PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
2504855-4	1989	Apolipoprotein B concentrations were lowered by 25.4% (pravastatin) and 22.0% (gemfibrozil).	Gemfibrozil	79-90	apolipoprotein B	Homo sapiens	0-16
2504855-8	1989	Gemfibrozil, in contrast, increased HDL3 cholesterol level by 9% because of an enrichment of HDL3 particles in both free cholesterol and cholesteryl esters and lowered the flotation rate of HDL3 (p less than 0.05).	Gemfibrozil	0-11	HDL3	Homo sapiens	36-40
2504855-8	1989	Gemfibrozil, in contrast, increased HDL3 cholesterol level by 9% because of an enrichment of HDL3 particles in both free cholesterol and cholesteryl esters and lowered the flotation rate of HDL3 (p less than 0.05).	Gemfibrozil	0-11	HDL3	Homo sapiens	93-97
2504855-8	1989	Gemfibrozil, in contrast, increased HDL3 cholesterol level by 9% because of an enrichment of HDL3 particles in both free cholesterol and cholesteryl esters and lowered the flotation rate of HDL3 (p less than 0.05).	Gemfibrozil	0-11	HDL3	Homo sapiens	93-97
3477829-2	1987	Three antilipidemic drugs, clofibrate, bezafibrate, and gemfibrozil, two of which had previously been shown to reduce Hb/O2 affinity in vitro, were tested in mice for their ability to affect Hb/O2 affinity and to alter the radiosensitivity of the RIF-1 sarcoma.	Gemfibrozil	56-67	replication timing regulatory factor 1	Mus musculus	247-252
3164977-3	1988	Type III HLP reasserted itself following an 8-week interruption of gemfibrozil therapy.	Gemfibrozil	67-78	HLP	Homo sapiens	9-12
2917701-6	1989	Addition of lovastatin to gemfibrozil effectively reduced total cholesterol (25%), LDL-chol (30%), and LDL-apoB (19%).	Gemfibrozil	26-37	apolipoprotein B	Homo sapiens	107-111
3162679-7	1988	In animals receiving the standard diet, fenofibrate, gemfibrozil and nicotinic acid decreased the triglyceride (TG) level (-28%, -31%, and -38%) by lowering VLDL-TG (-37%, -42%, and -49%), fenofibrate and gemfibrozil increased HDL-cholesterol by 18% and 31%, respectively.	Gemfibrozil	53-64	CD320 antigen	Mus musculus	157-161
3162679-7	1988	In animals receiving the standard diet, fenofibrate, gemfibrozil and nicotinic acid decreased the triglyceride (TG) level (-28%, -31%, and -38%) by lowering VLDL-TG (-37%, -42%, and -49%), fenofibrate and gemfibrozil increased HDL-cholesterol by 18% and 31%, respectively.	Gemfibrozil	205-216	CD320 antigen	Mus musculus	157-161
3464282-0	1986	Gemfibrozil treatment and the relationship between HDL cholesterol and apoE distribution in cholesterol-fed rats.	Gemfibrozil	0-11	apolipoprotein E	Rattus norvegicus	71-75
3555908-0	1987	Normalization of lipoprotein lipase and hepatic lipase by gemfibrozil results in correction of lipoprotein abnormalities in chronic renal failure.	Gemfibrozil	58-69	lipoprotein lipase	Homo sapiens	17-35
3555908-0	1987	Normalization of lipoprotein lipase and hepatic lipase by gemfibrozil results in correction of lipoprotein abnormalities in chronic renal failure.	Gemfibrozil	58-69	lipase C, hepatic type	Homo sapiens	40-54
3923042-5	1985	Gemfibrozil significantly increased plasma HDL cholesterol, apolipoprotein (apo) AI, and apo AII by 36%, 29%, and 38% from base line, respectively.	Gemfibrozil	0-11	apolipoprotein A1	Homo sapiens	60-83
3081014-0	1986	Gemfibrozil increases both apo A-I and apo E concentrations.	Gemfibrozil	0-11	apolipoprotein A1	Rattus norvegicus	27-44
3081014-5	1986	Only gemfibrozil increased plasma apo E levels which are characteristically low in this rat model.	Gemfibrozil	5-16	apolipoprotein E	Rattus norvegicus	34-39
3862732-0	1985	Apolipoprotein changes associated with the plasma lipid-regulating activity of gemfibrozil in cholesterol-fed rats.	Gemfibrozil	79-90	apolipoprotein E	Rattus norvegicus	0-14
3862732-6	1985	Whole plasma apoE and apoA-I concentrations were decreased and apoB increased due to cholesterol feeding as determined by electroimmunoassay, but again gemfibrozil treatment prevented these diet-induced alterations.	Gemfibrozil	152-163	apolipoprotein E	Rattus norvegicus	13-17
3862732-6	1985	Whole plasma apoE and apoA-I concentrations were decreased and apoB increased due to cholesterol feeding as determined by electroimmunoassay, but again gemfibrozil treatment prevented these diet-induced alterations.	Gemfibrozil	152-163	apolipoprotein B	Rattus norvegicus	63-67
3862732-8	1985	Gemfibrozil lowered the concentration of both apoB variants and prevented the shift of apoE from HDL to lower density lipoproteins.	Gemfibrozil	0-11	apolipoprotein B	Rattus norvegicus	46-50
3862732-8	1985	Gemfibrozil lowered the concentration of both apoB variants and prevented the shift of apoE from HDL to lower density lipoproteins.	Gemfibrozil	0-11	apolipoprotein E	Rattus norvegicus	87-91
3862732-10	1985	These methods also revealed a shift of apoA-IV from HDL to the d greater than 1.21 g/ml, lipoprotein-free fraction with gemfibrozil treatment when blood was taken from fasted or postabsorptive animals.	Gemfibrozil	120-131	apolipoprotein A4	Rattus norvegicus	39-46
3862732-11	1985	Since it was also noted that in chow-fed rats more apoA-IV was present in the d greater than 1.21 g/ml fraction in the postabsorptive or fed state compared to fasted animals, it could be postulated that the shift of apoA-IV into this fraction in gemfibrozil-treated rats is related to an accelerated clearance of chylomicrons.	Gemfibrozil	246-257	apolipoprotein A4	Rattus norvegicus	51-58
3862732-11	1985	Since it was also noted that in chow-fed rats more apoA-IV was present in the d greater than 1.21 g/ml fraction in the postabsorptive or fed state compared to fasted animals, it could be postulated that the shift of apoA-IV into this fraction in gemfibrozil-treated rats is related to an accelerated clearance of chylomicrons.	Gemfibrozil	246-257	apolipoprotein A4	Rattus norvegicus	216-223
3923042-8	1985	Gemfibrozil increased synthetic rates of apo AI and apo AII by 27% and 34%, respectively, without changing the fractional catabolic rates.	Gemfibrozil	0-11	apolipoprotein A1	Homo sapiens	41-47
3923042-9	1985	Stimulation of apo AI and apo AII synthesis by gemfibrozil was associated with the appearance in plasma of smaller (and heavier) HDL particles as assessed by gradient gel electrophoresis and HDL composition.	Gemfibrozil	47-58	apolipoprotein A1	Homo sapiens	15-21
7018466-1	1981	The lipid lowering drug Gemfibrozil significantly increased the levels of HDL-apoproteins, apoA-I and apoA-II in a group of 20 Swedish hyperlipemic males who were given 1200 mg daily of the drug for 8 weeks and thereafter submitted to a 4 weeks placebo period.	Gemfibrozil	24-35	apolipoprotein A1	Homo sapiens	91-97
6188330-2	1982	During gemfibrozil use, plasma prekallikrein and kininogen were increased significantly while kallikrein inhibitors increased only slightly.	Gemfibrozil	7-18	kallikrein B1	Homo sapiens	24-44
6188330-2	1982	During gemfibrozil use, plasma prekallikrein and kininogen were increased significantly while kallikrein inhibitors increased only slightly.	Gemfibrozil	7-18	kallikrein related peptidase 4	Homo sapiens	34-44
3907298-2	1985	Gemfibrozil also produces increases in both Apo AI and AII, and in kininogen and prekallikrein.	Gemfibrozil	0-11	apolipoprotein A1	Homo sapiens	44-50
3907298-2	1985	Gemfibrozil also produces increases in both Apo AI and AII, and in kininogen and prekallikrein.	Gemfibrozil	0-11	NLR family pyrin domain containing 3	Homo sapiens	55-58
6867010-4	1983	Gemfibrozil at 250 mg/kg/day for 4 weeks increased catalase by 86%.	Gemfibrozil	0-11	catalase	Rattus norvegicus	51-59
7010929-11	1981	Apoprotein A-I remained unchanged, but A-II increased by 20% during gemfibrozil treatment.	Gemfibrozil	68-79	NLR family pyrin domain containing 3	Homo sapiens	39-43
7018466-1	1981	The lipid lowering drug Gemfibrozil significantly increased the levels of HDL-apoproteins, apoA-I and apoA-II in a group of 20 Swedish hyperlipemic males who were given 1200 mg daily of the drug for 8 weeks and thereafter submitted to a 4 weeks placebo period.	Gemfibrozil	24-35	apolipoprotein A2	Homo sapiens	102-109
190608-9	1976	The postheparin plasma lipoprotein lipase and hepatic lipase activities, determined separately by an immunochemical method, increased during four weeks of gemfibrozil treatment (+18.1% and +20.6% respectively), but neither of these changes was significantly correlated with the changes in any of the serum lipid or lipoprotein levels.	Gemfibrozil	155-166	lipoprotein lipase	Homo sapiens	23-41
190608-9	1976	The postheparin plasma lipoprotein lipase and hepatic lipase activities, determined separately by an immunochemical method, increased during four weeks of gemfibrozil treatment (+18.1% and +20.6% respectively), but neither of these changes was significantly correlated with the changes in any of the serum lipid or lipoprotein levels.	Gemfibrozil	155-166	lipase C, hepatic type	Homo sapiens	46-60
32997809-1	2021	AIMS: The strong cytochrome P450 (CYP) 2C8 inhibitor gemfibrozil has been demonstrated to increase the area under the plasma concentration-time curve from 0 to infinity (AUC0-  ) of ACT-333679, an active metabolite of selexipag, by 11-fold.	Gemfibrozil	53-64	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	17-42
32997809-2	2021	Similarly as gemfibrozil, the CYP2C8 inhibitor clopidogrel also increases clopidogrel increased ACT-333679 concentration by 1.9-fold after a single loading dose (300 mg once daily) and 2.7-fold after repeated treatment with the maintenance dose (75 mg once daily) in Europeans.	Gemfibrozil	13-24	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	30-36
33514677-9	2021	These findings highlight the importance of PPARalpha-dependent astroglial GDNF pathway in gemfibrozil-mediated protection of dopaminergic neurons in an animal model of PD and suggest possible therapeutic use of gemfibrozil in PD patients.SIGNIFICANCE STATEMENT:Increasing the level of glial cell-derived neurotrophic factor (GDNF) in the brain is important for the protection of dopamine neurons in Parkinson"s disease (PD).	Gemfibrozil	90-101	peroxisome proliferator activated receptor alpha	Homo sapiens	43-52
33514677-9	2021	These findings highlight the importance of PPARalpha-dependent astroglial GDNF pathway in gemfibrozil-mediated protection of dopaminergic neurons in an animal model of PD and suggest possible therapeutic use of gemfibrozil in PD patients.SIGNIFICANCE STATEMENT:Increasing the level of glial cell-derived neurotrophic factor (GDNF) in the brain is important for the protection of dopamine neurons in Parkinson"s disease (PD).	Gemfibrozil	90-101	glial cell derived neurotrophic factor	Homo sapiens	74-78
33514677-0	2021	Gemfibrozil Protects Dopaminergic Neurons in a Mouse Model of Parkinson"s disease via PPARalpha-Dependent Astrocytic GDNF Pathway.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	86-95
33514677-9	2021	These findings highlight the importance of PPARalpha-dependent astroglial GDNF pathway in gemfibrozil-mediated protection of dopaminergic neurons in an animal model of PD and suggest possible therapeutic use of gemfibrozil in PD patients.SIGNIFICANCE STATEMENT:Increasing the level of glial cell-derived neurotrophic factor (GDNF) in the brain is important for the protection of dopamine neurons in Parkinson"s disease (PD).	Gemfibrozil	211-222	peroxisome proliferator activated receptor alpha	Homo sapiens	43-52
33514677-0	2021	Gemfibrozil Protects Dopaminergic Neurons in a Mouse Model of Parkinson"s disease via PPARalpha-Dependent Astrocytic GDNF Pathway.	Gemfibrozil	0-11	glial cell line derived neurotrophic factor	Mus musculus	117-121
33514677-9	2021	These findings highlight the importance of PPARalpha-dependent astroglial GDNF pathway in gemfibrozil-mediated protection of dopaminergic neurons in an animal model of PD and suggest possible therapeutic use of gemfibrozil in PD patients.SIGNIFICANCE STATEMENT:Increasing the level of glial cell-derived neurotrophic factor (GDNF) in the brain is important for the protection of dopamine neurons in Parkinson"s disease (PD).	Gemfibrozil	211-222	glial cell derived neurotrophic factor	Homo sapiens	74-78
33514677-7	2021	Gemfibrozil-mediated protection of the nigrostriatal and locomotor activities in WT but not PPARalpha-/- mice from MPTP intoxication suggests that gemfibrozil needs the involvement of PPARalpha in protecting dopaminergic neurons.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	184-193
33514677-11	2021	Here, we delineate that gemfibrozil, a lipid-lowering drug, stimulates GDNF in astrocytes via peroxisome proliferator-activated receptor alpha (PPARalpha).	Gemfibrozil	24-35	glial cell derived neurotrophic factor	Homo sapiens	71-75
33514677-8	2021	While investigating further mechanisms, we found that gemfibrozil stimulated the transcription of glial-derived neurotrophic factor (GDNF) gene in astrocytes via PPARalpha and that gemfibrozil protected nigral neurons, normalized striatal fibers and neurotransmitters, and improved locomotor activities in MPTP-intoxicated Gfaf cre mice, but not Gdnf Deltaastro mice lacking GDNF in astrocytes.	Gemfibrozil	54-65	glial cell line derived neurotrophic factor	Mus musculus	133-137
33514677-11	2021	Here, we delineate that gemfibrozil, a lipid-lowering drug, stimulates GDNF in astrocytes via peroxisome proliferator-activated receptor alpha (PPARalpha).	Gemfibrozil	24-35	peroxisome proliferator activated receptor alpha	Mus musculus	94-142
33514677-8	2021	While investigating further mechanisms, we found that gemfibrozil stimulated the transcription of glial-derived neurotrophic factor (GDNF) gene in astrocytes via PPARalpha and that gemfibrozil protected nigral neurons, normalized striatal fibers and neurotransmitters, and improved locomotor activities in MPTP-intoxicated Gfaf cre mice, but not Gdnf Deltaastro mice lacking GDNF in astrocytes.	Gemfibrozil	54-65	peroxisome proliferator activated receptor alpha	Mus musculus	162-171
33514677-8	2021	While investigating further mechanisms, we found that gemfibrozil stimulated the transcription of glial-derived neurotrophic factor (GDNF) gene in astrocytes via PPARalpha and that gemfibrozil protected nigral neurons, normalized striatal fibers and neurotransmitters, and improved locomotor activities in MPTP-intoxicated Gfaf cre mice, but not Gdnf Deltaastro mice lacking GDNF in astrocytes.	Gemfibrozil	54-65	glial cell line derived neurotrophic factor	Mus musculus	346-350
33514677-8	2021	While investigating further mechanisms, we found that gemfibrozil stimulated the transcription of glial-derived neurotrophic factor (GDNF) gene in astrocytes via PPARalpha and that gemfibrozil protected nigral neurons, normalized striatal fibers and neurotransmitters, and improved locomotor activities in MPTP-intoxicated Gfaf cre mice, but not Gdnf Deltaastro mice lacking GDNF in astrocytes.	Gemfibrozil	54-65	glial cell line derived neurotrophic factor	Mus musculus	375-379
33514677-11	2021	Here, we delineate that gemfibrozil, a lipid-lowering drug, stimulates GDNF in astrocytes via peroxisome proliferator-activated receptor alpha (PPARalpha).	Gemfibrozil	24-35	peroxisome proliferator activated receptor alpha	Homo sapiens	144-153
33514677-8	2021	While investigating further mechanisms, we found that gemfibrozil stimulated the transcription of glial-derived neurotrophic factor (GDNF) gene in astrocytes via PPARalpha and that gemfibrozil protected nigral neurons, normalized striatal fibers and neurotransmitters, and improved locomotor activities in MPTP-intoxicated Gfaf cre mice, but not Gdnf Deltaastro mice lacking GDNF in astrocytes.	Gemfibrozil	181-192	glial cell line derived neurotrophic factor	Mus musculus	346-350
33514677-8	2021	While investigating further mechanisms, we found that gemfibrozil stimulated the transcription of glial-derived neurotrophic factor (GDNF) gene in astrocytes via PPARalpha and that gemfibrozil protected nigral neurons, normalized striatal fibers and neurotransmitters, and improved locomotor activities in MPTP-intoxicated Gfaf cre mice, but not Gdnf Deltaastro mice lacking GDNF in astrocytes.	Gemfibrozil	181-192	glial cell line derived neurotrophic factor	Mus musculus	375-379
33514677-12	2021	Moreover, gemfibrozil protected nigral neurons, normalized striatal fibers and neurotransmitters, and improved locomotor activities from MPTP toxicity via PPARalpha-dependent astroglial GDNF pathway.	Gemfibrozil	10-21	peroxisome proliferator activated receptor alpha	Homo sapiens	155-164
33514677-12	2021	Moreover, gemfibrozil protected nigral neurons, normalized striatal fibers and neurotransmitters, and improved locomotor activities from MPTP toxicity via PPARalpha-dependent astroglial GDNF pathway.	Gemfibrozil	10-21	glial cell derived neurotrophic factor	Homo sapiens	186-190
32708962-9	2020	Erythropoietin levels were increased in the serum of gemfibrozil-treated animals, and we also observed an increased expression of hypoxia-inducible factor-2 alpha (HIF-2alpha) and erythropoietin in renal tissue, while PPAR-alpha knockout mice treated with gemfibrozil did not present increased levels of serum erythropoietin or tissue HIF-2alpha and erythropoietin mRNA levels in the kidneys.	Gemfibrozil	53-64	erythropoietin	Mus musculus	310-324
32540489-0	2020	Gemfibrozil improves lipid metabolism in Nile tilapia Oreochromis niloticus fed a high-carbohydrate diet through peroxisome proliferator activated receptor-alpha activation.	Gemfibrozil	0-11	peroxisome proliferator-activated receptor alpha	Oreochromis niloticus	113-161
32540489-10	2020	This study indicates that gemfibrozil can improve lipid metabolism and maintain high antioxidant and anti-inflammatory capacity through activating PPARalpha in Nile tilapia fed a high carbohydrate diet.	Gemfibrozil	26-37	peroxisome proliferator-activated receptor alpha	Oreochromis niloticus	147-156
32708962-0	2020	Gemfibrozil Induces Anemia, Leukopenia and Reduces Hematopoietic Stem Cells via PPAR-alpha in Mice.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	80-90
32708962-4	2020	Gemfibrozil is a fibrate that acts via peroxisome proliferator-activated receptor alpha to promote changes in lipid metabolism and decrease serum triglyceride levels.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	39-87
32708962-9	2020	Erythropoietin levels were increased in the serum of gemfibrozil-treated animals, and we also observed an increased expression of hypoxia-inducible factor-2 alpha (HIF-2alpha) and erythropoietin in renal tissue, while PPAR-alpha knockout mice treated with gemfibrozil did not present increased levels of serum erythropoietin or tissue HIF-2alpha and erythropoietin mRNA levels in the kidneys.	Gemfibrozil	53-64	endothelial PAS domain protein 1	Mus musculus	335-345
32708962-6	2020	Considering that gemfibrozil may lead to anemia and that gemfibrozil acts via peroxisome proliferator-activated receptor alpha, we treated wild-type and peroxisome proliferator-activated receptor alpha-knockout mice with gemfibrozil for four consecutive days.	Gemfibrozil	57-68	peroxisome proliferator activated receptor alpha	Mus musculus	78-126
32708962-6	2020	Considering that gemfibrozil may lead to anemia and that gemfibrozil acts via peroxisome proliferator-activated receptor alpha, we treated wild-type and peroxisome proliferator-activated receptor alpha-knockout mice with gemfibrozil for four consecutive days.	Gemfibrozil	57-68	peroxisome proliferator activated receptor alpha	Mus musculus	78-126
32708962-8	2020	PPAR-alpha-knockout mice were capable of reversing all of those reduced parameters induced by gemfibrozil treatment.	Gemfibrozil	94-105	peroxisome proliferator activated receptor alpha	Mus musculus	0-10
32708962-9	2020	Erythropoietin levels were increased in the serum of gemfibrozil-treated animals, and we also observed an increased expression of hypoxia-inducible factor-2 alpha (HIF-2alpha) and erythropoietin in renal tissue, while PPAR-alpha knockout mice treated with gemfibrozil did not present increased levels of serum erythropoietin or tissue HIF-2alpha and erythropoietin mRNA levels in the kidneys.	Gemfibrozil	53-64	erythropoietin	Mus musculus	310-324
32708962-9	2020	Erythropoietin levels were increased in the serum of gemfibrozil-treated animals, and we also observed an increased expression of hypoxia-inducible factor-2 alpha (HIF-2alpha) and erythropoietin in renal tissue, while PPAR-alpha knockout mice treated with gemfibrozil did not present increased levels of serum erythropoietin or tissue HIF-2alpha and erythropoietin mRNA levels in the kidneys.	Gemfibrozil	256-267	erythropoietin	Mus musculus	0-14
32708962-9	2020	Erythropoietin levels were increased in the serum of gemfibrozil-treated animals, and we also observed an increased expression of hypoxia-inducible factor-2 alpha (HIF-2alpha) and erythropoietin in renal tissue, while PPAR-alpha knockout mice treated with gemfibrozil did not present increased levels of serum erythropoietin or tissue HIF-2alpha and erythropoietin mRNA levels in the kidneys.	Gemfibrozil	53-64	erythropoietin	Mus musculus	0-14
32708962-9	2020	Erythropoietin levels were increased in the serum of gemfibrozil-treated animals, and we also observed an increased expression of hypoxia-inducible factor-2 alpha (HIF-2alpha) and erythropoietin in renal tissue, while PPAR-alpha knockout mice treated with gemfibrozil did not present increased levels of serum erythropoietin or tissue HIF-2alpha and erythropoietin mRNA levels in the kidneys.	Gemfibrozil	256-267	endothelial PAS domain protein 1	Mus musculus	164-174
32708962-9	2020	Erythropoietin levels were increased in the serum of gemfibrozil-treated animals, and we also observed an increased expression of hypoxia-inducible factor-2 alpha (HIF-2alpha) and erythropoietin in renal tissue, while PPAR-alpha knockout mice treated with gemfibrozil did not present increased levels of serum erythropoietin or tissue HIF-2alpha and erythropoietin mRNA levels in the kidneys.	Gemfibrozil	53-64	endothelial PAS domain protein 1	Mus musculus	130-162
32708962-9	2020	Erythropoietin levels were increased in the serum of gemfibrozil-treated animals, and we also observed an increased expression of hypoxia-inducible factor-2 alpha (HIF-2alpha) and erythropoietin in renal tissue, while PPAR-alpha knockout mice treated with gemfibrozil did not present increased levels of serum erythropoietin or tissue HIF-2alpha and erythropoietin mRNA levels in the kidneys.	Gemfibrozil	53-64	endothelial PAS domain protein 1	Mus musculus	164-174
32708962-11	2020	Here, we show for the first time that gemfibrozil treatment leads to anemia and leukopenia via peroxisome proliferator-activated receptor alpha in mice.	Gemfibrozil	38-49	peroxisome proliferator activated receptor alpha	Mus musculus	95-143
32708962-9	2020	Erythropoietin levels were increased in the serum of gemfibrozil-treated animals, and we also observed an increased expression of hypoxia-inducible factor-2 alpha (HIF-2alpha) and erythropoietin in renal tissue, while PPAR-alpha knockout mice treated with gemfibrozil did not present increased levels of serum erythropoietin or tissue HIF-2alpha and erythropoietin mRNA levels in the kidneys.	Gemfibrozil	53-64	erythropoietin	Mus musculus	180-194
32708962-9	2020	Erythropoietin levels were increased in the serum of gemfibrozil-treated animals, and we also observed an increased expression of hypoxia-inducible factor-2 alpha (HIF-2alpha) and erythropoietin in renal tissue, while PPAR-alpha knockout mice treated with gemfibrozil did not present increased levels of serum erythropoietin or tissue HIF-2alpha and erythropoietin mRNA levels in the kidneys.	Gemfibrozil	53-64	peroxisome proliferator activated receptor alpha	Mus musculus	218-228
32155958-5	2020	Notably, administration of gemfibrozil (GEM), a PPARalpha activator, significantly reduced the in vivo Mabc load and inflammatory response in mice.	Gemfibrozil	27-38	peroxisome proliferator activated receptor alpha	Mus musculus	48-57
32155958-5	2020	Notably, administration of gemfibrozil (GEM), a PPARalpha activator, significantly reduced the in vivo Mabc load and inflammatory response in mice.	Gemfibrozil	40-43	peroxisome proliferator activated receptor alpha	Mus musculus	48-57
30898012-6	2020	We found that pharmacological activation of PPARA by the PPARA agonists gemfibrozil and Wy14643 induces autophagy in human microglia (HM) cells and U251 human glioma cells stably expressing the human APP (amyloid beta precursor protein) mutant (APP-p.M671L) and this effect is PPARA-dependent.	Gemfibrozil	72-83	peroxisome proliferator activated receptor alpha	Homo sapiens	44-49
31287236-2	2020	A 3-arm, open-label, randomized, single-dose, fixed-sequence crossover study was conducted to characterize the effects of the strong inhibitors gemfibrozil (of CYP2C8) and itraconazole (of CYP3A) and the strong inducer rifampin (of CYP3A) on the single-dose pharmacokinetics of brigatinib.	Gemfibrozil	144-155	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	160-166
31963528-7	2020	Conversely, gemfibrozil, an agonist of PPARalpha, elicited the increase of PPARalpha, OCT-2, and MATE-1 expression by 115%, 144%, and 376%, respectively.	Gemfibrozil	12-23	peroxisome proliferator activated receptor alpha	Mus musculus	39-48
31963528-7	2020	Conversely, gemfibrozil, an agonist of PPARalpha, elicited the increase of PPARalpha, OCT-2, and MATE-1 expression by 115%, 144%, and 376%, respectively.	Gemfibrozil	12-23	peroxisome proliferator activated receptor alpha	Mus musculus	75-84
31963528-7	2020	Conversely, gemfibrozil, an agonist of PPARalpha, elicited the increase of PPARalpha, OCT-2, and MATE-1 expression by 115%, 144%, and 376%, respectively.	Gemfibrozil	12-23	POU domain, class 2, transcription factor 2	Mus musculus	86-91
31963528-7	2020	Conversely, gemfibrozil, an agonist of PPARalpha, elicited the increase of PPARalpha, OCT-2, and MATE-1 expression by 115%, 144%, and 376%, respectively.	Gemfibrozil	12-23	solute carrier family 47, member 1	Mus musculus	97-103
31926091-9	2020	Drug interactions may occur in patients who use premixed insulin with glimepiride, lisinopril, fenofibrate, candesartan, irbesartan, and gemfibrozil.	Gemfibrozil	137-148	insulin	Homo sapiens	57-64
30898012-6	2020	We found that pharmacological activation of PPARA by the PPARA agonists gemfibrozil and Wy14643 induces autophagy in human microglia (HM) cells and U251 human glioma cells stably expressing the human APP (amyloid beta precursor protein) mutant (APP-p.M671L) and this effect is PPARA-dependent.	Gemfibrozil	72-83	peroxisome proliferator activated receptor alpha	Homo sapiens	57-62
30898012-6	2020	We found that pharmacological activation of PPARA by the PPARA agonists gemfibrozil and Wy14643 induces autophagy in human microglia (HM) cells and U251 human glioma cells stably expressing the human APP (amyloid beta precursor protein) mutant (APP-p.M671L) and this effect is PPARA-dependent.	Gemfibrozil	72-83	peroxisome proliferator activated receptor alpha	Homo sapiens	57-62
30898012-9	2020	These results indicated that PPARA is an important factor regulating autophagy in the clearance of Abeta and suggested gemfibrozil be assessed as a possible treatment for AD.	Gemfibrozil	119-130	peroxisome proliferator activated receptor alpha	Homo sapiens	29-34
30074417-0	2019	Combined gemfibrozil (peroxisome proliferator-activated receptor alpha agonist) with reduced steroid dose gives a similar management picture as the full steroid dose in a rat adjuvant-induced arthritis model.	Gemfibrozil	9-20	peroxisome proliferator activated receptor alpha	Rattus norvegicus	22-70
31127527-5	2019	Our mRNA analyses followed by different immunoassays clearly indicated that PPARalpha agonist gemfibrozil strongly upregulated the expression of Nurr1 in wild-type, but not PPARalpha-/-, DA neurons.	Gemfibrozil	94-105	peroxisome proliferator activated receptor alpha	Mus musculus	76-85
31127527-5	2019	Our mRNA analyses followed by different immunoassays clearly indicated that PPARalpha agonist gemfibrozil strongly upregulated the expression of Nurr1 in wild-type, but not PPARalpha-/-, DA neurons.	Gemfibrozil	94-105	nuclear receptor subfamily 4, group A, member 2	Mus musculus	145-150
31127527-7	2019	Finally, oral administration of gemfibrozil increased Nurr1 expression in vivo in nigra of wild-type, but not PPARalpha-/-, mice identifying PPARalpha as a novel regulator of Nurr1 expression and associated protection of DA neurons.	Gemfibrozil	32-43	nuclear receptor subfamily 4, group A, member 2	Mus musculus	54-59
31127527-7	2019	Finally, oral administration of gemfibrozil increased Nurr1 expression in vivo in nigra of wild-type, but not PPARalpha-/-, mice identifying PPARalpha as a novel regulator of Nurr1 expression and associated protection of DA neurons.	Gemfibrozil	32-43	peroxisome proliferator activated receptor alpha	Mus musculus	141-150
31127527-7	2019	Finally, oral administration of gemfibrozil increased Nurr1 expression in vivo in nigra of wild-type, but not PPARalpha-/-, mice identifying PPARalpha as a novel regulator of Nurr1 expression and associated protection of DA neurons.	Gemfibrozil	32-43	nuclear receptor subfamily 4, group A, member 2	Mus musculus	175-180
31357780-12	2019	Four drugs (gemfibrozil, bezafibrate, omega-3 carboxylic acid and glycyrrhizic acid) were screened by L1000 and DrugBank to activate lipoprotein lipase.	Gemfibrozil	12-23	lipoprotein lipase	Homo sapiens	133-151
31129789-0	2019	Physiologically Based Pharmacokinetic Models for Prediction of Complex CYP2C8 and OATP1B1 (SLCO1B1) Drug-Drug-Gene Interactions: A Modeling Network of Gemfibrozil, Repaglinide, Pioglitazone, Rifampicin, Clarithromycin and Itraconazole.	Gemfibrozil	151-162	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	71-77
31129789-0	2019	Physiologically Based Pharmacokinetic Models for Prediction of Complex CYP2C8 and OATP1B1 (SLCO1B1) Drug-Drug-Gene Interactions: A Modeling Network of Gemfibrozil, Repaglinide, Pioglitazone, Rifampicin, Clarithromycin and Itraconazole.	Gemfibrozil	151-162	solute carrier organic anion transporter family member 1B1	Homo sapiens	82-89
31129789-0	2019	Physiologically Based Pharmacokinetic Models for Prediction of Complex CYP2C8 and OATP1B1 (SLCO1B1) Drug-Drug-Gene Interactions: A Modeling Network of Gemfibrozil, Repaglinide, Pioglitazone, Rifampicin, Clarithromycin and Itraconazole.	Gemfibrozil	151-162	solute carrier organic anion transporter family member 1B1	Homo sapiens	91-98
31129789-5	2019	METHODS: PBPK models of the CYP2C8 and organic-anion-transporting polypeptide (OATP) 1B1 perpetrator drug gemfibrozil (parent-metabolite model) and the CYP2C8 victim drugs repaglinide (also an OATP1B1 substrate) and pioglitazone were developed using a total of 103 clinical studies.	Gemfibrozil	106-117	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	28-34
31129789-5	2019	METHODS: PBPK models of the CYP2C8 and organic-anion-transporting polypeptide (OATP) 1B1 perpetrator drug gemfibrozil (parent-metabolite model) and the CYP2C8 victim drugs repaglinide (also an OATP1B1 substrate) and pioglitazone were developed using a total of 103 clinical studies.	Gemfibrozil	106-117	solute carrier organic anion transporter family member 1B1	Homo sapiens	39-88
31129789-5	2019	METHODS: PBPK models of the CYP2C8 and organic-anion-transporting polypeptide (OATP) 1B1 perpetrator drug gemfibrozil (parent-metabolite model) and the CYP2C8 victim drugs repaglinide (also an OATP1B1 substrate) and pioglitazone were developed using a total of 103 clinical studies.	Gemfibrozil	106-117	solute carrier organic anion transporter family member 1B1	Homo sapiens	193-200
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	solute carrier organic anion transporter family member 1B1	Homo sapiens	115-122
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
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 8	Homo sapiens	143-149
31259309-0	2019	Gemfibrozil, a Lipid-Lowering Drug, Lowers Amyloid Plaque Pathology and Enhances Memory in a Mouse Model of Alzheimer"s Disease via Peroxisome Proliferator-Activated Receptor alpha.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	132-180
31259309-6	2019	Finally, we delineate that gemfibrozil requires the transcription factor peroxisome proliferator-activated receptor alpha (PPARalpha) to exhibit its amyloid lowering and memory enhancing effects in 5XFAD mice.	Gemfibrozil	27-38	peroxisome proliferator activated receptor alpha	Mus musculus	73-121
31259309-6	2019	Finally, we delineate that gemfibrozil requires the transcription factor peroxisome proliferator-activated receptor alpha (PPARalpha) to exhibit its amyloid lowering and memory enhancing effects in 5XFAD mice.	Gemfibrozil	27-38	peroxisome proliferator activated receptor alpha	Mus musculus	123-132
29240983-6	2018	The formation of CAG was significantly inhibited by azidothymidine and gemfibrozil (well-characterized UGT2B7 substrates) in a concentration-dependent manner, or by fluconazole (a typical UGT2B7-selective inhibitor) in a time-dependent manner, for both HLMs and rUGT2B7, respectively.	Gemfibrozil	71-82	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	103-109
30500419-6	2019	Moreover, CS-induced (sub-chronic) ceramide-accumulation was significantly (p < 0.05) reduced by treatment with TFEB/autophagy-inducing drug, gemfibrozil (GEM), suggesting that autophagy regulates CS-induced ceramide-accumulation.	Gemfibrozil	142-153	transcription factor EB	Homo sapiens	112-116
30500419-6	2019	Moreover, CS-induced (sub-chronic) ceramide-accumulation was significantly (p < 0.05) reduced by treatment with TFEB/autophagy-inducing drug, gemfibrozil (GEM), suggesting that autophagy regulates CS-induced ceramide-accumulation.	Gemfibrozil	155-158	transcription factor EB	Homo sapiens	112-116
30260990-0	2018	Testing the PPAR hypothesis of tobacco use disorder in humans: A randomized trial of the impact of gemfibrozil (a partial PPARalpha agonist) in smokers.	Gemfibrozil	99-110	peroxisome proliferator activated receptor alpha	Homo sapiens	122-131
30260990-2	2018	Our goal was to investigate the potential of gemfibrozil, a PPARalpha agonist, on reducing tobacco smoking in humans.	Gemfibrozil	45-56	peroxisome proliferator activated receptor alpha	Homo sapiens	60-69
30023335-1	2018	Purpose: Gemfibrozil (GEM) apart from agonist activity at peroxisome proliferator-activated receptor-alpha (PPAR-alpha) has antioxidant and anti-inflammatory properties.	Gemfibrozil	9-20	peroxisome proliferator activated receptor alpha	Mus musculus	108-118
30023335-8	2018	Results: GEM led to significant decrease in serum ALT and AST activities and increase in catalase activity and hepatic GSH level and reduces malondialdehyde and ROS levels in the liver tissue.	Gemfibrozil	9-12	glutamic pyruvic transaminase, soluble	Mus musculus	50-53
30023335-8	2018	Results: GEM led to significant decrease in serum ALT and AST activities and increase in catalase activity and hepatic GSH level and reduces malondialdehyde and ROS levels in the liver tissue.	Gemfibrozil	9-12	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	58-61
29662003-9	2018	The PPAR system thus offers an important hope in the management of atherogenic dyslipidemias, although concerns regarding potential adverse events such as the rise of plasma creatinine, gallstone formation, drug-drug interactions (i.e., gemfibrozil) and myopathy should also be acknowledged.	Gemfibrozil	237-248	peroxisome proliferator activated receptor alpha	Homo sapiens	4-8
30630815-0	2019	Clopidogrel and Gemfibrozil Strongly Inhibit the CYP2C8-Dependent Formation of 3-Hydroxydesloratadine and Increase Desloratadine Exposure In Humans.	Gemfibrozil	16-27	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	49-55
30630815-3	2019	Glucuronide metabolites of clopidogrel and gemfibrozil act as time-dependent inhibitors of CYP2C8, but they have not been compared clinically.	Gemfibrozil	43-54	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	91-97
30680004-0	2019	Gemfibrozil reduces lipid accumulation in SMMC-7721 cells via the involvement of PPARalpha and SREBP1.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Homo sapiens	81-90
30680004-0	2019	Gemfibrozil reduces lipid accumulation in SMMC-7721 cells via the involvement of PPARalpha and SREBP1.	Gemfibrozil	0-11	sterol regulatory element binding transcription factor 1	Homo sapiens	95-101
30680004-6	2019	Upregulation of peroxisome proliferator-activated receptor alpha (PPARalpha) protein and sterol regulatory element-binding protein 1 (SREBP1) was detected following treatment with GEM.	Gemfibrozil	180-183	peroxisome proliferator activated receptor alpha	Homo sapiens	16-64
30680004-6	2019	Upregulation of peroxisome proliferator-activated receptor alpha (PPARalpha) protein and sterol regulatory element-binding protein 1 (SREBP1) was detected following treatment with GEM.	Gemfibrozil	180-183	peroxisome proliferator activated receptor alpha	Homo sapiens	66-75
30680004-6	2019	Upregulation of peroxisome proliferator-activated receptor alpha (PPARalpha) protein and sterol regulatory element-binding protein 1 (SREBP1) was detected following treatment with GEM.	Gemfibrozil	180-183	sterol regulatory element binding transcription factor 1	Homo sapiens	89-132
30680004-6	2019	Upregulation of peroxisome proliferator-activated receptor alpha (PPARalpha) protein and sterol regulatory element-binding protein 1 (SREBP1) was detected following treatment with GEM.	Gemfibrozil	180-183	sterol regulatory element binding transcription factor 1	Homo sapiens	134-140
30251457-3	2018	METHODS: In this study, wild-type and Ppara-null mice fed a medium-fat diet (MFD) were administered gemfibrozil and fenofibrate for 3 months respectively, to explore the effect and action mechanism.	Gemfibrozil	100-111	peroxisome proliferator activated receptor alpha	Mus musculus	38-43
30251457-6	2018	The STAT3 pathway was activated in adipose and hepatic tissues in positive control, and inhibited in groups treated with gemfibrozil and fenofibrate.	Gemfibrozil	121-132	signal transducer and activator of transcription 3	Mus musculus	4-9
30335192-10	2018	In the tDDI verification, the model reasonably predicted pravastatin tDDI caused by rifampicin and gemfibrozil OATP1B1/3 inhibition but under-predicted tDDI caused by cyclosporine.	Gemfibrozil	99-110	solute carrier organic anion transporter family member 1B1	Homo sapiens	111-118
29864903-6	2018	The data suggest that combined treatment with EPA and ATM is beneficial to endothelial function and was unique to EPA and ATM since similar improvements could not be recapitulated by substituting another O3FA docosahexaenoic acid (DHA) or other TG-lowering agents such as fenofibrate, niacin, or gemfibrozil.	Gemfibrozil	296-307	ATM serine/threonine kinase	Homo sapiens	54-57
29712725-8	2018	The DDIs were then simulated using the established PBPK models with previously obtained in vitro inhibition constants of CsA or GEM/GEM-glu against the OATP1B1 and cytochrome P450s.	Gemfibrozil	128-131	solute carrier organic anion transporter family member 1B1	Homo sapiens	152-159
29534628-0	2018	Gemfibrozil has antidepressant effects in mice: Involvement of the hippocampal brain-derived neurotrophic factor system.	Gemfibrozil	0-11	brain derived neurotrophic factor	Mus musculus	79-112
29534628-3	2018	Besides being a lipid-regulating agent, gemfibrozil is an agonist of peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	Gemfibrozil	40-51	peroxisome proliferator activated receptor alpha	Mus musculus	69-117
29534628-3	2018	Besides being a lipid-regulating agent, gemfibrozil is an agonist of peroxisome proliferator-activated receptor-alpha (PPAR-alpha).	Gemfibrozil	40-51	peroxisome proliferator activated receptor alpha	Homo sapiens	119-129
29534628-5	2018	The changes in brain-derived neurotrophic factor (BDNF) signaling cascade in the brain after CUMS and gemfibrozil treatment were further assessed.	Gemfibrozil	102-113	brain derived neurotrophic factor	Mus musculus	50-54
29534628-9	2018	Gemfibrozil treatment also restored CUMS-induced inhibition of the hippocampal BDNF signaling pathway.	Gemfibrozil	0-11	brain derived neurotrophic factor	Mus musculus	79-83
29534628-10	2018	Blocking PPAR-alpha and BDNF but not the serotonergic system abolished the antidepressant effects of gemfibrozil on mice.	Gemfibrozil	101-112	peroxisome proliferator activated receptor alpha	Mus musculus	9-19
29534628-10	2018	Blocking PPAR-alpha and BDNF but not the serotonergic system abolished the antidepressant effects of gemfibrozil on mice.	Gemfibrozil	101-112	brain derived neurotrophic factor	Mus musculus	24-28
29534628-11	2018	Gemfibrozil produced antidepressant effects in mice by promoting the hippocampal BDNF system.	Gemfibrozil	0-11	brain derived neurotrophic factor	Mus musculus	81-85
29240983-6	2018	The formation of CAG was significantly inhibited by azidothymidine and gemfibrozil (well-characterized UGT2B7 substrates) in a concentration-dependent manner, or by fluconazole (a typical UGT2B7-selective inhibitor) in a time-dependent manner, for both HLMs and rUGT2B7, respectively.	Gemfibrozil	71-82	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	188-194
29240983-6	2018	The formation of CAG was significantly inhibited by azidothymidine and gemfibrozil (well-characterized UGT2B7 substrates) in a concentration-dependent manner, or by fluconazole (a typical UGT2B7-selective inhibitor) in a time-dependent manner, for both HLMs and rUGT2B7, respectively.	Gemfibrozil	71-82	UDP glucuronosyltransferase family 2 member B7	Rattus norvegicus	262-269
28444890-2	2017	Prescribing information for VIEKIRA PAK contraindicates gemfibrozil, a strong CYP2C8 inhibitor, because coadministration significantly increases dasabuvir exposures, which may increase the risk of QT prolongation.	Gemfibrozil	56-67	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	78-84
28653847-5	2017	As interaction perpetrators with CYP2C8, glucuronides of gemfibrozil and clopidogrel showed marked clinical drug-drug interactions (e.g., with cerivastatin and repaglinide), which are more than expected from the parent drug.	Gemfibrozil	57-68	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	33-39
29874752-7	2018	In this study, there was significant induction of CYP19A2 in individual exposures of diltiazem, fluoxetine, gemfibrozil and metformin at concentrations measured in Lake Michigan.	Gemfibrozil	108-119	cytochrome P450, family 19, subfamily A, polypeptide 1b	Danio rerio	50-57
28752027-3	2017	PPARs constitute a recognized druggable target and indeed several classes of drugs used in the treatment of metabolic disease symptoms, such as dyslipidemia (fibrates, e.g. fenofibrate and gemfibrozil) and diabetes (thiazolidinediones, e.g. rosiglitazone and pioglitazone) are ligands for the various PPAR isoforms.	Gemfibrozil	189-200	peroxisome proliferator activated receptor alpha	Homo sapiens	0-4
28374976-0	2017	Peroxisome Proliferator-Activated Receptor alpha Activation Suppresses Cytochrome P450 Induction Potential in Mice Treated with Gemfibrozil.	Gemfibrozil	128-139	peroxisome proliferator activated receptor alpha	Mus musculus	0-48
28374976-0	2017	Peroxisome Proliferator-Activated Receptor alpha Activation Suppresses Cytochrome P450 Induction Potential in Mice Treated with Gemfibrozil.	Gemfibrozil	128-139	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	71-86
28374976-1	2017	Gemfibrozil, a peroxisome proliferator-activated receptor alpha (PPARalpha) agonist, is widely used for hypertriglyceridaemia and mixed hyperlipidaemia.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	15-63
28374976-1	2017	Gemfibrozil, a peroxisome proliferator-activated receptor alpha (PPARalpha) agonist, is widely used for hypertriglyceridaemia and mixed hyperlipidaemia.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	65-74
28374976-2	2017	Drug-drug interaction of gemfibrozil and other PPARalpha agonists has been reported.	Gemfibrozil	25-36	peroxisome proliferator activated receptor alpha	Mus musculus	47-56
28374976-4	2017	In this study, wild-type mice were first fed gemfibrozil-containing diets (0.375%, 0.75% and 1.5%) for 14 days to establish a dose-response relationship for CYP induction.	Gemfibrozil	45-56	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	157-160
28374976-6	2017	CYP3a, CYP2b and CYP2c were induced in a dose-dependent manner by gemfibrozil.	Gemfibrozil	66-77	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	0-5
28374976-6	2017	CYP3a, CYP2b and CYP2c were induced in a dose-dependent manner by gemfibrozil.	Gemfibrozil	66-77	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	7-12
28374976-6	2017	CYP3a, CYP2b and CYP2c were induced in a dose-dependent manner by gemfibrozil.	Gemfibrozil	66-77	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	17-22
28374976-8	2017	So, gemfibrozil induced CYP, and this action was inhibited by activated PPARalpha.	Gemfibrozil	4-15	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	24-27
28374976-8	2017	So, gemfibrozil induced CYP, and this action was inhibited by activated PPARalpha.	Gemfibrozil	4-15	peroxisome proliferator activated receptor alpha	Mus musculus	72-81
28479356-5	2017	The time profiles of RPG and the inhibitors were analyzed by PBPK models, considering the inhibition of OATP1B1 and CYP3A4 by CsA or OATP1B1 inhibition by GEM and its glucuronide and the mechanism-based inhibition of CYP2C8 by GEM glucuronide.	Gemfibrozil	155-158	solute carrier organic anion transporter family member 1B1	Homo sapiens	104-111
28479356-5	2017	The time profiles of RPG and the inhibitors were analyzed by PBPK models, considering the inhibition of OATP1B1 and CYP3A4 by CsA or OATP1B1 inhibition by GEM and its glucuronide and the mechanism-based inhibition of CYP2C8 by GEM glucuronide.	Gemfibrozil	155-158	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	116-122
28479356-5	2017	The time profiles of RPG and the inhibitors were analyzed by PBPK models, considering the inhibition of OATP1B1 and CYP3A4 by CsA or OATP1B1 inhibition by GEM and its glucuronide and the mechanism-based inhibition of CYP2C8 by GEM glucuronide.	Gemfibrozil	155-158	solute carrier organic anion transporter family member 1B1	Homo sapiens	133-140
27858342-6	2017	RESULTS: The statin models reasonably predicted the observed exposure change due to Organic Anion Transporting Polypeptide (OATP) 1B1 polymorphism or clinical DDIs with itraconazole, erythromycin, and gemfibrozil, while under-predicted the observed DDIs caused by rifampin and cyclosporine.	Gemfibrozil	201-212	solute carrier organic anion transporter family member 1B1	Homo sapiens	84-133
28199020-5	2017	Therefore, we administered gemfibrozil (gem), an food and drug administration (FDA)-approved lipid-lowering drug, which has been shown to stimulate lysosomal biogenesis and induce anti-inflammation, orally, at a dose of 7.5 mg/kg body wt/day to Cln2(-/-) mice.	Gemfibrozil	27-38	tripeptidyl peptidase I	Mus musculus	245-249
28623936-6	2017	Gemfibrozil has shown efficacy in an animal model of NCL known as CLN2 (late infantile classic juvenile) and has been shown to be safe for lowering lipids in children.	Gemfibrozil	0-11	tripeptidyl peptidase 1	Homo sapiens	66-70
28343425-5	2017	Expert opinion: In addition to the aim of improving lipid profile with fibrates, the interest in new PPAR-alpha activators stems from the need to overcome some of the clinical problems encountered with dose-dependent adverse events; a rise of plasma creatinine, gallstone formation, drug-drug interactions (i.e. gemfibrozil), and myopathy.	Gemfibrozil	312-323	peroxisome proliferator activated receptor alpha	Homo sapiens	101-111
28199020-6	2017	We observed that gem-fed Cln2(-/-) mice lived longer by more than 10 weeks and had better motor activity compared to vehicle (0.1% Methyl cellulose) treatment.	Gemfibrozil	17-20	tripeptidyl peptidase I	Mus musculus	25-29
27665778-5	2016	PPARalpha agonist activity of HDBB was elucidated by comparison with gene expression data of typical PPARalpha agonist, i.e. clofibrate, WY-14643, gemfibrozil, and fenofibrate, from TG GATEs database.	Gemfibrozil	147-158	peroxisome proliferator activated receptor alpha	Rattus norvegicus	0-9
28296193-6	2017	The predicted effects of gemfibrozil and its metabolite were moderate (1.88-fold increase in rosuvastatin AUC) and mediated primarily via inhibition of hepatic OATP1B1 and renal organic cation transporter 3.	Gemfibrozil	25-36	solute carrier organic anion transporter family member 1B1	Homo sapiens	160-167
27648490-5	2017	Clinical DDIs of montelukast were evaluated using physiologically based pharmacokinetic modeling; and simulation of the interactions with gemfibrozil-CYP2C8 and OATP1B1/1B3 inhibitor, clarithromycin-CYP3A and OATP1B1/1B3 inhibitor, and itraconazole-CYP3A inhibitor, implicated OATPs-CYP2C8-CYP2C8 interplay as the primary determinant of montelukast pharmacokinetics.	Gemfibrozil	138-149	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	150-156
27918198-0	2017	PPARalpha-dependent increase of mouse urine output by gemfibrozil and fenofibrate.	Gemfibrozil	54-65	peroxisome proliferator activated receptor alpha	Mus musculus	0-9
27918198-11	2017	These results revealed a new pharmacodynamic effect of clinically prescribed PPARalpha agonists and suggested the potential value of gemfibrozil in modification of blood pressure.	Gemfibrozil	133-144	peroxisome proliferator activated receptor alpha	Mus musculus	77-86
30090481-0	2017	Application research on PPARalpha-transgenic mice in preclinical safety evaluation of gemfibrozil.	Gemfibrozil	86-97	peroxisome proliferator activated receptor alpha	Mus musculus	24-33
27624558-7	2016	Antioxidants (glutathione and N-Acetylcysteine), Cyp3a inhibitor ketoconazole and SLCO1B1 inhibitor gemfibrozil suppressed cytotoxicity and ROS formation in primary hepatocytes of diabetic rats.	Gemfibrozil	100-111	solute carrier organic anion transporter family member 1B1	Homo sapiens	82-89
28340451-5	2017	Since enzalutamide is extensively metabolized by CYP2C8, its plasma levels are likely to be raised if coadministered with strong CYP2C8 inhibitors such as gemfibrozil or pioglitazone.	Gemfibrozil	155-166	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	49-55
28340451-5	2017	Since enzalutamide is extensively metabolized by CYP2C8, its plasma levels are likely to be raised if coadministered with strong CYP2C8 inhibitors such as gemfibrozil or pioglitazone.	Gemfibrozil	155-166	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	129-135
28065762-5	2017	We then developed a high-throughput screen and tested for correction of deficient cells with lentiviral-mediated CLN5 or CLN6 gene transfer and fibrate drugs, gemfibrozil and fenofibrate in CLN6 deficient neural cultures.	Gemfibrozil	159-170	ceroid-lipofuscinosis neuronal protein 6	Ovis aries	190-194
27259818-1	2016	CYP2C8 is involved in the metabolic clearance of several important drugs and recent reports have shown that acyl glucuronides of gemfibrozil and clopidogrel are potent time-dependent inhibitors of CYP2C8 activity.	Gemfibrozil	129-140	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	0-6
27259818-1	2016	CYP2C8 is involved in the metabolic clearance of several important drugs and recent reports have shown that acyl glucuronides of gemfibrozil and clopidogrel are potent time-dependent inhibitors of CYP2C8 activity.	Gemfibrozil	129-140	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	197-203
27462272-11	2016	Furthermore, incubation of zebrafish with another PPARalpha agonist, gemfibrozil, also increased expression of the mbp promoter-driven fluorescent reporter in an SREBF-dependent manner.	Gemfibrozil	69-80	peroxisome proliferator-activated receptor alpha b	Danio rerio	50-59
27462272-11	2016	Furthermore, incubation of zebrafish with another PPARalpha agonist, gemfibrozil, also increased expression of the mbp promoter-driven fluorescent reporter in an SREBF-dependent manner.	Gemfibrozil	69-80	myelin basic protein a	Danio rerio	115-118
27209701-0	2016	Gemfibrozil not fenofibrate decreases systemic glucose level via PPARalpha.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	65-74
27209701-8	2016	Secondary regulation on the transcription of pyruvate kinase, and gluconolactonase were observed following gemfibrozil treatment, which was differential between WT mice and KO mice.	Gemfibrozil	107-118	regucalcin	Mus musculus	66-82
27209701-9	2016	CONCLUSIONS: Gemfibrozil, not fenofibrate, down-regulates systemic glucose level and glycogen storage in the liver dependent on PPARalpha, suggesting its potential value for treatment of dyslipidemia with concurrent diabetes or high glucose levels.	Gemfibrozil	13-24	peroxisome proliferator activated receptor alpha	Mus musculus	128-137
26080426-7	2015	Gemfibrozil, an agonist of PPARalpha, induced the recruitment of PPARalpha:retinoid x receptor alpha, but not PPARgamma coactivator 1alpha (PGC1alpha), to the Adam10 promoter in wild-type mouse hippocampal neurons and shifted APP processing toward the alpha-secretase, as determined by augmented soluble APPalpha and decreased Abeta production.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	27-36
26721703-5	2016	In vivo, already a small dose of gemfibrozil, i.e., 10% of its therapeutic dose, is a strong, irreversible inhibitor of CYP2C8.	Gemfibrozil	33-44	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	120-126
26721703-6	2016	Interestingly, recent findings indicate that the acyl-beta-glucuronides of gemfibrozil and clopidogrel cause metabolism-dependent inactivation of CYP2C8, leading to a strong potential for drug interactions.	Gemfibrozil	75-86	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	146-152
26195223-2	2015	In the present study, gemfibrozil preincubation time-dependently inhibited the metabolism of pioglitazone in the cytochrome P450 (CYP)- and UDP-glucuronosyltransferase (UGT)-activated human liver microsomes.	Gemfibrozil	22-33	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	140-167
26195223-2	2015	In the present study, gemfibrozil preincubation time-dependently inhibited the metabolism of pioglitazone in the cytochrome P450 (CYP)- and UDP-glucuronosyltransferase (UGT)-activated human liver microsomes.	Gemfibrozil	22-33	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	169-172
26080426-7	2015	Gemfibrozil, an agonist of PPARalpha, induced the recruitment of PPARalpha:retinoid x receptor alpha, but not PPARgamma coactivator 1alpha (PGC1alpha), to the Adam10 promoter in wild-type mouse hippocampal neurons and shifted APP processing toward the alpha-secretase, as determined by augmented soluble APPalpha and decreased Abeta production.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	65-74
26080426-7	2015	Gemfibrozil, an agonist of PPARalpha, induced the recruitment of PPARalpha:retinoid x receptor alpha, but not PPARgamma coactivator 1alpha (PGC1alpha), to the Adam10 promoter in wild-type mouse hippocampal neurons and shifted APP processing toward the alpha-secretase, as determined by augmented soluble APPalpha and decreased Abeta production.	Gemfibrozil	0-11	retinoid X receptor alpha	Mus musculus	75-100
26080426-7	2015	Gemfibrozil, an agonist of PPARalpha, induced the recruitment of PPARalpha:retinoid x receptor alpha, but not PPARgamma coactivator 1alpha (PGC1alpha), to the Adam10 promoter in wild-type mouse hippocampal neurons and shifted APP processing toward the alpha-secretase, as determined by augmented soluble APPalpha and decreased Abeta production.	Gemfibrozil	0-11	a disintegrin and metallopeptidase domain 10	Mus musculus	159-165
26080426-7	2015	Gemfibrozil, an agonist of PPARalpha, induced the recruitment of PPARalpha:retinoid x receptor alpha, but not PPARgamma coactivator 1alpha (PGC1alpha), to the Adam10 promoter in wild-type mouse hippocampal neurons and shifted APP processing toward the alpha-secretase, as determined by augmented soluble APPalpha and decreased Abeta production.	Gemfibrozil	0-11	amyloid beta (A4) precursor protein	Mus musculus	327-332
25595597-6	2015	Other inhibitors of CYP2C8 (gemfibrozil, montelukast, clopidogrel glucuronide, repaglinide, and cerivastatin) also caused extensive inhibition of 3-hydroxydesloratadine formation (73%-100%).	Gemfibrozil	28-39	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	20-26
25750174-5	2015	This study demonstrates that gemfibrozil, an agonist of peroxisome proliferator-activated receptor (PPAR) alpha, alone and in conjunction with all-trans-retinoic acid is capable of enhancing TFEB in brain cells.	Gemfibrozil	29-40	peroxisome proliferator activated receptor alpha	Homo sapiens	56-111
25750174-5	2015	This study demonstrates that gemfibrozil, an agonist of peroxisome proliferator-activated receptor (PPAR) alpha, alone and in conjunction with all-trans-retinoic acid is capable of enhancing TFEB in brain cells.	Gemfibrozil	29-40	transcription factor EB	Homo sapiens	191-195
25750174-6	2015	We also observed that PPARalpha, but not PPARbeta and PPARgamma, is involved in gemfibrozil-mediated up-regulation of TFEB.	Gemfibrozil	80-91	peroxisome proliferator activated receptor alpha	Homo sapiens	22-31
25750174-6	2015	We also observed that PPARalpha, but not PPARbeta and PPARgamma, is involved in gemfibrozil-mediated up-regulation of TFEB.	Gemfibrozil	80-91	transcription factor EB	Homo sapiens	118-122
25499606-7	2015	Our data show that the CoA esters of bezafibrate and gemfibrozil reduce chain elongation by specifically inhibiting ELOVL1.	Gemfibrozil	53-64	ELOVL fatty acid elongase 1	Homo sapiens	116-122
25667670-6	2015	The LDH, AST and ALT values were significantly elevated following CLP compared with those in the sham group, and GFZ treatment was able to reduce these elevations.	Gemfibrozil	113-116	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	9-12
25667670-7	2015	GFZ also reduced the sepsis-induced elevations of TNF-alpha and IL-1.	Gemfibrozil	0-3	tumor necrosis factor	Rattus norvegicus	50-59
25414411-4	2015	Effects of cyclosporine A (CsA), rifampin, and gemfibrozil on OATP1B1-mediated uptake of 12 substrate drugs were examined in OATP1B1-expressing human embryonic kidney 293 cells.	Gemfibrozil	47-58	solute carrier organic anion transporter family member 1B1	Homo sapiens	62-69
25653502-4	2015	The increased uptake of catalposide via the OAT3, OATP1B1, and OATP1B3 transporters was decreased to basal levels in the presence of representative inhibitors such as probenecid, furosemide, and cimetidine (for OAT3) and cyclosporin A, gemfibrozil, and rifampin (for OATP1B1 and OATP1B3).	Gemfibrozil	236-247	solute carrier family 22 member 8	Homo sapiens	44-48
25653502-4	2015	The increased uptake of catalposide via the OAT3, OATP1B1, and OATP1B3 transporters was decreased to basal levels in the presence of representative inhibitors such as probenecid, furosemide, and cimetidine (for OAT3) and cyclosporin A, gemfibrozil, and rifampin (for OATP1B1 and OATP1B3).	Gemfibrozil	236-247	solute carrier organic anion transporter family member 1B3	Homo sapiens	63-70
25119429-6	2014	PPARalpha agonist Gemfibrozil improved the vacuolization but did not rescue CCR5(-/-) infected mice from high serum triglycerides levels and enhanced mortality.	Gemfibrozil	18-29	peroxisome proliferator activated receptor alpha	Mus musculus	0-9
25088042-7	2014	Oatp1d1 mediated the transport of diclofenac with very high affinity, followed by high affinity towards perfluorooctanesulfonic acid (PFOS), nonylphenol, gemfibrozil and 17alpha-ethinylestradiol; moderate affinity towards carbaryl, diazinon and caffeine; and low affinity towards metolachlor.	Gemfibrozil	154-165	solute carrier organic anion transporter family, member 1D1	Danio rerio	0-7
23657159-0	2013	Gemfibrozil impairs imatinib absorption and inhibits the CYP2C8-mediated formation of its main metabolite.	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	57-63
24306327-5	2014	Efflux in bacteria (NorA [S. aureus], Lde [L. monocytogenes]) and in macrophages (Mrp4) was assessed using the corresponding inhibitors reserpine and gemfibrozil, respectively.	Gemfibrozil	150-161	prolactin family 2, subfamily c, member 5	Mus musculus	82-86
24385052-0	2014	Gemfibrozil disrupts lysophosphatidylcholine and bile acid homeostasis via PPARalpha and its relevance to hepatotoxicity.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	75-84
24385052-1	2014	Gemfibrozil, a ligand of peroxisome proliferator-activated receptor alpha (PPARalpha), is one of the most widely prescribed anti-dyslipidemia fibrate drugs.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	25-73
24385052-1	2014	Gemfibrozil, a ligand of peroxisome proliferator-activated receptor alpha (PPARalpha), is one of the most widely prescribed anti-dyslipidemia fibrate drugs.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	75-84
24385052-4	2014	In this study, wild-type and Ppara-null mice were dosed with a gemfibrozil-containing diet for 14 days.	Gemfibrozil	63-74	peroxisome proliferator activated receptor alpha	Mus musculus	29-34
24385052-10	2014	These data suggest that PPARalpha mediates gemfibrozil-induced hepatotoxicity in part by disrupting phospholipid and bile acid homeostasis.	Gemfibrozil	43-54	peroxisome proliferator activated receptor alpha	Mus musculus	24-33
24591743-5	2013	This article deals with the development of a 2D QSAR model based on the inhibitory potential of gemfibrozil, its analogues and corresponding glucuronide conjugates in inhibiting the CYP2C8-catalysed amodiaquine N-deethylation.	Gemfibrozil	96-107	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	182-188
24271013-7	2014	Fenofibrate and gemfibrozil, previously reported to induce TPP1 activity in control cells, failed to increase TPP1 activity in patient iPSC-derived neural progenitor cells.	Gemfibrozil	16-27	tripeptidyl peptidase 1	Homo sapiens	59-63
24491572-2	2014	OBJECTIVE: The goal of these studies was to investigate potential drug-drug interactions between empagliflozin and gemfibrozil (an organic anion-transporting polypeptide 1B1 [OATP1B1]/1B3 and organic anion transporter 3 [OAT3] inhibitor), rifampicin (an OATP1B1/1B3 inhibitor), or probenecid (an OAT3 and uridine diphosphate glucuronosyltransferase inhibitor).	Gemfibrozil	115-126	solute carrier organic anion transporter family member 1B1	Homo sapiens	131-173
24491572-2	2014	OBJECTIVE: The goal of these studies was to investigate potential drug-drug interactions between empagliflozin and gemfibrozil (an organic anion-transporting polypeptide 1B1 [OATP1B1]/1B3 and organic anion transporter 3 [OAT3] inhibitor), rifampicin (an OATP1B1/1B3 inhibitor), or probenecid (an OAT3 and uridine diphosphate glucuronosyltransferase inhibitor).	Gemfibrozil	115-126	solute carrier organic anion transporter family member 1B1	Homo sapiens	175-182
24491572-2	2014	OBJECTIVE: The goal of these studies was to investigate potential drug-drug interactions between empagliflozin and gemfibrozil (an organic anion-transporting polypeptide 1B1 [OATP1B1]/1B3 and organic anion transporter 3 [OAT3] inhibitor), rifampicin (an OATP1B1/1B3 inhibitor), or probenecid (an OAT3 and uridine diphosphate glucuronosyltransferase inhibitor).	Gemfibrozil	115-126	solute carrier family 22 member 8	Homo sapiens	192-219
24491572-2	2014	OBJECTIVE: The goal of these studies was to investigate potential drug-drug interactions between empagliflozin and gemfibrozil (an organic anion-transporting polypeptide 1B1 [OATP1B1]/1B3 and organic anion transporter 3 [OAT3] inhibitor), rifampicin (an OATP1B1/1B3 inhibitor), or probenecid (an OAT3 and uridine diphosphate glucuronosyltransferase inhibitor).	Gemfibrozil	115-126	solute carrier family 22 member 8	Homo sapiens	221-225
24491572-2	2014	OBJECTIVE: The goal of these studies was to investigate potential drug-drug interactions between empagliflozin and gemfibrozil (an organic anion-transporting polypeptide 1B1 [OATP1B1]/1B3 and organic anion transporter 3 [OAT3] inhibitor), rifampicin (an OATP1B1/1B3 inhibitor), or probenecid (an OAT3 and uridine diphosphate glucuronosyltransferase inhibitor).	Gemfibrozil	115-126	solute carrier organic anion transporter family member 1B1	Homo sapiens	254-261
24491572-2	2014	OBJECTIVE: The goal of these studies was to investigate potential drug-drug interactions between empagliflozin and gemfibrozil (an organic anion-transporting polypeptide 1B1 [OATP1B1]/1B3 and organic anion transporter 3 [OAT3] inhibitor), rifampicin (an OATP1B1/1B3 inhibitor), or probenecid (an OAT3 and uridine diphosphate glucuronosyltransferase inhibitor).	Gemfibrozil	115-126	solute carrier family 22 member 8	Homo sapiens	296-300
24180432-4	2014	Chemical-specific and mechanistic data support concordance of temporal and dose-response relationships for the key events associated with many PPARalpha activators including a phthalate ester plasticizer di(2-ethylhexyl) phthalate (DEHP) and the drug gemfibrozil.	Gemfibrozil	251-262	peroxisome proliferator activated receptor alpha	Homo sapiens	143-152
25147562-2	2014	The present study aimed at evaluating how 3 PPARalpha agonists, namely, fenofibrate, gemfibrozil, and Wy14,643, affect bilirubin synthesis and metabolism.	Gemfibrozil	85-96	peroxisome proliferator activated receptor alpha	Homo sapiens	44-53
23111552-0	2013	Gemfibrozil and its combination with metformin on pleiotropic effect on IL-10 and adiponectin and anti-atherogenic treatment in insulin resistant type 2 diabetes mellitus rats.	Gemfibrozil	0-11	interleukin 10	Rattus norvegicus	72-77
23288702-6	2013	While the expression of NRF-1 and TFAM were induced in gemfibrozil-pretreated met-estrous females, they were suppressed in males.	Gemfibrozil	55-66	transcription factor A, mitochondrial	Rattus norvegicus	34-38
23288702-8	2013	In the mitogen-activated protein kinase (MAPKs) pathway, gemfibrozil pretreatment induced the expression of extracellular signal-regulated kinases (ERK1/2) in met-estrous females and reduced it in males.	Gemfibrozil	57-68	mitogen activated protein kinase 3	Rattus norvegicus	148-154
24575330-5	2013	After polarization of MBP-primed Th1 cells to Th2 by gemfibrozil and other drugs, we observed that MBP-primed Th2 cells dose dependently inhibited the production of interleukin-1beta (IL-1beta) and nitric oxide (NO) in LPS-stimulated microglia via cell-to-cell contact.	Gemfibrozil	53-64	myelin basic protein	Homo sapiens	22-25
24575330-5	2013	After polarization of MBP-primed Th1 cells to Th2 by gemfibrozil and other drugs, we observed that MBP-primed Th2 cells dose dependently inhibited the production of interleukin-1beta (IL-1beta) and nitric oxide (NO) in LPS-stimulated microglia via cell-to-cell contact.	Gemfibrozil	53-64	negative elongation factor complex member C/D	Homo sapiens	33-36
24575330-5	2013	After polarization of MBP-primed Th1 cells to Th2 by gemfibrozil and other drugs, we observed that MBP-primed Th2 cells dose dependently inhibited the production of interleukin-1beta (IL-1beta) and nitric oxide (NO) in LPS-stimulated microglia via cell-to-cell contact.	Gemfibrozil	53-64	myelin basic protein	Homo sapiens	99-102
24575330-5	2013	After polarization of MBP-primed Th1 cells to Th2 by gemfibrozil and other drugs, we observed that MBP-primed Th2 cells dose dependently inhibited the production of interleukin-1beta (IL-1beta) and nitric oxide (NO) in LPS-stimulated microglia via cell-to-cell contact.	Gemfibrozil	53-64	interleukin 1 beta	Homo sapiens	165-182
23288702-2	2013	The ability of Gemfibrozil, a fibrate, is investigated for the first time to modulate mitochondrial pro-survival factors involved in the mitochondrial biogenesis signaling pathway, including peroxisome proliferator-activated receptor coactivator-1alpha (PGC-1alpha), nuclear respiratory factor (NRF-1), and mitochondrial transcription factor A (TFAM) in the brain.	Gemfibrozil	15-26	PPARG coactivator 1 alpha	Rattus norvegicus	254-264
23288702-2	2013	The ability of Gemfibrozil, a fibrate, is investigated for the first time to modulate mitochondrial pro-survival factors involved in the mitochondrial biogenesis signaling pathway, including peroxisome proliferator-activated receptor coactivator-1alpha (PGC-1alpha), nuclear respiratory factor (NRF-1), and mitochondrial transcription factor A (TFAM) in the brain.	Gemfibrozil	15-26	nuclear respiratory factor 1	Rattus norvegicus	295-300
23288702-2	2013	The ability of Gemfibrozil, a fibrate, is investigated for the first time to modulate mitochondrial pro-survival factors involved in the mitochondrial biogenesis signaling pathway, including peroxisome proliferator-activated receptor coactivator-1alpha (PGC-1alpha), nuclear respiratory factor (NRF-1), and mitochondrial transcription factor A (TFAM) in the brain.	Gemfibrozil	15-26	transcription factor A, mitochondrial	Rattus norvegicus	345-349
23288702-6	2013	While the expression of NRF-1 and TFAM were induced in gemfibrozil-pretreated met-estrous females, they were suppressed in males.	Gemfibrozil	55-66	nuclear respiratory factor 1	Rattus norvegicus	24-29
23805127-6	2013	Inhibition assays using human liver microsomes (HLM) incubated with 19-norandrosterone and selective inhibitors confirmed that UGT2B7 and UGT2B15 are involved in 19-norandrosterone glucuronidation, since the presence of the specific UGT2B7 and UGT2B15 inhibitors gemfibrozil and valproic acid inhibited the 19-norandrosterone glucuronidation by 35 and 45%, respectively.	Gemfibrozil	263-274	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	127-133
23805127-6	2013	Inhibition assays using human liver microsomes (HLM) incubated with 19-norandrosterone and selective inhibitors confirmed that UGT2B7 and UGT2B15 are involved in 19-norandrosterone glucuronidation, since the presence of the specific UGT2B7 and UGT2B15 inhibitors gemfibrozil and valproic acid inhibited the 19-norandrosterone glucuronidation by 35 and 45%, respectively.	Gemfibrozil	263-274	UDP glucuronosyltransferase family 2 member B15	Homo sapiens	138-145
23111552-0	2013	Gemfibrozil and its combination with metformin on pleiotropic effect on IL-10 and adiponectin and anti-atherogenic treatment in insulin resistant type 2 diabetes mellitus rats.	Gemfibrozil	0-11	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	82-93
23111552-1	2013	AIM: Gemfibrozil is a PPAR-alpha ligand that inhibits the progression of atherosclerosis in insulin resistance type 2 diabetes mellitus (IR type 2 DM).	Gemfibrozil	5-16	peroxisome proliferator activated receptor alpha	Rattus norvegicus	22-32
23111552-8	2013	OVERALL CONCLUSIONS: Gemfibrozil plus metformin decrease MMP-9, increase IL-10 and adiponectin acting as anti-atherogenic, anti-inflammatory and immunomodulatory in IR type 2 DM.	Gemfibrozil	21-32	matrix metallopeptidase 9	Rattus norvegicus	57-62
23111552-8	2013	OVERALL CONCLUSIONS: Gemfibrozil plus metformin decrease MMP-9, increase IL-10 and adiponectin acting as anti-atherogenic, anti-inflammatory and immunomodulatory in IR type 2 DM.	Gemfibrozil	21-32	interleukin 10	Rattus norvegicus	73-78
23111552-8	2013	OVERALL CONCLUSIONS: Gemfibrozil plus metformin decrease MMP-9, increase IL-10 and adiponectin acting as anti-atherogenic, anti-inflammatory and immunomodulatory in IR type 2 DM.	Gemfibrozil	21-32	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	83-94
22625877-1	2013	AIM: The objective of this study was to determine the extent to which the CYP2C8*3 allele influences pharmacokinetic variability in the drug-drug interaction between gemfibrozil (CYP2C8 inhibitor) and pioglitazone (CYP2C8 substrate).	Gemfibrozil	166-177	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	74-80
22773136-10	2013	In contrast, gemfibrozil pretreatment was toxic to males, enhancing the expression of inflammatory factors such as tumor necrosis factor-alpha, nuclear factor-kappaB, and cyclooxygenase-2, and decreasing Nrf-2 expression and SOD activity, leading to hippocampal neurodegeneration.	Gemfibrozil	13-24	tumor necrosis factor	Rattus norvegicus	115-142
22773136-10	2013	In contrast, gemfibrozil pretreatment was toxic to males, enhancing the expression of inflammatory factors such as tumor necrosis factor-alpha, nuclear factor-kappaB, and cyclooxygenase-2, and decreasing Nrf-2 expression and SOD activity, leading to hippocampal neurodegeneration.	Gemfibrozil	13-24	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	171-187
22773136-10	2013	In contrast, gemfibrozil pretreatment was toxic to males, enhancing the expression of inflammatory factors such as tumor necrosis factor-alpha, nuclear factor-kappaB, and cyclooxygenase-2, and decreasing Nrf-2 expression and SOD activity, leading to hippocampal neurodegeneration.	Gemfibrozil	13-24	NFE2 like bZIP transcription factor 2	Rattus norvegicus	204-209
22625877-0	2013	Impact of the CYP2C8 *3 polymorphism on the drug-drug interaction between gemfibrozil and pioglitazone.	Gemfibrozil	74-85	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	14-20
22625877-1	2013	AIM: The objective of this study was to determine the extent to which the CYP2C8*3 allele influences pharmacokinetic variability in the drug-drug interaction between gemfibrozil (CYP2C8 inhibitor) and pioglitazone (CYP2C8 substrate).	Gemfibrozil	166-177	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	179-185
22625877-1	2013	AIM: The objective of this study was to determine the extent to which the CYP2C8*3 allele influences pharmacokinetic variability in the drug-drug interaction between gemfibrozil (CYP2C8 inhibitor) and pioglitazone (CYP2C8 substrate).	Gemfibrozil	166-177	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	179-185
22625877-7	2013	The relative change in pioglitazone plasma exposure following gemfibrozil administration was significantly influenced by CYP2C8 genotype.	Gemfibrozil	62-73	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	121-127
22625877-9	2013	CONCLUSION: CYP2C8*3 is associated with decreased pioglitazone plasma exposure in vivo and significantly influences the pharmacokinetic magnitude of the gemfibrozil-pioglitazone drug-drug interaction.	Gemfibrozil	153-164	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	12-18
22528839-4	2012	This study underlines the importance of PPARbeta/delta in mediating the anti-inflammatory effect of gemfibrozil, an FDA-approved lipid-lowering drug, in primary human microglia.	Gemfibrozil	100-111	peroxisome proliferator activated receptor delta	Homo sapiens	40-48
22989886-0	2012	Gemfibrozil and fenofibrate, Food and Drug Administration-approved lipid-lowering drugs, up-regulate tripeptidyl-peptidase 1 in brain cells via peroxisome proliferator-activated receptor alpha: implications for late infantile Batten disease therapy.	Gemfibrozil	0-11	tripeptidyl peptidase I	Mus musculus	101-124
22989886-0	2012	Gemfibrozil and fenofibrate, Food and Drug Administration-approved lipid-lowering drugs, up-regulate tripeptidyl-peptidase 1 in brain cells via peroxisome proliferator-activated receptor alpha: implications for late infantile Batten disease therapy.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	144-192
22989886-4	2012	This study reveals a novel use of gemfibrozil and fenofibrate, Food and Drug Administration-approved lipid-lowering drugs, in up-regulating TPP1 in brain cells.	Gemfibrozil	34-45	tripeptidyl peptidase I	Mus musculus	140-144
22989886-5	2012	Both gemfibrozil and fenofibrate up-regulated mRNA, protein, and enzymatic activity of TPP1 in primary mouse neurons and astrocytes as well as human astrocytes and neuronal cells.	Gemfibrozil	5-16	tripeptidyl peptidase I	Mus musculus	87-91
22989886-6	2012	Because gemfibrozil and fenofibrate are known to activate peroxisome proliferator-activated receptor-alpha (PPARalpha), the role of PPARalpha in gemfibrozil- and fenofibrate-mediated up-regulation of TPP1 was investigated revealing that both drugs up-regulated TPP1 mRNA, protein, and enzymatic activity both in vitro and in vivo in wild type (WT) and PPARbeta(-/-), but not PPARalpha(-/-), mice.	Gemfibrozil	8-19	peroxisome proliferator activated receptor alpha	Mus musculus	58-106
22989886-6	2012	Because gemfibrozil and fenofibrate are known to activate peroxisome proliferator-activated receptor-alpha (PPARalpha), the role of PPARalpha in gemfibrozil- and fenofibrate-mediated up-regulation of TPP1 was investigated revealing that both drugs up-regulated TPP1 mRNA, protein, and enzymatic activity both in vitro and in vivo in wild type (WT) and PPARbeta(-/-), but not PPARalpha(-/-), mice.	Gemfibrozil	8-19	peroxisome proliferator activated receptor alpha	Mus musculus	108-117
22989886-6	2012	Because gemfibrozil and fenofibrate are known to activate peroxisome proliferator-activated receptor-alpha (PPARalpha), the role of PPARalpha in gemfibrozil- and fenofibrate-mediated up-regulation of TPP1 was investigated revealing that both drugs up-regulated TPP1 mRNA, protein, and enzymatic activity both in vitro and in vivo in wild type (WT) and PPARbeta(-/-), but not PPARalpha(-/-), mice.	Gemfibrozil	145-156	peroxisome proliferator activated receptor alpha	Mus musculus	132-141
22989886-6	2012	Because gemfibrozil and fenofibrate are known to activate peroxisome proliferator-activated receptor-alpha (PPARalpha), the role of PPARalpha in gemfibrozil- and fenofibrate-mediated up-regulation of TPP1 was investigated revealing that both drugs up-regulated TPP1 mRNA, protein, and enzymatic activity both in vitro and in vivo in wild type (WT) and PPARbeta(-/-), but not PPARalpha(-/-), mice.	Gemfibrozil	145-156	peroxisome proliferator activated receptor alpha	Mus musculus	132-141
22989886-8	2012	Accordingly, all-trans-retinoic acid, alone or together with gemfibrozil, up-regulated TPP1.	Gemfibrozil	61-72	tripeptidyl peptidase I	Mus musculus	87-91
22879602-0	2012	Gemfibrozil, a lipid-lowering drug, increases myelin genes in human oligodendrocytes via peroxisome proliferator-activated receptor-beta.	Gemfibrozil	0-11	peroxisome proliferator activated receptor delta	Homo sapiens	89-136
22879602-3	2012	The current study identified another novel property of gemfibrozil in stimulating the expression of myelin-specific genes (myelin basic protein, myelin oligodendrocyte glycoprotein, 2",3"-cyclic-nucleotide 3"-phosphodiesterase, and proteolipid protein (PLP)) in primary human oligodendrocytes, mixed glial cells, and spinal cord organotypic cultures.	Gemfibrozil	55-66	myelin basic protein	Homo sapiens	123-143
22879602-3	2012	The current study identified another novel property of gemfibrozil in stimulating the expression of myelin-specific genes (myelin basic protein, myelin oligodendrocyte glycoprotein, 2",3"-cyclic-nucleotide 3"-phosphodiesterase, and proteolipid protein (PLP)) in primary human oligodendrocytes, mixed glial cells, and spinal cord organotypic cultures.	Gemfibrozil	55-66	myelin oligodendrocyte glycoprotein	Homo sapiens	145-180
22879602-3	2012	The current study identified another novel property of gemfibrozil in stimulating the expression of myelin-specific genes (myelin basic protein, myelin oligodendrocyte glycoprotein, 2",3"-cyclic-nucleotide 3"-phosphodiesterase, and proteolipid protein (PLP)) in primary human oligodendrocytes, mixed glial cells, and spinal cord organotypic cultures.	Gemfibrozil	55-66	proteolipid protein 1	Homo sapiens	232-257
22879602-4	2012	Although gemfibrozil is a known activator of peroxisome proliferator-activated receptor-alpha (PPAR-alpha), we were unable to detect PPAR-alpha in either gemfibrozil-treated or untreated human oligodendrocytes, and gemfibrozil increased the expression of myelin genes in oligodendrocytes isolated from both wild type and PPAR-alpha(-/-) mice.	Gemfibrozil	9-20	peroxisome proliferator activated receptor alpha	Homo sapiens	45-93
22879602-4	2012	Although gemfibrozil is a known activator of peroxisome proliferator-activated receptor-alpha (PPAR-alpha), we were unable to detect PPAR-alpha in either gemfibrozil-treated or untreated human oligodendrocytes, and gemfibrozil increased the expression of myelin genes in oligodendrocytes isolated from both wild type and PPAR-alpha(-/-) mice.	Gemfibrozil	9-20	peroxisome proliferator activated receptor alpha	Homo sapiens	95-105
22879602-5	2012	On the other hand, gemfibrozil markedly increased the expression of PPAR-beta but not PPAR-gamma.	Gemfibrozil	19-30	peroxisome proliferator activated receptor delta	Homo sapiens	68-77
22879602-6	2012	Consistently, antisense knockdown of PPAR-beta, but not PPAR-gamma, abrogated the stimulatory effect of gemfibrozil on myelin genes in human oligodendrocytes.	Gemfibrozil	104-115	peroxisome proliferator activated receptor delta	Homo sapiens	37-46
22879602-8	2012	Chromatin immunoprecipitation analysis showed that gemfibrozil induced the recruitment of PPAR-beta to the promoter of PLP and myelin oligodendrocyte glycoprotein genes in human oligodendrocytes.	Gemfibrozil	51-62	peroxisome proliferator activated receptor delta	Homo sapiens	90-99
22879602-8	2012	Chromatin immunoprecipitation analysis showed that gemfibrozil induced the recruitment of PPAR-beta to the promoter of PLP and myelin oligodendrocyte glycoprotein genes in human oligodendrocytes.	Gemfibrozil	51-62	proteolipid protein 1	Homo sapiens	119-122
22879602-8	2012	Chromatin immunoprecipitation analysis showed that gemfibrozil induced the recruitment of PPAR-beta to the promoter of PLP and myelin oligodendrocyte glycoprotein genes in human oligodendrocytes.	Gemfibrozil	51-62	myelin oligodendrocyte glycoprotein	Homo sapiens	127-162
22879602-9	2012	Furthermore, gemfibrozil treatment also led to the recruitment of PPAR-beta to the PLP promoter in vivo in the spinal cord of experimental autoimmune encephalomyelitis mice and suppression of experimental autoimmune encephalomyelitis symptoms in PLP-T cell receptor transgenic mice.	Gemfibrozil	13-24	peroxisome proliferator activator receptor delta	Mus musculus	66-75
22879602-9	2012	Furthermore, gemfibrozil treatment also led to the recruitment of PPAR-beta to the PLP promoter in vivo in the spinal cord of experimental autoimmune encephalomyelitis mice and suppression of experimental autoimmune encephalomyelitis symptoms in PLP-T cell receptor transgenic mice.	Gemfibrozil	13-24	proteolipid protein (myelin) 1	Mus musculus	83-86
22879602-9	2012	Furthermore, gemfibrozil treatment also led to the recruitment of PPAR-beta to the PLP promoter in vivo in the spinal cord of experimental autoimmune encephalomyelitis mice and suppression of experimental autoimmune encephalomyelitis symptoms in PLP-T cell receptor transgenic mice.	Gemfibrozil	13-24	proteolipid protein (myelin) 1	Mus musculus	246-249
22879602-10	2012	These results suggest that gemfibrozil stimulates the expression of myelin genes via PPAR-beta and that gemfibrozil, a prescribed drug for humans, may find further therapeutic use in demyelinating diseases.	Gemfibrozil	27-38	peroxisome proliferator activated receptor delta	Homo sapiens	85-94
22538052-8	2012	Rifamycin SV strongly, and gemfibrozil weakly, inhibited the OATP1B1-mediated transport of substrates.	Gemfibrozil	27-38	solute carrier organic anion transporter family member 1B1	Homo sapiens	61-68
22685291-0	2012	Gemfibrozil, a lipid-lowering drug, induces suppressor of cytokine signaling 3 in glial cells: implications for neurodegenerative disorders.	Gemfibrozil	0-11	suppressor of cytokine signaling 3	Mus musculus	44-78
22685291-4	2012	This study underlines the importance of gemfibrozil, a Food and Drug Administration-approved lipid-lowering drug, in up-regulating the expression of SOCS3 in glial cells.	Gemfibrozil	40-51	suppressor of cytokine signaling 3	Mus musculus	149-154
22685291-5	2012	Gemfibrozil increased the expression of Socs3 mRNA and protein in mouse astroglia and microglia in both a time- and dose-dependent manner.	Gemfibrozil	0-11	suppressor of cytokine signaling 3	Mus musculus	40-45
22685291-6	2012	Interestingly, gemfibrozil induced the activation of type IA phosphatidylinositol (PI) 3-kinase and AKT.	Gemfibrozil	15-26	thymoma viral proto-oncogene 1	Mus musculus	100-103
22685291-7	2012	Accordingly, inhibition of PI 3-kinase and AKT by chemical inhibitors abrogated gemfibrozil-mediated up-regulation of SOCS3.	Gemfibrozil	80-91	thymoma viral proto-oncogene 1	Mus musculus	43-46
22685291-7	2012	Accordingly, inhibition of PI 3-kinase and AKT by chemical inhibitors abrogated gemfibrozil-mediated up-regulation of SOCS3.	Gemfibrozil	80-91	suppressor of cytokine signaling 3	Mus musculus	118-123
22685291-8	2012	Furthermore, we demonstrated that gemfibrozil induced the activation of Kruppel-like factor 4 (KLF4) via the PI 3-kinase-AKT pathway and that siRNA knockdown of KLF4 abrogated gemfibrozil-mediated up-regulation of SOCS3.	Gemfibrozil	34-45	Kruppel-like factor 4 (gut)	Mus musculus	72-93
22685291-8	2012	Furthermore, we demonstrated that gemfibrozil induced the activation of Kruppel-like factor 4 (KLF4) via the PI 3-kinase-AKT pathway and that siRNA knockdown of KLF4 abrogated gemfibrozil-mediated up-regulation of SOCS3.	Gemfibrozil	34-45	Kruppel-like factor 4 (gut)	Mus musculus	95-99
22685291-8	2012	Furthermore, we demonstrated that gemfibrozil induced the activation of Kruppel-like factor 4 (KLF4) via the PI 3-kinase-AKT pathway and that siRNA knockdown of KLF4 abrogated gemfibrozil-mediated up-regulation of SOCS3.	Gemfibrozil	34-45	thymoma viral proto-oncogene 1	Mus musculus	121-124
22685291-8	2012	Furthermore, we demonstrated that gemfibrozil induced the activation of Kruppel-like factor 4 (KLF4) via the PI 3-kinase-AKT pathway and that siRNA knockdown of KLF4 abrogated gemfibrozil-mediated up-regulation of SOCS3.	Gemfibrozil	34-45	Kruppel-like factor 4 (gut)	Mus musculus	161-165
22685291-8	2012	Furthermore, we demonstrated that gemfibrozil induced the activation of Kruppel-like factor 4 (KLF4) via the PI 3-kinase-AKT pathway and that siRNA knockdown of KLF4 abrogated gemfibrozil-mediated up-regulation of SOCS3.	Gemfibrozil	34-45	suppressor of cytokine signaling 3	Mus musculus	214-219
22685291-8	2012	Furthermore, we demonstrated that gemfibrozil induced the activation of Kruppel-like factor 4 (KLF4) via the PI 3-kinase-AKT pathway and that siRNA knockdown of KLF4 abrogated gemfibrozil-mediated up-regulation of SOCS3.	Gemfibrozil	176-187	Kruppel-like factor 4 (gut)	Mus musculus	72-93
22685291-8	2012	Furthermore, we demonstrated that gemfibrozil induced the activation of Kruppel-like factor 4 (KLF4) via the PI 3-kinase-AKT pathway and that siRNA knockdown of KLF4 abrogated gemfibrozil-mediated up-regulation of SOCS3.	Gemfibrozil	176-187	Kruppel-like factor 4 (gut)	Mus musculus	95-99
22685291-8	2012	Furthermore, we demonstrated that gemfibrozil induced the activation of Kruppel-like factor 4 (KLF4) via the PI 3-kinase-AKT pathway and that siRNA knockdown of KLF4 abrogated gemfibrozil-mediated up-regulation of SOCS3.	Gemfibrozil	176-187	Kruppel-like factor 4 (gut)	Mus musculus	161-165
22685291-8	2012	Furthermore, we demonstrated that gemfibrozil induced the activation of Kruppel-like factor 4 (KLF4) via the PI 3-kinase-AKT pathway and that siRNA knockdown of KLF4 abrogated gemfibrozil-mediated up-regulation of SOCS3.	Gemfibrozil	176-187	suppressor of cytokine signaling 3	Mus musculus	214-219
22685291-9	2012	Gemfibrozil also induced the recruitment of KLF4 to the distal, but not proximal, KLF4-binding site of the Socs3 promoter.	Gemfibrozil	0-11	Kruppel-like factor 4 (gut)	Mus musculus	44-48
22685291-9	2012	Gemfibrozil also induced the recruitment of KLF4 to the distal, but not proximal, KLF4-binding site of the Socs3 promoter.	Gemfibrozil	0-11	Kruppel-like factor 4 (gut)	Mus musculus	82-86
22685291-9	2012	Gemfibrozil also induced the recruitment of KLF4 to the distal, but not proximal, KLF4-binding site of the Socs3 promoter.	Gemfibrozil	0-11	suppressor of cytokine signaling 3	Mus musculus	107-112
22685291-10	2012	This study delineates a novel property of gemfibrozil in up-regulating SOCS3 in glial cells via PI 3-kinase-AKT-mediated activation of KLF4 and suggests that gemfibrozil may find therapeutic application in neuroinflammatory and neurodegenerative disorders.	Gemfibrozil	42-53	suppressor of cytokine signaling 3	Mus musculus	71-76
22685291-10	2012	This study delineates a novel property of gemfibrozil in up-regulating SOCS3 in glial cells via PI 3-kinase-AKT-mediated activation of KLF4 and suggests that gemfibrozil may find therapeutic application in neuroinflammatory and neurodegenerative disorders.	Gemfibrozil	42-53	thymoma viral proto-oncogene 1	Mus musculus	108-111
22685291-10	2012	This study delineates a novel property of gemfibrozil in up-regulating SOCS3 in glial cells via PI 3-kinase-AKT-mediated activation of KLF4 and suggests that gemfibrozil may find therapeutic application in neuroinflammatory and neurodegenerative disorders.	Gemfibrozil	42-53	Kruppel-like factor 4 (gut)	Mus musculus	135-139
22685291-10	2012	This study delineates a novel property of gemfibrozil in up-regulating SOCS3 in glial cells via PI 3-kinase-AKT-mediated activation of KLF4 and suggests that gemfibrozil may find therapeutic application in neuroinflammatory and neurodegenerative disorders.	Gemfibrozil	158-169	suppressor of cytokine signaling 3	Mus musculus	71-76
22685291-10	2012	This study delineates a novel property of gemfibrozil in up-regulating SOCS3 in glial cells via PI 3-kinase-AKT-mediated activation of KLF4 and suggests that gemfibrozil may find therapeutic application in neuroinflammatory and neurodegenerative disorders.	Gemfibrozil	158-169	thymoma viral proto-oncogene 1	Mus musculus	108-111
22685291-10	2012	This study delineates a novel property of gemfibrozil in up-regulating SOCS3 in glial cells via PI 3-kinase-AKT-mediated activation of KLF4 and suggests that gemfibrozil may find therapeutic application in neuroinflammatory and neurodegenerative disorders.	Gemfibrozil	158-169	Kruppel-like factor 4 (gut)	Mus musculus	135-139
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
22538270-8	2012	In human hepatocytes and/or liver microsomes, gemfibrozil potently inhibited the hydroxylation of BRV-AC into BRV-OHAC (K(I) 12 muM) while having a marginal effect on BRV-OH formation (K(I) &gt;=153 muM).	Gemfibrozil	46-57	latexin	Homo sapiens	128-131
22538270-8	2012	In human hepatocytes and/or liver microsomes, gemfibrozil potently inhibited the hydroxylation of BRV-AC into BRV-OHAC (K(I) 12 muM) while having a marginal effect on BRV-OH formation (K(I) &gt;=153 muM).	Gemfibrozil	46-57	latexin	Homo sapiens	199-202
22528839-8	2012	Interestingly, either antisense knockdown of PPAR-beta or antagonism of PPAR-beta by a specific chemical antagonist abrogated gemfibrozil-mediated inhibition of microglial activation.	Gemfibrozil	126-137	peroxisome proliferator activated receptor delta	Homo sapiens	45-54
22528839-8	2012	Interestingly, either antisense knockdown of PPAR-beta or antagonism of PPAR-beta by a specific chemical antagonist abrogated gemfibrozil-mediated inhibition of microglial activation.	Gemfibrozil	126-137	peroxisome proliferator activated receptor delta	Homo sapiens	72-81
22528839-10	2012	These results highlight the fact that gemfibrozil regulates microglial activation by inhibiting inflammatory gene expression in a PPAR-beta dependent pathway and further reinforce its therapeutic application in several neuroinflammatory and neurodegenerative diseases.	Gemfibrozil	38-49	peroxisome proliferator activated receptor delta	Homo sapiens	130-139
23153186-8	2012	The strong CYP2C8 and OATP1B1 inhibitor gemfibrozil increases substantially the plasma concentrations of repaglinide and TZDs.	Gemfibrozil	40-51	solute carrier organic anion transporter family member 1B1	Homo sapiens	22-29
22528839-6	2012	However, gemfibrozil markedly suppressed proinflammatory molecules and CD11b in LPS-stimulated microglia.	Gemfibrozil	9-20	integrin subunit alpha M	Homo sapiens	71-76
22706077-4	2012	The present study underlines a novel application of gemfibrozil (gem), a Food and Drug Administration-approved lipid-lowering drug, in increasing the expression of IL-1Ra in primary mouse and human neurons.	Gemfibrozil	52-63	interleukin 1 receptor antagonist	Mus musculus	164-170
22706077-4	2012	The present study underlines a novel application of gemfibrozil (gem), a Food and Drug Administration-approved lipid-lowering drug, in increasing the expression of IL-1Ra in primary mouse and human neurons.	Gemfibrozil	52-55	interleukin 1 receptor antagonist	Mus musculus	164-170
22706077-10	2012	Taken together, these results highlight the importance of the PI3K-Akt-CREB pathway in mediating gem-induced upregulation of IL-1Ra in neurons and suggest gem as a possible therapeutic treatment for propagating neuronal self-defense in neuroinflammatory and neurodegenerative disorders.	Gemfibrozil	97-100	cAMP responsive element binding protein 1	Mus musculus	71-75
22706077-6	2012	Activation of type IA p110alpha PI3K and Akt by gem and abrogation of gem-induced upregulation of IL-1Ra by inhibitors of PI3K and Akt indicate a role of the PI3K-Akt pathway in the upregulation of IL-1Ra.	Gemfibrozil	48-51	thymoma viral proto-oncogene 1	Mus musculus	41-44
22706077-10	2012	Taken together, these results highlight the importance of the PI3K-Akt-CREB pathway in mediating gem-induced upregulation of IL-1Ra in neurons and suggest gem as a possible therapeutic treatment for propagating neuronal self-defense in neuroinflammatory and neurodegenerative disorders.	Gemfibrozil	97-100	interleukin 1 receptor antagonist	Mus musculus	125-131
22706077-6	2012	Activation of type IA p110alpha PI3K and Akt by gem and abrogation of gem-induced upregulation of IL-1Ra by inhibitors of PI3K and Akt indicate a role of the PI3K-Akt pathway in the upregulation of IL-1Ra.	Gemfibrozil	70-73	interleukin 1 receptor antagonist	Mus musculus	98-104
22706077-6	2012	Activation of type IA p110alpha PI3K and Akt by gem and abrogation of gem-induced upregulation of IL-1Ra by inhibitors of PI3K and Akt indicate a role of the PI3K-Akt pathway in the upregulation of IL-1Ra.	Gemfibrozil	70-73	thymoma viral proto-oncogene 1	Mus musculus	131-134
22706077-6	2012	Activation of type IA p110alpha PI3K and Akt by gem and abrogation of gem-induced upregulation of IL-1Ra by inhibitors of PI3K and Akt indicate a role of the PI3K-Akt pathway in the upregulation of IL-1Ra.	Gemfibrozil	70-73	thymoma viral proto-oncogene 1	Mus musculus	131-134
22706077-6	2012	Activation of type IA p110alpha PI3K and Akt by gem and abrogation of gem-induced upregulation of IL-1Ra by inhibitors of PI3K and Akt indicate a role of the PI3K-Akt pathway in the upregulation of IL-1Ra.	Gemfibrozil	70-73	interleukin 1 receptor antagonist	Mus musculus	198-204
22706077-7	2012	Gem also induced the activation of CREB via the PI3K-Akt pathway, and small interfering RNA attenuation of CREB abolished the gem-mediated increase in IL-1Ra.	Gemfibrozil	126-129	cAMP responsive element binding protein 1	Mus musculus	35-39
22706077-7	2012	Gem also induced the activation of CREB via the PI3K-Akt pathway, and small interfering RNA attenuation of CREB abolished the gem-mediated increase in IL-1Ra.	Gemfibrozil	126-129	cAMP responsive element binding protein 1	Mus musculus	107-111
22706077-7	2012	Gem also induced the activation of CREB via the PI3K-Akt pathway, and small interfering RNA attenuation of CREB abolished the gem-mediated increase in IL-1Ra.	Gemfibrozil	126-129	interleukin 1 receptor antagonist	Mus musculus	151-157
22706077-8	2012	Furthermore, gem was able to protect neurons from IL-1beta insult.	Gemfibrozil	13-16	interleukin 1 alpha	Mus musculus	50-58
22706077-9	2012	However, small interfering RNA knockdown of neuronal IL-1Ra abrogated the protective effect of gem against IL-1beta, suggesting that this drug increases the defense mechanism of cortical neurons via upregulation of IL-1Ra.	Gemfibrozil	95-98	interleukin 1 receptor antagonist	Mus musculus	53-59
22706077-9	2012	However, small interfering RNA knockdown of neuronal IL-1Ra abrogated the protective effect of gem against IL-1beta, suggesting that this drug increases the defense mechanism of cortical neurons via upregulation of IL-1Ra.	Gemfibrozil	95-98	interleukin 1 alpha	Mus musculus	107-115
22706077-9	2012	However, small interfering RNA knockdown of neuronal IL-1Ra abrogated the protective effect of gem against IL-1beta, suggesting that this drug increases the defense mechanism of cortical neurons via upregulation of IL-1Ra.	Gemfibrozil	95-98	interleukin 1 receptor antagonist	Mus musculus	215-221
21838784-5	2012	Plasma concentrations of montelukast, gemfibrozil, itraconazole and their metabolites were measured up to 72 h. RESULTS: The CYP2C8 inhibitor gemfibrozil increased the AUC(0, ) of montelukast 4.3-fold and its t(1/2) 2.1-fold (P &lt; 0.001).	Gemfibrozil	38-49	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	125-131
21838784-5	2012	Plasma concentrations of montelukast, gemfibrozil, itraconazole and their metabolites were measured up to 72 h. RESULTS: The CYP2C8 inhibitor gemfibrozil increased the AUC(0, ) of montelukast 4.3-fold and its t(1/2) 2.1-fold (P &lt; 0.001).	Gemfibrozil	142-153	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	125-131
21917557-10	2011	The adjusted IRR for a statin and fenofibrate was 3.26 (95% CI 1.21 to 8.80), while the adjusted IRR for a statin and gemfibrozil was 11.93 (95% CI 3.96 to 35.93) versus statin therapy alone.	Gemfibrozil	118-129	insulin receptor related receptor	Homo sapiens	97-100
21903140-6	2012	The importance of TG in producing these changes was supported by the finding that the TG-lowering medication gemfibrozil as compared to vehicle, when peripherally administered before consumption of a HiSat meal, significantly decreased the expression of OX, while increasing the expression of NPY and AgRP.	Gemfibrozil	109-120	hypocretin neuropeptide precursor	Rattus norvegicus	254-256
21903140-6	2012	The importance of TG in producing these changes was supported by the finding that the TG-lowering medication gemfibrozil as compared to vehicle, when peripherally administered before consumption of a HiSat meal, significantly decreased the expression of OX, while increasing the expression of NPY and AgRP.	Gemfibrozil	109-120	neuropeptide Y	Rattus norvegicus	293-296
21903140-6	2012	The importance of TG in producing these changes was supported by the finding that the TG-lowering medication gemfibrozil as compared to vehicle, when peripherally administered before consumption of a HiSat meal, significantly decreased the expression of OX, while increasing the expression of NPY and AgRP.	Gemfibrozil	109-120	agouti related neuropeptide	Rattus norvegicus	301-305
22028316-6	2012	Because the haloperidol O-glucuronidation in a panel of 17 HLM was significantly correlated (r = 0.732, p &lt; 0.01) with zidovudine O-glucuronidation, a probe activity of UGT2B7, and the activity in the pooled HLM was prominently inhibited (58% of control) by gemfibrozil, an inhibitor of UGT2B7, we surmised that the reaction would mainly be catalyzed by UGT2B7.	Gemfibrozil	261-272	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	172-178
21911547-0	2011	Studies to further investigate the inhibition of human liver microsomal CYP2C8 by the acyl-beta-glucuronide of gemfibrozil.	Gemfibrozil	111-122	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	72-78
21911547-1	2011	In previous studies, gemfibrozil acyl-beta-glucuronide, but not gemfibrozil, was found to be a mechanism-based inhibitor of cytochrome P450 2C8.	Gemfibrozil	21-32	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	124-143
21911547-5	2011	When the aromatic methyl groups on the gemfibrozil moiety were substituted with trifluoromethyls, the resulting glucuronide conjugate was a weaker inhibitor of CYP2C8 and mechanism-based inhibition was abolished.	Gemfibrozil	39-50	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	160-166
21963672-0	2011	The PPAR alpha agonist gemfibrozil is an ineffective treatment for spinal cord injured mice.	Gemfibrozil	23-34	peroxisome proliferator activated receptor alpha	Mus musculus	4-14
21963672-2	2011	Gemfibrozil, an agonist of PPAR-alpha, is a FDA approved drug for hyperlipidemia and has been shown to inhibit clinical signs in a rodent model of multiple sclerosis.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	27-37
21881934-6	2011	Gemfibrozil was discontinued and in a few days AST and ALT levels returned to normal.	Gemfibrozil	0-11	solute carrier family 17 member 5	Homo sapiens	47-50
21889235-0	2011	Discovery of gemfibrozil analogues that activate PPARalpha and enhance the expression of gene CPT1A involved in fatty acids catabolism.	Gemfibrozil	13-24	peroxisome proliferator activated receptor alpha	Homo sapiens	49-58
21889235-0	2011	Discovery of gemfibrozil analogues that activate PPARalpha and enhance the expression of gene CPT1A involved in fatty acids catabolism.	Gemfibrozil	13-24	carnitine palmitoyltransferase 1A	Homo sapiens	94-99
21889235-1	2011	A new series of gemfibrozil analogues conjugated with alpha-asarone, trans-stilbene, chalcone, and their bioisosteric modifications were synthesized and evaluated to develop PPARalpha agonists.	Gemfibrozil	16-27	peroxisome proliferator activated receptor alpha	Homo sapiens	174-183
21778352-0	2011	Dose-dependent interaction between gemfibrozil and repaglinide in humans: strong inhibition of CYP2C8 with subtherapeutic gemfibrozil doses.	Gemfibrozil	122-133	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	95-101
21778352-2	2011	We investigated the effect of gemfibrozil dose on CYP2C8 activity in humans using repaglinide as a probe drug.	Gemfibrozil	30-41	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	50-56
21778352-7	2011	The gemfibrozil-repaglinide interaction could be mainly explained by gemfibrozil 1-O-beta-glucuronide concentration-dependent, mechanism-based inhibition of CYP2C8, with a minor contribution by competitive inhibition of organic anion-transporting polypeptide 1B1 at the highest gemfibrozil dose.	Gemfibrozil	4-15	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	157-163
21778352-8	2011	The findings are consistent with ~50% inhibition of CYP2C8 already with a single 30-mg dose of gemfibrozil and &gt;95% inhibition with 900 mg.	Gemfibrozil	95-106	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	52-58
21778352-9	2011	In clinical drug-drug interaction studies, a single 900-mg dose of gemfibrozil can be used to achieve nearly complete inactivation of CYP2C8.	Gemfibrozil	67-78	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	134-140
21368757-0	2011	Mechanism-based inactivation of CYP2C8 by gemfibrozil occurs rapidly in humans.	Gemfibrozil	42-53	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	32-38
21652050-5	2011	Gemfibrozil exposure induced biomarkers of stress (glutathione S-transferase and metallothionein) at both concentrations 24h and 96 h after exposure, respectively.	Gemfibrozil	0-11	glutathione S-transferase kappa 1	Homo sapiens	51-76
21297316-6	2011	Gemfibrozil displays DDIs with some OATP1B1 substrates, although their extent is small.	Gemfibrozil	0-11	solute carrier organic anion transporter family member 1B1	Homo sapiens	36-43
21223511-3	2011	Because serum paraoxonase 1 (PON1) is an important enzyme with specific protective function on metabolism of lipid peroxides, we examined the influence of GEM on PON1 activity in liver and serum.	Gemfibrozil	155-158	paraoxonase 1	Rattus norvegicus	14-27
21223511-3	2011	Because serum paraoxonase 1 (PON1) is an important enzyme with specific protective function on metabolism of lipid peroxides, we examined the influence of GEM on PON1 activity in liver and serum.	Gemfibrozil	155-158	paraoxonase 1	Rattus norvegicus	162-166
21381897-8	2011	The present results demonstrated complex interactions between IFN-alpha2b and hepatocytes and the observed down-regulation of CYP1A2, OAT2 and UGT2B7 is consistent with reports of drug interactions between IFN-alpha2b and drugs such as theophylline, clozapine and gemfibrozil.	Gemfibrozil	264-275	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	126-132
21381897-8	2011	The present results demonstrated complex interactions between IFN-alpha2b and hepatocytes and the observed down-regulation of CYP1A2, OAT2 and UGT2B7 is consistent with reports of drug interactions between IFN-alpha2b and drugs such as theophylline, clozapine and gemfibrozil.	Gemfibrozil	264-275	solute carrier family 22 member 7	Homo sapiens	134-138
21381897-8	2011	The present results demonstrated complex interactions between IFN-alpha2b and hepatocytes and the observed down-regulation of CYP1A2, OAT2 and UGT2B7 is consistent with reports of drug interactions between IFN-alpha2b and drugs such as theophylline, clozapine and gemfibrozil.	Gemfibrozil	264-275	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	143-149
21368757-1	2011	To study the time to onset of mechanism-based inactivation of cytochrome P450 (CYP) 2C8 by gemfibrozil in vivo, we conducted a randomized five-phase crossover study in 10 healthy volunteers.	Gemfibrozil	91-102	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	62-87
21368757-5	2011	The strong inactivation of CYP2C8, evident as soon as 1 h after gemfibrozil dosing, has implications in clinical practice and in studies with gemfibrozil as a CYP2C8 model inhibitor.	Gemfibrozil	64-75	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	27-33
21368757-5	2011	The strong inactivation of CYP2C8, evident as soon as 1 h after gemfibrozil dosing, has implications in clinical practice and in studies with gemfibrozil as a CYP2C8 model inhibitor.	Gemfibrozil	142-153	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	27-33
21368757-5	2011	The strong inactivation of CYP2C8, evident as soon as 1 h after gemfibrozil dosing, has implications in clinical practice and in studies with gemfibrozil as a CYP2C8 model inhibitor.	Gemfibrozil	142-153	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	159-165
19628752-7	2009	In MRP3-expressing membrane vesicles, ATP-dependent uptakes of the glucuronide conjugates of estradiol, gemfibrozil, E3040, and troglitazone were markedly greater than those in controls, whereas MRP4-expressing membrane vesicles exhibited significant ATP-dependent uptake of gemfibrozil glucuronide and estradiol glucuronide.	Gemfibrozil	104-115	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	3-7
20931329-1	2011	PURPOSE: Gemfibrozil, a strong inhibitor of cytochrome P450 (CYP) 2C8 in vivo, was recently found to markedly increase the plasma concentrations of montelukast in humans.	Gemfibrozil	9-20	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	44-69
21175442-12	2010	CONCLUSIONS: Inhibition of UGT enzymes, especially UGT1A1, by gemfibrozil and its glucuronide is an additional mechanism to consider when rationalizing the interaction between repaglinide and gemfibrozil.	Gemfibrozil	62-73	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	27-30
21175442-12	2010	CONCLUSIONS: Inhibition of UGT enzymes, especially UGT1A1, by gemfibrozil and its glucuronide is an additional mechanism to consider when rationalizing the interaction between repaglinide and gemfibrozil.	Gemfibrozil	62-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
21175442-12	2010	CONCLUSIONS: Inhibition of UGT enzymes, especially UGT1A1, by gemfibrozil and its glucuronide is an additional mechanism to consider when rationalizing the interaction between repaglinide and gemfibrozil.	Gemfibrozil	192-203	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	27-30
21175442-12	2010	CONCLUSIONS: Inhibition of UGT enzymes, especially UGT1A1, by gemfibrozil and its glucuronide is an additional mechanism to consider when rationalizing the interaction between repaglinide and gemfibrozil.	Gemfibrozil	192-203	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
19779008-5	2010	This is of great interest since we have recently shown that gemfibrozil, a drug used to treat hyperlipidemia in humans and a synthetic ligand of PPAR alpha, significantly reduces the mortality associated with influenza infections in mice.	Gemfibrozil	60-71	peroxisome proliferator activated receptor alpha	Homo sapiens	145-155
20810571-8	2010	The relative potency of the compounds was different with each chemokine; for example, gemfibrozil exerted a 55% inhibition on CXCL11, whereas it had a weaker activity on CXCL9 (40% inhibition).	Gemfibrozil	86-97	C-X-C motif chemokine ligand 11	Homo sapiens	126-132
20949026-8	2010	A beneficial effect on aortic plaques was also obtained by treating ApoE(-/-) mice with gemfibrozil, a PPARalpha agonist.	Gemfibrozil	88-99	apolipoprotein E	Mus musculus	68-72
20949026-8	2010	A beneficial effect on aortic plaques was also obtained by treating ApoE(-/-) mice with gemfibrozil, a PPARalpha agonist.	Gemfibrozil	88-99	peroxisome proliferator activated receptor alpha	Mus musculus	103-112
20516252-9	2010	Further studies with this novel model demonstrated that OATP and cytochrome P450 have a synergistic effect on cerivastatin-gemfibrozil interactions.	Gemfibrozil	123-134	solute carrier organic anion transporter family member 1A2	Homo sapiens	56-60
20548972-0	2010	Effects of high sucrose diet, gemfibrozil, and their combination on plasma paraoxonase 1 activity and lipid levels in rats.	Gemfibrozil	30-41	paraoxonase 1	Rattus norvegicus	75-88
20953357-7	2010	These events are causally related to hepatotoxicity and hepatocarcinogenicity of gemfibrozil in rodents via peroxisome proliferator activated receptor-alpha (PPARalpha) activation; however, there is widespread evidence that activation of PPARalpha in humans results in expression of genes involved in lipid metabolism, but not in hepatocellular proliferation.	Gemfibrozil	81-92	peroxisome proliferator activated receptor alpha	Homo sapiens	108-156
20953357-7	2010	These events are causally related to hepatotoxicity and hepatocarcinogenicity of gemfibrozil in rodents via peroxisome proliferator activated receptor-alpha (PPARalpha) activation; however, there is widespread evidence that activation of PPARalpha in humans results in expression of genes involved in lipid metabolism, but not in hepatocellular proliferation.	Gemfibrozil	81-92	peroxisome proliferator activated receptor alpha	Homo sapiens	158-167
20953357-7	2010	These events are causally related to hepatotoxicity and hepatocarcinogenicity of gemfibrozil in rodents via peroxisome proliferator activated receptor-alpha (PPARalpha) activation; however, there is widespread evidence that activation of PPARalpha in humans results in expression of genes involved in lipid metabolism, but not in hepatocellular proliferation.	Gemfibrozil	81-92	peroxisome proliferator activated receptor alpha	Homo sapiens	238-247
19919292-10	2010	Bezafibrate and gemfibrozil exhibited concentration-dependent inhibition of OATP1B1-mediated uptake of [(3)H]-oestradiol 17beta-glucuronide with mean IC(50) values of 16 and 27 microM, respectively.	Gemfibrozil	16-27	solute carrier organic anion transporter family member 1B1	Homo sapiens	76-83
21966330-2	2011	Fibrates, including fenofibrate, gemfibrozil, benzafibrate, ciprofibrate, and clofibrate act on PPAR alpha to reduce the level of hypertriglyceridemia.	Gemfibrozil	33-44	peroxisome proliferator activated receptor alpha	Homo sapiens	96-106
20592724-0	2010	Gemfibrozil markedly increases the plasma concentrations of montelukast: a previously unrecognized role for CYP2C8 in the metabolism of montelukast.	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	108-114
20592724-6	2010	In conclusion, gemfibrozil markedly increases the plasma concentrations of montelukast, indicating that CYP2C8 is crucial in the elimination of montelukast.	Gemfibrozil	15-26	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	104-110
20006695-6	2010	(iii) Parallel changes of prestin mRNA and Gata-3,-2 mRNA levels were observed in response to thyroid hormone and to gemfibrozil application.	Gemfibrozil	117-128	solute carrier family 26 member 5	Rattus norvegicus	26-33
20006695-6	2010	(iii) Parallel changes of prestin mRNA and Gata-3,-2 mRNA levels were observed in response to thyroid hormone and to gemfibrozil application.	Gemfibrozil	117-128	GATA binding protein 3	Rattus norvegicus	43-52
20548972-4	2010	In the rats on CD and HSD, GEM caused a significant decrease of PON1 activity by 44% and 33%, while a significant decrease of TGs level by 38% (P&lt;0.05) was measured only in rats on CD.	Gemfibrozil	27-30	paraoxonase 1	Rattus norvegicus	64-68
20208386-4	2010	Studies with HLM under-predict the ability of gemfibrozil and bupropion to cause clinically significant inhibition of CYP2C8 and CYP2D6, respectively, and over-predict the ability of ezetimibe to cause clinically significant inhibition of CYP3A4.	Gemfibrozil	46-57	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	118-124
20208386-4	2010	Studies with HLM under-predict the ability of gemfibrozil and bupropion to cause clinically significant inhibition of CYP2C8 and CYP2D6, respectively, and over-predict the ability of ezetimibe to cause clinically significant inhibition of CYP3A4.	Gemfibrozil	46-57	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	129-135
20208386-5	2010	Gemfibrozil and bupropion represent examples of glucuronidation-dependent and reduction-dependent activation to metabolites that inhibit CYP2C8 and CYP2D6, respectively, whereas ezetimibe represents an example of glucuronidation-dependent protection against metabolism-dependent inhibition of CYP3A4.	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	137-143
20208386-5	2010	Gemfibrozil and bupropion represent examples of glucuronidation-dependent and reduction-dependent activation to metabolites that inhibit CYP2C8 and CYP2D6, respectively, whereas ezetimibe represents an example of glucuronidation-dependent protection against metabolism-dependent inhibition of CYP3A4.	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	148-154
20208386-5	2010	Gemfibrozil and bupropion represent examples of glucuronidation-dependent and reduction-dependent activation to metabolites that inhibit CYP2C8 and CYP2D6, respectively, whereas ezetimibe represents an example of glucuronidation-dependent protection against metabolism-dependent inhibition of CYP3A4.	Gemfibrozil	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	293-299
19628752-10	2009	Significant reductions in the basal-to-apical flux of the glucuronide conjugates of estradiol, gemfibrozil, E3040, and troglitazone were observed in the OATP1B1/MRP2/MRP3 triple transfectants compared with those in the double transfectants, whereas significant reduction was observed only for gemfibrozil glucuronide and estradiol glucuronide in the OATP1B1/MRP2/MRP4 triple transfectants.	Gemfibrozil	95-106	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	161-165
19628752-10	2009	Significant reductions in the basal-to-apical flux of the glucuronide conjugates of estradiol, gemfibrozil, E3040, and troglitazone were observed in the OATP1B1/MRP2/MRP3 triple transfectants compared with those in the double transfectants, whereas significant reduction was observed only for gemfibrozil glucuronide and estradiol glucuronide in the OATP1B1/MRP2/MRP4 triple transfectants.	Gemfibrozil	95-106	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	166-170
19628752-10	2009	Significant reductions in the basal-to-apical flux of the glucuronide conjugates of estradiol, gemfibrozil, E3040, and troglitazone were observed in the OATP1B1/MRP2/MRP3 triple transfectants compared with those in the double transfectants, whereas significant reduction was observed only for gemfibrozil glucuronide and estradiol glucuronide in the OATP1B1/MRP2/MRP4 triple transfectants.	Gemfibrozil	95-106	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	358-362
19628752-10	2009	Significant reductions in the basal-to-apical flux of the glucuronide conjugates of estradiol, gemfibrozil, E3040, and troglitazone were observed in the OATP1B1/MRP2/MRP3 triple transfectants compared with those in the double transfectants, whereas significant reduction was observed only for gemfibrozil glucuronide and estradiol glucuronide in the OATP1B1/MRP2/MRP4 triple transfectants.	Gemfibrozil	95-106	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	363-367
19801273-11	2009	In Experiment 4, the TG-lowering drug gemfibrozil also caused a significant reduction in the expression of the orexigenic peptide, OX, in the perifornical lateral hypothalamus.	Gemfibrozil	38-49	hypocretin neuropeptide precursor	Rattus norvegicus	131-133
19376321-4	2009	The objective of this study was to investigate whether the PPARalpha activator gemfibrozil prevents or delays the development of AF in patients with coronary heart disease.	Gemfibrozil	79-90	peroxisome proliferator activated receptor alpha	Homo sapiens	59-68
19307362-3	2009	In the present paper, we first show that ciprofloxacin-resistant cells display a faster efflux of ciprofloxacin which is inhibited by gemfibrozil (an unspecific MRP inhibitor).	Gemfibrozil	134-145	ATP-binding cassette, sub-family C (CFTR/MRP), member 1	Mus musculus	161-164
19492148-7	2009	In cultured preadipocytes and adipocytes gemfibrozil and fenofibrate significantly reduced PAI-1 protein expression by up to 55 +/- 5% and 34 +/- 4% under basal conditions and up to 56 +/- 6% and 31 +/- 6% under conditions of stimulation of the cells with 40 pM transforming growth factor (TGF)beta, respectively.	Gemfibrozil	41-52	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	91-96
19492148-7	2009	In cultured preadipocytes and adipocytes gemfibrozil and fenofibrate significantly reduced PAI-1 protein expression by up to 55 +/- 5% and 34 +/- 4% under basal conditions and up to 56 +/- 6% and 31 +/- 6% under conditions of stimulation of the cells with 40 pM transforming growth factor (TGF)beta, respectively.	Gemfibrozil	41-52	transforming growth factor, beta 1	Mus musculus	290-298
19492148-10	2009	The decrease in PAI-1 expression induced by gemfibrozil was inhibited by MK886, a PPARalpha inhibitor.	Gemfibrozil	44-55	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	16-21
19492148-10	2009	The decrease in PAI-1 expression induced by gemfibrozil was inhibited by MK886, a PPARalpha inhibitor.	Gemfibrozil	44-55	peroxisome proliferator activated receptor alpha	Mus musculus	82-91
19299749-2	2009	In this study, we investigated the mechanism by which the PPARalpha agonist gemfibrozil induces immune deviation and protects mice from EAE.	Gemfibrozil	76-87	peroxisome proliferator activated receptor alpha	Mus musculus	58-67
19299749-3	2009	We demonstrated that treatment with gemfibrozil increases expression of the Th2 transcription factor GATA-3 and decreases expression of the Th1 transcription factor T-bet in vitro and directly ex vivo.	Gemfibrozil	36-47	GATA binding protein 3	Mus musculus	101-107
19299749-3	2009	We demonstrated that treatment with gemfibrozil increases expression of the Th2 transcription factor GATA-3 and decreases expression of the Th1 transcription factor T-bet in vitro and directly ex vivo.	Gemfibrozil	36-47	negative elongation factor complex member C/D, Th1l	Mus musculus	140-143
19299749-3	2009	We demonstrated that treatment with gemfibrozil increases expression of the Th2 transcription factor GATA-3 and decreases expression of the Th1 transcription factor T-bet in vitro and directly ex vivo.	Gemfibrozil	36-47	delta/notch-like EGF repeat containing	Mus musculus	167-170
19166694-6	2009	The combination of nicotinic acid and gemfibrozil resulted in a further 17.8% reduction in apolipoprotein B (p = 0.06), a further 33.8% reduction in IDL (p = 0.06), and a greater reduction in the apolipoprotein B/apolipoprotein A-I ratio (p = 0.02).	Gemfibrozil	38-49	apolipoprotein B	Homo sapiens	91-107
19166694-6	2009	The combination of nicotinic acid and gemfibrozil resulted in a further 17.8% reduction in apolipoprotein B (p = 0.06), a further 33.8% reduction in IDL (p = 0.06), and a greater reduction in the apolipoprotein B/apolipoprotein A-I ratio (p = 0.02).	Gemfibrozil	38-49	apolipoprotein B	Homo sapiens	196-212
19166694-6	2009	The combination of nicotinic acid and gemfibrozil resulted in a further 17.8% reduction in apolipoprotein B (p = 0.06), a further 33.8% reduction in IDL (p = 0.06), and a greater reduction in the apolipoprotein B/apolipoprotein A-I ratio (p = 0.02).	Gemfibrozil	38-49	apolipoprotein A1	Homo sapiens	213-231
19166694-7	2009	The combination of nicotinic acid and gemfibrozil reduced atherogenic by IDL 71%, dense LDL-III by 52%, and apolipoprotein B by 37% and increased protective HDL(2) by 90%.	Gemfibrozil	38-49	apolipoprotein B	Homo sapiens	108-124
19166694-7	2009	The combination of nicotinic acid and gemfibrozil reduced atherogenic by IDL 71%, dense LDL-III by 52%, and apolipoprotein B by 37% and increased protective HDL(2) by 90%.	Gemfibrozil	38-49	junctophilin 3	Homo sapiens	157-163
19238654-2	2008	The mean increase in the repaglinide area under the plasma concentration-time curve from 0 h to infinity (AUC(0-infinity)) produced by gemfibrozil was larger in individuals with the SLCO1B1 c.521CC genotype (n = 6) than in those with the c.521TC (n = 6) and c.521TT (n = 12) genotypes, by factors of 1.56 (P = 0.004) and 1.54 (P = 0.002), respectively.	Gemfibrozil	135-146	solute carrier organic anion transporter family member 1B1	Homo sapiens	182-189
18799592-1	2008	The first generation peroxisome proliferator-activated receptor (PPAR) alpha agonist gemfibrozil reduces the risk of major cardiovascular events; therefore, more potent PPARalpha agonists for the treatment of cardiovascular diseases have been actively sought.	Gemfibrozil	85-96	peroxisome proliferator activated receptor alpha	Homo sapiens	65-69
18799592-1	2008	The first generation peroxisome proliferator-activated receptor (PPAR) alpha agonist gemfibrozil reduces the risk of major cardiovascular events; therefore, more potent PPARalpha agonists for the treatment of cardiovascular diseases have been actively sought.	Gemfibrozil	85-96	peroxisome proliferator activated receptor alpha	Mus musculus	169-178
19238654-6	2008	In conclusion, the extent of gemfibrozil-repaglinide interaction depends on SLCO1B1 genotype.	Gemfibrozil	29-40	solute carrier organic anion transporter family member 1B1	Homo sapiens	76-83
18325492-7	2008	Despite these differences, the C299S AKR1B10 mutant still manifests kinetics similar to the wild-type protein with other fibrates including zopolrestat, fenofibrate, Wy 14,346, gemfibrozil and ciprofibrate that show mixed non-competitive inhibition kinetics.	Gemfibrozil	177-188	aldo-keto reductase family 1 member B10	Homo sapiens	37-44
18678301-1	2008	The weak peroxisome proliferator activated receptor-alpha (PPAR-alpha) agonists gemfibrozil and fenofibrate achieve only small increases in high-density lipoprotein (HDL) cholesterol.	Gemfibrozil	80-91	peroxisome proliferator activated receptor alpha	Homo sapiens	9-57
18678301-1	2008	The weak peroxisome proliferator activated receptor-alpha (PPAR-alpha) agonists gemfibrozil and fenofibrate achieve only small increases in high-density lipoprotein (HDL) cholesterol.	Gemfibrozil	80-91	peroxisome proliferator activated receptor alpha	Homo sapiens	59-69
18420459-6	2008	An experimental study has shown that the fibrate gemfibrozil, a peroxisome proliferator-activated receptor (PPAR) alpha agonist, reduces mortality in H2N2 influenza virus-infected mice.	Gemfibrozil	49-60	peroxisome proliferator activated receptor alpha	Homo sapiens	108-112
18547436-7	2008	Changes in plasma PCSK9 following fenofibrate or gemfibrozil treatments (fibric acid derivatives) were inversely correlated with changes in LDLC levels (r = -0.558, p = 0.013).	Gemfibrozil	49-60	proprotein convertase subtilisin/kexin type 9	Homo sapiens	18-23
18547436-7	2008	Changes in plasma PCSK9 following fenofibrate or gemfibrozil treatments (fibric acid derivatives) were inversely correlated with changes in LDLC levels (r = -0.558, p = 0.013).	Gemfibrozil	49-60	component of oligomeric golgi complex 2	Homo sapiens	140-144
18356553-6	2008	Although gemfibrozil reduced Lp-PLA(2) only modestly (6.6%), at higher levels of Lp-PLA(2) gemfibrozil produced a significant reduction in CV events.	Gemfibrozil	9-20	phospholipase A2 group VII	Homo sapiens	29-37
18356553-6	2008	Although gemfibrozil reduced Lp-PLA(2) only modestly (6.6%), at higher levels of Lp-PLA(2) gemfibrozil produced a significant reduction in CV events.	Gemfibrozil	9-20	phospholipase A2 group VII	Homo sapiens	29-38
18356553-7	2008	CONCLUSIONS: In VA-HIT, a population with low HDL-C and LDL-C, high Lp-PLA(2) independently predicted CV events that were reduced by gemfibrozil.	Gemfibrozil	133-144	component of oligomeric golgi complex 2	Homo sapiens	56-61
18356553-7	2008	CONCLUSIONS: In VA-HIT, a population with low HDL-C and LDL-C, high Lp-PLA(2) independently predicted CV events that were reduced by gemfibrozil.	Gemfibrozil	133-144	phospholipase A2 group VII	Homo sapiens	68-76
17901929-5	2008	Gemfibrozil and cyclosporine inhibition data obtained in human embryonic kidney cells expressing OATP1B1 and hepatic input concentration ([I]in) were used for qualitative zoning of 14 transporter-mediated DDIs.	Gemfibrozil	0-11	solute carrier organic anion transporter family member 1B1	Homo sapiens	97-104
17335828-8	2008	CONCLUSIONS: In VA-HIT, gemfibrozil resulted in weight loss associated with reductions in insulin.	Gemfibrozil	24-35	insulin	Homo sapiens	90-97
18502109-5	2008	Gemfibrozil produces major modifications in fatty acid composition, which are both fatty acid and lipid class specific but generally decreases SFA and increases PUFA (mainly n6) and increases the proportion of fatty acids with chain length of 18C or more.	Gemfibrozil	0-11	pumilio RNA binding family member 3	Homo sapiens	161-165
18356690-5	2008	While fenofibrate and LY518674 showed exclusive dependency on PPARalpha for these activities, bezafibrate and gemfibrozil exhibited dependency on PPARbeta/delta and PPARgamma as well.	Gemfibrozil	110-121	peroxisome proliferator activated receptor delta	Homo sapiens	146-154
18356690-5	2008	While fenofibrate and LY518674 showed exclusive dependency on PPARalpha for these activities, bezafibrate and gemfibrozil exhibited dependency on PPARbeta/delta and PPARgamma as well.	Gemfibrozil	110-121	peroxisome proliferator activated receptor gamma	Homo sapiens	165-174
17625103-7	2007	The histological and immunohistochemical analyses also demonstrate the inhibitory effect of gemfibrozil on the invasion of T-bet-positive T cells into the spinal cord of EAE mice.	Gemfibrozil	92-103	T-box 21	Mus musculus	123-128
18092840-13	2008	In clinical trials of gemfibrozil, a PPARalpha ligand, significantly fewer patients treated with this lipid-lowering drug were diagnosed with melanoma as compared to those in the control group.	Gemfibrozil	22-33	peroxisome proliferator activated receptor alpha	Homo sapiens	37-46
17823123-3	2007	Here we describe that after Th2 polarization by gemfibrozil or other drugs, MBP-primed T cells induced the expression of neurotrophic molecules such as brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), but not proinflammatory molecules in microglia and astroglia via cell-to-cell contact.	Gemfibrozil	48-59	myelin basic protein	Homo sapiens	76-79
17823123-3	2007	Here we describe that after Th2 polarization by gemfibrozil or other drugs, MBP-primed T cells induced the expression of neurotrophic molecules such as brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), but not proinflammatory molecules in microglia and astroglia via cell-to-cell contact.	Gemfibrozil	48-59	brain derived neurotrophic factor	Homo sapiens	152-185
17965553-6	2007	In fact, WY-14,643, clofibrate, gemfibrozil and benzbromarone, reported to be PPARalpha activators, distributed to the former, whereas propylthiouracil, omeprazole, phenobarbital, thioacetamide, methapyrilene, sulfasalazine and coumarin did to the latter.	Gemfibrozil	32-43	peroxisome proliferator activated receptor alpha	Rattus norvegicus	78-87
18078862-5	2008	Analyses in the gemfibrozil arm showed that subjects with recurrent CVD events had significantly higher prebeta-1 and had significantly lower alpha-1 and alpha-2 HDL levels than those without such events.	Gemfibrozil	16-27	adrenoceptor alpha 1D	Homo sapiens	142-149
18078862-8	2008	Gemfibrozil treatment was associated with 3% to 6% decreases in the small, lipid-poor prebeta-1 HDL and in the large, lipid-rich alpha-1 and alpha-2 HDL and with increases in the small alpha-3 (3%) and prealpha-3 (16%) HDLs.	Gemfibrozil	0-11	adrenoceptor alpha 1D	Homo sapiens	129-136
17670842-0	2007	The UDP-glucuronosyltransferase 2B7 isozyme is responsible for gemfibrozil glucuronidation in the human liver.	Gemfibrozil	63-74	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	4-35
17670842-3	2007	Comprehensive assessment of the drug interaction between gemfibrozil and cytochrome P450 2C8 substrates requires a clear understanding of gemfibrozil glucuronidation.	Gemfibrozil	138-149	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	73-92
17670842-4	2007	However, the primary UDP-glucuronosyltransferase (UGT) isozymes responsible for gemfibrozil glucuronidation remain to be determined.	Gemfibrozil	80-91	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	21-48
17670842-4	2007	However, the primary UDP-glucuronosyltransferase (UGT) isozymes responsible for gemfibrozil glucuronidation remain to be determined.	Gemfibrozil	80-91	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	50-53
17670842-5	2007	Here, we identified the main UGT isozymes involved in gemfibrozil glucuronidation.	Gemfibrozil	54-65	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	29-32
17670842-6	2007	Evaluation of 12 recombinant human UGT isozymes shows gemfibrozil glucuronidation activity in UGT1A1, UGT1A3, UGT1A9, UGT2B4, UGT2B7, and UGT2B17, with UGT2B7 showing the highest activity.	Gemfibrozil	54-65	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	35-38
17670842-6	2007	Evaluation of 12 recombinant human UGT isozymes shows gemfibrozil glucuronidation activity in UGT1A1, UGT1A3, UGT1A9, UGT2B4, UGT2B7, and UGT2B17, with UGT2B7 showing the highest activity.	Gemfibrozil	54-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
17670842-6	2007	Evaluation of 12 recombinant human UGT isozymes shows gemfibrozil glucuronidation activity in UGT1A1, UGT1A3, UGT1A9, UGT2B4, UGT2B7, and UGT2B17, with UGT2B7 showing the highest activity.	Gemfibrozil	54-65	UDP glucuronosyltransferase family 1 member A3	Homo sapiens	102-108
17670842-6	2007	Evaluation of 12 recombinant human UGT isozymes shows gemfibrozil glucuronidation activity in UGT1A1, UGT1A3, UGT1A9, UGT2B4, UGT2B7, and UGT2B17, with UGT2B7 showing the highest activity.	Gemfibrozil	54-65	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	110-116
17670842-6	2007	Evaluation of 12 recombinant human UGT isozymes shows gemfibrozil glucuronidation activity in UGT1A1, UGT1A3, UGT1A9, UGT2B4, UGT2B7, and UGT2B17, with UGT2B7 showing the highest activity.	Gemfibrozil	54-65	UDP glucuronosyltransferase family 2 member B4	Homo sapiens	118-124
17670842-6	2007	Evaluation of 12 recombinant human UGT isozymes shows gemfibrozil glucuronidation activity in UGT1A1, UGT1A3, UGT1A9, UGT2B4, UGT2B7, and UGT2B17, with UGT2B7 showing the highest activity.	Gemfibrozil	54-65	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	126-132
17670842-6	2007	Evaluation of 12 recombinant human UGT isozymes shows gemfibrozil glucuronidation activity in UGT1A1, UGT1A3, UGT1A9, UGT2B4, UGT2B7, and UGT2B17, with UGT2B7 showing the highest activity.	Gemfibrozil	54-65	UDP glucuronosyltransferase family 2 member B17	Homo sapiens	138-145
17670842-6	2007	Evaluation of 12 recombinant human UGT isozymes shows gemfibrozil glucuronidation activity in UGT1A1, UGT1A3, UGT1A9, UGT2B4, UGT2B7, and UGT2B17, with UGT2B7 showing the highest activity.	Gemfibrozil	54-65	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	152-158
17670842-8	2007	The high affinity K(m) value was 2.5 microM, which is similar to the K(m) value of gemfibrozil glucuronidation in recombinant UGT2B7 (2.2 microM).	Gemfibrozil	83-94	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	126-132
17670842-11	2007	These results suggest that UGT2B7 is the main isozyme responsible for gemfibrozil glucuronidation in humans.	Gemfibrozil	70-81	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	27-33
17625103-1	2007	The present study underlines the importance of gemfibrozil, a lipid-lowering drug and an activator of peroxisome proliferator-activated receptor-alpha (PPAR-alpha), in inhibiting the disease process of adoptively transferred experimental allergic encephalomyelitis (EAE), an animal model of relapsing-remitting multiple sclerosis.	Gemfibrozil	47-58	peroxisome proliferator activated receptor alpha	Mus musculus	102-150
17625103-1	2007	The present study underlines the importance of gemfibrozil, a lipid-lowering drug and an activator of peroxisome proliferator-activated receptor-alpha (PPAR-alpha), in inhibiting the disease process of adoptively transferred experimental allergic encephalomyelitis (EAE), an animal model of relapsing-remitting multiple sclerosis.	Gemfibrozil	47-58	peroxisome proliferator activated receptor alpha	Mus musculus	152-162
17625103-4	2007	Gemfibrozil also inhibited the encephalitogenicity of MBP-primed T cells and switched the immune response from a Th1 to a Th2 profile independent of PPAR-alpha.	Gemfibrozil	0-11	myelin basic protein	Mus musculus	54-57
17625103-4	2007	Gemfibrozil also inhibited the encephalitogenicity of MBP-primed T cells and switched the immune response from a Th1 to a Th2 profile independent of PPAR-alpha.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	149-159
17625103-5	2007	Gemfibrozil consistently inhibited the expression and DNA-binding activity of T-bet, a key regulator of interferon-gamma (IFN-gamma) expression and stimulated the expression and DNA-binding activity of GATA3, a key regulator of IL-4.	Gemfibrozil	0-11	T-box 21	Mus musculus	78-83
17625103-5	2007	Gemfibrozil consistently inhibited the expression and DNA-binding activity of T-bet, a key regulator of interferon-gamma (IFN-gamma) expression and stimulated the expression and DNA-binding activity of GATA3, a key regulator of IL-4.	Gemfibrozil	0-11	interferon gamma	Mus musculus	104-120
17625103-8	2007	Furthermore, we demonstrate that the differential effect of gemfibrozil on the expression of T-bet and GATA3 was due to its inhibitory effect on NO production.	Gemfibrozil	60-71	T-box 21	Mus musculus	93-98
17625103-5	2007	Gemfibrozil consistently inhibited the expression and DNA-binding activity of T-bet, a key regulator of interferon-gamma (IFN-gamma) expression and stimulated the expression and DNA-binding activity of GATA3, a key regulator of IL-4.	Gemfibrozil	0-11	interferon gamma	Mus musculus	122-131
17625103-5	2007	Gemfibrozil consistently inhibited the expression and DNA-binding activity of T-bet, a key regulator of interferon-gamma (IFN-gamma) expression and stimulated the expression and DNA-binding activity of GATA3, a key regulator of IL-4.	Gemfibrozil	0-11	GATA binding protein 3	Mus musculus	202-207
17625103-5	2007	Gemfibrozil consistently inhibited the expression and DNA-binding activity of T-bet, a key regulator of interferon-gamma (IFN-gamma) expression and stimulated the expression and DNA-binding activity of GATA3, a key regulator of IL-4.	Gemfibrozil	0-11	interleukin 4	Mus musculus	228-232
17625103-8	2007	Furthermore, we demonstrate that the differential effect of gemfibrozil on the expression of T-bet and GATA3 was due to its inhibitory effect on NO production.	Gemfibrozil	60-71	GATA binding protein 3	Mus musculus	103-108
17470528-0	2007	Substrate-dependent drug-drug interactions between gemfibrozil, fluvastatin and other organic anion-transporting peptide (OATP) substrates on OATP1B1, OATP2B1, and OATP1B3.	Gemfibrozil	51-62	solute carrier organic anion transporter family member 1A2	Homo sapiens	86-120
17625103-6	2007	Gemfibrozil treatment decreased the number of T-bet-positive T cells and increased the number of GATA3-positive T cells in spleen of donor mice.	Gemfibrozil	0-11	T-box transcription factor 21	Homo sapiens	46-51
17625103-6	2007	Gemfibrozil treatment decreased the number of T-bet-positive T cells and increased the number of GATA3-positive T cells in spleen of donor mice.	Gemfibrozil	0-11	GATA binding protein 3	Homo sapiens	97-102
17470528-8	2007	Recombinant OATP1B1-, OATP2B1-, and OATP1B3-mediated fluvastatin transport was inhibited to 97, 70, and 62% by gemfibrozil (200 microM), respectively, whereas only a small inhibitory effect by gemfibrozil (200 microM) on fluvastatin uptake into primary human hepatocytes was observed (27% inhibition).	Gemfibrozil	193-204	solute carrier organic anion transporter family member 1B1	Homo sapiens	12-19
17785853-0	2007	Involvement of phosphatidylinositol 3-kinase-mediated up-regulation of I kappa B alpha in anti-inflammatory effect of gemfibrozil in microglia.	Gemfibrozil	118-129	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	71-86
17785853-2	2007	Gemfibrozil inhibited LPS-induced expression of inducible NO synthase (iNOS) and proinflammatory cytokines in mouse BV-2 microglial cells and primary microglia.	Gemfibrozil	0-11	nitric oxide synthase 2, inducible	Mus musculus	48-69
17785853-2	2007	Gemfibrozil inhibited LPS-induced expression of inducible NO synthase (iNOS) and proinflammatory cytokines in mouse BV-2 microglial cells and primary microglia.	Gemfibrozil	0-11	nitric oxide synthase 2, inducible	Mus musculus	71-75
17785853-3	2007	By overexpressing wild-type and dominant-negative constructs of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) in microglial cells and isolating primary microglia from PPAR-alpha-/- mice, we have demonstrated that gemfibrozil inhibits the activation of microglia independent of PPAR-alpha.	Gemfibrozil	229-240	peroxisome proliferator activated receptor alpha	Mus musculus	64-112
17785853-3	2007	By overexpressing wild-type and dominant-negative constructs of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) in microglial cells and isolating primary microglia from PPAR-alpha-/- mice, we have demonstrated that gemfibrozil inhibits the activation of microglia independent of PPAR-alpha.	Gemfibrozil	229-240	peroxisome proliferator activated receptor alpha	Mus musculus	114-124
17785853-4	2007	Interestingly, gemfibrozil induced the activation of p85alpha-associated PI3K (p110beta but not p110alpha) and inhibition of that PI3K by either chemical inhibitors or dominant-negative mutants abrogated the inhibitory effect of gemfibrozil.	Gemfibrozil	15-26	phosphoinositide-3-kinase regulatory subunit 1	Mus musculus	53-61
17785853-4	2007	Interestingly, gemfibrozil induced the activation of p85alpha-associated PI3K (p110beta but not p110alpha) and inhibition of that PI3K by either chemical inhibitors or dominant-negative mutants abrogated the inhibitory effect of gemfibrozil.	Gemfibrozil	15-26	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta	Mus musculus	79-87
17785853-4	2007	Interestingly, gemfibrozil induced the activation of p85alpha-associated PI3K (p110beta but not p110alpha) and inhibition of that PI3K by either chemical inhibitors or dominant-negative mutants abrogated the inhibitory effect of gemfibrozil.	Gemfibrozil	229-240	phosphoinositide-3-kinase regulatory subunit 1	Mus musculus	53-61
17785853-5	2007	Conversely, overexpression of the constitutively active mutant of p110 enhanced the inhibitory effect of gemfibrozil on LPS-induced expression of proinflammatory molecules.	Gemfibrozil	105-116	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Mus musculus	66-70
17785853-6	2007	Similarly, gemfibrozil also inhibited fibrillar amyloid beta (Abeta)-, prion peptide (PrP)-, dsRNA (poly IC)-, HIV-1 Tat-, and 1-methyl-4-phenylpyridinium (MPP+)-, but not IFN-gamma-, induced microglial expression of iNOS.	Gemfibrozil	11-22	prion protein	Mus musculus	86-89
17785853-6	2007	Similarly, gemfibrozil also inhibited fibrillar amyloid beta (Abeta)-, prion peptide (PrP)-, dsRNA (poly IC)-, HIV-1 Tat-, and 1-methyl-4-phenylpyridinium (MPP+)-, but not IFN-gamma-, induced microglial expression of iNOS.	Gemfibrozil	11-22	interferon gamma	Mus musculus	172-181
17785853-6	2007	Similarly, gemfibrozil also inhibited fibrillar amyloid beta (Abeta)-, prion peptide (PrP)-, dsRNA (poly IC)-, HIV-1 Tat-, and 1-methyl-4-phenylpyridinium (MPP+)-, but not IFN-gamma-, induced microglial expression of iNOS.	Gemfibrozil	11-22	nitric oxide synthase 2, inducible	Mus musculus	217-221
17785853-7	2007	Inhibition of PI3K also abolished the inhibitory effect of gemfibrozil on Abeta-, PrP-, poly IC-, Tat-, and MPP+-induced microglial expression of iNOS.	Gemfibrozil	59-70	prion protein	Mus musculus	82-85
17785853-7	2007	Inhibition of PI3K also abolished the inhibitory effect of gemfibrozil on Abeta-, PrP-, poly IC-, Tat-, and MPP+-induced microglial expression of iNOS.	Gemfibrozil	59-70	nitric oxide synthase 2, inducible	Mus musculus	146-150
17470528-8	2007	Recombinant OATP1B1-, OATP2B1-, and OATP1B3-mediated fluvastatin transport was inhibited to 97, 70, and 62% by gemfibrozil (200 microM), respectively, whereas only a small inhibitory effect by gemfibrozil (200 microM) on fluvastatin uptake into primary human hepatocytes was observed (27% inhibition).	Gemfibrozil	193-204	solute carrier organic anion transporter family member 2B1	Homo sapiens	22-29
17470528-8	2007	Recombinant OATP1B1-, OATP2B1-, and OATP1B3-mediated fluvastatin transport was inhibited to 97, 70, and 62% by gemfibrozil (200 microM), respectively, whereas only a small inhibitory effect by gemfibrozil (200 microM) on fluvastatin uptake into primary human hepatocytes was observed (27% inhibition).	Gemfibrozil	193-204	solute carrier organic anion transporter family member 1B3	Homo sapiens	36-43
17470528-0	2007	Substrate-dependent drug-drug interactions between gemfibrozil, fluvastatin and other organic anion-transporting peptide (OATP) substrates on OATP1B1, OATP2B1, and OATP1B3.	Gemfibrozil	51-62	solute carrier organic anion transporter family member 1A2	Homo sapiens	122-126
17470528-0	2007	Substrate-dependent drug-drug interactions between gemfibrozil, fluvastatin and other organic anion-transporting peptide (OATP) substrates on OATP1B1, OATP2B1, and OATP1B3.	Gemfibrozil	51-62	solute carrier organic anion transporter family member 1B1	Homo sapiens	142-149
17470528-0	2007	Substrate-dependent drug-drug interactions between gemfibrozil, fluvastatin and other organic anion-transporting peptide (OATP) substrates on OATP1B1, OATP2B1, and OATP1B3.	Gemfibrozil	51-62	solute carrier organic anion transporter family member 2B1	Homo sapiens	151-158
17470528-0	2007	Substrate-dependent drug-drug interactions between gemfibrozil, fluvastatin and other organic anion-transporting peptide (OATP) substrates on OATP1B1, OATP2B1, and OATP1B3.	Gemfibrozil	51-62	solute carrier organic anion transporter family member 1B3	Homo sapiens	164-171
17470528-5	2007	For OATP1B1 the inhibition by gemfibrozil was substrate-dependent as the transport of fluvastatin (IC(50) of 63 microM), pravastatin, simvastatin, and taurocholate was inhibited by gemfibrozil, whereas the transport of estrone-3-sulfate and troglitazone sulfate (both used at 3 microM) was not affected.	Gemfibrozil	30-41	solute carrier organic anion transporter family member 1B1	Homo sapiens	4-11
17470528-5	2007	For OATP1B1 the inhibition by gemfibrozil was substrate-dependent as the transport of fluvastatin (IC(50) of 63 microM), pravastatin, simvastatin, and taurocholate was inhibited by gemfibrozil, whereas the transport of estrone-3-sulfate and troglitazone sulfate (both used at 3 microM) was not affected.	Gemfibrozil	181-192	solute carrier organic anion transporter family member 1B1	Homo sapiens	4-11
17470528-8	2007	Recombinant OATP1B1-, OATP2B1-, and OATP1B3-mediated fluvastatin transport was inhibited to 97, 70, and 62% by gemfibrozil (200 microM), respectively, whereas only a small inhibitory effect by gemfibrozil (200 microM) on fluvastatin uptake into primary human hepatocytes was observed (27% inhibition).	Gemfibrozil	111-122	solute carrier organic anion transporter family member 1B1	Homo sapiens	12-19
17470528-8	2007	Recombinant OATP1B1-, OATP2B1-, and OATP1B3-mediated fluvastatin transport was inhibited to 97, 70, and 62% by gemfibrozil (200 microM), respectively, whereas only a small inhibitory effect by gemfibrozil (200 microM) on fluvastatin uptake into primary human hepatocytes was observed (27% inhibition).	Gemfibrozil	111-122	solute carrier organic anion transporter family member 2B1	Homo sapiens	22-29
17470528-8	2007	Recombinant OATP1B1-, OATP2B1-, and OATP1B3-mediated fluvastatin transport was inhibited to 97, 70, and 62% by gemfibrozil (200 microM), respectively, whereas only a small inhibitory effect by gemfibrozil (200 microM) on fluvastatin uptake into primary human hepatocytes was observed (27% inhibition).	Gemfibrozil	111-122	solute carrier organic anion transporter family member 1B3	Homo sapiens	36-43
17633905-7	2007	Other lipid-lowering agents reported to reduce CRP include niacin, fibrates, and gemfibrozil.	Gemfibrozil	81-92	C-reactive protein	Homo sapiens	47-50
17333159-2	2007	We studied the possible effect of gemfibrozil, an in vivo inhibitor of CYP2C8, on the pharmacokinetics of ibuprofen in healthy volunteers.	Gemfibrozil	34-45	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	71-77
17333159-10	2007	CONCLUSIONS: Gemfibrozil moderately increases the AUC(0-infinity) of R-ibuprofen and prolongs its t (1/2), indicating that R-ibuprofen is partially metabolised by CYP2C8.	Gemfibrozil	13-24	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	163-169
17333159-0	2007	Stereoselective interaction between the CYP2C8 inhibitor gemfibrozil and racemic ibuprofen.	Gemfibrozil	57-68	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	40-46
16782410-4	2006	PPARalpha is activated by polyunsaturated fatty acids and by fibrate drugs (fenofibrate and gemfibrozil) and controls expression of genes involved in lipid metabolism.	Gemfibrozil	92-103	peroxisome proliferator activated receptor alpha	Homo sapiens	0-9
17897018-4	2007	Fenofibrate and gemfibrozil are two drugs that act as PPARalpha agonists and are currently in use in the clinical setting.	Gemfibrozil	16-27	peroxisome proliferator activated receptor alpha	Homo sapiens	54-63
17897018-8	2007	These studies have shown both PPARalpha agonists, gemfibrozil and fenofibrate, confer anti-atherosclerotic effects, partly independent of their metabolic effects.	Gemfibrozil	50-61	peroxisome proliferator activated receptor alpha	Homo sapiens	30-39
17202761-2	2006	In the present study, the data of three ligands of peroxisome proliferator activated receptor alpha (PPARalpha), i.e., clofibrate, WY-14643 and gemfibrozil in our database were analyzed.	Gemfibrozil	144-155	peroxisome proliferator activated receptor alpha	Rattus norvegicus	51-99
17202761-2	2006	In the present study, the data of three ligands of peroxisome proliferator activated receptor alpha (PPARalpha), i.e., clofibrate, WY-14643 and gemfibrozil in our database were analyzed.	Gemfibrozil	144-155	peroxisome proliferator activated receptor alpha	Rattus norvegicus	101-110
16764943-2	2006	Recently, we demonstrated that administration of the PPAR-alpha agonists gemfibrozil and fenofibrate, inhibit the clinical signs of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS).	Gemfibrozil	73-84	peroxisome proliferator activated receptor alpha	Mus musculus	53-63
16764943-8	2006	Interestingly, a combination of 9-cis RA and the PPAR-alpha agonists fenofibrate or gemfibrozil cooperatively inhibited NO, TNF-alpha, IL-1beta, IL-6, and MCP-1 production by these cells.	Gemfibrozil	84-95	peroxisome proliferator activated receptor alpha	Mus musculus	49-59
16764943-8	2006	Interestingly, a combination of 9-cis RA and the PPAR-alpha agonists fenofibrate or gemfibrozil cooperatively inhibited NO, TNF-alpha, IL-1beta, IL-6, and MCP-1 production by these cells.	Gemfibrozil	84-95	tumor necrosis factor	Mus musculus	124-133
16764943-8	2006	Interestingly, a combination of 9-cis RA and the PPAR-alpha agonists fenofibrate or gemfibrozil cooperatively inhibited NO, TNF-alpha, IL-1beta, IL-6, and MCP-1 production by these cells.	Gemfibrozil	84-95	interleukin 1 beta	Mus musculus	135-143
16764943-8	2006	Interestingly, a combination of 9-cis RA and the PPAR-alpha agonists fenofibrate or gemfibrozil cooperatively inhibited NO, TNF-alpha, IL-1beta, IL-6, and MCP-1 production by these cells.	Gemfibrozil	84-95	interleukin 6	Mus musculus	145-149
16764943-8	2006	Interestingly, a combination of 9-cis RA and the PPAR-alpha agonists fenofibrate or gemfibrozil cooperatively inhibited NO, TNF-alpha, IL-1beta, IL-6, and MCP-1 production by these cells.	Gemfibrozil	84-95	mast cell protease 1	Mus musculus	155-160
17523051-0	2007	Gemfibrozil and its glucuronide inhibit the hepatic uptake of pravastatin mediated by OATP1B1.	Gemfibrozil	0-11	solute carrier organic anion transporter family member 1B1	Homo sapiens	86-93
17523051-7	2007	Considering the plasma concentrations of gemfibrozil and gem-glu in humans, the inhibition of OATP1B1-mediated hepatic uptake of pravastatin by gem-glu would contribute, at least in part, to the elevation of plasma concentration of pravastatin by the concomitant use of gemfibrozil.	Gemfibrozil	41-52	solute carrier organic anion transporter family member 1B1	Homo sapiens	94-101
17523051-7	2007	Considering the plasma concentrations of gemfibrozil and gem-glu in humans, the inhibition of OATP1B1-mediated hepatic uptake of pravastatin by gem-glu would contribute, at least in part, to the elevation of plasma concentration of pravastatin by the concomitant use of gemfibrozil.	Gemfibrozil	270-281	solute carrier organic anion transporter family member 1B1	Homo sapiens	94-101
17455113-0	2007	Inhibition of human organic anion transporter 3 mediated pravastatin transport by gemfibrozil and the metabolites in humans.	Gemfibrozil	82-93	solute carrier family 22 member 8	Homo sapiens	20-47
17455113-5	2007	Gemfibrozil and its glucuronide and carboxylic metabolite forms inhibited the uptake of pravastatin by hOAT3 with IC(50) values of 6.8 microM, 19.7 microM and 5.4 microM, respectively.	Gemfibrozil	0-11	solute carrier family 22 member 8	Homo sapiens	103-108
17455113-6	2007	Considering the plasma concentrations of gemfibrozil and its metabolites in humans, the inhibition of hOAT3-mediated pravastatin transport by gemfibrozil and its metabolites would lead to a decrease in the renal clearance of pravastatin in clinical settings.	Gemfibrozil	41-52	solute carrier family 22 member 8	Homo sapiens	102-107
17455113-6	2007	Considering the plasma concentrations of gemfibrozil and its metabolites in humans, the inhibition of hOAT3-mediated pravastatin transport by gemfibrozil and its metabolites would lead to a decrease in the renal clearance of pravastatin in clinical settings.	Gemfibrozil	142-153	solute carrier family 22 member 8	Homo sapiens	102-107
17253883-15	2007	The most impressive pharmacokinetic interaction was reported with combined administration of gemfibrozil (a strong CYP2C8 inhibitor) and repaglinide (8-fold increase in repaglinide AUC).	Gemfibrozil	93-104	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	115-121
17178259-10	2006	Gemfibrozil and its glucuronide inhibit CYP2C8 and OATP1B1.	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	40-46
17178259-10	2006	Gemfibrozil and its glucuronide inhibit CYP2C8 and OATP1B1.	Gemfibrozil	0-11	solute carrier organic anion transporter family member 1B1	Homo sapiens	51-58
17178262-8	2006	Furthermore, estrone-3-sulfate transport into OATP2B1-overexpressing Madin-Darby canine kidney II cells was inhibited by various drugs, including atorvastatin, simvastatin, cerivastatin, glyburide (INN, glibenclamide), and gemfibrozil, with the most pronounced effect being found for atorvastatin (inhibition constant, 0.7 +/- 0.4 micromol/L).	Gemfibrozil	223-234	solute carrier organic anion transporter family member 2B1	Homo sapiens	46-53
16828346-2	2006	Treatment with a fibrate such as gemfibrozil (a PPAR alpha agonist) has been shown to be especially effective in people with low HDL-C and other features of the metabolic syndrome.	Gemfibrozil	33-44	peroxisome proliferator activated receptor alpha	Homo sapiens	48-58
16832679-0	2006	The CYP2C8 inhibitor gemfibrozil does not increase the plasma concentrations of zopiclone.	Gemfibrozil	21-32	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	4-10
16832679-2	2006	We studied the possible effect of gemfibrozil, an inhibitor of CYP2C8, on the pharmacokinetics and pharmacodynamics of zopiclone.	Gemfibrozil	34-45	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	63-69
16221474-1	2006	BACKGROUND: The Veterans Affairs HDL Intervention Trial (VA-HIT) showed that gemfibrozil, which activates peroxisome proliferator-activator receptor alpha (PPARalpha), significantly reduced the risk of cardiovascular (CV) events in men with low HDL cholesterol (&lt; 40 mg/dl) and established coronary heart disease.	Gemfibrozil	77-88	peroxisome proliferator activated receptor alpha	Homo sapiens	156-165
16299161-0	2006	Glucuronidation converts gemfibrozil to a potent, metabolism-dependent inhibitor of CYP2C8: implications for drug-drug interactions.	Gemfibrozil	25-36	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	84-90
16463048-10	2006	In addition, gemfibrozil reduced the expression of the genes encoding the NADPH oxidase subunits p47phox, gp91phox and Rac-1.	Gemfibrozil	13-24	neutrophil cytosolic factor 1	Mus musculus	97-104
16463048-10	2006	In addition, gemfibrozil reduced the expression of the genes encoding the NADPH oxidase subunits p47phox, gp91phox and Rac-1.	Gemfibrozil	13-24	cytochrome b-245, beta polypeptide	Mus musculus	106-114
16463048-10	2006	In addition, gemfibrozil reduced the expression of the genes encoding the NADPH oxidase subunits p47phox, gp91phox and Rac-1.	Gemfibrozil	13-24	Rac family small GTPase 1	Mus musculus	119-124
16463048-11	2006	In addition, gemfibrozil reduced the expression of the genes encoding nuclear factor kappa B (NF-kappaB) subunit, p65, the NF-kappaB-dependent chemokine monocyte chemoattractant protein-1, and tissue factor.	Gemfibrozil	13-24	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	70-92
16463048-11	2006	In addition, gemfibrozil reduced the expression of the genes encoding nuclear factor kappa B (NF-kappaB) subunit, p65, the NF-kappaB-dependent chemokine monocyte chemoattractant protein-1, and tissue factor.	Gemfibrozil	13-24	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	94-103
16463048-11	2006	In addition, gemfibrozil reduced the expression of the genes encoding nuclear factor kappa B (NF-kappaB) subunit, p65, the NF-kappaB-dependent chemokine monocyte chemoattractant protein-1, and tissue factor.	Gemfibrozil	13-24	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	114-117
16463048-11	2006	In addition, gemfibrozil reduced the expression of the genes encoding nuclear factor kappa B (NF-kappaB) subunit, p65, the NF-kappaB-dependent chemokine monocyte chemoattractant protein-1, and tissue factor.	Gemfibrozil	13-24	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	123-132
16463048-11	2006	In addition, gemfibrozil reduced the expression of the genes encoding nuclear factor kappa B (NF-kappaB) subunit, p65, the NF-kappaB-dependent chemokine monocyte chemoattractant protein-1, and tissue factor.	Gemfibrozil	13-24	coagulation factor III	Mus musculus	193-206
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
16299161-1	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 8	Homo sapiens	47-53
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
16299161-4	2006	Unexpectedly, gemfibrozil glucuronide, but not gemfibrozil, was found to be a metabolism-dependent inhibitor of CYP2C8 only.	Gemfibrozil	14-25	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	112-118
16299161-7	2006	Potent inhibition of CYP2C8 was also achieved by first incubating gemfibrozil with alamethicin-activated human liver microsomes and UDP-glucuronic acid (to form gemfibrozil glucuronide), followed by a second incubation with NADPH.	Gemfibrozil	66-77	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	21-27
16299161-9	2006	The results described have important implications for the mechanism of the clinical interaction reported between gemfibrozil and CYP2C8 substrates such as cerivastatin, repaglinide, rosiglitazone, and pioglitazone.	Gemfibrozil	113-124	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	129-135
16883221-10	2006	vWF activity did not change in controls and significantly increased in gemfibrozil group by days 7, 14, but from lower baseline level.	Gemfibrozil	71-82	von Willebrand factor	Homo sapiens	0-3
17668698-6	2006	RESULTS: Gemfibrozil elevated significantly apolipoprotein A-I, but decreased the total cholesterol, LDL cholesterol, triglycerides, the lipid indices, the ADP-induced platelet aggregation, plasminogen, alpha2-antiplasmin and hematocrit.	Gemfibrozil	9-20	apolipoprotein A1	Homo sapiens	44-62
17668698-6	2006	RESULTS: Gemfibrozil elevated significantly apolipoprotein A-I, but decreased the total cholesterol, LDL cholesterol, triglycerides, the lipid indices, the ADP-induced platelet aggregation, plasminogen, alpha2-antiplasmin and hematocrit.	Gemfibrozil	9-20	serpin family F member 2	Homo sapiens	203-221
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 8	Homo sapiens	115-121
16507380-0	2005	Potential drug-drug interaction between interferon alfa-2b and gemfibrozil in a patient with malignant melanoma.	Gemfibrozil	63-74	interferon alpha 1	Homo sapiens	40-50
16507380-4	2005	OBJECTIVE: The aim of this report was to describe a potential drug-drug interaction between IFN alfa-2b and gemfibrozil in a patient with malignant melanoma.	Gemfibrozil	108-119	interferon alpha 1	Homo sapiens	92-95
16507380-10	2005	RESULTS: In this case of a possible drug-drug interaction between IFN alfa 11 MU TIW and gemfibrozil 600 mg BID in a patient undergoing treatment for IFN-induced hypertriglyceridemia, the Naranjo Adverse Drug Reactions (ADR) Probability Scale score was 7 (ie, ADR possibly related to treatment).	Gemfibrozil	89-100	interferon alpha 1	Homo sapiens	66-69
16507380-10	2005	RESULTS: In this case of a possible drug-drug interaction between IFN alfa 11 MU TIW and gemfibrozil 600 mg BID in a patient undergoing treatment for IFN-induced hypertriglyceridemia, the Naranjo Adverse Drug Reactions (ADR) Probability Scale score was 7 (ie, ADR possibly related to treatment).	Gemfibrozil	89-100	BH3 interacting domain death agonist	Homo sapiens	108-111
16507380-10	2005	RESULTS: In this case of a possible drug-drug interaction between IFN alfa 11 MU TIW and gemfibrozil 600 mg BID in a patient undergoing treatment for IFN-induced hypertriglyceridemia, the Naranjo Adverse Drug Reactions (ADR) Probability Scale score was 7 (ie, ADR possibly related to treatment).	Gemfibrozil	89-100	interferon alpha 1	Homo sapiens	150-153
16507380-11	2005	CONCLUSIONS: Both IFN and gemfibrozil inhibit the activity of the hepatic enzymes CYP1A2 and CYP2C19.	Gemfibrozil	26-37	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	82-88
16507380-11	2005	CONCLUSIONS: Both IFN and gemfibrozil inhibit the activity of the hepatic enzymes CYP1A2 and CYP2C19.	Gemfibrozil	26-37	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-100
16507380-12	2005	A possible drug-drug interaction between IFN alfa 11 MU TIW and gemfibrozil 600 mg BID was reported in a patient undergoing treatment for IFN-induced hypertriglyceridemia.	Gemfibrozil	64-75	interferon alpha 1	Homo sapiens	41-44
16507380-12	2005	A possible drug-drug interaction between IFN alfa 11 MU TIW and gemfibrozil 600 mg BID was reported in a patient undergoing treatment for IFN-induced hypertriglyceridemia.	Gemfibrozil	64-75	BH3 interacting domain death agonist	Homo sapiens	83-86
16507380-12	2005	A possible drug-drug interaction between IFN alfa 11 MU TIW and gemfibrozil 600 mg BID was reported in a patient undergoing treatment for IFN-induced hypertriglyceridemia.	Gemfibrozil	64-75	interferon alpha 1	Homo sapiens	138-141
16226225-1	2005	Fibrates such as bezafibrate, gemfibrozil, clofibric acid, ciprofibrate and fenofibrate, are ligands for peroxisome proliferator-activated receptor alpha (PPARalpha), and are used as therapeutic agents in the treatment of hyperlipidemia.	Gemfibrozil	30-41	peroxisome proliferator activated receptor alpha	Homo sapiens	105-153
16226225-1	2005	Fibrates such as bezafibrate, gemfibrozil, clofibric acid, ciprofibrate and fenofibrate, are ligands for peroxisome proliferator-activated receptor alpha (PPARalpha), and are used as therapeutic agents in the treatment of hyperlipidemia.	Gemfibrozil	30-41	peroxisome proliferator activated receptor alpha	Homo sapiens	155-164
16226225-4	2005	Bezafibrate and gemfibrozil displayed a mixed non-competitive inhibition pattern in the glyceraldehyde reduction activity and pure non-competitive inhibition pattern in the benzyl alcohol oxidation activity of AR.	Gemfibrozil	16-27	aldo-keto reductase family 1 member B	Homo sapiens	210-212
16235714-2	2005	evening dose) and gemfibrozil (600 mg/kg, po twice) for 30 days produced significant decrease in the level of reduced glutathione, superoxide dismutase, catalase and increase in the level of lipid peroxidation and various serum parameters (creatine phosphokinase, lactate dehydrogenase, serum glutamate oxaloacetate transaminase, creatinine, urea and blood urea nitrogen).	Gemfibrozil	18-29	catalase	Rattus norvegicus	153-161
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.	Gemfibrozil	20-31	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	115-121
16042675-1	2005	BACKGROUND AND AIMS: Gemfibrozil, and particularly its combination with itraconazole, greatly increases the area under the plasma concentration-time curve [AUC(0, infinity)] and response to the cytochrome P450 (CYP) 2C8 and 3A4 substrate repaglinide.	Gemfibrozil	21-32	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	194-219
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
16042675-2	2005	In vitro, gemfibrozil is a more potent inhibitor of CYP2C9 than of CYP2C8.	Gemfibrozil	10-21	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	67-73
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.	Gemfibrozil	46-57	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	209-215
16283275-1	2005	OBJECTIVE: Our objective was to study the effects of gemfibrozil on the pharmacokinetics of pioglitazone and the active compounds, which are all the substrates of CYP2C8 and CYP3A4.	Gemfibrozil	53-64	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	163-169
16283275-1	2005	OBJECTIVE: Our objective was to study the effects of gemfibrozil on the pharmacokinetics of pioglitazone and the active compounds, which are all the substrates of CYP2C8 and CYP3A4.	Gemfibrozil	53-64	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	174-180
16176562-10	2005	Gemfibrozil is only a moderate inhibitor of CYP2C8 and does not inhibit CYP3A4; inhibition of CYP-enzymes by parent gemfibrozil alone does not explain its interaction with repaglinide in vivo.	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	44-50
16193754-5	2005	Agonists of both PPARalpha (WY14,643 and gemfibrozil) and PPARbeta (bezafibrate) induced luciferase activity, while rosiglitazone, a PPARgamma agonist, was not effective.	Gemfibrozil	41-52	peroxisome proliferator-activated receptor alpha b	Oncorhynchus mykiss	17-26
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
15968640-2	2005	Recently, we demonstrated that administration of the PPAR-alpha agonists gemfibrozil and fenofibrate, inhibit the clinical signs of experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS).	Gemfibrozil	73-84	peroxisome proliferator activated receptor alpha	Mus musculus	53-63
15968640-4	2005	Our studies demonstrated that the PPAR-alpha agonists ciprofibrate, fenofibrate, gemfibrozil, and WY 14,643 each inhibited NO production by cytokine-stimulated microglia in a dose-dependent manner.	Gemfibrozil	81-92	peroxisome proliferator activated receptor alpha	Mus musculus	34-44
16101410-2	2005	The physiological effects of several marketed drugs for the treatment of dyslipidemia (fenofibrate and gemfibrozil) and diabetes (rosiglitazone and pioglitazone) have now been shown to be mediated through PPARalpha and PPARgamma respectively.	Gemfibrozil	103-114	peroxisome proliferator activated receptor alpha	Homo sapiens	205-214
16101410-2	2005	The physiological effects of several marketed drugs for the treatment of dyslipidemia (fenofibrate and gemfibrozil) and diabetes (rosiglitazone and pioglitazone) have now been shown to be mediated through PPARalpha and PPARgamma respectively.	Gemfibrozil	103-114	peroxisome proliferator activated receptor gamma	Homo sapiens	219-228
15292370-5	2004	On gemfibrozil, carriers of the LPL N9 allele in VA-HIT had lower levels of large LDL (-32%; P &lt; 0.01) but higher levels of small, dense LDL (+59%; P &lt; 0.003) than did noncarriers.	Gemfibrozil	3-14	lipoprotein lipase	Homo sapiens	32-35
15998575-1	2005	Eighteen-month-old Sprague-Dawley rats present age-related alterations in lipid and glucose metabolism and are resistant to the effect of PPARalpha-activating hypolipidemic drugs, such as gemfibrozil.	Gemfibrozil	188-199	peroxisome proliferator activated receptor alpha	Rattus norvegicus	138-147
15998575-4	2005	Although gemfibrozil induced mild effects on hepatic PPARalpha, HNF-4, and LXRalpha, only rosiglitazone significantly reduced plasma TG (59%), glucose (19%), insulin (61%), and leptin (66%), and liver TG (43%), CE (49%), and NEFA (27%).	Gemfibrozil	9-20	peroxisome proliferator activated receptor alpha	Rattus norvegicus	53-62
16316932-11	2005	Considering the plasma protein binding and IC50 values for OATP1B1, only gemfibrozil appeared to have a potential to cause drug-drug interactions by inhibiting OATP1B1 at clinically relevant concentrations.	Gemfibrozil	73-84	solute carrier organic anion transporter family member 1B1	Homo sapiens	160-167
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
15618549-0	2005	Regulation of human apoA-I by gemfibrozil and fenofibrate through selective peroxisome proliferator-activated receptor alpha modulation.	Gemfibrozil	30-41	apolipoprotein A1	Homo sapiens	20-26
15618549-0	2005	Regulation of human apoA-I by gemfibrozil and fenofibrate through selective peroxisome proliferator-activated receptor alpha modulation.	Gemfibrozil	30-41	peroxisome proliferator activated receptor alpha	Homo sapiens	76-124
15345331-7	2004	GFB increased also by 80% the cortex PPARalpha content in old males.	Gemfibrozil	0-3	peroxisome proliferator activated receptor alpha	Rattus norvegicus	37-46
15900215-11	2005	Patients who were homozygous for CYP3A5*3 demonstrated greater serum CK levels than patients who were heterozygous for CYP3A5*3, when concomitant lipid-lowering agents were sequentially removed from the analysis (P=0.025 without gemfibrozil, P=0.010 without gemfibrozil and niacin).	Gemfibrozil	229-240	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	33-39
15900215-11	2005	Patients who were homozygous for CYP3A5*3 demonstrated greater serum CK levels than patients who were heterozygous for CYP3A5*3, when concomitant lipid-lowering agents were sequentially removed from the analysis (P=0.025 without gemfibrozil, P=0.010 without gemfibrozil and niacin).	Gemfibrozil	258-269	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	33-39
15900286-11	2005	CONCLUSIONS: Gemfibrozil elevates the plasma concentrations of pioglitazone, probably by inhibition of its CYP2C8-mediated metabolism.	Gemfibrozil	13-24	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	107-113
15618549-1	2005	OBJECTIVE: The objective of this trial was to study the effects of fenofibrate (FF) and gemfibrozil (GF), the most commonly used fibrates, on high-density lipoprotein (HDL) and apolipoprotein (apo) A-I.	Gemfibrozil	88-99	apolipoprotein A1	Homo sapiens	177-201
15771232-8	2005	However, in contrast to the mRNA induction, marked decreases (&gt;60%) in CYP2C8 activity were obtained with gemfibrozil treatment.	Gemfibrozil	109-120	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	74-80
15771232-13	2005	Gemfibrozil is also an inducer of CYP3A4, but acts as both an inducer and an inhibitor of CYP2C8.	Gemfibrozil	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	34-40
15771232-13	2005	Gemfibrozil is also an inducer of CYP3A4, but acts as both an inducer and an inhibitor of CYP2C8.	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	90-96
15363580-4	2004	CYP2C7 gene expression was dramatically down-regulated in the livers of rats treated for 13 weeks by WY-14,643 (WY; 500 ppm) or gemfibrozil (GEM; 8000 ppm).	Gemfibrozil	128-139	cytochrome P450, family 2, subfamily c, polypeptide 7	Rattus norvegicus	0-6
15292370-7	2004	In men with low HDL-C and CHD: 1) the LPL N9 and S291 alleles are more frequent than in CHD-free men with normal HDL-C, whereas the X447 allele is less frequent, and 2) the LPL N9 allele is associated with the LDL subclass response to gemfibrozil.	Gemfibrozil	235-246	lipoprotein lipase	Homo sapiens	38-41
15292370-7	2004	In men with low HDL-C and CHD: 1) the LPL N9 and S291 alleles are more frequent than in CHD-free men with normal HDL-C, whereas the X447 allele is less frequent, and 2) the LPL N9 allele is associated with the LDL subclass response to gemfibrozil.	Gemfibrozil	235-246	lipoprotein lipase	Homo sapiens	173-176
15322734-5	2004	In addition, the hypothesis that gemfibrozil-mediated inhibition of P-glycoprotein contributes to the interaction between gemfibrozil and cerivastatin was tested in Caco-2 cells.	Gemfibrozil	33-44	ATP binding cassette subfamily B member 1	Homo sapiens	68-82
15194707-0	2004	Gemfibrozil and its glucuronide inhibit the organic anion transporting polypeptide 2 (OATP2/OATP1B1:SLC21A6)-mediated hepatic uptake and CYP2C8-mediated metabolism of cerivastatin: analysis of the mechanism of the clinically relevant drug-drug interaction between cerivastatin and gemfibrozil.	Gemfibrozil	0-11	solute carrier organic anion transporter family member 1B1	Homo sapiens	44-84
15194707-0	2004	Gemfibrozil and its glucuronide inhibit the organic anion transporting polypeptide 2 (OATP2/OATP1B1:SLC21A6)-mediated hepatic uptake and CYP2C8-mediated metabolism of cerivastatin: analysis of the mechanism of the clinically relevant drug-drug interaction between cerivastatin and gemfibrozil.	Gemfibrozil	0-11	solute carrier organic anion transporter family member 1B1	Homo sapiens	86-91
15194707-0	2004	Gemfibrozil and its glucuronide inhibit the organic anion transporting polypeptide 2 (OATP2/OATP1B1:SLC21A6)-mediated hepatic uptake and CYP2C8-mediated metabolism of cerivastatin: analysis of the mechanism of the clinically relevant drug-drug interaction between cerivastatin and gemfibrozil.	Gemfibrozil	0-11	solute carrier organic anion transporter family member 1B1	Homo sapiens	92-99
15194707-0	2004	Gemfibrozil and its glucuronide inhibit the organic anion transporting polypeptide 2 (OATP2/OATP1B1:SLC21A6)-mediated hepatic uptake and CYP2C8-mediated metabolism of cerivastatin: analysis of the mechanism of the clinically relevant drug-drug interaction between cerivastatin and gemfibrozil.	Gemfibrozil	0-11	solute carrier organic anion transporter family member 1B1	Homo sapiens	100-107
15194707-0	2004	Gemfibrozil and its glucuronide inhibit the organic anion transporting polypeptide 2 (OATP2/OATP1B1:SLC21A6)-mediated hepatic uptake and CYP2C8-mediated metabolism of cerivastatin: analysis of the mechanism of the clinically relevant drug-drug interaction between cerivastatin and gemfibrozil.	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	137-143
15194707-0	2004	Gemfibrozil and its glucuronide inhibit the organic anion transporting polypeptide 2 (OATP2/OATP1B1:SLC21A6)-mediated hepatic uptake and CYP2C8-mediated metabolism of cerivastatin: analysis of the mechanism of the clinically relevant drug-drug interaction between cerivastatin and gemfibrozil.	Gemfibrozil	281-292	solute carrier organic anion transporter family member 1B1	Homo sapiens	44-84
15194707-0	2004	Gemfibrozil and its glucuronide inhibit the organic anion transporting polypeptide 2 (OATP2/OATP1B1:SLC21A6)-mediated hepatic uptake and CYP2C8-mediated metabolism of cerivastatin: analysis of the mechanism of the clinically relevant drug-drug interaction between cerivastatin and gemfibrozil.	Gemfibrozil	281-292	solute carrier organic anion transporter family member 1B1	Homo sapiens	86-91
15194707-0	2004	Gemfibrozil and its glucuronide inhibit the organic anion transporting polypeptide 2 (OATP2/OATP1B1:SLC21A6)-mediated hepatic uptake and CYP2C8-mediated metabolism of cerivastatin: analysis of the mechanism of the clinically relevant drug-drug interaction between cerivastatin and gemfibrozil.	Gemfibrozil	281-292	solute carrier organic anion transporter family member 1B1	Homo sapiens	92-99
15194707-0	2004	Gemfibrozil and its glucuronide inhibit the organic anion transporting polypeptide 2 (OATP2/OATP1B1:SLC21A6)-mediated hepatic uptake and CYP2C8-mediated metabolism of cerivastatin: analysis of the mechanism of the clinically relevant drug-drug interaction between cerivastatin and gemfibrozil.	Gemfibrozil	281-292	solute carrier organic anion transporter family member 1B1	Homo sapiens	100-107
15194707-2	2004	In the present study, we examined the inhibitory effects of GEM and its metabolites, M3 and gemfibrozil 1-O-beta-glucuronide (GEM-1-O-glu), on the uptake of CER by human organic anion transporting polypeptide 2 (OATP2)-expressing cells and its metabolism in cytochrome P450 expression systems.	Gemfibrozil	60-63	solute carrier organic anion transporter family member 1B1	Homo sapiens	170-210
15194707-2	2004	In the present study, we examined the inhibitory effects of GEM and its metabolites, M3 and gemfibrozil 1-O-beta-glucuronide (GEM-1-O-glu), on the uptake of CER by human organic anion transporting polypeptide 2 (OATP2)-expressing cells and its metabolism in cytochrome P450 expression systems.	Gemfibrozil	60-63	solute carrier organic anion transporter family member 1B1	Homo sapiens	212-217
15194707-3	2004	Uptake studies showed that GEM and GEM-1-O-glu significantly inhibited the OATP2-mediated uptake of CER with IC(50) values of 72 and 24 microM, respectively.	Gemfibrozil	27-30	solute carrier organic anion transporter family member 1B1	Homo sapiens	75-80
15194707-5	2004	GEM and GEM-1-O-glu minimally inhibited the CYP3A4-mediated metabolism of CER.	Gemfibrozil	0-3	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	44-50
15194707-7	2004	However, considering the possibly concentrated high unbound concentrations of GEM-1-O-glu in the liver and its relatively larger plasma unbound fraction compared with GEM itself, the glucuronide inhibition of the CYP2C8-mediated metabolism of CER appears to be the main mechanism for the clinically relevant drug-drug interaction.	Gemfibrozil	78-81	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	213-219
15289377-8	2004	A selective CFTR channel blocker, gemfibrozil, abrogated the protective effect of IPC.	Gemfibrozil	34-45	cystic fibrosis transmembrane conductance regulator	Mus musculus	12-16
15322734-5	2004	In addition, the hypothesis that gemfibrozil-mediated inhibition of P-glycoprotein contributes to the interaction between gemfibrozil and cerivastatin was tested in Caco-2 cells.	Gemfibrozil	122-133	ATP binding cassette subfamily B member 1	Homo sapiens	68-82
15215125-6	2004	Cells made resistant to probenecid and showing a marked overexpression of MRP1 (by Western blot analysis and confocal microscopy) accumulated ciprofloxacin to almost the same extent as did control cells, but efflux was inhibited less by probenecid, gemfibrozil, and MK571.	Gemfibrozil	249-260	ATP-binding cassette, sub-family C (CFTR/MRP), member 1	Mus musculus	74-78
15194003-0	2004	PPARalpha agonists clofibrate and gemfibrozil inhibit cell growth, down-regulate hCG and up-regulate progesterone secretions in immortalized human trophoblast cells.	Gemfibrozil	34-45	peroxisome proliferator activated receptor alpha	Homo sapiens	0-9
15194003-0	2004	PPARalpha agonists clofibrate and gemfibrozil inhibit cell growth, down-regulate hCG and up-regulate progesterone secretions in immortalized human trophoblast cells.	Gemfibrozil	34-45	chorionic gonadotropin subunit beta 5	Homo sapiens	81-84
15116058-13	2004	The in vitro results indicate that the maximum gemfibrozil inhibition of rosuvastatin OATP2-mediated uptake was 50%; the inhibition constant for the inhibitory process was 4.0 +/- 1.3 micromol/L.	Gemfibrozil	47-58	solute carrier organic anion transporter family member 1B1	Homo sapiens	86-91
15142970-4	2004	PPARalpha is activated by polyunsaturated fatty acids and oxidized derivatives and by lipid-modifying drugs of the fibrate family, including fenofibrate or gemfibrozil.	Gemfibrozil	156-167	peroxisome proliferator activated receptor alpha	Homo sapiens	0-9
15116058-15	2004	Gemfibrozil inhibition of OATP2-mediated rosuvastatin hepatic uptake may contribute to the mechanism of the drug-drug interaction.	Gemfibrozil	0-11	solute carrier organic anion transporter family member 1B1	Homo sapiens	26-31
15100326-3	2004	The PPAR alpha agonists, gemfibrozil, ciprofibrate, and fenofibrate, have an excellent track history as oral agents used to treat hypertriglyceridemia.	Gemfibrozil	25-36	peroxisome proliferator activated receptor alpha	Homo sapiens	4-14
14698041-5	2004	We tested whether gemfibrozil, fenofibrate, fenofibric acid, and bezafibrate inhibit Pgp in vitro using a calcein acetoxymethylester (calcein-AM) uptake assay and confocal laser scanning microscopy with bodipy-verapamil as substrate in L-MDR1 cells, which overexpress human Pgp.	Gemfibrozil	18-29	ATP binding cassette subfamily B member 1	Homo sapiens	85-88
14685799-5	2004	RESULTS: Bezafibrate, fenofibrate and gemfibrozil significantly reduced CYP7A1 mRNA levels.	Gemfibrozil	38-49	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	72-78
15100326-6	2004	More importantly, gemfibrozil was shown to shift the cytokine secretion of human T cell lines by inhibiting IFN-gamma and promoting IL-4 secretion.	Gemfibrozil	18-29	interferon gamma	Homo sapiens	108-117
15100326-6	2004	More importantly, gemfibrozil was shown to shift the cytokine secretion of human T cell lines by inhibiting IFN-gamma and promoting IL-4 secretion.	Gemfibrozil	18-29	interleukin 4	Homo sapiens	132-136
15100326-7	2004	These results suggest that PPAR alpha agonists such as gemfibrozil and fenofibrate, may be attractive candidates for use in human inflammatory conditions such as multiple sclerosis.	Gemfibrozil	55-66	peroxisome proliferator activated receptor alpha	Homo sapiens	27-37
15283301-5	2004	In the presence of gemfibrozil, the CYP- or UGT-mediated metabolism of pitavastatin was inhibited in vitro.	Gemfibrozil	19-30	peptidylprolyl isomerase G	Homo sapiens	36-39
15283301-5	2004	In the presence of gemfibrozil, the CYP- or UGT-mediated metabolism of pitavastatin was inhibited in vitro.	Gemfibrozil	19-30	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	44-47
14555339-0	2003	Metabolism and disposition of gemfibrozil in Wistar and multidrug resistance-associated protein 2-deficient TR- rats.	Gemfibrozil	30-41	ATP binding cassette subfamily C member 2	Rattus norvegicus	56-97
14709251-10	2003	Ritonavir partially inhibited induction of PPAR target genes by gemfibrozil and rosiglitazone.	Gemfibrozil	64-75	peroxisome proliferator activated receptor alpha	Mus musculus	43-47
14555339-2	2003	The roles of multidrug resistance-associated protein (Mrp) 2 deficiency and Mrp3 up-regulation were evaluated on the metabolism and disposition of gemfibrozil.	Gemfibrozil	147-158	ATP binding cassette subfamily C member 3	Rattus norvegicus	76-80
14555339-4	2003	Results from in vitro studies in microsomes showed that the hepatic intrinsic clearance (CLint) for the oxidative metabolism of gemfibrozil was slightly higher (1.5-fold) in male TR- rats, which are deficient in Mrp2, than in wild-type Wistar rats, whereas CLint for glucuronidation was similar in both strains.	Gemfibrozil	128-139	ATP binding cassette subfamily C member 2	Rattus norvegicus	212-216
14555339-11	2003	Overall, it was demonstrated that alterations in the expression of the transporters Mrp2 and Mrp3 significantly affected the excretion as well as the secondary metabolism and distribution of [14C]gemfibrozil.	Gemfibrozil	196-207	ATP binding cassette subfamily C member 2	Rattus norvegicus	84-88
14555339-11	2003	Overall, it was demonstrated that alterations in the expression of the transporters Mrp2 and Mrp3 significantly affected the excretion as well as the secondary metabolism and distribution of [14C]gemfibrozil.	Gemfibrozil	196-207	ATP binding cassette subfamily C member 3	Rattus norvegicus	93-97
12935323-6	2003	These data suggest that FLPs and gemfibrozil not only lower lipid intolerance but also reduce diabetic-dyslipidemic complications by activating peroxisome proliferator-activated receptors (PPAR).	Gemfibrozil	33-44	peroxisome proliferator activated receptor alpha	Rattus norvegicus	144-187
12935323-6	2003	These data suggest that FLPs and gemfibrozil not only lower lipid intolerance but also reduce diabetic-dyslipidemic complications by activating peroxisome proliferator-activated receptors (PPAR).	Gemfibrozil	33-44	peroxisome proliferator activated receptor alpha	Rattus norvegicus	189-193
12692010-0	2003	Gemfibrozil reduces plasma C-reactive protein levels in abdominally obese men with the atherogenic dyslipidemia of the metabolic syndrome.	Gemfibrozil	0-11	C-reactive protein	Homo sapiens	27-45
12763281-0	2003	Gemfibrozil reduces release of tumor necrosis factor-alpha in peripheral blood mononuclear cells from healthy subjects and patients with coronary heart disease.	Gemfibrozil	0-11	tumor necrosis factor	Homo sapiens	31-58
12763281-3	2003	But little is known about the effect of gemfibrozil on tumor necrosis factor (TNF)-alpha secretion in peripheral blood mononuclear cells (PBMC) from patients with coronary heart disease.	Gemfibrozil	40-51	tumor necrosis factor	Homo sapiens	55-76
12763281-3	2003	But little is known about the effect of gemfibrozil on tumor necrosis factor (TNF)-alpha secretion in peripheral blood mononuclear cells (PBMC) from patients with coronary heart disease.	Gemfibrozil	40-51	tumor necrosis factor	Homo sapiens	78-88
12763281-11	2003	Gemfibrozil (10(-5),10(-4) mol/l) significantly inhibited TNF-alpha secretion in both groups (P&lt;0.05).	Gemfibrozil	0-11	tumor necrosis factor	Homo sapiens	58-67
12763281-12	2003	CONCLUSIONS: Our data demonstrated that gemfibrozil reduced release of TNF-alpha in PBMC both from CHD patients and controls.	Gemfibrozil	40-51	tumor necrosis factor	Homo sapiens	71-80
12746275-5	2003	PPARalpha potentiates fatty acid catabolism in the liver and is the molecular target of the lipid-lowering fibrates (e.g. fenofibrate and gemfibrozil), whereas PPARgamma is essential for adipocyte differentiation and mediates the activity of the insulin-sensitizing thiazolidinediones (e.g. rosiglitazone and pioglitazone).	Gemfibrozil	138-149	peroxisome proliferator activated receptor alpha	Homo sapiens	0-9
12834305-0	2003	Preparation of antiserum against rat delta6-desaturase and its use to evaluate the desaturase protein levels in rats treated with gemfibrozil, a ligand for peroxisome proliferator-activated receptor alpha.	Gemfibrozil	130-141	fatty acid desaturase 2	Rattus norvegicus	37-54
12834305-0	2003	Preparation of antiserum against rat delta6-desaturase and its use to evaluate the desaturase protein levels in rats treated with gemfibrozil, a ligand for peroxisome proliferator-activated receptor alpha.	Gemfibrozil	130-141	peroxisome proliferator activated receptor alpha	Rattus norvegicus	156-204
12834305-3	2003	Subsequently, the antiserum was used to demonstrate that gemfibrozil, a ligand for peroxisome proliferator-activated receptor alpha, is involved in activating delta6-desaturase gene expression, thereby elevating the protein level and the activity.	Gemfibrozil	57-68	peroxisome proliferator activated receptor alpha	Rattus norvegicus	83-131
12834305-3	2003	Subsequently, the antiserum was used to demonstrate that gemfibrozil, a ligand for peroxisome proliferator-activated receptor alpha, is involved in activating delta6-desaturase gene expression, thereby elevating the protein level and the activity.	Gemfibrozil	57-68	fatty acid desaturase 2	Rattus norvegicus	159-176
12716814-5	2003	Throughout both lower and higher ranges of HDL cholesterol and triglycerides, the rate of new cardiovascular events and the reduction of events with gemfibrozil was greater in subjects with insulin resistance than without, despite the finding that an increase in HDL cholesterol and a decrease in triglycerides with gemfibrozil was less with insulin resistance than without insulin resistance.	Gemfibrozil	149-160	insulin	Homo sapiens	190-197
12623126-5	2003	Paradoxically, under the same treatment conditions in male rats, liver P450R protein levels decreased after exposure to the PPs Wy-14,643 ([4-chloro-6-(2,3-xylidino)pyrimidynylthio]acetic acid) (WY) or gemfibrozil (GEM).	Gemfibrozil	202-213	cytochrome p450 oxidoreductase	Rattus norvegicus	71-76
12623126-5	2003	Paradoxically, under the same treatment conditions in male rats, liver P450R protein levels decreased after exposure to the PPs Wy-14,643 ([4-chloro-6-(2,3-xylidino)pyrimidynylthio]acetic acid) (WY) or gemfibrozil (GEM).	Gemfibrozil	215-218	cytochrome p450 oxidoreductase	Rattus norvegicus	71-76
12623126-6	2003	The down-regulation of the P450R protein was sex- and tissue-specific in that exposure to PPs led to increases in P450R protein in female rat livers [di-n-butyl phthalate (DBP) only] and male rat kidneys (WY, GEM, DBP).	Gemfibrozil	209-212	cytochrome p450 oxidoreductase	Rattus norvegicus	27-32
14727929-10	2003	The use of combined therapy with an HMG-CoA reductase inhibitor and a fibric acid derivative requires the respect of some rules such as avoiding the prescription in patients with concomitant conditions like renal failure and avoiding the use of gemfibrozil as a fibric acid derivative in such a combination.	Gemfibrozil	245-256	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	36-53
12640339-11	2003	In addition, the percentage increment of MCP-1 was higher in patients treated with gemfibrozil than in patients who received bezafibrate.	Gemfibrozil	83-94	C-C motif chemokine ligand 2	Homo sapiens	41-46
12640339-13	2003	This finding was associated with increased HDL-C. Fibrates, especially gemfibrozil, increased MCP-1 concentrations.	Gemfibrozil	71-82	C-C motif chemokine ligand 2	Homo sapiens	94-99
12433802-0	2002	Gemfibrozil inhibits CYP2C8-mediated cerivastatin metabolism in human liver microsomes.	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	21-27
14682608-4	2003	Several CYP enzymes were shown to be principally responsible for the metabolism of gemfibrozil in contrast to other fibrates.	Gemfibrozil	83-94	peptidylprolyl isomerase G	Homo sapiens	8-11
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 8	Homo sapiens	118-124
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
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 3 subfamily A member 4	Homo sapiens	139-145
14682608-6	2003	We propose that the increase of plasma concentration caused by co-administration of gemfibrozil and statins is at least partially due to CYP-mediated inhibition.	Gemfibrozil	84-95	peptidylprolyl isomerase G	Homo sapiens	137-140
12496749-7	2002	Gemfibrozil increased the AUC(0-infinity) of cerivastatin lactone, on average, to 440% (94% to 594%; P =.0024) and that of metabolite M-1 to 435% (216% to 802%; P =.0002) of the control (placebo) values, whereas the AUC(0-24) of metabolite M-23 was decreased to 22% (11% to 74%; P =.0017).	Gemfibrozil	0-11	myoregulin	Homo sapiens	134-137
12496749-8	2002	CONCLUSIONS: Gemfibrozil greatly increases plasma concentrations of cerivastatin, cerivastatin lactone, and metabolite M-1, whereas the level of metabolite M-23 is markedly reduced by gemfibrozil.	Gemfibrozil	13-24	myoregulin	Homo sapiens	119-122
12496749-9	2002	Gemfibrozil therefore inhibits the formation of M-23, which is thought to be dependent on CYP2C8.	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	90-96
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
12456232-2	2002	OBJECTIVES: To determine the efficacy of gemfibrozil in subjects with varying levels of glucose tolerance or hyperinsulinemia and to examine the association between diabetes status and glucose and insulin levels and risk of cardiovascular outcomes.	Gemfibrozil	41-52	insulin	Homo sapiens	114-121
12456232-10	2002	Among individuals without diabetes, gemfibrozil was most efficacious for those in the highest fasting plasma insulin level quartile (risk reduction, 35%; P =.04).	Gemfibrozil	36-47	insulin	Homo sapiens	109-116
12456232-11	2002	CONCLUSION: In men with CHD and a low high-density lipoprotein cholesterol level, gemfibrozil use was associated with a reduction in major cardiovascular events in persons with diabetes and in nondiabetic subjects with a high fasting plasma insulin level.	Gemfibrozil	82-93	insulin	Homo sapiens	241-248
12433802-5	2002	The present in vitro findings suggest that inhibition of CYP2C8 activity by gemfibrozil at least partially explains the interaction between gemfibrozil and cerivastatin.	Gemfibrozil	76-87	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	57-63
12433802-5	2002	The present in vitro findings suggest that inhibition of CYP2C8 activity by gemfibrozil at least partially explains the interaction between gemfibrozil and cerivastatin.	Gemfibrozil	140-151	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	57-63
12433802-7	2002	Inhibition of CYP2C8-mediated metabolism by gemfibrozil warrants further in vivo exploration.	Gemfibrozil	44-55	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	14-20
12433802-4	2002	Additionally, gemfibrozil inhibited paclitaxel 6 alpha-hydroxylation [K(i) (IC(50)) = 75 micro M (91 micro M)], a CYP2C8 marker reaction, but did not inhibit testosterone 6 beta-hydroxylation (CYP3A4).	Gemfibrozil	14-25	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	114-120
12433802-4	2002	Additionally, gemfibrozil inhibited paclitaxel 6 alpha-hydroxylation [K(i) (IC(50)) = 75 micro M (91 micro M)], a CYP2C8 marker reaction, but did not inhibit testosterone 6 beta-hydroxylation (CYP3A4).	Gemfibrozil	14-25	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	193-199
12244038-1	2002	Gemfibrozil, a lipid-lowering drug, inhibited cytokine-induced production of NO and the expression of inducible nitric-oxide synthase (iNOS) in human U373MG astroglial cells and primary astrocytes.	Gemfibrozil	0-11	nitric oxide synthase 2	Homo sapiens	102-133
12244038-4	2002	Since gemfibrozil is known to activate peroxisome proliferator-activated receptor-alpha (PPAR-alpha), we investigated the role of PPAR-alpha in gemfibrozil-mediated inhibition of iNOS.	Gemfibrozil	144-155	nitric oxide synthase 2	Homo sapiens	179-183
12244038-1	2002	Gemfibrozil, a lipid-lowering drug, inhibited cytokine-induced production of NO and the expression of inducible nitric-oxide synthase (iNOS) in human U373MG astroglial cells and primary astrocytes.	Gemfibrozil	0-11	nitric oxide synthase 2	Homo sapiens	135-139
12244038-5	2002	Gemfibrozil induced peroxisome proliferator-responsive element (PPRE)-dependent luciferase activity, which was inhibited by the expression of DeltahPPAR-alpha, the dominant-negative mutant of human PPAR-alpha.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Homo sapiens	148-158
12244038-2	2002	Similar to gemfibrozil, clofibrate, another fibrate drug, also inhibited the expression of iNOS.	Gemfibrozil	11-22	nitric oxide synthase 2	Homo sapiens	91-95
12244038-6	2002	However, DeltahPPAR-alpha was unable to abrogate gemfibrozil-mediated inhibition of iNOS suggesting that gemfibrozil inhibits iNOS independent of PPAR-alpha.	Gemfibrozil	105-116	nitric oxide synthase 2	Homo sapiens	126-130
12244038-3	2002	Inhibition of human iNOS promoter-driven luciferase activity by gemfibrozil in cytokine-stimulated U373MG astroglial cells suggests that this compound inhibits the transcription of iNOS.	Gemfibrozil	64-75	nitric oxide synthase 2	Homo sapiens	20-24
12244038-9	2002	Interestingly, gemfibrozil strongly inhibited the activation of NF-kappaB, AP-1, and C/EBPbeta but not that of GAS in cytokine-stimulated astroglial cells.	Gemfibrozil	15-26	nuclear factor kappa B subunit 1	Homo sapiens	64-73
12244038-3	2002	Inhibition of human iNOS promoter-driven luciferase activity by gemfibrozil in cytokine-stimulated U373MG astroglial cells suggests that this compound inhibits the transcription of iNOS.	Gemfibrozil	64-75	nitric oxide synthase 2	Homo sapiens	181-185
12244038-9	2002	Interestingly, gemfibrozil strongly inhibited the activation of NF-kappaB, AP-1, and C/EBPbeta but not that of GAS in cytokine-stimulated astroglial cells.	Gemfibrozil	15-26	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	75-79
12244038-4	2002	Since gemfibrozil is known to activate peroxisome proliferator-activated receptor-alpha (PPAR-alpha), we investigated the role of PPAR-alpha in gemfibrozil-mediated inhibition of iNOS.	Gemfibrozil	6-17	peroxisome proliferator activated receptor alpha	Homo sapiens	39-87
12244038-9	2002	Interestingly, gemfibrozil strongly inhibited the activation of NF-kappaB, AP-1, and C/EBPbeta but not that of GAS in cytokine-stimulated astroglial cells.	Gemfibrozil	15-26	CCAAT enhancer binding protein beta	Homo sapiens	85-94
12244038-4	2002	Since gemfibrozil is known to activate peroxisome proliferator-activated receptor-alpha (PPAR-alpha), we investigated the role of PPAR-alpha in gemfibrozil-mediated inhibition of iNOS.	Gemfibrozil	6-17	peroxisome proliferator activated receptor alpha	Homo sapiens	89-99
12244038-10	2002	These results suggest that gemfibrozil inhibits the induction of iNOS probably by inhibiting the activation of NF-kappaB, AP-1, and C/EBPbeta and that gemfibrozil, a prescribed drug for humans, may further find its therapeutic use in neuroinflammatory diseases.	Gemfibrozil	27-38	nitric oxide synthase 2	Homo sapiens	65-69
12386136-2	2002	Gemfibrozil (GFZ) modestly affected the formation of beta-oxidative products and CYP3A4-mediated oxidative metabolites of simvastatin hydroxy acid (SVA) but markedly inhibited the glucuronidation-mediated lactonization of SVA and the glucuronidation of a beta-oxidation product (IC(50) approximately 50 and 15 microM, respectively).	Gemfibrozil	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	81-87
12244038-10	2002	These results suggest that gemfibrozil inhibits the induction of iNOS probably by inhibiting the activation of NF-kappaB, AP-1, and C/EBPbeta and that gemfibrozil, a prescribed drug for humans, may further find its therapeutic use in neuroinflammatory diseases.	Gemfibrozil	27-38	nuclear factor kappa B subunit 1	Homo sapiens	111-120
12244038-10	2002	These results suggest that gemfibrozil inhibits the induction of iNOS probably by inhibiting the activation of NF-kappaB, AP-1, and C/EBPbeta and that gemfibrozil, a prescribed drug for humans, may further find its therapeutic use in neuroinflammatory diseases.	Gemfibrozil	27-38	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	122-126
12244038-10	2002	These results suggest that gemfibrozil inhibits the induction of iNOS probably by inhibiting the activation of NF-kappaB, AP-1, and C/EBPbeta and that gemfibrozil, a prescribed drug for humans, may further find its therapeutic use in neuroinflammatory diseases.	Gemfibrozil	27-38	CCAAT enhancer binding protein beta	Homo sapiens	132-141
12386136-2	2002	Gemfibrozil (GFZ) modestly affected the formation of beta-oxidative products and CYP3A4-mediated oxidative metabolites of simvastatin hydroxy acid (SVA) but markedly inhibited the glucuronidation-mediated lactonization of SVA and the glucuronidation of a beta-oxidation product (IC(50) approximately 50 and 15 microM, respectively).	Gemfibrozil	13-16	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	81-87
12386136-6	2002	While GFZ is not an inhibitor of CYP3A4, it is a competitive inhibitor (K(i) = 87 microM) of CYP2C8, a major catalyzing enzyme for CVA oxidation.	Gemfibrozil	6-9	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	93-99
12386136-7	2002	These results suggest that 1) the pharmacokinetic interaction observed between GFZ and statins was not likely mediated by the inhibitory effect of GFZ on the beta-oxidation, but rather by its effect primarily on the glucuronidation and non-CYP3A-mediated oxidation of statin hydroxy acids, and 2) there is a potential difference between fibrates in their ability to affect the pharmacokinetics of statins, and among statins in their susceptibility to metabolic interactions with GFZ in humans.	Gemfibrozil	79-82	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	240-245
12172398-0	2002	Influences of the PPAR alpha-L162V polymorphism on plasma HDL(2)-cholesterol response of abdominally obese men treated with gemfibrozil.	Gemfibrozil	124-135	peroxisome proliferator activated receptor alpha	Homo sapiens	18-28
12204791-0	2002	Effect of gemfibrozil on apolipoprotein B secretion and diacylglycerol acyltransferase activity in human hepatoblastoma (HepG2) cells.	Gemfibrozil	10-21	apolipoprotein B	Homo sapiens	25-41
12204791-1	2002	The mechanism of action of a widely used drug gemfibrozil to reduce triglycerides (TG) and apolipoprotein B (apo B) is incompletely understood.	Gemfibrozil	46-57	apolipoprotein B	Homo sapiens	91-107
12204791-1	2002	The mechanism of action of a widely used drug gemfibrozil to reduce triglycerides (TG) and apolipoprotein B (apo B) is incompletely understood.	Gemfibrozil	46-57	apolipoprotein B	Homo sapiens	109-114
12204791-2	2002	Using human hepatoblastoma (HepG2) cells, we examined the effect of gemfibrozil on apo B secretion and TG synthesis catalyzed by diacylglycerol acyltransferase (DGAT), primary processes associated with the secretion of LDL.	Gemfibrozil	68-79	apolipoprotein B	Homo sapiens	83-88
12204791-2	2002	Using human hepatoblastoma (HepG2) cells, we examined the effect of gemfibrozil on apo B secretion and TG synthesis catalyzed by diacylglycerol acyltransferase (DGAT), primary processes associated with the secretion of LDL.	Gemfibrozil	68-79	diacylglycerol O-acyltransferase 1	Homo sapiens	129-159
12204791-2	2002	Using human hepatoblastoma (HepG2) cells, we examined the effect of gemfibrozil on apo B secretion and TG synthesis catalyzed by diacylglycerol acyltransferase (DGAT), primary processes associated with the secretion of LDL.	Gemfibrozil	68-79	diacylglycerol O-acyltransferase 1	Homo sapiens	161-165
12204791-3	2002	Gemfibrozil significantly decreased apo B secretion by HepG2 cells.	Gemfibrozil	0-11	apolipoprotein B	Homo sapiens	36-41
12204791-4	2002	It decreased oleate-induced stimulation of apo B secretion, suggesting that gemfibrozil-mediated inhibition of apo B secretion may be dependent on the synthesis of TG catalyzed by DGAT.	Gemfibrozil	76-87	apolipoprotein B	Homo sapiens	43-48
12204791-4	2002	It decreased oleate-induced stimulation of apo B secretion, suggesting that gemfibrozil-mediated inhibition of apo B secretion may be dependent on the synthesis of TG catalyzed by DGAT.	Gemfibrozil	76-87	apolipoprotein B	Homo sapiens	111-116
12204791-4	2002	It decreased oleate-induced stimulation of apo B secretion, suggesting that gemfibrozil-mediated inhibition of apo B secretion may be dependent on the synthesis of TG catalyzed by DGAT.	Gemfibrozil	76-87	diacylglycerol O-acyltransferase 1	Homo sapiens	180-184
12204791-5	2002	Pre-incubation of HepG2 cells with gemfibrozil (200-400 micromol/l for 48 h) significantly inhibited microsomal DGAT activity.	Gemfibrozil	35-46	diacylglycerol O-acyltransferase 1	Homo sapiens	112-116
12204791-6	2002	When added directly to the DGAT assay system containing control microsomes, gemfibrozil significantly inhibited the activity of DGAT by 14-25%.	Gemfibrozil	76-87	diacylglycerol O-acyltransferase 1	Homo sapiens	27-31
12204791-6	2002	When added directly to the DGAT assay system containing control microsomes, gemfibrozil significantly inhibited the activity of DGAT by 14-25%.	Gemfibrozil	76-87	diacylglycerol O-acyltransferase 1	Homo sapiens	128-132
12204791-8	2002	The data indicate that gemfibrozil inhibits DGAT activity resulting in decreased synthesis of TG and its availability for apo B lipidation rendering it susceptible to intracellular apo B degradation leading to the decreased secretion.	Gemfibrozil	23-34	diacylglycerol O-acyltransferase 1	Homo sapiens	44-48
12204791-8	2002	The data indicate that gemfibrozil inhibits DGAT activity resulting in decreased synthesis of TG and its availability for apo B lipidation rendering it susceptible to intracellular apo B degradation leading to the decreased secretion.	Gemfibrozil	23-34	apolipoprotein B	Homo sapiens	122-127
12204791-8	2002	The data indicate that gemfibrozil inhibits DGAT activity resulting in decreased synthesis of TG and its availability for apo B lipidation rendering it susceptible to intracellular apo B degradation leading to the decreased secretion.	Gemfibrozil	23-34	apolipoprotein B	Homo sapiens	181-186
12204791-9	2002	These in-vitro data suggest a novel additional mechanism by which gemfibrozil lowers plasma TG and atherogenic apo B lipoproteins in dyslipidemic patients.	Gemfibrozil	66-77	apolipoprotein B	Homo sapiens	111-116
12147264-5	2002	Non-cross-reacting ACS1, ACS4, and ACS5 peptide antibodies showed that ACS4 was the only ACS isoform present in peroxisomes isolated from livers of gemfibrozil-treated rats.	Gemfibrozil	148-159	acyl-CoA synthetase long-chain family member 4	Rattus norvegicus	71-75
12104084-13	2002	Lag time, the principle measure of lipoprotein susceptibility to oxidation, was decreased by gemfibrozil.	Gemfibrozil	93-104	stathmin 1	Homo sapiens	0-3
12104084-15	2002	CONCLUSION: These data support the notion that gemfibrozil increases the proportion of polyunsaturated fatty acids in plasma lipids and that this increase is associated with an increase in lipoprotein oxidative susceptibility as measured by lag time in hypertriglyceridemia.	Gemfibrozil	47-58	stathmin 1	Homo sapiens	241-244
12123487-8	2002	The results of this study suggest that the ACE I/D polymorphism influences the effect of gemfibrozil on plasma HDL-C levels.	Gemfibrozil	89-100	angiotensin I converting enzyme	Homo sapiens	43-46
12172398-1	2002	PURPOSE: The effect of gemfibrozil is mediated by the activation of peroxisome proliferator-activated receptor alpha (PPAR alpha).	Gemfibrozil	23-34	peroxisome proliferator activated receptor alpha	Homo sapiens	68-116
12172398-1	2002	PURPOSE: The effect of gemfibrozil is mediated by the activation of peroxisome proliferator-activated receptor alpha (PPAR alpha).	Gemfibrozil	23-34	peroxisome proliferator activated receptor alpha	Homo sapiens	118-128
12172398-2	2002	The objective of this study was to determine whether the lipid response to gemfibrozil therapy is influenced by the PPAR alpha-L162V polymorphism.	Gemfibrozil	75-86	peroxisome proliferator activated receptor alpha	Homo sapiens	116-126
12172398-5	2002	CONCLUSION: These results suggest that the HDL(2)-C response to gemfibrozil is modulated by the PPAR alpha-L162V polymorphism.	Gemfibrozil	64-75	peroxisome proliferator activated receptor alpha	Homo sapiens	96-106
12023536-5	2002	In dog and human liver microsomes, GFZ exerted a minimal inhibitory effect on CYP3A-mediated SVA oxidation, but did inhibit SVA glucuronidation.	Gemfibrozil	35-38	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	78-83
12163133-7	2002	This suggests that ciprofibrate and gemfibrozil induce a different conformation to the receptor-PGC-1 and receptor-CBP complex, respectively.	Gemfibrozil	36-47	PPARG coactivator 1 alpha	Homo sapiens	96-101
12163133-7	2002	This suggests that ciprofibrate and gemfibrozil induce a different conformation to the receptor-PGC-1 and receptor-CBP complex, respectively.	Gemfibrozil	36-47	CREB binding protein	Homo sapiens	115-118
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
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
12023536-8	2002	Among six human UGT isozymes tested, UGT1A1 and 1A3 were capable of catalyzing the glucuronidation of both GFZ and SVA.	Gemfibrozil	107-110	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	16-19
12023536-8	2002	Among six human UGT isozymes tested, UGT1A1 and 1A3 were capable of catalyzing the glucuronidation of both GFZ and SVA.	Gemfibrozil	107-110	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-51
12023536-9	2002	Further studies conducted in human liver microsomes with atorvastatin (AVA) showed that, as with SVA, GFZ was a less potent inhibitor of the CYP3A4-mediated oxidation of this drug than its glucuronidation.	Gemfibrozil	102-105	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	141-147
12023536-10	2002	However, with cerivastatin (CVA), the glucuronidation as well as the CYP2C8- and CYP3A4-mediated oxidation pathways were much more susceptible to inhibition by GFZ than was observed with SVA or AVA.	Gemfibrozil	160-163	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	69-75
12023536-10	2002	However, with cerivastatin (CVA), the glucuronidation as well as the CYP2C8- and CYP3A4-mediated oxidation pathways were much more susceptible to inhibition by GFZ than was observed with SVA or AVA.	Gemfibrozil	160-163	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	81-87
11858378-8	2002	At the end of the fourth month, gemfibrozil reduced total cholesterol by 34%, LDL by 30%, apo B by 21% and triglycerides by 53% (p &lt; 0.05).	Gemfibrozil	32-43	apolipoprotein B	Homo sapiens	90-95
12025914-10	2002	Fibrates (with the exception of gemfibrozil) also consistently lower plasma fibrinogen levels.	Gemfibrozil	32-43	fibrinogen beta chain	Homo sapiens	76-86
11947905-5	2002	In low and high glucose media, gemfibrozil (100 micromol/l) reduced total PG production in the presence of TGF-beta 1, which was associated with a decrease in the apparent size of PGs.	Gemfibrozil	31-42	transforming growth factor beta 1	Homo sapiens	107-117
11947905-6	2002	Gemfibrozil and another PPAR-alpha ligand, WY-14643, significantly inhibited basal and TGF-beta1 stimulated GAG synthesis.	Gemfibrozil	0-11	transforming growth factor beta 1	Homo sapiens	87-96
11947915-3	2002	The reduction of total cholesterol (TC), betaquant LDL and LDL cholesterol (LDL-C) was significantly greater in patients treated with pravastatin than with gemfibrozil.	Gemfibrozil	156-167	component of oligomeric golgi complex 2	Homo sapiens	59-74
11947915-3	2002	The reduction of total cholesterol (TC), betaquant LDL and LDL cholesterol (LDL-C) was significantly greater in patients treated with pravastatin than with gemfibrozil.	Gemfibrozil	156-167	component of oligomeric golgi complex 2	Homo sapiens	76-81
12047397-6	2002	CONCLUSIONS: Gemfibrozil does not affect insulin sensitivity to glucose or fat metabolism in type 2 diabetes but enhances the lowering of plasma NEFA concentrations by insulin, probably by reducing hepatic fatty acid synthesis.	Gemfibrozil	13-24	insulin	Homo sapiens	168-175
11942772-9	2002	CONCLUSION: Fenofibrate and gemfibrozil induced similar variations from baseline values in triglycerides, HDL cholesterol, apolipoprotein B, and fibrinogen, but the decreases in total and LDL cholesterol levels were greater with fenofibrate, in this group of patients with primary hyperlipidemia.	Gemfibrozil	28-39	apolipoprotein B	Homo sapiens	123-139
11942772-9	2002	CONCLUSION: Fenofibrate and gemfibrozil induced similar variations from baseline values in triglycerides, HDL cholesterol, apolipoprotein B, and fibrinogen, but the decreases in total and LDL cholesterol levels were greater with fenofibrate, in this group of patients with primary hyperlipidemia.	Gemfibrozil	28-39	fibrinogen beta chain	Homo sapiens	145-155
11947915-6	2002	Both gemfibrozil and pravastatin reduced the concentrations of trigylceride-rich Lp-Bc (-12.2 and -13.3%, respectively) and Lp-A-II;B;C;D;E (-19 and -12.7%, respectively) particles and their characteristic apoC-III constituent (-10.0 and -7.0%, respectively).	Gemfibrozil	5-16	apolipoprotein C3	Homo sapiens	206-214
11947915-8	2002	Both pravastatin and gemfibrozil significantly increased the levels of apoA-I and, with both drugs, the elevated concentrations of apoA-I were due to significantly increased levels of Lp-A-I;A-II particles.	Gemfibrozil	21-32	apolipoprotein A1	Homo sapiens	71-77
11947915-8	2002	Both pravastatin and gemfibrozil significantly increased the levels of apoA-I and, with both drugs, the elevated concentrations of apoA-I were due to significantly increased levels of Lp-A-I;A-II particles.	Gemfibrozil	21-32	apolipoprotein A1	Homo sapiens	131-137
12047397-0	2002	Effects of gemfibrozil on insulin resistance to fat metabolism in subjects with type 2 diabetes and hypertriglyceridaemia.	Gemfibrozil	11-22	insulin	Homo sapiens	26-33
12047397-1	2002	AIM: To examine whether lowering of plasma triglyceride concentrations using the fibrate peroxisome proliferator-activated receptor (PPAR)alpha agonist gemfibrozil would influence insulin sensitivity to various aspects of intermediary metabolism among subjects with type 2 diabetes mellitus.	Gemfibrozil	152-163	insulin	Homo sapiens	180-187
11914252-2	2002	METHODS AND RESULTS: We investigated the association between the leucine 162 to valine (L162V) polymorphism and a G to C transversion in intron 7 of the PPARalpha gene and progression of atherosclerosis in the Lopid Coronary Angiography Trial (LOCAT), a trial examining the effect of gemfibrozil treatment on progression of atherosclerosis after bypass surgery and on risk of IHD in the second Northwick Park Heart Study (NPHS2), a prospective study of healthy middle-aged men in the United Kingdom.	Gemfibrozil	284-295	peroxisome proliferator activated receptor alpha	Homo sapiens	153-162
11694861-8	2001	RESULTS: After three months, it was observed that under the effect of gemfibrozil, serum triglyceride level was significantly decreased (from median: 3.46 mmol/l quartiles: q1=2.92 q3=5.28 to median 2.20 mmol/l quartiles: q1=1.79 q3=3.65; p&lt;0.001) while protective high-density lipoprotein (from 1.02 +/- 0.22 mmol/l to 1.13 +/- 0.28 mmol/l; p=0.05) and apolipoprotein A(1) (from 1.56 +/- 0.33 g/l to 1.72 +/- 0.29; p&lt;0.01) levels were significantly increased.	Gemfibrozil	70-81	apolipoprotein A1	Homo sapiens	357-376
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
11602509-4	2001	In addition, gemfibrozil exhibited somewhat smaller inhibitory effects on CYP2C19 and CYP1A2 activities, with K(i) (IC(50)) values of 24 (47) microM and 82 (136) microM, respectively.	Gemfibrozil	13-24	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	74-81
11602509-4	2001	In addition, gemfibrozil exhibited somewhat smaller inhibitory effects on CYP2C19 and CYP1A2 activities, with K(i) (IC(50)) values of 24 (47) microM and 82 (136) microM, respectively.	Gemfibrozil	13-24	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	86-92
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
11602509-8	2001	Gemfibrozil may also impair clearance of CYP2C19 and CYP1A2 substrates, but inhibition of other CYP isoforms is unlikely.	Gemfibrozil	0-11	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	41-48
11602509-8	2001	Gemfibrozil may also impair clearance of CYP2C19 and CYP1A2 substrates, but inhibition of other CYP isoforms is unlikely.	Gemfibrozil	0-11	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	53-59
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
11712864-6	2001	PPAR-alpha activators (gemfibrozil) decrease the risk of coronary heart disease in patients with normal LDL-cholesterol and low HDL-cholesterol (VA-HIT) and they slow the progression of premature coronary atherosclerosis (BECAIT) (bezafibrate), particularly in patients with type 2 diabetes (DAIS) (fenofibrate).	Gemfibrozil	23-34	peroxisome proliferator activated receptor alpha	Homo sapiens	0-10
11816722-5	2001	Gemfibrozil inhibited basal PAI-1 expression by 23% (p = ns) and TGF-beta-induced PAI-1 expression by 52% (p = 0.017) whereas t-PA and total protein synthesis was not affected.	Gemfibrozil	0-11	serpin family E member 1	Homo sapiens	28-33
11816722-5	2001	Gemfibrozil inhibited basal PAI-1 expression by 23% (p = ns) and TGF-beta-induced PAI-1 expression by 52% (p = 0.017) whereas t-PA and total protein synthesis was not affected.	Gemfibrozil	0-11	transforming growth factor beta 1	Homo sapiens	65-73
11816722-5	2001	Gemfibrozil inhibited basal PAI-1 expression by 23% (p = ns) and TGF-beta-induced PAI-1 expression by 52% (p = 0.017) whereas t-PA and total protein synthesis was not affected.	Gemfibrozil	0-11	serpin family E member 1	Homo sapiens	82-87
11816722-6	2001	Changes in PAI-1 protein accumulation reflected PAI-1 gene expression attributable to modulation of half-life of PAI-1 mRNA by gemfibrozil.	Gemfibrozil	127-138	serpin family E member 1	Homo sapiens	11-16
11816722-8	2001	Gemfibrozil specifically attenuates TGF-beta-induced PAI-1 expression in human arterial smooth muscle cells.	Gemfibrozil	0-11	transforming growth factor beta 1	Homo sapiens	36-44
11816722-8	2001	Gemfibrozil specifically attenuates TGF-beta-induced PAI-1 expression in human arterial smooth muscle cells.	Gemfibrozil	0-11	serpin family E member 1	Homo sapiens	53-58
11385362-6	2001	Gemfibrozil effectively lowered concentrations of plasma lipid, apolipoprotein (apo) B, and apo E.	Gemfibrozil	0-11	apolipoprotein B	Homo sapiens	64-86
11780395-6	2001	PDGF-B detected by immuno-histochemistry and RT-PCR analysis showed that the release of PDGF-B was inhibited by simvastatin and gemfibrozil after de-endothelialization.	Gemfibrozil	128-139	platelet-derived growth factor subunit B	Oryctolagus cuniculus	0-6
11780395-6	2001	PDGF-B detected by immuno-histochemistry and RT-PCR analysis showed that the release of PDGF-B was inhibited by simvastatin and gemfibrozil after de-endothelialization.	Gemfibrozil	128-139	platelet-derived growth factor subunit B	Oryctolagus cuniculus	88-94
11522369-4	2001	Chronic exposure to the PP WY-14,643 (WY) and gemfibrozil (GEM), but not di-n-butyl phthalate (DBP), led to decreases in ES-4 in male rat livers.	Gemfibrozil	46-57	carboxylesterase 1C	Mus musculus	121-125
11522369-4	2001	Chronic exposure to the PP WY-14,643 (WY) and gemfibrozil (GEM), but not di-n-butyl phthalate (DBP), led to decreases in ES-4 in male rat livers.	Gemfibrozil	59-62	carboxylesterase 1C	Mus musculus	121-125
11551527-0	2001	Increase in hepatic expression of SREBP-2 by gemfibrozil administration to rats.	Gemfibrozil	45-56	sterol regulatory element binding transcription factor 2	Rattus norvegicus	34-41
11551527-4	2001	As a part of a compensatory homeostatic response, we report for the first time that gemfibrozil administration to rats increased the hepatic sterol regulatory element binding protein-2 (SREBP-2) mRNA (2.9-fold) and mature protein (2.2-fold) levels.	Gemfibrozil	84-95	sterol regulatory element binding transcription factor 2	Rattus norvegicus	141-184
11551527-4	2001	As a part of a compensatory homeostatic response, we report for the first time that gemfibrozil administration to rats increased the hepatic sterol regulatory element binding protein-2 (SREBP-2) mRNA (2.9-fold) and mature protein (2.2-fold) levels.	Gemfibrozil	84-95	sterol regulatory element binding transcription factor 2	Rattus norvegicus	186-193
11551527-5	2001	An early increase in the transcriptional activity of SREBP-2 elicited by gemfibrozil administration might be responsible for the observed changes in HMG-CoA reductase, phosphatidate phosphohydrolase, and SREBP-2 expression.	Gemfibrozil	73-84	sterol regulatory element binding transcription factor 2	Rattus norvegicus	53-60
11551527-5	2001	An early increase in the transcriptional activity of SREBP-2 elicited by gemfibrozil administration might be responsible for the observed changes in HMG-CoA reductase, phosphatidate phosphohydrolase, and SREBP-2 expression.	Gemfibrozil	73-84	sterol regulatory element binding transcription factor 2	Rattus norvegicus	204-211
11385362-6	2001	Gemfibrozil effectively lowered concentrations of plasma lipid, apolipoprotein (apo) B, and apo E.	Gemfibrozil	0-11	apolipoprotein E	Homo sapiens	92-97
11385362-8	2001	The surface-to-core ratio and apo E/apo B ratio of VLDL particles were increased after gemfibrozil treatment.	Gemfibrozil	87-98	apolipoprotein E	Homo sapiens	30-35
11385362-8	2001	The surface-to-core ratio and apo E/apo B ratio of VLDL particles were increased after gemfibrozil treatment.	Gemfibrozil	87-98	apolipoprotein B	Homo sapiens	36-41
11474570-5	2001	PPAR-alpha activators (fibrates) improve plasma lipid levels and decrease CHD risk in patients with low HDL-cholesterol (gemfibrozil).	Gemfibrozil	121-132	peroxisome proliferator activated receptor alpha	Homo sapiens	0-10
11248139-9	2001	In gemfibrozil treated rats and hamsters, a decrease in alpha-tocopherol content and an increase in DT-diaphorase activity were observed.	Gemfibrozil	3-14	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	100-113
11159800-4	2001	Intrinsic clearance values for human UGT1A1 and UGT2B7 substrates were an order of magnitude higher in DLM than in HLM (e.g., gemfibrozil: 31 microl/min/mg versus 3.0 microl/min/mg; ketoprofen: 2.4 microl/min/mg versus 0.2 microl/min/mg).	Gemfibrozil	126-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
11159800-4	2001	Intrinsic clearance values for human UGT1A1 and UGT2B7 substrates were an order of magnitude higher in DLM than in HLM (e.g., gemfibrozil: 31 microl/min/mg versus 3.0 microl/min/mg; ketoprofen: 2.4 microl/min/mg versus 0.2 microl/min/mg).	Gemfibrozil	126-137	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	48-54
11159800-4	2001	Intrinsic clearance values for human UGT1A1 and UGT2B7 substrates were an order of magnitude higher in DLM than in HLM (e.g., gemfibrozil: 31 microl/min/mg versus 3.0 microl/min/mg; ketoprofen: 2.4 microl/min/mg versus 0.2 microl/min/mg).	Gemfibrozil	126-137	oxysterol binding protein 2	Homo sapiens	115-118
14728015-9	2001	Fibric acid derivatives and HMG-CoA reductase inhibitor therapy can be combined with care, provided that gemfibrozil is avoided, fibric acid derivatives are given in the mornings and shorter half -life HMG-CoA reductase inhibitors are used at night.	Gemfibrozil	105-116	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	28-45
10657576-5	2000	Gemfibrozil treatment did not affect plasma fibrinolysis or fibrinogen levels, despite marked reduction of plasma triglycerides and improvement of the insulin sensitivity associated with triglyceride normalization.	Gemfibrozil	0-11	insulin	Homo sapiens	151-158
11120871-5	2000	Some evidence also indicates that APO E2 individuals are more likely to respond favorably to gemfibrozil and cholestyramine.	Gemfibrozil	93-104	apolipoprotein E	Homo sapiens	34-40
10789612-8	2000	Effects on plasma fibrinogen levels were significantly favorable for Niaspan compared with gemfibrozil (P&lt;.02), as gemfibrozil increased the fibrinogen level (from 5% to 9%) and Niaspan tended to decrease the fibrinogen level (from -1% to -6%).	Gemfibrozil	91-102	fibrinogen beta chain	Homo sapiens	18-28
10789612-8	2000	Effects on plasma fibrinogen levels were significantly favorable for Niaspan compared with gemfibrozil (P&lt;.02), as gemfibrozil increased the fibrinogen level (from 5% to 9%) and Niaspan tended to decrease the fibrinogen level (from -1% to -6%).	Gemfibrozil	118-129	fibrinogen beta chain	Homo sapiens	144-154
10789612-8	2000	Effects on plasma fibrinogen levels were significantly favorable for Niaspan compared with gemfibrozil (P&lt;.02), as gemfibrozil increased the fibrinogen level (from 5% to 9%) and Niaspan tended to decrease the fibrinogen level (from -1% to -6%).	Gemfibrozil	118-129	fibrinogen beta chain	Homo sapiens	144-154
10744143-5	2000	tPA and PAI-1 antigen increased significantly in the gemfibrozil group (+11.3% and + 16.4%, respectively, p &lt; 0.001), whereas there was no treatment effect on PAI-1 activity (median change 0.0%).	Gemfibrozil	53-64	serpin family E member 1	Homo sapiens	8-13
10744143-7	2000	Furthermore, pronounced long-term lowering of serum triglycerides by gemfibrozil treatment does not significantly affect the plasma PAI-1 activity level but increases the plasma tPA and PAI-1 antigen concentrations.	Gemfibrozil	69-80	serpin family E member 1	Homo sapiens	186-191
10910008-8	2000	After 6 months, gemfibrozil therapy versus placebo had a marked lipid-lowering effect, significantly decreased triglycerides (61%), VLDL cholesterol (72%), apoB (28%), and apoE (55%), and increased high-density lipoprotein (44%) and apoA-I (18%).	Gemfibrozil	16-27	apolipoprotein B	Homo sapiens	156-160
10910008-8	2000	After 6 months, gemfibrozil therapy versus placebo had a marked lipid-lowering effect, significantly decreased triglycerides (61%), VLDL cholesterol (72%), apoB (28%), and apoE (55%), and increased high-density lipoprotein (44%) and apoA-I (18%).	Gemfibrozil	16-27	apolipoprotein E	Homo sapiens	172-176
10910008-8	2000	After 6 months, gemfibrozil therapy versus placebo had a marked lipid-lowering effect, significantly decreased triglycerides (61%), VLDL cholesterol (72%), apoB (28%), and apoE (55%), and increased high-density lipoprotein (44%) and apoA-I (18%).	Gemfibrozil	16-27	apolipoprotein A1	Homo sapiens	233-239
10910008-9	2000	Furthermore, gemfibrozil affected the apoprotein composition of VLDL: total protein increased by 28%, the molar ratio of apoE to apoB decreased 64%, and apoE content decreased 55%.	Gemfibrozil	13-24	apolipoprotein E	Homo sapiens	121-125
10910008-9	2000	Furthermore, gemfibrozil affected the apoprotein composition of VLDL: total protein increased by 28%, the molar ratio of apoE to apoB decreased 64%, and apoE content decreased 55%.	Gemfibrozil	13-24	apolipoprotein B	Homo sapiens	129-133
10910008-9	2000	Furthermore, gemfibrozil affected the apoprotein composition of VLDL: total protein increased by 28%, the molar ratio of apoE to apoB decreased 64%, and apoE content decreased 55%.	Gemfibrozil	13-24	apolipoprotein E	Homo sapiens	153-157
10657576-0	2000	Effects of gemfibrozil on insulin sensitivity and on haemostatic variables in hypertriglyceridemic patients.	Gemfibrozil	11-22	insulin	Homo sapiens	26-33
10656170-10	1999	Small fibrinogen (t0, t2, t6, t8), PAI-1 (t6) and AT III (t0-t8) increases were observed after gemfibrozil, while simvastatin did not significantly modify these parameters.	Gemfibrozil	95-106	serpin family E member 1	Homo sapiens	35-40
11111964-6	2000	F and G combined treatment is safe and useful in patients who do not respond satisfactorily to monotherapy with F. Gemfibrozil augments the effect of F on TC, LDL-C, and triglyceride levels.	Gemfibrozil	115-126	component of oligomeric golgi complex 2	Homo sapiens	159-164
10521386-6	1999	In the gemfibrozil group, there was a significant decrease in F1+2, while TAT complexes did not change.	Gemfibrozil	7-18	coagulation factor XII	Homo sapiens	62-66
10656170-10	1999	Small fibrinogen (t0, t2, t6, t8), PAI-1 (t6) and AT III (t0-t8) increases were observed after gemfibrozil, while simvastatin did not significantly modify these parameters.	Gemfibrozil	95-106	serpin family C member 1	Homo sapiens	50-56
10494028-7	1999	Under serum conditions allowing apo CIII secretion, treatment with the peroxisome-proliferator activated receptor (PPAR)alpha activators fenofibrate, gemfibrozil and Wy-14643 result in a marked lowering of apo CIII secretion and gene expression, this effect being most pronounced with Wy-14643.	Gemfibrozil	150-161	apolipoprotein C3	Homo sapiens	32-40
10364093-7	1999	In contrast, both fenofibric acid and gemfibrozil markedly decreased PAI-1 transcription and secretion from HUVECs and EA.hy926 cells.	Gemfibrozil	38-49	serpin family E member 1	Homo sapiens	69-74
10494028-7	1999	Under serum conditions allowing apo CIII secretion, treatment with the peroxisome-proliferator activated receptor (PPAR)alpha activators fenofibrate, gemfibrozil and Wy-14643 result in a marked lowering of apo CIII secretion and gene expression, this effect being most pronounced with Wy-14643.	Gemfibrozil	150-161	peroxisome proliferator activated receptor alpha	Homo sapiens	115-125
10494028-7	1999	Under serum conditions allowing apo CIII secretion, treatment with the peroxisome-proliferator activated receptor (PPAR)alpha activators fenofibrate, gemfibrozil and Wy-14643 result in a marked lowering of apo CIII secretion and gene expression, this effect being most pronounced with Wy-14643.	Gemfibrozil	150-161	apolipoprotein C3	Homo sapiens	206-214
9791843-7	1998	CONCLUSION: In patients with risk of pancreatitis due to severe hypertriglyceridemia, immediate reduction of the triglyceride level is achievable by using a single dose of regular insulin (0.1 unit/kg, subcutaneous) while long-term maintenance therapy can be provided by gemfibrozil.	Gemfibrozil	271-282	insulin	Homo sapiens	180-187
9853402-4	1998	At 1 mM, gemfibrozil decreased not only the activity of HMG-CoA reductase and cholesterol synthesis, but also the protein content of the cells and peroxisomal enzyme activity, indicating nonspecific inhibition at this concentration.	Gemfibrozil	9-20	3-hydroxy-3-methylglutaryl-CoA reductase	Rattus norvegicus	56-73
9853402-6	1998	With respect to the direct effect on HMG-CoA reductase in the cell homogenate, gemfibrozil at 0.25 mm did not affect the activity, but it clearly inhibited the activity at 2 mM and above.	Gemfibrozil	79-90	3-hydroxy-3-methylglutaryl-CoA reductase	Rattus norvegicus	37-54
9853402-11	1998	In contrast to whole body results, gemfibrozil may suppress cholesterol synthesis from [14C]acetate through the inhibition of HMG-CoA reductase at the culture cell level.	Gemfibrozil	35-46	3-hydroxy-3-methylglutaryl-CoA reductase	Rattus norvegicus	126-143
9853402-3	1998	Gemfibrozil at 0.25 mM increased the activity of some peroxisomal enzymes (catalase and the cyanide-insensitive fatty acyl-CoA oxidizing system) after incubation for 72 h. However, contrary to whole body experiments, gemfibrozil decreased the activity of HMG-CoA reductase and cholesterol synthesis from [14C]acetate.	Gemfibrozil	0-11	3-hydroxy-3-methylglutaryl-CoA reductase	Rattus norvegicus	255-272
9608883-5	1998	Gemfibrozil had no effect on plasma total cholesterol levels but gave significant dose-dependent decreases in plasma (VLDL) triglyceride levels (up to -53%).	Gemfibrozil	0-11	CD320 antigen	Mus musculus	118-122
9699891-0	1998	The 5A/6A polymorphism in the promoter of the stromelysin-1 (MMP-3) gene predicts progression of angiographically determined coronary artery disease in men in the LOCAT gemfibrozil study.	Gemfibrozil	169-180	matrix metallopeptidase 3	Homo sapiens	46-59
9699891-0	1998	The 5A/6A polymorphism in the promoter of the stromelysin-1 (MMP-3) gene predicts progression of angiographically determined coronary artery disease in men in the LOCAT gemfibrozil study.	Gemfibrozil	169-180	matrix metallopeptidase 3	Homo sapiens	61-66
9678787-13	1998	Serum apolipoprotein A1 (apo A1) was increased (P &lt; 0.05) by bezafibrate compared to gemfibrozil (placebo 103 +/- 26, bezafibrate 111 +/- 28 and gemfibrozil 102 +/- 25 mg/dl) and CETA from HDL to VLDL and LDL was decreased (P &lt; 0.05) by bezafibrate compared to placebo, but the apparent decrease with gemfibrozil did not achieve statistical significance (placebo 39.6 +/- 17.7, bezafibrate 32.3 +/- 14.7 and gemfibrozil 33.8 +/- 15.0 nmol/ml/h).	Gemfibrozil	148-159	apolipoprotein A1	Homo sapiens	6-23
9678787-13	1998	Serum apolipoprotein A1 (apo A1) was increased (P &lt; 0.05) by bezafibrate compared to gemfibrozil (placebo 103 +/- 26, bezafibrate 111 +/- 28 and gemfibrozil 102 +/- 25 mg/dl) and CETA from HDL to VLDL and LDL was decreased (P &lt; 0.05) by bezafibrate compared to placebo, but the apparent decrease with gemfibrozil did not achieve statistical significance (placebo 39.6 +/- 17.7, bezafibrate 32.3 +/- 14.7 and gemfibrozil 33.8 +/- 15.0 nmol/ml/h).	Gemfibrozil	148-159	apolipoprotein A1	Homo sapiens	25-31
9678787-13	1998	Serum apolipoprotein A1 (apo A1) was increased (P &lt; 0.05) by bezafibrate compared to gemfibrozil (placebo 103 +/- 26, bezafibrate 111 +/- 28 and gemfibrozil 102 +/- 25 mg/dl) and CETA from HDL to VLDL and LDL was decreased (P &lt; 0.05) by bezafibrate compared to placebo, but the apparent decrease with gemfibrozil did not achieve statistical significance (placebo 39.6 +/- 17.7, bezafibrate 32.3 +/- 14.7 and gemfibrozil 33.8 +/- 15.0 nmol/ml/h).	Gemfibrozil	148-159	apolipoprotein A1	Homo sapiens	6-23
9678787-13	1998	Serum apolipoprotein A1 (apo A1) was increased (P &lt; 0.05) by bezafibrate compared to gemfibrozil (placebo 103 +/- 26, bezafibrate 111 +/- 28 and gemfibrozil 102 +/- 25 mg/dl) and CETA from HDL to VLDL and LDL was decreased (P &lt; 0.05) by bezafibrate compared to placebo, but the apparent decrease with gemfibrozil did not achieve statistical significance (placebo 39.6 +/- 17.7, bezafibrate 32.3 +/- 14.7 and gemfibrozil 33.8 +/- 15.0 nmol/ml/h).	Gemfibrozil	148-159	apolipoprotein A1	Homo sapiens	25-31
9678787-13	1998	Serum apolipoprotein A1 (apo A1) was increased (P &lt; 0.05) by bezafibrate compared to gemfibrozil (placebo 103 +/- 26, bezafibrate 111 +/- 28 and gemfibrozil 102 +/- 25 mg/dl) and CETA from HDL to VLDL and LDL was decreased (P &lt; 0.05) by bezafibrate compared to placebo, but the apparent decrease with gemfibrozil did not achieve statistical significance (placebo 39.6 +/- 17.7, bezafibrate 32.3 +/- 14.7 and gemfibrozil 33.8 +/- 15.0 nmol/ml/h).	Gemfibrozil	148-159	apolipoprotein A1	Homo sapiens	6-23
9678787-13	1998	Serum apolipoprotein A1 (apo A1) was increased (P &lt; 0.05) by bezafibrate compared to gemfibrozil (placebo 103 +/- 26, bezafibrate 111 +/- 28 and gemfibrozil 102 +/- 25 mg/dl) and CETA from HDL to VLDL and LDL was decreased (P &lt; 0.05) by bezafibrate compared to placebo, but the apparent decrease with gemfibrozil did not achieve statistical significance (placebo 39.6 +/- 17.7, bezafibrate 32.3 +/- 14.7 and gemfibrozil 33.8 +/- 15.0 nmol/ml/h).	Gemfibrozil	148-159	apolipoprotein A1	Homo sapiens	25-31
9678787-15	1998	Plasma fibrinogen was increased (P &lt; 0.05) by gemfibrozil (placebo 4.16 (3.38-4.71) and gemfibrozil 4.65 (4.05-5.77) g/l) and was significantly lower (P &lt; 0.001) on bezafibrate (3.60 (3.18-4.54) g/l) than on gemfibrozil treatment.	Gemfibrozil	49-60	fibrinogen beta chain	Homo sapiens	7-17
9678787-15	1998	Plasma fibrinogen was increased (P &lt; 0.05) by gemfibrozil (placebo 4.16 (3.38-4.71) and gemfibrozil 4.65 (4.05-5.77) g/l) and was significantly lower (P &lt; 0.001) on bezafibrate (3.60 (3.18-4.54) g/l) than on gemfibrozil treatment.	Gemfibrozil	91-102	fibrinogen beta chain	Homo sapiens	7-17
9678787-15	1998	Plasma fibrinogen was increased (P &lt; 0.05) by gemfibrozil (placebo 4.16 (3.38-4.71) and gemfibrozil 4.65 (4.05-5.77) g/l) and was significantly lower (P &lt; 0.001) on bezafibrate (3.60 (3.18-4.54) g/l) than on gemfibrozil treatment.	Gemfibrozil	91-102	fibrinogen beta chain	Homo sapiens	7-17
9678787-20	1998	The two drugs also had different effects on the plasma fibrinogen levels, which increased with gemfibrozil and tended to decrea	Gemfibrozil	95-106	fibrinogen beta chain	Homo sapiens	55-65
18370512-1	1998	OBJECTIVE: This pilot study investigated the efficacy of high-dose gemfibrozil (2400 mg/day) in treating patients with elevated lipoprotein (a) [Lp(a)].	Gemfibrozil	67-78	lipoprotein(a)	Homo sapiens	145-150
9514936-5	1998	The addition of gemfibrozil to cultures of monkey and human hepatocytes had no effect on apo(a) synthesis, but resulted in a dose- and time-dependent increase of apo A-I synthesis and mRNA.	Gemfibrozil	16-27	apolipoprotein A1	Homo sapiens	162-169
9514936-7	1998	Similar results were obtained by using human hepatocytes; apo(a) synthesis remained unchanged, while apo A-I secretion was 2.0-fold increased at 1 mM gemfibrozil.	Gemfibrozil	150-161	apolipoprotein A1	Homo sapiens	101-108
9484993-3	1998	Fibrates like gemfibrozil are well-known PPARalpha activators and are used in the treatment of hyperlipidemia.	Gemfibrozil	14-25	peroxisome proliferator activated receptor alpha	Homo sapiens	41-50
9484993-4	1998	We show that the RXR ligand LGD1069 (Targretin), like gemfibrozil, can activate the PPARalpha/RXR signal-transduction pathway, including transactivation of the bifunctional enzyme or acyl-CoA oxidase response elements in a cotransfection assay.	Gemfibrozil	54-65	retinoid X receptor alpha	Homo sapiens	17-20
9484993-4	1998	We show that the RXR ligand LGD1069 (Targretin), like gemfibrozil, can activate the PPARalpha/RXR signal-transduction pathway, including transactivation of the bifunctional enzyme or acyl-CoA oxidase response elements in a cotransfection assay.	Gemfibrozil	54-65	peroxisome proliferator activated receptor alpha	Homo sapiens	84-93
9484993-4	1998	We show that the RXR ligand LGD1069 (Targretin), like gemfibrozil, can activate the PPARalpha/RXR signal-transduction pathway, including transactivation of the bifunctional enzyme or acyl-CoA oxidase response elements in a cotransfection assay.	Gemfibrozil	54-65	retinoid X receptor alpha	Homo sapiens	94-97
9507986-1	1998	Previously, we demonstrated that protein-DNA interactions at the drug response element (DRE) in the human apoA-I promoter were important for the induction of apoA-I gene expression by gemfibrozil.	Gemfibrozil	184-195	apolipoprotein A1	Homo sapiens	106-112
9507986-1	1998	Previously, we demonstrated that protein-DNA interactions at the drug response element (DRE) in the human apoA-I promoter were important for the induction of apoA-I gene expression by gemfibrozil.	Gemfibrozil	184-195	apolipoprotein A1	Homo sapiens	158-164
9507986-9	1998	Together these observations indicate that HSmuBP2 acts as a transcription factor that regulates apoA-I gene expression in hepatoma cells and whose activity may be stimulated by gemfibrozil treatment.	Gemfibrozil	177-188	apolipoprotein A1	Homo sapiens	96-102
9364979-8	1997	However, after twelve weeks, gemfibrozil enhanced functional fibrinogen levels by 7.2% (p &lt;0.05) as assessed by the Clauss mechanical assay, but decreased functional fibrinogen levels by 12.5% (p &lt;0.0001) when a Clauss assay based on turbidity was used.	Gemfibrozil	29-40	fibrinogen beta chain	Homo sapiens	169-179
9409246-0	1997	Upregulation of low density lipoprotein receptor by gemfibrozil, a hypolipidemic agent, in human hepatoma cells through stabilization of mRNA transcripts.	Gemfibrozil	52-63	low density lipoprotein receptor	Homo sapiens	16-48
9409246-3	1997	Exposure to gemfibrozil, 40 mumol/L, for 3 days increased the binding of 125I-LDL to the surface of three lines of human hepatoma cell, HepG2, HuH7, and HLE by 1.5- to 2.0-fold.	Gemfibrozil	12-23	MIR7-3 host gene	Homo sapiens	143-147
9409246-7	1997	Gemfibrozil increased the levels of LDL receptor mRNA and protein in HepG2 cells.	Gemfibrozil	0-11	low density lipoprotein receptor	Homo sapiens	36-48
9409246-11	1997	The expression of LDL receptor regulated by the sterol regulatory element was increased by pravastatin, but not by gemfibrozil.	Gemfibrozil	115-126	low density lipoprotein receptor	Homo sapiens	18-30
9409246-13	1997	Gemfibrozil prolonged the half-life of the mRNA for LDL receptor but not that for the EGF receptor.	Gemfibrozil	0-11	low density lipoprotein receptor	Homo sapiens	52-64
9409246-14	1997	Stabilization of the LDL receptor mRNA is suggested to be the novel mode of action of gemfibrozil.	Gemfibrozil	86-97	low density lipoprotein receptor	Homo sapiens	21-33
9361689-7	1997	The postprandial TRL apo B increase was reduced with gemfibrozil (from 11.6 +/- 2.8 to 20.7 +/- 5.0 mg/dL with therapy v 19.0 +/- 7.6 to 33.0 +/- 12.5 mg/dL before therapy, P &lt; .05, respectively) with a proportionally greater increase in apo B-48 (119% and 169%, respectively) compared with apo B-100 (64% and 64%, respectively).	Gemfibrozil	53-64	apolipoprotein B	Homo sapiens	294-303
9364979-0	1997	Effects of gemfibrozil and ciprofibrate on plasma levels of tissue-type plasminogen activator, plasminogen activator inhibitor-1 and fibrinogen in hyperlipidaemic patients.	Gemfibrozil	11-22	plasminogen activator, tissue type	Homo sapiens	60-93
9497506-5	1997	RESULTS: Gemfibrozil reduced TC (-21%), LDL-C (-26%), triglycerides (TG)(-48%) and Lp(a) (-25%), increased HDL-C (+48%)(p &lt; 0.001).	Gemfibrozil	9-20	component of oligomeric golgi complex 2	Homo sapiens	40-45
9364979-3	1997	We sought to learn more about this variability by examining the effects of gemfibrozil and ciprofibrate on plasma levels of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1) and fibrinogen in primary hyperlipidaemic patients after six and twelve weeks of treatment using different assay systems for PAI-1 and fibrinogen.	Gemfibrozil	75-86	plasminogen activator, tissue type	Homo sapiens	124-157
9364979-6	1997	Fibrinogen antigen levels were elevated by 17.6% (p &lt;0.05) and 24.3% (p &lt;0.001) with gemfibrozil after six and twelve weeks, respectively, whereas with ciprofibrate there was no effect.	Gemfibrozil	91-102	fibrinogen beta chain	Homo sapiens	0-10
9364979-8	1997	However, after twelve weeks, gemfibrozil enhanced functional fibrinogen levels by 7.2% (p &lt;0.05) as assessed by the Clauss mechanical assay, but decreased functional fibrinogen levels by 12.5% (p &lt;0.0001) when a Clauss assay based on turbidity was used.	Gemfibrozil	29-40	fibrinogen beta chain	Homo sapiens	61-71
9294990-12	1997	Simvastatin + ciprofibrate was more effective than pravastatin + gemfibrozil in reducing LDL, TG, and plasma fibrinogen levels.	Gemfibrozil	65-76	fibrinogen beta chain	Homo sapiens	109-119
9298501-2	1997	Several drugs and other compounds, e.g. phenobarbital, gemfibrozil, fenofibrate, prednisone, estrogen and alcohol, induce apolipoprotein A-I synthesis.	Gemfibrozil	55-66	apolipoprotein A1	Homo sapiens	122-140
9497506-7	1997	CONCLUSION: Besides reducing plasma LDL-C, TG and increasing HDL-C, gemfibrozil effectively lowers Lp(a) levels.	Gemfibrozil	68-79	lipoprotein(a)	Homo sapiens	99-104
9327717-4	1997	In contrast, plasma plasminogen activator inhibitor-1 antigen (36.9 +/- 12.4 vs 27.3 +/- 11.4 ng/ml; p = 0.008) and activity (15.5 +/- 5.5 vs 11.8 +/- 3.0 IU/ml; p = 0.009) and tissue plasminogen activator antigen (13.2 +/- 4.0 vs 10.4 +/- 3.7 ng/ml; p = 0.007) were significantly depressed, and tissue plasimogen activator activity (0.57 +/- 0.31 vs 0.69 +/- 0.38 IU/ml; p = 0.015) was significantly elevated by gemfibrozil.	Gemfibrozil	413-424	serpin family E member 1	Homo sapiens	20-53
9024157-0	1997	Attenuation by gemfibrozil of expression of plasminogen activator inhibitor type 1 induced by insulin and its precursors.	Gemfibrozil	15-26	serpin family E member 1	Homo sapiens	44-82
9145201-5	1997	The hydroxymethylglutaryl-CoA (HMG-CoA) reductase (rate-limiting enzyme of cholesterol synthesis) activity of peroxisomes and microsomes was greatly increased by in vivo treatment with gemfibrozil, but was decreased by addition of the agent to the assay mixture of the enzyme.	Gemfibrozil	185-196	3-hydroxy-3-methylglutaryl-CoA reductase	Rattus norvegicus	4-49
9105566-12	1997	Lp(a) (P = 0.04) and plasma insulin concentrations (P = 0.03) were negative predictors of percentage triglyceride-lowering with gemfibrozil.	Gemfibrozil	128-139	lipoprotein(a)	Homo sapiens	0-5
9105566-12	1997	Lp(a) (P = 0.04) and plasma insulin concentrations (P = 0.03) were negative predictors of percentage triglyceride-lowering with gemfibrozil.	Gemfibrozil	128-139	insulin	Homo sapiens	28-35
9024157-0	1997	Attenuation by gemfibrozil of expression of plasminogen activator inhibitor type 1 induced by insulin and its precursors.	Gemfibrozil	15-26	insulin	Homo sapiens	94-101
9024157-4	1997	METHODS AND RESULTS: In Hep G2 cells, 500 (700) mumol/L gemfibrozil decreased basal secretion of PAI-1 by 26% (43%) (P = .012 and P = .021, respectively) and attenuated insulin-induced (10 nmol/L) augmentation of PAI-1 in conditioned media by 61% (109%) (P = .010) within 24 hours.	Gemfibrozil	56-67	serpin family E member 1	Homo sapiens	97-102
9024157-4	1997	METHODS AND RESULTS: In Hep G2 cells, 500 (700) mumol/L gemfibrozil decreased basal secretion of PAI-1 by 26% (43%) (P = .012 and P = .021, respectively) and attenuated insulin-induced (10 nmol/L) augmentation of PAI-1 in conditioned media by 61% (109%) (P = .010) within 24 hours.	Gemfibrozil	56-67	insulin	Homo sapiens	169-176
9024157-4	1997	METHODS AND RESULTS: In Hep G2 cells, 500 (700) mumol/L gemfibrozil decreased basal secretion of PAI-1 by 26% (43%) (P = .012 and P = .021, respectively) and attenuated insulin-induced (10 nmol/L) augmentation of PAI-1 in conditioned media by 61% (109%) (P = .010) within 24 hours.	Gemfibrozil	56-67	serpin family E member 1	Homo sapiens	213-218
9024157-6	1997	Gemfibrozil attenuated the augmentation of PAI-1 secretion induced by proinsulin (&gt; 100%), by des(31,32)proinsulin (75%), and by des(64,65) proinsulin (77%) as well (10 nmol/L each).	Gemfibrozil	0-11	serpin family E member 1	Homo sapiens	43-48
9024157-6	1997	Gemfibrozil attenuated the augmentation of PAI-1 secretion induced by proinsulin (&gt; 100%), by des(31,32)proinsulin (75%), and by des(64,65) proinsulin (77%) as well (10 nmol/L each).	Gemfibrozil	0-11	insulin	Homo sapiens	70-80
9024157-6	1997	Gemfibrozil attenuated the augmentation of PAI-1 secretion induced by proinsulin (&gt; 100%), by des(31,32)proinsulin (75%), and by des(64,65) proinsulin (77%) as well (10 nmol/L each).	Gemfibrozil	0-11	insulin	Homo sapiens	107-117
9024157-6	1997	Gemfibrozil attenuated the augmentation of PAI-1 secretion induced by proinsulin (&gt; 100%), by des(31,32)proinsulin (75%), and by des(64,65) proinsulin (77%) as well (10 nmol/L each).	Gemfibrozil	0-11	insulin	Homo sapiens	107-117
9024157-10	1997	CONCLUSIONS: Gemfibrozil attenuated the augmentation of synthesis and secretion of PAI-1 induced by insulin and its precursors directly and specifically.	Gemfibrozil	13-24	serpin family E member 1	Homo sapiens	83-88
9024157-10	1997	CONCLUSIONS: Gemfibrozil attenuated the augmentation of synthesis and secretion of PAI-1 induced by insulin and its precursors directly and specifically.	Gemfibrozil	13-24	insulin	Homo sapiens	100-107
9012633-4	1997	Different fibrates showed different potency in suppressing PAI-1 production: gemfibrozil and clofibric acid, at a concentration of 1 mmol/L, reduced PAI-1 synthesis over 24 hours to 52 +/- 20% and 60 +/- 5%, while clofibrate and bezafibrate lowered PAI-1 synthesis to only 86 +/- 17% and 84 +/- 15% of control values, respectively.	Gemfibrozil	77-88	plasminogen activator inhibitor 1	Macaca fascicularis	59-64
9012633-4	1997	Different fibrates showed different potency in suppressing PAI-1 production: gemfibrozil and clofibric acid, at a concentration of 1 mmol/L, reduced PAI-1 synthesis over 24 hours to 52 +/- 20% and 60 +/- 5%, while clofibrate and bezafibrate lowered PAI-1 synthesis to only 86 +/- 17% and 84 +/- 15% of control values, respectively.	Gemfibrozil	77-88	plasminogen activator inhibitor 1	Macaca fascicularis	149-154
9012633-4	1997	Different fibrates showed different potency in suppressing PAI-1 production: gemfibrozil and clofibric acid, at a concentration of 1 mmol/L, reduced PAI-1 synthesis over 24 hours to 52 +/- 20% and 60 +/- 5%, while clofibrate and bezafibrate lowered PAI-1 synthesis to only 86 +/- 17% and 84 +/- 15% of control values, respectively.	Gemfibrozil	77-88	plasminogen activator inhibitor 1	Macaca fascicularis	149-154
9006809-2	1996	Although both drugs lowered plasma triglycerides (TG) to about the same extent in chow-fed rats, gemfibrozil lowered liver TG as well as plasma total and LDL-cholesterol (LDL-C), but elevated HDL-cholesterol (HDL-C) and plasma apo E concentrations.	Gemfibrozil	97-108	apolipoprotein E	Rattus norvegicus	227-232
9069450-14	1997	Furthermore, gemfibrozil treatment resulted in the reduction of plasma concentrations of complex (LP-Bc) and simple (LP-B) apoB-containing lipoprotein particles by 22 and 7%, respectively.	Gemfibrozil	13-24	apolipoprotein B	Homo sapiens	123-127
9069450-19	1997	CONCLUSIONS: Gemfibrozil treatment significantly reduces both plasma lipids and apoB, apoC-III and apoE concentrations in patients with moderately advanced renal insufficiency.	Gemfibrozil	13-24	apolipoprotein B	Homo sapiens	80-84
9069450-19	1997	CONCLUSIONS: Gemfibrozil treatment significantly reduces both plasma lipids and apoB, apoC-III and apoE concentrations in patients with moderately advanced renal insufficiency.	Gemfibrozil	13-24	apolipoprotein C3	Homo sapiens	86-94
9069450-19	1997	CONCLUSIONS: Gemfibrozil treatment significantly reduces both plasma lipids and apoB, apoC-III and apoE concentrations in patients with moderately advanced renal insufficiency.	Gemfibrozil	13-24	apolipoprotein E	Homo sapiens	99-103
9069450-20	1997	The results of this study indicate that gemfibrozil enhances the clearance of apoB-containing triglyceride-rich lipoproteins.	Gemfibrozil	40-51	apolipoprotein B	Homo sapiens	78-82
9031453-0	1997	Modulation of plasma fibrinogen levels by ciprofibrate and gemfibrozil in primary hyperlipidaemia.	Gemfibrozil	59-70	fibrinogen beta chain	Homo sapiens	21-31
9006809-7	1996	From these data we postulate that, although similar with regard to TG lowering activity and mechanisms thereof, gemfibrozil and bezafibrate produce fundamentally different effects on LDL, HDL and apolipoprotein metabolism (apo B and apo E) in rats which may relate to potential differential effects on reverse cholesterol transport and atherogenesis.	Gemfibrozil	112-123	apolipoprotein B	Rattus norvegicus	188-238
8900208-1	1996	Previously, we demonstrated that when two human hepatoma cell lines, Hep3B and HepG2, were exposed to gemfibrozil, a hypolipidemic drug, a 2-fold induction in apolipoprotein A-I (apoA-I) mRNA levels resulted.	Gemfibrozil	102-113	apolipoprotein A1	Homo sapiens	159-177
8902147-0	1996	Effects of gemfibrozil administration on very low density lipoprotein receptor mRNA levels in rabbits.	Gemfibrozil	11-22	very low-density lipoprotein receptor	Oryctolagus cuniculus	41-78
8902147-1	1996	To elucidate the regulation of very low density lipoprotein (VLDL) receptor gene expression, we administered to rabbits for 14 days gemfibrozil, a fabric acid derivative and a lipid lowering drug that is also included among peroxisome proliferators.	Gemfibrozil	132-143	very low-density lipoprotein receptor	Oryctolagus cuniculus	31-75
8902147-3	1996	The VLDL receptor mRNA levels in retroperitoneal adipose tissue and in gastrocnemius muscle were increased 6.9-fold and 3.7-fold, respectively, with gemfibrozil treatment, but no marked changes were observed in the heart, the organ in which VLDL receptor is most highly expressed.	Gemfibrozil	149-160	very low-density lipoprotein receptor	Oryctolagus cuniculus	4-17
8902147-3	1996	The VLDL receptor mRNA levels in retroperitoneal adipose tissue and in gastrocnemius muscle were increased 6.9-fold and 3.7-fold, respectively, with gemfibrozil treatment, but no marked changes were observed in the heart, the organ in which VLDL receptor is most highly expressed.	Gemfibrozil	149-160	very low-density lipoprotein receptor	Oryctolagus cuniculus	241-254
8900208-1	1996	Previously, we demonstrated that when two human hepatoma cell lines, Hep3B and HepG2, were exposed to gemfibrozil, a hypolipidemic drug, a 2-fold induction in apolipoprotein A-I (apoA-I) mRNA levels resulted.	Gemfibrozil	102-113	apolipoprotein A1	Homo sapiens	179-185
8900208-4	1996	However, nuclear run-off assays indicated that the transcription rate of the apoA-I gene was increased 2-fold in gemfibrozil-treated cells.	Gemfibrozil	113-124	apolipoprotein A1	Homo sapiens	77-83
8900208-5	1996	Transient transfection experiments also indicated that the induction of apoA-I mRNA level in response to gemfibrozil is mediated at the transcriptional level.	Gemfibrozil	105-116	apolipoprotein A1	Homo sapiens	72-78
8900208-6	1996	We have identified two copies of the "drug-responsive element" (DRE) in the apoA-I promoter region that may be responsible for the increase in apoA-I transcriptional activity by gemfibrozil.	Gemfibrozil	178-189	apolipoprotein A1	Homo sapiens	76-82
8900208-6	1996	We have identified two copies of the "drug-responsive element" (DRE) in the apoA-I promoter region that may be responsible for the increase in apoA-I transcriptional activity by gemfibrozil.	Gemfibrozil	178-189	apolipoprotein A1	Homo sapiens	143-149
8900208-15	1996	These results implicate protein-DNA interactions at the DRE region in the transcriptional induction of human apoA-I gene expression by gemfibrozil.	Gemfibrozil	135-146	apolipoprotein A1	Homo sapiens	109-115
8696946-3	1996	Since the liver is the major organ involved in HDL production and removal, we assessed the effect of gemfibrozil on the modulation of apoA-I (a major protein of HDL)-containing particles by a human hepatoblastoma cell line (Hep G2).	Gemfibrozil	101-112	apolipoprotein A1	Homo sapiens	134-140
8790349-5	1996	SCD1 mRNA was analyzed from the livers of BALB/c mice that had been fed diets supplemented with clofibrate or gemfibrozil.	Gemfibrozil	110-121	stearoyl-Coenzyme A desaturase 1	Mus musculus	0-4
8879439-4	1996	Gemfibrozil significantly affected VLDL composition: protein increased 26%, molar ratio of apoE to apoB reduced 48%, apoC-II increased 19%, and apoC-III decreased 9%.	Gemfibrozil	0-11	apolipoprotein E	Homo sapiens	91-95
8879439-4	1996	Gemfibrozil significantly affected VLDL composition: protein increased 26%, molar ratio of apoE to apoB reduced 48%, apoC-II increased 19%, and apoC-III decreased 9%.	Gemfibrozil	0-11	apolipoprotein B	Homo sapiens	99-103
8879439-4	1996	Gemfibrozil significantly affected VLDL composition: protein increased 26%, molar ratio of apoE to apoB reduced 48%, apoC-II increased 19%, and apoC-III decreased 9%.	Gemfibrozil	0-11	apolipoprotein C2	Homo sapiens	117-124
8879439-4	1996	Gemfibrozil significantly affected VLDL composition: protein increased 26%, molar ratio of apoE to apoB reduced 48%, apoC-II increased 19%, and apoC-III decreased 9%.	Gemfibrozil	0-11	apolipoprotein C3	Homo sapiens	144-152
8879439-9	1996	Taken together, these results suggest that treatment with gemfibrozil reduces plasma concentrations of VLDL and alters the apoprotein composition of VLDL in a manner that may favor LDL- and VLDL-receptor-mediated clearance of the apoE-rich VLDL subfraction, thereby reducing TG-rich particle concentrations, and possibly reducing risk for coronary heart disease.	Gemfibrozil	58-69	very low density lipoprotein receptor	Homo sapiens	190-203
8879439-9	1996	Taken together, these results suggest that treatment with gemfibrozil reduces plasma concentrations of VLDL and alters the apoprotein composition of VLDL in a manner that may favor LDL- and VLDL-receptor-mediated clearance of the apoE-rich VLDL subfraction, thereby reducing TG-rich particle concentrations, and possibly reducing risk for coronary heart disease.	Gemfibrozil	58-69	apolipoprotein E	Homo sapiens	230-234
8696946-5	1996	These data indicate that gemfibrozil stabilizes apoA-I mRNA transcripts, resulting in increased translation of functional apoA-I-containing particles capable of effluxing cellular cholesterol, thus defining a major mechanism by which gemfibrozil increases HDL.	Gemfibrozil	25-36	apolipoprotein A1	Homo sapiens	48-54
8696946-5	1996	These data indicate that gemfibrozil stabilizes apoA-I mRNA transcripts, resulting in increased translation of functional apoA-I-containing particles capable of effluxing cellular cholesterol, thus defining a major mechanism by which gemfibrozil increases HDL.	Gemfibrozil	25-36	apolipoprotein A1	Homo sapiens	122-128
8696946-5	1996	These data indicate that gemfibrozil stabilizes apoA-I mRNA transcripts, resulting in increased translation of functional apoA-I-containing particles capable of effluxing cellular cholesterol, thus defining a major mechanism by which gemfibrozil increases HDL.	Gemfibrozil	234-245	apolipoprotein A1	Homo sapiens	48-54
8696946-5	1996	These data indicate that gemfibrozil stabilizes apoA-I mRNA transcripts, resulting in increased translation of functional apoA-I-containing particles capable of effluxing cellular cholesterol, thus defining a major mechanism by which gemfibrozil increases HDL.	Gemfibrozil	234-245	apolipoprotein A1	Homo sapiens	122-128
8946270-0	1996	Effects of gemfibrozil therapy on glucose tolerance, insulin sensitivity and plasma plasminogen activator inhibitor activity in hypertriglyceridaemia.	Gemfibrozil	11-22	insulin	Homo sapiens	53-60
8824106-7	1996	In keeping with a more effective reduction of VLDL particles, a more pronounced reduction of apo-CIII also was observed after gemfibrozil, which correlated with the reduction in plasma triglycerides.	Gemfibrozil	126-137	apolipoprotein C3	Homo sapiens	93-101
8865525-0	1996	Gemfibrozil reduces thrombin generation in patients with combined hyperlipidaemia, without influencing plasma fibrinogen, fibrin gel structure or coagulation factor VII.	Gemfibrozil	0-11	coagulation factor II, thrombin	Homo sapiens	20-28
8675576-0	1996	Gemfibrozil treatment of endogenous hypertriglyceridemia: effect on insulin-mediated glucose disposal and plasma insulin concentrations.	Gemfibrozil	0-11	insulin	Homo sapiens	68-75
8865525-4	1996	Gemfibrozil reduced the plasma concentrations of thrombin-antithrombin complex (TAT) and prothrombin fragment F1 + 2 (F1 + 2), both at rest and during mental stress.	Gemfibrozil	0-11	coagulation factor XII	Homo sapiens	49-124
8865525-7	1996	Thus, gemfibrozil reduced thrombin generation in men with combined hyperlipoproteinaemia, without influencing the plasma levels of fibrinogen, VIIa and XIIa, or fibrin gel structure.	Gemfibrozil	6-17	coagulation factor II, thrombin	Homo sapiens	26-34
8865525-8	1996	Attenuation of thrombin generation may contribute to the primary-preventive effects of gemfibrozil on coronary heart disease.	Gemfibrozil	87-98	coagulation factor II, thrombin	Homo sapiens	15-23
8831919-9	1996	Ciprofibrate therapy significantly reduced (-8.33%) and gemfibrozil therapy significantly increased (+6.97%) plasma fibrinogen levels (P &lt; 0.001 compared with baseline in each case).	Gemfibrozil	56-67	fibrinogen beta chain	Homo sapiens	116-126
8675576-0	1996	Gemfibrozil treatment of endogenous hypertriglyceridemia: effect on insulin-mediated glucose disposal and plasma insulin concentrations.	Gemfibrozil	0-11	insulin	Homo sapiens	113-120
8647932-10	1996	When transgenic mice were treated with gemfibrozil (0.5% wt/wt) plasma human apo A-I and HDL-cholesterol levels increased 32 and 73%, respectively, above control levels.	Gemfibrozil	39-50	apolipoprotein A1	Homo sapiens	77-84
8808764-8	1996	These results indicate i) that the levels of Lp[a] are about 2 times higher in type IIa than IIb subjects, and ii) that although gemfibrozil elicits a rather uniform decrease in fasting and post-prandial triglyceride levels in type IIa and IIb patients, the drug causes heterogeneous changes in Lp[a], suggesting that different metabolic mechanisms may be dominant in subjects showing opposing effects.	Gemfibrozil	129-140	lipoprotein(a)	Homo sapiens	45-49
8808764-8	1996	These results indicate i) that the levels of Lp[a] are about 2 times higher in type IIa than IIb subjects, and ii) that although gemfibrozil elicits a rather uniform decrease in fasting and post-prandial triglyceride levels in type IIa and IIb patients, the drug causes heterogeneous changes in Lp[a], suggesting that different metabolic mechanisms may be dominant in subjects showing opposing effects.	Gemfibrozil	129-140	lipoprotein(a)	Homo sapiens	295-299
8808764-2	1996	Previous studies have provided evidence that the levels of Lp[a] and triglyceride are related, suggesting that Lp[a] might be altered by gemfibrozil, a drug well known for its efficacy in reducing plasma triglycerides.	Gemfibrozil	137-148	lipoprotein(a)	Homo sapiens	59-63
8620056-3	1995	This study presents data of an ongoing study to dissect the role of the apolipoprotein E gene locus in the response to low fat/low cholesterol diet combined with gemfibrozil treatment.	Gemfibrozil	162-173	apolipoprotein E	Homo sapiens	72-88
8808764-2	1996	Previous studies have provided evidence that the levels of Lp[a] and triglyceride are related, suggesting that Lp[a] might be altered by gemfibrozil, a drug well known for its efficacy in reducing plasma triglycerides.	Gemfibrozil	137-148	lipoprotein(a)	Homo sapiens	111-115
9072407-6	1995	Gemfibrozil effectively increased high density lipoprotein (HDL) subfraction rich in apoE (apoE-HDL) and significantly decreased very low density lipoprotein (VLDL) in normocholesterolaemic SHRSP.	Gemfibrozil	0-11	apolipoprotein E	Rattus norvegicus	85-89
9072407-6	1995	Gemfibrozil effectively increased high density lipoprotein (HDL) subfraction rich in apoE (apoE-HDL) and significantly decreased very low density lipoprotein (VLDL) in normocholesterolaemic SHRSP.	Gemfibrozil	0-11	apolipoprotein E	Rattus norvegicus	91-99
9072407-10	1995	On the other hand, it significantly increased the contents of apoA-I, A-IV and E in the HDL fraction compared with the control group, suggesting that gemfibrozil effectively increases anti-atherogenic HDL subfractions rich in apoA-I, A-IV or E. In the liver of hypercholesterolaemic SHRSP, gemfibrozil markedly prevented lipid accumulation.	Gemfibrozil	150-161	apolipoprotein A1	Rattus norvegicus	62-68
9072407-10	1995	On the other hand, it significantly increased the contents of apoA-I, A-IV and E in the HDL fraction compared with the control group, suggesting that gemfibrozil effectively increases anti-atherogenic HDL subfractions rich in apoA-I, A-IV or E. In the liver of hypercholesterolaemic SHRSP, gemfibrozil markedly prevented lipid accumulation.	Gemfibrozil	150-161	apolipoprotein A1	Rattus norvegicus	226-232
8620056-0	1995	Apolipoprotein E and complement C3 polymorphism and their role in the response to gemfibrozil and low fat low cholesterol therapy.	Gemfibrozil	82-93	apolipoprotein E	Homo sapiens	0-16
8620056-0	1995	Apolipoprotein E and complement C3 polymorphism and their role in the response to gemfibrozil and low fat low cholesterol therapy.	Gemfibrozil	82-93	complement C3	Homo sapiens	21-34
8615769-3	1996	Increased levels of mdr2 mRNA were observed in the liver of mice treated with different fibrates: ciprofibrate, 660+/-155% (as compared with control group); clofibrate, 611+/-77%; bezafibrate, 410+/-47%; fenofibrate, 310+/-52%; gemfibrozil, 190+/-25% (P &lt;0.05 compared with control group).	Gemfibrozil	228-239	ATP-binding cassette, sub-family B (MDR/TAP), member 4	Mus musculus	20-24
8847480-5	1995	In the current studies, we sought to determine whether the selected fibrates, bezafibrate, clofibrate, fenofibrate, and gemfibrozil, could reduce hepatic apoC-III mRNA and plasma apoC-III levels.	Gemfibrozil	120-131	apolipoprotein C3	Homo sapiens	154-162
8847480-5	1995	In the current studies, we sought to determine whether the selected fibrates, bezafibrate, clofibrate, fenofibrate, and gemfibrozil, could reduce hepatic apoC-III mRNA and plasma apoC-III levels.	Gemfibrozil	120-131	apolipoprotein C3	Homo sapiens	179-187
8847480-9	1995	Gemfibrozil strongly reduced plasma triglyceride levels and had an intermediate but significant effect on apoC-III mRNA and plasma apoC-III levels.	Gemfibrozil	0-11	apolipoprotein C3	Homo sapiens	106-114
8847480-9	1995	Gemfibrozil strongly reduced plasma triglyceride levels and had an intermediate but significant effect on apoC-III mRNA and plasma apoC-III levels.	Gemfibrozil	0-11	apolipoprotein C3	Homo sapiens	131-139
8847480-10	1995	Some of the fibrates, especially gemfibrozil also reduced plasma apoC-II levels, an effect that could contribute to the observed triglyceride-lowering effect.	Gemfibrozil	33-44	apolipoprotein C2	Homo sapiens	65-72
7578896-5	1995	In the gemfibrozil-treated group a significant decrease of total cholesterol and triglycerides and a significant increase of HDL-C and HDL2-C were found.	Gemfibrozil	7-18	junctophilin 3	Homo sapiens	135-139
7595182-6	1995	RESULTS: Gemfibrozil increased the concentration of HDL cholesterol (+11.1%) because of the rise of HDL3 cholesterol (34.5%, P &lt; 0.01).	Gemfibrozil	9-20	HDL3	Homo sapiens	100-104
7595182-9	1995	Gemfibrozil increased LPL and HL activities by 18.2% (P &lt; 0.05) and by 19.6%, respectively.	Gemfibrozil	0-11	lipoprotein lipase	Homo sapiens	22-25
7595182-9	1995	Gemfibrozil increased LPL and HL activities by 18.2% (P &lt; 0.05) and by 19.6%, respectively.	Gemfibrozil	0-11	lipase C, hepatic type	Homo sapiens	30-32
7595182-10	1995	Plasma CETP activity was also increased during gemfibrozil treatment (+15.8%, P &lt; 0.05).	Gemfibrozil	47-58	cholesteryl ester transfer protein	Homo sapiens	7-11
7595182-11	1995	CONCLUSION: The gemfibrozil-induced elevation of HDL3 and apoA-II may reflect the combined action of LPL, HL and CETP on plasma HDL metabolism.	Gemfibrozil	16-27	HDL3	Homo sapiens	49-53
7595182-11	1995	CONCLUSION: The gemfibrozil-induced elevation of HDL3 and apoA-II may reflect the combined action of LPL, HL and CETP on plasma HDL metabolism.	Gemfibrozil	16-27	apolipoprotein A2	Homo sapiens	58-65
7595182-11	1995	CONCLUSION: The gemfibrozil-induced elevation of HDL3 and apoA-II may reflect the combined action of LPL, HL and CETP on plasma HDL metabolism.	Gemfibrozil	16-27	lipoprotein lipase	Homo sapiens	101-104
7595182-11	1995	CONCLUSION: The gemfibrozil-induced elevation of HDL3 and apoA-II may reflect the combined action of LPL, HL and CETP on plasma HDL metabolism.	Gemfibrozil	16-27	lipase C, hepatic type	Homo sapiens	106-108
7595182-11	1995	CONCLUSION: The gemfibrozil-induced elevation of HDL3 and apoA-II may reflect the combined action of LPL, HL and CETP on plasma HDL metabolism.	Gemfibrozil	16-27	cholesteryl ester transfer protein	Homo sapiens	113-117
7578896-7	1995	After 12 weeks of treatment in the gemfibrozil group the release of t-PA:Ag in response to venous occlusion was significantly higher and plasma PAI activity was significantly lower than in placebo group.	Gemfibrozil	35-46	plasminogen activator, tissue type	Homo sapiens	68-72
7578896-7	1995	After 12 weeks of treatment in the gemfibrozil group the release of t-PA:Ag in response to venous occlusion was significantly higher and plasma PAI activity was significantly lower than in placebo group.	Gemfibrozil	35-46	serpin family B member 2	Homo sapiens	144-147
8595642-7	1995	Gemfibrozil was significantly more effective than lovastatin in raising total HDL and HDL3 levels and in lowering the IDL plus VLDL:HDL ratio.	Gemfibrozil	0-11	HDL3	Homo sapiens	86-90
7755647-0	1995	Insulin action and glucose metabolism are improved by gemfibrozil treatment in hypertriglyceridemic patients.	Gemfibrozil	54-65	insulin	Homo sapiens	0-7
7641354-3	1995	We and others have observed attenuation of PAI-1 expression by gemfibrozil both in vivo and in vitro.	Gemfibrozil	63-74	serpin family E member 1	Homo sapiens	43-48
7666007-3	1995	Lp[a] reduction was directly related to blood gemfibrozil concentration (range 36-428 microM, r = 0.969) and occurred without concomitant changes in apolipoprotein B.	Gemfibrozil	46-57	apolipoprotein(a)	Macaca fascicularis	0-4
7666007-7	1995	However, both Lp[a] and apo[a] mRNA in primary cynomolgus monkey hepatocytes were coordinately lowered in a dose-dependent fashion by gemfibrozil.	Gemfibrozil	134-145	apolipoprotein(a)	Macaca fascicularis	14-18
7666007-8	1995	Thus, Lp[a] can be regulated by gemfibrozil at the level of apo[a] mRNA expression.	Gemfibrozil	32-43	apolipoprotein(a)	Macaca fascicularis	6-10
7788039-15	1995	This beneficial effect of gemfibrozil, which was expressed by the third month and was evident for some time afterwards, was attributed to a significant reduction of triglyceride and fibrinogen levels, an increase of HDL cholesterol concentrations and a moderate decrease of total cholesterol and LDL cholesterol levels.	Gemfibrozil	26-37	fibrinogen beta chain	Homo sapiens	182-192
8595642-5	1995	Gemfibrozil significantly decreased triglyceride, very-low-density lipoprotein (VLDL), and intermediate-density lipoprotein (IDL) levels, the total cholesterol:HDL ratio, and the IDL plus VLDL;HDL ratio, and significantly increased levels of HDL, HDL2, and HDL3.	Gemfibrozil	0-11	junctophilin 3	Homo sapiens	247-251
8595642-5	1995	Gemfibrozil significantly decreased triglyceride, very-low-density lipoprotein (VLDL), and intermediate-density lipoprotein (IDL) levels, the total cholesterol:HDL ratio, and the IDL plus VLDL;HDL ratio, and significantly increased levels of HDL, HDL2, and HDL3.	Gemfibrozil	0-11	HDL3	Homo sapiens	257-261
7752906-7	1995	The rate of insulin-induced whole-body glucose disposal increased similarly both before (basal 10.8 +/- 1.8, low-dose insulin 10.5 +/- 2.1, and high-dose insulin 20.9 +/- 11.9 mumol.kg-1.min-1) and after (11.1 +/- 1.7, 10.7 +/- 1.2, and 18.6 +/- 7.9, respectively) gemfibrozil treatment.	Gemfibrozil	265-276	insulin	Homo sapiens	12-19
7662602-0	1995	Gemfibrozil and Mediterranean diet for patients with high plasma levels of lipoprotein [Lp(a)] and cholesterol--pilot study.	Gemfibrozil	0-11	lipoprotein(a)	Homo sapiens	88-93
7662602-3	1995	We have evaluated a combination of medical treatment with Gemfibrozil (600 mg bid) and a Mediterranean diet for 2 months in 15 patients with both hypercholesterolemia (&gt; 240 mg/dl) and high levels of Lp(a) (&gt; 30 mg/dl).	Gemfibrozil	58-69	BH3 interacting domain death agonist	Homo sapiens	78-81
7662602-3	1995	We have evaluated a combination of medical treatment with Gemfibrozil (600 mg bid) and a Mediterranean diet for 2 months in 15 patients with both hypercholesterolemia (&gt; 240 mg/dl) and high levels of Lp(a) (&gt; 30 mg/dl).	Gemfibrozil	58-69	lipoprotein(a)	Homo sapiens	203-208
7755644-9	1995	Furthermore, gemfibrozil increased HDL cholesterol (P &lt; 0.05) and normalised the elevated HDL2 and HDL3 TG content.	Gemfibrozil	13-24	junctophilin 3	Homo sapiens	93-97
7755644-9	1995	Furthermore, gemfibrozil increased HDL cholesterol (P &lt; 0.05) and normalised the elevated HDL2 and HDL3 TG content.	Gemfibrozil	13-24	HDL3	Homo sapiens	102-106
7749807-4	1995	Moreover, the urinary excretion of 11-dehydro-thromboxane-B2 was 54% higher during treatment with gemfibrozil (P &lt; .001), whereas the excretion of beta-thromboglobulin in urine was unaltered.	Gemfibrozil	98-109	pro-platelet basic protein	Homo sapiens	150-170
7869918-0	1995	A comparison between the effects of gemfibrozil and simvastatin on insulin sensitivity in patients with non-insulin-dependent diabetes mellitus and hyperlipoproteinemia.	Gemfibrozil	36-47	insulin	Homo sapiens	67-74
7869918-2	1995	After gemfibrozil treatment, the insulin concentration was increased during the major part of the intravenous glucose tolerance test (IVGTT) and during the hyperinsulinemic euglycemic clamp.	Gemfibrozil	6-17	insulin	Homo sapiens	33-40
7869918-4	1995	Insulin sensitivity decreased by 27% and 28% during gemfibrozil and simvastatin treatment, respectively.	Gemfibrozil	52-63	insulin	Homo sapiens	0-7
7869918-8	1995	After gemfibrozil treatment, lipoprotein(a) [Lp(a)] was decreased by 24%, and the plasma free fatty acid (FFA) concentration was increased by 20% and skeletal muscle lipoprotein lipase activity (LPLA) by 37%.	Gemfibrozil	6-17	lipoprotein(a)	Homo sapiens	29-43
8071873-8	1994	Thus, in this rodent model of hypertension and dyslipidemia, gemfibrozil lowers plasma TG levels by 50% with no effect on TG secretion; the hypotriglyceridemic effect is due mainly to an increase in TG removal rate associated with a post-transcriptional increase in LPL activity in skeletal muscle.	Gemfibrozil	61-72	lipoprotein lipase	Rattus norvegicus	266-269
7826893-2	1994	We compare here the effects of gemfibrozil and placebo on the serum levels of dehydroepiandrosterone (DHEA), its sulfate (DHEAS), their metabolite androstanediol glucuronide (3 alpha-AdiolG), androstenedione, cortisol, testosterone, and sex-hormone binding globulin (SHBG) in non-smokers.	Gemfibrozil	31-42	sex hormone binding globulin	Homo sapiens	237-265
7826893-2	1994	We compare here the effects of gemfibrozil and placebo on the serum levels of dehydroepiandrosterone (DHEA), its sulfate (DHEAS), their metabolite androstanediol glucuronide (3 alpha-AdiolG), androstenedione, cortisol, testosterone, and sex-hormone binding globulin (SHBG) in non-smokers.	Gemfibrozil	31-42	sex hormone binding globulin	Homo sapiens	267-271
7826893-5	1994	The mean SHBG levels decreased from 46.4 to 41.7 nmol/l; P = 0.03 with gemfibrozil treatment.	Gemfibrozil	71-82	sex hormone binding globulin	Homo sapiens	9-13
8077896-0	1994	An interaction between Gemfibrozil and alpha 1-antitrypsin.	Gemfibrozil	23-34	serpin family A member 1	Homo sapiens	39-58
8077896-3	1994	Gemfibrozil treatment in non-PiZ patients also resulted in a reduction of alpha 1-AT activity which could be reproduced in vitro.	Gemfibrozil	0-11	serpin family A member 1	Homo sapiens	74-84
7917468-5	1994	When HDL of the subjects studied were recombined with the CETP fraction and VLDL/LDL isolated from the control plasma pool, the rate of EC transfer was decreased by 43% after gemfibrozil administration.	Gemfibrozil	175-186	cholesteryl ester transfer protein	Homo sapiens	58-62
8017467-6	1994	Gemfibrozil reduced LDL-C by 15.8%, TC by 13.4%, VLDL-C by 32.2%, LDL-C:HDL-C by 24.8%, and TG by 34.2%, and increased HDL-C by 13.9% (all changes were statistically significant, p &lt; 0.001) compared with baseline.	Gemfibrozil	0-11	component of oligomeric golgi complex 2	Homo sapiens	20-25
8017467-6	1994	Gemfibrozil reduced LDL-C by 15.8%, TC by 13.4%, VLDL-C by 32.2%, LDL-C:HDL-C by 24.8%, and TG by 34.2%, and increased HDL-C by 13.9% (all changes were statistically significant, p &lt; 0.001) compared with baseline.	Gemfibrozil	0-11	component of oligomeric golgi complex 2	Homo sapiens	50-55
8017467-7	1994	Gemfibrozil produced significantly greater changes in VLDL-C (p &lt; 0.01), HDL-C (p &lt; 0.001), and TG (p &lt; 0.001), but not in LDL-C: HDL-C, compared with fluvastatin.	Gemfibrozil	0-11	component of oligomeric golgi complex 2	Homo sapiens	55-60
8017467-9	1994	At the end of the study, 43.8% of fluvastatin patients and 45% of gemfibrozil patients achieved a reduction of &gt; 20% in LDL-C levels.	Gemfibrozil	66-77	component of oligomeric golgi complex 2	Homo sapiens	123-128
8017467-10	1994	Normalization of LDL-C levels was achieved (according to European Atherosclerosis Society guidelines) by 13.4% of fluvastatin- and 14.6% of gemfibrozil-treated patients.	Gemfibrozil	140-151	component of oligomeric golgi complex 2	Homo sapiens	17-22
8304363-11	1994	CONCLUSION: Gemfibrozil treatment in patients with familial dysbetalipoproteinemia resulted in a marked reduction of the concentrations of large VLDL, small VLDL, and IDL, and an increase in the levels of HDL, apo A-I, and apo A-II.	Gemfibrozil	12-23	apolipoprotein A2	Homo sapiens	223-231
8222487-5	1993	These differences may have a physiologic background because the main effect of gemfibrozil is in the stable HDL3 subfraction, rather than in the variable HDL2.	Gemfibrozil	79-90	HDL3	Homo sapiens	108-112
8231846-0	1993	Effect of gemfibrozil on adipose tissue and muscle lipoprotein lipase.	Gemfibrozil	10-21	lipoprotein lipase	Homo sapiens	51-69
7509512-0	1993	Inhibition of endothelial cell expression of plasminogen activator inhibitor type-1 by gemfibrozil.	Gemfibrozil	87-98	serpin family E member 1	Homo sapiens	45-83
7509512-2	1993	In pilot studies designed to identify pharmacologic approaches capable of diminishing such increases, we found that gemfibrozil attenuated the stimulation of synthesis of PAI-1 in a human, immortal, hepatoma cell line (Hep G2) induced by platelets.	Gemfibrozil	116-127	serpin family E member 1	Homo sapiens	171-176
7509512-5	1993	Gemfibrozil, 100 microM, suppressed basal PAI-1 production by 15% and attenuated the augmentation of synthesis of PAI-1 induced by lysates from platelets (4 x 10(7)/ml) by 36% over 24 h without inhibiting overall protein synthesis.	Gemfibrozil	0-11	serpin family E member 1	Homo sapiens	42-47
7509512-5	1993	Gemfibrozil, 100 microM, suppressed basal PAI-1 production by 15% and attenuated the augmentation of synthesis of PAI-1 induced by lysates from platelets (4 x 10(7)/ml) by 36% over 24 h without inhibiting overall protein synthesis.	Gemfibrozil	0-11	serpin family E member 1	Homo sapiens	114-119
8236126-4	1993	After 1 month of therapy, plasma fibrinogen significantly decreased by 9% and 15% in fenofibrate and bezafibrate groups respectively and increased by 19% in gemfibrozil treated patients.	Gemfibrozil	157-168	fibrinogen beta chain	Homo sapiens	33-43
8458531-2	1993	In the present study we examined whether gemfibrozil, by lowering triglyceride levels, improves the glucoregulatory and antilipolytic action of insulin in Type 2 (non-insulin-dependent) diabetes mellitus.	Gemfibrozil	41-52	insulin	Homo sapiens	144-151
8509712-5	1993	However, immunoblot analysis of tissue homogenates revealed that SCP2 protein is decreased by 75% in the livers of gemfibrozil-treated animals and increased by 5-fold at 48 h in regenerating liver and in the remaining kidney after unilateral nephrectomy.	Gemfibrozil	115-126	sterol carrier protein 2	Rattus norvegicus	65-69
8509712-6	1993	Taken together these results suggest that SCP2 gene expression is developmentally regulated and modulated translationally or post-translationally in the adult rat by gemfibrozil and compensatory cell growth.	Gemfibrozil	166-177	sterol carrier protein 2	Rattus norvegicus	42-46
8318063-6	1993	Postheparin lipoprotein lipase (LPL) and hepatic lipase (HL) activities were increased by gemfibrozil therapy while only a mild elevation in LPL activity alone was seen on lovastatin therapy.	Gemfibrozil	90-101	lipoprotein lipase	Homo sapiens	12-30
8318063-6	1993	Postheparin lipoprotein lipase (LPL) and hepatic lipase (HL) activities were increased by gemfibrozil therapy while only a mild elevation in LPL activity alone was seen on lovastatin therapy.	Gemfibrozil	90-101	lipoprotein lipase	Homo sapiens	32-35
8318063-6	1993	Postheparin lipoprotein lipase (LPL) and hepatic lipase (HL) activities were increased by gemfibrozil therapy while only a mild elevation in LPL activity alone was seen on lovastatin therapy.	Gemfibrozil	90-101	lipase C, hepatic type	Homo sapiens	41-55
8257455-6	1993	Gemfibrozil increased the concentration of HDL cholesterol (P &lt; 0.01), which was due to the rise of HDL3 cholesterol (+16%), while in the placebo group these values remained unchanged.	Gemfibrozil	0-11	HDL3	Homo sapiens	103-107
8257455-7	1993	Gemfibrozil increased the concentrations of apo A-I(+12.6%, NS), apo A-II (+28.2%, P &lt; 0.01) and Lp A-I:A-II particles (+21.6%, P &lt; 0.06) but there were no changes in the placebo group.	Gemfibrozil	0-11	apolipoprotein A1	Homo sapiens	44-51
8257455-7	1993	Gemfibrozil increased the concentrations of apo A-I(+12.6%, NS), apo A-II (+28.2%, P &lt; 0.01) and Lp A-I:A-II particles (+21.6%, P &lt; 0.06) but there were no changes in the placebo group.	Gemfibrozil	0-11	apolipoprotein A2	Homo sapiens	65-73
8257455-7	1993	Gemfibrozil increased the concentrations of apo A-I(+12.6%, NS), apo A-II (+28.2%, P &lt; 0.01) and Lp A-I:A-II particles (+21.6%, P &lt; 0.06) but there were no changes in the placebo group.	Gemfibrozil	0-11	lipoprotein(a)	Homo sapiens	100-104
8257455-11	1993	Gemfibrozil increased LPL and HL activities by 14.7% (P &lt; 0.05) and by 18.8% (P &lt; 0.01), respectively, while in the placebo group LPL and HL activities remained unchanged.	Gemfibrozil	0-11	lipoprotein lipase	Homo sapiens	22-25
8257455-11	1993	Gemfibrozil increased LPL and HL activities by 14.7% (P &lt; 0.05) and by 18.8% (P &lt; 0.01), respectively, while in the placebo group LPL and HL activities remained unchanged.	Gemfibrozil	0-11	lipase C, hepatic type	Homo sapiens	30-32
8257455-12	1993	Plasma CETP activity was also increased during gemfibrozil treatment while in the placebo group it remained unchanged.	Gemfibrozil	47-58	cholesteryl ester transfer protein	Homo sapiens	7-11
8257455-14	1993	The gemfibrozil-induced elevation of HDL3 and dense HDL subpopulations may reflect the concerted action of LPL, HL and CETP on plasma HDL metabolism.	Gemfibrozil	4-15	HDL3	Homo sapiens	37-41
8257455-14	1993	The gemfibrozil-induced elevation of HDL3 and dense HDL subpopulations may reflect the concerted action of LPL, HL and CETP on plasma HDL metabolism.	Gemfibrozil	4-15	lipoprotein lipase	Homo sapiens	107-110
8257455-14	1993	The gemfibrozil-induced elevation of HDL3 and dense HDL subpopulations may reflect the concerted action of LPL, HL and CETP on plasma HDL metabolism.	Gemfibrozil	4-15	lipase C, hepatic type	Homo sapiens	112-114
8257455-14	1993	The gemfibrozil-induced elevation of HDL3 and dense HDL subpopulations may reflect the concerted action of LPL, HL and CETP on plasma HDL metabolism.	Gemfibrozil	4-15	cholesteryl ester transfer protein	Homo sapiens	119-123
8458531-2	1993	In the present study we examined whether gemfibrozil, by lowering triglyceride levels, improves the glucoregulatory and antilipolytic action of insulin in Type 2 (non-insulin-dependent) diabetes mellitus.	Gemfibrozil	41-52	insulin	Homo sapiens	167-174
8458531-9	1993	Rate of whole body glucose disposal during a low-dose insulin infusion (serum insulin -90 pmol/l) (pre- vs post-gemfibrozil 11.9 +/- 1.1 vs 11.1 +/- 0.7, pre- vs post-placebo 9.9 +/- 1.1 vs 10.8 +/- 0.8 mumol.kg-1.min-1, NS for both) and a high-dose insulin infusion (serum insulin approximately 500 pmol/l) (16.2 +/- 1.7 vs 17.7 +/- 2.7, 17.1 +/- 4.2 vs 17.4 +/- 2.9 mumol.kg-1 x min-1, respectively, NS for both) remained unchanged.	Gemfibrozil	112-123	insulin	Homo sapiens	54-61
1397665-2	1992	After oral treatment with 450 mg gemfibrozil twice daily for 28 days, triglyceride concentrations were reduced in serum, chylomicrons, VLDL and low-density lipoprotein, and total cholesterol concentrations were reduced in serum, chylomicrons and VLDL, and increased in HDL2 plus HDL3.	Gemfibrozil	33-44	HDL3	Homo sapiens	279-283
8418887-4	1993	A phosphocholine cytidylyltransferase-mediated rise in cellular CDP choline content may explain the gemfibrozil-dependent rise in phosphatidylcholine biosynthesis since homogenates of monolayers incubated with CDP choline preferentially incorporate labeled diacylglycerol into phosphatidylcholine rather than triacylglycerol.	Gemfibrozil	100-111	cut-like homeobox 1	Rattus norvegicus	64-67
8418887-4	1993	A phosphocholine cytidylyltransferase-mediated rise in cellular CDP choline content may explain the gemfibrozil-dependent rise in phosphatidylcholine biosynthesis since homogenates of monolayers incubated with CDP choline preferentially incorporate labeled diacylglycerol into phosphatidylcholine rather than triacylglycerol.	Gemfibrozil	100-111	cut-like homeobox 1	Rattus norvegicus	210-213
1613316-3	1992	Gemfibrozil and lovastatin caused primarily similar alterations in HDL components in HDL2 and HDL3 subfractions.	Gemfibrozil	0-11	junctophilin 3	Homo sapiens	85-89
1613316-3	1992	Gemfibrozil and lovastatin caused primarily similar alterations in HDL components in HDL2 and HDL3 subfractions.	Gemfibrozil	0-11	HDL3	Homo sapiens	94-98
1613316-6	1992	Gemfibrozil increased the cholesterol concentrations of HDL2 and HDL3 (p less than 0.05 for both), and lovastatin caused significant increases in HDL2 (p less than 0.05) and HDL3 phospholipids (p less than 0.01).	Gemfibrozil	0-11	junctophilin 3	Homo sapiens	56-60
1613316-6	1992	Gemfibrozil increased the cholesterol concentrations of HDL2 and HDL3 (p less than 0.05 for both), and lovastatin caused significant increases in HDL2 (p less than 0.05) and HDL3 phospholipids (p less than 0.01).	Gemfibrozil	0-11	HDL3	Homo sapiens	65-69
1397665-4	1992	It is concluded that gemfibrozil is effective in lowering triglycerides and cholesterol, particularly in triglyceride-rich particles, and raising the cholesterol content of HDL2 plus HDL3.	Gemfibrozil	21-32	HDL3	Homo sapiens	183-187
1534991-4	1992	These new observations suggest that gemfibrozil treatment increases the production and turnover of DHEA and DHEAS and may in addition stimulate the 5 alpha-reduction of androgens.	Gemfibrozil	36-47	sulfotransferase family 2A member 1	Homo sapiens	108-113
1519208-4	1992	Plasma prothrombin fragment F1 + 2 concentration, a marker of the in vivo rate of generation of thrombin, was 25 (12 to 37)% lower on average while on gemfibrozil than during the placebo phase.	Gemfibrozil	151-162	coagulation factor II, thrombin	Homo sapiens	10-18
1572044-6	1992	METHODS AND RESULTS: To determine whether pharmacological concentrations of gemfibrozil directly affect PAI-1 synthesis, we characterized its effects on a human hepatoma cell line (Hep G2) in vitro.	Gemfibrozil	76-87	serpin family E member 1	Homo sapiens	104-109
1572044-7	1992	Gemfibrozil decreased basal PAI-1 secretion by 43% and attenuated the augmentation of PAI-1 synthesis over 24 hours induced by EGF and TGF-beta by 37% and 39% without altering overall protein synthesis.	Gemfibrozil	0-11	serpin family E member 1	Homo sapiens	28-33
1572044-7	1992	Gemfibrozil decreased basal PAI-1 secretion by 43% and attenuated the augmentation of PAI-1 synthesis over 24 hours induced by EGF and TGF-beta by 37% and 39% without altering overall protein synthesis.	Gemfibrozil	0-11	serpin family E member 1	Homo sapiens	86-91
1572044-7	1992	Gemfibrozil decreased basal PAI-1 secretion by 43% and attenuated the augmentation of PAI-1 synthesis over 24 hours induced by EGF and TGF-beta by 37% and 39% without altering overall protein synthesis.	Gemfibrozil	0-11	epidermal growth factor	Homo sapiens	127-130
1572044-10	1992	CONCLUSIONS: Beneficial effects of gemfibrozil in reducing coronary events in hypertriglyceridemic patients may depend, in part, on potentiation of fibrinolysis by direct diminution of synthesis of endogenous PAI-1.	Gemfibrozil	35-46	serpin family E member 1	Homo sapiens	209-214
1534991-2	1992	Simultaneously we studied the effects of gemfibrozil treatment on the serum levels of dehydroepiandrosterone (DHEA), its sulfate (DHEAS), and their metabolite androstanediol glucuronide (3 alpha AdiolG) with those of placebo.	Gemfibrozil	41-52	sulfotransferase family 2A member 1	Homo sapiens	130-135
1619364-4	1992	In contrast, hepatic LCAT mRNA levels decreased to 67%, 64%, and 46% of the control levels after treatment with the fibric acid derivatives clofibrate, gemfibrozil, and fenofibrate, respectively.	Gemfibrozil	152-163	lecithin cholesterol acyltransferase	Rattus norvegicus	21-25
1547188-9	1992	Both clofibrate and gemfibrozil had effects comparable to those of fenofibrate on liver and intestinal apolipoprotein mRNA levels except for liver apo A-II mRNA, which decreased only marginally.	Gemfibrozil	20-31	apolipoprotein E	Rattus norvegicus	103-117
1547188-10	1992	Compared with fenofibrate, clofibrate caused similar changes in plasma cholesterol, apo A-I, apo A-IV, and apo E concentrations, whereas gemfibrozil increased plasma cholesterol and apo E without changing apo A-I and apo A-IV concentrations.	Gemfibrozil	137-148	apolipoprotein E	Rattus norvegicus	182-187
1811554-1	1991	Exposure of HepG2 and Hep3B cells to gemfibrozil (40 micrograms/ml), a hypolipidemic drug, resulted in a 2-fold induction of apo AI mRNA and, a one-third reduction in apo B mRNA but had no significant effect on apo E mRNA levels.	Gemfibrozil	37-48	apolipoprotein A1	Homo sapiens	125-131
1471924-2	1992	They were treated with gemfibrozil (600 mg BID) for 12 weeks.	Gemfibrozil	23-34	BH3 interacting domain death agonist	Homo sapiens	43-46
1789808-9	1991	It is suggested that the HMG-CoA reductase inhibition observed in mononuclear cells during gemfibrozil treatment is due to changes in LDL structure affecting LDL receptor binding rather than direct effects of the drug on cellular cholesterol metabolism.	Gemfibrozil	91-102	low density lipoprotein receptor	Homo sapiens	158-170
1811554-2	1991	The hypothesis that the mechanism of action of gemfibrozil involved the cytochrome P-450 system was tested by using ketoconazole, a P-450 inhibitor, which blocks the formation of endogenous polar sterols.	Gemfibrozil	47-58	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	72-88
1811554-8	1991	The induction of apo AI mRNA by gemfibrozil was not apparent when the cells were simultaneously treated with ketoconazole.	Gemfibrozil	32-43	apolipoprotein A1	Homo sapiens	17-23
1907081-10	1991	Gemfibrozil significantly increased plasma HDL cholesterol, apolipoprotein (apo) AI, and apo AII by 36%, 29%, and 38% from baseline, respectively.	Gemfibrozil	0-11	apolipoprotein A1	Homo sapiens	60-83
1678324-0	1991	DNA polymorphisms of apolipoprotein B and AI/CIII genes and response to gemfibrozil treatment.	Gemfibrozil	72-83	apolipoprotein B	Homo sapiens	21-37
1678324-6	1991	These data indicate that common polymorphisms of the apolipoprotein B and apolipoprotein AI/CIII gene loci influence serum lipid levels by mechanisms that are amenable to an intervention with gemfibrozil.	Gemfibrozil	192-203	apolipoprotein B	Homo sapiens	53-91
1793455-0	1991	Effects of gemfibrozil on serum apolipoprotein E distribution in hypercholesterolemic patients.	Gemfibrozil	11-22	apolipoprotein E	Homo sapiens	32-48
1992957-5	1991	Filicol and gemfibrozil caused similar decrements of total cholesterol (14% for both), low-density lipoprotein cholesterol (20% and 18%, respectively), and apolipoprotein B (16% and 21%, respectively).	Gemfibrozil	12-23	apolipoprotein B	Homo sapiens	156-172
1992957-7	1991	Gemfibrozil, but not filicol, significantly increased plasma high-density lipoprotein cholesterol (16%) and apolipoprotein A-I (17%) levels and reduced triglyceride levels (35%).	Gemfibrozil	0-11	apolipoprotein A1	Homo sapiens	108-126
1907081-12	1991	Gemfibrozil increased synthetic rates of apo AI and apo AII by 27% and 34%, respectively, without changing the FCR.	Gemfibrozil	0-11	apolipoprotein A1	Homo sapiens	41-47
2073911-6	1990	Ultracentrifuge analysis in a subsample of the cohort revealed that gemfibrozil raised the level of HDL3-cholesterol but had little effect on HDL2-cholesterol.	Gemfibrozil	68-79	HDL3	Homo sapiens	100-104
2025787-5	1991	Gemfibrozil lowered plasma triglycerides, VLDL cholesterol and apolipoprotein B (apoB), increased HDL cholesterol and apoAI levels in both groups, and induced a very substantial reduction in LDL cholesterol in type IIa patients only.	Gemfibrozil	0-11	apolipoprotein B	Homo sapiens	63-79
2025787-5	1991	Gemfibrozil lowered plasma triglycerides, VLDL cholesterol and apolipoprotein B (apoB), increased HDL cholesterol and apoAI levels in both groups, and induced a very substantial reduction in LDL cholesterol in type IIa patients only.	Gemfibrozil	0-11	apolipoprotein B	Homo sapiens	81-85
1898694-7	1991	Apolipoprotein B decrease was 21% with pravastatin and 13% with gemfibrozil.	Gemfibrozil	64-75	apolipoprotein B	Homo sapiens	0-16
1997786-2	1991	The most noteworthy finding was the 50% decrease in the cytoplasmic desmin fraction in cells treated with gemfibrozil in comparison to control cultures, and the 19% increase in the cytoskeletal fraction in cultures treated with gemfibrozil and with bezafibrate.	Gemfibrozil	106-117	desmin	Gallus gallus	68-74
1997786-3	1991	Vimentin accumulation by cells treated with bezafibrate was similar to that in control cultures, however the cytoskeletal vimentin fraction rose by 26% after treatment with gemfibrozil, and fell 13% after treatment with fenofibrate.	Gemfibrozil	173-184	vimentin	Gallus gallus	122-130
2203245-7	1990	Gemfibrozil additionally stimulates apolipoprotein AI synthesis.	Gemfibrozil	0-11	apolipoprotein A1	Homo sapiens	36-53
2407250-6	1990	Gemfibrozil increased the level of HDL-cholesterol with the main effect on HDL3-subfraction.	Gemfibrozil	0-11	HDL3	Homo sapiens	75-79
2256470-9	1990	The fibric acid derivative gemfibrozil inhibits adipose lipolysis and enhances lipoprotein lipase activity thus decreasing LDL synthesis and increasing its removal.	Gemfibrozil	27-38	lipoprotein lipase	Homo sapiens	79-97
2076620-6	1990	Furthermore, plasma fibrinogen levels increased by a mean of 17.6%, a potentially adverse effect of gemfibrozil that has not been previously reported.	Gemfibrozil	100-111	fibrinogen beta chain	Homo sapiens	20-30
34365128-2	2021	A series of new gemfibrozil derivatives were synthesized and evaluated for sGC activation.	Gemfibrozil	16-27	serglycin	Mus musculus	75-78
2343430-0	1990	[Post-heparin LPL and HL activities after two months" treatment with gemfibrozil.	Gemfibrozil	69-80	lipoprotein lipase	Homo sapiens	14-17
2343430-3	1990	Though lipidic parameters were not modified after treatment, gemfibrozil increased the LPL and HL plasmatic activities measured 10 minutes after heparin injection.	Gemfibrozil	61-72	lipoprotein lipase	Homo sapiens	87-90
23008696-2	2012	The PPARalpha agonists GW7647, WY14643, and gemfibrozil acutely relaxed aortas held under isometric tension and dilated pressurized MCAs with the following order of potency: GW7647&gt;&gt;WY14643&gt;gemfibrozil.	Gemfibrozil	44-55	peroxisome proliferator activated receptor alpha	Mus musculus	4-13
23008696-2	2012	The PPARalpha agonists GW7647, WY14643, and gemfibrozil acutely relaxed aortas held under isometric tension and dilated pressurized MCAs with the following order of potency: GW7647&gt;&gt;WY14643&gt;gemfibrozil.	Gemfibrozil	199-210	peroxisome proliferator activated receptor alpha	Mus musculus	4-13
34365128-3	2021	The structure-activity relationship study identified the positions in gemfibrozil"s scaffold that are detrimental for sGC activation and those that are amendable for optimizing modifications.	Gemfibrozil	70-81	serglycin	Mus musculus	118-121
34365128-4	2021	Compared with gemfibrozil, compounds 7c and 15b were more potent activators of cGMP-forming activity of purified sGC and exhibited enhanced relaxation of preconstricted mouse thoracic aorta rings.	Gemfibrozil	14-25	serglycin	Mus musculus	113-116
34365128-5	2021	These studies established the overall framework needed for futher improvement of sGC activators based on gemfibrozil scaffold.	Gemfibrozil	105-116	serglycin	Mus musculus	81-84
34499887-5	2021	Gemfibrozil, a pharmacological agonist of PPARalpha, increased PPARalpha levels and activity in podocytes.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	42-51
34499887-5	2021	Gemfibrozil, a pharmacological agonist of PPARalpha, increased PPARalpha levels and activity in podocytes.	Gemfibrozil	0-11	peroxisome proliferator activated receptor alpha	Mus musculus	63-72
34499887-11	2021	This study identified a novel mechanism of the PPARalpha agonist gemfibrozil that exerts its protective effects by inhibiting PAN-induced apoptosis and cytoskeleton rearrangements through inhibition of ANGPTL3 expression.	Gemfibrozil	65-76	peroxisome proliferator activated receptor alpha	Mus musculus	47-56
34499887-11	2021	This study identified a novel mechanism of the PPARalpha agonist gemfibrozil that exerts its protective effects by inhibiting PAN-induced apoptosis and cytoskeleton rearrangements through inhibition of ANGPTL3 expression.	Gemfibrozil	65-76	angiopoietin-like 3	Mus musculus	202-209
35163693-0	2022	Structural Analysis of Human Serum Albumin in Complex with the Fibrate Drug Gemfibrozil.	Gemfibrozil	76-87	albumin	Homo sapiens	29-42
35163693-4	2022	Most of them appear to be related to the ability of GEM to bind with high affinity human serum albumin (HSA), the major drug-carrier protein in blood plasma.	Gemfibrozil	52-55	albumin	Homo sapiens	89-102
34303168-7	2021	In the presence of Cl-, we found that Cl2 - and in particular ClO  were responsible for the enhanced degradation with increasing Cl- concentrations due to the considerable ClO  reactivity of gemfibrozil (1.93 x 109 M-1 s-1) and naproxen (9.24 x 109 M-1 s-1) and the rapid transformation of Cl2 - to ClO .	Gemfibrozil	191-202	endogenous retrovirus group W member 5	Homo sapiens	38-41