PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
2578101-8	1985	The residual 7-OH-MTX tetraglutamate remained bound to a site with a molecular weight of approximately 25,000 to 35,000 as assessed by Bio-Gel P-60 analysis and could not be displaced by folic acid, 5-formyltetrahydrofolate, 7-OH-MTX, or the tetraglutamate of MTX.	7-hydroxymethotrexate	13-21	interferon induced protein with tetratricopeptide repeats 3	Homo sapiens	143-147
10385213-2	1999	The goals of this study were to determine the role of aldehyde oxidase in the metabolism of methotrexate to 7-hydroxymethotrexate in the liver and to study the effects of inhibitors and other substrates on the metabolism of methotrexate.	7-hydroxymethotrexate	108-129	aldehyde oxidase 1	Homo sapiens	54-70
10385213-5	1999	In-vitro aldehyde oxidase from the liver of man catalyses the oxidation of methotrexate to 7-hydroxymethotrexate, but the turnover is low.	7-hydroxymethotrexate	91-112	aldehyde oxidase 1	Homo sapiens	9-25
10385213-6	1999	However, formation of 7-hydroxy-methotrexate from all forms of methotrexate by the liver in guinea-pig and man was significantly inhibited in the presence of 100 microM menadione and chlorpromazine, potent inhibitors of aldehyde oxidase.	7-hydroxymethotrexate	22-44	aldehyde oxidase 1	Homo sapiens	220-236
10385213-10	1999	Although aldehyde oxidase is also responsible for some of this conversion, it is also possible that the closely related xanthine oxidase is responsible for the formation of 7-hydroxymethotrexate.	7-hydroxymethotrexate	173-194	aldehyde oxidase 1	Homo sapiens	9-25
8194163-2	1994	After only 5 h, the 7-OH-MTX-treated rats demonstrated 2.6-fold increases in serum creatinine values and 2-fold elevations in serum aspartate aminotransferase (ASAT) levels as compared with the controls.	7-hydroxymethotrexate	20-28	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	132-158
2244925-2	1990	We show that 7-hydroxymethotrexate and dideazafolates require the prior binding of dUMP or its fluorinated derivative FdUMP to bind to thymidylate synthase, as does methotrexate.	7-hydroxymethotrexate	13-34	thymidylate synthetase	Homo sapiens	135-155
2244925-6	1990	In the presence of FdUMP or dUMP, all the studied compounds except 7-hydroxymethotrexate exhibited a large negative enthalpy variation when binding to thymidylate synthase (from -44 to -91 kJ/mol).	7-hydroxymethotrexate	67-88	thymidylate synthetase	Homo sapiens	151-171
3502454-9	1987	These results confirm the protein binding of metabolite to serum albumin and may suggest that distribution of 7-hydroxy-methotrexate is different from unchanged drug or that the metabolite can be eliminated by another route, such as bile.	7-hydroxymethotrexate	110-132	albumin	Homo sapiens	65-72
6201178-1	1984	7-Hydroxymethotrexate, an important metabolite of methotrexate, is a substrate for folylpolyglutamate synthetase (FPGS) isolated from rat liver and several human leukemia cell lines.	7-hydroxymethotrexate	0-21	folylpolyglutamate synthase	Rattus norvegicus	83-112
6201178-1	1984	7-Hydroxymethotrexate, an important metabolite of methotrexate, is a substrate for folylpolyglutamate synthetase (FPGS) isolated from rat liver and several human leukemia cell lines.	7-hydroxymethotrexate	0-21	folylpolyglutamate synthase	Rattus norvegicus	114-118
6201178-4	1984	The pattern of polyglutamate products synthesized by rat liver FPGS was nearly identical with both 7-hydroxymethotrexate and methotrexate.	7-hydroxymethotrexate	99-120	folylpolyglutamate synthase	Rattus norvegicus	63-67
6956440-1	1982	The pharmacokinetics of methotrexate (MXT) and 7-hydroxymethotrexate (7-OH-MTX) has been studied in seven patients treated for osteosarcoma with up to 27 cycles of MTX at doses of 140-350 mg/kg of body weight.	7-hydroxymethotrexate	47-68	metaxin 1	Homo sapiens	75-78
6698654-1	1984	The pharmacokinetics of methotrexate and its metabolite, 7-hydroxymethotrexate (7-OH-MTX), were evaluated by a specific HPLC assay in patients receiving low dose (40 mg/m2) or high dose (750-1500 mg/m2) MTX.	7-hydroxymethotrexate	57-78	metaxin 1	Homo sapiens	85-88
6838652-2	1983	In order to explain the difference of inhibition of dihydrofolate reductase (DHFR) by methotrexate (MTX) and its metabolites 7-hydroxymethotrexate [7OH (MTX)] and polyglutamate derivatives [MTX (G1) and MTX (G2)], direct determinations of binding parameters to beef liver DHFR were performed.	7-hydroxymethotrexate	125-146	dihydrofolate reductase	Homo sapiens	52-75
6838652-2	1983	In order to explain the difference of inhibition of dihydrofolate reductase (DHFR) by methotrexate (MTX) and its metabolites 7-hydroxymethotrexate [7OH (MTX)] and polyglutamate derivatives [MTX (G1) and MTX (G2)], direct determinations of binding parameters to beef liver DHFR were performed.	7-hydroxymethotrexate	125-146	dihydrofolate reductase	Homo sapiens	77-81
31913347-3	2020	The latter was mainly metabolized by AOX to form hepatotoxic 7-hydroxymethotrexate (7-OH MTX).	7-hydroxymethotrexate	61-82	acyl-CoA oxidase 1	Rattus norvegicus	37-40
29618584-7	2018	Mrp2/3/4 alteration changed the distribution of MTX and 7OH MTX in plasma and tissues.	7-hydroxymethotrexate	56-63	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	0-4
30593388-7	2019	MTX is irreversibly hydroxylated to form 7-hydroxy methotrexate (7-OH-MTX) by aldehyde oxidase (EC 1.2.3.1) (AOX).	7-hydroxymethotrexate	41-63	aldehyde oxidase 1	Homo sapiens	78-94
30593388-7	2019	MTX is irreversibly hydroxylated to form 7-hydroxy methotrexate (7-OH-MTX) by aldehyde oxidase (EC 1.2.3.1) (AOX).	7-hydroxymethotrexate	41-63	acyl-CoA oxidase 1	Homo sapiens	109-112
30593388-7	2019	MTX is irreversibly hydroxylated to form 7-hydroxy methotrexate (7-OH-MTX) by aldehyde oxidase (EC 1.2.3.1) (AOX).	7-hydroxymethotrexate	65-73	aldehyde oxidase 1	Homo sapiens	78-94
30593388-7	2019	MTX is irreversibly hydroxylated to form 7-hydroxy methotrexate (7-OH-MTX) by aldehyde oxidase (EC 1.2.3.1) (AOX).	7-hydroxymethotrexate	65-73	acyl-CoA oxidase 1	Homo sapiens	109-112
30593388-16	2019	Our hypothesis is that in postmenopausal women with RA and osteoporosis treated with MTX and raloxifene, the inhibition of AOX with resultant decreased formation of 7-OH MTX; will increase MTX levels and improve MTX efficacy.	7-hydroxymethotrexate	165-173	acyl-CoA oxidase 1	Homo sapiens	123-126
19644884-7	2009	RESULTS: Folic acid inhibited aldehyde oxidase (AO), the enzyme that produces 7-OH-MTX, but folinic acid did not.	7-hydroxymethotrexate	78-86	aldehyde oxidase 1	Homo sapiens	30-46
21566011-2	2011	We have shown before that ABCC2, ABCC3, and ABCG2 together influence the pharmacokinetics of the anticancer and antirheumatic drug methotrexate (MTX) and its toxic metabolite 7-hydroxymethotrexate (7OH-MTX) after intravenous MTX administration.	7-hydroxymethotrexate	175-196	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	26-31
21566011-2	2011	We have shown before that ABCC2, ABCC3, and ABCG2 together influence the pharmacokinetics of the anticancer and antirheumatic drug methotrexate (MTX) and its toxic metabolite 7-hydroxymethotrexate (7OH-MTX) after intravenous MTX administration.	7-hydroxymethotrexate	175-196	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	33-38
21566011-2	2011	We have shown before that ABCC2, ABCC3, and ABCG2 together influence the pharmacokinetics of the anticancer and antirheumatic drug methotrexate (MTX) and its toxic metabolite 7-hydroxymethotrexate (7OH-MTX) after intravenous MTX administration.	7-hydroxymethotrexate	175-196	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	44-49
21566011-2	2011	We have shown before that ABCC2, ABCC3, and ABCG2 together influence the pharmacokinetics of the anticancer and antirheumatic drug methotrexate (MTX) and its toxic metabolite 7-hydroxymethotrexate (7OH-MTX) after intravenous MTX administration.	7-hydroxymethotrexate	198-205	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	26-31
21566011-2	2011	We have shown before that ABCC2, ABCC3, and ABCG2 together influence the pharmacokinetics of the anticancer and antirheumatic drug methotrexate (MTX) and its toxic metabolite 7-hydroxymethotrexate (7OH-MTX) after intravenous MTX administration.	7-hydroxymethotrexate	198-205	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	44-49
21841039-4	2011	The absence of Abcc2 caused a decrease in total clearance of MTX relative to WT mice at all dose levels yet was accompanied by compensatory increases in renal excretion and metabolism to 7-hydroxymethotrexate (7OH-MTX).	7-hydroxymethotrexate	187-208	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	15-20
21566011-7	2011	The absence of Abcc2 and/or Abcg2 also led to significantly increased liver and kidney levels of 7OH-MTX.	7-hydroxymethotrexate	97-104	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	15-20
21566011-7	2011	The absence of Abcc2 and/or Abcg2 also led to significantly increased liver and kidney levels of 7OH-MTX.	7-hydroxymethotrexate	97-104	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	28-33
19996279-0	2009	Abcc2 (Mrp2), Abcc3 (Mrp3), and Abcg2 (Bcrp1) are the main determinants for rapid elimination of methotrexate and its toxic metabolite 7-hydroxymethotrexate in vivo.	7-hydroxymethotrexate	135-156	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	0-5
19996279-0	2009	Abcc2 (Mrp2), Abcc3 (Mrp3), and Abcg2 (Bcrp1) are the main determinants for rapid elimination of methotrexate and its toxic metabolite 7-hydroxymethotrexate in vivo.	7-hydroxymethotrexate	135-156	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	7-11
19996279-0	2009	Abcc2 (Mrp2), Abcc3 (Mrp3), and Abcg2 (Bcrp1) are the main determinants for rapid elimination of methotrexate and its toxic metabolite 7-hydroxymethotrexate in vivo.	7-hydroxymethotrexate	135-156	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	14-19
19996279-0	2009	Abcc2 (Mrp2), Abcc3 (Mrp3), and Abcg2 (Bcrp1) are the main determinants for rapid elimination of methotrexate and its toxic metabolite 7-hydroxymethotrexate in vivo.	7-hydroxymethotrexate	135-156	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	21-25
19996279-0	2009	Abcc2 (Mrp2), Abcc3 (Mrp3), and Abcg2 (Bcrp1) are the main determinants for rapid elimination of methotrexate and its toxic metabolite 7-hydroxymethotrexate in vivo.	7-hydroxymethotrexate	135-156	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	32-37
19996279-0	2009	Abcc2 (Mrp2), Abcc3 (Mrp3), and Abcg2 (Bcrp1) are the main determinants for rapid elimination of methotrexate and its toxic metabolite 7-hydroxymethotrexate in vivo.	7-hydroxymethotrexate	135-156	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	39-44
19996279-7	2009	Furthermore, the urinary and fecal excretion of the nephrotoxic metabolite 7OH-MTX were increased 27- and 7-fold, respectively, in Abcc2;Abcc3;Abcg2-/- mice.	7-hydroxymethotrexate	75-82	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	131-136
19996279-7	2009	Furthermore, the urinary and fecal excretion of the nephrotoxic metabolite 7OH-MTX were increased 27- and 7-fold, respectively, in Abcc2;Abcc3;Abcg2-/- mice.	7-hydroxymethotrexate	75-82	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	137-142
19996279-7	2009	Furthermore, the urinary and fecal excretion of the nephrotoxic metabolite 7OH-MTX were increased 27- and 7-fold, respectively, in Abcc2;Abcc3;Abcg2-/- mice.	7-hydroxymethotrexate	75-82	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	143-148
19996279-8	2009	Thus, Abcc2, Abcc3, and Abcg2 together mediate the rapid elimination of MTX and 7OH-MTX after i.v.	7-hydroxymethotrexate	80-87	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	6-11
19996279-8	2009	Thus, Abcc2, Abcc3, and Abcg2 together mediate the rapid elimination of MTX and 7OH-MTX after i.v.	7-hydroxymethotrexate	80-87	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	13-18
19996279-8	2009	Thus, Abcc2, Abcc3, and Abcg2 together mediate the rapid elimination of MTX and 7OH-MTX after i.v.	7-hydroxymethotrexate	80-87	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	24-29
19644884-7	2009	RESULTS: Folic acid inhibited aldehyde oxidase (AO), the enzyme that produces 7-OH-MTX, but folinic acid did not.	7-hydroxymethotrexate	78-86	aldehyde oxidase 1	Homo sapiens	48-50
19088030-11	2008	7OH-MTX accumulated substantially in the liver of Abcc2(-/-) and especially Abcc2;Abcc3(-/-) mice.	7-hydroxymethotrexate	0-7	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	76-81
19383815-0	2009	Functionally overlapping roles of Abcg2 (Bcrp1) and Abcc2 (Mrp2) in the elimination of methotrexate and its main toxic metabolite 7-hydroxymethotrexate in vivo.	7-hydroxymethotrexate	130-151	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	34-39
19383815-0	2009	Functionally overlapping roles of Abcg2 (Bcrp1) and Abcc2 (Mrp2) in the elimination of methotrexate and its main toxic metabolite 7-hydroxymethotrexate in vivo.	7-hydroxymethotrexate	130-151	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	41-46
19383815-0	2009	Functionally overlapping roles of Abcg2 (Bcrp1) and Abcc2 (Mrp2) in the elimination of methotrexate and its main toxic metabolite 7-hydroxymethotrexate in vivo.	7-hydroxymethotrexate	130-151	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	52-57
19383815-0	2009	Functionally overlapping roles of Abcg2 (Bcrp1) and Abcc2 (Mrp2) in the elimination of methotrexate and its main toxic metabolite 7-hydroxymethotrexate in vivo.	7-hydroxymethotrexate	130-151	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	59-63
19383815-2	2009	We investigated the possibly overlapping roles of Abcg2 and Abcc2 in the elimination of the anticancer drug methotrexate (MTX) and its toxic metabolite 7-hydroxymethotrexate (7OH-MTX).	7-hydroxymethotrexate	152-173	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	50-55
19383815-2	2009	We investigated the possibly overlapping roles of Abcg2 and Abcc2 in the elimination of the anticancer drug methotrexate (MTX) and its toxic metabolite 7-hydroxymethotrexate (7OH-MTX).	7-hydroxymethotrexate	152-173	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	60-65
19383815-10	2009	We additionally found that in the absence of Abcc2, Abcg2 mediated substantial urinary excretion of MTX and 7OH-MTX.	7-hydroxymethotrexate	108-115	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	52-57
19383815-11	2009	CONCLUSIONS: Abcc2 and Abcg2 together are major determinants of MTX and 7OH-MTX pharmacokinetics.	7-hydroxymethotrexate	72-79	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	13-18
19383815-11	2009	CONCLUSIONS: Abcc2 and Abcg2 together are major determinants of MTX and 7OH-MTX pharmacokinetics.	7-hydroxymethotrexate	72-79	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	23-28
19426680-1	2009	In vitro treatment of human T-cell leukemia cells with 7-hydroxymethotrexate, the major metabolite of methotrexate resulted in acquired resistance as a result of the complete loss of folypolyglutamate synthetase (FPGS) activity.	7-hydroxymethotrexate	55-76	folylpolyglutamate synthase	Homo sapiens	213-217
19426680-5	2009	The dramatic loss of FPGS activity in 7-hydroxymethotrexate-resistant cells was associated with alterations in the expression of various genes aimed at preserving reduced folates and/or enhancing purine nucleotide biosynthesis, e.g. methylene tetrahydrofolate reductase, glycinamide ribonucleotide formyltransferase, adenosine deaminase, cystathionine beta synthase, as well as the ATP-dependent folate exporters BCRP/ABCG2 and MRP1/ABCC1.	7-hydroxymethotrexate	38-59	folylpolyglutamate synthase	Homo sapiens	21-25
19426680-5	2009	The dramatic loss of FPGS activity in 7-hydroxymethotrexate-resistant cells was associated with alterations in the expression of various genes aimed at preserving reduced folates and/or enhancing purine nucleotide biosynthesis, e.g. methylene tetrahydrofolate reductase, glycinamide ribonucleotide formyltransferase, adenosine deaminase, cystathionine beta synthase, as well as the ATP-dependent folate exporters BCRP/ABCG2 and MRP1/ABCC1.	7-hydroxymethotrexate	38-59	cystathionine beta-synthase	Homo sapiens	338-365
19426680-5	2009	The dramatic loss of FPGS activity in 7-hydroxymethotrexate-resistant cells was associated with alterations in the expression of various genes aimed at preserving reduced folates and/or enhancing purine nucleotide biosynthesis, e.g. methylene tetrahydrofolate reductase, glycinamide ribonucleotide formyltransferase, adenosine deaminase, cystathionine beta synthase, as well as the ATP-dependent folate exporters BCRP/ABCG2 and MRP1/ABCC1.	7-hydroxymethotrexate	38-59	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	413-417
19426680-5	2009	The dramatic loss of FPGS activity in 7-hydroxymethotrexate-resistant cells was associated with alterations in the expression of various genes aimed at preserving reduced folates and/or enhancing purine nucleotide biosynthesis, e.g. methylene tetrahydrofolate reductase, glycinamide ribonucleotide formyltransferase, adenosine deaminase, cystathionine beta synthase, as well as the ATP-dependent folate exporters BCRP/ABCG2 and MRP1/ABCC1.	7-hydroxymethotrexate	38-59	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	418-423
19426680-5	2009	The dramatic loss of FPGS activity in 7-hydroxymethotrexate-resistant cells was associated with alterations in the expression of various genes aimed at preserving reduced folates and/or enhancing purine nucleotide biosynthesis, e.g. methylene tetrahydrofolate reductase, glycinamide ribonucleotide formyltransferase, adenosine deaminase, cystathionine beta synthase, as well as the ATP-dependent folate exporters BCRP/ABCG2 and MRP1/ABCC1.	7-hydroxymethotrexate	38-59	ATP binding cassette subfamily C member 1	Homo sapiens	428-432
19426680-5	2009	The dramatic loss of FPGS activity in 7-hydroxymethotrexate-resistant cells was associated with alterations in the expression of various genes aimed at preserving reduced folates and/or enhancing purine nucleotide biosynthesis, e.g. methylene tetrahydrofolate reductase, glycinamide ribonucleotide formyltransferase, adenosine deaminase, cystathionine beta synthase, as well as the ATP-dependent folate exporters BCRP/ABCG2 and MRP1/ABCC1.	7-hydroxymethotrexate	38-59	ATP binding cassette subfamily C member 1	Homo sapiens	433-438
19088030-0	2008	Impact of Abcc2 (Mrp2) and Abcc3 (Mrp3) on the in vivo elimination of methotrexate and its main toxic metabolite 7-hydroxymethotrexate.	7-hydroxymethotrexate	113-134	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	10-15
19088030-0	2008	Impact of Abcc2 (Mrp2) and Abcc3 (Mrp3) on the in vivo elimination of methotrexate and its main toxic metabolite 7-hydroxymethotrexate.	7-hydroxymethotrexate	113-134	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	27-32
19088030-0	2008	Impact of Abcc2 (Mrp2) and Abcc3 (Mrp3) on the in vivo elimination of methotrexate and its main toxic metabolite 7-hydroxymethotrexate.	7-hydroxymethotrexate	113-134	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	34-38
19088030-9	2008	The plasma AUCi.v.s of 7OH-MTX were 6.0-fold and 4.3-fold increased in Abcc2(-/-) and Abcc2;Abcc3(-/-) mice, respectively, leading to increased urinary excretion.	7-hydroxymethotrexate	23-30	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	71-76
19088030-9	2008	The plasma AUCi.v.s of 7OH-MTX were 6.0-fold and 4.3-fold increased in Abcc2(-/-) and Abcc2;Abcc3(-/-) mice, respectively, leading to increased urinary excretion.	7-hydroxymethotrexate	23-30	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	86-91
19088030-9	2008	The plasma AUCi.v.s of 7OH-MTX were 6.0-fold and 4.3-fold increased in Abcc2(-/-) and Abcc2;Abcc3(-/-) mice, respectively, leading to increased urinary excretion.	7-hydroxymethotrexate	23-30	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	92-97
19088030-10	2008	The biliary excretion of 7OH-MTX was 5.8-fold reduced in Abcc2(-/-) but unchanged in Abcc2;Abcc3(-/-) mice.	7-hydroxymethotrexate	25-32	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	57-62
19088030-11	2008	7OH-MTX accumulated substantially in the liver of Abcc2(-/-) and especially Abcc2;Abcc3(-/-) mice.	7-hydroxymethotrexate	0-7	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	50-55
19088030-11	2008	7OH-MTX accumulated substantially in the liver of Abcc2(-/-) and especially Abcc2;Abcc3(-/-) mice.	7-hydroxymethotrexate	0-7	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	82-87
19088030-12	2008	CONCLUSIONS: Abcc2 is important for (biliary) excretion of MTX and its toxic metabolite 7OH-MTX.	7-hydroxymethotrexate	88-95	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	13-18
19088030-13	2008	When Abcc2 is absent, Abcc3 transports MTX and 7OH-MTX back from the liver into the circulation, leading to increased plasma levels and urinary excretion.	7-hydroxymethotrexate	47-54	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	5-10
19088030-13	2008	When Abcc2 is absent, Abcc3 transports MTX and 7OH-MTX back from the liver into the circulation, leading to increased plasma levels and urinary excretion.	7-hydroxymethotrexate	47-54	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	22-27
19088030-14	2008	Variation in ABCC2 and/or ABCC3 activity may therefore have profound effects on the elimination and severity of toxicity of MTX and 7OH-MTX after MTX treatment of patients.	7-hydroxymethotrexate	132-139	ATP binding cassette subfamily C member 2	Homo sapiens	13-18
19088030-14	2008	Variation in ABCC2 and/or ABCC3 activity may therefore have profound effects on the elimination and severity of toxicity of MTX and 7OH-MTX after MTX treatment of patients.	7-hydroxymethotrexate	132-139	ATP binding cassette subfamily C member 3	Homo sapiens	26-31
15868145-0	2005	Effects and interaction of 7-hydroxy methotrexate and methotrexate in leukaemic cells ex vivo measured by the thymidylate synthase inhibition assay.	7-hydroxymethotrexate	27-49	thymidylate synthetase	Homo sapiens	110-130
15868145-4	2005	However, a statistically significant increase of TS inhibition (p<0.05) was observed for a 1:1 mixture of MTX and 7-OH MTX as compared to the effect of MTX alone.	7-hydroxymethotrexate	117-125	thymidylate synthetase	Homo sapiens	49-51
12730515-6	2003	RESULTS: In the 30 patients, coadministration of CSA and MTX led to a 26% increase in mean peak plasma MTX concentration (P < 0.01), an 18% increase in the mean plasma MTX concentration area under the curve (AUC, P=0.01) and an 80% decrease in plasma 7-OH-MTX AUC (P < 0.01).	7-hydroxymethotrexate	254-262	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	49-52
12730515-7	2003	In 13 patients receiving a 10 mg MTX dose, CSA reduced urinary 7-OH-MTX excretion by 87% (P < 0.01) without altering MTX excretion.	7-hydroxymethotrexate	63-71	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	43-46
12730515-9	2003	CONCLUSION: CSA may block oxidation of MTX to its relatively inactive metabolite, 7-OH-MTX, thereby potentiating MTX efficacy.	7-hydroxymethotrexate	82-90	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	12-15
15313923-3	2004	We hypothesized that benzimidazoles interfere with the clearance of MTX and/or 7-hydroxymethotrexate by inhibition of the ATP-binding cassette drug transporters BCRP and/or MRP2, two transporters known to transport MTX and located in apical membranes of epithelia involved in drug disposition.	7-hydroxymethotrexate	79-100	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	161-165
15313923-3	2004	We hypothesized that benzimidazoles interfere with the clearance of MTX and/or 7-hydroxymethotrexate by inhibition of the ATP-binding cassette drug transporters BCRP and/or MRP2, two transporters known to transport MTX and located in apical membranes of epithelia involved in drug disposition.	7-hydroxymethotrexate	79-100	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	173-177