to these variants.	Warfarin	20-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
26409440-5	2015	Significant promotions were also demonstrated in the syntheses of albumin and urea and the activities of phase I (CYP 3A11 and CYP 2C9) and phase II enzymes.	Urea	78-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-134
30620511-5	2016	Flu-voxamine inhibits CYPlA2 and CYP2C9 activity, and paroxetine inhibits CYP2D6 activity.	Fluvoxamine	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
26677906-5	2016	Formation of 5-CA and S-777469 5-hydroxymethyl (5-HM), a precursor metabolite of 5-CA, was catalyzed by CYP2C9.	S-777469	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
26677906-5	2016	Formation of 5-CA and S-777469 5-hydroxymethyl (5-HM), a precursor metabolite of 5-CA, was catalyzed by CYP2C9.	5-hydroxymethyl	31-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
26677906-5	2016	Formation of 5-CA and S-777469 5-hydroxymethyl (5-HM), a precursor metabolite of 5-CA, was catalyzed by CYP2C9.	5-hydroxymethyl tolterodine	48-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
26677906-6	2016	Arachidonic acid, alpha-linolenic acid, oleic acid and myristic acid, which have been reported to exist in liver microsomes, inhibited S-777469 oxidation by CYP2C9, but serum albumin enhanced this reactions.	Arachidonic Acid	0-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
26677906-6	2016	Arachidonic acid, alpha-linolenic acid, oleic acid and myristic acid, which have been reported to exist in liver microsomes, inhibited S-777469 oxidation by CYP2C9, but serum albumin enhanced this reactions.	alpha-Linolenic Acid	18-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
26677906-6	2016	Arachidonic acid, alpha-linolenic acid, oleic acid and myristic acid, which have been reported to exist in liver microsomes, inhibited S-777469 oxidation by CYP2C9, but serum albumin enhanced this reactions.	Oleic Acid	40-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
26677906-6	2016	Arachidonic acid, alpha-linolenic acid, oleic acid and myristic acid, which have been reported to exist in liver microsomes, inhibited S-777469 oxidation by CYP2C9, but serum albumin enhanced this reactions.	Myristic Acid	55-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	157-163
26677906-11	2016	CYP2C9 was the enzyme responsible for S-777469 oxidation in human livers.	Sulfur	38-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
26712778-2	2015	This study evaluated the effect of GA on the activity of five P450(CYP450) cytochrome enzymes: CYP2A6, CYP2C9, CYP2C19, CYP2D6, and CYP3A4, in human liver microsomes (HLMs) and recombinant cDNA-expressed enzyme systems using a HPLC-MS/MS CYP-specific probe substrate assay.	Glycyrrhetinic Acid	35-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
26712778-6	2015	Moreover, CYP2C9 and CYP2C19 could also be inhibited significantly by GA with IC50 of 42.89 and 40.26 muM in HLMs, respectively.	Glycyrrhetinic Acid	70-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
26377995-10	2015	CONCLUSIONS: The genotyping of polymorphic variants in VKORC1 and CYP2C9, together with clinical and demographic parameters, can serve for more precise definition of the individual starting and maintenance doses of coumarin derivatives in each patient.	coumarin	215-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
26348733-6	2015	Several compounds, including loratadine, showed high selectivity to cynomolgus monkey CYP2C19, and all of these have been reported as human CYP2C19 and/or CYP2C9 substrates.	Loratadine	29-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
26223945-7	2015	Similarly, in the subpopulation of AA carriers in the CYP2C9 gene, patients with the T allele required significantly higher doses of warfarin than those with other genotypes of rs887829 (6.5 +- 2.4 vs. 5.3 +- 1.5 mg, P = 0.002).	Warfarin	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
26344676-1	2015	Genetic variation in the pharmacokinetics of metoprolol and torsemide due to polymorphisms in CYP2D6, CYP2C9, and OATP1B1 has been extensively studied.	Metoprolol	45-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
26264702-5	2015	RESULTS: In vitro, evacetrapib inhibited all of the major CYPs, with inhibition constants (K(i)) ranging from 0.57 microM (CYP2C9) to 7.6 microM (CYP2C19).	evacetrapib	19-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
26344676-1	2015	Genetic variation in the pharmacokinetics of metoprolol and torsemide due to polymorphisms in CYP2D6, CYP2C9, and OATP1B1 has been extensively studied.	Torsemide	60-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
26374173-3	2015	Kinetic and inhibition experiments performed at therapeutically relevant concentrations reveal that CYP2C8 and CYP2C9 are the principal enzymes responsible for montelukast 36-hydroxylation to 1,2-diol.	montelukast	160-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
26781925-6	2015	This was a prospective hospital based study in which allele and genotypic frequencies of CYP2C9 gene polymorphisms; 430C&gt;T and 1075A&gt;C and VKORC1 gene polymorphisms; 1639G&gt;A, 9041G&gt;A and 6009C&gt;T in 106 alleles of north Indian patients with valve replacement on acenocoumarol were determined and their effect on acenocoumarol dosing was studied.	Acenocoumarol	276-289	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
26781925-6	2015	This was a prospective hospital based study in which allele and genotypic frequencies of CYP2C9 gene polymorphisms; 430C&gt;T and 1075A&gt;C and VKORC1 gene polymorphisms; 1639G&gt;A, 9041G&gt;A and 6009C&gt;T in 106 alleles of north Indian patients with valve replacement on acenocoumarol were determined and their effect on acenocoumarol dosing was studied.	Acenocoumarol	326-339	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
26781925-8	2015	In 53 patients with valve replacement on acenocoumarol with stable INR, the allele frequency of CYP2C9*2 and CYP2C9*3 gene polymorphisms was 0.05 and 0.17 respectively and that of VKORC1 *2,*3 and *4 gene polymorphisms was 0.15, 0.72 and 0.11 respectively.	Acenocoumarol	41-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
26781925-9	2015	The presence of CYP2C9*3 or VKORC1*2 gene polymorphism were associated with decrease in acenocoumarol dose requirements (p values 0.03 and 0.02 respectively).This study confirmed the association of lower mean weekly dosages of acenocoumarol in patients with CYP2C9*3 and VKORC1*2 gene polymorphisms.	Acenocoumarol	88-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
26781925-9	2015	The presence of CYP2C9*3 or VKORC1*2 gene polymorphism were associated with decrease in acenocoumarol dose requirements (p values 0.03 and 0.02 respectively).This study confirmed the association of lower mean weekly dosages of acenocoumarol in patients with CYP2C9*3 and VKORC1*2 gene polymorphisms.	Acenocoumarol	88-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	258-264
26781925-9	2015	The presence of CYP2C9*3 or VKORC1*2 gene polymorphism were associated with decrease in acenocoumarol dose requirements (p values 0.03 and 0.02 respectively).This study confirmed the association of lower mean weekly dosages of acenocoumarol in patients with CYP2C9*3 and VKORC1*2 gene polymorphisms.	Acenocoumarol	227-240	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
26781925-9	2015	The presence of CYP2C9*3 or VKORC1*2 gene polymorphism were associated with decrease in acenocoumarol dose requirements (p values 0.03 and 0.02 respectively).This study confirmed the association of lower mean weekly dosages of acenocoumarol in patients with CYP2C9*3 and VKORC1*2 gene polymorphisms.	Acenocoumarol	227-240	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	258-264
26409163-8	2015	The in-vitro metabolism assay with the human CYP2C9 isoform led to the formation of THCOH and THCCOOH of Delta(8)-THC and Delta(9)-THC.	thcoh	84-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
26409163-8	2015	The in-vitro metabolism assay with the human CYP2C9 isoform led to the formation of THCOH and THCCOOH of Delta(8)-THC and Delta(9)-THC.	11-nor-delta(9)-tetrahydrocannabinol-9-carboxylic acid	94-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
26409163-8	2015	The in-vitro metabolism assay with the human CYP2C9 isoform led to the formation of THCOH and THCCOOH of Delta(8)-THC and Delta(9)-THC.	delta-8-tetrahydrocannabinol	105-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
26409163-8	2015	The in-vitro metabolism assay with the human CYP2C9 isoform led to the formation of THCOH and THCCOOH of Delta(8)-THC and Delta(9)-THC.	Dronabinol	122-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
26374173-3	2015	Kinetic and inhibition experiments performed at therapeutically relevant concentrations reveal that CYP2C8 and CYP2C9 are the principal enzymes responsible for montelukast 36-hydroxylation to 1,2-diol.	MLS002693268	192-200	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
26669712-6	2015	The CYP2C9 phenotype was determined using a single oral dose of 50 mg losartan.	Losartan	70-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
26669712-8	2015	The urinary losartan to its metabolite E-3174 metabolic ratio (MR) was used as an index of CYP2C9 metabolic activity.	Losartan	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
27047214-0	2015	The influence of VKORC1 and CYP2C9 mutations on warfarin response after total hip and knee arthroplasty.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
26360837-2	2015	The aim of this study was to evaluate the influence of the genetic polymorphisms of CYP2C9, CYP2D6 and CYP3A4 on the pharmacokinetics (PK) of celecoxib and its two main metabolites, hydroxyl-celecoxib and carboxy-celecoxib, in healthy Chinese subjects, based on a bioequivalence study of celecoxib.	Celecoxib	191-200	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
26593908-7	2015	Human CYP1A2 followed by CYP2C9, 3A4 and 1A1 were the major enzymes contributing to AAI oxidation in human liver, while CYP2C and 1A were most important in rat liver.	aristolochic acid I	84-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
26360837-2	2015	The aim of this study was to evaluate the influence of the genetic polymorphisms of CYP2C9, CYP2D6 and CYP3A4 on the pharmacokinetics (PK) of celecoxib and its two main metabolites, hydroxyl-celecoxib and carboxy-celecoxib, in healthy Chinese subjects, based on a bioequivalence study of celecoxib.	Celecoxib	142-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
26360837-8	2015	Therefore, the influence of the CYP2C9*3 and CYP2D6*10 on the PK of celecoxib and its metabolites in Chinese was studied.	Celecoxib	68-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
26360837-9	2015	Compared with CYP2C9*1/*1 group, pharmacokinetic parameters of celecoxib such as AUC0-48 and Cmax was increased by 90.6% and 45.8%, the t1/2 was extended by 21.8% and the CL/F was decreased by 51.1% in CYP2C9*1/*3 group.	Celecoxib	63-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
26360837-2	2015	The aim of this study was to evaluate the influence of the genetic polymorphisms of CYP2C9, CYP2D6 and CYP3A4 on the pharmacokinetics (PK) of celecoxib and its two main metabolites, hydroxyl-celecoxib and carboxy-celecoxib, in healthy Chinese subjects, based on a bioequivalence study of celecoxib.	hydroxyl-celecoxib	182-200	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
26360837-9	2015	Compared with CYP2C9*1/*1 group, pharmacokinetic parameters of celecoxib such as AUC0-48 and Cmax was increased by 90.6% and 45.8%, the t1/2 was extended by 21.8% and the CL/F was decreased by 51.1% in CYP2C9*1/*3 group.	Celecoxib	63-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	202-208
26360837-2	2015	The aim of this study was to evaluate the influence of the genetic polymorphisms of CYP2C9, CYP2D6 and CYP3A4 on the pharmacokinetics (PK) of celecoxib and its two main metabolites, hydroxyl-celecoxib and carboxy-celecoxib, in healthy Chinese subjects, based on a bioequivalence study of celecoxib.	carboxy-celecoxib	205-222	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
26360837-10	2015	In terms of hydroxy-celecoxib, compared with CYP2C9*1/*1 group, the Cmax was decreased by 17.2%, the t1/2 prolonged 42.1% in CYP2C9*1/*3 group.	hydroxy-celecoxib	12-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
26360837-10	2015	In terms of hydroxy-celecoxib, compared with CYP2C9*1/*1 group, the Cmax was decreased by 17.2%, the t1/2 prolonged 42.1% in CYP2C9*1/*3 group.	hydroxy-celecoxib	12-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
26360837-11	2015	In terms of carboxy-celecoxib, the AUC0-48 was increased by 25.2%, the t1/2 prolonged 16.1% and the CL/F was decreased by 21.2% in CYP2C9*1/*3 group.	carboxy-celecoxib	12-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
26360837-11	2015	In terms of carboxy-celecoxib, the AUC0-48 was increased by 25.2%, the t1/2 prolonged 16.1% and the CL/F was decreased by 21.2% in CYP2C9*1/*3 group.	Fluorine	103-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
26995878-4	2015	Recent pharmacogenomic (PGx) studies have shown that several single nucleotide polymorphisms (SNPs) in CYP2C9 (warfarin metabolic enzyme) and VKORC1 (warfarin target enzyme) are responsible for an individual"s warfarin sensitivity.	Warfarin	111-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
26296708-1	2015	In this study, IC50 shift and time-dependent inhibition (TDI) experiments were carried out to measure the ability of amiodarone (AMIO), and its circulating human metabolites, to reversibly and irreversibly inhibit CYP1A2, CYP2C9, CYP2D6, and CYP3A4 activities in human liver microsomes.	Amiodarone	117-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	222-228
26296708-1	2015	In this study, IC50 shift and time-dependent inhibition (TDI) experiments were carried out to measure the ability of amiodarone (AMIO), and its circulating human metabolites, to reversibly and irreversibly inhibit CYP1A2, CYP2C9, CYP2D6, and CYP3A4 activities in human liver microsomes.	Amiodarone	129-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	222-228
26296708-3	2015	Based on these values, the minor metabolite N,N-didesethylamiodarone (DDEA) is predicted to be the major cause of DDIs with xenobiotics primarily metabolized by CYP1A2, CYP2C9, or CYP3A4, while AMIO and its N-monodesethylamiodarone (MDEA) derivative are the most likely cause of interactions involving inhibition of CYP2D6 metabolism.	n,n-didesethylamiodarone	44-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
26296708-3	2015	Based on these values, the minor metabolite N,N-didesethylamiodarone (DDEA) is predicted to be the major cause of DDIs with xenobiotics primarily metabolized by CYP1A2, CYP2C9, or CYP3A4, while AMIO and its N-monodesethylamiodarone (MDEA) derivative are the most likely cause of interactions involving inhibition of CYP2D6 metabolism.	Di-N-desethylamiodarone	70-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
26296708-3	2015	Based on these values, the minor metabolite N,N-didesethylamiodarone (DDEA) is predicted to be the major cause of DDIs with xenobiotics primarily metabolized by CYP1A2, CYP2C9, or CYP3A4, while AMIO and its N-monodesethylamiodarone (MDEA) derivative are the most likely cause of interactions involving inhibition of CYP2D6 metabolism.	Amiodarone	194-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
26296708-3	2015	Based on these values, the minor metabolite N,N-didesethylamiodarone (DDEA) is predicted to be the major cause of DDIs with xenobiotics primarily metabolized by CYP1A2, CYP2C9, or CYP3A4, while AMIO and its N-monodesethylamiodarone (MDEA) derivative are the most likely cause of interactions involving inhibition of CYP2D6 metabolism.	desethylamiodarone	207-231	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
26296708-3	2015	Based on these values, the minor metabolite N,N-didesethylamiodarone (DDEA) is predicted to be the major cause of DDIs with xenobiotics primarily metabolized by CYP1A2, CYP2C9, or CYP3A4, while AMIO and its N-monodesethylamiodarone (MDEA) derivative are the most likely cause of interactions involving inhibition of CYP2D6 metabolism.	desethylamiodarone	233-237	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	169-175
26360116-7	2015	These findings provided for the development of a low-cost, simple, and fast direct whole blood genotyping method that uses Pfu DNA polymerase combined with phosphorothioate AS primers for CYP2C9*3 and VKORC1(-1639) loci.	Parathion	156-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	188-194
26757860-2	2015	Pharmacogenetic studies have shown that common variants in genes CYP2C9 (*2 and *3) and VKORC1 (-1639G&gt;A) are associated with lower requirements of OAC.	SDZ 33-243	151-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
26433837-2	2015	Genetic polymorphisms in CYP2C9, VKORC1 and CYP4F2 have been shown to play an important role in variations in the warfarin maintenance dose in adults, but their effects in children remain unclear.	Warfarin	114-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
25929560-6	2015	Enzalutamide reduced the AUC  of oral S-warfarin, omeprazole, and midazolam by 56, 70, and 86 %, respectively; therefore, enzalutamide is a moderate inducer of CYP2C9 and CYP2C19 and a strong inducer of CYP3A4.	enzalutamide	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
26431339-9	2015	Sensitivity analysis suggested changes in CYP2C9 activity, and to a lesser extent UGT2B7, as the primary factor contributing to differences in indomethacin disposition between pregnancy and non-pregnancy.	Indomethacin	143-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
26423799-5	2015	We found that the formation of 4OH-NDM-TOR was catalyzed both by CYP2C9 and CYP2D6, whereas the formation of 4OH-TAM and endoxifen was specifically catalyzed by CYP2D6 in HLMs.	4oh-ndm-tor	31-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
25929560-6	2015	Enzalutamide reduced the AUC  of oral S-warfarin, omeprazole, and midazolam by 56, 70, and 86 %, respectively; therefore, enzalutamide is a moderate inducer of CYP2C9 and CYP2C19 and a strong inducer of CYP3A4.	enzalutamide	122-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
25929560-8	2015	It is recommended to avoid concomitant use of enzalutamide with narrow therapeutic index drugs metabolized by CYP2C9, CYP2C19, or CYP3A4, as enzalutamide may decrease their exposure.	enzalutamide	46-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
25929560-8	2015	It is recommended to avoid concomitant use of enzalutamide with narrow therapeutic index drugs metabolized by CYP2C9, CYP2C19, or CYP3A4, as enzalutamide may decrease their exposure.	enzalutamide	141-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
26423799-5	2015	We found that the formation of 4OH-NDM-TOR was catalyzed both by CYP2C9 and CYP2D6, whereas the formation of 4OH-TAM and endoxifen was specifically catalyzed by CYP2D6 in HLMs.	4-hydroxy-N-desmethyltamoxifen	121-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
26233334-6	2015	Phenotyping of CYP2C9 was performed by administration of a 50-mg single oral dose of losartan and by calculating the urinary metabolic ratio (MR) of probe drug to its metabolite E-3174.	Losartan	85-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
26418980-9	2015	VKORC1 -1639G/A, CYP2C9 430C/T, CYP2C9 1075A/C and CYP4F2 V433M polymorphisms have significant influence on stable warfarin dosage.	Warfarin	115-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
26865929-0	2015	Identification of CYP2C9 and VKORC1 polymorphisms in Iranian patients who are under warfarin therapy.	Warfarin	84-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
26865929-12	2015	CONCLUSION: In this study, samples were characterized by higher frequencies of CYP2C9*1 and VKORC1 G/A, determined as higher warfarin taking doses.	Warfarin	125-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
26865929-13	2015	The results showed a significant relationship of the VCORC1 and CYP2C9 polymorphisms with warfarin sensitivity and severe side effects.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
26516586-1	2015	Our previous studies revealed that sesamin caused a mechanism-based inhibition (MBI) of CYP2C9 in human liver microsomes.	sesamin	35-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
26516586-5	2015	These results suggest that the MI complex of cytochrome P450 and sesamin is unstable, and the effects of sesamin on human CYP2C9- or rat CYP2C-mediated drug metabolism may be small.	sesamin	105-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
26837174-6	2015	Among them, the body weight (WT), CYP2C9 and VKORC1 genotype had conspicuous effect on warfarin PK/PD parameters.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
26418980-9	2015	VKORC1 -1639G/A, CYP2C9 430C/T, CYP2C9 1075A/C and CYP4F2 V433M polymorphisms have significant influence on stable warfarin dosage.	Warfarin	115-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
24920353-1	2015	Rosuvastatin is used to treat dyslipidemia and is metabolized by CYP2C9 that shows variable metabolic activity in males and females.	Rosuvastatin Calcium	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
26543813-0	2015	Adverse events in a newborn on valproate therapy due to loss-of-function mutations in CYP2C9.	Valproic Acid	31-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
26543813-6	2015	The patient was demonstrated to carry two loss-of-function mutations in CYP2C9 (CYP2C9*3/*3) resulting in exaggerated blood concentrations of valproate.	Valproic Acid	142-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
26543813-6	2015	The patient was demonstrated to carry two loss-of-function mutations in CYP2C9 (CYP2C9*3/*3) resulting in exaggerated blood concentrations of valproate.	Valproic Acid	142-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
26543813-7	2015	The present case highlights the importance of assaying inborn errors in CYP2C9 gene in pediatric patients to avoid valproate-evoked serious side effects.	Valproic Acid	115-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
26138612-8	2015	TMP 3"-demethylation was catalyzed by multiple P450s, including CYP2C9, correlated with CYP2C9 activity, and was inhibited by sulfaphenazole (up to 40%).	Trimethoprim	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
26138612-8	2015	TMP 3"-demethylation was catalyzed by multiple P450s, including CYP2C9, correlated with CYP2C9 activity, and was inhibited by sulfaphenazole (up to 40%).	Trimethoprim	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
26138612-8	2015	TMP 3"-demethylation was catalyzed by multiple P450s, including CYP2C9, correlated with CYP2C9 activity, and was inhibited by sulfaphenazole (up to 40%).	Sulfaphenazole	126-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
26138612-9	2015	Overall, CYP2C9 and CYP3A4 appear to be the most significant contributors to TMP primary metabolism.	Trimethoprim	77-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
25940823-3	2015	Tamoxifen is bioactivated by cytochrome P450 (CYP) enzymes such as CYP2B6, CYP2C9, CYP2C19, CYP2D6 and CYP3A4/5, resulting in the formation of active metabolites, including 4-hydroxy-tamoxifen and endoxifen.	Tamoxifen	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
26302287-3	2015	Warfarin metabolism is affected by variations in the cytochrome P450 2C9 (CYP2C9) and the vitamin K epoxide reductase complex 1 (VKORC1) genotypes.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-72
26302287-3	2015	Warfarin metabolism is affected by variations in the cytochrome P450 2C9 (CYP2C9) and the vitamin K epoxide reductase complex 1 (VKORC1) genotypes.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
25940823-3	2015	Tamoxifen is bioactivated by cytochrome P450 (CYP) enzymes such as CYP2B6, CYP2C9, CYP2C19, CYP2D6 and CYP3A4/5, resulting in the formation of active metabolites, including 4-hydroxy-tamoxifen and endoxifen.	4'-hydroxytamoxifen	173-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
25994031-1	2015	CYP2C9, one of the most important drug-metabolizing enzymes, is responsible for metabolizing approximately 15% of clinically important drugs, including warfarin, diclofenac, and losartan.	Warfarin	152-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25940823-3	2015	Tamoxifen is bioactivated by cytochrome P450 (CYP) enzymes such as CYP2B6, CYP2C9, CYP2C19, CYP2D6 and CYP3A4/5, resulting in the formation of active metabolites, including 4-hydroxy-tamoxifen and endoxifen.	4-hydroxy-N-desmethyltamoxifen	197-206	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
25994031-1	2015	CYP2C9, one of the most important drug-metabolizing enzymes, is responsible for metabolizing approximately 15% of clinically important drugs, including warfarin, diclofenac, and losartan.	Diclofenac	162-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25994031-1	2015	CYP2C9, one of the most important drug-metabolizing enzymes, is responsible for metabolizing approximately 15% of clinically important drugs, including warfarin, diclofenac, and losartan.	Losartan	178-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25994031-4	2015	This base transversion leads to an Ile-to-Phe amino acid substitution at codon 434 within the CYP2C9 protein, and this new variant has been named a novel allele, CYP2C9*59, by the Human CYP Allele Nomenclature Committee (http://www.cypalleles.ki.se/cyp2c9.htm).	Isoleucine	35-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
25994031-4	2015	This base transversion leads to an Ile-to-Phe amino acid substitution at codon 434 within the CYP2C9 protein, and this new variant has been named a novel allele, CYP2C9*59, by the Human CYP Allele Nomenclature Committee (http://www.cypalleles.ki.se/cyp2c9.htm).	Isoleucine	35-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
25994031-4	2015	This base transversion leads to an Ile-to-Phe amino acid substitution at codon 434 within the CYP2C9 protein, and this new variant has been named a novel allele, CYP2C9*59, by the Human CYP Allele Nomenclature Committee (http://www.cypalleles.ki.se/cyp2c9.htm).	Isoleucine	35-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	249-255
25994031-4	2015	This base transversion leads to an Ile-to-Phe amino acid substitution at codon 434 within the CYP2C9 protein, and this new variant has been named a novel allele, CYP2C9*59, by the Human CYP Allele Nomenclature Committee (http://www.cypalleles.ki.se/cyp2c9.htm).	Phenylalanine	42-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
25994031-4	2015	This base transversion leads to an Ile-to-Phe amino acid substitution at codon 434 within the CYP2C9 protein, and this new variant has been named a novel allele, CYP2C9*59, by the Human CYP Allele Nomenclature Committee (http://www.cypalleles.ki.se/cyp2c9.htm).	Phenylalanine	42-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
25994031-4	2015	This base transversion leads to an Ile-to-Phe amino acid substitution at codon 434 within the CYP2C9 protein, and this new variant has been named a novel allele, CYP2C9*59, by the Human CYP Allele Nomenclature Committee (http://www.cypalleles.ki.se/cyp2c9.htm).	Phenylalanine	42-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	249-255
25815675-0	2015	Improvements in CYP2C9 Genotyping Accuracy Are Needed: A Report of the First Proficiency Testing for Warfarin-related CYP2C9 and VKORC1 Genotyping in China.	Warfarin	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
25815675-0	2015	Improvements in CYP2C9 Genotyping Accuracy Are Needed: A Report of the First Proficiency Testing for Warfarin-related CYP2C9 and VKORC1 Genotyping in China.	Warfarin	101-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
25815675-2	2015	The cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex 1 (VKORC1) genotypes have been confirmed to be associated with warfarin dose requirements.	Warfarin	136-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-23
25815675-2	2015	The cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex 1 (VKORC1) genotypes have been confirmed to be associated with warfarin dose requirements.	Warfarin	136-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
25904339-0	2015	Analysis of CYP2C9 polymorphisms (*2 and *3) in warfarin therapy patients in Pakistan.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
25994870-0	2015	Association analysis of CYP2C9*3 and phenytoin-induced severe cutaneous adverse reactions (SCARs) in Thai epilepsy children.	Phenytoin	37-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
25994870-6	2015	The association between CYP2C9*3 with phenytoin-induced SCARs and phenobarbital-induced SCARs were analyzed in comparison with tolerances and healthy samples.	Phenytoin	38-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
25994870-7	2015	Significant association between phenytoin-induced SCARs and CYP2C9*3 was discovered (odds ratio=14.52; 95% confidence interval (CI)=1.18- , P-value=0.044).	Phenytoin	32-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
25994870-9	2015	This study is the first report of CYP2C9*3 association to phenytoin-induced SCARs in Thai epileptic children.	Phenytoin	58-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
25994870-10	2015	The CYP2C9*3 is a reasonable predictive genetic marker to anticipate SCARs from phenytoin.	Phenytoin	80-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
26010205-0	2015	Influence of CYP2C9 polymorphism on the fall in International Normalized Ratio in patients interrupting warfarin therapy before elective surgery.	Warfarin	104-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
26010205-3	2015	OBJECTIVES: The aim of this study was to investigate the potential influence of CYP2C9 polymorphism on the variable rate of fall in the International Normalized Ratio (INR) in patients withdrawing from warfarin treatment prior to elective surgery.	Warfarin	202-210	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
26010205-9	2015	CONCLUSION: A genotype-guided protocol to tailor warfarin withdrawal according to an individual patient"s CYP2C9 genotype could reduce cancellation or delays of planned procedures, and could also be beneficial when transitioning patients from warfarin to one of the new oral anticoagulants.	Warfarin	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
26010205-9	2015	CONCLUSION: A genotype-guided protocol to tailor warfarin withdrawal according to an individual patient"s CYP2C9 genotype could reduce cancellation or delays of planned procedures, and could also be beneficial when transitioning patients from warfarin to one of the new oral anticoagulants.	Warfarin	243-251	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
25904339-1	2015	Association of CYP2C9 polymorphisms (*2 and*3) with warfarin dose, age, PT and INR.	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
25904339-3	2015	Single nucleotide polymorphisms in hepatic VKORC1 and CYP2C9 genes causes decreased and increased metabolism of warfarin respectively.	Warfarin	112-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
25904339-11	2015	Statistical analysis showed that low warfarin dose (weekly) is significantly associated with *1/*2 and *1/*3 genotypes (p value &gt;= 0.001), whereas PT/INR showed no significant association with the any genotypes of CYP2C9.	Warfarin	37-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	217-223
25904339-12	2015	Our study suggest that polymorphic variants of CYP2C9 (*2 and *3) might influence warfarin dose requirements and associated with the low dose of warfarin in patients.	Warfarin	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
25904339-12	2015	Our study suggest that polymorphic variants of CYP2C9 (*2 and *3) might influence warfarin dose requirements and associated with the low dose of warfarin in patients.	Warfarin	145-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
26448196-2	2015	Genetic variants of the enzymes that metabolize warfarin, i.e. cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1), contribute to differences in patients" responses to various warfarin doses.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-82
26186657-0	2015	Clinical Practice Recommendations on Genetic Testing of CYP2C9 and VKORC1 Variants in Warfarin Therapy.	Warfarin	86-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
26186657-4	2015	METHODS: A systematic literature search was performed for VKORC1 and CYP2C9 and their association with warfarin therapy.	Warfarin	103-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
26448196-2	2015	Genetic variants of the enzymes that metabolize warfarin, i.e. cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1), contribute to differences in patients" responses to various warfarin doses.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
26448196-2	2015	Genetic variants of the enzymes that metabolize warfarin, i.e. cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1), contribute to differences in patients" responses to various warfarin doses.	Warfarin	194-202	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-82
26448196-2	2015	Genetic variants of the enzymes that metabolize warfarin, i.e. cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1), contribute to differences in patients" responses to various warfarin doses.	Warfarin	194-202	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
25758405-3	2015	Both had variant cytochrome P2C9 (CYP2C9) alleles which reduce the metabolic capacity of the CYP2C9 enzyme responsible for the metabolism of the S-warfarin enantiomer.	Warfarin	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-32
26024874-5	2015	Warfarin dose was influenced by age, BSA, CKD, amiodarone use, and CYP2C9*3 and VKORC1 variants in both races, by CYP2C9*2 and CYP4F2 variants in European Americans, and by rs12777823 in African Americans.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
26024874-5	2015	Warfarin dose was influenced by age, BSA, CKD, amiodarone use, and CYP2C9*3 and VKORC1 variants in both races, by CYP2C9*2 and CYP4F2 variants in European Americans, and by rs12777823 in African Americans.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
26469104-1	2015	BACKGROUND: Warfarin dose requirements are partly determined by common single nucleotide polymorphisms in VKORC1 and CYP2C9 genes.	Warfarin	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
26469104-9	2015	CONCLUSIONS: The presence of CYP2C9*2 and/or *3 genotypes is associated with unstable warfarin treatment in patients after heart valve replacement, regardless of the type of INR testing.	Warfarin	86-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
25758405-3	2015	Both had variant cytochrome P2C9 (CYP2C9) alleles which reduce the metabolic capacity of the CYP2C9 enzyme responsible for the metabolism of the S-warfarin enantiomer.	Warfarin	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
25758405-3	2015	Both had variant cytochrome P2C9 (CYP2C9) alleles which reduce the metabolic capacity of the CYP2C9 enzyme responsible for the metabolism of the S-warfarin enantiomer.	Warfarin	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
25758405-4	2015	Need for preoperative administration of vitamin K or postponement of an operation because of an INR &gt;1.5 could be explained by variant alleles for CYP2C9 and age.	Vitamin K	40-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
25808545-5	2015	We show that vitamin K2 and lithocholic acid, a by-product of intestinal flora, activate pregnane X receptor (PXR) and subsequent CYP3A4 and CYP2C9 expression in hPSC-derived and isolated fetal hepatocytes.	Vitamin K 2	13-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
26125664-1	2015	Polymorphisms for VKORC1 and CYP2C9 are associated with increased warfarin sensitivity.	Warfarin	66-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
26125664-8	2015	One or more polymorphisms for VKORC1 or CYP2C9 (associated with warfarin sensitivity) were found in 67.7% of MCS patients.	Warfarin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
26125664-8	2015	One or more polymorphisms for VKORC1 or CYP2C9 (associated with warfarin sensitivity) were found in 67.7% of MCS patients.	mcs	109-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
25699611-0	2015	Impact of CYP2C9 and VKORC1 genetic polymorphisms upon warfarin dose requirements in Egyptian patients with acute coronary syndrome.	Warfarin	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
25699611-2	2015	Cytochrome P450-2C9 (CYP2C9) and vitamin K epoxide reductase-oxidaxe complex subunit 1 (VKORC1) contribute significantly to the variability of warfarin dose requirements among patients.	Warfarin	143-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
25699611-2	2015	Cytochrome P450-2C9 (CYP2C9) and vitamin K epoxide reductase-oxidaxe complex subunit 1 (VKORC1) contribute significantly to the variability of warfarin dose requirements among patients.	Warfarin	143-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
25699611-3	2015	We investigated the impact of CYP2C9 and VKORC1 polymorphisms on the variability of warfarin dosage requirements in Egyptian patients with acute coronary syndrome and their association with other nongenetic factors.	Warfarin	84-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
25699611-9	2015	Regression analysis revealed that age, height, CYP2C9 and VKORC1 genotypes were significantly associated with warfarin dose.	Warfarin	110-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
25699611-10	2015	Genetic polymorphisms in VKORC1, CYP2C9 along with age and height are determinants of warfarin dose requirements in Egyptian population acute coronary syndrome.	Warfarin	86-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
25699611-11	2015	Higher warfarin loading dose is required for both wild CYP2C9 and VKORC1 gene variants which may contribute to warfarin-resistant cases.	Warfarin	7-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
25699611-11	2015	Higher warfarin loading dose is required for both wild CYP2C9 and VKORC1 gene variants which may contribute to warfarin-resistant cases.	Warfarin	111-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
25948712-8	2015	Although efavirenz is known as a marker substrate for human CYP2B6, efavirenz was not oxidized by CYP2B6 but by CYP2C9 in monkeys.	efavirenz	68-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
25808545-5	2015	We show that vitamin K2 and lithocholic acid, a by-product of intestinal flora, activate pregnane X receptor (PXR) and subsequent CYP3A4 and CYP2C9 expression in hPSC-derived and isolated fetal hepatocytes.	Lithocholic Acid	28-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
26142522-11	2015	Previous studies have also pointed out CYP2C9 polymorphism being responsible for such inter-individual differences in S-warfarin metabolism.	Warfarin	120-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
25936586-3	2015	CTXA reversibly inhibited the CYP1A2-catalyzed phenacetin O-deethylation, CYP2C8-catalyzed paclitaxel 6-hydroxylation, and CYP2C9-catalyzed diclofenac 4"-hydroxylation with half-maximal inhibitory concentration (IC50) values of 3.9, 4.7, and 2.9 microM, respectively.	cudratricusxanthone A	0-4	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
25943175-0	2015	Clinical relevance of genetic polymorphism in CYP2C9 gene to pharmacodynamics and pharmacokinetics of phenytoin in epileptic patients: validatory pharmacogenomic approach to pharmacovigilance.	Phenytoin	102-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
25943175-10	2015	CYP2C9 genotype based phenytoin therapy is highly relevant in Kashmiri population due to a high incidence of genetic variations associated with therapeutic and adverse responses to phenytoin.	Phenytoin	22-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25943175-10	2015	CYP2C9 genotype based phenytoin therapy is highly relevant in Kashmiri population due to a high incidence of genetic variations associated with therapeutic and adverse responses to phenytoin.	Phenytoin	181-190	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
26142522-12	2015	So plasma warfarin S/R ratio may serve as a useful phenotypic test for CYP2C9 polymorphism.	Warfarin	10-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
25946405-0	2015	Variation in genes controlling warfarin disposition and response in American Indian and Alaska Native people: CYP2C9, VKORC1, CYP4F2, CYP4F11, GGCX.	Warfarin	31-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
25946405-4	2015	Therefore, we were interested in variation in CYP2C9, VKORC1, CYP4F2, CYP4F11, and GGCX, which encode enzymes important for the activity of warfarin and synthesis of vitamin K-dependent blood clotting factors.	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
25946405-4	2015	Therefore, we were interested in variation in CYP2C9, VKORC1, CYP4F2, CYP4F11, and GGCX, which encode enzymes important for the activity of warfarin and synthesis of vitamin K-dependent blood clotting factors.	Vitamin K	166-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
26267945-4	2015	Cytochromes P450 (CYP) 2C9 and 3A4 are involved in the metabolism of tetrahydrocannabinol and cannabidiol, which implies possible DDI with CYP450 inhibitor and inducer, such as anticonvulsivants and HIV protease inhibitors, which may be prescribed in patients with neuropathic pain.	Dronabinol	69-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-26
26267945-4	2015	Cytochromes P450 (CYP) 2C9 and 3A4 are involved in the metabolism of tetrahydrocannabinol and cannabidiol, which implies possible DDI with CYP450 inhibitor and inducer, such as anticonvulsivants and HIV protease inhibitors, which may be prescribed in patients with neuropathic pain.	Cannabidiol	94-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-26
28930203-8	2015	Results: Vinpocetine showed a strong inhibition of P-gp (EC50 8 microM) and a moderate inhibition of recombinant CYP3A4 and CYP2D6 (IC50 2.8 and 6.5 microM) with no activity towards CYP2C9, CYP2C19 and CYP1A2 enzymes.	vinpocetine	9-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	182-188
26179835-4	2015	The possible mechanism is speculated to be due to noni juiceinduced cytochrome P-450 2C9 metabolism of phenytoin.	Phenytoin	103-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-88
25769357-13	2015	INTERPRETATION: CYP2C9 and VKORC1 genotypes identify patients who are more likely to experience early bleeding with warfarin and who derive a greater early safety benefit from edoxaban compared with warfarin.	Warfarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
25986145-2	2015	S-warfarin is metabolized to 7-S-hydroxywarfarin by the cytochrome P450 isoform 2C9 encoded by CYP2C9 gene.	Warfarin	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
25712887-0	2015	Effects of CYP2C9*1/*3 genotype on the pharmacokinetics of flurbiprofen in Korean subjects.	Flurbiprofen	59-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
25712887-1	2015	The aim of this study was to investigate the impact of CYP2C9*1/*3 genotype on the pharmacokinetics of flurbiprofen and its metabolite.	Flurbiprofen	103-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
25712887-5	2015	AUCinf of flurbiprofen was significantly higher and its clearance was significantly lower in the CYP2C9*1/*3 individuals than in those with CYP2C9*1/*1.	Flurbiprofen	10-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
25712887-5	2015	AUCinf of flurbiprofen was significantly higher and its clearance was significantly lower in the CYP2C9*1/*3 individuals than in those with CYP2C9*1/*1.	Flurbiprofen	10-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	140-146
25712887-6	2015	The AUC ratio of 4"-hydroxyflurbiprofen to flurbiprofen was significantly lower in the CYP2C9*1/*3 individuals than in those with CYP2C9*1/*1.	4'-hydroxyflurbiprofen	17-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
25986145-2	2015	S-warfarin is metabolized to 7-S-hydroxywarfarin by the cytochrome P450 isoform 2C9 encoded by CYP2C9 gene.	7-s-hydroxywarfarin	29-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
25712887-6	2015	The AUC ratio of 4"-hydroxyflurbiprofen to flurbiprofen was significantly lower in the CYP2C9*1/*3 individuals than in those with CYP2C9*1/*1.	4'-hydroxyflurbiprofen	17-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
25712887-6	2015	The AUC ratio of 4"-hydroxyflurbiprofen to flurbiprofen was significantly lower in the CYP2C9*1/*3 individuals than in those with CYP2C9*1/*1.	Flurbiprofen	27-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
25712887-6	2015	The AUC ratio of 4"-hydroxyflurbiprofen to flurbiprofen was significantly lower in the CYP2C9*1/*3 individuals than in those with CYP2C9*1/*1.	Flurbiprofen	27-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
25986145-10	2015	The S-7-hydroxywarfarin was lower in carriers of the VKORC1 c.-1639A allele (p = 0.0005) and CYP2C9*3 (p = 0.047).	7-hydroxywarfarin	4-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
25712887-7	2015	These results indicate that the individuals carrying of CYP2C9*3 have significant reduction in flurbiprofen metabolism.	Flurbiprofen	95-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
25986145-11	2015	The S-7-hydroxywarfarin/S-warfarin ratio was lower in the carriers of CYP2C9*3 (p = 0.008), but not in those with VKORC1 -c.1639A allele.	7-hydroxywarfarin	4-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
26053779-4	2015	Metronidazole and fluconazole inhibit the metabolism of warfarin by blocking cytochrome P-450 2C9 (CYP-2C9), the major metabolic pathway of warfarin, with the end result being dramatic increases in patients" international normalized ratios (INRs) and potentially fatal bleeding.	Metronidazole	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-97
25986145-11	2015	The S-7-hydroxywarfarin/S-warfarin ratio was lower in the carriers of CYP2C9*3 (p = 0.008), but not in those with VKORC1 -c.1639A allele.	Sulfur	4-5	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
25986145-11	2015	The S-7-hydroxywarfarin/S-warfarin ratio was lower in the carriers of CYP2C9*3 (p = 0.008), but not in those with VKORC1 -c.1639A allele.	Warfarin	15-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
26053779-4	2015	Metronidazole and fluconazole inhibit the metabolism of warfarin by blocking cytochrome P-450 2C9 (CYP-2C9), the major metabolic pathway of warfarin, with the end result being dramatic increases in patients" international normalized ratios (INRs) and potentially fatal bleeding.	Metronidazole	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-106
26053779-4	2015	Metronidazole and fluconazole inhibit the metabolism of warfarin by blocking cytochrome P-450 2C9 (CYP-2C9), the major metabolic pathway of warfarin, with the end result being dramatic increases in patients" international normalized ratios (INRs) and potentially fatal bleeding.	Fluconazole	18-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-97
26053779-4	2015	Metronidazole and fluconazole inhibit the metabolism of warfarin by blocking cytochrome P-450 2C9 (CYP-2C9), the major metabolic pathway of warfarin, with the end result being dramatic increases in patients" international normalized ratios (INRs) and potentially fatal bleeding.	Fluconazole	18-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-106
26053779-4	2015	Metronidazole and fluconazole inhibit the metabolism of warfarin by blocking cytochrome P-450 2C9 (CYP-2C9), the major metabolic pathway of warfarin, with the end result being dramatic increases in patients" international normalized ratios (INRs) and potentially fatal bleeding.	Warfarin	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-97
26053779-4	2015	Metronidazole and fluconazole inhibit the metabolism of warfarin by blocking cytochrome P-450 2C9 (CYP-2C9), the major metabolic pathway of warfarin, with the end result being dramatic increases in patients" international normalized ratios (INRs) and potentially fatal bleeding.	Warfarin	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-106
26053779-4	2015	Metronidazole and fluconazole inhibit the metabolism of warfarin by blocking cytochrome P-450 2C9 (CYP-2C9), the major metabolic pathway of warfarin, with the end result being dramatic increases in patients" international normalized ratios (INRs) and potentially fatal bleeding.	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-97
26053779-4	2015	Metronidazole and fluconazole inhibit the metabolism of warfarin by blocking cytochrome P-450 2C9 (CYP-2C9), the major metabolic pathway of warfarin, with the end result being dramatic increases in patients" international normalized ratios (INRs) and potentially fatal bleeding.	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-106
25967074-0	2015	Clinical significance of CYP2C9-status guided valproic acid therapy in children.	Valproic Acid	46-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
25967074-3	2015	Thus, patients" CYP2C9-status may account for the predisposition to adverse reactions, and testing CYP2C9-status may contribute to the improvement and rationalization of VPA therapy in children.	Valproic Acid	170-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
25967074-6	2015	When the results of CYP2C9 genotyping and CYP2C9 expression were combined, the patients" VPA-metabolizing capacity was predicted, and VPA dosing was adjusted to the patients" CYP2C9-status.	Valproic Acid	89-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
25967074-6	2015	When the results of CYP2C9 genotyping and CYP2C9 expression were combined, the patients" VPA-metabolizing capacity was predicted, and VPA dosing was adjusted to the patients" CYP2C9-status.	Valproic Acid	89-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
25967074-6	2015	When the results of CYP2C9 genotyping and CYP2C9 expression were combined, the patients" VPA-metabolizing capacity was predicted, and VPA dosing was adjusted to the patients" CYP2C9-status.	Valproic Acid	89-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
25967074-11	2015	SIGNIFICANCE: The knowledge of pediatric patients" CYP2C9-status can contribute to the optimization of VPA dosing and to the avoidance of misdosing-induced side effects.	Valproic Acid	103-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
25884291-0	2015	In vitro assessment of 39 CYP2C9 variants found in the Chinese population on the metabolism of the model substrate fluoxetine and a summary of their effects on other substrates.	Fluoxetine	115-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
26219158-1	2015	BACKGROUND: Polymorphisms in cytochrome P450 2C9 and vitamin K epoxide reductase complex, subunit 1 genes (CYP2C9 and VKORC1, respectively) were previously shown to affect the warfarin dose required in anticoagulant therapy of deep vein thrombosis (DVT).	Warfarin	176-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-48
26219158-1	2015	BACKGROUND: Polymorphisms in cytochrome P450 2C9 and vitamin K epoxide reductase complex, subunit 1 genes (CYP2C9 and VKORC1, respectively) were previously shown to affect the warfarin dose required in anticoagulant therapy of deep vein thrombosis (DVT).	Warfarin	176-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
26219158-3	2015	OBJECTIVE: To identify the effect of CYP2C9 and VKORC1 genetic variants on warfarin dosage in the Thai population with DVT.	Warfarin	75-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
25884291-2	2015	The objective of this study was to assess the catalytic characteristics of 39 CYP2C9 isoforms found in the Chinese population and their effects on the metabolism of the model substrate fluoxetine in vitro.	Fluoxetine	185-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
25884291-9	2015	In addition, 28 CYP2C9 isoforms including CYP2C9*3 exhibited a trend towards substrate inhibition for fluoxetine.	Fluoxetine	102-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
25884291-9	2015	In addition, 28 CYP2C9 isoforms including CYP2C9*3 exhibited a trend towards substrate inhibition for fluoxetine.	Fluoxetine	102-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
25884291-10	2015	WHAT IS NEW AND CONCLUSION: This study provides the most comprehensive data on the enzymatic activities associated with all reported CYP2C9 variants in the Chinese population with regard to the widely used antidepressant drug, fluoxetine.	Fluoxetine	227-237	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
25884291-11	2015	Our data indicate that more attention should be paid to subjects carrying the corresponding infrequent CYP2C9 alleles when administering fluoxetine in the clinic.	Fluoxetine	137-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
25858232-10	2015	Stratified analyses demonstrated increased alcohol-related major bleeding risk in patients on warfarin for &gt;=1 year and in those with a low-dose genotype (CYP2C9*2/*3, VKORC1(1173G&gt;A), CYP4F2*1), but not in other sub-groups evaluated.	Alcohols	43-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
25977991-3	2015	CYP2C9 genotype-based dose recommendations (e.g., for warfarin) is advocated.	Warfarin	54-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25977991-6	2015	CYP2C9 genotype and phenotype was determined in 148 Swedes and 146 Koreans using losartan as a probe.	Losartan	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25977991-7	2015	CYP2C9 enzyme activity was assessed using urinary losartan/metabolite E-3174 ratio.	Losartan	50-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25977991-7	2015	CYP2C9 enzyme activity was assessed using urinary losartan/metabolite E-3174 ratio.	losartan carboxylic acid	70-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25077812-3	2015	CYP2C9 and CYP2E1 specifically metabolised sulfonylurea herbicides and halogenated hydrocarbons respectively.	Sulfonylurea Compounds	43-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25077812-3	2015	CYP2C9 and CYP2E1 specifically metabolised sulfonylurea herbicides and halogenated hydrocarbons respectively.	Hydrocarbons	83-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
29771647-0	2015	Phenoconversion of CYP2C9 in epilepsy limits the predictive value of CYP2C9 genotype in optimizing valproate therapy.	Valproic Acid	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
29771647-0	2015	Phenoconversion of CYP2C9 in epilepsy limits the predictive value of CYP2C9 genotype in optimizing valproate therapy.	Valproic Acid	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
29771647-1	2015	AIM: Since prominent role in valproate metabolism is assigned to CYP2C9 in pediatric patients, the association between children"s CYP2C9-status and serum valproate concentrations or dose-requirements was evaluated.	Valproic Acid	29-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
29771647-1	2015	AIM: Since prominent role in valproate metabolism is assigned to CYP2C9 in pediatric patients, the association between children"s CYP2C9-status and serum valproate concentrations or dose-requirements was evaluated.	Valproic Acid	154-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
29771647-2	2015	MATERIALS &amp; METHODS: The contribution of CYP2C9 genotype and CYP2C9 expression in children (n = 50, Caucasian) with epilepsy to valproate pharmacokinetics was analyzed.	Valproic Acid	132-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
29771647-3	2015	RESULTS: Valproate concentrations were significantly lower in normal expressers with CYP2C9*1/*1 than in low expressers or in patients carrying polymorphic CYP2C9 alleles.	Valproic Acid	9-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
29771647-3	2015	RESULTS: Valproate concentrations were significantly lower in normal expressers with CYP2C9*1/*1 than in low expressers or in patients carrying polymorphic CYP2C9 alleles.	Valproic Acid	9-18	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
29771647-6	2015	CONCLUSION: Due to the substantial downregulation of CYP2C9 expression in epilepsy, inferring patients" valproate metabolizing phenotype merely from CYP2C9 genotype results in false prediction.	Valproic Acid	104-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
29771647-6	2015	CONCLUSION: Due to the substantial downregulation of CYP2C9 expression in epilepsy, inferring patients" valproate metabolizing phenotype merely from CYP2C9 genotype results in false prediction.	Valproic Acid	104-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
29771648-2	2015	RESULTS &amp; DISCUSSION: It was found that VKORC-1639G&gt;A (25.5%), CYP2C9*2 (7.8%), CYP2C9*3 (6.1%), age (13.6%) and diagnosis (6.0%) significantly affected acenocoumarol dose variability in the derivation cohort.	Adenosine Monophosphate	9-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
25747538-6	2015	The multiple linear regression model including VKORC1, CYP4F2, and CYP2C9 genetic variants, age, and weight could explain 42% of the variability in warfarin dosage.	Warfarin	148-156	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
25499099-0	2015	Novel single nucleotide polymorphism in CYP2C9 is associated with changes in warfarin clearance and CYP2C9 expression levels in African Americans.	Warfarin	77-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
25499099-1	2015	Warfarin is a widely used anticoagulant whose active S-enantiomer is primarily metabolized by the CYP2C9 enzyme.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
25499099-2	2015	The CYP2C9*2 and CYP2C9*3 alleles are associated with lower warfarin dose requirement and decreased enzyme activity.	Warfarin	60-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
25499099-2	2015	The CYP2C9*2 and CYP2C9*3 alleles are associated with lower warfarin dose requirement and decreased enzyme activity.	Warfarin	60-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
25499099-3	2015	In contrast, we previously identified a novel single-nucleotide polymorphism (SNP) (rs7089580A &gt; T) in CYP2C9 that is associated with higher warfarin dose requirement in African Americans (AAs).	Warfarin	144-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
25499099-7	2015	Our findings indicate that rs7089580 is associated with higher S-warfarin clearance and CYP2C9 expression and may help explain the higher dose requirement of warfarin in AAs.	Warfarin	158-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
25466603-1	2015	BACKGROUND AND OBJECTIVES: Approximately 50% of inter-individual variation in warfarin dose requirements is attributed to the polymorphisms of cytochrome P450 (CYP) 2C9 (CYP2C9) and vitamin K epoxide reductase complex, subunit 1 (VKORC1) genotypes.	Warfarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-168
25466603-1	2015	BACKGROUND AND OBJECTIVES: Approximately 50% of inter-individual variation in warfarin dose requirements is attributed to the polymorphisms of cytochrome P450 (CYP) 2C9 (CYP2C9) and vitamin K epoxide reductase complex, subunit 1 (VKORC1) genotypes.	Warfarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-176
25466603-7	2015	RESULTS: Using 437 warfarin measurements obtained from 325 patients, we found a correlation between plasma warfarin concentration and warfarin dose (r (2) = 0.356; P &lt; 0.001) and a significant difference in the warfarin/7-hydroxywarfarin ratios of the CYP2C9*1/*1 and CYP2C9*1/*3 genotypes combined with drugs that inhibited warfarin (P = 0.003).	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	255-261
25466603-7	2015	RESULTS: Using 437 warfarin measurements obtained from 325 patients, we found a correlation between plasma warfarin concentration and warfarin dose (r (2) = 0.356; P &lt; 0.001) and a significant difference in the warfarin/7-hydroxywarfarin ratios of the CYP2C9*1/*1 and CYP2C9*1/*3 genotypes combined with drugs that inhibited warfarin (P = 0.003).	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	271-277
25466603-7	2015	RESULTS: Using 437 warfarin measurements obtained from 325 patients, we found a correlation between plasma warfarin concentration and warfarin dose (r (2) = 0.356; P &lt; 0.001) and a significant difference in the warfarin/7-hydroxywarfarin ratios of the CYP2C9*1/*1 and CYP2C9*1/*3 genotypes combined with drugs that inhibited warfarin (P = 0.003).	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	255-261
25466603-7	2015	RESULTS: Using 437 warfarin measurements obtained from 325 patients, we found a correlation between plasma warfarin concentration and warfarin dose (r (2) = 0.356; P &lt; 0.001) and a significant difference in the warfarin/7-hydroxywarfarin ratios of the CYP2C9*1/*1 and CYP2C9*1/*3 genotypes combined with drugs that inhibited warfarin (P = 0.003).	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	271-277
25466603-7	2015	RESULTS: Using 437 warfarin measurements obtained from 325 patients, we found a correlation between plasma warfarin concentration and warfarin dose (r (2) = 0.356; P &lt; 0.001) and a significant difference in the warfarin/7-hydroxywarfarin ratios of the CYP2C9*1/*1 and CYP2C9*1/*3 genotypes combined with drugs that inhibited warfarin (P = 0.003).	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	255-261
25466603-7	2015	RESULTS: Using 437 warfarin measurements obtained from 325 patients, we found a correlation between plasma warfarin concentration and warfarin dose (r (2) = 0.356; P &lt; 0.001) and a significant difference in the warfarin/7-hydroxywarfarin ratios of the CYP2C9*1/*1 and CYP2C9*1/*3 genotypes combined with drugs that inhibited warfarin (P = 0.003).	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	271-277
25466603-7	2015	RESULTS: Using 437 warfarin measurements obtained from 325 patients, we found a correlation between plasma warfarin concentration and warfarin dose (r (2) = 0.356; P &lt; 0.001) and a significant difference in the warfarin/7-hydroxywarfarin ratios of the CYP2C9*1/*1 and CYP2C9*1/*3 genotypes combined with drugs that inhibited warfarin (P = 0.003).	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	255-261
25466603-7	2015	RESULTS: Using 437 warfarin measurements obtained from 325 patients, we found a correlation between plasma warfarin concentration and warfarin dose (r (2) = 0.356; P &lt; 0.001) and a significant difference in the warfarin/7-hydroxywarfarin ratios of the CYP2C9*1/*1 and CYP2C9*1/*3 genotypes combined with drugs that inhibited warfarin (P = 0.003).	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	271-277
25585969-6	2015	RESULTS: Pharmacogenetic testing revealed a relation between this adverse event and an allelic variant of cytochrome P450, CYP2C9, subsequently leading to discontinuation of the drug along with counseling to caution the patient to avoid the use of celecoxib and other drugs metabolized by the same enzyme.	Celecoxib	248-257	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
25515945-2	2015	The impact of activity of the genes encoding CYP3A4, CYP3A5, and CYP2C9 on the pharmacokinetics of voriconazole cannot be ignored because, second to CYP2C19, they are the most important enzymes involved in voriconazole metabolism.	Voriconazole	99-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
25470432-8	2015	In both cells, the expressions of CYP2C8, CYP2C9, CYP3A4 and constitutive androstane receptor (CAR) were decreased by MTZ treatment.	Metronidazole	118-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
25470432-11	2015	Our findings suggest that the interaction between MTZ and S-warfarin may be due to the MTZ-induced down-regulation of CYP2C9, the primary enzyme responsible for S-warfarin hydroxylation, and CAR, which regulates CYP2C9 expression.	Metronidazole	50-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
25470432-11	2015	Our findings suggest that the interaction between MTZ and S-warfarin may be due to the MTZ-induced down-regulation of CYP2C9, the primary enzyme responsible for S-warfarin hydroxylation, and CAR, which regulates CYP2C9 expression.	Metronidazole	50-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
25470432-11	2015	Our findings suggest that the interaction between MTZ and S-warfarin may be due to the MTZ-induced down-regulation of CYP2C9, the primary enzyme responsible for S-warfarin hydroxylation, and CAR, which regulates CYP2C9 expression.	Warfarin	58-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
25470432-11	2015	Our findings suggest that the interaction between MTZ and S-warfarin may be due to the MTZ-induced down-regulation of CYP2C9, the primary enzyme responsible for S-warfarin hydroxylation, and CAR, which regulates CYP2C9 expression.	Warfarin	58-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
25470432-11	2015	Our findings suggest that the interaction between MTZ and S-warfarin may be due to the MTZ-induced down-regulation of CYP2C9, the primary enzyme responsible for S-warfarin hydroxylation, and CAR, which regulates CYP2C9 expression.	Metronidazole	87-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
25470432-11	2015	Our findings suggest that the interaction between MTZ and S-warfarin may be due to the MTZ-induced down-regulation of CYP2C9, the primary enzyme responsible for S-warfarin hydroxylation, and CAR, which regulates CYP2C9 expression.	Metronidazole	87-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
25470432-11	2015	Our findings suggest that the interaction between MTZ and S-warfarin may be due to the MTZ-induced down-regulation of CYP2C9, the primary enzyme responsible for S-warfarin hydroxylation, and CAR, which regulates CYP2C9 expression.	Warfarin	60-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
25470432-11	2015	Our findings suggest that the interaction between MTZ and S-warfarin may be due to the MTZ-induced down-regulation of CYP2C9, the primary enzyme responsible for S-warfarin hydroxylation, and CAR, which regulates CYP2C9 expression.	Warfarin	60-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	212-218
25804257-6	2015	The inhibitor sulfaphenazole, in addition to the previously studied aniline, increased the barrier height for electron transfer and thereby makes CYP2C9 reduction more difficult and inhibits metabolism.	Sulfaphenazole	14-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
25804257-6	2015	The inhibitor sulfaphenazole, in addition to the previously studied aniline, increased the barrier height for electron transfer and thereby makes CYP2C9 reduction more difficult and inhibits metabolism.	aniline	68-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
25875957-0	2015	Correction: CYP2C9 genotype vs. metabolic phenotype for individual drug dosing--a correlation analysis using flurbiprofen as probe drug.	Flurbiprofen	109-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
25623616-9	2015	Compared to conventional in vitro BDI methodologies of assessment, the introduction of human plasma into the in vitro study model changed the observed inhibitory effect of silybin A, silybin B and hydrastine and berberine on CYP2C9 and CYP3A4/5, respectively, results which more closely mirrored those generated in clinical study.	Silybin	172-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	225-231
25623616-9	2015	Compared to conventional in vitro BDI methodologies of assessment, the introduction of human plasma into the in vitro study model changed the observed inhibitory effect of silybin A, silybin B and hydrastine and berberine on CYP2C9 and CYP3A4/5, respectively, results which more closely mirrored those generated in clinical study.	Silybin	183-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	225-231
25623616-9	2015	Compared to conventional in vitro BDI methodologies of assessment, the introduction of human plasma into the in vitro study model changed the observed inhibitory effect of silybin A, silybin B and hydrastine and berberine on CYP2C9 and CYP3A4/5, respectively, results which more closely mirrored those generated in clinical study.	Berberine	212-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	225-231
24517573-0	2015	Inhibitory effects of curcumin on activity of cytochrome P450 2C9 enzyme in human and 2C11 in rat liver microsomes.	Curcumin	22-30	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-65
24517573-1	2015	Cytochrome P450 2C9 (CYP2C9), one of the most important phase I drug metabolizing enzymes, could catalyze the reactions that convert diclofenanc into diclofenac 4"-hydroxylation.	diclofenanc	133-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
24517573-1	2015	Cytochrome P450 2C9 (CYP2C9), one of the most important phase I drug metabolizing enzymes, could catalyze the reactions that convert diclofenanc into diclofenac 4"-hydroxylation.	diclofenanc	133-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
24517573-1	2015	Cytochrome P450 2C9 (CYP2C9), one of the most important phase I drug metabolizing enzymes, could catalyze the reactions that convert diclofenanc into diclofenac 4"-hydroxylation.	diclofenac 4"	150-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
24517573-1	2015	Cytochrome P450 2C9 (CYP2C9), one of the most important phase I drug metabolizing enzymes, could catalyze the reactions that convert diclofenanc into diclofenac 4"-hydroxylation.	diclofenac 4"	150-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
24517573-3	2015	The objective of this work was to investigate the effects of curcumin on CYP2C9 in human and cytochrome P450 2C11 (CYP2C11) in rat liver microsomes.	Curcumin	61-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
24517573-4	2015	The results showed that curcumin inhibited CYP2C9 activity (10 micromol L(-1) diclofenac) with half-maximal inhibition or a half-maximal inhibitory concentration (IC50) of 15.25 micromol L(-1) and Ki = 4.473 micromol L(-1) in human liver microsomes.	Curcumin	24-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
24517573-4	2015	The results showed that curcumin inhibited CYP2C9 activity (10 micromol L(-1) diclofenac) with half-maximal inhibition or a half-maximal inhibitory concentration (IC50) of 15.25 micromol L(-1) and Ki = 4.473 micromol L(-1) in human liver microsomes.	Diclofenac	78-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
24517573-5	2015	Curcumin"s mode of action on CYP2C9 activity was noncompetitive for the substrate diclofenanc and uncompetitive for the cofactor NADPH.	Curcumin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
24517573-5	2015	Curcumin"s mode of action on CYP2C9 activity was noncompetitive for the substrate diclofenanc and uncompetitive for the cofactor NADPH.	diclofenanc	82-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
24517573-5	2015	Curcumin"s mode of action on CYP2C9 activity was noncompetitive for the substrate diclofenanc and uncompetitive for the cofactor NADPH.	NADP	129-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
24517573-7	2015	The observations imply that curcumin has the inhibitory effects on CYP2C9 activity in human.	Curcumin	28-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
25652102-6	2015	The genotypes of VKORC1, CYP2C9, and CYP2C19, together with non-genetic factors (age, sex, and body weight) explained 52% of the variability in warfarin INR/daily dose, of which CYP2C19 genotypes accounted for 7%.	Warfarin	144-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
25515945-2	2015	The impact of activity of the genes encoding CYP3A4, CYP3A5, and CYP2C9 on the pharmacokinetics of voriconazole cannot be ignored because, second to CYP2C19, they are the most important enzymes involved in voriconazole metabolism.	Voriconazole	206-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
25515945-3	2015	The influence of genetic polymorphisms in CYP3A4, CYP3A5, and CYP2C9 on the plasma concentrations of voriconazole was evaluated in the present study.	Voriconazole	101-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
25656643-6	2015	The specific cytochrome P450 (CYP) 2C9 inhibitor, sulfaphenazole, counteracted both oxidative stress and mitochondrial membrane depolarization, providing EC protection against resveratrol-elicited pro-oxidant effects.	Sulfaphenazole	50-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-38
25656643-6	2015	The specific cytochrome P450 (CYP) 2C9 inhibitor, sulfaphenazole, counteracted both oxidative stress and mitochondrial membrane depolarization, providing EC protection against resveratrol-elicited pro-oxidant effects.	Resveratrol	176-187	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-38
25656643-7	2015	Our findings strongly suggest that CYP2C9 mediates resveratrol-induced oxidative stress leading to mitochondria impairment and EC death.	Resveratrol	51-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
25449227-2	2015	In vitro studies indicated that faldaprevir inhibited CYP2B6, CYP2C9, and CYP3A, and was a weak-to-moderate inactivator of CYP3A4.	faldaprevir	32-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
25595525-1	2015	INTRODUCTION: A large proportion of the coumarin dose variability is explained by environmental factors and by common genetic variants in the VKORC1 and CYP2C9 genes.	coumarin	40-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	153-159
25449227-6	2015	These studies suggest that faldaprevir shows a dose-dependent inhibition of CYP3A and CYP2C9, and does not induce CYP isoforms.	faldaprevir	27-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
28294900-2	2015	In the group with PG selection we took into consideration the result of preliminary genotyping of polymorphisms of VKORC1 and CYP2C9 genes known to be associated with individual warfarin dose.	Warfarin	178-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
28294900-6	2015	Carriers of *2 and/or *3 of CYP2C9 associated with lowering of activity of this cytochrome had greater lability of INR values during course of therapy with warfarin.	Warfarin	156-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
25449654-1	2015	The induction of CYP2C9 by dabrafenib using S-warfarin as a probe and the effects of a CYP3A inhibitor (ketoconazole) and a CYP2C8 inhibitor (gemfibrozil) on dabrafenib pharmacokinetics were evaluated in patients with BRAF V600 mutation-positive tumors.	dabrafenib	27-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
25162219-0	2015	Individualized phenytoin therapy for Japanese pediatric patients with epilepsy based on CYP2C9 and CYP2C19 genotypes.	Phenytoin	15-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
25162219-1	2015	BACKGROUND: The aims of this study were to identify the target dose of phenytoin (PHT) and to compare the treatment continuation rate between patients receiving conventional therapy and patients receiving individualized therapy based on genotyping of the CYP2C9*3, CYP2C19*2, and CYP2C19*3 alleles.	Phenytoin	71-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	255-261
25162219-6	2015	If the patients had the CYP2C9*3, CYP2C19*2, or CYP2C19*3 alleles, the initial dose of PHT was reduced by 10%-50% according to previous reports.	Phenytoin	87-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
25775139-0	2015	CYP2C9 genotype vs. metabolic phenotype for individual drug dosing--a correlation analysis using flurbiprofen as probe drug.	Flurbiprofen	97-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25758259-4	2015	Owing to the unique hydrophobic feature of a ZnO NW that provides a desirable "microenvironment" for the immobilization of biomolecules, our device can effectively stimulate the tolbutamide metabolism by decorating a ZnO NW with cytochrome P4502C9/CYPs reductase (CYP2C9/CPR) microsomes.	Zinc Oxide	45-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	264-270
25758259-4	2015	Owing to the unique hydrophobic feature of a ZnO NW that provides a desirable "microenvironment" for the immobilization of biomolecules, our device can effectively stimulate the tolbutamide metabolism by decorating a ZnO NW with cytochrome P4502C9/CYPs reductase (CYP2C9/CPR) microsomes.	Tolbutamide	178-189	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	264-270
25758259-4	2015	Owing to the unique hydrophobic feature of a ZnO NW that provides a desirable "microenvironment" for the immobilization of biomolecules, our device can effectively stimulate the tolbutamide metabolism by decorating a ZnO NW with cytochrome P4502C9/CYPs reductase (CYP2C9/CPR) microsomes.	Zinc Oxide	217-220	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	264-270
25560189-0	2015	Genotype frequencies of VKORC1 and CYP2C9 in native and Mestizo populations from Mexico, potential impact for coumarin dosing.	coumarin	110-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-41
25304014-0	2015	Effect of CYP2C9, CYP4F2 and VKORC1 genetic polymorphisms on pharmacokinetics and pharmacodynamics of mean daily maintenance dose of warfarin in Chinese patients.	Warfarin	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
25578229-9	2015	In PHH, a low CYP2C9 activity, the major IBU-metabolising CYP, led to an increased cytotoxicity.	Ibuprofen	41-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
25304014-7	2015	There were significant differences in the concentrations of S-WF and 7-OH-S-WF among the CYP2C9 variants.	7-oh-s	69-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
25669612-1	2015	OBJECTIVE: Our aim was to determinate the acenocoumarol dose requirement in highly sensitive geriatric patients, based on a minimum of genotype (VKORC1 and CYP2C9) data.	Acenocoumarol	42-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
25618289-6	2015	Genetic variants of other CYP enzymes, including CYP3A4 and CYP2C9/19, as well as co-medication interfering with the metabolic activity of CYP2D6 and CYP3A4 have been shown to affect endoxifen concentrations and may also contribute to the variability in response to tamoxifen.	4-hydroxy-N-desmethyltamoxifen	183-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
25618289-6	2015	Genetic variants of other CYP enzymes, including CYP3A4 and CYP2C9/19, as well as co-medication interfering with the metabolic activity of CYP2D6 and CYP3A4 have been shown to affect endoxifen concentrations and may also contribute to the variability in response to tamoxifen.	Tamoxifen	266-275	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
25187307-0	2015	Effect of CYP2C9-VKORC1 interaction on warfarin stable dosage and its predictive algorithm.	Warfarin	39-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
25187307-1	2015	This study aimed to identify the effect of CYP2C9-VKORC1 interaction on warfarin dosage requirement and its predictive algorithm by investigating four populations.	Warfarin	72-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
25311916-8	2015	The highest mean phenytoin level (27.95 +- 1.85 microg/ml) was detected in the G8 genotype group (CYP2C9*1/*3-CYP2C19*2/*3) and the G1 genotype group showed the lowest mean phenytoin level (7.43 +- 0.73 microg/ml).	Phenytoin	17-26	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	98-104
28962416-0	2015	In vitro modulatory effects of Terminalia arjuna, arjunic acid, arjunetin and arjungenin on CYP3A4, CYP2D6 and CYP2C9 enzyme activity in human liver microsomes.	arjunic acid	50-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
28962416-0	2015	In vitro modulatory effects of Terminalia arjuna, arjunic acid, arjunetin and arjungenin on CYP3A4, CYP2D6 and CYP2C9 enzyme activity in human liver microsomes.	arjunetin	64-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
28962416-3	2015	Alcoholic and aqueous bark extracts of T. arjuna, arjunic acid, arjunetin and arjungenin were evaluated for their potential to inhibit CYP3A4, CYP2D6 and CYP2C9 enzymes in human liver microsomes.	arjunic acid	50-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
28962416-3	2015	Alcoholic and aqueous bark extracts of T. arjuna, arjunic acid, arjunetin and arjungenin were evaluated for their potential to inhibit CYP3A4, CYP2D6 and CYP2C9 enzymes in human liver microsomes.	arjunetin	64-73	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
28962416-3	2015	Alcoholic and aqueous bark extracts of T. arjuna, arjunic acid, arjunetin and arjungenin were evaluated for their potential to inhibit CYP3A4, CYP2D6 and CYP2C9 enzymes in human liver microsomes.	arjungenin	78-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
28962416-7	2015	Our findings suggest strongly that arjuna extracts significantly inhibit the activity of CYP3A4, CYP2D6 and CYP2C9 enzymes, which is likely to cause clinically significant drug-drug interactions mediated via inhibition of the major CYP isozymes.	arjuna	35-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
25663116-2	2015	The dosage of warfarin is strongly affected by genetic variants of CYP2C9 and VKORC1 genes.	Warfarin	14-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
25597548-3	2015	Genetic polymorphisms of CYP2C9 and 2C19 are reasonably common and further prolong the elimination of phenytoin.	Phenytoin	102-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-40
25533629-7	2015	VMY-2-95 2HCl showed significant inhibition of CYP2C9 and 2C19, but weak or no effect on 1A2, 2D6, and 3A4.	vmy-2-95 2hcl	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
25052959-3	2015	HS-23 slightly inhibited CYP2A6, CYP2B6, CYP2C9, CYP2C19, and CYP3A4 enzyme activities in human liver microsomes with IC50 values of 80.6, 160.7, 169.5, 85.4, and 76.6 mug/mL, respectively.	hs-23	0-5	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
25681367-7	2015	Phenytoin is metabolized in the liver, primarily by the CYP2C9 isozyme, which can be competitively inhibited by capecitabine.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
25681367-7	2015	Phenytoin is metabolized in the liver, primarily by the CYP2C9 isozyme, which can be competitively inhibited by capecitabine.	Capecitabine	112-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
25324279-7	2015	The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered.	Simvastatin	47-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	300-306
25181036-8	2015	Genetic polymorphisms in the gene encoding cytochrome P450 2C9 (CYP2C9) and those in the target gene responsible for the warfarin anticoagulant effect, vitamin K epoxide reductase (VKORC1), account for much of the variability in the warfarin maintenance dose; however, routine genotyping in warfarin therapy remains controversial.	Warfarin	233-241	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-62
25181036-8	2015	Genetic polymorphisms in the gene encoding cytochrome P450 2C9 (CYP2C9) and those in the target gene responsible for the warfarin anticoagulant effect, vitamin K epoxide reductase (VKORC1), account for much of the variability in the warfarin maintenance dose; however, routine genotyping in warfarin therapy remains controversial.	Warfarin	233-241	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
25181036-8	2015	Genetic polymorphisms in the gene encoding cytochrome P450 2C9 (CYP2C9) and those in the target gene responsible for the warfarin anticoagulant effect, vitamin K epoxide reductase (VKORC1), account for much of the variability in the warfarin maintenance dose; however, routine genotyping in warfarin therapy remains controversial.	Warfarin	233-241	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-62
25181036-8	2015	Genetic polymorphisms in the gene encoding cytochrome P450 2C9 (CYP2C9) and those in the target gene responsible for the warfarin anticoagulant effect, vitamin K epoxide reductase (VKORC1), account for much of the variability in the warfarin maintenance dose; however, routine genotyping in warfarin therapy remains controversial.	Warfarin	233-241	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
25324279-7	2015	The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered.	Amiodarone	106-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	300-306
25324279-7	2015	The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered.	MDEA	115-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	300-306
25324279-7	2015	The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered.	Dextromethorphan	148-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	300-306
25324279-7	2015	The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered.	Amiodarone	207-211	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	300-306
25324279-7	2015	The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered.	MDEA	268-272	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	300-306
25324279-7	2015	The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered.	Warfarin	308-316	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	300-306
25324279-7	2015	The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered.	Amiodarone	207-211	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	300-306
25324279-7	2015	The closest prediction was obtained for CYP3A (simvastatin) DDI when the competitive inhibition from both AMIO and MDEA was considered, for CYP2D6 (dextromethorphan) DDI when the competitive inhibition from AMIO and the competitive plus time-dependent inhibition from MDEA were incorporated, and for CYP2C9 (warfarin) DDI when the competitive plus time-dependent inhibition from AMIO and the competitive inhibition from MDEA were considered.	MDEA	268-272	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	300-306
25760542-2	2015	Cynomolgus CYP2C9 (formerly known as CYP2C43) is predominantly expressed in liver and encodes a drug-metabolizing enzyme that metabolizes human CYP2C substrates such as S-mephenytoin and progesterone.	Mephenytoin	169-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
25480923-7	2015	Enzyme activities of CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, and CYP3A4 were reduced upon 48-72 hours exposure to IL-6 in PHH and HepaRG.	4,5,6,7-tetrachlorophthalide	123-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
25760542-2	2015	Cynomolgus CYP2C9 (formerly known as CYP2C43) is predominantly expressed in liver and encodes a drug-metabolizing enzyme that metabolizes human CYP2C substrates such as S-mephenytoin and progesterone.	Mephenytoin	169-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-16
25480923-7	2015	Enzyme activities of CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, and CYP3A4 were reduced upon 48-72 hours exposure to IL-6 in PHH and HepaRG.	heparg	131-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
25760542-2	2015	Cynomolgus CYP2C9 (formerly known as CYP2C43) is predominantly expressed in liver and encodes a drug-metabolizing enzyme that metabolizes human CYP2C substrates such as S-mephenytoin and progesterone.	Progesterone	187-199	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
25760542-2	2015	Cynomolgus CYP2C9 (formerly known as CYP2C43) is predominantly expressed in liver and encodes a drug-metabolizing enzyme that metabolizes human CYP2C substrates such as S-mephenytoin and progesterone.	Progesterone	187-199	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-16
25760542-3	2015	In addition, cynomolgus CYP2C9 also metabolizes caffeine, resulting in the formation of the metabolite that is not generated efficiently in humans.	Caffeine	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
24962733-1	2015	Previous studies have raised interest in using the genotyping of CYP2C9 and VKORC1 to guide warfarin dosing.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
25519826-1	2015	OBJECTIVE: The objective of this study was to determine the influence of CYP2C9, VKORC1, CYP4F2, and GGCX genetic polymorphisms on mean daily dose of acenocoumarol in South Indian patients and to develop a new pharmacogenetic algorithm based on clinical and genetic factors.	Acenocoumarol	150-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
25519826-6	2015	The genetic variants of CYP2C9 and GGCX (rs11676382) were found to be associated with lower acenocoumarol dose, whereas CYP4F2 (rs2108622) was associated with higher doses.	Acenocoumarol	92-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
25519826-7	2015	Age, body mass index (BMI), variation of CYP2C9, VKORC1, CYP4F2, and GGCX were the major determinants of acenocoumarol maintenance dose, accounting for 61.8 % of its variability (adjusted r (2) = 0.615, p &lt; 0.0001).	Acenocoumarol	105-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
25727956-7	2015	CYP2C9 and CYP2C19 activities were inhibited down to 75-80% (at the same rocuronium concentration).	Rocuronium	73-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25026456-1	2015	Interindividual variability in stable warfarin doses is largely attributed to VKORC1 and CYP2C9 variants.	Warfarin	38-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
25026456-5	2015	This study revealed that GATA4 can be predictive of stable warfarin dose and extended warfarin pharmacogenetics further to the regulation of CYP2C9 expression.	Warfarin	59-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
25026456-5	2015	This study revealed that GATA4 can be predictive of stable warfarin dose and extended warfarin pharmacogenetics further to the regulation of CYP2C9 expression.	Warfarin	86-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	141-147
25091503-4	2015	CYP2C19 and CYP2C9 correlated with norendoxifen and (Z)-4-hydroxytamoxifen concentrations, respectively (P&lt;0.001).	N,N-didesmethyl-4-hydroxytamoxifen	35-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
25560582-3	2015	CYP2C8, CYP2C9 and CYP2J2 gene involved in the metabolism of arachidonic acid, generates epoxyeicosatrienoic acids (EETs) that mediate dilation of coronary arteries improving post-ischemic cardiac contractile function, reduce vascular inflammation, and increase intravascular fibrinolysis.	Arachidonic Acid	61-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
25560582-3	2015	CYP2C8, CYP2C9 and CYP2J2 gene involved in the metabolism of arachidonic acid, generates epoxyeicosatrienoic acids (EETs) that mediate dilation of coronary arteries improving post-ischemic cardiac contractile function, reduce vascular inflammation, and increase intravascular fibrinolysis.	epoxyeicosatrienoic acids	89-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
25091503-4	2015	CYP2C19 and CYP2C9 correlated with norendoxifen and (Z)-4-hydroxytamoxifen concentrations, respectively (P&lt;0.001).	hydroxytamoxifen	52-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
25462116-7	2015	CYP2C9 and CYP3A4, which metabolize DF to p-benzoquinone imines, were tested to investigate the applicability of human P450s.	1,4-benzoquinoneimine	42-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
26632190-1	2015	Arachidonic acid (AA) is metabolized to epoxyeicosatrienoic acids (EETs) via cytochrome enzymes such as CYP 2C9, 2C8 and 2J2.	Arachidonic Acid	0-16	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-111
25391650-0	2015	Epigenetic modification of histone 3 lysine 27: mediator subunit MED25 is required for the dissociation of polycomb repressive complex 2 from the promoter of cytochrome P450 2C9.	Lysine	37-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-177
25391650-9	2015	Formaldehyde-assisted isolation of regulatory elements (FAIRE) revealed chromatin conformation changes that were reliant on MED25, indicating that MED25 induced a permissive chromatin state that reflected increases in CYP2C9 mRNA.	Formaldehyde	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
26632190-1	2015	Arachidonic acid (AA) is metabolized to epoxyeicosatrienoic acids (EETs) via cytochrome enzymes such as CYP 2C9, 2C8 and 2J2.	epoxyeicosatrienoic acids	40-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-111
26632190-1	2015	Arachidonic acid (AA) is metabolized to epoxyeicosatrienoic acids (EETs) via cytochrome enzymes such as CYP 2C9, 2C8 and 2J2.	eets	67-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-111
25832633-0	2015	Impact of CYP2C9 polymorphism found in the Chinese population on the metabolism of propofol in vitro.	Propofol	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
25832633-1	2015	The microsomal CYP2C9 alleles involved in the biotransformation of propofol, a widely used anesthetic agent, were investigated in vitro.	Propofol	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
25832633-2	2015	To examine the enzymatic activity of the CYP2C9 alleles, kinetic parameters for propofol 4-hydroxylation were determined in recombinant human P450s CYP2C9 microsomes from Sf21 insects cells carrying CYP2C9*1 and other variants.	Propofol	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
25832633-6	2015	This study is the first to report these rare alleles for propofol metabolism, providing fundamental data for further clinical studies on CYP2C9 alleles for propofol metabolism in vivo.	Propofol	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
25832633-6	2015	This study is the first to report these rare alleles for propofol metabolism, providing fundamental data for further clinical studies on CYP2C9 alleles for propofol metabolism in vivo.	Propofol	156-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	137-143
26554252-0	2015	CYP2C9 Genetic Polymorphism is a Potential Predictive Marker for the Efficacy of Rosuvastatin Therapy.	Rosuvastatin Calcium	81-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25757926-0	2015	In vitro inhibition of CYP2C9-mediated warfarin 7-hydroxylation by iguratimod: possible mechanism of iguratimod-warfarin interaction.	Warfarin	39-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
25757926-0	2015	In vitro inhibition of CYP2C9-mediated warfarin 7-hydroxylation by iguratimod: possible mechanism of iguratimod-warfarin interaction.	Warfarin	112-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
25757926-13	2015	These results indicated that iguratimod is a potent direct inhibitor of CYP2C9-mediated warfarin 7-hydroxylation and that its inhibitory effect on CYP2C9.1 was more sensitive than that on CYP2C9.3.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
26554252-3	2015	This study aimed to evaluate the associations of CYP2C9 genetic polymorphism with the efficacy and safety of rosuvastatin in Chinese patients with hyperlipidemia.	Rosuvastatin Calcium	109-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
26554252-15	2015	CONCLUSIONS: This study suggests that the CYP2C9 polymorphism may be involved in the lipid-lowering efficacy of rosuvastatin in patients with hyperlipidemia.	Rosuvastatin Calcium	112-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
25144335-0	2015	Effect of CYP2C9 genetic polymorphism on the metabolism of flurbiprofen in vitro.	Flurbiprofen	59-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
25144335-2	2015	To examine the enzymatic activity of the CYP2C9 alleles, kinetic parameters for 4"-hydroxyflurbiprofen were determined using recombinant human P450s CYP2C9 microsomes from insect cells Sf21 carrying wild-type CYP2C9*1 and other variants.	4'-hydroxyflurbiprofen	80-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
25144335-2	2015	To examine the enzymatic activity of the CYP2C9 alleles, kinetic parameters for 4"-hydroxyflurbiprofen were determined using recombinant human P450s CYP2C9 microsomes from insect cells Sf21 carrying wild-type CYP2C9*1 and other variants.	4'-hydroxyflurbiprofen	80-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
25144335-2	2015	To examine the enzymatic activity of the CYP2C9 alleles, kinetic parameters for 4"-hydroxyflurbiprofen were determined using recombinant human P450s CYP2C9 microsomes from insect cells Sf21 carrying wild-type CYP2C9*1 and other variants.	4'-hydroxyflurbiprofen	80-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
25144335-5	2015	This study provided the most comprehensive data on the enzymatic activities of all reported CYP2C9 variants in the Chinese population with regard to the commonly used non-steroidal anti-inflammatory drug, flurbiprofen (FP).	Flurbiprofen	205-217	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
26037375-2	2015	This article reviews the contribution of genetic polymorphisms affecting the activity of CYP2C9, the main enzyme responsible for phenytoin metabolism, to the variation in phenytoin clearance and susceptibility to adverse effects.	Phenytoin	129-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
26037375-2	2015	This article reviews the contribution of genetic polymorphisms affecting the activity of CYP2C9, the main enzyme responsible for phenytoin metabolism, to the variation in phenytoin clearance and susceptibility to adverse effects.	Phenytoin	171-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
26037375-3	2015	AREAS COVERED: Comprehensive and critical review of available evidence concerning the influence of CYP2C9 genetic polymorphism on phenytoin pharmacokinetic and safety profile.	Phenytoin	130-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
26037375-4	2015	EXPERT OPINION: There is extensive evidence that CYP2C9 polymorphisms are an important determinant of the rate of phenytoin metabolism, although other factors including expression of other enzymes such as CYP2C19 and the influence of drug interactions, physiological and disease-related factors may also play a role.	Phenytoin	114-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
26037375-6	2015	The clinical value and cost-effectiveness of CYP2C9 genotyping in improving the safety of phenytoin therapy, however, have not been clearly established and require formal testing in well-designed prospective studies.	Phenytoin	90-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
26058399-6	2015	Fluvastatin is metabolized by CYP2C9, while pravastatin, rosuvastatin and pitavastatin are not susceptible to inhibition by any CYP.	Fluvastatin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
26502504-2	2015	In the group with PG selection we took into consideration the result of preliminary genotyping of polymorphisms of VKORC1 and CYP2C9 genes known to be associated with individual warfarin dose.	Warfarin	178-186	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
25345887-4	2015	EXPERT OPINION: Gene candidate studies in Brazilian patients verified consistently the association of warfarin and pheprocoumon stable dose requirements with CYP2C9 and VKORC1 polymorphisms, and minor or no influence of other pharmacogenes (e.g., CYP4F2 and F7).	Warfarin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
25103957-2	2015	A series of in vitro experiments conducted early in the development of ivacaftor indicated ivacaftor and metabolites may have the potential to inhibit cytochrome P450 (CYP) 2C8, CYP2C9, CYP3A, and CYP2D6, as well as P-glycoprotein (P-gp).	ivacaftor	91-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	178-184
25103957-7	2015	Based on these results, caution and appropriate monitoring are recommended when concomitant substrates of CYP2C9, CYP3A and/or P-gp are used during treatment with ivacaftor, particularly drugs with a narrow therapeutic index, such as warfarin.	ivacaftor	163-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
25103957-7	2015	Based on these results, caution and appropriate monitoring are recommended when concomitant substrates of CYP2C9, CYP3A and/or P-gp are used during treatment with ivacaftor, particularly drugs with a narrow therapeutic index, such as warfarin.	Warfarin	234-242	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
26517138-0	2015	The Implication of the Polymorphisms of COX-1, UGT1A6, and CYP2C9 among Cardiovascular Disease (CVD) Patients Treated with Aspirin.	Aspirin	123-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
26517138-1	2015	PURPOSE:   Enzymes potentially responsible for the pharmacokinetic variations of aspirin include cyclooxygenase-1 (COX-1), UDP-glucuronosyltransferase (UGT1A6) and P450 (CYP) (CYP2C9).	Aspirin	81-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
26517138-10	2015	CONCLUSION: Screening of patients with defective genetic variants of UGT1A6 and CYP2C9*3 helps in identifying patients at risk of aspirin induced gastritis.	Aspirin	130-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
26502504-6	2015	Carriers of *2 and/or *3 of CYP2C9 associated with lowering of activity of this cytochrome had greater lability of INR values during course of therapy with warfarin.	Warfarin	156-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
25823787-0	2015	Mechanistic insights into the effect of CYP2C9*2 and CYP2C9*3 variants on the 7-hydroxylation of warfarin.	Warfarin	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
25560470-5	2015	Polymorphisms of genes involved in drug metabolism, such as CYP2C9, CYP2C8 and SLCO1B1, may influence the efficacy of glinides and the incidence of adverse effects.	glinides	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
25823787-0	2015	Mechanistic insights into the effect of CYP2C9*2 and CYP2C9*3 variants on the 7-hydroxylation of warfarin.	Warfarin	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
25823787-1	2015	AIM: To evaluate the impact of CYP2C9*2 and CYP2C9*3 variants on binding and hydroxylation of warfarin.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
25823787-1	2015	AIM: To evaluate the impact of CYP2C9*2 and CYP2C9*3 variants on binding and hydroxylation of warfarin.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	Warfarin	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	Warfarin	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	Warfarin	55-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	7-hydroxywarfarin	64-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
26122864-0	2015	Effect of gender and CYP2C9 and CYP2C8 polymorphisms on the pharmacokinetics of ibuprofen enantiomers.	Ibuprofen	80-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	7-hydroxywarfarin	64-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
26122864-1	2015	AIM: To evaluate the effect of polymorphisms in CYP2C9 and CYP2C8 and gender on the pharmacokinetics of the enantiomeric forms of ibuprofen.	Ibuprofen	130-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
26122864-4	2015	CYP2C9*3 and CYP2C9*2 carriers had a lower S-ibuprofen clearance and a higher S-ibuprofen AUC and half-life.	Ibuprofen	43-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	7-hydroxywarfarin	64-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
26122864-4	2015	CYP2C9*3 and CYP2C9*2 carriers had a lower S-ibuprofen clearance and a higher S-ibuprofen AUC and half-life.	Ibuprofen	43-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	Hydrogen	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
26122864-4	2015	CYP2C9*3 and CYP2C9*2 carriers had a lower S-ibuprofen clearance and a higher S-ibuprofen AUC and half-life.	Ibuprofen	78-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
26122864-4	2015	CYP2C9*3 and CYP2C9*2 carriers had a lower S-ibuprofen clearance and a higher S-ibuprofen AUC and half-life.	Ibuprofen	78-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	Hydrogen	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
26122864-5	2015	R-ibuprofen clearance was decreased in CYP2C9*3 carriers.	Ibuprofen	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
26122864-7	2015	Multiple regression analysis showed that CYP2C9*2, CYP2C9*3 and gender were associated with S-ibuprofen clearance, but only CYP2C9*3 was associated with R-ibuprofen clearance.	Ibuprofen	92-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	Hydrogen	147-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
26122864-7	2015	Multiple regression analysis showed that CYP2C9*2, CYP2C9*3 and gender were associated with S-ibuprofen clearance, but only CYP2C9*3 was associated with R-ibuprofen clearance.	Ibuprofen	92-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
26122864-7	2015	Multiple regression analysis showed that CYP2C9*2, CYP2C9*3 and gender were associated with S-ibuprofen clearance, but only CYP2C9*3 was associated with R-ibuprofen clearance.	Ibuprofen	92-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
26122864-8	2015	CONCLUSION: The pharmacokinetics of S-ibuprofen and R-ibuprofen is affected by CYP2C9 polymorphisms and gender.	Ibuprofen	36-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
26122864-8	2015	CONCLUSION: The pharmacokinetics of S-ibuprofen and R-ibuprofen is affected by CYP2C9 polymorphisms and gender.	Ibuprofen	52-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
25823787-4	2015	RESULTS: CYP2C9*2 and CYP2C9*3 variants exhibited high warfarin/7-hydroxywarfarin (multiple linear regression model), dose-dependent disruption of hydrogen bonds with warfarin, dose-dependent increase in the distance between C7 of S-warfarin and Fe-O of CYP2C9, dose-dependent decrease in the glide scores (in silico).	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
25823787-5	2015	CONCLUSION: CYP2C9*2 and CYP2C9*3 variants result in disruption of hydrogen bonding interactions with warfarin and longer distance between C7 and Fe-O thus impairing warfarin 7-hydroxylation due to lower binding affinity of warfarin.	Hydrogen	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
25823787-5	2015	CONCLUSION: CYP2C9*2 and CYP2C9*3 variants result in disruption of hydrogen bonding interactions with warfarin and longer distance between C7 and Fe-O thus impairing warfarin 7-hydroxylation due to lower binding affinity of warfarin.	Hydrogen	67-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
25823787-5	2015	CONCLUSION: CYP2C9*2 and CYP2C9*3 variants result in disruption of hydrogen bonding interactions with warfarin and longer distance between C7 and Fe-O thus impairing warfarin 7-hydroxylation due to lower binding affinity of warfarin.	Warfarin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
25823787-5	2015	CONCLUSION: CYP2C9*2 and CYP2C9*3 variants result in disruption of hydrogen bonding interactions with warfarin and longer distance between C7 and Fe-O thus impairing warfarin 7-hydroxylation due to lower binding affinity of warfarin.	Warfarin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
25823787-5	2015	CONCLUSION: CYP2C9*2 and CYP2C9*3 variants result in disruption of hydrogen bonding interactions with warfarin and longer distance between C7 and Fe-O thus impairing warfarin 7-hydroxylation due to lower binding affinity of warfarin.	Warfarin	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
25823787-5	2015	CONCLUSION: CYP2C9*2 and CYP2C9*3 variants result in disruption of hydrogen bonding interactions with warfarin and longer distance between C7 and Fe-O thus impairing warfarin 7-hydroxylation due to lower binding affinity of warfarin.	Warfarin	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
25823787-5	2015	CONCLUSION: CYP2C9*2 and CYP2C9*3 variants result in disruption of hydrogen bonding interactions with warfarin and longer distance between C7 and Fe-O thus impairing warfarin 7-hydroxylation due to lower binding affinity of warfarin.	Warfarin	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
25823787-5	2015	CONCLUSION: CYP2C9*2 and CYP2C9*3 variants result in disruption of hydrogen bonding interactions with warfarin and longer distance between C7 and Fe-O thus impairing warfarin 7-hydroxylation due to lower binding affinity of warfarin.	Warfarin	166-174	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
25833162-4	2015	The results showed that MXC and HPTE inhibited both human CYP2C9 and rat liver CYP2C11 activity, with half-maximal inhibitory concentration (IC50) values of 15.47 +- 0.36 (MXC) and 8.87 +- 0.53 mumol/l (HPTE) for human CYP2C9, and of 22.45 +- 1.48 (MXC) and 24.63 +- 1.35 mumol/l (HPTE) for rat CYP2C11.	2,2-bis(4-hydroxyphenyl)-1,1,1-trichloroethane	32-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
25833162-4	2015	The results showed that MXC and HPTE inhibited both human CYP2C9 and rat liver CYP2C11 activity, with half-maximal inhibitory concentration (IC50) values of 15.47 +- 0.36 (MXC) and 8.87 +- 0.53 mumol/l (HPTE) for human CYP2C9, and of 22.45 +- 1.48 (MXC) and 24.63 +- 1.35 mumol/l (HPTE) for rat CYP2C11.	2,2-bis(4-hydroxyphenyl)-1,1,1-trichloroethane	32-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	219-225
25584932-4	2015	Black and Hispanic populations are known to have a higher prevalence of cardiovascular risk factors and disease, and a substantial proportion of black and Hispanic individuals possess genotypes of the cytochrome P450 (CYP) 2C9 enzyme involved in the metabolism of many NSAIDs and the CYP2D6 enzyme involved in metabolism of the dual opioid agonist/norepinephrine-serotonin reuptake inhibitor tramadol.	Norepinephrine	348-362	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	201-226
26255664-0	2015	Identification and characterization of a novel CYP2C9 allelic variant in a warfarin-sensitive patient.	Warfarin	75-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
26255664-6	2015	When expressed in yeast and insect cells, compared with wild-type enzyme, variant CYP2C9.60 exhibited lower protein expression capacity and showed significantly decreased metabolic activities for the hydroxylation of S-warfarin, tolbutamide and diclofenac.	Warfarin	219-227	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
26255664-6	2015	When expressed in yeast and insect cells, compared with wild-type enzyme, variant CYP2C9.60 exhibited lower protein expression capacity and showed significantly decreased metabolic activities for the hydroxylation of S-warfarin, tolbutamide and diclofenac.	Tolbutamide	229-240	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
26255664-6	2015	When expressed in yeast and insect cells, compared with wild-type enzyme, variant CYP2C9.60 exhibited lower protein expression capacity and showed significantly decreased metabolic activities for the hydroxylation of S-warfarin, tolbutamide and diclofenac.	Diclofenac	245-255	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
26265036-7	2015	CONCLUSION: We confirmed the important role of VKORC1 and CYP2C9 polymorphisms in warfarin dose.	Warfarin	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
25584932-4	2015	Black and Hispanic populations are known to have a higher prevalence of cardiovascular risk factors and disease, and a substantial proportion of black and Hispanic individuals possess genotypes of the cytochrome P450 (CYP) 2C9 enzyme involved in the metabolism of many NSAIDs and the CYP2D6 enzyme involved in metabolism of the dual opioid agonist/norepinephrine-serotonin reuptake inhibitor tramadol.	Serotonin	363-372	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	201-226
25584932-4	2015	Black and Hispanic populations are known to have a higher prevalence of cardiovascular risk factors and disease, and a substantial proportion of black and Hispanic individuals possess genotypes of the cytochrome P450 (CYP) 2C9 enzyme involved in the metabolism of many NSAIDs and the CYP2D6 enzyme involved in metabolism of the dual opioid agonist/norepinephrine-serotonin reuptake inhibitor tramadol.	Tramadol	392-400	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	201-226
26827407-9	2015	DISCUSSION: The metabolism of warfarin involves several cytochrome P450 isoenzymes, including CYP1A2, CYP2C9, CYP2C19, and CYP3A4.	Warfarin	30-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
25282448-1	2015	The cytochrome P450 (CYP) 2C9 and vitamin K epoxide reductase complex 1 (VKORC1) genotypes have been strongly and consistently associated with warfarin dose requirements, and dosing algorithms incorporating genetic and clinical information have been shown to be predictive of stable warfarin dose.	Warfarin	143-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-29
26053557-11	2015	A cocktail assay showed that CYP1A2, CYP2C9, CYP2C19, CYP2E1 and CYP3A4 can be inhibited by rutaecarpine in human liver microsomes.	rutecarpine	92-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
25312789-5	2014	RESULTS: CYP2C9*2, CYP2C9*3, VKORC1-1639G&gt;A, and APOE *epsilon4 were associated with lower warfarin doses.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
26422867-2	2015	We evaluated an existing warfarin dosing algorithm developed for Malaysian patients that was based only on VKORC1 and CYP2C9 genes.	Warfarin	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
25372302-4	2014	In addition to the major metabolite 3"-OH-methyl-MFA, resulting from the benzylic hydroxylation by CYP2C9, 4"-hydroxy-MFA and 5-hydroxy-MFA were identified as metabolites resulting from oxidative metabolism of both aromatic rings of MFA.	3"-oh-methyl-mfa	36-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
25372302-4	2014	In addition to the major metabolite 3"-OH-methyl-MFA, resulting from the benzylic hydroxylation by CYP2C9, 4"-hydroxy-MFA and 5-hydroxy-MFA were identified as metabolites resulting from oxidative metabolism of both aromatic rings of MFA.	Mefenamic Acid	49-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-105
25372302-6	2014	The major GSH conjugate was identified as 4"-OH-5"-glutathionyl-MFA and was formed at the highest activity by CYP1A2 and to a lesser extent by CYP2C9 and CYP3A4.	Glutathione	10-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
25372302-6	2014	The major GSH conjugate was identified as 4"-OH-5"-glutathionyl-MFA and was formed at the highest activity by CYP1A2 and to a lesser extent by CYP2C9 and CYP3A4.	4"-oh-5"-glutathionyl-mfa	42-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
25224009-7	2014	Furthermore, VT-1161 weakly inhibited human CYP2C9, CYP2C19, and CYP3A4, suggesting a low drug-drug interaction potential.	VT-1161	13-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
24891132-12	2014	The patients with CYP2C9*2 had a higher concentration of propofol at the time of LOC (p = 0.02).	Propofol	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
25312789-5	2014	RESULTS: CYP2C9*2, CYP2C9*3, VKORC1-1639G&gt;A, and APOE *epsilon4 were associated with lower warfarin doses.	Warfarin	94-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
25312789-10	2014	CONCLUSION: CYP2C9*2, CYP2C9*3, VKORC1-1639G&gt;A, and APOE *epsilon4 were associated with lower warfarin doses, while MDR1 3435C&gt;T and UGT1A1(TA) n polymorphisms were associated with a requirement for higher doses.	Warfarin	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
25312789-10	2014	CONCLUSION: CYP2C9*2, CYP2C9*3, VKORC1-1639G&gt;A, and APOE *epsilon4 were associated with lower warfarin doses, while MDR1 3435C&gt;T and UGT1A1(TA) n polymorphisms were associated with a requirement for higher doses.	Warfarin	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
25001883-2	2014	Previous studies have produced estimates of the effect of polymorphisms in Cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) on stable warfarin dosing, but data on time in therapeutic range, initial dosing and adverse effects are limited.	Warfarin	173-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-94
25001883-2	2014	Previous studies have produced estimates of the effect of polymorphisms in Cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase complex subunit 1 (VKORC1) on stable warfarin dosing, but data on time in therapeutic range, initial dosing and adverse effects are limited.	Warfarin	173-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
25001883-7	2014	These data show novel associations between VKORC1-1639 and CYP2C9*2 and INR values in children taking warfarin, as well as replicating previous findings with regard to stable dose requirements.	Warfarin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
25951663-3	2014	The purpose of the present study was to clarify the role of 36 CYP2C9 alleles, 21 novel alleles (*36-*56) found in the Chinese population, in the oxidative metabolism of diclofenac in vitro.	Diclofenac	170-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
25521356-4	2014	In the 214 (85.6%) cases with a major bleed 30 or more days after warfarin initiation, CYP2C9*3 was the only variant associated with bleeding (adjusted odds ratio: 2.05; 95% CI: 1.04, 4.04).	Warfarin	66-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
25951663-8	2014	Thus, this study demonstrated that more attention should be given to subjects carrying these CYP2C9 alleles when administering diclofena.	diclofena	127-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
25521356-5	2014	CONCLUSION: The CYP2C9*3 allele may double the risk of major bleeding among patients taking warfarin for 30 or more days.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
25951663-0	2014	The role of CYP2C9 genetic polymorphisms in the oxidative metabolism of diclofenac in vitro.	Diclofenac	72-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
25196644-5	2014	Both caffeic acid and quercetin were potent competitive inhibitors of CYP1A2 (Ki = 1.16 and 0.93 muM, respectively) and CYP2C9 (Ki = 0.95 and 1.67 muM, respectively).	caffeic acid	5-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
25196644-5	2014	Both caffeic acid and quercetin were potent competitive inhibitors of CYP1A2 (Ki = 1.16 and 0.93 muM, respectively) and CYP2C9 (Ki = 0.95 and 1.67 muM, respectively).	Quercetin	22-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	120-126
25361167-3	2014	The activities of CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4 were attenuated by EEP-B55 in a concentration-dependent manner, and artepillin C, kaempferide, dihydrokaempferide, isosakuranetin, and kaempferol were estimated to have potential for CYP inhibition.	isosakuranetin	177-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
25427198-7	2014	The results suggested that MH was simultaneously a substrate and an inhibitor of CYP1A2 and CYP2C9, and MH had the potential to perpetrate drug-drug interactions with other CYP1A2 and CYP2C19 substrates.	meranzin hydrate	27-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
25361167-3	2014	The activities of CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4 were attenuated by EEP-B55 in a concentration-dependent manner, and artepillin C, kaempferide, dihydrokaempferide, isosakuranetin, and kaempferol were estimated to have potential for CYP inhibition.	eep-b55	81-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
25361167-3	2014	The activities of CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4 were attenuated by EEP-B55 in a concentration-dependent manner, and artepillin C, kaempferide, dihydrokaempferide, isosakuranetin, and kaempferol were estimated to have potential for CYP inhibition.	kaempferol	197-207	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
25332267-2	2014	Bosentan is metabolized by the cytochrome CYP2C9 and inhibits the bile salt export pump, which is encoded by ABCB11.	Bosentan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
25361167-3	2014	The activities of CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4 were attenuated by EEP-B55 in a concentration-dependent manner, and artepillin C, kaempferide, dihydrokaempferide, isosakuranetin, and kaempferol were estimated to have potential for CYP inhibition.	Dihydrokaempferide	157-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
25332267-3	2014	This suggests that genetic variants of CYP2C9 and/or ABCB11 may predispose patients to bosentan-induced liver injury.	Bosentan	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
25332267-9	2014	CONCLUSION: Our data indicate hepatotoxicity of bosentan from decreased hepatic metabolism due to common variants of CYP2C9.	Bosentan	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
25142093-0	2014	Influence of proton pump inhibitors and VKORC1 mutations on CYP2C9-mediated dose requirements of vitamin K antagonist therapy: a pilot study.	Vitamin K	97-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
25142093-1	2014	Interindividual variations in dose requirements of oral vitamin K antagonists (VKA) are attributed to several factors, including genetic variant alleles of vitamin K epoxide reductase complex subunit 1 (VKORC1) and cytochrome P450 2C9 (CYP2C9), but also interaction with co-medications.	Vitamin K	56-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	215-234
25142093-1	2014	Interindividual variations in dose requirements of oral vitamin K antagonists (VKA) are attributed to several factors, including genetic variant alleles of vitamin K epoxide reductase complex subunit 1 (VKORC1) and cytochrome P450 2C9 (CYP2C9), but also interaction with co-medications.	Vitamin K	56-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	236-242
25099164-1	2014	Phenytoin is a widely used antiepileptic drug with a narrow therapeutic index and large interpatient variability, partly due to genetic variations in the gene encoding cytochrome P450 (CYP)2C9 (CYP2C9).	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-192
25099164-1	2014	Phenytoin is a widely used antiepileptic drug with a narrow therapeutic index and large interpatient variability, partly due to genetic variations in the gene encoding cytochrome P450 (CYP)2C9 (CYP2C9).	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	194-200
25099164-3	2014	We summarize evidence from the published literature supporting these associations and provide recommendations for the use of phenytoin based on CYP2C9 and/or HLA-B genotype (also available on PharmGKB: http://www.pharmgkb.org).	Phenytoin	125-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
25142737-0	2014	Effects of cytochrome P450 2C9 polymorphism on bosentan metabolism.	Bosentan	47-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-30
25142737-3	2014	The aim of this study was to assess the catalytic activities of 38 human CYP2C9 alleles, including 24 novel alleles (*36-*60) found in the Han Chinese population, toward bosentan (BOS) in vitro.	Bosentan	170-178	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
25142737-3	2014	The aim of this study was to assess the catalytic activities of 38 human CYP2C9 alleles, including 24 novel alleles (*36-*60) found in the Han Chinese population, toward bosentan (BOS) in vitro.	Bosentan	180-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
25142737-8	2014	These findings suggest that more attention should be directed to subjects carrying these infrequent CYP2C9 alleles when administering BOS in the clinic.	Bosentan	134-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	100-106
25187484-0	2014	Mechanistic studies of the cationic binding pocket of CYP2C9 in vitro and in silico: metabolism of nonionizable analogs of tienilic acid.	Ticrynafen	123-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
24944083-7	2014	CYP2C9 and CYP2C19 inhibitors strongly inhibited R(+)-NAF metabolism, and CYP1A2, CYP2C8, CYP2D6 and CYP3A4/5 inhibitors moderately inhibited R(+)-NAF metabolism.	r(+)-naf	49-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25187484-1	2014	Tienilic acid (TA) is selectively oxidized at the C-5 position of the thiophene ring by the human liver enzyme cytochrome P450 2C9 (CYP2C9).	Ticrynafen	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-130
25187484-1	2014	Tienilic acid (TA) is selectively oxidized at the C-5 position of the thiophene ring by the human liver enzyme cytochrome P450 2C9 (CYP2C9).	Ticrynafen	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
25187484-1	2014	Tienilic acid (TA) is selectively oxidized at the C-5 position of the thiophene ring by the human liver enzyme cytochrome P450 2C9 (CYP2C9).	Ticrynafen	15-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-130
25187484-1	2014	Tienilic acid (TA) is selectively oxidized at the C-5 position of the thiophene ring by the human liver enzyme cytochrome P450 2C9 (CYP2C9).	Ticrynafen	15-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
25187484-1	2014	Tienilic acid (TA) is selectively oxidized at the C-5 position of the thiophene ring by the human liver enzyme cytochrome P450 2C9 (CYP2C9).	Thiophenes	70-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-130
25187484-1	2014	Tienilic acid (TA) is selectively oxidized at the C-5 position of the thiophene ring by the human liver enzyme cytochrome P450 2C9 (CYP2C9).	Thiophenes	70-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
25187484-3	2014	In this study, we investigated how chemical modification of TA influences the bioactivation by CYP2C9.	Ticrynafen	60-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
24944083-7	2014	CYP2C9 and CYP2C19 inhibitors strongly inhibited R(+)-NAF metabolism, and CYP1A2, CYP2C8, CYP2D6 and CYP3A4/5 inhibitors moderately inhibited R(+)-NAF metabolism.	r(+)-naf	142-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24944083-8	2014	CYP2C9 inhibitors strongly inhibited S(-)-NAF metabolism, and CYP2C8, CYP2C19 and CYP3A4/5 inhibitors moderately inhibited S(-)-NAF metabolism.	naftopidil	37-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24944083-9	2014	Consistent with the results of chemical inhibitors experiments, recombinant human CYP2C9 and CYP2C19 contributed greatly to R(+)-NAF metabolism, and CYP2C9 contributed greatly to S(-)-NAF metabolism.	r(+)-naf	124-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
24944083-9	2014	Consistent with the results of chemical inhibitors experiments, recombinant human CYP2C9 and CYP2C19 contributed greatly to R(+)-NAF metabolism, and CYP2C9 contributed greatly to S(-)-NAF metabolism.	Sulfur	179-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
24944083-9	2014	Consistent with the results of chemical inhibitors experiments, recombinant human CYP2C9 and CYP2C19 contributed greatly to R(+)-NAF metabolism, and CYP2C9 contributed greatly to S(-)-NAF metabolism.	naftopidil	180-187	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	149-155
24944083-11	2014	CYP2C9 plays the most important role in the demethylation and hydroxylation of both NAF enantiomers, CYP2C19 is another major CYP isoform that is involved in R(+)-NAF metabolism.	naftopidil	84-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24944083-11	2014	CYP2C9 plays the most important role in the demethylation and hydroxylation of both NAF enantiomers, CYP2C19 is another major CYP isoform that is involved in R(+)-NAF metabolism.	naftopidil	159-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
25280537-0	2014	Creatine kinase elevation caused by a combination of fluvastatin and telmisartan in a patient heterozygous for the CYP2C9*3 and ABCC2 -24C &gt; T variants: a case report.	Fluvastatin	53-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
25069408-2	2014	CYP2C9, VKROC1, and CYP4F2 play important roles in warfarin metabolism, and their genetic polymorphisms are related to the variability in dose determination.	Warfarin	51-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24882266-2	2014	The main human CYP epoxygenases, i.e. CYP2C8, CYP2C9, CYP2C19 and CYP2J2, convert AA to four regioisomer epoxyeicosatrienoic acids (EETs).	epoxyeicosatrienoic acids	105-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
24882266-2	2014	The main human CYP epoxygenases, i.e. CYP2C8, CYP2C9, CYP2C19 and CYP2J2, convert AA to four regioisomer epoxyeicosatrienoic acids (EETs).	eets	132-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
24590863-6	2014	The standardized EJE was incubated with pooled human liver microsomes to assess the CYP2C9-, CYP2D6-, and CYP3A4-mediated metabolism of diclofenac, dextromethorphan, and testosterone, respectively.	Diclofenac	136-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
24590863-9	2014	The selectivity of EJE for CYP2C9 rather than CYP3A4 and CYP2D6 led to perform the enzyme kinetics to explicate the mechanism underlying the inhibition of CYP2C9-mediated diclofenac 4"-hydroxylation.	Diclofenac	171-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
24590863-9	2014	The selectivity of EJE for CYP2C9 rather than CYP3A4 and CYP2D6 led to perform the enzyme kinetics to explicate the mechanism underlying the inhibition of CYP2C9-mediated diclofenac 4"-hydroxylation.	Diclofenac	171-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-161
25272989-4	2014	The reaction phenotype study showed that CYP3A4, CYP2C9, and CYP1A2 were the major cytochrome P450 isozymes in the metabolism of CSA.	3-hydroxy-4-prenyl-5-methoxystilbene-2-carboxylic acid	129-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
25272989-8	2014	CSA reversibly inhibited CYP3A4 and CYP2C9 activities in human liver microsomes with IC50 values of 28.3 and 31.3 muM, respectively, but exhibited no inhibition activities to CYP1A2, CYP2A6, CYP2C19, CYP2D6, and CYP2E1.	3-hydroxy-4-prenyl-5-methoxystilbene-2-carboxylic acid	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
25280537-0	2014	Creatine kinase elevation caused by a combination of fluvastatin and telmisartan in a patient heterozygous for the CYP2C9*3 and ABCC2 -24C &gt; T variants: a case report.	Telmisartan	69-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
24612223-4	2014	For example, SP 600125 was a potent inhibitor for CYP1A2, but enhanced the activity of CYP2C9 fourfolds.	pyrazolanthrone	13-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-93
25079360-3	2014	Variation in warfarin pharmacokinetic and pharmacodynamic genes, such as CYP2C9 and VKORC1, do not fully explain the dose variability in African Americans.	Warfarin	13-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
24750390-4	2014	It is known that variability in two genes (CYP2C9 and VKORC1) has a significant effect on individual response to warfarin dose.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
26052198-0	2014	Warfarin dose requirement in Turkish patients: the influences of patient characteristics and polymorphisms in CYP2C9, VKORC1 and factor VII.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	110-116
26052198-5	2014	RESULTS: The mean daily warfarin dosage was significantly higher in patients with the CYP2C9*1/*1 genotype than in the CYP2C9*2/*2 and CYP2C9*1/*3 groups (p &lt;= 0.05).	Warfarin	24-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
26052198-5	2014	RESULTS: The mean daily warfarin dosage was significantly higher in patients with the CYP2C9*1/*1 genotype than in the CYP2C9*2/*2 and CYP2C9*1/*3 groups (p &lt;= 0.05).	Warfarin	24-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
26052198-5	2014	RESULTS: The mean daily warfarin dosage was significantly higher in patients with the CYP2C9*1/*1 genotype than in the CYP2C9*2/*2 and CYP2C9*1/*3 groups (p &lt;= 0.05).	Warfarin	24-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
26052198-9	2014	CONCLUSIONS: Polymorphisms in CYP2C9, VKORC1 and factor VII did partially affect daily warfarin dose requirements, while age, gender, BMI and INR do not.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
25089947-1	2014	AIM: To develop an acenocoumarol (ACN) dosing algorithm for patients with atrial fibrillation or venous thromboembolism, considering the influence on the stable ACN dose of clinical factors and gene polymorphisms, including CYP2C9*2/*3, VKORC1, CYP4F2*3, ABCB1, APOE, CYP2C19*2/*17, and GGCX.	Acenocoumarol	19-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	224-230
24663076-2	2014	In this study, we evaluate, for the first time, the influence of CYP2D6, CYP2C9 and ABCB1 genotypes on the steady-state plasma concentrations of fluoxetine and its active metabolite (S)-norfluoxetine, and on the clinical improvement in children and adolescent patients receiving fluoxetine treatment.	Fluoxetine	145-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
25089947-4	2014	CONCLUSION: The variability in the stable ACN dose was better explained by a pharmacogenetic algorithm including clinical and genetic factors (CYP2C9, VKORC1, and APOE) than by a clinical algorithm, providing a more accurate dosage prediction.	Acenocoumarol	42-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
25932358-10	2014	Our results indicated that the PCR-CTPP could be one of the alternative methods for genotyping VKORC1 G-1639A and CYP2C9 A1075C for Asians and Africans with similar allele frequencies to Japanese.	ctpp	35-39	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
24779639-2	2014	In this article, the modulatory effects of extracts from vinegar-baked Radix Bupleuri (VBRB) and saikosaponins on the activity of CYP1A2, CYP2C9 and CYP3A4 were investigated in vitro.	saikosaponin D	97-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
25932358-0	2014	A PCR method for VKORC1 G-1639A and CYP2C9 A1075C genotyping useful to warfarin therapy among Japanese.	Warfarin	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
25182955-1	2014	BACKGROUND: Cytochrome P450 (CYP) 2C9 is expressed in the vascular endothelium and metabolizes arachidonic acid to biologically active epoxyeicosatrienoic acids (EETs), which have the crucial role in the modulation of cardiovascular homeostasis.	Arachidonic Acid	95-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-37
25182955-1	2014	BACKGROUND: Cytochrome P450 (CYP) 2C9 is expressed in the vascular endothelium and metabolizes arachidonic acid to biologically active epoxyeicosatrienoic acids (EETs), which have the crucial role in the modulation of cardiovascular homeostasis.	epoxyeicosatrienoic acids	135-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-37
25182955-1	2014	BACKGROUND: Cytochrome P450 (CYP) 2C9 is expressed in the vascular endothelium and metabolizes arachidonic acid to biologically active epoxyeicosatrienoic acids (EETs), which have the crucial role in the modulation of cardiovascular homeostasis.	eets	162-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-37
24548191-6	2014	Fenofibrate was a potent in vitro inhibitor of CYP2C19 (IC50 = 0.2 mum) and CYP2B6 (IC50 = 0.7 mum) and a moderate inhibitor of CYP2C9 (IC50 = 9.7 mum).	Fenofibrate	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
24919870-10	2014	In conclusion, VKORC1, CYP2C9*3, APOE and ABCB1 genotypes should be considered in prevention of overanticoagulation and bleeding events in the initiation of acenocoumarol therapy.	Acenocoumarol	157-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
25088191-2	2014	A lead molecule was identified that has improved agonist efficacy relative to our clinical compound (APD597) and possesses reduced CYP2C9 inhibitory potential.	APD597	101-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
24986093-0	2014	Drug-drug interaction of losartan and glimepiride metabolism by recombinant microsome CYP2C9*1, 2C9*3, 2C9*13, and 2C9*16 in vitro.	Losartan	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
24986093-0	2014	Drug-drug interaction of losartan and glimepiride metabolism by recombinant microsome CYP2C9*1, 2C9*3, 2C9*13, and 2C9*16 in vitro.	glimepiride	38-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	86-92
24986093-2	2014	METHODS: In this study, we characterized the drug-drug interactions of losartan (LOS) and glimepiride (GLP) using recombinant cytochrome P450 (CYP) 2C9 enzymes (CYP2C9*1, CYP2C9*3, CYP2C9*13, and CYP2C9*16).	Losartan	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-151
24986093-2	2014	METHODS: In this study, we characterized the drug-drug interactions of losartan (LOS) and glimepiride (GLP) using recombinant cytochrome P450 (CYP) 2C9 enzymes (CYP2C9*1, CYP2C9*3, CYP2C9*13, and CYP2C9*16).	Losartan	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
24986093-2	2014	METHODS: In this study, we characterized the drug-drug interactions of losartan (LOS) and glimepiride (GLP) using recombinant cytochrome P450 (CYP) 2C9 enzymes (CYP2C9*1, CYP2C9*3, CYP2C9*13, and CYP2C9*16).	Losartan	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
24986093-2	2014	METHODS: In this study, we characterized the drug-drug interactions of losartan (LOS) and glimepiride (GLP) using recombinant cytochrome P450 (CYP) 2C9 enzymes (CYP2C9*1, CYP2C9*3, CYP2C9*13, and CYP2C9*16).	Losartan	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
24986093-2	2014	METHODS: In this study, we characterized the drug-drug interactions of losartan (LOS) and glimepiride (GLP) using recombinant cytochrome P450 (CYP) 2C9 enzymes (CYP2C9*1, CYP2C9*3, CYP2C9*13, and CYP2C9*16).	Losartan	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
24986093-2	2014	METHODS: In this study, we characterized the drug-drug interactions of losartan (LOS) and glimepiride (GLP) using recombinant cytochrome P450 (CYP) 2C9 enzymes (CYP2C9*1, CYP2C9*3, CYP2C9*13, and CYP2C9*16).	Losartan	81-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-151
24986093-2	2014	METHODS: In this study, we characterized the drug-drug interactions of losartan (LOS) and glimepiride (GLP) using recombinant cytochrome P450 (CYP) 2C9 enzymes (CYP2C9*1, CYP2C9*3, CYP2C9*13, and CYP2C9*16).	Losartan	81-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
24986093-2	2014	METHODS: In this study, we characterized the drug-drug interactions of losartan (LOS) and glimepiride (GLP) using recombinant cytochrome P450 (CYP) 2C9 enzymes (CYP2C9*1, CYP2C9*3, CYP2C9*13, and CYP2C9*16).	glimepiride	90-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-151
24986093-2	2014	METHODS: In this study, we characterized the drug-drug interactions of losartan (LOS) and glimepiride (GLP) using recombinant cytochrome P450 (CYP) 2C9 enzymes (CYP2C9*1, CYP2C9*3, CYP2C9*13, and CYP2C9*16).	glimepiride	90-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	161-167
24986093-2	2014	METHODS: In this study, we characterized the drug-drug interactions of losartan (LOS) and glimepiride (GLP) using recombinant cytochrome P450 (CYP) 2C9 enzymes (CYP2C9*1, CYP2C9*3, CYP2C9*13, and CYP2C9*16).	glimepiride	90-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
24986093-2	2014	METHODS: In this study, we characterized the drug-drug interactions of losartan (LOS) and glimepiride (GLP) using recombinant cytochrome P450 (CYP) 2C9 enzymes (CYP2C9*1, CYP2C9*3, CYP2C9*13, and CYP2C9*16).	glimepiride	90-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
24986093-2	2014	METHODS: In this study, we characterized the drug-drug interactions of losartan (LOS) and glimepiride (GLP) using recombinant cytochrome P450 (CYP) 2C9 enzymes (CYP2C9*1, CYP2C9*3, CYP2C9*13, and CYP2C9*16).	glimepiride	90-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
24986093-3	2014	RESULTS: Metabolism of losartan by recombinant CYP2C9* 1, CYP2C9*3, CYP2C9*13, and CYP2C9* 16 was inhibited by glimepiride competitively with IC50 values of 0.669 +- 0.055 microM, 0.424 +- 0.032 microM, 2.557 +- 0.058 microM, and 0.667 +- 0.039 microM, respectively.	Losartan	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
24986093-3	2014	RESULTS: Metabolism of losartan by recombinant CYP2C9* 1, CYP2C9*3, CYP2C9*13, and CYP2C9* 16 was inhibited by glimepiride competitively with IC50 values of 0.669 +- 0.055 microM, 0.424 +- 0.032 microM, 2.557 +- 0.058 microM, and 0.667 +- 0.039 microM, respectively.	Losartan	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
24986093-3	2014	RESULTS: Metabolism of losartan by recombinant CYP2C9* 1, CYP2C9*3, CYP2C9*13, and CYP2C9* 16 was inhibited by glimepiride competitively with IC50 values of 0.669 +- 0.055 microM, 0.424 +- 0.032 microM, 2.557 +- 0.058 microM, and 0.667 +- 0.039 microM, respectively.	Losartan	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
24986093-3	2014	RESULTS: Metabolism of losartan by recombinant CYP2C9* 1, CYP2C9*3, CYP2C9*13, and CYP2C9* 16 was inhibited by glimepiride competitively with IC50 values of 0.669 +- 0.055 microM, 0.424 +- 0.032 microM, 2.557 +- 0.058 microM, and 0.667 +- 0.039 microM, respectively.	Losartan	23-31	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
24986093-3	2014	RESULTS: Metabolism of losartan by recombinant CYP2C9* 1, CYP2C9*3, CYP2C9*13, and CYP2C9* 16 was inhibited by glimepiride competitively with IC50 values of 0.669 +- 0.055 microM, 0.424 +- 0.032 microM, 2.557 +- 0.058 microM, and 0.667 +- 0.039 microM, respectively.	glimepiride	111-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
24986093-3	2014	RESULTS: Metabolism of losartan by recombinant CYP2C9* 1, CYP2C9*3, CYP2C9*13, and CYP2C9* 16 was inhibited by glimepiride competitively with IC50 values of 0.669 +- 0.055 microM, 0.424 +- 0.032 microM, 2.557 +- 0.058 microM, and 0.667 +- 0.039 microM, respectively.	glimepiride	111-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
24986093-3	2014	RESULTS: Metabolism of losartan by recombinant CYP2C9* 1, CYP2C9*3, CYP2C9*13, and CYP2C9* 16 was inhibited by glimepiride competitively with IC50 values of 0.669 +- 0.055 microM, 0.424 +- 0.032 microM, 2.557 +- 0.058 microM, and 0.667 +- 0.039 microM, respectively.	glimepiride	111-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
24986093-3	2014	RESULTS: Metabolism of losartan by recombinant CYP2C9* 1, CYP2C9*3, CYP2C9*13, and CYP2C9* 16 was inhibited by glimepiride competitively with IC50 values of 0.669 +- 0.055 microM, 0.424 +- 0.032 microM, 2.557 +- 0.058 microM, and 0.667 +- 0.039 microM, respectively.	glimepiride	111-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
24986093-4	2014	The inhibitory effect of glimepiride on losartan metabolism by CYP2C9*13 was marginal.	glimepiride	25-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
24986093-5	2014	The apparent Ki value of glimepiride with CYP2C9*3 (0.0416 +- 0.0059 microM) was significantly lower than with CYP2C9*1 (0.1476 +- 0.0219 microM) and CYP2C9*16 (0.2671 +- 0.0456 microM).	glimepiride	25-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
24986093-5	2014	The apparent Ki value of glimepiride with CYP2C9*3 (0.0416 +- 0.0059 microM) was significantly lower than with CYP2C9*1 (0.1476 +- 0.0219 microM) and CYP2C9*16 (0.2671 +- 0.0456 microM).	glimepiride	25-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
24986093-5	2014	The apparent Ki value of glimepiride with CYP2C9*3 (0.0416 +- 0.0059 microM) was significantly lower than with CYP2C9*1 (0.1476 +- 0.0219 microM) and CYP2C9*16 (0.2671 +- 0.0456 microM).	glimepiride	25-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
24986093-7	2014	The potencies for inhibition of glimepiride hydroxylation were determined to be CYP2C9*1~CYP2C9*3~CYP2C9*16 &gt; CYP2C9*13 by 4 microM losartan.	glimepiride	32-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
24986093-7	2014	The potencies for inhibition of glimepiride hydroxylation were determined to be CYP2C9*1~CYP2C9*3~CYP2C9*16 &gt; CYP2C9*13 by 4 microM losartan.	glimepiride	32-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
24986093-7	2014	The potencies for inhibition of glimepiride hydroxylation were determined to be CYP2C9*1~CYP2C9*3~CYP2C9*16 &gt; CYP2C9*13 by 4 microM losartan.	glimepiride	32-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
24986093-7	2014	The potencies for inhibition of glimepiride hydroxylation were determined to be CYP2C9*1~CYP2C9*3~CYP2C9*16 &gt; CYP2C9*13 by 4 microM losartan.	glimepiride	32-43	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
24986093-9	2014	CONCLUSIONS: Given these results, the potential inhibition of losartan metabolism by CYP2C9*3, CYP2C9*13, and CYP2C9*16 in vivo by glimepiride deserves further investigation.	Losartan	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
24986093-9	2014	CONCLUSIONS: Given these results, the potential inhibition of losartan metabolism by CYP2C9*3, CYP2C9*13, and CYP2C9*16 in vivo by glimepiride deserves further investigation.	Losartan	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
24986093-9	2014	CONCLUSIONS: Given these results, the potential inhibition of losartan metabolism by CYP2C9*3, CYP2C9*13, and CYP2C9*16 in vivo by glimepiride deserves further investigation.	Losartan	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
24986093-9	2014	CONCLUSIONS: Given these results, the potential inhibition of losartan metabolism by CYP2C9*3, CYP2C9*13, and CYP2C9*16 in vivo by glimepiride deserves further investigation.	glimepiride	131-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
25298588-0	2014	CYP2C9*3 polymorphism presenting as lethal subdural hematoma with low-dose warfarin.	Warfarin	75-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24986093-9	2014	CONCLUSIONS: Given these results, the potential inhibition of losartan metabolism by CYP2C9*3, CYP2C9*13, and CYP2C9*16 in vivo by glimepiride deserves further investigation.	glimepiride	131-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
24986093-9	2014	CONCLUSIONS: Given these results, the potential inhibition of losartan metabolism by CYP2C9*3, CYP2C9*13, and CYP2C9*16 in vivo by glimepiride deserves further investigation.	glimepiride	131-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
25246753-0	2014	Extremely elevated international normalized ratio of warfarin in a patient with CYP2C9*1/*3 and thyrotoxicosis.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
24730468-1	2014	OBJECTIVES: The aim of this study is to establish the inhibitory effects of 14 commonly used complementary and alternative medicines (CAM) on the metabolism of cytochrome P450 2C9 (CYP2C9) substrates 7-methoxy-4-trifluoromethyl coumarine (MFC) and tolbutamide.	7-methoxy-4-trifluoromethyl coumarine	200-237	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
24730468-1	2014	OBJECTIVES: The aim of this study is to establish the inhibitory effects of 14 commonly used complementary and alternative medicines (CAM) on the metabolism of cytochrome P450 2C9 (CYP2C9) substrates 7-methoxy-4-trifluoromethyl coumarine (MFC) and tolbutamide.	mfc	239-242	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
24730468-1	2014	OBJECTIVES: The aim of this study is to establish the inhibitory effects of 14 commonly used complementary and alternative medicines (CAM) on the metabolism of cytochrome P450 2C9 (CYP2C9) substrates 7-methoxy-4-trifluoromethyl coumarine (MFC) and tolbutamide.	Tolbutamide	248-259	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
24730468-5	2014	In human liver microsomes (HLM) the inhibition of CYP2C9-mediated metabolism of tolbutamide was determined, using liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS).	Tolbutamide	80-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
25244877-9	2014	CONCLUSION: The association of CYP2C9 and VKORC1 genotypes and risks for adverse events due to exposure to warfarin was examined for the first time in Puerto Ricans.	Warfarin	107-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
25317394-2	2014	Phenytoin, one of the common drugs implicated in gingival enlargement, is metabolized mainly by cytochrome P450 (CYP)2C9 and partly by CYP2C19.	Phenytoin	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-120
25317394-4	2014	AIMS: The present study was undertaken to investigate the influence of the CYP2C9*2 and *3 variant genotypes on phenytoin hydroxylation in subjects diagnosed with epilepsy from South India, thus establishing the genetic polymorphisms leading to its defective hydroxylation process.	Phenytoin	112-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
25410896-1	2014	The CYP2C9 c.449G&gt;A (p.R150H, rs7900194) polymorphism, which confers the CYP2C9*8 allele, is common in persons of African descent and results in reduced clearance of the narrow therapeutic index drugs, warfarin and phenytoin.	Warfarin	205-213	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
25410896-1	2014	The CYP2C9 c.449G&gt;A (p.R150H, rs7900194) polymorphism, which confers the CYP2C9*8 allele, is common in persons of African descent and results in reduced clearance of the narrow therapeutic index drugs, warfarin and phenytoin.	Warfarin	205-213	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
25410896-1	2014	The CYP2C9 c.449G&gt;A (p.R150H, rs7900194) polymorphism, which confers the CYP2C9*8 allele, is common in persons of African descent and results in reduced clearance of the narrow therapeutic index drugs, warfarin and phenytoin.	Phenytoin	218-227	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
25410896-1	2014	The CYP2C9 c.449G&gt;A (p.R150H, rs7900194) polymorphism, which confers the CYP2C9*8 allele, is common in persons of African descent and results in reduced clearance of the narrow therapeutic index drugs, warfarin and phenytoin.	Phenytoin	218-227	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
24908449-2	2014	Polymorphisms in two genes i.e. CYP2C9 (Cytochrome P450 2C9) and VKORC1 (Vitamin K epoxide reductase complex subunit 1) play a major role in warfarin dose variation and its related adverse effects.	Warfarin	141-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
24908449-2	2014	Polymorphisms in two genes i.e. CYP2C9 (Cytochrome P450 2C9) and VKORC1 (Vitamin K epoxide reductase complex subunit 1) play a major role in warfarin dose variation and its related adverse effects.	Warfarin	141-149	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-59
24910189-4	2014	As measured by liquid chromatography-electrospray ionization tandem mass spectrometry, ethambutol exhibited strong inhibitory potential against CYP1A2 and CYP2E1, moderate against CYP2C19 and CYP2D6 and weak against CYP2A6, CYP2C9 and CYP3A4, based on the IC50 values.	Ethambutol	87-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	224-230
25042728-1	2014	INTRODUCTION: VKORC1 and cytochrome CYP2C9 genetic variants contribute largely to inter-individual variations in vitamin K antagonists (VKAs) dose requirements.	Vitamin K	113-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
25042728-6	2014	Carriers of 2 and/or 3 variant alleles for CYP2C9 also required a lower dose of warfarin as compared with 1 1 carriers (35.0 [31.5-52.5] vs. 43.8 [35.0-60.2] mg/week, p=0.02; 35.0 [23.5-35.0] vs. 43.8 [35.0-60.2] mg/week, p&lt;0.0001, respectively).	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
25202272-3	2014	The purpose of this study was to find out whether CYP2C9 was involved in this herb-herb interaction by using tolbutamide as a probe substrate in vivo and in vitro.	Tolbutamide	109-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
25126975-3	2014	Only VKORC1 and CYP2C9 SNPs were observed to be significantly associated with warfarin dose.	Warfarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
25096692-10	2014	Direct sequencing of CYP2C identified missense variant rs1057910 (CYP2C9*3) that showed significant association with phenytoin-related severe cutaneous adverse reactions (odds ratio, 12; 95% CI, 6.6-20; P=1.1 x 10(-17)).	Phenytoin	117-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
24974237-0	2014	Prevalence of genetic polymorphisms of CYP2C9 and VKORC1 - implications for warfarin management and outcome in Croatian patients with acute stroke.	Warfarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
24974237-1	2014	BACKGROUND: Data on the prevalence of CYP2C9 and VKORC1 genes and their influence on anticoagulant effect and warfarin dose in stroke patients are scarce.	Warfarin	110-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
24974237-8	2014	Warfarin dosage complications were slightly more frequent among the carriers of CYP2C9 2, 3 compared to the carriers of VKORC1 1173T alleles (68.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
25096692-11	2014	The statistically significant association between CYP2C9*3 and phenytoin-related severe cutaneous adverse reactions was observed in additional samples from Taiwan, Japan, and Malaysia.	Phenytoin	63-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
25096692-12	2014	A meta-analysis using the data from the 3 populations showed an overall odds ratio of 11 (95% CI, 6.2-18; z=8.58; P &lt; .00001) for CYP2C9*3 association with phenytoin-related severe cutaneous adverse reactions.	Phenytoin	159-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	133-139
25096692-13	2014	Delayed clearance of plasma phenytoin was detected in patients with severe cutaneous adverse reactions, especially CYP2C9*3 carriers, providing a functional link of the associated variants to the disease.	Phenytoin	28-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
25096692-14	2014	CONCLUSIONS AND RELEVANCE: This study identified CYP2C variants, including CYP2C9*3, known to reduce drug clearance, as important genetic factors associated with phenytoin-related severe cutaneous adverse reactions.	Phenytoin	162-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
25014006-2	2014	Herein, a nanotube array enzymatic reactor (CYP2C9/Au/TNA) was constructed by electrostatically adsorbing enzyme on the inner wall of TiO2 nanotube arrays (TNAs).	titanium dioxide	134-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
25014006-5	2014	The cytochrome P450 2C9 enzyme (CYP2C9) was confined inside TNAs as a model.	tnas	60-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-23
25014006-5	2014	The cytochrome P450 2C9 enzyme (CYP2C9) was confined inside TNAs as a model.	tnas	60-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
24797541-0	2014	Frequency of CYP2C9 and VKORC1 gene polymorphisms and their influence on warfarin dose in Egyptian pediatric patients.	Warfarin	73-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
24830941-2	2014	Initial studies using primary human hepatocytes showed induction of both the CYP2C9 and CYP2C19 genes by tert-butylhydroquinone (tBHQ).	2-tert-butylhydroquinone	105-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
24830941-2	2014	Initial studies using primary human hepatocytes showed induction of both the CYP2C9 and CYP2C19 genes by tert-butylhydroquinone (tBHQ).	2-tert-butylhydroquinone	129-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	77-83
24830941-6	2014	Using specific kinase inhibitors for mitogen-activated protein kinase, we showed that extracellular signal-regulated kinase and Jun N-terminal kinase are essential for tBHQ-induced expression of CYP2C9.	2-tert-butylhydroquinone	168-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
24322786-0	2014	High warfarin sensitivity in carriers of CYP2C9*35 is determined by the impaired interaction with P450 oxidoreductase.	Warfarin	5-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
24322786-1	2014	Cytochrome P450 2C9 (CYP2C9) metabolizes many clinically important drugs including warfarin and diclofenac.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
24322786-1	2014	Cytochrome P450 2C9 (CYP2C9) metabolizes many clinically important drugs including warfarin and diclofenac.	Warfarin	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
24322786-1	2014	Cytochrome P450 2C9 (CYP2C9) metabolizes many clinically important drugs including warfarin and diclofenac.	Diclofenac	96-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
24322786-1	2014	Cytochrome P450 2C9 (CYP2C9) metabolizes many clinically important drugs including warfarin and diclofenac.	Diclofenac	96-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
24322786-2	2014	We have recently reported a new allelic variant, CYP2C9*35, found in a warfarin hypersensitive patient with Arg125Leu and Arg144Cys mutations.	Warfarin	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
24322786-4	2014	CYP2C9.1 and CYP2C9-Arg144Cys expressed in human embryonic kidney 293 cells effectively metabolized both S-warfarin and diclofenac in NADPH-dependent reactions, whereas CYP2C9-Arg125Leu or CYP2C9.35 were catalytically silent.	Warfarin	105-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24322786-4	2014	CYP2C9.1 and CYP2C9-Arg144Cys expressed in human embryonic kidney 293 cells effectively metabolized both S-warfarin and diclofenac in NADPH-dependent reactions, whereas CYP2C9-Arg125Leu or CYP2C9.35 were catalytically silent.	Warfarin	105-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
24322786-4	2014	CYP2C9.1 and CYP2C9-Arg144Cys expressed in human embryonic kidney 293 cells effectively metabolized both S-warfarin and diclofenac in NADPH-dependent reactions, whereas CYP2C9-Arg125Leu or CYP2C9.35 were catalytically silent.	Warfarin	105-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
24322786-4	2014	CYP2C9.1 and CYP2C9-Arg144Cys expressed in human embryonic kidney 293 cells effectively metabolized both S-warfarin and diclofenac in NADPH-dependent reactions, whereas CYP2C9-Arg125Leu or CYP2C9.35 were catalytically silent.	Warfarin	105-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
24322786-4	2014	CYP2C9.1 and CYP2C9-Arg144Cys expressed in human embryonic kidney 293 cells effectively metabolized both S-warfarin and diclofenac in NADPH-dependent reactions, whereas CYP2C9-Arg125Leu or CYP2C9.35 were catalytically silent.	Diclofenac	120-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24322786-4	2014	CYP2C9.1 and CYP2C9-Arg144Cys expressed in human embryonic kidney 293 cells effectively metabolized both S-warfarin and diclofenac in NADPH-dependent reactions, whereas CYP2C9-Arg125Leu or CYP2C9.35 were catalytically silent.	Diclofenac	120-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
24322786-4	2014	CYP2C9.1 and CYP2C9-Arg144Cys expressed in human embryonic kidney 293 cells effectively metabolized both S-warfarin and diclofenac in NADPH-dependent reactions, whereas CYP2C9-Arg125Leu or CYP2C9.35 were catalytically silent.	Diclofenac	120-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
24322786-4	2014	CYP2C9.1 and CYP2C9-Arg144Cys expressed in human embryonic kidney 293 cells effectively metabolized both S-warfarin and diclofenac in NADPH-dependent reactions, whereas CYP2C9-Arg125Leu or CYP2C9.35 were catalytically silent.	Diclofenac	120-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
24322786-4	2014	CYP2C9.1 and CYP2C9-Arg144Cys expressed in human embryonic kidney 293 cells effectively metabolized both S-warfarin and diclofenac in NADPH-dependent reactions, whereas CYP2C9-Arg125Leu or CYP2C9.35 were catalytically silent.	NADP	134-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24322786-4	2014	CYP2C9.1 and CYP2C9-Arg144Cys expressed in human embryonic kidney 293 cells effectively metabolized both S-warfarin and diclofenac in NADPH-dependent reactions, whereas CYP2C9-Arg125Leu or CYP2C9.35 were catalytically silent.	NADP	134-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
24322786-4	2014	CYP2C9.1 and CYP2C9-Arg144Cys expressed in human embryonic kidney 293 cells effectively metabolized both S-warfarin and diclofenac in NADPH-dependent reactions, whereas CYP2C9-Arg125Leu or CYP2C9.35 were catalytically silent.	NADP	134-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
24322786-4	2014	CYP2C9.1 and CYP2C9-Arg144Cys expressed in human embryonic kidney 293 cells effectively metabolized both S-warfarin and diclofenac in NADPH-dependent reactions, whereas CYP2C9-Arg125Leu or CYP2C9.35 were catalytically silent.	NADP	134-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
24322786-5	2014	However, when NADPH was replaced by a direct electron donor to CYPs, cumene hydroperoxide, hereby bypassing the CYP oxidoreductase (POR), all variant enzymes were active, indicating unproductive interactions between CYP2C9.35 and POR.	NADP	14-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	216-222
24322786-5	2014	However, when NADPH was replaced by a direct electron donor to CYPs, cumene hydroperoxide, hereby bypassing the CYP oxidoreductase (POR), all variant enzymes were active, indicating unproductive interactions between CYP2C9.35 and POR.	cumene hydroperoxide	69-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	216-222
24322786-7	2014	In conclusion, our data strongly suggest that the Arg125Leu mutation in CYP2C9.35 prevents CYP2C9-POR interactions resulting in the absence of NADPH-dependent CYP2C9-catalyzed activity in vivo, thus influencing the warfarin sensitivity in the carriers of this allele.	NADP	143-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
24322786-7	2014	In conclusion, our data strongly suggest that the Arg125Leu mutation in CYP2C9.35 prevents CYP2C9-POR interactions resulting in the absence of NADPH-dependent CYP2C9-catalyzed activity in vivo, thus influencing the warfarin sensitivity in the carriers of this allele.	NADP	143-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
24322786-7	2014	In conclusion, our data strongly suggest that the Arg125Leu mutation in CYP2C9.35 prevents CYP2C9-POR interactions resulting in the absence of NADPH-dependent CYP2C9-catalyzed activity in vivo, thus influencing the warfarin sensitivity in the carriers of this allele.	NADP	143-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
24322786-7	2014	In conclusion, our data strongly suggest that the Arg125Leu mutation in CYP2C9.35 prevents CYP2C9-POR interactions resulting in the absence of NADPH-dependent CYP2C9-catalyzed activity in vivo, thus influencing the warfarin sensitivity in the carriers of this allele.	Warfarin	215-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
24322786-7	2014	In conclusion, our data strongly suggest that the Arg125Leu mutation in CYP2C9.35 prevents CYP2C9-POR interactions resulting in the absence of NADPH-dependent CYP2C9-catalyzed activity in vivo, thus influencing the warfarin sensitivity in the carriers of this allele.	Warfarin	215-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
24322786-7	2014	In conclusion, our data strongly suggest that the Arg125Leu mutation in CYP2C9.35 prevents CYP2C9-POR interactions resulting in the absence of NADPH-dependent CYP2C9-catalyzed activity in vivo, thus influencing the warfarin sensitivity in the carriers of this allele.	Warfarin	215-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
25303293-0	2014	Relationship between the CYP2C9 IVS8-109A&gt;T polymorphism and high losartan hydroxylation in healthy Ecuadorian volunteers.	Losartan	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
25003537-0	2014	Impact of CYP2C9*3/*3 genotype on the pharmacokinetics and pharmacodynamics of oxicam NSAIDs.	oxicam	79-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
25003538-0	2014	Response to Suarez-Kurtz"s comments on strongly increased exposure of meloxicam in CYP2C9*3/*3 individuals.	Meloxicam	70-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
25303293-1	2014	AIM: The CYP2C9 IVS8-109T allele was recently found to be more frequent among Swedish individuals, who have the highest losartan metabolic ratio (MR; losartan:E-3174).	Losartan	120-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
25303293-1	2014	AIM: The CYP2C9 IVS8-109T allele was recently found to be more frequent among Swedish individuals, who have the highest losartan metabolic ratio (MR; losartan:E-3174).	Losartan	150-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	9-15
25303293-2	2014	Thus, the influence of the CYP2C9 IVS8-109A&gt;T polymorphism on the losartan MR was evaluated among healthy Ecuadorians.	Losartan	69-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
25303293-7	2014	Further investigation needs to be carried out in order to clarify the relevance of the SNP of CYP2C9 IVS8-109A&gt;T on losartan hydroxylation across populations and its potential implications in CYP2C9 activity.	Losartan	119-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
25303293-7	2014	Further investigation needs to be carried out in order to clarify the relevance of the SNP of CYP2C9 IVS8-109A&gt;T on losartan hydroxylation across populations and its potential implications in CYP2C9 activity.	Losartan	119-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	195-201
25197954-0	2014	Inhibition of cytochrome P450 2C9 expression and activity in vitro by allyl isothiocyanate.	allyl isothiocyanate	70-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-33
25197954-4	2014	In this study, we found that allyl isothiocyanate reduced catalytic activity, messenger ribonucleic acid, and protein expression of cytochrome P450 2C9 in HepaRG cells.	allyl isothiocyanate	29-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-151
25197954-5	2014	An investigation of the transcriptional activity of the pregnane X receptor and the constitutive androstane receptor revealed that allyl isothiocyanate disrupted the transcriptional coregulation effects of the pregnane X receptor/constitutive androstane receptor with several important coregulators and interfered with the assembly of transcriptional complexes of the cytochrome P450 2C9 pregnane X receptor/constitutive androstane receptor-response element.	isothiocyanic acid	137-151	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	368-387
25197954-6	2014	The decrease of cytochrome P450 2C9 expression and activity mediated by allyl isothiocyanate suggested that this agent could alter the metabolism of drugs metabolized by cytochrome P450 2C9.	allyl isothiocyanate	72-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-35
25197954-6	2014	The decrease of cytochrome P450 2C9 expression and activity mediated by allyl isothiocyanate suggested that this agent could alter the metabolism of drugs metabolized by cytochrome P450 2C9.	allyl isothiocyanate	72-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	170-189
24821498-1	2014	On the basis of the photo-induced electron transfer (PET) from CdTe quantum dots (QDs) to cytochrome P450 2C9 (CYP2C9), a light-controlled drug metabolism system was successfully designed by using CYP2C9 functionalized-CdTe QDs as photocatalysts.	cadmium telluride	63-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-109
24821498-1	2014	On the basis of the photo-induced electron transfer (PET) from CdTe quantum dots (QDs) to cytochrome P450 2C9 (CYP2C9), a light-controlled drug metabolism system was successfully designed by using CYP2C9 functionalized-CdTe QDs as photocatalysts.	cadmium telluride	63-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
24821498-1	2014	On the basis of the photo-induced electron transfer (PET) from CdTe quantum dots (QDs) to cytochrome P450 2C9 (CYP2C9), a light-controlled drug metabolism system was successfully designed by using CYP2C9 functionalized-CdTe QDs as photocatalysts.	cadmium telluride	63-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
25117329-6	2014	We were able to correctly infer genotypes for the warfarin-related loci VKORC1 and CYP2C9 alleles 2, 3, 5, and 11 and also clopidogrel-related CYP2C19 alleles 2 and 17 for a small sample of Brazilian individuals, as well as for HapMap samples.	Warfarin	50-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
24821498-1	2014	On the basis of the photo-induced electron transfer (PET) from CdTe quantum dots (QDs) to cytochrome P450 2C9 (CYP2C9), a light-controlled drug metabolism system was successfully designed by using CYP2C9 functionalized-CdTe QDs as photocatalysts.	cadmium telluride	219-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-109
24821498-1	2014	On the basis of the photo-induced electron transfer (PET) from CdTe quantum dots (QDs) to cytochrome P450 2C9 (CYP2C9), a light-controlled drug metabolism system was successfully designed by using CYP2C9 functionalized-CdTe QDs as photocatalysts.	cadmium telluride	219-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
24821498-1	2014	On the basis of the photo-induced electron transfer (PET) from CdTe quantum dots (QDs) to cytochrome P450 2C9 (CYP2C9), a light-controlled drug metabolism system was successfully designed by using CYP2C9 functionalized-CdTe QDs as photocatalysts.	cadmium telluride	219-223	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
24794636-0	2014	Structural and energetic analysis to provide insight residues of CYP2C9, 2C11 and 2E1 involved in valproic acid dehydrogenation selectivity.	Valproic Acid	98-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
24794636-2	2014	In this study, both methods were combined to predict the regioselectivity in the binding mode of valproic acid (VPA) on three cytochrome P-450 (CYP) isoforms CYP2C9, CYP2C11, and CYP2E1, which are involved in the biotransformation of VPA yielding reactive hepatotoxic intermediate 2-n-propyl-4-pentenoic acid (4nVPA).	Valproic Acid	97-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
24794636-2	2014	In this study, both methods were combined to predict the regioselectivity in the binding mode of valproic acid (VPA) on three cytochrome P-450 (CYP) isoforms CYP2C9, CYP2C11, and CYP2E1, which are involved in the biotransformation of VPA yielding reactive hepatotoxic intermediate 2-n-propyl-4-pentenoic acid (4nVPA).	Valproic Acid	112-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
25221392-4	2014	We hypothesize that the polymorphisms in ABCB1, Cyp2C9, Cyp2C19 and methylene tetrahydrofolate reductase (MTHFR) might result in differential expression resulting in differential drug transport, drug metabolism and folate metabolism, which in turn may contribute to the teratogenic impact of AEDs.	Folic Acid	88-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
24839071-4	2014	In vitro, glyburide is metabolized (intrinsic clearance, 52.9 muL/min/mg-microsomal protein) by CYP3A4, CYP2C9, and CYP2C8 with fraction metabolism of 0.53, 0.36, and 0.11, respectively.	Glyburide	10-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	104-110
24760401-3	2014	The objective of this study was to evaluate the effect of IPE on the pharmacokinetic and anticoagulation pharmacodynamics of warfarin, a substrate of cytochrome P450 2C9-mediated metabolism.	eicosapentaenoic acid ethyl ester	58-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-169
24590592-9	2014	Since other sulfonylureas in clinical use are substrates of CYP2C9, their hepatic CLint changes have the potential to cause clinically relevant pharmacokinetic changes in a hyperlipidemic state.	Sulfonylurea Compounds	12-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
24942396-1	2014	Observational studies have overwhelmingly shown that variants in the genes CYP2C9 and VKORC1 are significant determinants of individual dose of coumarin anticoagulants needed to maintain a therapeutic international normalized ratio (INR).	coumarin	144-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
24760401-3	2014	The objective of this study was to evaluate the effect of IPE on the pharmacokinetic and anticoagulation pharmacodynamics of warfarin, a substrate of cytochrome P450 2C9-mediated metabolism.	Warfarin	125-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-169
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
25155935-0	2014	Genetic epidemiology of pharmacogenetic variations in CYP2C9, CYP4F2 and VKORC1 genes associated with warfarin dosage in the Indian population.	Warfarin	102-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
24757038-2	2014	Voriconazole, a second-generation triazole antifungal agent, is both a substrate and potent inhibitor of CYP isoenzymes, specifically CYP2C19, CYP2C9, and CYP3A4; thus, the potential for drug-drug interactions with voriconazole is high.	Voriconazole	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
24594507-5	2014	The hepatic cytochrome P450 (CYP) 2C protein expression level in the menthol administration group was significantly increased compared to that in the control group.	Menthol	69-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-36
25136521-0	2014	Association of cytochrome P450 2C9 polymorphism with locally advanced head and neck squamous cell carcinoma and response to concurrent cisplatin-based radical chemoradiation.	Cisplatin	135-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-34
25136521-1	2014	AIMS: The aim of the present study is to investigate the association between polymorphism of cytochrome P450 2C9 (CYP2C9) enzyme with head and neck squamous cell carcinoma (HNSCC) and response in patients receiving cisplatin-based radical chemoradiation (CT-RT).	Cisplatin	215-224	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-112
25136521-1	2014	AIMS: The aim of the present study is to investigate the association between polymorphism of cytochrome P450 2C9 (CYP2C9) enzyme with head and neck squamous cell carcinoma (HNSCC) and response in patients receiving cisplatin-based radical chemoradiation (CT-RT).	Cisplatin	215-224	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
25136521-5	2014	Tobacco intake in the form of chewing or smoking and alcohol intake resulted in several folds increase in the risk to HNSCC in the cases carrying variant genotypes of CYP2C9*2 or CYP2C9*013.	Alcohols	53-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	167-173
25136521-5	2014	Tobacco intake in the form of chewing or smoking and alcohol intake resulted in several folds increase in the risk to HNSCC in the cases carrying variant genotypes of CYP2C9*2 or CYP2C9*013.	Alcohols	53-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	179-185
25136521-6	2014	Further, majority of the cases assessed for response (n = 436) carrying variant alleles of CYP2C9*2 (69.6%) or CYP2C9*3 (65.2%) were found to respond poorly to cisplatin-based radical CT-RT.	Cisplatin	160-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
25136521-6	2014	Further, majority of the cases assessed for response (n = 436) carrying variant alleles of CYP2C9*2 (69.6%) or CYP2C9*3 (65.2%) were found to respond poorly to cisplatin-based radical CT-RT.	Cisplatin	160-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
24601977-2	2014	We performed a retrospective, cross-sectional study to examine the effect of variant CYP2C9 and VKORC1 genotypes on warfarin dose in 100 children.	Warfarin	116-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
24594507-7	2014	The addition of menthol to human hepatic cells, HepaRG cells, caused an increase in the mRNA expression level of CYP2C9.	Menthol	16-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
23800980-2	2014	CYP2C9 and VKORC1 are two major genetic factors associated with inter-individual and inter-ethnic variability in the warfarin dose.	Warfarin	117-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24842639-0	2014	CYP2C9, SLCO1B1, SLCO1B3, and ABCB11 polymorphisms in patients with bosentan-induced liver toxicity.	Bosentan	68-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24842639-4	2014	We conducted a nested case-control study to further explore the relationship between functional polymorphisms of gene products involved in bosentan pharmacokinetics (OATP1B1, OATP1B3, and CYP2C9) or hepatobiliary transporters affected by bosentan (ABCB11) and bosentan-induced liver toxicity.	Bosentan	139-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	188-194
23800980-3	2014	AIM: This study aims to assess the impact of VKORC1-1639G&gt;A polymorphism and the most common CYP2C9 variant alleles (*2 and *3) on warfarin response in Egyptian patients.	Warfarin	134-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
23800980-7	2014	RESULTS: Patients carrying VKORC1 and CYP2C9 variant genotypes needed a 44.8 % lower mean daily warfarin dose as compared to wild types.	Warfarin	96-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
23800980-10	2014	Multiple regression analysis showed that, VKORC1-1639G&gt;A, age, CYP2C9*3, and smoking status explained 43.4 % of the overall variability in the warfarin dose.	Warfarin	146-154	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
23800980-11	2014	CONCLUSION: VKORC1-1639G&gt;A and CYP2C9 polymorphisms contribute to the difference in warfarin dose requirements and quality of anticoagulation amongst Egyptian patients.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
24602049-2	2014	This study aimed to evaluate the effect of gene polymorphisms of CYP2C9, VKORC1, thrombomodulin (THBD) and C-reactive protein (CRP) on the risk of bleeding complications of warfarin at therapeutic INR in Korean patients with mechanical cardiac valves.	Warfarin	173-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
24612117-10	2014	WHAT IS NEW AND CONCLUSION: The patient required a high warfarin dose because of the VKORC1 genotype, and induction of CYP2C9 by carbamazepine.	Carbamazepine	129-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
24574079-9	2014	ANN analysis identified several predictors of warfarin dosage including race; age; height; weight; cytochrome P450 (CYP)2C9 genotype; VKORC1 genotype; sulfonamide, azole antifungals, or macrolide administration; carbamazepine, phenytoin, or rifampicin administration; and amiodarone administration.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	99-123
24474498-0	2014	VKORC1 and CYP2C9 genotypes are predictors of warfarin-related outcomes in children.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
24474498-9	2014	CYP2C9*3 carriers were also at increased risk of major bleeding while receiving warfarin (adjusted OR = 11.28).	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24474498-10	2014	An additional variant in CYP2C9 (rs7089580) was significantly associated with warfarin dose (P = 0.020) in a multivariate clinical and genetic model.	Warfarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
24474498-11	2014	CONCLUSIONS: This study confirms the importance of VKORC1/CYP2C9 genotypes for warfarin dosing in a young pediatric cohort and demonstrates an impact of genetic factors on clinical outcomes in children.	Warfarin	79-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
24474498-12	2014	Furthermore, we identified an additional variant in CYP2C9 of potential relevance for warfarin dosing in children.	Warfarin	86-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
24018621-1	2014	Using a derivation cohort (N=349), we developed the first warfarin dosing algorithm that includes recently discovered polymorphisms in VKORC1 and CYP2C9 associated with warfarin dose requirement in African Americans (AAs).	Warfarin	58-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
24018621-1	2014	Using a derivation cohort (N=349), we developed the first warfarin dosing algorithm that includes recently discovered polymorphisms in VKORC1 and CYP2C9 associated with warfarin dose requirement in African Americans (AAs).	Warfarin	169-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	146-152
24165757-12	2014	These results suggest that CYP2C9 has a role in the oxidation reactions of THT and indicate that it may be possible to predict the efficacy of Bu-based myeloablative conditioning before HSCT on the basis of CYP genotypes and Bu MRs.	tetrahydrothiophene	75-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
24165757-12	2014	These results suggest that CYP2C9 has a role in the oxidation reactions of THT and indicate that it may be possible to predict the efficacy of Bu-based myeloablative conditioning before HSCT on the basis of CYP genotypes and Bu MRs.	Busulfan	143-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
24974574-4	2014	Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19.	Simvastatin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
24974574-4	2014	Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19.	Simvastatin	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
24974574-4	2014	Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19.	Atorvastatin	13-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
24974574-4	2014	Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19.	Atorvastatin	13-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
24974574-4	2014	Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19.	Lovastatin	30-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
24974574-4	2014	Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19.	Lovastatin	30-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
24974574-4	2014	Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19.	Fluvastatin	68-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
24974574-4	2014	Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19.	Rosuvastatin Calcium	97-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
24928022-6	2014	RESULTS: VKORC1 and CYP2C9 gene polymorphisms could explain more than 50% Warfarin maintenance dose variation in recruited patients, while CYP4F2 gene polymorphisms could only explain 1%.	Warfarin	74-82	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
24928022-8	2014	VKORC1 and CYP2C9 gene polymorphisms have a greater impact on Warfarin maintenance dose compared with demographic characteristics and concomitant medications.	Warfarin	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
24928022-9	2014	CONCLUSION: VKORC1 and CYP2C9 gene polymorphisms have a significant impact on Warfarin maintenance dose in Chinese Han population.	Warfarin	78-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
24956244-0	2014	Warfarin dose requirements in a patient with the CYP2C9*14 allele.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
24799042-4	2014	The device enables users to manipulate the expression of individual and multiple human metabolizing-enzyme genes (such as CYP3A4, CYP2D6, CYP2C9, CYP1A2, CYP2E1 and UGT1A4) in THLE-2 cell microarrays.	thle	176-180	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
24802986-3	2014	In this study, the in vitro inhibitory effects of scutellarin on six major human CYPs (CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6, and CYP3A4) and six rat CYPs (CYP1A2, CYP2C7, CYP2C11, CYP2C79, CYP2D4, and CYP3A2) activities were examined by using liquid chromatography-tandem mass spectrometry.	scutellarin	50-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
24550229-0	2014	1-Aminobenzotriazole coincubated with (S)-warfarin results in potent inactivation of CYP2C9.	1-aminobenzotriazole	0-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
24550229-0	2014	1-Aminobenzotriazole coincubated with (S)-warfarin results in potent inactivation of CYP2C9.	Warfarin	38-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
24550229-3	2014	Here we propose that ABT preferentially binds to the warfarin-binding pocket in the CYP2C9 active-site cavity; thus, ABT bioactivation and subsequent inactivation is not favored.	1-aminobenzotriazole	21-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
24550229-3	2014	Here we propose that ABT preferentially binds to the warfarin-binding pocket in the CYP2C9 active-site cavity; thus, ABT bioactivation and subsequent inactivation is not favored.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
24550229-4	2014	Therefore, coincubation with (S)-warfarin would result in displacement of ABT from the warfarin-binding pocket and subsequent binding to the active site, converting ABT into a potent inactivator of CYP2C9.	Warfarin	29-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	198-204
24550229-4	2014	Therefore, coincubation with (S)-warfarin would result in displacement of ABT from the warfarin-binding pocket and subsequent binding to the active site, converting ABT into a potent inactivator of CYP2C9.	1-aminobenzotriazole	74-77	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	198-204
24550229-4	2014	Therefore, coincubation with (S)-warfarin would result in displacement of ABT from the warfarin-binding pocket and subsequent binding to the active site, converting ABT into a potent inactivator of CYP2C9.	Warfarin	33-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	198-204
24550229-4	2014	Therefore, coincubation with (S)-warfarin would result in displacement of ABT from the warfarin-binding pocket and subsequent binding to the active site, converting ABT into a potent inactivator of CYP2C9.	1-aminobenzotriazole	165-168	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	198-204
24550229-5	2014	To test this hypothesis, in vitro studies were conducted using various coincubation combinations of ABT and (S)-warfarin or diclofenac to modulate the effectiveness of CYP2C9 inactivation by ABT.	1-aminobenzotriazole	100-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
24550229-5	2014	To test this hypothesis, in vitro studies were conducted using various coincubation combinations of ABT and (S)-warfarin or diclofenac to modulate the effectiveness of CYP2C9 inactivation by ABT.	Warfarin	108-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
24550229-5	2014	To test this hypothesis, in vitro studies were conducted using various coincubation combinations of ABT and (S)-warfarin or diclofenac to modulate the effectiveness of CYP2C9 inactivation by ABT.	Diclofenac	124-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
24550229-5	2014	To test this hypothesis, in vitro studies were conducted using various coincubation combinations of ABT and (S)-warfarin or diclofenac to modulate the effectiveness of CYP2C9 inactivation by ABT.	1-aminobenzotriazole	191-194	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
24550229-7	2014	The kinetic parameters of time-dependent inhibition of ABT for CYP2C9 in the absence and presence of (S)-warfarin (20 muM) were 0.0826 and 0.273 min(-1) for kinact and 3.49 and 0.157 mM for KI, respectively.	1-aminobenzotriazole	55-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
24550229-7	2014	The kinetic parameters of time-dependent inhibition of ABT for CYP2C9 in the absence and presence of (S)-warfarin (20 muM) were 0.0826 and 0.273 min(-1) for kinact and 3.49 and 0.157 mM for KI, respectively.	Warfarin	101-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
24956244-6	2014	This report adds to the limited data of the effects of the CYP2C9*14 allele on warfarin dose requirements.	Warfarin	79-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
24530212-0	2014	Influence of CYP2C9 polymorphism and phenytoin co-administration on acenocoumarol dose in patients with cerebral venous thrombosis.	Acenocoumarol	68-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
24530212-6	2014	During the initiation phase of anticoagulation the CYP2C9*2 allele was independently associated with low acenocoumarol dose requirement (Adjusted OR 5.38; 95%CI 1.65-17.49; p=0.005).	Acenocoumarol	105-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
24530212-12	2014	CONCLUSION: This study emphasizes the fact that polymorphisms in CYP2C9 gene and co-medication with phenytoin alter the anticoagulant effect of acenocoumarol.	Phenytoin	100-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
24530212-12	2014	CONCLUSION: This study emphasizes the fact that polymorphisms in CYP2C9 gene and co-medication with phenytoin alter the anticoagulant effect of acenocoumarol.	Acenocoumarol	144-157	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
24165884-7	2014	These data suggest that etravirine is a weak CYP3A isozyme inducer and minimally inhibits CYP2C9, 2C19, and P-glycoprotein activity.	etravirine	24-34	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	90-96
25042915-9	2014	CONCLUSION: Our algorithm based on VKORC1, CYP2C9 and CYP4F2 polymorphisms can help to predict the warfarin maintenance dose in Chinese Han Population.	Warfarin	99-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
24966969-1	2014	Single nucleotide polymorphisms (SNPs) of VKORC (1173T/C, rs9934438) and CYP2C9 (1075A/C, rs1057910) are major contributory factors on the sensitivity of warfarin in Chinese.	Warfarin	154-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	73-79
24118918-0	2014	In vitro assessment of 36 CYP2C9 allelic isoforms found in the Chinese population on the metabolism of glimepiride.	glimepiride	103-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
24118918-9	2014	This study provided the most comprehensive data on the enzymatic activities of all reported CYP2C9 variants in the Chinese population with regard to the commonly used antidiabetic drug, glimepiride.	glimepiride	186-197	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
24118918-10	2014	Our results indicate that most of the tested rare alleles significantly decrease the catalytic activity of CYP2C9 variants towards glimepiride hydroxylation in vitro.	glimepiride	131-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	107-113
24224579-3	2014	Phenprocoumon metabolism is mediated by CYP2C9 and CYP3A enzymes.	Phenprocoumon	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
24519941-5	2014	Sulfaphenazole (SFZ), a selective inhibitor of human cytochrome P450 (CYP) 2C9 isozyme, was identified as a novel and leading cytoprotective compound.	Sulfaphenazole	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-78
24337438-9	2014	In conclusion, in addition to body-weight and amiodarone-intake, pharmacogenetic factors (VKORC1, CYP4F2, ABCB1) related to the pharmacodynamic effect and transport of fluindione significantly influenced the dose requirement in elderly patients while CYP2C9 did not.	fluindione	168-178	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	251-257
24337438-10	2014	Studies are required to know whether fluindione could be an alternative VKA in carriers of polymorphic CYP2C9 alleles, hypersensitive to coumarins.	fluindione	37-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
24337438-10	2014	Studies are required to know whether fluindione could be an alternative VKA in carriers of polymorphic CYP2C9 alleles, hypersensitive to coumarins.	Coumarins	137-146	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
24723938-1	2014	CYP2C8 and CYP2C9 are involved in the inactivation of several non-steroidal anti-inflammatory drugs, including ibuprofen.	Ibuprofen	111-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
24519941-5	2014	Sulfaphenazole (SFZ), a selective inhibitor of human cytochrome P450 (CYP) 2C9 isozyme, was identified as a novel and leading cytoprotective compound.	Sulfaphenazole	16-19	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-78
24342125-4	2014	Isoxanthohumol from hops was the most potent inhibitor of CYP2C8 with an IC50 of 0.2 muM, whereas 8-prenylnaringenin was the most potent inhibitor of CYP1A2, CYP2C9 and CYP2C19 with IC50 values of 1.1 muM, 1.1 muM and 0.4 muM, respectively.	8-prenylnaringenin	98-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
24593903-1	2014	BACKGROUND: Two variants in the gene encoding the cytochrome P450 2C9 enzyme (CYP2C9) are considered the most significant genetic risk factors associated with bleeding after warfarin prescription.	Warfarin	174-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-69
24593903-0	2014	Genetic polymorphisms in warfarin and tacrolimus-related genes VKORC1, CYP2C9 and CYP3A5 in the Greek-Cypriot population.	Warfarin	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
24593903-0	2014	Genetic polymorphisms in warfarin and tacrolimus-related genes VKORC1, CYP2C9 and CYP3A5 in the Greek-Cypriot population.	Tacrolimus	38-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
24594849-2	2014	Isozyme CYP2C9 is reported to be inhibited by benzbromarone (BzBr) and this phenomenon was hitherto explained by classical active-site binding.	Benzbromarone	46-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
24594849-2	2014	Isozyme CYP2C9 is reported to be inhibited by benzbromarone (BzBr) and this phenomenon was hitherto explained by classical active-site binding.	Benzbromarone	61-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
24594849-5	2014	In silico docking of various BzBr analogs with known crystal structure of CYP2C9 did not provide any evidence in support of active-site based inhibition hypothesis.	Benzbromarone	29-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
24594849-10	2014	Further, amphipathic derivatives of vitamins C &amp; E (scavengers of diffusible reactive oxygen species or DROS) effectively inhibited CYP2C9 reactions in different reaction setups.	vitamins c &amp	36-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
24594849-10	2014	Further, amphipathic derivatives of vitamins C &amp; E (scavengers of diffusible reactive oxygen species or DROS) effectively inhibited CYP2C9 reactions in different reaction setups.	Reactive Oxygen Species	81-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
24594849-10	2014	Further, amphipathic derivatives of vitamins C &amp; E (scavengers of diffusible reactive oxygen species or DROS) effectively inhibited CYP2C9 reactions in different reaction setups.	dros	108-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
24357089-6	2014	The PG/PK study of indapamide demonstrated that the polymorphic SNPs CYP2C9 rs4918758 and CYP2C19 rs4244285 appeared to confer lowered enzyme activity, as indicated by increased C max (25% ~ 64%), increased area under the plasma level-time curves (30~76%), increased area under the time infinity (43% ~ 80%), and lower apparent clearance values than PK for wild-type indapamide.	Indapamide	19-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
24357089-6	2014	The PG/PK study of indapamide demonstrated that the polymorphic SNPs CYP2C9 rs4918758 and CYP2C19 rs4244285 appeared to confer lowered enzyme activity, as indicated by increased C max (25% ~ 64%), increased area under the plasma level-time curves (30~76%), increased area under the time infinity (43% ~ 80%), and lower apparent clearance values than PK for wild-type indapamide.	Indapamide	367-377	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
24357089-7	2014	Our results reinforce the biochemical support of CYP2C19 in indapamide metabolism and identify a possible new participating enzyme CYP2C9.	Indapamide	60-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	131-137
24593903-1	2014	BACKGROUND: Two variants in the gene encoding the cytochrome P450 2C9 enzyme (CYP2C9) are considered the most significant genetic risk factors associated with bleeding after warfarin prescription.	Warfarin	174-182	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
24387348-5	2014	Current evidence suggests that garlic and ginkgo can be safely co-administered, whereas CYP2C9 substrates (e.g., warfarin) should be monitored closely when ginseng therapy is started.	Warfarin	113-121	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
24464553-0	2014	Characterizing the effect of cytochrome P450 (CYP) 2C8, CYP2C9, and CYP2D6 genetic polymorphisms on stereoselective N-demethylation of fluoxetine.	Fluoxetine	135-145	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
24464553-6	2014	Five CYP2C9 variants and CYP2D6.1 exhibited significantly stereoselective kinetic profiles prior to R-FLX, and CYP2C8.3 showed a slight stereoselectivity.	r-flx	100-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	5-11
24464553-8	2014	Together, these findings suggest that CYP2C9 and CYP2D6 polymorphism may play an important role in the clearance of FLX and also in the stereoselective kinetic profiles of FLX enantiomers.	Fluoxetine	116-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
24322971-4	2014	Nevertheless, VKORC1, CYP2C9, and CYP4F2 variants have been associated with warfarin dose requirements, and CYP2C19 variants have been associated with perturbed antiplatelet response to clopidogrel.	Warfarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	22-28
24660123-1	2014	Warfarin is the most common anticoagulant prescribed and its metabolism has been linked to two specific genes, CYP2C9 and VKORC1.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
24368832-2	2014	Levonorgestrel, a commonly employed progestin component of combined oral contraceptives, was implicated in drug-drug interactions mediated via CYP2C9.	Levonorgestrel	0-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
24368832-4	2014	In the current study, we examined the phenotypic status of CYP2C9 using low-dose (125 mg) tolbutamide before and after oral contraceptive use in reproductive age women.	Tolbutamide	90-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
24368832-6	2014	The natural logarithm of tolbutamide C24, a metric for CYP2C9 phenotype, was found to be equivalent (within 80%-125% equivalency boundaries) before and after oral contraceptive use.	Tolbutamide	25-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
23932726-0	2014	Frequency of CYP2C9 polymorphisms in Polynesian people and potential relevance to management of gout with benzbromarone.	Benzbromarone	106-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
23932726-2	2014	The uricosuric drug benzbromarone is an alternative treatment but CYP2C9 poor metabolisers (PMs) may be at a heightened risk of benzbromarone-induced hepatotoxicity.	pms	92-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
23932726-2	2014	The uricosuric drug benzbromarone is an alternative treatment but CYP2C9 poor metabolisers (PMs) may be at a heightened risk of benzbromarone-induced hepatotoxicity.	Benzbromarone	128-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
23932726-10	2014	CONCLUSION: Prospective CYP2C9 genotyping of Caucasian gout patients may be warranted for benzbromarone, whereas the low frequencies of CYP2C9 PM alleles in Polynesians suggests that the CYP2C9 polymorphism may be of little or no relevance to benzbromarone prescribing in this population.	Benzbromarone	90-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
24360850-1	2014	BACKGROUND: Genetic polymorphisms in the CYP2C9 and VKORC1 genes have been linked to sensitivity of the anticoagulant drug warfarin.	Warfarin	123-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
23844998-0	2014	Effect of 36 CYP2C9 variants found in the Chinese population on losartan metabolism in vitro.	Losartan	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
23844998-4	2014	The aim of this study was to assess the catalytic activities of 36 CYP2C9 variants found in the Chinese population toward losartan in vitro.	Losartan	122-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
23844998-6	2014	Insect microsomes expressing the 36 CYP2C9 variants were incubated with 0.5-25 muM losartan for 30 min at 37  C. Next, the products were extracted, and signal detection was performed using high-performance liquid chromatography.	Losartan	83-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
23844998-11	2014	These findings suggest that more attention should be paid to subjects carrying these infrequent CYP2C9 alleles when administering losartan in the clinic.	Losartan	130-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
24615047-0	2014	Effect of CYP2C9*3 mutant variants on meloxicam pharmacokinetics in a healthy Chinese population.	Meloxicam	38-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
24615047-1	2014	The aim of this study was to investigate the effect of the CYP2C9*3 (CYP2C9 1075 A&gt;C) polymorphism on meloxicam pharmacokinetics in a Chinese population.	Meloxicam	105-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	59-65
24615047-1	2014	The aim of this study was to investigate the effect of the CYP2C9*3 (CYP2C9 1075 A&gt;C) polymorphism on meloxicam pharmacokinetics in a Chinese population.	Meloxicam	105-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
24615047-8	2014	CYP2C9*3 was found to play an important role in the metabolism of meloxicam by reducing its enzymatic activity.	Meloxicam	66-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24498291-6	2014	The calculated binding equilibrium of APAP within the compact active site of CYP2A6 is able to predict the experimentally documented product ratios and is also applied to explain APAP regioselectivity in CYP1A2 and CYP2C9.	Acetaminophen	38-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	215-221
24166101-3	2014	Here, we describe a bioreactor that is made by immobilizing cytochrome P450 2C9 (CYP2C9) to a poly(methyl methacrylate) surface and, as an alternative to traditional chemical synthesis, can be used to biosynthesize P450 metabolites in a plug flow bioreactor.	Polymethyl Methacrylate	94-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-79
24498291-4	2014	In CYP2C9 and CYP3A4, weak interactions in an overall large active site cavity result in a fairly small binding free energy difference between APAP reactive binding states, consistent with experimental results that show little preference for resulting metabolites.	Acetaminophen	143-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	3-9
24166101-3	2014	Here, we describe a bioreactor that is made by immobilizing cytochrome P450 2C9 (CYP2C9) to a poly(methyl methacrylate) surface and, as an alternative to traditional chemical synthesis, can be used to biosynthesize P450 metabolites in a plug flow bioreactor.	Polymethyl Methacrylate	94-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
24753822-2	2014	In the present study, the inhibitory effects of polyozellin and thelephoric acid on 9 cytochrome P450 (CYP) family members (CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4) were examined in pooled human liver microsomes (HLMs) using a cocktail probe assay.	polyozellin	48-59	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
24166101-6	2014	Our results show that the immobilization of CYP2C9 enzymes to a PMMA surface represents a viable and alternative approach to the preparation of CYP2C9 metabolites for toxicity testing.	Polymethyl Methacrylate	64-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
24166101-6	2014	Our results show that the immobilization of CYP2C9 enzymes to a PMMA surface represents a viable and alternative approach to the preparation of CYP2C9 metabolites for toxicity testing.	Polymethyl Methacrylate	64-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
24186263-10	2014	RESULTS: In vitro AZD2066 inhibited CYP1A2, CYP2B6, CYP2C9, CYP2C19 and CYP2D6.	AZD2066	18-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
24160757-5	2014	Clinical pharmacogenetic data further support CYP2C9 as a significant contributor to THC metabolism, and a pharmacokinetic interaction study using ketoconazole with oromucosal cannabis extract further supports CYP3A4 as a significant metabolic pathway for THC and CBD.	Dronabinol	85-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
24322170-0	2014	Strongly increased exposure of meloxicam in CYP2C9*3/*3 individuals.	Meloxicam	31-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
24287930-0	2014	Variability of warfarin dose response associated with CYP2C9 and VKORC1 gene polymorphisms in Chinese patients.	Warfarin	15-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
24038489-8	2014	The CYP2C9 pathway (4-hydroxyflurbiprofen formation clearance) was similar in all the patients with CKD and was concordant with previous reports of patients with end-stage renal disease (ESRD) and healthy controls.	4'-hydroxyflurbiprofen	20-41	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
24322170-4	2014	RESULTS: A nine-fold lower apparent oral clearance and an eight-fold higher AUC0-  of single-dose meloxicam were observed in CYP2C9*3/*3 individuals when compared with CYP2C9*1/*1 individuals.	Meloxicam	98-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
24322170-5	2014	CYP2C9*3/*3 individuals also showed markedly increased inhibition of thromboxane B2 generation by meloxicam.	Thromboxane B2	69-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24322170-5	2014	CYP2C9*3/*3 individuals also showed markedly increased inhibition of thromboxane B2 generation by meloxicam.	Meloxicam	98-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24533715-1	2014	Clinical factors, demographic variables and variations in two genes, CYP2C9 and VKORC1, have been shown to contribute to the variability in warfarin dose requirements among adult patients.	Warfarin	140-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
24322170-6	2014	CONCLUSION: These results indicate that CYP2C9*3/*3 individuals may be at a higher risk for concentration-dependent adverse effects during long-term treatment with standard doses of meloxicam.	Meloxicam	182-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
24302581-3	2014	In this study, we show that targeting the formation of proangiogenic epoxyeicosatrienoic acids (EET) by the cytochrome P450 arachidonic acid epoxygenases (Cyp2c) represents a new and safe mechanism to treat NSCLC growth and progression.	epoxyeicosatrienoic acids	69-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-160
24387788-0	2014	Effects of anthocyanidins and anthocyanins on the expression and catalytic activities of CYP2A6, CYP2B6, CYP2C9, and CYP3A4 in primary human hepatocytes and human liver microsomes.	Anthocyanins	11-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
24387788-0	2014	Effects of anthocyanidins and anthocyanins on the expression and catalytic activities of CYP2A6, CYP2B6, CYP2C9, and CYP3A4 in primary human hepatocytes and human liver microsomes.	Anthocyanins	30-42	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
24387788-3	2014	The current study evaluated the effects of anthocyanidins and anthocyanins on the expression and catalytic activity of major drug-metabolizing enzymes CYP2C9, CYP2A6, CYP2B6, and CYP3A4 in primary cultures of human hepatocytes and human liver microsomes.	Anthocyanins	43-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	151-157
24387788-3	2014	The current study evaluated the effects of anthocyanidins and anthocyanins on the expression and catalytic activity of major drug-metabolizing enzymes CYP2C9, CYP2A6, CYP2B6, and CYP3A4 in primary cultures of human hepatocytes and human liver microsomes.	Anthocyanins	62-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	151-157
24387788-8	2014	Catalytic activities of CYP2C9, CYP2A6, CYP2B6, and CYP3A4 enzymes were inhibited by all anthocyanidins to different extents (e.g., delphinidin inhibits CYP3A4 by &gt;90% at 100 muM with IC50 = 32 muM).	Anthocyanins	89-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
24387788-8	2014	Catalytic activities of CYP2C9, CYP2A6, CYP2B6, and CYP3A4 enzymes were inhibited by all anthocyanidins to different extents (e.g., delphinidin inhibits CYP3A4 by &gt;90% at 100 muM with IC50 = 32 muM).	delphinidin	132-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
24302581-3	2014	In this study, we show that targeting the formation of proangiogenic epoxyeicosatrienoic acids (EET) by the cytochrome P450 arachidonic acid epoxygenases (Cyp2c) represents a new and safe mechanism to treat NSCLC growth and progression.	EET	96-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	155-160
24636047-7	2014	One of the main factors affecting the efficacy of Clopidogrel is the phenotype associated with polymorphisms in the gene CYP 2C9.	Clopidogrel	50-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-128
26161443-0	2014	A chiral HPLC-MS/MS method for simultaneous quantification of warfarin enantiomers and its major hydroxylation metabolites of CYP2C9 and CYP3A4 in human plasma.	Warfarin	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	126-132
26161443-2	2014	Enantiomeric separation and quantification of warfarin enantiomers and clinically important major hydroxylation metabolites are essential for drug interaction studies and phenotypic characterization of CYP2C9 and CYP3A4, the major cytochrome P450 (CYP) enzymes involved in warfarin metabolism.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	202-208
26161443-3	2014	Here, we describe the development and validation of a chiral high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS)-based quantification of R-warfarin, S-warfarin, S-7-hydroxywarfarin (the major CYP2C9 metabolite) and (9R;10S)-10-hydroxywarfarin (the CYP3A4 metabolite) in human plasma.	7-hydroxywarfarin	186-205	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	217-223
25318916-0	2014	Frequencies of polymorphisms in CYP2C9 and VKORC1 genes influencing warfarin metabolism in Slovak population: implication for clinical practice.	Warfarin	68-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
24423593-2	2014	P-gp (fexofenadine) and CYP-specific substrates (caffeine for CYP1A2, bupropion for CYP2B6, flurbiprofen for CYP2C9, omeprazole for CYP2C19, dextromethorphan for CYP2D6 and midazolam for CYP3A4) and their metabolites were extracted from DBS (10 microl) using methanol.	Flurbiprofen	92-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	109-115
25318916-1	2014	OBJECTIVES: The study was aimed at establishing an effective molecular-genetic method for detecting polymorphisms in genes CYP2C9 and VKORC1, which affect the pharmacogenetics of warfarin, and at determining their prevalence in Slovak population.	Warfarin	179-187	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	123-129
25318916-4	2014	It was proven that genetic variability in two genes, CYP2C9 a VKORC1, has a significant influence on the individual"s response to the dosage of warfarin.	Warfarin	144-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
25318916-6	2014	RESULTS: Due to the combination of frequent alleles CYP2C9*2, CYP2C9*3 and VKORC1*2 in Slovak population we determine that 25% of population need a standard 5-mg daily dose of warfarin, while 44%, 23%, and 8% need 4 mg, 3 mg and 2 mg of warfarin per day.	Warfarin	176-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
25318916-6	2014	RESULTS: Due to the combination of frequent alleles CYP2C9*2, CYP2C9*3 and VKORC1*2 in Slovak population we determine that 25% of population need a standard 5-mg daily dose of warfarin, while 44%, 23%, and 8% need 4 mg, 3 mg and 2 mg of warfarin per day.	Warfarin	176-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
24479689-6	2014	Moreover, an integrated in silico approach for the prediction of Phase I metabolism of the flavonoids quercetin, rutin, naringenin and naringin, which provided useful information about the most likely metabolites of these flavonoids and their interactions with amino acid residues of CYP2C9, is described.	Flavonoids	91-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	284-290
24627811-0	2014	Warfarin Dosing in a Patient with CYP2C9(*)3(*)3 and VKORC1-1639 AA Genotypes.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
24627811-1	2014	Genetic factors most correlated with warfarin dose requirements are variations in the genes encoding the enzymes cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKOR).	Warfarin	37-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-132
24627811-1	2014	Genetic factors most correlated with warfarin dose requirements are variations in the genes encoding the enzymes cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKOR).	Warfarin	37-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
24627811-2	2014	Patients receiving warfarin who possess one or more genetic variations in CYP2C9 and VKORC1 are at increased risk of adverse drug events and require significant dose reductions to achieve a therapeutic international normalized ratio (INR).	Warfarin	19-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
24492587-4	2014	The amino acids in these positions have opposite charges in CYP2C9 and 2C19; the former has lysines in both positions (Lys72 and Lys241), and the latter has glutamic acids (Glu72 and Glu241).	Lysine	92-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
24479689-6	2014	Moreover, an integrated in silico approach for the prediction of Phase I metabolism of the flavonoids quercetin, rutin, naringenin and naringin, which provided useful information about the most likely metabolites of these flavonoids and their interactions with amino acid residues of CYP2C9, is described.	Quercetin	102-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	284-290
24479689-6	2014	Moreover, an integrated in silico approach for the prediction of Phase I metabolism of the flavonoids quercetin, rutin, naringenin and naringin, which provided useful information about the most likely metabolites of these flavonoids and their interactions with amino acid residues of CYP2C9, is described.	Rutin	113-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	284-290
24479689-6	2014	Moreover, an integrated in silico approach for the prediction of Phase I metabolism of the flavonoids quercetin, rutin, naringenin and naringin, which provided useful information about the most likely metabolites of these flavonoids and their interactions with amino acid residues of CYP2C9, is described.	naringenin	120-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	284-290
25109798-3	2014	Extensive evidence suggests that common genetic variants in CYP2C9 and VKORC1 genes together with a number of clinical factors are important determinants of the coumarin dose variability.	coumarin	161-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
24479689-6	2014	Moreover, an integrated in silico approach for the prediction of Phase I metabolism of the flavonoids quercetin, rutin, naringenin and naringin, which provided useful information about the most likely metabolites of these flavonoids and their interactions with amino acid residues of CYP2C9, is described.	naringin	135-143	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	284-290
24479689-6	2014	Moreover, an integrated in silico approach for the prediction of Phase I metabolism of the flavonoids quercetin, rutin, naringenin and naringin, which provided useful information about the most likely metabolites of these flavonoids and their interactions with amino acid residues of CYP2C9, is described.	Flavonoids	222-232	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	284-290
24695277-3	2014	Sequential metabolic reactions by Phase I and then Phase II enzymes were found in diclofenac [CYP2C9 and UDP-glucuronyltransferases (UGTs)], midazolam (CYP3A4 and UGTs) and propranolol (CYP1A2/2D6 and UGTs).	Diclofenac	82-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
25429674-5	2014	In in vivo pharmacokinetic studies, itraconazole was found to be a potent clinically important inhibitor of CYP3A4/5 substrates, and fluconazole and voriconazole increased the blood/plasma concentrations of not only CYP3A4/5 substrates but also CYP2C9 substrates.	Itraconazole	36-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	245-251
25429674-5	2014	In in vivo pharmacokinetic studies, itraconazole was found to be a potent clinically important inhibitor of CYP3A4/5 substrates, and fluconazole and voriconazole increased the blood/plasma concentrations of not only CYP3A4/5 substrates but also CYP2C9 substrates.	Fluconazole	133-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	245-251
25429674-5	2014	In in vivo pharmacokinetic studies, itraconazole was found to be a potent clinically important inhibitor of CYP3A4/5 substrates, and fluconazole and voriconazole increased the blood/plasma concentrations of not only CYP3A4/5 substrates but also CYP2C9 substrates.	Voriconazole	149-161	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	245-251
25429674-6	2014	Miconazole was a potent inhibitor of all P450s investigated in vitro, although there are few detailed studies on the clinical significance of this except for CYP2C9.	Miconazole	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
24695277-3	2014	Sequential metabolic reactions by Phase I and then Phase II enzymes were found in diclofenac [CYP2C9 and UDP-glucuronyltransferases (UGTs)], midazolam (CYP3A4 and UGTs) and propranolol (CYP1A2/2D6 and UGTs).	Propranolol	173-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
24825094-1	2014	CYP2C9 metabolizes approximately 20% of clinically used drugs, including the narrow therapeutic window drugs warfarin and phenytoin.	Warfarin	109-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24825094-1	2014	CYP2C9 metabolizes approximately 20% of clinically used drugs, including the narrow therapeutic window drugs warfarin and phenytoin.	Phenytoin	122-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24019055-8	2014	CONCLUSION: Genetic polymorphisms of CYP2C9, VKORC1, CYP4F2 and GGCX are important predictive factors of warfarin maintenance dose, and the developed algorithm will be useful to predict the required maintenance and/or starting warfarin dose in South Indian populations.	Warfarin	105-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
24019055-0	2014	Effect of CYP2C9, VKORC1, CYP4F2 and GGCX genetic variants on warfarin maintenance dose and explicating a new pharmacogenetic algorithm in South Indian population.	Warfarin	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
24019055-5	2014	Patients with the CYP2C9*1/*2, *1/*3 and *2/*3 variant genotypes required a 51.0 (2.8 mg), 60.9 (2.3 mg) and 62.2 % (2.2 mg) lower daily maintenance dose of warfarin, respectively, than those patients with the CYP2C9*1/*1 wild-type genotype (5.2 mg) (p&lt;0.0001).	Warfarin	157-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
24019055-8	2014	CONCLUSION: Genetic polymorphisms of CYP2C9, VKORC1, CYP4F2 and GGCX are important predictive factors of warfarin maintenance dose, and the developed algorithm will be useful to predict the required maintenance and/or starting warfarin dose in South Indian populations.	Warfarin	227-235	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
24019055-6	2014	The genetic variants of CYP2C9, VKORC1 and GGCX were associated with decreased warfarin dose, except for rs7196161, rs7294 and rs2108622 which were associated with an increased warfarin dose.	Warfarin	79-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
24899908-1	2014	Cytochrome P450 2C9 (CYP2C9) metabolizes dehydroepiandrosterone-sulfate (DHEA-S), but in elderly people the amount of DHEA-S remaining after CYP2C9 metabolization may be insufficient for optimal health.	Dehydroepiandrosterone Sulfate	41-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
24899908-1	2014	Cytochrome P450 2C9 (CYP2C9) metabolizes dehydroepiandrosterone-sulfate (DHEA-S), but in elderly people the amount of DHEA-S remaining after CYP2C9 metabolization may be insufficient for optimal health.	Dehydroepiandrosterone Sulfate	41-71	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
24899908-4	2014	The interaction between 4-methoxymagndialdehyde and CYP2C9 is more intense than with other TCM compounds, but the simulation is longer.	4'-methoxymagndialdehyde	24-47	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
25061471-11	2014	Fisetin showed potent inhibitory effects on CYP2C9, CYP2C19, and CYP1A2.	fisetin	0-7	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
24464600-0	2014	CYP2C9*2 allele increases risk for hypoglycemia in POR*1/*1 type 2 diabetic patients treated with sulfonylureas.	Sulfonylurea Compounds	98-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24464600-10	2014	Therefore, POR*28 allele is an important source of CYP2C9 activity variability and combined with CYP2C9 gene poly-morphisms may explain individual variability in the effect of sulfonylureas.	Sulfonylurea Compounds	176-189	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
24799741-0	2014	Investigating the Role of Plasma Glucose Concentration as a Phenotypic Marker for CYP2C9 Genetic Variants, in the Diabetic Population of Gujarat.	Glucose	33-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
24799741-7	2014	Patients with CYP2C9*1/*3 genotype showed greater mean glucose drop per milligram of drug values than patients with CYP2C9*1/*1 wild-type genotype for both glipizide and glimepiride while patients with CYP2C9*2/*3 genotype showed greater drop than patients with CYP2C9*1/*1 genotype only in the glipizide-treatment group.	Glucose	55-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
24799741-7	2014	Patients with CYP2C9*1/*3 genotype showed greater mean glucose drop per milligram of drug values than patients with CYP2C9*1/*1 wild-type genotype for both glipizide and glimepiride while patients with CYP2C9*2/*3 genotype showed greater drop than patients with CYP2C9*1/*1 genotype only in the glipizide-treatment group.	Glipizide	156-165	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
24799741-7	2014	Patients with CYP2C9*1/*3 genotype showed greater mean glucose drop per milligram of drug values than patients with CYP2C9*1/*1 wild-type genotype for both glipizide and glimepiride while patients with CYP2C9*2/*3 genotype showed greater drop than patients with CYP2C9*1/*1 genotype only in the glipizide-treatment group.	glimepiride	170-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
24799741-7	2014	Patients with CYP2C9*1/*3 genotype showed greater mean glucose drop per milligram of drug values than patients with CYP2C9*1/*1 wild-type genotype for both glipizide and glimepiride while patients with CYP2C9*2/*3 genotype showed greater drop than patients with CYP2C9*1/*1 genotype only in the glipizide-treatment group.	Glipizide	295-304	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
24799741-8	2014	The presence of CYP2C9*3 allele significantly affected plasma glucose drop per milligram of drug values in patients taking glipizide and glimepiride, while effects of CYP2C9*2 allele were insignificant.	Glucose	62-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
24799741-8	2014	The presence of CYP2C9*3 allele significantly affected plasma glucose drop per milligram of drug values in patients taking glipizide and glimepiride, while effects of CYP2C9*2 allele were insignificant.	Glipizide	123-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
24799741-8	2014	The presence of CYP2C9*3 allele significantly affected plasma glucose drop per milligram of drug values in patients taking glipizide and glimepiride, while effects of CYP2C9*2 allele were insignificant.	glimepiride	137-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
24799741-9	2014	Further studies are needed to confirm the effects of CYP2C9*2 allele on plasma glucose drop per milligram of drug values.	Glucose	79-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
25075423-0	2014	Characterization of a novel CYP2C9 mutation (1009C&gt;A) detected in a warfarin-sensitive patient.	Warfarin	71-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	28-34
25075423-2	2014	Recent studies have shown that polymorphic alleles within the CYP2C9, VKORC1, and CYP4F2 genes are related to the warfarin dosage requirement.	Warfarin	114-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
25075423-3	2014	In this study, a novel non-synonymous mutation (1009C&gt;A) in CYP2C9 was detected in a warfarin-hypersensitive patient, while the other two candidate genes were both found to be homozygous for the wild-type alleles.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
25075423-5	2014	When expressed in insect cell microsomes, the relative intrinsic clearance values of the CYP2C9.58 variant for tolbutamide and losartan were quite similar to those of the typical defective variant CYP2C9.3, whereas the clearance value of CYP2C9.58 for diclofenac was slightly higher than that of another typical defective variant CYP2C9.2.	Tolbutamide	111-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
25075423-5	2014	When expressed in insect cell microsomes, the relative intrinsic clearance values of the CYP2C9.58 variant for tolbutamide and losartan were quite similar to those of the typical defective variant CYP2C9.3, whereas the clearance value of CYP2C9.58 for diclofenac was slightly higher than that of another typical defective variant CYP2C9.2.	Tolbutamide	111-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
25075423-5	2014	When expressed in insect cell microsomes, the relative intrinsic clearance values of the CYP2C9.58 variant for tolbutamide and losartan were quite similar to those of the typical defective variant CYP2C9.3, whereas the clearance value of CYP2C9.58 for diclofenac was slightly higher than that of another typical defective variant CYP2C9.2.	Tolbutamide	111-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
25075423-5	2014	When expressed in insect cell microsomes, the relative intrinsic clearance values of the CYP2C9.58 variant for tolbutamide and losartan were quite similar to those of the typical defective variant CYP2C9.3, whereas the clearance value of CYP2C9.58 for diclofenac was slightly higher than that of another typical defective variant CYP2C9.2.	Tolbutamide	111-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
25075423-5	2014	When expressed in insect cell microsomes, the relative intrinsic clearance values of the CYP2C9.58 variant for tolbutamide and losartan were quite similar to those of the typical defective variant CYP2C9.3, whereas the clearance value of CYP2C9.58 for diclofenac was slightly higher than that of another typical defective variant CYP2C9.2.	Losartan	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
25075423-5	2014	When expressed in insect cell microsomes, the relative intrinsic clearance values of the CYP2C9.58 variant for tolbutamide and losartan were quite similar to those of the typical defective variant CYP2C9.3, whereas the clearance value of CYP2C9.58 for diclofenac was slightly higher than that of another typical defective variant CYP2C9.2.	Losartan	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
25075423-5	2014	When expressed in insect cell microsomes, the relative intrinsic clearance values of the CYP2C9.58 variant for tolbutamide and losartan were quite similar to those of the typical defective variant CYP2C9.3, whereas the clearance value of CYP2C9.58 for diclofenac was slightly higher than that of another typical defective variant CYP2C9.2.	Losartan	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
25075423-5	2014	When expressed in insect cell microsomes, the relative intrinsic clearance values of the CYP2C9.58 variant for tolbutamide and losartan were quite similar to those of the typical defective variant CYP2C9.3, whereas the clearance value of CYP2C9.58 for diclofenac was slightly higher than that of another typical defective variant CYP2C9.2.	Losartan	127-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	197-203
25075423-5	2014	When expressed in insect cell microsomes, the relative intrinsic clearance values of the CYP2C9.58 variant for tolbutamide and losartan were quite similar to those of the typical defective variant CYP2C9.3, whereas the clearance value of CYP2C9.58 for diclofenac was slightly higher than that of another typical defective variant CYP2C9.2.	Diclofenac	252-262	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
25343299-7	2014	Only thujopsene was found to be a mechanism-based inhibitor of CYP2C8, CYP2C9, and CYP2C19.	thujopsene	5-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
25343299-8	2014	Cedrol and thujopsene weakly inhibited CYP2C8, CYP2C9, and CYP2C19 activities, but beta-cedrene did not.	cedrol	0-6	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
25343299-8	2014	Cedrol and thujopsene weakly inhibited CYP2C8, CYP2C9, and CYP2C19 activities, but beta-cedrene did not.	thujopsene	11-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
25335408-1	2014	The goal of this work was to study cytochrome-450 (CYP) 2C9 (CYP2C9) gene polymorphism in patients with tuberculosis (TB) and its meaning for development, progress, and outcome of TB, for the pharmacokinetics of the antituberculosis antibiotic rifampicin on the basis of the southern region of Ukraine.	Rifampin	244-254	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	35-59
25335408-1	2014	The goal of this work was to study cytochrome-450 (CYP) 2C9 (CYP2C9) gene polymorphism in patients with tuberculosis (TB) and its meaning for development, progress, and outcome of TB, for the pharmacokinetics of the antituberculosis antibiotic rifampicin on the basis of the southern region of Ukraine.	Rifampin	244-254	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
24245489-5	2014	Genotyping for various CYP single-nucleotide polymorphisms showed that the patient carried mutant alleles encoding enzymes CYP2B6 and CYP2C9 involved in prasugrel metabolic pathway.	Prasugrel Hydrochloride	153-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
25185986-5	2014	In this review, we discuss the implications of polymorphisms in the cytochrome P-450 enzyme 2C9 (CYP2C9) and Vitamin K Epoxide Reductase Enzyme Complex subunit 1 (VKORC1) as they relate to therapeutic warfarin dosing.	Warfarin	201-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-95
25185986-5	2014	In this review, we discuss the implications of polymorphisms in the cytochrome P-450 enzyme 2C9 (CYP2C9) and Vitamin K Epoxide Reductase Enzyme Complex subunit 1 (VKORC1) as they relate to therapeutic warfarin dosing.	Warfarin	201-209	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	97-103
25492821-4	2014	VKORC1 and CYP2C9 are two genes responsible for warfarin metabolism.	Warfarin	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
24464600-1	2014	It is previously shown that carriers of the defective allele CYP2C9*3 that leads to impaired sulfonylurea metabolism are at increased sulfonylurea-induced hypoglycemia risk due to diminished drug metabolism, whereas no effect of CYP2C9*2 allele was found.	Sulfonylurea Compounds	93-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
24464600-8	2014	In a model adjusted for age, BMI, duration of T2DM and renal function, and POR*1/*1 entered as a selection variable, CYP2C9*2 allele increased the hypoglycemia risk in response to sulfonylurea (odds ratio: 3.218, p=0.031).	Sulfonylurea Compounds	180-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
24464600-9	2014	In conclusion, our results suggest that POR*28 allele is masking the association of CYP2C9*2 allele with sulfonyl-urea-induced hypoglycemia.	Sulfonylurea Compounds	105-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
23863877-0	2013	Association of CYP2C9*2 with bosentan-induced liver injury.	Bosentan	29-37	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
24043253-3	2013	We tested the hypothesis that regional inhibition of endothelium-derived hyperpolarizing factor with the cytochrome P-450 2C9 antagonist fluconazole, alone or combined with the NO synthase antagonist N(G)-monomethyl-L-arginine (L-NMMA), attenuates hypoxia-induced vasodilation.	Fluconazole	137-148	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-125
23863877-6	2013	Bosentan metabolism by CYP2C9*2 in vitro was significantly reduced compared with CYP2C9*1 and was comparable to that by CYP2C9*3.	Bosentan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
23863877-7	2013	These results suggest that CYP2C9*2 is a potential genetic marker for prediction of bosentan-induced liver injury and warrants investigation for the optimization of bosentan treatment.	Bosentan	84-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
23863877-7	2013	These results suggest that CYP2C9*2 is a potential genetic marker for prediction of bosentan-induced liver injury and warrants investigation for the optimization of bosentan treatment.	Bosentan	165-173	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
23863877-6	2013	Bosentan metabolism by CYP2C9*2 in vitro was significantly reduced compared with CYP2C9*1 and was comparable to that by CYP2C9*3.	Bosentan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
23863877-6	2013	Bosentan metabolism by CYP2C9*2 in vitro was significantly reduced compared with CYP2C9*1 and was comparable to that by CYP2C9*3.	Bosentan	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
24046330-6	2013	Spectral scanning of the reaction between CYP2C9 and noscapine revealed the formation of an absorption spectrum at 458 nm, indicating the formation of a metabolite-intermediate complex.	Noscapine	53-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
23974699-7	2013	CYP1A2 and CYP2D6 enzyme activities showed no significant changes, and CYP2C9 enzyme activity was increased with rifampicin administration, with a tendency toward statistical significance.	Rifampin	113-123	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
24046330-4	2013	Our enzyme kinetics data obtained from human liver microsomes and recombinant CYP2C9 proteins indicate that noscapine is a competitive inhibitor of the (S)-warfarin 7-hydroxylation reaction by CYP2C9.	Noscapine	108-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
24046330-7	2013	Surprisingly, noscapine is a 2- to 3-fold more efficient inactivator of CYP2C9.2 and CYP2C9.3 variants than it is of the wild type, by unknown mechanisms.	Noscapine	14-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
24046330-4	2013	Our enzyme kinetics data obtained from human liver microsomes and recombinant CYP2C9 proteins indicate that noscapine is a competitive inhibitor of the (S)-warfarin 7-hydroxylation reaction by CYP2C9.	Noscapine	108-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	193-199
24046330-4	2013	Our enzyme kinetics data obtained from human liver microsomes and recombinant CYP2C9 proteins indicate that noscapine is a competitive inhibitor of the (S)-warfarin 7-hydroxylation reaction by CYP2C9.	Warfarin	152-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-84
24046330-7	2013	Surprisingly, noscapine is a 2- to 3-fold more efficient inactivator of CYP2C9.2 and CYP2C9.3 variants than it is of the wild type, by unknown mechanisms.	Noscapine	14-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-91
24046330-4	2013	Our enzyme kinetics data obtained from human liver microsomes and recombinant CYP2C9 proteins indicate that noscapine is a competitive inhibitor of the (S)-warfarin 7-hydroxylation reaction by CYP2C9.	Warfarin	152-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	193-199
24046330-8	2013	Based on the inhibitory kinetic data, (S)-warfarin exposure is predicted to increase up to 7-fold (depending on CYP2C9 genotypes) upon noscapine coadministration, mainly due to mechanism-based inactivation of CYP2C9 by noscapine.	Warfarin	38-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
24046330-8	2013	Based on the inhibitory kinetic data, (S)-warfarin exposure is predicted to increase up to 7-fold (depending on CYP2C9 genotypes) upon noscapine coadministration, mainly due to mechanism-based inactivation of CYP2C9 by noscapine.	Warfarin	38-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	209-215
24046330-8	2013	Based on the inhibitory kinetic data, (S)-warfarin exposure is predicted to increase up to 7-fold (depending on CYP2C9 genotypes) upon noscapine coadministration, mainly due to mechanism-based inactivation of CYP2C9 by noscapine.	Noscapine	135-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
24046330-8	2013	Based on the inhibitory kinetic data, (S)-warfarin exposure is predicted to increase up to 7-fold (depending on CYP2C9 genotypes) upon noscapine coadministration, mainly due to mechanism-based inactivation of CYP2C9 by noscapine.	Noscapine	135-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	209-215
24046330-9	2013	Together, these results indicate that mechanism-based inhibition of CYP2C9 by noscapine may dramatically alter pharmacokinetics of warfarin and provide a basis for warfarin dosage adjustment when noscapine is coadministered.	Noscapine	78-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
24046330-9	2013	Together, these results indicate that mechanism-based inhibition of CYP2C9 by noscapine may dramatically alter pharmacokinetics of warfarin and provide a basis for warfarin dosage adjustment when noscapine is coadministered.	Warfarin	131-139	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
24046330-9	2013	Together, these results indicate that mechanism-based inhibition of CYP2C9 by noscapine may dramatically alter pharmacokinetics of warfarin and provide a basis for warfarin dosage adjustment when noscapine is coadministered.	Warfarin	164-172	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
24046330-9	2013	Together, these results indicate that mechanism-based inhibition of CYP2C9 by noscapine may dramatically alter pharmacokinetics of warfarin and provide a basis for warfarin dosage adjustment when noscapine is coadministered.	Noscapine	196-205	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	68-74
23941071-7	2013	CONCLUSION: These findings indicate that individuals carrying the CYP2C19 rs3814637CC or CYP2C9 rs1057910AA or GGCX rs699664AA genotype needed higher warfarin doses in the Chinese population.	Warfarin	150-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
23996211-0	2013	Evaluation of the relationship between polymorphisms in CYP2C8 and CYP2C9 and the pharmacokinetics of celecoxib.	Celecoxib	102-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
23996211-1	2013	Celecoxib is metabolized by enzymes of the cytochrome P450 (CYP450) superfamily, mainly CYP2C9 and CYP3A4.	Celecoxib	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
23996211-2	2013	Polymorphisms in the CYP2C9 gene have been associated with decreased enzyme activity and alteration of celecoxib pharmacokinetic parameters.	Celecoxib	103-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
23996211-8	2013	In conclusion, the recommended dose of celecoxib should be decreased in CYP2C9*3 carriers, especially in homozygous subjects.	Celecoxib	39-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
25505570-9	2013	Additional studies were done to ascertain if ajulemic acid can inhibit the activities of five principal human cytochrome P450 isozymes; CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4/5.	lenabasum	45-58	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	144-150
23839801-10	2013	SYBR Green-based multiplex allele-specific real-time PCR was used for genotyping of CYP2C9 (1075A&gt;C) and VKORC1 (1173C&gt;T) polymorphisms.	sybr green	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
23839801-11	2013	Linear regression analysis, including the variables age, gender, CYP2C9 and VKORC1 SNP genotypes, was run to derive the best model for estimating the warfarin dose that achieves an INR of 2-3.	Warfarin	150-158	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
23839801-14	2013	RESULTS: In the study cohort, warfarin dose/week in VKORC1 TT subjects was statistically significantly lower than in VKORC1 CC/CT subjects (p=0.032), while there was no statistically significant difference in warfarin dose/week between CYP2C9*1*1 and *1*3 (p=0.925).	Warfarin	30-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	236-242
24503429-0	2013	[A randomized controlled study of the VKORC1 and CYP2C9 genotypes in guiding warfarin therapy for pulmonary thromboembolism].	Warfarin	77-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
24521898-2	2013	METHODS: Genomic DNAs were extracted from the warfarin hypersensitive patient and used for genetic screening of CYP2C9, VKORC1 and CYP4F2 by direct sequencing.	Warfarin	46-54	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	112-118
23679834-0	2013	Monkey liver cytochrome P450 2C9 is involved in caffeine 7-N-demethylation to form theophylline.	Caffeine	48-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-32
23679834-0	2013	Monkey liver cytochrome P450 2C9 is involved in caffeine 7-N-demethylation to form theophylline.	Theophylline	83-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-32
24521898-11	2013	When expressed in insect cell microsomes, the relative clearance values of CYP2C9 *2, *3, *13 and L467P variants to tolbutamide were 91.58%, 13.55%, 0.11% and 1.59% to that of wild-type protein respectively.	Tolbutamide	116-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	75-81
23807523-0	2013	Effects of amiodarone, thyroid hormones and CYP2C9 and VKORC1 polymorphisms on warfarin metabolism: a review of the literature.	Warfarin	79-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	44-50
23872824-8	2013	CONCLUSIONS: Substantial inhibition of CYP3A- and modest induction of CYP2C9- activity were observed with danoprevir/r and low-dose ritonavir.	danoprevir	106-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
23872824-8	2013	CONCLUSIONS: Substantial inhibition of CYP3A- and modest induction of CYP2C9- activity were observed with danoprevir/r and low-dose ritonavir.	r	89-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
23872824-8	2013	CONCLUSIONS: Substantial inhibition of CYP3A- and modest induction of CYP2C9- activity were observed with danoprevir/r and low-dose ritonavir.	Ritonavir	132-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
23649958-1	2013	Warfarin, an anticoagulant with a narrow therapeutic window, is largely metabolized by cytochrome P450 2C9.	Warfarin	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-106
24071466-8	2013	Polymorphism of CYP2C9 and VKORC1 were related to the dosage of warfarin but not determinant of TTR.	Warfarin	64-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
24380239-5	2013	Seven subjects (2.97%) were poor metabolites (PMs) for CYP2C9 because of the *2/*2 and *3/*3 genotype.	pms	46-49	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	55-61
24222221-0	2013	Genetic contribution of CYP2C9, CYP2C19, and APOE variants in acenocoumarol response.	Acenocoumarol	62-75	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
24222221-4	2013	The objective of this study was to determine the contribution of CYP2C9, CYP2C19, and APOE polymorphisms to the variations in response to the doses of acenocoumarol, which is the main anticoagulant prescribed to the Mexican population.	Acenocoumarol	151-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
23852652-5	2013	Roles for CYP3A4, CYP2C9, CYP2C19 and CYP2B6 in the metabolism of ospemifene and its two main metabolites, 4--hydroxyospemifene and 4"-hydroxyospemifene, were confirmed.	Ospemifene	66-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
23932037-0	2013	Influence of CYP2C9 and VKORC1 genotypes on the risk of hemorrhagic complications in warfarin-treated patients: a systematic review and meta-analysis.	Warfarin	85-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
23932037-14	2013	CONCLUSIONS: Both CYP2C9 and VKORC1 genotypes are associated with an increased risk for warfarin over-anticoagulation, with VKORC1 c. -1639G &gt; A more sensitive early in the course of anticoagulation.	Warfarin	88-96	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
23932037-15	2013	CYP2C9*3 is the main genetic risk factor for warfarin hemorrhagic complications.	Warfarin	45-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
23852652-8	2013	Strong CYP3A or CYP2C9 inducers (e.g. rifampicin) would be expected to decrease the exposure to ospemifene.	Rifampin	38-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
23852652-8	2013	Strong CYP3A or CYP2C9 inducers (e.g. rifampicin) would be expected to decrease the exposure to ospemifene.	Ospemifene	96-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
24174816-2	2013	AIMS: This study was conducted to determine the inhibitory effects of mitragynine on cytochrome P450 2C9, 2D6 and 3A4 activities.	mitragynine	70-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	85-104
24174816-6	2013	RESULTS: Assessment using recombinant enzymes showed that mitragynine gave the strongest inhibitory effect on CYP2D6 with an IC50 value of 0.45+-0.33 mM, followed by CYP2C9 and CYP3A4 with IC50 values of 9.70+-4.80 and 41.32+-6.74 muM respectively.	mitragynine	58-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	166-172
24174816-7	2013	Positive inhibitors appropriate for CYP2C9, CYP2D6, and CYP3A4 which are sulfaphenazole, quinidine and ketoconazole were used respectively.	Sulfaphenazole	73-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
24174816-7	2013	Positive inhibitors appropriate for CYP2C9, CYP2D6, and CYP3A4 which are sulfaphenazole, quinidine and ketoconazole were used respectively.	Quinidine	89-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
24174816-7	2013	Positive inhibitors appropriate for CYP2C9, CYP2D6, and CYP3A4 which are sulfaphenazole, quinidine and ketoconazole were used respectively.	Ketoconazole	103-115	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
24174816-10	2013	Mitragynine noncompetitively inhibits CYP2C9 and CYP2D6 activities with the Ki values of 61.48 and 12.86 muM respectively.	mitragynine	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
23688605-0	2013	First report of warfarin dose requirements in patients possessing the CYP2C9*12 allele.	Warfarin	16-24	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	70-76
23688605-3	2013	Cytochrome P450 (CYP) 2C9 is the enzyme primarily responsible for the metabolism of S-warfarin.	Warfarin	84-94	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-25
23688605-12	2013	This is the first report of patients with the rare CYP2C9*12 genotype and lower warfarin dose requirements.	Warfarin	80-88	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
24005963-5	2013	These in vitro results indicate that honokiol has the potential to cause pharmacokinetic drug interactions with other co-administered drugs metabolized by CYP1A2, CYP2C8, CYP2C9, CYP2C19, and UGT1A9.	honokiol	37-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	171-177
24023924-0	2013	Distal effect of amino acid substitutions in CYP2C9 polymorphic variants causes differences in interatomic interactions against (S)-warfarin.	Warfarin	128-140	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
24023924-5	2013	To relate distal effects of these mutations and defective drug metabolisms, simulations of CYP2C9 binding to anti-coagulant (S)-warfarin were performed as a system model.	Sulfur	124-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
24023924-5	2013	To relate distal effects of these mutations and defective drug metabolisms, simulations of CYP2C9 binding to anti-coagulant (S)-warfarin were performed as a system model.	Warfarin	128-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	91-97
23287855-4	2013	In vitro analysis suggested that the purified CYP102A5 metabolizes typical substrates of human CYP2C9, CYP2D6, CYP2E1, and CYP3A4, such as coumarin, propranolol, aniline, chlorzoxazone, p-nitrophenol, and nifedipine.	coumarin	139-147	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
23770984-5	2013	RESULTS: All three gingerols potently inhibited CYP2C9 activity, exerted moderate inhibition on CYP2C19 and CYP3A4, and weak inhibion on CYP2D6.	gingerol	19-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	48-54
23770984-6	2013	8-Gingerol was the most potent in inhibition of P450 enzymes with IC50 values of 6.8, 12.5, 8.7, and 42.7 mumol/L for CYP2C9, CYP2C19, CYP3A4, and CYP2D6, respectively.	8-gingerol	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-124
23287855-4	2013	In vitro analysis suggested that the purified CYP102A5 metabolizes typical substrates of human CYP2C9, CYP2D6, CYP2E1, and CYP3A4, such as coumarin, propranolol, aniline, chlorzoxazone, p-nitrophenol, and nifedipine.	Propranolol	149-160	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
23287855-4	2013	In vitro analysis suggested that the purified CYP102A5 metabolizes typical substrates of human CYP2C9, CYP2D6, CYP2E1, and CYP3A4, such as coumarin, propranolol, aniline, chlorzoxazone, p-nitrophenol, and nifedipine.	aniline	162-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
23287855-4	2013	In vitro analysis suggested that the purified CYP102A5 metabolizes typical substrates of human CYP2C9, CYP2D6, CYP2E1, and CYP3A4, such as coumarin, propranolol, aniline, chlorzoxazone, p-nitrophenol, and nifedipine.	Chlorzoxazone	171-184	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
23287855-4	2013	In vitro analysis suggested that the purified CYP102A5 metabolizes typical substrates of human CYP2C9, CYP2D6, CYP2E1, and CYP3A4, such as coumarin, propranolol, aniline, chlorzoxazone, p-nitrophenol, and nifedipine.	4-nitrophenol	186-199	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
23287855-4	2013	In vitro analysis suggested that the purified CYP102A5 metabolizes typical substrates of human CYP2C9, CYP2D6, CYP2E1, and CYP3A4, such as coumarin, propranolol, aniline, chlorzoxazone, p-nitrophenol, and nifedipine.	Nifedipine	205-215	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
23504614-6	2013	SPZ also prevented CA-induced mitochondrial membrane depolarization and ECs death, implicating CYP2C9 in mediating the cellular response upon CA treatment.	Sulfaphenazole	0-3	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
23436703-2	2013	However, multiple genes are likely to contribute, either acting independently or epistatically, with the CYP2C9-VKORC1-warfarin test panel, an example of a clinically used gene-gene-dug interaction.	Warfarin	119-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
23726967-1	2013	PURPOSE: The aim of the present study was to investigate the genetic variability of VKORC1, CYP2C9 and CYP4F2 genes in patients who required a very low and high warfarin dose, in order to identify novel variants that could help to explain the particular extreme dose requirements.	Warfarin	161-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
23682017-4	2013	In this review, we focus on the important CYP2C9 and VKORC1 variants involved in warfarin response, our current understanding of warfarin disposition and pharmacogenomics, and recent warfarin pharmacogenetic studies in pediatric patients.	Warfarin	81-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	42-48
24024895-0	2013	CYP2C9 and ABCG2 polymorphisms as risk factors for developing adverse drug reactions in renal transplant patients taking fluvastatin: a case-control study.	Fluvastatin	121-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
24024895-1	2013	AIM: To investigate whether an association exists between fluvastatin-induced adverse drug reactions (ADRs) and polymorphisms in genes encoding the metabolizing enzyme CYP2C9 and the drug transporter ABCG2 in renal transplant recipients (RTRs).	Fluvastatin	58-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
24024895-8	2013	CONCLUSION: Our preliminary data demonstrate an association between fluvastatin-induced ADRs in RTRs and genetic variants in the CYP2C9 and ABCG2 genes.	Fluvastatin	68-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
23755828-1	2013	BACKGROUND: VKORC1 and CYP2C9 are important contributors to warfarin dose variability, but explain less variability for individuals of African descent than for those of European or Asian descent.	Warfarin	60-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
23755828-14	2013	INTERPRETATION: A novel CYP2C single nucleotide polymorphism exerts a clinically relevant effect on warfarin dose in African Americans, independent of CYP2C9*2 and CYP2C9*3.	Warfarin	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	151-157
23755828-14	2013	INTERPRETATION: A novel CYP2C single nucleotide polymorphism exerts a clinically relevant effect on warfarin dose in African Americans, independent of CYP2C9*2 and CYP2C9*3.	Warfarin	100-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	164-170
23441978-1	2013	OBJECTIVES: Etravirine is a substrate and inducer of cytochrome P450 (CYP) 3A and a substrate and inhibitor of CYP2C9 and CYPC2C19.	etravirine	12-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
23441978-3	2013	Artemether and lumefantrine are primarily metabolized by CYP3A; artemether is also metabolized to a lesser extent by CYP2B6, CYP2C9 and CYP2C19.	Artemether	64-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	125-131
23930675-0	2013	Effects of polymorphisms in ABCG2, SLCO1B1, SLC10A1 and CYP2C9/19 on plasma concentrations of rosuvastatin and lipid response in Chinese patients.	Rosuvastatin Calcium	94-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	56-62
23545481-4	2013	Estimates of CLint for the production of mono(2-ethyl-5-hydroxyhexyl) phthalate and mono(2-ethyl-5-oxohexyl) phthalate by human CYP2C9 1 were 4.2- and 2.6-fold greater than those by rat CYP2C6, respectively.	mono(2-ethyl-5-hydroxyhexyl) phthalate	41-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
23545481-4	2013	Estimates of CLint for the production of mono(2-ethyl-5-hydroxyhexyl) phthalate and mono(2-ethyl-5-oxohexyl) phthalate by human CYP2C9 1 were 4.2- and 2.6-fold greater than those by rat CYP2C6, respectively.	mono(2-ethyl-5-oxohexyl)phthalate	84-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
23727057-5	2013	A microdose of (14)C-tolbutamide (100 mug) was administered orally to healthy volunteers with the CYP2C9(*)1/(*)1 or CYP2C9(*)1/(*)3 diplotype.	Tolbutamide	21-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	117-123
23688499-0	2013	Pregnane X receptor dependent up-regulation of CYP2C9 and CYP3A4 in tumor cells by antitumor acridine agents, C-1748 and C-1305, selectively diminished under hypoxia.	Acridines	93-101	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
23688499-0	2013	Pregnane X receptor dependent up-regulation of CYP2C9 and CYP3A4 in tumor cells by antitumor acridine agents, C-1748 and C-1305, selectively diminished under hypoxia.	9-(2'-hydroxyethylamino)-4-methyl-1-nitroacridine	110-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
23688499-0	2013	Pregnane X receptor dependent up-regulation of CYP2C9 and CYP3A4 in tumor cells by antitumor acridine agents, C-1748 and C-1305, selectively diminished under hypoxia.	C 1305	121-127	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	47-53
23688499-6	2013	C-1748-mediated CYP3A4 and CYP2C9 mRNA induction equal to rifampicin occurred at extremely low concentrations (0.001 and 0.01muM), whereas 10muM C-1305 induced three-times higher CYP3A4 and CYP2C9 mRNA levels than rifampicin did.	9-(2'-hydroxyethylamino)-4-methyl-1-nitroacridine	0-6	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
23688499-6	2013	C-1748-mediated CYP3A4 and CYP2C9 mRNA induction equal to rifampicin occurred at extremely low concentrations (0.001 and 0.01muM), whereas 10muM C-1305 induced three-times higher CYP3A4 and CYP2C9 mRNA levels than rifampicin did.	9-(2'-hydroxyethylamino)-4-methyl-1-nitroacridine	0-6	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	190-196
23880855-4	2013	Ospemifene and its main metabolites 4-hydroxyospemifene and 4"-hydroxyospemifene weakly inhibited a number of CYPs (CYP2B6, CYP2C9, CYP2C19, CYP2C8, and CYP2D6) in vitro.	Ospemifene	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
23880855-4	2013	Ospemifene and its main metabolites 4-hydroxyospemifene and 4"-hydroxyospemifene weakly inhibited a number of CYPs (CYP2B6, CYP2C9, CYP2C19, CYP2C8, and CYP2D6) in vitro.	4-hydroxyospemifene	36-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
23880855-4	2013	Ospemifene and its main metabolites 4-hydroxyospemifene and 4"-hydroxyospemifene weakly inhibited a number of CYPs (CYP2B6, CYP2C9, CYP2C19, CYP2C8, and CYP2D6) in vitro.	4-hydroxyospemifene	60-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
23880855-5	2013	However, only CYP2C9 activity was inhibited by 4-hydroxyospemifene at clinically relevant concentrations.	4-hydroxyospemifene	47-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
23737517-4	2013	The pharmacokinetics of the probe drug cocktail (flurbiprofen/fexofenadine) were altered, with formation clearance of flurbiprofen (CYP2C9 function) lower in our patient versus the average value in our study cohort, suggesting a reduction in activity.	Flurbiprofen	118-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-138
24052784-1	2013	BACKGROUND: Warfarin dosage regimens using CYP2C9 and VKORC1 polymorphisms have been extensively studied in adults and is included in US Food and Drug Administration-approved warfarin labeling.	Warfarin	12-20	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
24052784-1	2013	BACKGROUND: Warfarin dosage regimens using CYP2C9 and VKORC1 polymorphisms have been extensively studied in adults and is included in US Food and Drug Administration-approved warfarin labeling.	Warfarin	175-183	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
24052784-11	2013	CONCLUSIONS: The proposed pediatric warfarin dosage scheme based on individual CYP2C9 (alleles *1,*2,*3) and VKORC1 rs9923231 (-1639 G&gt;A) genotypes may offer improved dosage compared to current treatment strategies, especially in patients with variant CYP2C9 and VKORC1 alleles.	Warfarin	36-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
24052784-11	2013	CONCLUSIONS: The proposed pediatric warfarin dosage scheme based on individual CYP2C9 (alleles *1,*2,*3) and VKORC1 rs9923231 (-1639 G&gt;A) genotypes may offer improved dosage compared to current treatment strategies, especially in patients with variant CYP2C9 and VKORC1 alleles.	Warfarin	36-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	255-261
24082701-0	2013	Cytochrome P450 2C9 gene polymorphism in phenytoin induced gingival enlargement: A case report.	Phenytoin	41-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
24082701-7	2013	Individuals with poor metaboliser alleles of CYP2C9 gene were shown to have a reduced metabolism of phenytoin compared with wild-type alleles.	Phenytoin	100-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
23615745-16	2013	In conclusion, CYP2B6 and CYP2C9 polymorphisms seem to be associated with prasugrel low-response.	Prasugrel Hydrochloride	74-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	26-32
27181593-1	2016	AIMS/INTRODUCTION: The objective of the present study was to investigate the effects of CYP2C9*3 polymorphisms on the therapeutic response to gliclazide in type 2 diabetes patients.	Gliclazide	142-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
27275407-2	2014	The frequency of heterozygous or homozygous genotypes of CYP2C9*2 &amp; CYP2C9*3, which leads to the poor metabolizer (PM) genotype was significantly higher in HNSCC cases when compared to the healthy controls resulting in significantly increased risk in the cases.	Adenosine Monophosphate	67-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	57-63
27275407-2	2014	The frequency of heterozygous or homozygous genotypes of CYP2C9*2 &amp; CYP2C9*3, which leads to the poor metabolizer (PM) genotype was significantly higher in HNSCC cases when compared to the healthy controls resulting in significantly increased risk in the cases.	Adenosine Monophosphate	67-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
27275407-4	2014	Likewise, alcohol intake in cases with variant genotypes of CYP2C9*2 or CYP2C9*3 also significantly increased the HNSCC risk in cases when compared to non-alcohol users.	Alcohols	10-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
27275407-4	2014	Likewise, alcohol intake in cases with variant genotypes of CYP2C9*2 or CYP2C9*3 also significantly increased the HNSCC risk in cases when compared to non-alcohol users.	Alcohols	10-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
27275407-4	2014	Likewise, alcohol intake in cases with variant genotypes of CYP2C9*2 or CYP2C9*3 also significantly increased the HNSCC risk in cases when compared to non-alcohol users.	Alcohols	155-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
27275407-4	2014	Likewise, alcohol intake in cases with variant genotypes of CYP2C9*2 or CYP2C9*3 also significantly increased the HNSCC risk in cases when compared to non-alcohol users.	Alcohols	155-162	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
22641027-1	2013	Pharmacogenetic studies have shown that genetic defects in drug-metabolizing enzymes encoded by CYP2C9, CYP2C19 genes and by the transporter ABCB1 gene can influence phenytoin (PTH) plasma levels and toxicity.	Phenytoin	166-175	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
23587916-5	2013	The CYP2C9*2 allele frequencies in the Mestizo, Nahua and Teenek populations were 0.051, 0.007 and 0.005, respectively.	nahua	48-53	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	4-10
23515956-5	2013	Based on in vitro enzyme kinetic parameters for S-warfarin metabolism, demographic data for Han Chinese and some scaling factors, the S-warfarin clearance (CL) was predicted for patients in the cohort with different CYP2C9 genotypes using IVIVE.	Warfarin	136-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	216-222
23515956-7	2013	The warfarin maintenance dose was then predicted based on the demographic data and genotypes of CYP2C9 and VKORC1 for each patient and using the observed steady-state INR (INRss) as a target value.	Warfarin	4-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
23515956-10	2013	There were significant differences in the mean warfarin daily dose in patients with different CYP2C9 and VKORC1 genotypes.	Warfarin	47-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
23515956-11	2013	Using IVIVE, the predicted mean CL of S-warfarin for patients with CYP2C9*1/*3 (0.092 l/h, n = 11) was 57 % less than for those with wild-type *1/*1 (0.215 l/h, n = 186).	Warfarin	40-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
23515956-15	2013	The mean predicted/observed warfarin doses (mg/day) for different combinations of CYP2C9 and VKORC1 genotypes were 1.54/3.75 (n = 1) for *1/*1 and GG, 3.33/3.66 (n = 36) for *1/*1 and AG, 2.31/2.41 (n = 136) for *1/*1 and AA, and 1.56/1.69 (n = 10) for *1/*3 and AA, respectively.	Warfarin	28-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	82-88
23515956-16	2013	Sensitivity analysis indicated BW and genetic polymorphisms of CYP2C9 and VKORC1 were important factors affecting the warfarin maintenance dose in the study population.	Warfarin	118-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	63-69
23515956-17	2013	CONCLUSION: The mechanistic model reported is the first to integrate IVIVE with a pharmacokinetic-pharmacodynamic model to describe the association of the warfarin maintenance dose with sex, age, BW and the genotypes of CYP2C9 and VKORC1.	Warfarin	155-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	220-226
23602689-0	2013	Influence of CYP2C9 and VKORC1 gene polymorphisms on warfarin dosage, over anticoagulation and other adverse outcomes in Indian population.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	13-19
23602689-8	2013	Our results suggest that both VKORC1 and CYP2C9 genotypes showed significant impact on warfarin dose requirement, over anticoagulation in the first month of anticoagulation and number of bleeding episodes.	Warfarin	87-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
22075408-3	2013	It has been shown that besides CYP2C19, CYP2C9 is involved in the hepatic biotransformation of clopidogrel to its active metabolite.	Clopidogrel	95-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-46
22075408-4	2013	Consequently, CYP2C9 polymorphisms may also affect the extent of clopidogrel-mediated platelet inhibition.	Clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	14-20
22075408-5	2013	We therefore studied the influence of CYP2C9 allelic variants on clopidogrel-mediated platelet inhibition as assessed by 5 platelet function tests.	Clopidogrel	65-76	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	38-44
22075408-10	2013	CONCLUSION: Results from the VerifyNow P2Y12 assay are significantly influenced by CYP2C9 LOF variants leading to decreased clopidogrel-mediated platelet inhibition and an increased rate of HRPR.	Clopidogrel	124-135	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
23579966-6	2013	Prospective randomized clinical trials are currently underway utilizing dosing algorithms that incorporate genetic polymorphisms in cytochrome P450 (CYP)2C9 and vitamin k epoxide reductase (VKORC1) to determine warfarin dosages.	Warfarin	211-219	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	132-156
23579966-7	2013	Polymorphisms in CYP2C9 and VKORC1 account for approximately 40 % of the variance in warfarin dose.	Warfarin	85-93	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
23525712-7	2013	In PE-constricted arteries, the H2S donor NaHS caused vasodilation that was inhibited by ryanodine (RyR blocker), abluminal or luminal iberiotoxin (IbTx, BKCa blocker), endothelial cell (EC) disruption, and sulfaphenazole [cytochrome P-450 2C (Cyp2C) inhibitor].	Hydrogen Sulfide	32-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	223-242
23525712-7	2013	In PE-constricted arteries, the H2S donor NaHS caused vasodilation that was inhibited by ryanodine (RyR blocker), abluminal or luminal iberiotoxin (IbTx, BKCa blocker), endothelial cell (EC) disruption, and sulfaphenazole [cytochrome P-450 2C (Cyp2C) inhibitor].	Hydrogen Sulfide	32-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	244-249
23525712-7	2013	In PE-constricted arteries, the H2S donor NaHS caused vasodilation that was inhibited by ryanodine (RyR blocker), abluminal or luminal iberiotoxin (IbTx, BKCa blocker), endothelial cell (EC) disruption, and sulfaphenazole [cytochrome P-450 2C (Cyp2C) inhibitor].	sodium bisulfide	42-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	223-242
23525712-7	2013	In PE-constricted arteries, the H2S donor NaHS caused vasodilation that was inhibited by ryanodine (RyR blocker), abluminal or luminal iberiotoxin (IbTx, BKCa blocker), endothelial cell (EC) disruption, and sulfaphenazole [cytochrome P-450 2C (Cyp2C) inhibitor].	sodium bisulfide	42-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	244-249
23604525-6	2013	Clomiphene, tamoxifen and toremifene were biotransformed to 22, 23 and 18 metabolites respectively, these phase I reactions being catalyzed mainly by CYP3A4 and CYP2D6 isoforms and, to a lesser degree, by CYP3A5, CYP2B6, CYP2C9, CYP2C19 isoforms.	Clomiphene	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	221-227
23604525-6	2013	Clomiphene, tamoxifen and toremifene were biotransformed to 22, 23 and 18 metabolites respectively, these phase I reactions being catalyzed mainly by CYP3A4 and CYP2D6 isoforms and, to a lesser degree, by CYP3A5, CYP2B6, CYP2C9, CYP2C19 isoforms.	Tamoxifen	12-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	221-227
23604525-6	2013	Clomiphene, tamoxifen and toremifene were biotransformed to 22, 23 and 18 metabolites respectively, these phase I reactions being catalyzed mainly by CYP3A4 and CYP2D6 isoforms and, to a lesser degree, by CYP3A5, CYP2B6, CYP2C9, CYP2C19 isoforms.	Toremifene	26-36	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	221-227
23509226-13	2013	Apatinib was metabolized primarily by CYP3A4/5 and, to a lesser extent, by CYP2D6, CYP2C9, and CYP2E1.	apatinib	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
23539296-6	2013	In addition to CYP2B6, anisomycin cotreatment potentiated an increase in CYP2A7 and CYP2C9 mRNAs but not CYP3A4 or UDP-glucuronosyltransferase 1A1 mRNAs.	Anisomycin	23-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
23500771-4	2013	The results showed that SAG was a potent noncompetitive inhibitor of CYP2C8 activity (Ki=8.9 muM), and competitive inhibitor of CYP1A2, CYP2C9 and CYP3A4 activities (Ki=2.7, 3.8 and 2.0 muM, respectively).	sanguinarine	24-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	136-142
23500771-7	2013	In vitro-in vivo extrapolation (IV-IVE) from HLM data showed that more than 35.9% of CYP1A2, CYP2C9, CYP2C8 and CYP3A4 activities in vivo could be inhibited by SAG, suggesting that harmful DDIs could occur when SAG or its medical preparations are co-administered with drugs primarily cleared by these CYP isoforms.	sanguinarine	160-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
23500771-7	2013	In vitro-in vivo extrapolation (IV-IVE) from HLM data showed that more than 35.9% of CYP1A2, CYP2C9, CYP2C8 and CYP3A4 activities in vivo could be inhibited by SAG, suggesting that harmful DDIs could occur when SAG or its medical preparations are co-administered with drugs primarily cleared by these CYP isoforms.	sanguinarine	211-214	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
23657428-4	2013	There is overwhelming evidence that an individual"s warfarin maintenance is associated with clinical factors and genetic variations, most notably polymorphisms in cytochrome P450 2C9 and vitamin K epoxide reductase subunit 1.	Warfarin	52-60	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-182
23588782-15	2013	CYP2C9 is responsible for metabolising vitamin K antagonists (VKAs), non-steroidal anti-inflammatory drugs (NSAIDs), sulfonylureas, angiotensin II receptor antagonists and phenytoin.	Vitamin K	39-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
23588782-15	2013	CYP2C9 is responsible for metabolising vitamin K antagonists (VKAs), non-steroidal anti-inflammatory drugs (NSAIDs), sulfonylureas, angiotensin II receptor antagonists and phenytoin.	Sulfonylurea Compounds	117-130	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
23588782-15	2013	CYP2C9 is responsible for metabolising vitamin K antagonists (VKAs), non-steroidal anti-inflammatory drugs (NSAIDs), sulfonylureas, angiotensin II receptor antagonists and phenytoin.	Phenytoin	172-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
23588782-19	2013	A relationship between CYP2C9 polymorphisms and the pharmacokinetics of sulfonylureas and angiotensin II receptor antagonists has also been observed.	Sulfonylurea Compounds	72-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
23588782-21	2013	Finally, homozygous and heterozygous carriers of CYP2C9 variant alleles require lower doses of phenytoin to reach therapeutic plasma concentrations, and are at increased risk of toxicity.	Phenytoin	95-104	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
23602689-1	2013	The aim of this study was to determine the frequencies of SNPs in the vitamin K epoxide reductase complex subunit 1 (VKORC1) and cytochrome P450 2C9 (CYP2C9) genes and their effect on warfarin dose requirement, over anticoagulation and other adverse outcomes in Indian population.	Warfarin	184-192	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	150-156
23602689-2	2013	A total of 145 warfarin treated patients for various clinical conditions were screened for VKORC1 and CYP2C9 gene polymorphisms by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique.	Warfarin	15-23	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	102-108
23201087-0	2013	Effect of different genetics variants: CYP2C9*2, CYP2C9*3 of cytochrome P-450 CYP2C9 and 1639G&gt;A of the VKORC1 gene; On acenocoumarol requirement in Moroccan patients.	Acenocoumarol	123-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
23201087-0	2013	Effect of different genetics variants: CYP2C9*2, CYP2C9*3 of cytochrome P-450 CYP2C9 and 1639G&gt;A of the VKORC1 gene; On acenocoumarol requirement in Moroccan patients.	Acenocoumarol	123-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
23201087-0	2013	Effect of different genetics variants: CYP2C9*2, CYP2C9*3 of cytochrome P-450 CYP2C9 and 1639G&gt;A of the VKORC1 gene; On acenocoumarol requirement in Moroccan patients.	Acenocoumarol	123-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	49-55
23582453-0	2013	Implication of novel CYP2C9*57 (p.Asn204His) variant in coumarin hypersensitivity.	coumarin	56-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
23582453-5	2013	The pharmacoproteomic significance of the novel genetic variant was elucidated by structural demonstration of binding of coumarin molecules within the mutant CYP2C9 204His protein model and in silico bioinformatic evolutionary analyses.	coumarin	121-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	158-164
23666577-4	2013	O-demethylation is catalyzed by the highly polymorphic CYP2D6 and N-demethylation by several enzymes, CYP2C19, CYP2C9, and CYP3A4.	Nitrogen	66-67	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
23582453-10	2013	Analysis of 3D structure model of the mutant protein revealed that the substituted His204 led to restricted binding of the coumarin drug within the binding site of CYP2C9 enzyme, thereby inhibiting its metabolic clearance and thus explaining the enhanced pharmacologic effect and bleeding in the patient.	coumarin	123-131	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	164-170
23666577-5	2013	The observed overall pharmacokinetic effect was most probably the result of decreased N-demethylation of venlafaxine by (1) reduced expression of CYP2C19 due to a genetic deficit and (2) inhibition of CYP2C9 by cotrimoxazole.	Nitrogen	86-87	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	201-207
23582453-11	2013	CONCLUSIONS: The study elucidates the structurally deleterious role of the novel CYP2C9*57 missense mutation in coumarin toxicity.	coumarin	112-120	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
23666577-5	2013	The observed overall pharmacokinetic effect was most probably the result of decreased N-demethylation of venlafaxine by (1) reduced expression of CYP2C19 due to a genetic deficit and (2) inhibition of CYP2C9 by cotrimoxazole.	Venlafaxine Hydrochloride	105-116	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	201-207
23641937-4	2013	Here we present a comprehensive study of the oxidation of three widely used pharmaceutical compounds (S-ibuprofen, diclofenac, and S-warfarin) by one of the major drug-metabolizing P450 isoforms, CYP2C9.	Sulfur	102-103	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
23666577-5	2013	The observed overall pharmacokinetic effect was most probably the result of decreased N-demethylation of venlafaxine by (1) reduced expression of CYP2C19 due to a genetic deficit and (2) inhibition of CYP2C9 by cotrimoxazole.	Trimethoprim, Sulfamethoxazole Drug Combination	211-224	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	201-207
23201087-6	2013	The results showed that the allelic frequencies of the three mutations studied was varies, most of patients having CYP2C9*2 and CYP2C9*3 mutations belong to a group with low dose of acenocoumarol, with P-value of 0.0082 and the single patient with CYP2C9*3 on homozygous form belongs to the same group and carried the A allele for VKORC1 gene.	Acenocoumarol	182-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	115-121
23201087-6	2013	The results showed that the allelic frequencies of the three mutations studied was varies, most of patients having CYP2C9*2 and CYP2C9*3 mutations belong to a group with low dose of acenocoumarol, with P-value of 0.0082 and the single patient with CYP2C9*3 on homozygous form belongs to the same group and carried the A allele for VKORC1 gene.	Acenocoumarol	182-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
23201087-6	2013	The results showed that the allelic frequencies of the three mutations studied was varies, most of patients having CYP2C9*2 and CYP2C9*3 mutations belong to a group with low dose of acenocoumarol, with P-value of 0.0082 and the single patient with CYP2C9*3 on homozygous form belongs to the same group and carried the A allele for VKORC1 gene.	Acenocoumarol	182-195	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	128-134
23641937-4	2013	Here we present a comprehensive study of the oxidation of three widely used pharmaceutical compounds (S-ibuprofen, diclofenac, and S-warfarin) by one of the major drug-metabolizing P450 isoforms, CYP2C9.	Ibuprofen	104-113	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
23641937-4	2013	Here we present a comprehensive study of the oxidation of three widely used pharmaceutical compounds (S-ibuprofen, diclofenac, and S-warfarin) by one of the major drug-metabolizing P450 isoforms, CYP2C9.	Diclofenac	115-125	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
23641937-4	2013	Here we present a comprehensive study of the oxidation of three widely used pharmaceutical compounds (S-ibuprofen, diclofenac, and S-warfarin) by one of the major drug-metabolizing P450 isoforms, CYP2C9.	Sulfur	131-132	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
23641937-4	2013	Here we present a comprehensive study of the oxidation of three widely used pharmaceutical compounds (S-ibuprofen, diclofenac, and S-warfarin) by one of the major drug-metabolizing P450 isoforms, CYP2C9.	Warfarin	133-141	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
23641937-9	2013	The carboxylate of diclofenac interacts strongly with the CYP2C9 Arg108 side chain in the transition state for formation of the observed metabolite-but not in that for the competing pathway.	carboxylate	4-15	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
23641937-9	2013	The carboxylate of diclofenac interacts strongly with the CYP2C9 Arg108 side chain in the transition state for formation of the observed metabolite-but not in that for the competing pathway.	Diclofenac	19-29	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
23691226-2	2013	Three polymorphisms in two genes, VKORC1 and CYP2C9, are the main coumarin dose determinants and no additional polymorphisms of any relevant pharmacogenetic importance have been identified.	coumarin	66-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
23208322-6	2013	RESULTS: Warfarin dose was partially correlated with the VKORC1 rs7294, CYP2C9 rs1057910 and ORM1 rs17650 polymorphisms.	Warfarin	9-17	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
27122712-5	2013	Clinical and genetic factors such as polymorphisms in CYP2C9 and VKORC1 associated with an individual"s warfarin maintenance have been identified.	Warfarin	104-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
23519598-8	2013	RESULTS: The model confirmed CYP2C9 and VKORC1 variants as the major predictors of variability in phenprocoumon concentrations and effects, together with body weight, age, comedication with CYP3A modifiers (i.e. inhibitors or inducers) and presence of atrial fibrillation.	Phenprocoumon	98-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-35
23559402-9	2013	Polymorphisms in CYP2C9, TPMT, UGT1A1, MDR1, and 5-HTR2A were related to some adverse effects of olanzapine.	Olanzapine	97-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	17-23
24324947-0	2013	VKORC1 and CYP2C9 Genotype Variations in Relation to Warfarin Dosing in Korean Stroke Patients.	Warfarin	53-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
24324947-2	2013	We sought to establish a warfarin dosing formula for individualized target International Normalization Ratio of Prothrombin Times (INRs) using data from single nucleotide polymorphisms (SNPs) in VKORC1 and CYP2C9 in Korean patients.	Warfarin	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	206-212
23651023-0	2013	Impact of CYP2C9 polymorphisms on the vulnerability to pharmacokinetic drug-drug interactions during acenocoumarol treatment.	Acenocoumarol	101-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
22767428-5	2013	CYP3A4, CYP2C9 and CYP1A2 were identified to be the main CYP isoforms involved in the metabolism of evodiamine in human liver microsomes.	evodiamine	100-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
23651023-1	2013	AIM: The objective of this study was to investigate the impact of CYP2C9 polymorphisms and drug-drug interactions on the risk of overanticoagulation in patients treated with acenocoumarol, a vitamin K antagonist.	Acenocoumarol	174-187	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
23651023-1	2013	AIM: The objective of this study was to investigate the impact of CYP2C9 polymorphisms and drug-drug interactions on the risk of overanticoagulation in patients treated with acenocoumarol, a vitamin K antagonist.	Vitamin K	191-200	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-72
23399640-6	2013	In contrast to PTI, indomethacin is primarily O-demethylated by CYP2C9, which prefers acidic substrates.	Indomethacin	20-32	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
22943633-1	2013	AIM: The present study evaluated the possibility of drug interactions involving blueberry juice (BBJ) and substrate drugs whose clearance is dependent on cytochromes P4503A (CYP3A) and P4502C9 (CYP2C9).	blueberry juice	80-95	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	194-200
22943633-1	2013	AIM: The present study evaluated the possibility of drug interactions involving blueberry juice (BBJ) and substrate drugs whose clearance is dependent on cytochromes P4503A (CYP3A) and P4502C9 (CYP2C9).	epacadostat	97-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	194-200
22943633-2	2013	METHODS: A 50:50 mixture of lowbush and highbush BBJ was evaluated in vitro as an inhibitor of CYP3A activity (hydroxylation of triazolam and dealkylation of buspirone) and of CYP2C9 activity (flurbiprofen hydroxylation) using human liver microsomes.	epacadostat	49-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	176-182
22943633-4	2013	RESULTS: BBJ inhibited CYP3A and CYP2C9 activity in vitro, with 50% inhibitory concentrations (IC50 ) of less than 2%, but without evidence of mechanism-based (irreversible) inhibition.	epacadostat	9-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	33-39
22943633-9	2013	In the study of flurbiprofen (CYP2C9 substrate), the positive control inhibitor fluconazole significantly increased flurbiprofen AUC (GMR = 1.71), but BBJ had no significant effect (GMR = 1.03).	Flurbiprofen	16-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
22943633-9	2013	In the study of flurbiprofen (CYP2C9 substrate), the positive control inhibitor fluconazole significantly increased flurbiprofen AUC (GMR = 1.71), but BBJ had no significant effect (GMR = 1.03).	Fluconazole	80-91	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
22943633-9	2013	In the study of flurbiprofen (CYP2C9 substrate), the positive control inhibitor fluconazole significantly increased flurbiprofen AUC (GMR = 1.71), but BBJ had no significant effect (GMR = 1.03).	Flurbiprofen	116-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	30-36
23845193-6	2013	The complete inhibition of the CYP2C9 and CYP3A4 mediated metabolic pathway of glibenclamide through sorafenib might have resulted in a rapid accumulation of glibenclamide.	Glyburide	79-92	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
23845193-6	2013	The complete inhibition of the CYP2C9 and CYP3A4 mediated metabolic pathway of glibenclamide through sorafenib might have resulted in a rapid accumulation of glibenclamide.	Sorafenib	101-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
23845193-6	2013	The complete inhibition of the CYP2C9 and CYP3A4 mediated metabolic pathway of glibenclamide through sorafenib might have resulted in a rapid accumulation of glibenclamide.	Glyburide	158-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
22990331-0	2013	CYP2C9 and VKORC1 polymorphisms influence warfarin dose variability in patients on long-term anticoagulation.	Warfarin	42-50	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
22990331-1	2013	OBJECTIVES: The main aim of this study was to determine whether CYP2C9 and VKORC1 polymorphisms influence warfarin dose variability during initial dose-finding phase and during maintenance treatment after 360 days.	Warfarin	106-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
22990331-4	2013	RESULTS: During the first 30 days of anticoagulation, the relative variability of warfarin dose was significantly associated with CYP2C9*2 and CYP2C9*3 polymorphisms (p = 0.02) and with VKORC1 1639G &gt;A genotypes (p = 0.04).	Warfarin	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
22990331-4	2013	RESULTS: During the first 30 days of anticoagulation, the relative variability of warfarin dose was significantly associated with CYP2C9*2 and CYP2C9*3 polymorphisms (p = 0.02) and with VKORC1 1639G &gt;A genotypes (p = 0.04).	Warfarin	82-90	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	143-149
22990331-8	2013	CONCLUSIONS: Genetic information on CYP2C9 and VKORC1 is important both for the initial dose-finding phase and during maintenance treatment with warfarin.	Warfarin	145-153	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
23183958-2	2013	Single gene polymorphisms in cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1) have been shown to impact warfarin dosing in adults.	Warfarin	125-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	29-48
23380426-0	2013	Evaluation of the pharmacokinetic interaction between ticagrelor and tolbutamide, a cytochrome P450 2C9 substrate, in healthy volunteers.	Ticagrelor	54-64	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-103
23380426-0	2013	Evaluation of the pharmacokinetic interaction between ticagrelor and tolbutamide, a cytochrome P450 2C9 substrate, in healthy volunteers.	Tolbutamide	69-80	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-103
23380426-1	2013	OBJECTIVES: To assess the effect of ticagrelor on the pharmacokinetics of tolbutamide (a CYP2C9 substrate), and the effect of tolbutamide on ticagrelor pharmacokinetics.	Tolbutamide	74-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
23183958-2	2013	Single gene polymorphisms in cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1) have been shown to impact warfarin dosing in adults.	Warfarin	125-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	50-56
23376925-1	2013	Cytochrome P450 2C9 (CYP2C9) c.449G&gt;A (*8) is common in African Americans and is associated with decreased warfarin clearance.	Warfarin	110-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-19
23376925-1	2013	Cytochrome P450 2C9 (CYP2C9) c.449G&gt;A (*8) is common in African Americans and is associated with decreased warfarin clearance.	Warfarin	110-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-27
23376925-7	2013	These data suggest that promoter region polymorphisms inherited with 449G&gt;A decrease CYP2C9 expression and contribute to CYP2C9*8 effects on warfarin clearance and dose requirements.	Warfarin	144-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	88-94
23376925-7	2013	These data suggest that promoter region polymorphisms inherited with 449G&gt;A decrease CYP2C9 expression and contribute to CYP2C9*8 effects on warfarin clearance and dose requirements.	Warfarin	144-152	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	124-130
23556443-0	2013	Combining genetic variations in CYP2C9 and VKORC1 with clinical factors for warfarin dosing determination improved clinical effectiveness.	Warfarin	76-84	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
27536444-5	2013	METHODS: The ability of 4-AP to inhibit CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4/5 in a direct and time-dependent manner was evaluated using pooled human liver microsomes.	4-Aminopyridine	24-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
23298603-0	2013	The role of CYP2C9 polymorphisms in phenytoin-related cerebellar atrophy.	Phenytoin	36-45	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	12-18
23298603-2	2013	It is also known that a CYP2C9 mutation (*2 or *3) reduces phenytoin metabolism by 25-50% and can increase the risk of phenytoin-related side effects.	Phenytoin	59-68	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
23298603-2	2013	It is also known that a CYP2C9 mutation (*2 or *3) reduces phenytoin metabolism by 25-50% and can increase the risk of phenytoin-related side effects.	Phenytoin	119-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	24-30
23298603-8	2013	CONCLUSION: Our study is the first to report evidence linking CYP2C9 polymorphism and a reduction in cerebellar volume in epileptic users of phenytoin.	Phenytoin	141-150	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	62-68
23473641-0	2013	Effect of CYP2C9 and VKORC1 genetic polymorphisms on mean daily maintenance dose of acenocoumarol in South Indian patients.	Acenocoumarol	84-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
23473641-1	2013	AIM: To determine the effect of CYP2C9 and VKORC1 genetic polymorphisms on mean daily maintenance dose of acenocoumarol in South Indian patients with heart valve replacement.	Acenocoumarol	106-119	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	32-38
23473641-4	2013	RESULTS: Patients with at least one variant allele of CYP2C9 (*1*2 or *1*3) required 44% and 28.2% lower daily maintenance dose of acenocoumarol (2.0mg and 2.5mg, respectively) than the normal CYP2C9*1*1 genotype group (3.4mg) (p&lt;0.05).	Acenocoumarol	131-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
23473641-4	2013	RESULTS: Patients with at least one variant allele of CYP2C9 (*1*2 or *1*3) required 44% and 28.2% lower daily maintenance dose of acenocoumarol (2.0mg and 2.5mg, respectively) than the normal CYP2C9*1*1 genotype group (3.4mg) (p&lt;0.05).	Acenocoumarol	131-144	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	193-199
23473641-7	2013	The clinical (age, body mass index) and genetic variables (VKORC1-1639 G&gt;A, CYP2C9*2, CYP2C9*3) contribute together to predict 30.4% of the required maintenance dose of acenocoumarol.	Acenocoumarol	172-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
23473641-7	2013	The clinical (age, body mass index) and genetic variables (VKORC1-1639 G&gt;A, CYP2C9*2, CYP2C9*3) contribute together to predict 30.4% of the required maintenance dose of acenocoumarol.	Acenocoumarol	172-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	89-95
23473641-8	2013	CONCLUSION: The genetic polymorphisms of CYP2C9 and VKORC1 results in decreased requirement of daily maintenance dose of acenocoumarol.	Acenocoumarol	121-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	41-47
23153057-3	2013	The cocktail strategy (in situ incubation) was used to assess the induction of CYP1A2, CYP2B6, CYP2C9 and CYP3A4 by using the recommended probe substrate, i.e. phenacetin, bupropion, diclofenac and midazolam, respectively.	Bupropion	172-181	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
23153057-3	2013	The cocktail strategy (in situ incubation) was used to assess the induction of CYP1A2, CYP2B6, CYP2C9 and CYP3A4 by using the recommended probe substrate, i.e. phenacetin, bupropion, diclofenac and midazolam, respectively.	Diclofenac	183-193	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
23153057-3	2013	The cocktail strategy (in situ incubation) was used to assess the induction of CYP1A2, CYP2B6, CYP2C9 and CYP3A4 by using the recommended probe substrate, i.e. phenacetin, bupropion, diclofenac and midazolam, respectively.	Midazolam	198-207	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	95-101
23427827-6	2013	Fitting of the data with the Poole-Frenkel model indicates a correlation between the barrier height for electron transfer and the ease of CYP2C9-mediated metabolism of the bound substrates, though the spin state of iron is not well correlated.	Iron	215-219	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	138-144
23376975-2	2013	There is now a large body of published data showing that genotype for certain common polymorphisms in the genes encoding the target vitamin K epoxide reductase (G-1639A/C1173T) and the main metabolizing enzyme CYP2C9 (CYP2C9*2 and *3 alleles) are important determinants of the individual coumarin anticoagulant dose requirement.	coumarin	288-296	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	210-216
23376975-2	2013	There is now a large body of published data showing that genotype for certain common polymorphisms in the genes encoding the target vitamin K epoxide reductase (G-1639A/C1173T) and the main metabolizing enzyme CYP2C9 (CYP2C9*2 and *3 alleles) are important determinants of the individual coumarin anticoagulant dose requirement.	coumarin	288-296	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	218-224
23061746-8	2013	In our study, in addition to age, genetic variants of CYP2C9, VKORC1 and CYP4F2 were found to be significant predictor variables for the maintenance dose for warfarin, explaining 39.3% of dose variability.	Warfarin	158-166	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	54-60
23061746-0	2013	Impact of genetic factors (CYP2C9, VKORC1 and CYP4F2) on warfarin dose requirement in the Turkish population.	Warfarin	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	27-33
23061746-3	2013	The main objective of this study was to determine whether and to what extent variability in warfarin dose requirements was determined by polymorphisms in CYP2C9, VKORC1, CYP4F2 (rs2108622) and EPHX1 (rs2292566) in the Turkish population.	Warfarin	92-100	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	154-160
23159639-0	2013	The impact of the CYP2C9 and VKORC1 polymorphisms on acenocoumarol dose requirements in a Romanian population.	Acenocoumarol	53-66	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	18-24
23159639-10	2013	CONCLUSION: The stable therapeutic dose of acenocoumarol is dependent of patient"s age, the presence of the CYP2C9*3 allele and the c.-1639G&gt;A polymorphism of VKORC1.	Acenocoumarol	43-56	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	108-114
23826879-7	2013	Amitifadine was a moderate inhibitor of the human isoforms of the major drug metabolizing enzymes CYP2D6, CYP3A4, CYP2C9, and CYP2C19 (IC50 = 9 - 100 muM), but was a potent inhibitor of human CYP2B6 (IC50 = 1.8 muM).	1-(3,4-dichlorophenyl)-3-azabicyclo-(3.1.0)hexane hydrochloride	0-11	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
24329780-3	2013	The present study extends these findings by testing the hypothesis that CYP2C9- and 1A2-selective chemical inhibitors, sulfaphenazole (SFZ) and alpha-naphthoflavone (ANF), block oxidation of JWH-018 and AM2201 in human liver microsomes (HLM).	Sulfaphenazole	119-133	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
24329780-3	2013	The present study extends these findings by testing the hypothesis that CYP2C9- and 1A2-selective chemical inhibitors, sulfaphenazole (SFZ) and alpha-naphthoflavone (ANF), block oxidation of JWH-018 and AM2201 in human liver microsomes (HLM).	Sulfaphenazole	135-138	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
24329780-3	2013	The present study extends these findings by testing the hypothesis that CYP2C9- and 1A2-selective chemical inhibitors, sulfaphenazole (SFZ) and alpha-naphthoflavone (ANF), block oxidation of JWH-018 and AM2201 in human liver microsomes (HLM).	alpha-naphthoflavone	144-164	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
24329780-3	2013	The present study extends these findings by testing the hypothesis that CYP2C9- and 1A2-selective chemical inhibitors, sulfaphenazole (SFZ) and alpha-naphthoflavone (ANF), block oxidation of JWH-018 and AM2201 in human liver microsomes (HLM).	alpha-naphthoflavone	166-169	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
24329780-3	2013	The present study extends these findings by testing the hypothesis that CYP2C9- and 1A2-selective chemical inhibitors, sulfaphenazole (SFZ) and alpha-naphthoflavone (ANF), block oxidation of JWH-018 and AM2201 in human liver microsomes (HLM).	1-pentyl-3-(1-naphthoyl)indole	191-198	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
22855348-5	2013	The S-warfarin concentration was significantly higher in patients with CYP2C9*1/*3 than in those with *1/*1 (p &lt; 0.05).	Warfarin	6-14	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
22855348-8	2013	CONCLUSION: For low-dose warfarin treatment, the VKORC1-1639 G &gt; A and CYP2C9 genotype variations affected the pharmacokinetics and pharmacodynamics of warfarin, while we could not find significant effects of CYP4F2 or CYP2C19 genotype variations on warfarin (metabolite) concentrations or PT-INR.	Warfarin	25-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
22855348-8	2013	CONCLUSION: For low-dose warfarin treatment, the VKORC1-1639 G &gt; A and CYP2C9 genotype variations affected the pharmacokinetics and pharmacodynamics of warfarin, while we could not find significant effects of CYP4F2 or CYP2C19 genotype variations on warfarin (metabolite) concentrations or PT-INR.	Warfarin	155-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
22855348-8	2013	CONCLUSION: For low-dose warfarin treatment, the VKORC1-1639 G &gt; A and CYP2C9 genotype variations affected the pharmacokinetics and pharmacodynamics of warfarin, while we could not find significant effects of CYP4F2 or CYP2C19 genotype variations on warfarin (metabolite) concentrations or PT-INR.	Warfarin	155-163	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
23556337-0	2013	CYP2C9*3(1075A &gt; C), ABCB1 and SLCO1B1 genetic polymorphisms and gender are determinants of inter-subject variability in pitavastatin pharmacokinetics.	pitavastatin	124-136	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
23556337-6	2013	Compared to CYP2C9*1/*1 carriers, CYP2C9*1/*3 carriers had higher AUC(0-infinity) and Cmax of pitavastatin acid and AUC(0-infinity) of pitavastatin lactone (P&lt;0.05).	7-(2-Cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl)-3,5-dihydroxyhept-6-enoic acid	94-111	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
23556337-6	2013	Compared to CYP2C9*1/*1 carriers, CYP2C9*1/*3 carriers had higher AUC(0-infinity) and Cmax of pitavastatin acid and AUC(0-infinity) of pitavastatin lactone (P&lt;0.05).	pitavastatin	135-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
23102508-4	2013	Miltirone showed moderate inhibition on CYP1A2 (IC(50)=1.73 muM) and CYP2C9 (IC(50)=8.61 muM), and weak inhibition on CYP2D6 (IC(50)=30.20 muM) and CYP3A4 (IC(50)=33.88 muM).	miltirone	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
23102508-5	2013	Enzyme kinetic studies showed that miltirone competitively inhibited CYP2C9 (K(i)=1.48 muM), and displayed mixed type inhibitions on CYP1A2, CYP2D6 and CYP3A4 with K(i) values of 3.17 muM, 24.25 muM and 35.09 muM, respectively.	miltirone	35-44	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	69-75
23260576-8	2013	The monomethyl and dimethyl analogues were shown to have enhanced activity in terms of cytotoxicity, CYP2C9 inhibitory potency, and antiviral activity (up to 6-fold increased potency) compared to the parent compound, silybin B.	Ethane	19-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
22963393-7	2013	Cynomolgus CYP2C19 exhibits higher activity for DFOH than cynomolgus CYP2C9 although this reaction is a marker reaction of human CYP2C9.	dfoh	48-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-135
22963393-9	2013	Cynomolgus CYP2C76 metabolizes non-CYP2C substrates, 7-ethoxyresorufin (human CYP1A substrate) and bufuralol (human CYP2D6 substrate).	ethoxyresorufin	53-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-16
22963393-9	2013	Cynomolgus CYP2C76 metabolizes non-CYP2C substrates, 7-ethoxyresorufin (human CYP1A substrate) and bufuralol (human CYP2D6 substrate).	bufuralol	99-108	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-16
22837389-6	2013	Estradiol also increased enzyme activities of CYP2C9 and CYP2E1 without affecting the mRNA expression levels by unknown mechanisms.	Estradiol	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	46-52
23429588-4	2013	Treprostinil is primarily metabolized by cytochrome (CYP) P450 2C8 with minor contribution from CYP2C9.	treprostinil	0-12	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
23429588-5	2013	Sildenafil is metabolized by CYP3A4 with minor contribution from CYP2C9.	Sildenafil Citrate	0-10	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	65-71
22842957-0	2013	Effect of CYP2C9 and SLCO1B1 polymorphisms on the pharmacokinetics and pharmacodynamics of nateglinide in healthy Chinese male volunteers.	Nateglinide	91-102	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	10-16
22842957-2	2013	Our objective was to assess the association between CYP2C9 and SLCO1B1 polymorphisms and the metabolism of nateglinide in healthy Chinese male volunteers.	Nateglinide	107-118	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	52-58
22842957-6	2013	CYP2C9*3 and 521 T&gt;C polymorphisms were the significant predictors of the AUC(0- ) and CL/F of nateglinide (adjusted multiple R(2) = 34 % and 43 %, respectively) according to multiple linear regression analyses, but they have no significant association with changes in the blood glucose-lowering effect of nateglinide.	Nateglinide	98-109	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
22842957-7	2013	CONCLUSIONS: Both SLCO1B1 521 T&gt;C and the CYP2C9*3 polymorphisms can significantly affect the pharmacokinetics of nateglinide, but they could only partially explain the interindividual variability of plasma concentration of nateglinide.	Nateglinide	117-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
22855348-0	2013	Responsiveness to low-dose warfarin associated with genetic variants of VKORC1, CYP2C9, CYP2C19, and CYP4F2 in an Indonesian population.	Warfarin	27-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	80-86
22855348-1	2013	PURPOSE: The aim of this study was to assess the pharmacokinetics and pharmacodynamics of warfarin associated with genetic polymorphisms in VKORC1, CYP2C9, CYP2C19, and CYP4F2 in Indonesian patients treated with low-dose warfarin.	Warfarin	90-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	148-154
23159358-0	2013	Role of CYP2C9 polymorphism in phenytoin-related metabolic abnormalities and subclinical atherosclerosis in young adult epileptic patients.	Phenytoin	31-40	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	8-14
23159358-4	2013	The mean serum total triglyceride and LDL levels were significantly higher in the wild type gene subjects than in the CYP 2C9 polymorphism gene subjects.	Triglycerides	21-33	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	118-125
23276529-0	2013	Repeated bleeding complications during therapy with vitamin K antagonists in a patient with the VKORC1*2A and the CYP2C9*3/*3 alleles: genetic testing to support switching to new oral anticoagulants.	Vitamin K	52-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	114-120
22725836-2	2013	Previous in vitro studies indicate that curcuminoids and piperine (a black pepper derivative that enhances curcuminoid bioavailability) could inhibit human CYP3A, CYP2C9, UGT and SULT dependent drug metabolism.	curcuminoids	40-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-169
22725836-2	2013	Previous in vitro studies indicate that curcuminoids and piperine (a black pepper derivative that enhances curcuminoid bioavailability) could inhibit human CYP3A, CYP2C9, UGT and SULT dependent drug metabolism.	piperine	57-65	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-169
22725836-2	2013	Previous in vitro studies indicate that curcuminoids and piperine (a black pepper derivative that enhances curcuminoid bioavailability) could inhibit human CYP3A, CYP2C9, UGT and SULT dependent drug metabolism.	curcuminoid	40-51	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	163-169
23206182-2	2013	AIM: To determine the clinical effectiveness of CYP2D6, CYP3A4, CYP2C9/19, and UGT polymorphism on the steady-state plasma concentrations and therapeutic outcome of rivastigmine monotherapy and combination therapy in patients with Alzheimer"s disease.	Rivastigmine	165-177	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	64-70
23061746-9	2013	VKORC1 and CYP2C9 genotypes remain predictor variables of the warfarin dose, and we first found that CYP4F2 (rs2108622) contributes to dose variability in the Turkish population as well.	Warfarin	62-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17