PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
10901697-0	2000	Mibefradil is a P-glycoprotein substrate and a potent inhibitor of both P-glycoprotein and CYP3A in vitro.	Mibefradil	0-10	ATP binding cassette subfamily B member 1	Homo sapiens	16-30
10901697-0	2000	Mibefradil is a P-glycoprotein substrate and a potent inhibitor of both P-glycoprotein and CYP3A in vitro.	Mibefradil	0-10	ATP binding cassette subfamily B member 1	Homo sapiens	72-86
10901697-0	2000	Mibefradil is a P-glycoprotein substrate and a potent inhibitor of both P-glycoprotein and CYP3A in vitro.	Mibefradil	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	91-96
10901697-2	2000	Mibefradil is known to inhibit various cytochrome P450 enzymes involved in drug metabolism, particularly CYP3A.	Mibefradil	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	105-110
10901697-3	2000	However, the extent and the severity of the observed drug interactions in humans suggest that inhibition of additional systems important to drug disposition, such as the drug transporter P-glycoprotein (P-gp), may also have contributed to the severity of the mibefradil interactions.	Mibefradil	259-269	ATP binding cassette subfamily B member 1	Homo sapiens	187-201
10901697-3	2000	However, the extent and the severity of the observed drug interactions in humans suggest that inhibition of additional systems important to drug disposition, such as the drug transporter P-glycoprotein (P-gp), may also have contributed to the severity of the mibefradil interactions.	Mibefradil	259-269	ATP binding cassette subfamily B member 1	Homo sapiens	203-207
10901697-6	2000	Using a human intestinal cancer-derived cell line Caco-2, which constitutively expresses P-gp, mibefradil was shown to be a potent inhibitor of P-gp-mediated digoxin transport, with an IC50 of 1.6 microM.	Mibefradil	95-105	ATP binding cassette subfamily B member 1	Homo sapiens	89-93
10901697-6	2000	Using a human intestinal cancer-derived cell line Caco-2, which constitutively expresses P-gp, mibefradil was shown to be a potent inhibitor of P-gp-mediated digoxin transport, with an IC50 of 1.6 microM.	Mibefradil	95-105	ATP binding cassette subfamily B member 1	Homo sapiens	144-148
10901697-7	2000	Additionally, the effect of mibefradil on CYP3A was assessed using human liver microsomes.	Mibefradil	28-38	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-47
10901697-8	2000	Mibefradil inhibited CYP3A-mediated nifedipine oxidase activity with an IC50 of 0.8 microM, and a Ki of 0.6 microM.	Mibefradil	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	21-26
10901697-9	2000	Thus, mibefradil is not only a P-gp substrate, but also a potent inhibitor of both P-gp and CYP3A.	Mibefradil	6-16	ATP binding cassette subfamily B member 1	Homo sapiens	31-35
10901697-9	2000	Thus, mibefradil is not only a P-gp substrate, but also a potent inhibitor of both P-gp and CYP3A.	Mibefradil	6-16	ATP binding cassette subfamily B member 1	Homo sapiens	83-87
10901697-9	2000	Thus, mibefradil is not only a P-gp substrate, but also a potent inhibitor of both P-gp and CYP3A.	Mibefradil	6-16	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	92-97
10821797-7	2000	Mibefradil and its analogue RO40-6040 had high affinity for neuronal voltage-gated Na(+)-channels as confirmed in binding (apparent K(i) values of 17 and 1.0 nM, respectively) and functional experiments (40% use-dependent inhibition of Na(+)-channel current by 1 microM mibefradil in GH3 cells).	Mibefradil	0-10	sodium voltage-gated channel alpha subunit 8	Rattus norvegicus	83-96
10821797-7	2000	Mibefradil and its analogue RO40-6040 had high affinity for neuronal voltage-gated Na(+)-channels as confirmed in binding (apparent K(i) values of 17 and 1.0 nM, respectively) and functional experiments (40% use-dependent inhibition of Na(+)-channel current by 1 microM mibefradil in GH3 cells).	Mibefradil	270-280	sodium voltage-gated channel alpha subunit 8	Rattus norvegicus	83-96
10821797-9	2000	More lipophilic mibefradil analogues may possess neuroprotective properties like other nonselective Ca(2+)-/Na(+)-channel blockers.	Mibefradil	16-26	sodium voltage-gated channel alpha subunit 8	Rattus norvegicus	108-121
10614640-11	2000	Administration of mibefradil significantly reduced the TTN-evoked stimulation of steroid production, whereas nifedipine was devoid of effect.	Mibefradil	18-28	TTN	Canis lupus familiaris	55-58
10974418-5	2000	Additionally, NPPB (50-100 microM) and mibefradil (10-30 microM) significantly inhibited bFGF (10 ng/ml) + TNFalpha (2.5 ng/ml)-stimulated microvessel formation by human microvascular endothelial cells plated on fibrin by 30-70%.	Mibefradil	39-49	fibroblast growth factor 2	Homo sapiens	89-93
10974418-5	2000	Additionally, NPPB (50-100 microM) and mibefradil (10-30 microM) significantly inhibited bFGF (10 ng/ml) + TNFalpha (2.5 ng/ml)-stimulated microvessel formation by human microvascular endothelial cells plated on fibrin by 30-70%.	Mibefradil	39-49	tumor necrosis factor	Homo sapiens	107-115
10614640-8	2000	Incubation of the cells with the T-type calcium channel blocker mibefradil significantly reduced the TTN-evoked [Ca2+]i increase, whereas the L-type calcium channel blocker nifedipine and the N-type calcium channel blocker omega-conotoxin GVIA had no effect.	Mibefradil	64-74	TTN	Canis lupus familiaris	101-104
10882033-2	2000	In particular, Ca(V)3.2 (or alpha1H) was cloned from a human heart library, its message was found abundantly in cardiac tissue, and expressed Ca(V)3.2 was shown to conduct low voltage-activated currents, which inactivate rapidly and are sensitive to Ni2+ and mibefradil.	Mibefradil	259-269	immunoglobulin lambda variable 7-43	Homo sapiens	15-23
10882033-2	2000	In particular, Ca(V)3.2 (or alpha1H) was cloned from a human heart library, its message was found abundantly in cardiac tissue, and expressed Ca(V)3.2 was shown to conduct low voltage-activated currents, which inactivate rapidly and are sensitive to Ni2+ and mibefradil.	Mibefradil	259-269	immunoglobulin lambda variable 7-43	Homo sapiens	142-150
10882033-6	2000	(2) The half-maximal blocking concentration (IC50) of mibefradil on Ca(V)3.2 is near that on native-T and the block is similarly voltage-dependent.	Mibefradil	54-64	immunoglobulin lambda variable 7-43	Homo sapiens	68-76
10640508-7	2000	Unlike the observations with mibefradil, a potent irreversible inhibitor of CYP3A, the NADPH-dependent inhibition of CYP3A activity by nicardipine and verapamil was completely reversible on dialysis, whereas that by diltiazem was partially restored (80%).	Mibefradil	29-39	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	76-81
10640508-7	2000	Unlike the observations with mibefradil, a potent irreversible inhibitor of CYP3A, the NADPH-dependent inhibition of CYP3A activity by nicardipine and verapamil was completely reversible on dialysis, whereas that by diltiazem was partially restored (80%).	Mibefradil	29-39	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	117-122
10218730-4	1999	Restoration of the proliferative response in mibefradil- or nifedipine-treated cells was investigated by addition of exogenous interleukin-2.	Mibefradil	45-55	interleukin 2	Homo sapiens	127-140
10791290-5	2000	Restoration of the proliferative response in nifedipine- or mibefradil-treated cells was investigated by addition of exogenous IL-2.	Mibefradil	60-70	interleukin 2	Homo sapiens	127-131
10791290-8	2000	The proliferative response of nifedipine- or mibefradil-treated cells was restored by addition of exogenous IL-2.	Mibefradil	45-55	interleukin 2	Homo sapiens	108-112
10791290-9	2000	The normal expression of IL-2 receptors was preserved while the IL-2 production was blocked in the presence of nifedipine or mibefradil.	Mibefradil	125-135	interleukin 2	Homo sapiens	64-68
28008517-3	2000	The potency (IC50) of mibefradil was 6.5 muM and of lacidipine 82.4 nM.	Mibefradil	22-32	latexin	Homo sapiens	41-44
10399131-5	1999	The proliferative response of nifedipine- or mibefradil-treated cells was restored by addition of phorbol-12-myristate-13-acetate (PMA), an exogenous PKC activator.	Mibefradil	45-55	proline rich transmembrane protein 2	Homo sapiens	150-153
10860024-3	2000	HERG is blocked by bepridil (EC50 = 0.55 microM), verapamil (EC50 = 0.83 microM) and mibefradil (EC50 = 1.43 microM), whereas nitrendipine and diltiazem have negligible effects.	Mibefradil	85-95	potassium voltage-gated channel subfamily H member 2	Homo sapiens	0-4
10860024-5	2000	Similarly, KvLQT1-IsK is inhibited by bepridil (EC50 = 10.0 microM) and mibefradil (EC50 = 11.8 microM), whilst being insensitive to nitrendipine, diltiazem or verapamil.	Mibefradil	72-82	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	11-17
10860024-5	2000	Similarly, KvLQT1-IsK is inhibited by bepridil (EC50 = 10.0 microM) and mibefradil (EC50 = 11.8 microM), whilst being insensitive to nitrendipine, diltiazem or verapamil.	Mibefradil	72-82	potassium voltage-gated channel subfamily E regulatory subunit 1	Homo sapiens	18-21
10546924-0	1999	Mibefradil but not isradipine substantially elevates the plasma concentrations of the CYP3A4 substrate triazolam.	Mibefradil	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	86-92
10546924-1	1999	BACKGROUND: The calcium channel blockers mibefradil and isradipine inhibit CYP3A4 in vitro.	Mibefradil	41-51	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	75-81
10546924-11	1999	CONCLUSION: Mibefradil but not isradipine markedly increases the plasma concentrations of triazolam and thereby enhances and prolongs its pharmacodynamic effects, consistent with potent inhibition of CYP3A4.	Mibefradil	12-22	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	200-206
10218730-13	1999	The proliferative response of mibefradil- or nifedipine-treated cells is restored by addition of exogenous interleukin-2.	Mibefradil	30-40	interleukin 2	Homo sapiens	107-120
10218730-14	1999	The normal expression of interleukin-2 receptors was preserved, whereas the interleukin-2 production was blocked in the presence of mibefradil or nifedipine.	Mibefradil	132-142	interleukin 2	Homo sapiens	76-89
10218737-4	1999	Mibefradil (n = 22; titration, 13 patients) reduced mean 24-h ABP from 159+/-14/102+/-7 mm Hg to 140+/-10/89+/-7 mm Hg after 12 weeks.	Mibefradil	0-10	amine oxidase copper containing 1	Homo sapiens	62-65
10218737-6	1999	Trough-to-peak ratios in DBP were 86% for mibefradil and 75% with enalapril.	Mibefradil	42-52	D-box binding PAR bZIP transcription factor	Homo sapiens	25-28
10218737-8	1999	Mibefradil matched enalapril in 24-h ABP control.	Mibefradil	0-10	amine oxidase copper containing 1	Homo sapiens	37-40
10215754-3	1999	RESULTS: Mibefradil inhibited, in a concentration-dependent fashion, the metabolism of the four statins (simvastatin, lovastatin, atorvastatin and cerivastatin) known to be substrates for CYP3A.	Mibefradil	9-19	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	188-193
10215754-4	1999	The potency of inhibition was such that the IC50 values (<1 microM) for inhibition of all of the CYP3A substrates fell within the therapeutic plasma concentrations of mibefradil, and was comparable with that of ketoconazole.	Mibefradil	170-180	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	100-105
10215754-8	1999	CONCLUSION: Mibefradil, at therapeutically relevant concentrations, strongly suppressed the metabolism in human liver microsomes of simvastatin, lovastatin, atorvastatin and cerivastatin through its inhibitory effects on CYP3A4/5, while the effects of mibefradil on fluvastatin, a substrate for CYP2C8/9, were minimal in this system.	Mibefradil	12-22	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	295-301
10215754-9	1999	Since mibefradil is a potent mechanism-based inhibitor of CYP3A4/5, it is anticipated that clinically significant drug-drug interactions will likely ensue when mibefradil is coadministered with agents which are cleared primarily by CYP3A-mediated pathways.	Mibefradil	6-16	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-64
10215754-6	1999	Based on the kinetics of its inhibition of hepatic testosterone 6beta-hydroxylase activity, mibefradil was judged to be a powerful mechanism-based inhibitor of CYP3A4/5, with values for Kinactivation, Ki and partition ratio (moles of mibefradil metabolized per moles of enzyme inactivated) of 0.4 min(-1), 2.3 microM and 1.7, respectively.	Mibefradil	92-102	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	160-166
10215754-8	1999	CONCLUSION: Mibefradil, at therapeutically relevant concentrations, strongly suppressed the metabolism in human liver microsomes of simvastatin, lovastatin, atorvastatin and cerivastatin through its inhibitory effects on CYP3A4/5, while the effects of mibefradil on fluvastatin, a substrate for CYP2C8/9, were minimal in this system.	Mibefradil	12-22	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	221-227
10215754-9	1999	Since mibefradil is a potent mechanism-based inhibitor of CYP3A4/5, it is anticipated that clinically significant drug-drug interactions will likely ensue when mibefradil is coadministered with agents which are cleared primarily by CYP3A-mediated pathways.	Mibefradil	6-16	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-63
10215754-9	1999	Since mibefradil is a potent mechanism-based inhibitor of CYP3A4/5, it is anticipated that clinically significant drug-drug interactions will likely ensue when mibefradil is coadministered with agents which are cleared primarily by CYP3A-mediated pathways.	Mibefradil	160-170	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-64
10215754-9	1999	Since mibefradil is a potent mechanism-based inhibitor of CYP3A4/5, it is anticipated that clinically significant drug-drug interactions will likely ensue when mibefradil is coadministered with agents which are cleared primarily by CYP3A-mediated pathways.	Mibefradil	160-170	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-63
9811158-2	1998	The recommended doses for treatment of hypertension and chronic stable angina pectoris are 50 or 100 mg. Mibefradil is metabolized via parallel pathways of esterase-catalysed hydrolysis and cytochrome P450 3A4-mediated oxidation.	Mibefradil	105-115	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	190-209
10226769-2	1999	The aim of the present study was to investigate the effects of mibefradil, a potent CYP3A inhibitor, on pravastatin pharmacokinetics.	Mibefradil	63-73	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	84-89
9765513-5	1998	Similarly, KvLQT1/IsK is inhibited by bepridil (EC50 = 10.0 microM) and mibefradil (EC50 = 11.8 microM), while being insensitive to nitrendipine, diltiazem, or verapamil.	Mibefradil	72-82	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	11-17
9765513-5	1998	Similarly, KvLQT1/IsK is inhibited by bepridil (EC50 = 10.0 microM) and mibefradil (EC50 = 11.8 microM), while being insensitive to nitrendipine, diltiazem, or verapamil.	Mibefradil	72-82	potassium voltage-gated channel subfamily E regulatory subunit 1	Homo sapiens	18-21
9765513-1	1998	We examined the effects of the calcium channel blockers nitrendipine, diltiazem, verapamil, bepridil, and mibefradil on the cloned HERG and KvLQT1/IsK K+ channels.	Mibefradil	106-116	potassium voltage-gated channel subfamily H member 2	Homo sapiens	131-135
9765513-1	1998	We examined the effects of the calcium channel blockers nitrendipine, diltiazem, verapamil, bepridil, and mibefradil on the cloned HERG and KvLQT1/IsK K+ channels.	Mibefradil	106-116	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	140-146
9765513-3	1998	When expressed in transfected COS cells, HERG is blocked in a concentration-dependent manner by bepridil (EC50 = 0.55 microM), verapamil (EC50 = 0.83 microM), and mibefradil (EC50 = 1.43 microM), whereas nitrendipine and diltiazem have negligible effects.	Mibefradil	163-173	potassium voltage-gated channel subfamily H member 2	Homo sapiens	41-45
9811158-3	1998	Mibefradil also inhibits cytochrome P450 3A4 and consequently inhibits its own metabolism, a property illustrated by three studies performed early in the drug"s development.	Mibefradil	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	25-44
9681729-8	1998	CONCLUSIONS: These results confirm previous findings of cytochrome P-450 3A4 inhibition by mibefradil and suggest that, for patients receiving CsA, its dose must be adjusted and its plasma concentration must be monitored when adding or stopping mibefradil.	Mibefradil	91-101	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	56-76
8842500-3	1996	For this purpose, the influence of the renin angiotensin system on the effects of mibefradil (30 mg/kg po) and cilazapril (10 mg/kg po) on neointima formation after carotid injury were evaluated in normotensive rats (normal renin angiotensin system) and DOCA hypertensive rats (suppressed renin angiotensin system).	Mibefradil	82-92	renin	Rattus norvegicus	39-44
9647484-7	1998	Mibefradil significantly lowered PRA and renin mRNA levels at 5 mg kg(-1) and moderately increased both parameters at a dose of 45 mg kg(-1), when PRA and renin mRNA levels were increased by 100% and 30%, respectively.	Mibefradil	0-10	renin	Rattus norvegicus	41-46
9647484-7	1998	Mibefradil significantly lowered PRA and renin mRNA levels at 5 mg kg(-1) and moderately increased both parameters at a dose of 45 mg kg(-1), when PRA and renin mRNA levels were increased by 100% and 30%, respectively.	Mibefradil	0-10	renin	Rattus norvegicus	155-160
9647484-11	1998	In contrast mibefradil (5 mg kg(-1) and 15 mg kg(-1) day(-1)) significantly attenuated the rise of PRA and renin mRNA levels, whilst amlodipine (15 mg kg(-1)) additionally elevated the rise of PRA and renin mRNA levels in response to renal artery clipping.	Mibefradil	12-22	renin	Rattus norvegicus	107-112
9647484-11	1998	In contrast mibefradil (5 mg kg(-1) and 15 mg kg(-1) day(-1)) significantly attenuated the rise of PRA and renin mRNA levels, whilst amlodipine (15 mg kg(-1)) additionally elevated the rise of PRA and renin mRNA levels in response to renal artery clipping.	Mibefradil	12-22	renin	Rattus norvegicus	201-206
9818292-8	1998	For non-DHP (verapamil, mibefradil) reflex tachycardia probably is prevented by a direct effect on the conductive tissue in the myocardium.	Mibefradil	24-34	dihydropyrimidinase	Rattus norvegicus	8-11
9286852-14	1997	In conclusion, the effectiveness of mibefradil in improving all 3 ETT parameters was greater than that of amlodipine and equivalent to that of diltiazem SR.	Mibefradil	36-46	paired box 5	Homo sapiens	60-65
8934362-5	1996	Mibefradil treatment resulted in lower blood pressure, reduced cardiac hypertrophy, near-normal structure of conduit and small arteries and lower endothelin-1 mRNA abundance.	Mibefradil	0-10	endothelin 1	Rattus norvegicus	146-158
34224697-0	2021	Mibefradil reduces hepatic glucose output in HepG2 cells via Ca2+/calmodulin-dependent protein kinase II-dependent Akt/forkhead box O1signaling.	Mibefradil	0-10	AKT serine/threonine kinase 1	Homo sapiens	115-118
8850387-2	1995	Therefore, the effect of mibefradil on increases in intracellular Ca2+ concentrations and aggregation of human platelets induced by platelet activating factor (PAF) was examined.	Mibefradil	25-35	PCNA clamp associated factor	Homo sapiens	160-163
8850387-4	1995	Mibefradil totally and dose dependently inhibited PAF-induced Ca2+ influx with a maximal effective concentration of 10 microM, but at this concentration only reduced Ca2+ mobilization from intracellular stores.	Mibefradil	0-10	PCNA clamp associated factor	Homo sapiens	50-53
8850387-6	1995	In the same range of concentrations, mibefradil inhibited Ca(2+)-dependent platelet aggregation induced by PAF.	Mibefradil	37-47	PCNA clamp associated factor	Homo sapiens	107-110
7594436-9	1995	Mibefradil and enalapril equally prevented the morphological consequences of hypertension (i.e. medial hypertrophy and the decreased elastin:collagen ratio).	Mibefradil	0-10	elastin	Rattus norvegicus	133-140
7594436-12	1995	This suggests that the changes observed in the aorta are directly related to blood pressure or to other mechanisms independent of the renin-angiotensin system, which could be blocked by a calcium antagonist such as mibefradil.	Mibefradil	215-225	renin	Rattus norvegicus	134-139
7694155-3	1993	Ro 40-5967 caused a concentration-dependent suppression of Ca2+ channel currents in muscle cells from both arteries, with greater potency on coronary than saphenous arterial cells.	Mibefradil	0-10	carbonic anhydrase 2	Canis lupus familiaris	59-62
34224697-6	2021	In HepG2 cells and mouse liver tissues, mibefradil decreased PA-induced cytoplasmic calcium levels and CaMKII phosphorylation, but increased the phosphorylation of Akt and FoxO1, thereby contributing to the cytoplasmic localization of FoxO1.	Mibefradil	40-50	calcium/calmodulin-dependent protein kinase II, beta	Mus musculus	103-109
34224697-6	2021	In HepG2 cells and mouse liver tissues, mibefradil decreased PA-induced cytoplasmic calcium levels and CaMKII phosphorylation, but increased the phosphorylation of Akt and FoxO1, thereby contributing to the cytoplasmic localization of FoxO1.	Mibefradil	40-50	thymoma viral proto-oncogene 1	Mus musculus	164-167
8603130-0	1996	Protein kinase C mechanism enhances vascular muscle relaxation by the Ca2+ antagonist, Ro 40-5967.	Mibefradil	87-97	proline rich transmembrane protein 2	Homo sapiens	0-16
8603130-9	1996	These data suggest that there is an important direct PKC inhibitory action of Ro 40-5967 that would at least partially explain relaxation of ET-induced contractions.	Mibefradil	78-88	proline rich transmembrane protein 2	Homo sapiens	53-56
7475057-4	1995	In epicardial vessels contracted with KCl, the thromboxane analogue U 46619, or endothelin-1 (ET-1), relaxations to the Ca2+ antagonist mibefradil were most effective after precontraction with KCl, followed by U 46619 and ET-1.	Mibefradil	136-146	endothelin 1	Homo sapiens	80-92
7475057-4	1995	In epicardial vessels contracted with KCl, the thromboxane analogue U 46619, or endothelin-1 (ET-1), relaxations to the Ca2+ antagonist mibefradil were most effective after precontraction with KCl, followed by U 46619 and ET-1.	Mibefradil	136-146	endothelin 1	Homo sapiens	94-98
7475057-4	1995	In epicardial vessels contracted with KCl, the thromboxane analogue U 46619, or endothelin-1 (ET-1), relaxations to the Ca2+ antagonist mibefradil were most effective after precontraction with KCl, followed by U 46619 and ET-1.	Mibefradil	136-146	endothelin 1	Homo sapiens	222-226
7475057-8	1995	However, epicardial but not intramyocardial vessels incubated with mibefradil exhibited enhanced relaxations to bradykinin (BK) and sodium nitroprusside (SNP) as compared with control.	Mibefradil	67-77	kininogen 1	Homo sapiens	112-122
7475057-8	1995	However, epicardial but not intramyocardial vessels incubated with mibefradil exhibited enhanced relaxations to bradykinin (BK) and sodium nitroprusside (SNP) as compared with control.	Mibefradil	67-77	kininogen 1	Homo sapiens	124-126
8069408-0	1994	Chronic treatment with the CA2+ channel inhibitor RO 40-5967 potentiates endothelium-dependent relaxations in the aorta of the hypertensive salt sensitive Dahl rat.	Mibefradil	50-60	carbonic anhydrase 2	Rattus norvegicus	27-30
34438468-5	2022	Incubation with nifedipine or mibefradil decreased the protein level of Cx43 in HL-1 cells.	Mibefradil	30-40	gap junction protein alpha 1	Homo sapiens	72-76
34224697-6	2021	In HepG2 cells and mouse liver tissues, mibefradil decreased PA-induced cytoplasmic calcium levels and CaMKII phosphorylation, but increased the phosphorylation of Akt and FoxO1, thereby contributing to the cytoplasmic localization of FoxO1.	Mibefradil	40-50	forkhead box O1	Mus musculus	172-177
34224697-6	2021	In HepG2 cells and mouse liver tissues, mibefradil decreased PA-induced cytoplasmic calcium levels and CaMKII phosphorylation, but increased the phosphorylation of Akt and FoxO1, thereby contributing to the cytoplasmic localization of FoxO1.	Mibefradil	40-50	forkhead box O1	Mus musculus	235-240
34224697-7	2021	Additionally, mibefradil alleviated PA-induced glucose output and insulin resistance through increased glucose consumption and glycogen synthesis, while decreasing the expression of key gluconeogenesis enzymes, including PEPCK and G6Pase.	Mibefradil	14-24	insulin	Homo sapiens	66-73
34224697-7	2021	Additionally, mibefradil alleviated PA-induced glucose output and insulin resistance through increased glucose consumption and glycogen synthesis, while decreasing the expression of key gluconeogenesis enzymes, including PEPCK and G6Pase.	Mibefradil	14-24	phosphoenolpyruvate carboxykinase 1, cytosolic	Mus musculus	221-226
34224697-0	2021	Mibefradil reduces hepatic glucose output in HepG2 cells via Ca2+/calmodulin-dependent protein kinase II-dependent Akt/forkhead box O1signaling.	Mibefradil	0-10	forkhead box O1	Homo sapiens	119-134
34224697-7	2021	Additionally, mibefradil alleviated PA-induced glucose output and insulin resistance through increased glucose consumption and glycogen synthesis, while decreasing the expression of key gluconeogenesis enzymes, including PEPCK and G6Pase.	Mibefradil	14-24	glucose-6-phosphatase, catalytic	Mus musculus	231-237
34224697-8	2021	Mibefradil may help to control blood sugar levels by reducing glucose output and insulin resistance, and the mechanism of action may involve the Ca2+-CaMKII-dependent Akt/FoxO1 signaling pathway.	Mibefradil	0-10	insulin	Homo sapiens	81-88
34224697-8	2021	Mibefradil may help to control blood sugar levels by reducing glucose output and insulin resistance, and the mechanism of action may involve the Ca2+-CaMKII-dependent Akt/FoxO1 signaling pathway.	Mibefradil	0-10	calcium/calmodulin-dependent protein kinase II, beta	Mus musculus	150-156
34224697-8	2021	Mibefradil may help to control blood sugar levels by reducing glucose output and insulin resistance, and the mechanism of action may involve the Ca2+-CaMKII-dependent Akt/FoxO1 signaling pathway.	Mibefradil	0-10	thymoma viral proto-oncogene 1	Mus musculus	167-170
34168192-9	2021	Furthermore, inhibition of T-type calcium channels with mibefradil or ML218 reduced diameter, volume and BNP levels in HL-1 cells.	Mibefradil	56-66	natriuretic peptide type B	Mus musculus	105-108
34224697-8	2021	Mibefradil may help to control blood sugar levels by reducing glucose output and insulin resistance, and the mechanism of action may involve the Ca2+-CaMKII-dependent Akt/FoxO1 signaling pathway.	Mibefradil	0-10	forkhead box O1	Mus musculus	171-176
31480231-0	2019	Structural Insights into the Interaction of Cytochrome P450 3A4 with Suicide Substrates: Mibefradil, Azamulin and 6",7"-Dihydroxybergamottin.	Mibefradil	89-99	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	44-63
32215948-6	2020	Tetraethylammonium was used in order to induce long term potentiation and T-type Ca2+ channel activity was assessed in the presence of mibefradil.	Mibefradil	135-145	carbonic anhydrase 2	Rattus norvegicus	81-84
32433360-0	2020	Mibefradil alleviates high glucose-induced cardiac hypertrophy by inhibiting PI3K/Akt/mTOR-mediated autophagy.	Mibefradil	0-10	AKT serine/threonine kinase 1	Rattus norvegicus	82-85
32433360-0	2020	Mibefradil alleviates high glucose-induced cardiac hypertrophy by inhibiting PI3K/Akt/mTOR-mediated autophagy.	Mibefradil	0-10	mechanistic target of rapamycin kinase	Rattus norvegicus	86-90
32433360-7	2020	Our results indicate that mibefradil reduced the size of H9c2 cells, decreased mRNA expression of ANP, BNP, and beta-MHC, and decreased the level of autophagic flux.	Mibefradil	26-36	natriuretic peptide A	Rattus norvegicus	98-101
32433360-7	2020	Our results indicate that mibefradil reduced the size of H9c2 cells, decreased mRNA expression of ANP, BNP, and beta-MHC, and decreased the level of autophagic flux.	Mibefradil	26-36	natriuretic peptide B	Rattus norvegicus	103-106
32433360-9	2020	In conclusion, mibefradil ameliorated high-glucose-induced cardiac hypertrophy by activating the PI3K/Akt/mTOR pathway and inhibiting excessive autophagy.	Mibefradil	15-25	AKT serine/threonine kinase 1	Rattus norvegicus	102-105
32433360-9	2020	In conclusion, mibefradil ameliorated high-glucose-induced cardiac hypertrophy by activating the PI3K/Akt/mTOR pathway and inhibiting excessive autophagy.	Mibefradil	15-25	mechanistic target of rapamycin kinase	Rattus norvegicus	106-110
35438819-7	2022	Pharmacological inhibition of CatSper with either mibefradil or NNC 55-0396 leads to the same loss in swim path chirality.	Mibefradil	50-60	cation channel, sperm associated 1	Mus musculus	30-37
33953843-6	2021	Here, we show that mibefradil inhibits DNA repair independent of its CCB activity, and report a series of mibefradil analogues which lack CCB activity and demonstrate reduced hERG and CYP activity while retaining potency as DNA repair inhibitors.	Mibefradil	106-116	ETS transcription factor ERG	Homo sapiens	175-179
33223955-4	2020	In LPS challenged mice, mibefradil (20 and 40 mg/kg) dramatically decreased the total cell number, as well as the productions of TNF-alpha and IL-6 in bronchoalveolar lavage fluid (BALF).	Mibefradil	24-34	tumor necrosis factor	Mus musculus	129-138
33223955-4	2020	In LPS challenged mice, mibefradil (20 and 40 mg/kg) dramatically decreased the total cell number, as well as the productions of TNF-alpha and IL-6 in bronchoalveolar lavage fluid (BALF).	Mibefradil	24-34	interleukin 6	Mus musculus	143-147
33223955-5	2020	Mibefradil also suppressed total protein concentration in BALF, attenuated Evans blue extravasation, MPO activity, and NF-kappaB activation in lung tissue.	Mibefradil	0-10	myeloperoxidase	Mus musculus	101-104
33223955-5	2020	Mibefradil also suppressed total protein concentration in BALF, attenuated Evans blue extravasation, MPO activity, and NF-kappaB activation in lung tissue.	Mibefradil	0-10	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	119-128
32331852-7	2020	Typical inhibitors, ketoconazole, nicardipine, mibefradil and GF-I-1 shared mutuality on their sittings, in which the inhibitor molecules hold a CYP3A4 residue from dual sides on Template.	Mibefradil	47-57	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	145-151
31271653-8	2019	KEY RESULTS: Mibefradil inhibited Orai1, Orai2, and Orai3 currents dose-dependently.	Mibefradil	13-23	ORAI calcium release-activated calcium modulator 1	Homo sapiens	34-39
31271653-8	2019	KEY RESULTS: Mibefradil inhibited Orai1, Orai2, and Orai3 currents dose-dependently.	Mibefradil	13-23	ORAI calcium release-activated calcium modulator 2	Homo sapiens	41-46
31271653-8	2019	KEY RESULTS: Mibefradil inhibited Orai1, Orai2, and Orai3 currents dose-dependently.	Mibefradil	13-23	ORAI calcium release-activated calcium modulator 3	Homo sapiens	52-57
31480231-4	2019	This study provides the first direct insights into the interaction of CYP3A4 with three suicide substrates: mibefradil, an antihypertensive drug quickly withdrawn from the market; a semi-synthetic antibiotic azamulin; and a natural furanocoumarin, 6",7"-dihydroxybergamottin.	Mibefradil	108-118	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	70-76
28371832-11	2017	18F-FLT PET imaging showed a significant decline in standardized uptake value (SUV) signal in 2 of 10 patients after 7 days of treatment with MIB.	Mibefradil	142-145	fms related receptor tyrosine kinase 1	Homo sapiens	4-7
29044427-6	2017	Subsequent treatment of bull sperm with either the calcium chelator ethylene glycol tetraacetic acid; mibefradil, a specific blocker of CatSper channels in human sperm; or CATSPER1 antibody all significantly inhibited caffeine-induced hyperactivation and the rheotactic response, supporting the concept that the calcium influx occurs via CatSper channels.	Mibefradil	102-112	cation channel sperm associated 1	Homo sapiens	136-143
29044427-6	2017	Subsequent treatment of bull sperm with either the calcium chelator ethylene glycol tetraacetic acid; mibefradil, a specific blocker of CatSper channels in human sperm; or CATSPER1 antibody all significantly inhibited caffeine-induced hyperactivation and the rheotactic response, supporting the concept that the calcium influx occurs via CatSper channels.	Mibefradil	102-112	cation channel sperm associated 1	Homo sapiens	338-345
27255432-2	2017	Given that mibefradil (Mb) is also known to inhibit K+ channels, we decided to study the interaction between this organic compound and the tumor-related Kv10.1 channel.	Mibefradil	11-21	potassium voltage-gated channel modifier subfamily G member 3	Homo sapiens	153-159
27255432-2	2017	Given that mibefradil (Mb) is also known to inhibit K+ channels, we decided to study the interaction between this organic compound and the tumor-related Kv10.1 channel.	Mibefradil	23-25	potassium voltage-gated channel modifier subfamily G member 3	Homo sapiens	153-159
27255432-6	2017	Our observations suggest that Mb binds to the voltage sensor domain of Kv10.1 channels, thereby modifying the gating of the channels in a way that in some, but not all, aspects opposes to the gating effects exerted by divalent cations.	Mibefradil	30-32	potassium voltage-gated channel modifier subfamily G member 3	Homo sapiens	71-77
29207174-8	2018	Furthermore, an intravitreal injection of the Ca2+ channel blocker Mibefradil (3 microM) reduced EphB2-fragment crystallizable region-induced RGC apoptosis in normal rats.	Mibefradil	67-77	Eph receptor B2	Rattus norvegicus	97-102
29167643-8	2017	Conversely, loss of ICCs may explain the lower amounts of adenosine detected in TNBS-treated preparations, since blockade of Cav3 (T-type) channels existing in ICCs with mibefradil (3 muM) or inhibition of the equilibrative nucleoside transporter 1 with dipyridamole (0.5 muM), both decreased extracellular adenosine.	Mibefradil	170-180	caveolin 3	Rattus norvegicus	125-129
28741432-7	2017	Moreover, disruption of the interaction between USP5 and Cav3.2 with TAT peptides suppressed acute nocifensive responses produced by interleukin-1 beta, which was similar to that achieved by elimination of T-type channel activity with the channel blockers, mibefradil, or TTA-A2.	Mibefradil	257-267	ubiquitin specific peptidase 5 (isopeptidase T)	Mus musculus	48-52
28069437-10	2017	RESULTS: Both, nimodipine and mibefradil prevented recall facilitating effects of subsequently injected Ang IV.	Mibefradil	30-40	angiogenin	Rattus norvegicus	104-107
28741432-7	2017	Moreover, disruption of the interaction between USP5 and Cav3.2 with TAT peptides suppressed acute nocifensive responses produced by interleukin-1 beta, which was similar to that achieved by elimination of T-type channel activity with the channel blockers, mibefradil, or TTA-A2.	Mibefradil	257-267	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	57-63
27765616-9	2016	Compared with the saline-treated group, rats receiving mibefradil or ethosuximide showed significant lower CaV3.2 expression in the spinal cord and DRG.	Mibefradil	55-65	caveolin 3	Rattus norvegicus	107-111
27765616-11	2016	CONCLUSION: In this study, we demonstrate that SNL-induced CaV3.2 upregulation in the spinal cord and DRG was attenuated by intrathecal infusion of mibefradil or ethosuximide.	Mibefradil	148-158	caveolin 3	Rattus norvegicus	59-63
27258646-0	2016	CACNA1H(M1549V) Mutant Calcium Channel Causes Autonomous Aldosterone Production in HAC15 Cells and Is Inhibited by Mibefradil.	Mibefradil	115-125	calcium voltage-gated channel subunit alpha1 H	Homo sapiens	0-7
26755813-7	2016	Although both TRPC1 and CAV1.2 expression levels were increased in PDGF-stimulated PASMCs on mibefradil and sildenafil treatment, it was not statistically significant (p=0.086 and 1.000, respectively).	Mibefradil	93-103	transient receptor potential cation channel subfamily C member 1	Homo sapiens	14-19
26669310-0	2016	Mibefradil represents a new class of benzimidazole TRPM7 channel agonists.	Mibefradil	0-10	transient receptor potential cation channel subfamily M member 7	Homo sapiens	51-56
26669310-8	2016	Here, we demonstrate that mibefradil and NNC 50-0396, two benzimidazole relatives of the TRPM7 inhibitor NS8593, are positive modulators of TRPM7.	Mibefradil	26-36	transient receptor potential cation channel subfamily M member 7	Homo sapiens	89-94
26669310-8	2016	Here, we demonstrate that mibefradil and NNC 50-0396, two benzimidazole relatives of the TRPM7 inhibitor NS8593, are positive modulators of TRPM7.	Mibefradil	26-36	transient receptor potential cation channel subfamily M member 7	Homo sapiens	140-145
26669310-9	2016	Using Ca(2+) imaging and the patch-clamp technique, we show that mibefradil activates TRPM7-mediated Ca(2+) entry and whole-cell currents.	Mibefradil	65-75	transient receptor potential cation channel subfamily M member 7	Homo sapiens	86-91
26669310-11	2016	In contrast to naltriben, mibefradil efficiently activates TRPM7 currents only at physiological intracellular Mg(2+) concentrations, and its stimulatory effect was fully abrogated by high internal Mg(2+) levels.	Mibefradil	26-36	transient receptor potential cation channel subfamily M member 7	Homo sapiens	59-64
26669310-13	2016	Finally, we observed that the effect of mibefradil was selective for TRPM7 when various TRP channels were tested.	Mibefradil	40-50	transient receptor potential cation channel subfamily M member 7	Homo sapiens	69-74
26669310-14	2016	Taken together, mibefradil acts as a Mg(2+)-regulated agonist of the TRPM7 channel and, hence, uncovers a new class of TRPM7 agonists.	Mibefradil	16-26	transient receptor potential cation channel subfamily M member 7	Homo sapiens	69-74
26669310-14	2016	Taken together, mibefradil acts as a Mg(2+)-regulated agonist of the TRPM7 channel and, hence, uncovers a new class of TRPM7 agonists.	Mibefradil	16-26	transient receptor potential cation channel subfamily M member 7	Homo sapiens	119-124
26875775-6	2016	But the inhibitory effect of mibefradil (mibe, a blocker for L-type (CaV1.2) and T-type calcium channels (CaV3.2)) on PE-, 5-HT-induced vasoconstriction was significantly greater than progesterone or nifedipine in Krebs solution.	Mibefradil	29-39	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	69-75
26755813-7	2016	Although both TRPC1 and CAV1.2 expression levels were increased in PDGF-stimulated PASMCs on mibefradil and sildenafil treatment, it was not statistically significant (p=0.086 and 1.000, respectively).	Mibefradil	93-103	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	24-30
26483387-7	2015	Pharmacological inhibition of CaV3.2 in wild-type CF-1 strain eggs using mibefradil or pimozide reduced Ca(2+) store accumulation during oocyte maturation and reduced Ca(2+) oscillation persistence, frequency and number following IVF.	Mibefradil	73-83	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	30-36
26690767-10	2015	Tau is using the early success of mibefradil as a proof of concept to build a platform technology of Cav3 blockers for broad antitumor applications in combination with new targeted cancer therapies, well-established chemotherapies, and radiation.	Mibefradil	34-44	caveolin 3	Homo sapiens	101-105
24479199-4	2010	Mibefradil (Posicor), a potent inhibitor of CYP3A4, was withdrawn from the market after numerous reports of serious drug-drug interactions.	Mibefradil	12-19	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	44-50
25989794-6	2015	In addition, we observed a reduced phosphorylation of ERK1/2 in MOLT-4 cells in response to mibefradil and NNC-55-0396 treatment.	Mibefradil	92-102	mitogen-activated protein kinase 3	Homo sapiens	54-60
25267397-5	2015	As did mibefradil, a T-channel inhibitor, in our previous report, AP18 prevented the Fos expression following ductal NaHS, an H(2)S donor.	Mibefradil	7-17	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	85-88
24479199-4	2010	Mibefradil (Posicor), a potent inhibitor of CYP3A4, was withdrawn from the market after numerous reports of serious drug-drug interactions.	Mibefradil	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	44-50
26602811-6	2015	Strikingly, pharmacological blockade and silencing of Cav3.2 T-type calcium channel by mibefradil, ascorbic acid, zinc chloride or Cav3.2 siRNA dramatically decreased NaHS-evoked scratching.	Mibefradil	87-97	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	54-60
23623968-5	2013	The activation of AKT in response to progesterone is calcium dependent and the CatSper channel inhibitor mibefradil significantly reduced progesterone mediated AKT phosphorylation.	Mibefradil	105-115	AKT serine/threonine kinase 1	Homo sapiens	18-21
24705276-0	2014	CaV3.2 T-type calcium channels in peripheral sensory neurons are important for mibefradil-induced reversal of hyperalgesia and allodynia in rats with painful diabetic neuropathy.	Mibefradil	79-89	caveolin 3	Rattus norvegicus	0-4
24705276-9	2014	We conclude that antihyperalgesic and antiallodynic effects of mibefradil in PDN are at least partly mediated by inhibition of CaV3.2 channels in peripheral nociceptors.	Mibefradil	63-73	caveolin 3	Rattus norvegicus	127-131
24048572-5	2013	Increasing intracellular pH induced a rise in intracellular calcium, which was inhibited by the known CatSper blocker mibefradil, supporting the presence of a pH-gated calcium channel, presumably CatSper.	Mibefradil	118-128	cation channel, sperm associated 1	Mus musculus	102-109
24048572-5	2013	Increasing intracellular pH induced a rise in intracellular calcium, which was inhibited by the known CatSper blocker mibefradil, supporting the presence of a pH-gated calcium channel, presumably CatSper.	Mibefradil	118-128	cation channel, sperm associated 1	Mus musculus	196-203
23623968-5	2013	The activation of AKT in response to progesterone is calcium dependent and the CatSper channel inhibitor mibefradil significantly reduced progesterone mediated AKT phosphorylation.	Mibefradil	105-115	AKT serine/threonine kinase 1	Homo sapiens	160-163
21575684-5	2011	We found that the inhibitory effect of VEGF on the osmotic swelling of retinal glial cells, used as an indicator of glutamate release, is prevented in the presence of selective blockers of T-type VGCCs (kurtoxin, mibefradil, Ni2+) and Na(v) channels (TTX, saxitoxin, phenytoin).	Mibefradil	213-223	vascular endothelial growth factor A	Rattus norvegicus	39-43
22251131-6	2013	The proliferation of HPLFs induced by bFGF was decreased significantly by treatment with Mibefradil.	Mibefradil	89-99	fibroblast growth factor 2	Homo sapiens	38-42
21354272-14	2011	TPEN caused prompt phosphorylation of ERK in the spinal dorsal horn, an effect blocked by mibefradil.	Mibefradil	90-100	mitogen-activated protein kinase 1	Mus musculus	38-41
21039820-0	2011	Two structurally different T-type Ca 2+ channel inhibitors, mibefradil and pimozide, protect CA1 neurons from delayed death after global ischemia in rats.	Mibefradil	60-70	carbonic anhydrase 1	Rattus norvegicus	93-96
21447734-3	2011	Mibefradil has previously been shown to be a potent reversible (IC(50) = 0.3-2 muM) and mechanism-based (K(i) = 2.3 muM; k(inact) = 0.4 min(-1)) inhibitor of CYP3A4-catalyzed statin metabolism.	Mibefradil	0-10	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	158-164
21447734-5	2011	Mechanism-based inactivation experiments and spectral studies were used to examine the mechanism of CYP3A4 inactivation by mibefradil and its major metabolite, des-methoxyacetyl mibefradil (Ro 40-5966), in vitro.	Mibefradil	123-133	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	100-106
21447734-8	2011	Approximately 70% of CYP3A4 activity was lost in the first minute of incubation with mibefradil, and inactivation was nonlinear after 2 min.	Mibefradil	85-95	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	21-27
21447734-10	2011	The decrease in CYP3A4 activity in the presence of mibefradil and NADPH was subsequently shown to have a good correlation with the time-dependent loss of CO binding, which, coupled with the lack of stable heme and/or apoprotein adducts, suggests heme destruction as the mechanism of inactivation of CYP3A4 by mibefradil.	Mibefradil	51-61	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	16-22
21447734-10	2011	The decrease in CYP3A4 activity in the presence of mibefradil and NADPH was subsequently shown to have a good correlation with the time-dependent loss of CO binding, which, coupled with the lack of stable heme and/or apoprotein adducts, suggests heme destruction as the mechanism of inactivation of CYP3A4 by mibefradil.	Mibefradil	51-61	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	299-305
21447734-10	2011	The decrease in CYP3A4 activity in the presence of mibefradil and NADPH was subsequently shown to have a good correlation with the time-dependent loss of CO binding, which, coupled with the lack of stable heme and/or apoprotein adducts, suggests heme destruction as the mechanism of inactivation of CYP3A4 by mibefradil.	Mibefradil	309-319	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	16-22
21474682-5	2011	Inactivation studies of mibefradil against the two isozymes showed that the maximal inactivation rate constants (k(inact)) were considerable in both isozymes (0.231-0.565 min(-1)), whereas the inhibitor concentration producing half the k(inact) (K(I, app)) of CYP3A2 (0.263-0.410 muM) was a good deal lower than that for CYP2C11 (6.82-11.4 muM).	Mibefradil	24-34	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	260-266
21474682-5	2011	Inactivation studies of mibefradil against the two isozymes showed that the maximal inactivation rate constants (k(inact)) were considerable in both isozymes (0.231-0.565 min(-1)), whereas the inhibitor concentration producing half the k(inact) (K(I, app)) of CYP3A2 (0.263-0.410 muM) was a good deal lower than that for CYP2C11 (6.82-11.4 muM).	Mibefradil	24-34	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	321-328
20806405-6	2010	Mibefradil, a T-type Ca(2+) channel blocker, abolished the phosphorylation of ERK caused by intraductal NaHS but not SLIGRL-NH(2).	Mibefradil	0-10	Eph receptor B1	Rattus norvegicus	78-81
20694017-6	2010	In the presence of 1.0 mmol L(-1) extracellular Ca(2+), hCG at 1 to 100 IU noticeably elevated both StAR mRNA level and testosterone secretion (P < 0.05), and the stimulatory effects of hCG were markedly diminished by mibefradil in a dose-dependent manner (P < 0.05).	Mibefradil	221-231	chorionic gonadotropin subunit beta 5	Homo sapiens	56-59
18805956-7	2008	The stretch-induced increase in P-selectin expression was substantially decreased by pretreatment with the T-type Ca(2+) channel inhibitor mibefradil (76% inhibition).	Mibefradil	139-149	selectin, platelet	Mus musculus	32-42
20457833-5	2010	Whole cell recordings of 3T3-L1 preadipocytes showed low-threshold Ca(V), which could be inhibited by mibefradil, Ni(2+) (IC(50) of 200 muM), and NNC55-0396.	Mibefradil	102-112	caveolin 1, caveolae protein	Mus musculus	67-72
20457833-10	2010	Mibefradil, NNC55-0396, a selective T-type Ca(V) blocker, but not diltiazem, inhibited cell proliferation in response to serum.	Mibefradil	0-10	caveolin 1, caveolae protein	Mus musculus	43-48
19508428-8	2009	Further data reveal that the immediate PACAP-evoked stimulation involves a phospholipase C and protein kinase C-dependent pathway to facilitate calcium influx through a Ni2+ and mibefradil-sensitive calcium conductance that results in catecholamine release.	Mibefradil	178-188	adenylate cyclase activating polypeptide 1	Homo sapiens	39-44
19051152-3	2008	The high-profile withdrawal of drugs such as mibefradil from the market because of unfavorable drug-drug interaction profiles has focused efforts on screening for cytochrome P450 (CYP)-mediated drug interactions early in the discovery paradigm and on predicting the impact of inhibition on the in vivo situation.	Mibefradil	45-55	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	163-178
19051152-3	2008	The high-profile withdrawal of drugs such as mibefradil from the market because of unfavorable drug-drug interaction profiles has focused efforts on screening for cytochrome P450 (CYP)-mediated drug interactions early in the discovery paradigm and on predicting the impact of inhibition on the in vivo situation.	Mibefradil	45-55	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	180-183
20456010-7	2010	NaHS, but not dibutyryl cAMP, actually caused phosphorylation of Src, an effect blocked by 1,2-bis(2-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid acetoxymethyl, an intracellular Ca(2+) chelator, mibefradil or ascorbic acid.	Mibefradil	197-207	Rous sarcoma oncogene	Mus musculus	65-68
20394732-7	2010	Our findings showed that Ni(2+) and mibefradil at concentrations that block T-type or Ca(V)3 channels, and nimodipine and diltiazem that block L-type or Ca(V)1 channels, significantly inhibited the rhZP3-initiated AR.	Mibefradil	36-46	caveolin 3	Homo sapiens	86-92
20394732-7	2010	Our findings showed that Ni(2+) and mibefradil at concentrations that block T-type or Ca(V)3 channels, and nimodipine and diltiazem that block L-type or Ca(V)1 channels, significantly inhibited the rhZP3-initiated AR.	Mibefradil	36-46	caveolin 1	Homo sapiens	153-159
20028346-6	2010	Pre-treatment with Mibefradil abolishes Ang II -induced cell migration.	Mibefradil	19-29	angiotensinogen	Homo sapiens	40-46
20453553-7	2010	The intrathecal administration of Mib significantly suppressed thermal hyperalgesia and allodynia in CCD rats (p< 0.01), and the inhibitory effect lasted for 2 h. However, only Cav3.2 and Cav3.3 T-type calcium channel mRNA were detected in the lumbar spinal cord of rats, and there were no Cav3.1 calcium channels.	Mibefradil	34-37	caveolin 3	Rattus norvegicus	180-184
20453553-7	2010	The intrathecal administration of Mib significantly suppressed thermal hyperalgesia and allodynia in CCD rats (p< 0.01), and the inhibitory effect lasted for 2 h. However, only Cav3.2 and Cav3.3 T-type calcium channel mRNA were detected in the lumbar spinal cord of rats, and there were no Cav3.1 calcium channels.	Mibefradil	34-37	caveolin 3	Rattus norvegicus	191-195
20453553-7	2010	The intrathecal administration of Mib significantly suppressed thermal hyperalgesia and allodynia in CCD rats (p< 0.01), and the inhibitory effect lasted for 2 h. However, only Cav3.2 and Cav3.3 T-type calcium channel mRNA were detected in the lumbar spinal cord of rats, and there were no Cav3.1 calcium channels.	Mibefradil	34-37	caveolin 3	Rattus norvegicus	191-195
19787244-6	2009	Furthermore, the persistent increase of phosphorylated ERK1/2 in SNU449 cells was found when treated with Mibefradil.	Mibefradil	106-116	mitogen-activated protein kinase 3	Homo sapiens	55-61
19787244-9	2009	The cell proliferation reduction of SNU449 with Mibefradil treatment is possibly associated with the persistent increase of phosphorylated ERK1/2.	Mibefradil	48-58	mitogen-activated protein kinase 3	Homo sapiens	139-145
18974361-4	2009	The goal of this study was to identify compounds that block the Ca(v)3.2 T-type channel with high affinity, focusing on two classes of compounds: phenylalkylamines (e.g., mibefradil) and dihydropyridines (e.g., efonidipine).	Mibefradil	171-181	immunoglobulin lambda variable 7-43	Homo sapiens	64-72
18411403-0	2008	The mibefradil derivative NNC55-0396, a specific T-type calcium channel antagonist, exhibits less CYP3A4 inhibition than mibefradil.	Mibefradil	4-14	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	98-104
18498041-9	2008	Finally, islet release of IL-1beta in response to high glucose could be abrogated by nimodipine, mibefradil, or PD98059.	Mibefradil	97-107	interleukin 1 beta	Rattus norvegicus	26-34
18411403-4	2008	Our results show that CYP3A4 and CYP2D6 are the two P450s most affected by mibefradil, Ro40-5966, and NNC55-0396.	Mibefradil	75-85	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	22-28
18278483-3	2008	Furthermore, we compared the effects of R(-) efonidipine with those of flunarizine and mibefradil on both T-type and HVA Ca2+ channels in rat hippocampal CA1 neurons by using the nystatin perforated-patch clamp technique.	Mibefradil	87-97	carbonic anhydrase 2	Rattus norvegicus	121-124
18411403-4	2008	Our results show that CYP3A4 and CYP2D6 are the two P450s most affected by mibefradil, Ro40-5966, and NNC55-0396.	Mibefradil	75-85	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	33-39
18278483-3	2008	Furthermore, we compared the effects of R(-) efonidipine with those of flunarizine and mibefradil on both T-type and HVA Ca2+ channels in rat hippocampal CA1 neurons by using the nystatin perforated-patch clamp technique.	Mibefradil	87-97	carbonic anhydrase 1	Rattus norvegicus	154-157
18278483-4	2008	Flunarizine and mibefradil nonselectively inhibited both T-type and HVA Ca2+ channels, though the dose-dependent blocking potency of flunarizine on T-type Ca2+ channels was slightly stronger than that of mibefradil.	Mibefradil	16-26	carbonic anhydrase 2	Homo sapiens	72-75
17392390-8	2007	In addition, we established an automated assay to distinguish quasi-irreversible and irreversible binding to CYP3A in which the quasi-irreversible inhibitors such as diltiazem, verapamil, and nicardipine were dissociated from CYP3A by the addition of potassium ferricyanide, whereas the irreversible inhibitors such as clozapine, delavirdine, and mibefradil were not.	Mibefradil	347-357	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	109-114
18473851-4	2008	Some drugs (e.g. mibefradil) have been withdrawn from the market since they are eventually identified as CYP3A4 inactivators that can cause toxicity-related fatal events.	Mibefradil	17-27	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	105-111
18188587-0	2008	Facilitation of Ca2+-activated K+ channels (IKCa1) by mibefradil in B lymphocytes.	Mibefradil	54-64	potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4	Mus musculus	44-49
18188587-7	2008	In the inside-out patch clamp study with cloned murine IKCa1 (mIKCa1) in HEK-293, mibefradil increased both Ca2+ sensitivity and maximum activity of mIKCa1.	Mibefradil	82-92	potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4	Mus musculus	55-60
18188587-7	2008	In the inside-out patch clamp study with cloned murine IKCa1 (mIKCa1) in HEK-293, mibefradil increased both Ca2+ sensitivity and maximum activity of mIKCa1.	Mibefradil	82-92	potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4	Mus musculus	62-68
18188587-7	2008	In the inside-out patch clamp study with cloned murine IKCa1 (mIKCa1) in HEK-293, mibefradil increased both Ca2+ sensitivity and maximum activity of mIKCa1.	Mibefradil	82-92	potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4	Mus musculus	149-155
17172292-6	2007	Expression of recombinant Cav3.1 subunit in PAECs resulted in pronounced increase in thrombin-stimulated Ca2+ entry, which is sensitive to mibefradil.	Mibefradil	139-149	coagulation factor II	Rattus norvegicus	85-93
17190903-4	2007	NaN/Nav1.9 was inhibited by inorganic I(Ca) blockers as follows (IC(50), microM): La(3+) (46) > Cd(2+) (233) > Ni(2+) (892) and by mibefradil, a non-dihydropyridine I(Ca)T antagonist.	Mibefradil	137-147	sodium voltage-gated channel alpha subunit 11	Homo sapiens	0-3
17190903-4	2007	NaN/Nav1.9 was inhibited by inorganic I(Ca) blockers as follows (IC(50), microM): La(3+) (46) > Cd(2+) (233) > Ni(2+) (892) and by mibefradil, a non-dihydropyridine I(Ca)T antagonist.	Mibefradil	137-147	sodium voltage-gated channel alpha subunit 11	Homo sapiens	4-10
16951550-4	2006	Indeed, the level of cytotoxic reactive oxygen species (ROS) and the expression of pro-apoptotic Bax increased in response to oxidative stress in haloperidol-treated cells, and these effects were inhibited by verapamil, a specific L-type calcium channel blocker, but not by the T-type calcium channel blocker, mibefradil.	Mibefradil	310-320	BCL2 associated X, apoptosis regulator	Homo sapiens	97-100
16842760-7	2006	Angiotensin II-induced migration of endothelial cells in a wound healing model was inhibited by incubation with mibefradil, a T-type Ca2+ channel blocker.	Mibefradil	112-122	angiotensinogen	Homo sapiens	0-14
16354767-4	2006	Mibefradil, zinc, and mercuric ions inhibited TRESK expressed in Xenopus laevis oocytes with IC50 values lower than 10 microM.	Mibefradil	0-10	potassium channel, two pore domain subfamily K, member 18 L homeolog	Xenopus laevis	46-51
16706840-3	2006	MPOs were dependent on CaV3.3 channel activity given that they were recorded from a potential range of -55 to -70 mV, blocked by nickel and mibefradil, as well as by low external Ca2+ concentration.	Mibefradil	140-150	calcium channel, voltage-dependent, alpha 1I subunit	Mus musculus	23-29
16640832-7	2006	For example, the CL(hep, in-vivo) of mibefradil in donor GNG was 4.27 mL min(-1) kg(-1) in the presence of serum and 0.46 mL min(-1) kg(-1) in the absence of serum (4.88 mL min(-1) kg(-1) observed in-vivo).	Mibefradil	37-47	CD59 molecule (CD59 blood group)	Homo sapiens	73-79
16640832-7	2006	For example, the CL(hep, in-vivo) of mibefradil in donor GNG was 4.27 mL min(-1) kg(-1) in the presence of serum and 0.46 mL min(-1) kg(-1) in the absence of serum (4.88 mL min(-1) kg(-1) observed in-vivo).	Mibefradil	37-47	CD59 molecule (CD59 blood group)	Homo sapiens	125-131
16640832-7	2006	For example, the CL(hep, in-vivo) of mibefradil in donor GNG was 4.27 mL min(-1) kg(-1) in the presence of serum and 0.46 mL min(-1) kg(-1) in the absence of serum (4.88 mL min(-1) kg(-1) observed in-vivo).	Mibefradil	37-47	CD59 molecule (CD59 blood group)	Homo sapiens	125-131
16077260-7	2005	The pretreatment with thapsigargin (a blocker of IP3-mediated intracellular calcium release) prevented the angiotensin II-induced afferent arteriolar constriction in WKY, but caused a significant constriction of afferent arterioles in SHR and efferent arterioles in WKY and SHR; in this setting, mibefradil did not alter efferent arteriolar tone.	Mibefradil	296-306	angiotensinogen	Rattus norvegicus	107-121
16424797-6	2006	Notably, efonidipine and mibefradil also significantly suppressed Ang II- and K+-induced mRNA expression of 11-beta-hydroxylase and aldosterone synthase, which catalyze the final two steps in the aldosterone synthesis, whereas nifedipine reduced only K+-induced enzyme expression.	Mibefradil	25-35	angiotensinogen	Homo sapiens	66-72
16424797-6	2006	Notably, efonidipine and mibefradil also significantly suppressed Ang II- and K+-induced mRNA expression of 11-beta-hydroxylase and aldosterone synthase, which catalyze the final two steps in the aldosterone synthesis, whereas nifedipine reduced only K+-induced enzyme expression.	Mibefradil	25-35	cytochrome P450 family 11 subfamily B member 2	Homo sapiens	132-152
15860655-8	2005	Direct comparison of known mechanism-based inactivators and quasi-irreversible inhibitors, based on our screening of apparent partition ratios, has identified ritonavir, mibefradil, and azamulin as highly effective mechanism-based inactivators; e.g., 1 mol of CYP3A4 was inactivated on turnover of about 2 mol of compound.	Mibefradil	170-180	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	260-266
16306443-6	2006	These results demonstrate that the effect of the putative T-type Ca2+ channel-selective blocker mibefradil on blood pressure and small vessel myogenic tone is mediated by the Cav1.2 L-type Ca2+ channel.	Mibefradil	96-106	calcium channel, voltage-dependent, L type, alpha 1C subunit	Mus musculus	175-181
12382075-6	2002	Mibefradil also inhibited the Na(+)/Ca(2+) exchanger-mediated Ca(2+) uptake, although at 3.7 times lower potency (IC(23%)=26 microM).	Mibefradil	0-10	solute carrier family 8 member A1	Homo sapiens	30-52
15562257-3	2004	Mibefradil blocked Nav1.5 in a use/frequency-dependent manner, indicating preferential binding to states visited during depolarization.	Mibefradil	0-10	sodium voltage-gated channel alpha subunit 5	Homo sapiens	19-25
15562257-4	2004	Mibefradil blocked currents of all Na+ channel isoforms with similar affinity and a dependence on holding potential, and drug off-rate was slowed at depolarized potentials (k(off) was 0.024/s at -130 mV and 0.007/s at -100 mV for Nav1.5).	Mibefradil	0-10	sodium voltage-gated channel alpha subunit 5	Homo sapiens	230-236
15562257-5	2004	We further probed the interaction of mibefradil with inactivated Nav1.5 channels.	Mibefradil	37-47	sodium voltage-gated channel alpha subunit 5	Homo sapiens	65-71
15562257-9	2004	When selectively applied to channels after inducing slow inactivation with a 60-s pulse to -10 mV, mibefradil (1 microM) produced 45% fractional block in Nav1.5 and greater block (88%) in an isoform (Nav1.4) that slow-inactivates more completely.	Mibefradil	99-109	sodium voltage-gated channel alpha subunit 5	Homo sapiens	154-160
15562257-9	2004	When selectively applied to channels after inducing slow inactivation with a 60-s pulse to -10 mV, mibefradil (1 microM) produced 45% fractional block in Nav1.5 and greater block (88%) in an isoform (Nav1.4) that slow-inactivates more completely.	Mibefradil	99-109	sodium voltage-gated channel alpha subunit 4	Homo sapiens	200-206
14639089-1	2003	Although nifedipine and other conventional calcium antagonists elicit preferential vasodilation of renal afferent arterioles, we demonstrate that mibefradil and nickel, T-type calcium channel blockers, reverse the angiotensin II-induced constriction of both afferent and efferent arterioles.	Mibefradil	146-156	angiotensinogen	Rattus norvegicus	214-228
14639089-2	2003	Since the angiotensin II-induced vasoconstriction involves inositol trisphosphate (IP3)-induced calcium release from the sarcoplasmic reticulum in the afferent arteriole, and both IP3- and protein kinase C (PKC)-mediated pathways in the efferent arteriole, we investigated the cellular mechanism for the mibefradil-induced dilation of angiotensin II-constricted renal arterioles, using the isolated perfused hydronephrotic rat kidney.	Mibefradil	304-314	angiotensinogen	Rattus norvegicus	10-24
14639089-3	2003	Mibefradil caused a dose-dependent dilation of angiotensin II-constricted afferent and efferent arterioles, with 88 +/- 9% and 74 +/- 10% reversal observed at 1 micromol/L, respectively.	Mibefradil	0-10	angiotensinogen	Rattus norvegicus	47-61
14639089-8	2003	In summary, mibefradil markedly dilates the angiotensin II-induced renal arteriolar constriction; the action of mibefradil is most likely mediated by the inhibition of the IP3-mediated pathway, but the inhibitory action on the PKC pathway appears modest.	Mibefradil	12-22	angiotensinogen	Rattus norvegicus	44-58
14639089-8	2003	In summary, mibefradil markedly dilates the angiotensin II-induced renal arteriolar constriction; the action of mibefradil is most likely mediated by the inhibition of the IP3-mediated pathway, but the inhibitory action on the PKC pathway appears modest.	Mibefradil	112-122	angiotensinogen	Rattus norvegicus	44-58
12895515-3	2003	Local reverse dialysis administration of 0.1-10 microM of the Ca(v)2.3 inhibitor SNX-482, or 100 microM of mibefradil, decreased the concentrations of dopamine and its metabolites in dialysate from substantia nigra, whereas 1 microM mibefradil or 40-80 microM nickel(II) induced an increase in nigral dialysate dopamine concentrations.	Mibefradil	233-243	calcium voltage-gated channel subunit alpha1 E	Rattus norvegicus	62-70
15589991-3	2005	Both serum starvation and application of mibefradil, a selective T-type calcium channel antagonist, resulted in a 50% decrease in the expression of alpha1G and alpha1H and a 700-900% increase in levels of cyclin D1 in U87MG and N1E-115 cells, respectively.	Mibefradil	41-51	cyclin D1	Homo sapiens	205-214
15069564-9	2004	RESULTS: Mibefradil induced apoptosis in hLEC.	Mibefradil	9-19	C-C motif chemokine ligand 16	Homo sapiens	41-45
11854450-0	2002	Single-channel pharmacology of mibefradil in human native T-type and recombinant Ca(v)3.2 calcium channels.	Mibefradil	31-41	immunoglobulin lambda variable 7-43	Homo sapiens	81-89
11854450-11	2002	Along all criteria examined (mechanisms of block, extent of block), recombinant Ca(v)3.2 interact with mibefradil in the same way as their native counterparts expressed in hMTC cells.	Mibefradil	103-113	immunoglobulin lambda variable 7-43	Homo sapiens	80-88
11728963-6	2001	Of note, P(GC) also was reduced by a similar extent (and to the sham value) with both mibefradil (58 +/- 2 mm Hg; P < 0.001) and amlodipine (61 +/- 2 mm Hg; P < 0.005) versus untreated DOCA-salt rats (70 +/- 1 mm Hg).	Mibefradil	86-96	progastricsin	Rattus norvegicus	9-14
11719851-0	2001	State-dependent inhibition of inactivation-deficient Ca(V)1.2 and Ca(V)2.3 channels by mibefradil.	Mibefradil	87-97	immunoglobulin lambda variable 2-8	Homo sapiens	53-61
11719851-0	2001	State-dependent inhibition of inactivation-deficient Ca(V)1.2 and Ca(V)2.3 channels by mibefradil.	Mibefradil	87-97	calcium voltage-gated channel subunit alpha1 E	Homo sapiens	66-74
11719851-4	2001	In the presence of mibefradil, Ca(V)1.2 and Ca(V)2.3 experienced significant use-dependent inhibition (0.1 to 1 Hz) and slower recovery from inactivation suggesting mibefradil could promote transition(s) to an absorbing inactivated state.	Mibefradil	19-29	immunoglobulin lambda variable 2-8	Homo sapiens	31-39
11719851-4	2001	In the presence of mibefradil, Ca(V)1.2 and Ca(V)2.3 experienced significant use-dependent inhibition (0.1 to 1 Hz) and slower recovery from inactivation suggesting mibefradil could promote transition(s) to an absorbing inactivated state.	Mibefradil	19-29	calcium voltage-gated channel subunit alpha1 E	Homo sapiens	44-52
11719851-4	2001	In the presence of mibefradil, Ca(V)1.2 and Ca(V)2.3 experienced significant use-dependent inhibition (0.1 to 1 Hz) and slower recovery from inactivation suggesting mibefradil could promote transition(s) to an absorbing inactivated state.	Mibefradil	165-175	immunoglobulin lambda variable 2-8	Homo sapiens	31-39
11719851-4	2001	In the presence of mibefradil, Ca(V)1.2 and Ca(V)2.3 experienced significant use-dependent inhibition (0.1 to 1 Hz) and slower recovery from inactivation suggesting mibefradil could promote transition(s) to an absorbing inactivated state.	Mibefradil	165-175	calcium voltage-gated channel subunit alpha1 E	Homo sapiens	44-52
11719851-9	2001	The slower Ca(V)1.2 wild-type and Ca(V)1.2 Q473K channels responded to higher doses of mibefradil with IC(50) approximately 100-120 microm.	Mibefradil	87-97	immunoglobulin lambda variable 2-8	Homo sapiens	11-19
11719851-9	2001	The slower Ca(V)1.2 wild-type and Ca(V)1.2 Q473K channels responded to higher doses of mibefradil with IC(50) approximately 100-120 microm.	Mibefradil	87-97	immunoglobulin lambda variable 2-8	Homo sapiens	34-42
11719851-10	2001	Mibefradil was also found to significantly speed up the inactivation kinetics of slower channels (Ca(V)1.2, CEEE) with little effect on the inactivation kinetics of faster-inactivating channels (Ca(V)2.3).	Mibefradil	0-10	immunoglobulin lambda variable 2-8	Homo sapiens	98-106
11046117-2	2000	Mibefradil inhibited in a concentration-dependent manner the hKv1.5 current with a K(D) value of 0.78 +/- 0.05 microM and a Hill coefficient of 0.97 +/- 0.06.	Mibefradil	0-10	potassium voltage-gated channel subfamily A member 5	Homo sapiens	61-67
11046117-8	2000	In the presence of mibefradil, recovery of inactivation was faster than under control conditions, suggesting that mibefradil might compete with the inactivation gate of hKv1.5.	Mibefradil	19-29	potassium voltage-gated channel subfamily A member 5	Homo sapiens	169-175
12374895-7	2002	Mibefradil was able to significantly inhibit the formyl-methionyl-leucyl-phenylalanine (fMLP) induced calcium rise, which suggests that mibefradil interfered with integrin signaling through blocking the intracellular calcium rise.	Mibefradil	0-10	formyl peptide receptor 1	Homo sapiens	88-92
12374895-7	2002	Mibefradil was able to significantly inhibit the formyl-methionyl-leucyl-phenylalanine (fMLP) induced calcium rise, which suggests that mibefradil interfered with integrin signaling through blocking the intracellular calcium rise.	Mibefradil	136-146	formyl peptide receptor 1	Homo sapiens	88-92
11325526-14	2001	Mibefradil inhibited K+- and AngII-induced secretion at concentrations similar to that for T channel inhibition; at high concentrations (10 microM) mibefradil inhibited AngII-induced secretion by 88% and completely inhibited K+-induced secretion.	Mibefradil	0-10	angiotensinogen	Rattus norvegicus	29-34
11325526-14	2001	Mibefradil inhibited K+- and AngII-induced secretion at concentrations similar to that for T channel inhibition; at high concentrations (10 microM) mibefradil inhibited AngII-induced secretion by 88% and completely inhibited K+-induced secretion.	Mibefradil	148-158	angiotensinogen	Rattus norvegicus	169-174
11325526-16	2001	Mibefradil exhibited an IC50 of 1.1 microM for inhibition of secretion at all AngII concentrations examined (0.1, 1.0, and 10 nM).	Mibefradil	0-10	angiotensinogen	Rattus norvegicus	78-83
11325526-17	2001	Mibefradil also exhibited multiple nonspecific effects, which complicated the assessment of T channel function, including; inhibition of leak and voltage-dependent K+ conductances, inhibition of Ca2+-independent aldosterone secretion, and inhibition of secretion under conditions expected to completely inactivate T channels (10 nM AngII or 20 mM K+).	Mibefradil	0-10	angiotensinogen	Rattus norvegicus	332-337
11087244-11	2000	Mibefradil inhibited ANP secretion and ANP concentration in contrast with the L-type Ca(2+) channel inhibitor.	Mibefradil	0-10	natriuretic peptides A	Oryctolagus cuniculus	21-24
11087244-11	2000	Mibefradil inhibited ANP secretion and ANP concentration in contrast with the L-type Ca(2+) channel inhibitor.	Mibefradil	0-10	natriuretic peptides A	Oryctolagus cuniculus	39-42