PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
23221912-6	2013	In this study, we show that block of WT HERG by bepridil and terfenadine, two drugs previously shown to be trapped inside the HERG channel after the channel closes, is insensitive to extracellular potassium over the range of 0 mM to 20 mM.	Bepridil	48-56	potassium voltage-gated channel subfamily H member 2	Homo sapiens	40-44
24260442-6	2013	This led to the identification of Bepridil, a calcium channel antagonist drug in addition to four further lead structures capable of normalizing the potentiated FAD-PS1-induced calcium release from ER.	Bepridil	34-42	presenilin 1	Homo sapiens	165-168
24260442-6	2013	This led to the identification of Bepridil, a calcium channel antagonist drug in addition to four further lead structures capable of normalizing the potentiated FAD-PS1-induced calcium release from ER.	Bepridil	34-42	epiregulin	Homo sapiens	198-200
24260442-7	2013	Interestingly, it has recently been reported that Bepridil can reduce Abeta production by lowering BACE1 activity.	Bepridil	50-58	amyloid beta precursor protein	Homo sapiens	70-75
24260442-7	2013	Interestingly, it has recently been reported that Bepridil can reduce Abeta production by lowering BACE1 activity.	Bepridil	50-58	beta-secretase 1	Homo sapiens	99-104
24260442-8	2013	Indeed, we also detected lowered Abeta, increased sAPPalpha and decreased sAPPbeta fragment levels upon Bepridil treatment.	Bepridil	104-112	amyloid beta precursor protein	Homo sapiens	33-38
24574578-4	2013	Bepridil decreased the protein levels of both Bax and cytochrome c of cells expressing E334K MyBPC-GFP with no changes in p53 and Bcl-2, while amiodarone decreased cytochrome c but did not influence Bax except in its highest concentration.	Bepridil	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	46-49
24574578-4	2013	Bepridil decreased the protein levels of both Bax and cytochrome c of cells expressing E334K MyBPC-GFP with no changes in p53 and Bcl-2, while amiodarone decreased cytochrome c but did not influence Bax except in its highest concentration.	Bepridil	0-8	cytochrome c, somatic	Homo sapiens	54-66
24574578-4	2013	Bepridil decreased the protein levels of both Bax and cytochrome c of cells expressing E334K MyBPC-GFP with no changes in p53 and Bcl-2, while amiodarone decreased cytochrome c but did not influence Bax except in its highest concentration.	Bepridil	0-8	myosin binding protein C3	Homo sapiens	93-98
24574578-4	2013	Bepridil decreased the protein levels of both Bax and cytochrome c of cells expressing E334K MyBPC-GFP with no changes in p53 and Bcl-2, while amiodarone decreased cytochrome c but did not influence Bax except in its highest concentration.	Bepridil	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	199-202
23740383-5	2013	While the beta blocker carvedilol (1 muM) normalized the level of p53 and Bcl-2 and the calcium channel blocker (CCB) bepridil (0.5 muM) normalized that of Bcl-2, both the CCB azelnidipine (1 muM) and the angiotensin receptor blocker (ARB) olmesartan (10 muM) normalized those of p53, Bax, cytochrome c, and Bcl-XL.	Bepridil	118-126	latexin	Homo sapiens	132-135
23740383-5	2013	While the beta blocker carvedilol (1 muM) normalized the level of p53 and Bcl-2 and the calcium channel blocker (CCB) bepridil (0.5 muM) normalized that of Bcl-2, both the CCB azelnidipine (1 muM) and the angiotensin receptor blocker (ARB) olmesartan (10 muM) normalized those of p53, Bax, cytochrome c, and Bcl-XL.	Bepridil	118-126	BCL2 apoptosis regulator	Homo sapiens	156-161
23740383-5	2013	While the beta blocker carvedilol (1 muM) normalized the level of p53 and Bcl-2 and the calcium channel blocker (CCB) bepridil (0.5 muM) normalized that of Bcl-2, both the CCB azelnidipine (1 muM) and the angiotensin receptor blocker (ARB) olmesartan (10 muM) normalized those of p53, Bax, cytochrome c, and Bcl-XL.	Bepridil	118-126	latexin	Homo sapiens	132-135
23740383-5	2013	While the beta blocker carvedilol (1 muM) normalized the level of p53 and Bcl-2 and the calcium channel blocker (CCB) bepridil (0.5 muM) normalized that of Bcl-2, both the CCB azelnidipine (1 muM) and the angiotensin receptor blocker (ARB) olmesartan (10 muM) normalized those of p53, Bax, cytochrome c, and Bcl-XL.	Bepridil	118-126	latexin	Homo sapiens	132-135
23221912-6	2013	In this study, we show that block of WT HERG by bepridil and terfenadine, two drugs previously shown to be trapped inside the HERG channel after the channel closes, is insensitive to extracellular potassium over the range of 0 mM to 20 mM.	Bepridil	48-56	potassium voltage-gated channel subfamily H member 2	Homo sapiens	126-130
23221912-7	2013	We also show that bepridil block of the HERG mutant D540K, a mutant channel that is unable to trap drugs, is dependent on extracellular potassium, correlates with the permeant ion, and is independent of HERG inactivation.	Bepridil	18-26	potassium voltage-gated channel subfamily H member 2	Homo sapiens	40-44
21586280-8	2011	Rg(3) actions were blocked by bepridil, a hERG K(+) channel antagonist.	Bepridil	30-38	ETS transcription factor ERG	Homo sapiens	42-46
22805236-7	2012	Conversely, bepridil treatment restored seladin-1/DHCR24 expression in the ipsilateral thalamus.	Bepridil	12-20	24-dehydrocholesterol reductase	Rattus norvegicus	40-49
22805236-7	2012	Conversely, bepridil treatment restored seladin-1/DHCR24 expression in the ipsilateral thalamus.	Bepridil	12-20	24-dehydrocholesterol reductase	Rattus norvegicus	50-56
21193236-11	2012	Down-regulation of Cx43 was partly suppressed in the Olm group while that of LCC, SCN5A, and Cx43 was suppressed in the Olm+Bep group.	Bepridil	124-127	gap junction protein alpha 1	Canis lupus familiaris	19-23
21193236-11	2012	Down-regulation of Cx43 was partly suppressed in the Olm group while that of LCC, SCN5A, and Cx43 was suppressed in the Olm+Bep group.	Bepridil	124-127	sodium voltage-gated channel alpha subunit 5	Canis lupus familiaris	82-87
21193236-11	2012	Down-regulation of Cx43 was partly suppressed in the Olm group while that of LCC, SCN5A, and Cx43 was suppressed in the Olm+Bep group.	Bepridil	124-127	gap junction protein alpha 1	Canis lupus familiaris	93-97
21332124-5	2011	The results indicated that bepridil binding within the hydrophobic pocket of cardiac TnC decreases the interaction of TnC with TnI at both the N-domain of TnC and the C-domain of TnC, and decreases the correlations of motions among the segments of the troponin subunits.	Bepridil	27-35	tenascin C	Homo sapiens	85-88
21696229-4	2011	Bepridil, identified as a calcium sensitizer to TnC, has been experimentally found to bind to the N-domain pocket of TnC but with negative cooperativity.	Bepridil	0-8	tenascin C	Homo sapiens	48-51
21696229-4	2011	Bepridil, identified as a calcium sensitizer to TnC, has been experimentally found to bind to the N-domain pocket of TnC but with negative cooperativity.	Bepridil	0-8	tenascin C	Homo sapiens	117-120
21332124-5	2011	The results indicated that bepridil binding within the hydrophobic pocket of cardiac TnC decreases the interaction of TnC with TnI at both the N-domain of TnC and the C-domain of TnC, and decreases the correlations of motions among the segments of the troponin subunits.	Bepridil	27-35	tenascin C	Homo sapiens	118-121
21332124-5	2011	The results indicated that bepridil binding within the hydrophobic pocket of cardiac TnC decreases the interaction of TnC with TnI at both the N-domain of TnC and the C-domain of TnC, and decreases the correlations of motions among the segments of the troponin subunits.	Bepridil	27-35	tenascin C	Homo sapiens	118-121
21332124-5	2011	The results indicated that bepridil binding within the hydrophobic pocket of cardiac TnC decreases the interaction of TnC with TnI at both the N-domain of TnC and the C-domain of TnC, and decreases the correlations of motions among the segments of the troponin subunits.	Bepridil	27-35	tenascin C	Homo sapiens	118-121
21332124-6	2011	The estimated calcium-binding affinities using MMPBSA showed that bepridil has a sensitizing effect for the isolated system of TnC, but loses this effect for the complex.	Bepridil	66-74	tenascin C	Homo sapiens	127-130
20625312-0	2010	Efficacy of low-dose bepridil for prevention of ventricular fibrillation in patients with Brugada syndrome with and without SCN5A mutation.	Bepridil	21-29	sodium voltage-gated channel alpha subunit 5	Homo sapiens	124-129
21289198-5	2011	Furthermore, clinically used alkalizing drugs, including chloroquine, bepridil, and amiodarone, similarly stimulate GRN production.	Bepridil	70-78	granulin precursor	Homo sapiens	116-119
21292685-9	2011	Furthermore, subtoxic doses of bepridil and cibenzoline, two other anti-arrhythmic drugs with NCX-inhibitor activity, also sensitized glioma cells to TRAIL-mediated apoptosis, via the upregulation of both CHOP and DR5.	Bepridil	31-39	TNF superfamily member 10	Homo sapiens	150-155
21292685-9	2011	Furthermore, subtoxic doses of bepridil and cibenzoline, two other anti-arrhythmic drugs with NCX-inhibitor activity, also sensitized glioma cells to TRAIL-mediated apoptosis, via the upregulation of both CHOP and DR5.	Bepridil	31-39	DNA damage inducible transcript 3	Homo sapiens	205-209
21292685-9	2011	Furthermore, subtoxic doses of bepridil and cibenzoline, two other anti-arrhythmic drugs with NCX-inhibitor activity, also sensitized glioma cells to TRAIL-mediated apoptosis, via the upregulation of both CHOP and DR5.	Bepridil	31-39	TNF receptor superfamily member 10b	Homo sapiens	214-217
20647042-5	2010	In fact, inhibition of the Na(+)/Ca(++) exchanger with bepridil or with KB-R7943, which selectively blocks the reverse mode of the exchanger, reduced the frequency of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from striatal neurons in EAE mice but not in control animals.	Bepridil	55-63	solute carrier family 8 (sodium/calcium exchanger), member 1	Mus musculus	27-49
20647042-6	2010	In the presence of tetrodotoxin (TTX), a blocker of voltage-dependent Na(+) channels, the effect of bepridil was normalized in acute (25 days post-immunization) EAE mice, indicating that axonal accumulation of Na(+) ions flowing through voltage-dependent Na(+) channels plays a role in the abnormal activity of the Na(+)/Ca(++) exchanger in EAE.	Bepridil	100-108	solute carrier family 8 (sodium/calcium exchanger), member 1	Mus musculus	315-337
20625312-3	2010	Among 130 patients with Brugada-type electrocardiogram (ECG), low-dose bepridil was administered to seven patients because of repetitive VF episodes, including three with and four without SCN5A mutation.	Bepridil	71-79	sodium voltage-gated channel alpha subunit 5	Homo sapiens	188-193
20625312-5	2010	Frequencies of VF episodes were reduced after treatment with low-dose bepridil in all three patients with the SCN5A mutation (before: 0.33 versus after: 0.02 episodes/month, P < 0.01), but not in all four patients without the SCN5A mutation (before: 0.43 versus after: 2.94 episodes/month, P = nonsignificant).	Bepridil	70-78	sodium voltage-gated channel alpha subunit 5	Homo sapiens	110-115
20625312-5	2010	Frequencies of VF episodes were reduced after treatment with low-dose bepridil in all three patients with the SCN5A mutation (before: 0.33 versus after: 0.02 episodes/month, P < 0.01), but not in all four patients without the SCN5A mutation (before: 0.43 versus after: 2.94 episodes/month, P = nonsignificant).	Bepridil	70-78	sodium voltage-gated channel alpha subunit 5	Homo sapiens	229-234
20625312-7	2010	Treatment with bepridil prevented recurrence of VF along with improvement of ST elevation and LAS40 in patients with Brugada syndrome with the SCN5A mutation.	Bepridil	15-23	sodium voltage-gated channel alpha subunit 5	Homo sapiens	143-148
19498275-4	2009	Amiodarone and bepridil potently inhibited the HCN4 channel current with IC50 values of 4.5 and 4.9 microM, respectively, which were close to their therapeutic concentrations.	Bepridil	15-23	hyperpolarization activated cyclic nucleotide gated potassium channel 4	Homo sapiens	47-51
19371335-12	2009	CONCLUSIONS AND IMPLICATIONS: We conclude that long-term exposure of cardiomyocytes to bepridil at therapeutic concentrations inhibits calmodulin action, which decreased degradation of the Na(v)1.5 alpha-subunit, which in turn increased Na+ current.	Bepridil	87-95	immunoglobulin lambda variable 2-18	Homo sapiens	189-197
20381614-6	2010	The most potent inhibitors of rOatp and rOct1 were dantrolene sodium (K(i)=2 +/- 9 microM) and bepridil (K(i)=14 +/- 2 microM), respectively.	Bepridil	95-103	solute carrier family 22 member 1	Rattus norvegicus	40-45
18277608-7	2008	Furthermore, we found that the response is inhibited by bepridil and Ni2+, specific inhibitors of Na+-Ca2+-exchanger, suggesting involvement of Na+-Ca2+ exchanger in the DMS-induced [Ca2+]i increase in colon cancer cells.	Bepridil	56-64	solute carrier family 8 member A1	Homo sapiens	144-162
18219173-12	2008	The mRNA downregulation of the LCC and SCN5A was negated by bepridil administration in the RA; but not in the LA; however, the data showed similar tendencies.	Bepridil	60-68	sodium voltage-gated channel alpha subunit 5	Canis lupus familiaris	39-44
17267549-4	2007	Extracellular application of nicotine, bepridil, correolide, and endothelin-1 (ET-1) all significantly and reversibly reduced the Kv1.5 currents, while nicotine and bepridil also accelerated the inactivation kinetics of the currents.	Bepridil	39-47	potassium voltage-gated channel subfamily A member 5	Homo sapiens	130-135
17267549-4	2007	Extracellular application of nicotine, bepridil, correolide, and endothelin-1 (ET-1) all significantly and reversibly reduced the Kv1.5 currents, while nicotine and bepridil also accelerated the inactivation kinetics of the currents.	Bepridil	165-173	endothelin 1	Homo sapiens	65-77
17267549-4	2007	Extracellular application of nicotine, bepridil, correolide, and endothelin-1 (ET-1) all significantly and reversibly reduced the Kv1.5 currents, while nicotine and bepridil also accelerated the inactivation kinetics of the currents.	Bepridil	165-173	potassium voltage-gated channel subfamily A member 5	Homo sapiens	130-135
17395860-6	2007	RESULTS: Bepridil, an inhibitor of NCX, reduced in a concentration-dependent manner (IC(50)=68 micromol/L) the field potential amplitude recorded from the peri-infarct area of corticostriatal slices.	Bepridil	9-17	solute carrier family 8 member A1	Rattus norvegicus	35-38
17395860-8	2007	The effect of bepridil was mimicked by 5-(N-4-chlorobenzyl)-2",4"-dimethylbenzamil (CB-DMB) (IC(50)=6 micromol/L), a more selective inhibitor of NCX.	Bepridil	14-22	solute carrier family 8 member A1	Rattus norvegicus	145-148
16876206-4	2006	Two known blockers of KNa channels, bepridil and quinidine, inhibited Slack currents in a concentration-dependent manner and decreased channel activity in excised membrane patches.	Bepridil	36-44	potassium sodium-activated channel subfamily T member 1	Homo sapiens	70-75
16876114-4	2006	The expressed current of KCNQ4 showed the half-maximal activation (V(1/2)) was -17.8 mV and blocked almost completely by KCNQ4 channel blockers, linopirdine (300 microM) or bepridil (200 microM).	Bepridil	173-181	potassium voltage-gated channel subfamily Q member 4	Homo sapiens	25-30
16876114-7	2006	Furthermore, the increased effect of ionomycin on KCNQ4 current is abolished by pretreatment of linopirdine or bepridil.	Bepridil	111-119	potassium voltage-gated channel subfamily Q member 4	Homo sapiens	50-55
16876206-5	2006	The inhibition by bepridil was potent, with an IC50 of 1.0 microM for inhibition of Slack currents in HEK cells.	Bepridil	18-26	potassium sodium-activated channel subfamily T member 1	Homo sapiens	84-89
16174795-8	2006	Bepridil (10 microM) completely inhibited the pinacidil-induced Kir6.2+SUR2A channel current expressed in HEK 293 cells.	Bepridil	0-8	potassium inwardly rectifying channel subfamily J member 11	Homo sapiens	64-70
16603928-4	2006	Here, we demonstrate that bepridil-sensitive Ca extrusion (indicative of Na(+)/Ca(2+) exchanger activity) is suppressed following 24 h hypoxia (2.5 or 1% O2) owing to a loss of Na(+)/Ca(2+) exchanger expression, as determined using immunocytochemistry and Western blots.	Bepridil	26-34	nascent polypeptide associated complex subunit alpha 2	Homo sapiens	73-84
16603928-4	2006	Here, we demonstrate that bepridil-sensitive Ca extrusion (indicative of Na(+)/Ca(2+) exchanger activity) is suppressed following 24 h hypoxia (2.5 or 1% O2) owing to a loss of Na(+)/Ca(2+) exchanger expression, as determined using immunocytochemistry and Western blots.	Bepridil	26-34	solute carrier family 8 member A1	Homo sapiens	73-95
16508157-6	2006	In addition, aprindine seemed to reduce the oral clearance of bepridil in the patients with the CYP2D6*10 allele.	Bepridil	62-70	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	96-102
16474003-2	2006	Here, we characterized the molecular mechanism of hERG block by two low-potency drugs (Nifekalant and bepridil) and two high-potency drugs 1-[2-(6-methyl-2pyridyl)ethyl]-4-(4-methylsulfonyl aminobenzoyl)piperidine (E-4031) and dofetilide).	Bepridil	102-110	ETS transcription factor ERG	Homo sapiens	50-54
15855830-0	2005	Voltage-dependent and frequency-independent inhibition of recombinant Cav3.2 T-type Ca2+ channel by bepridil.	Bepridil	100-108	calcium voltage-gated channel subunit alpha1 H	Homo sapiens	70-76
15855830-1	2005	Effects of bepridil on the low voltage-activated T-type Ca2+ channel (CaV3.2) current stably expressed in human embryonic kidney (HEK)-293 cells were examined using patch-clamp techniques.	Bepridil	11-19	calcium voltage-gated channel subunit alpha1 H	Homo sapiens	70-76
15351857-6	2004	The calcium rise is mediated primarily by induction of a calcium entry mechanism involving the Na(+)-Ca(2+) exchanger operating in reverse mode, since it was blocked by inhibitors of Na(+)-Ca(2+) exchange, bepridil and 5 mM NiCl(2).	Bepridil	206-214	solute carrier family 8 member A1	Homo sapiens	95-117
15730865-6	2005	And the Ca2+ influx resulting from the reverse mode of NCX was significantly reduced by 2-[2-[4-(4-nitrobenyloxy) phenyl] ethyl] isothiourea methanesulfonate, while the Ca2+ efflux via forward mode was inhibited by bepridil.	Bepridil	215-223	solute carrier family 8 member A1	Rattus norvegicus	55-58
14975699-8	2004	All NCX inhibitors, GLU-XIP, CB-DMB and bepridil, caused a worsening of the brain infarct lesion.	Bepridil	40-48	solute carrier family 8 member A1	Rattus norvegicus	4-7
14716203-1	2004	Whole-cell patch-clamp techniques were employed to examine the effects of bepridil, a Ca2+ channel blocker with Vaughan Williams class III action, on a slow component of cardiac delayed rectifier K+ current (IKs), which was reconstituted in HEK293 cells by transfecting KCNQ1 and KCNE1.	Bepridil	74-82	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	270-275
14716203-1	2004	Whole-cell patch-clamp techniques were employed to examine the effects of bepridil, a Ca2+ channel blocker with Vaughan Williams class III action, on a slow component of cardiac delayed rectifier K+ current (IKs), which was reconstituted in HEK293 cells by transfecting KCNQ1 and KCNE1.	Bepridil	74-82	potassium voltage-gated channel subfamily E regulatory subunit 1	Homo sapiens	280-285
14716203-2	2004	Micromolar bepridil inhibited tail currents carried by KCNQ1/KCNE1 channels in a concentration-dependent manner (IC50 = 5.3 +/- 0.7 microM at -40 mV from 1000 milliseconds test pulse).	Bepridil	11-19	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	55-60
14716203-2	2004	Micromolar bepridil inhibited tail currents carried by KCNQ1/KCNE1 channels in a concentration-dependent manner (IC50 = 5.3 +/- 0.7 microM at -40 mV from 1000 milliseconds test pulse).	Bepridil	11-19	potassium voltage-gated channel subfamily E regulatory subunit 1	Homo sapiens	61-66
12297528-5	2002	The increase in the [Ca(2+)](i) was due to Ca(2+) influx since it was abolished in the absence of extracellular Ca(2+), and the increase was mediated by the Na(+)/Ca(2+) exchanger since it was blocked by the application of amiloride or bepridil, inhibitors of Na(+)/Ca(2+) exchange.	Bepridil	236-244	solute carrier family 8 member A1	Homo sapiens	157-179
12887970-9	2003	The half-time for decay of the ET-1 and ATP calcium peak was increased several folds by bepridil, ouabain and low-sodium conditions.	Bepridil	88-96	endothelin 1	Homo sapiens	31-35
11591369-0	2001	Interaction of bepridil with the cardiac troponin C/troponin I complex.	Bepridil	15-23	troponin C1, slow skeletal and cardiac type	Homo sapiens	33-51
12060657-0	2002	Structure of the regulatory N-domain of human cardiac troponin C in complex with human cardiac troponin I147-163 and bepridil.	Bepridil	117-125	troponin C1, slow skeletal and cardiac type	Homo sapiens	46-64
12060657-5	2002	In this work, we used two-dimensional (1)H,(15)N-heteronuclear single quantum coherence (HSQC) NMR spectroscopy to examine the binding of bepridil to cNTnC.Ca(2+) in the absence and presence of cTnI(147-163) and of cTnI(147-163) to cNTnC.Ca(2+) in the absence and presence of bepridil.	Bepridil	138-146	troponin I3, cardiac type	Homo sapiens	194-198
12060657-5	2002	In this work, we used two-dimensional (1)H,(15)N-heteronuclear single quantum coherence (HSQC) NMR spectroscopy to examine the binding of bepridil to cNTnC.Ca(2+) in the absence and presence of cTnI(147-163) and of cTnI(147-163) to cNTnC.Ca(2+) in the absence and presence of bepridil.	Bepridil	138-146	troponin I3, cardiac type	Homo sapiens	215-219
12060657-7	2002	The affinity of cTnI(147-163) for cNTnC.Ca(2+) is reduced approximately 3.5-fold by bepridil and vice versa.	Bepridil	84-92	troponin I3, cardiac type	Homo sapiens	16-20
12060657-8	2002	Using multinuclear and multidimensional NMR spectroscopy, we have determined the structure of the cNTnC.Ca(2+).cTnI(147-163).bepridil ternary complex.	Bepridil	125-133	troponin I3, cardiac type	Homo sapiens	111-115
12060657-10	2002	In the structure, the N terminus of the peptide clashes with part of the bepridil molecule, which explains the negative cooperativity between cTnI(147-163) and bepridil for cNTnC.Ca(2+).	Bepridil	73-81	troponin I3, cardiac type	Homo sapiens	142-146
11711026-0	2001	Inhibitory effect of bepridil on hKv1.5 channel current: comparison with amiodarone and E-4031.	Bepridil	21-29	potassium voltage-gated channel subfamily A member 5	Homo sapiens	33-39
11711026-4	2001	Bepridil also inhibited the hKv1.5 channel current with the IC(50) value of 6.6 microM.	Bepridil	0-8	potassium voltage-gated channel subfamily A member 5	Homo sapiens	28-34
11711026-8	2001	Thus, bepridil inhibits hKv1.5 channel current and the inhibitory effect may be useful for the treatment of atrial fibrillation.	Bepridil	6-14	potassium voltage-gated channel subfamily A member 5	Homo sapiens	24-30
14588286-8	2002	Bepridil (Research Biochemical Inc., Natick, MA, USA) (a less selective NCX inhibitor), when applied at 10 microM and 50 microM concentration promoted CAP amplitude recovery only to 46.8 +/- 7.8% and 29.9 +/- 3.3% of control, respectively, after hypoxic/ischemic injury to dorsal column white matter.	Bepridil	0-8	solute carrier family 8 member A1	Rattus norvegicus	72-75
11591369-1	2001	We have investigated the binding of bepridil to calcium-saturated cardiac troponin C in a cardiac troponin C/troponin I complex.	Bepridil	36-44	troponin C1, slow skeletal and cardiac type	Homo sapiens	66-84
11591369-1	2001	We have investigated the binding of bepridil to calcium-saturated cardiac troponin C in a cardiac troponin C/troponin I complex.	Bepridil	36-44	troponin C1, slow skeletal and cardiac type	Homo sapiens	90-108
11591369-2	2001	Nuclear magnetic resonance spectroscopy and [(15)N,(2)H]cardiac troponin C permitted the mapping of bepridil-induced amide proton chemical shifts.	Bepridil	100-108	troponin C1, slow skeletal and cardiac type	Homo sapiens	56-74
11591369-4	2001	In the presence of cardiac troponin I, bepridil binding to the C domain of cardiac troponin C was not detected.	Bepridil	39-47	troponin C1, slow skeletal and cardiac type	Homo sapiens	75-93
11162903-15	2000	Bepridil (antagonist of Na-Na exchange of the Na+/Ca2+ exchanger) and Na-free medium had powerful effect on increase of [Ca2+](i).	Bepridil	0-8	solute carrier family 8 member A1	Homo sapiens	46-64
11245603-6	2001	The antiarrhythmic KCNQ1 channel blocker bepridil inhibited KCNQ4 with an IC(50) value of 9.4 microM, whereas clofilium was without significant effect at 100 microM.	Bepridil	41-49	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	19-24
11245603-6	2001	The antiarrhythmic KCNQ1 channel blocker bepridil inhibited KCNQ4 with an IC(50) value of 9.4 microM, whereas clofilium was without significant effect at 100 microM.	Bepridil	41-49	potassium voltage-gated channel subfamily Q member 4	Homo sapiens	60-65
11245677-9	2001	Furthermore, blockade of the Na(+)-Ca(2+) exchanger with bepridil modestly reduced the calcium influx after injury.	Bepridil	57-65	nascent polypeptide associated complex subunit alpha	Homo sapiens	29-37
11181077-8	2001	Inhibitors of Na(+), Ca(2+)-exchanger, bepridil, and benzamil significantly prevented both [Ca(2+)](i) increase and apoptosis induced by Pin.	Bepridil	39-47	dynein light chain LC8-type 1	Homo sapiens	137-140
11090126-2	2000	The Ca(2+)-sensor protein troponin C (TnC) exerts a key role in the regulation of muscle contraction, and constitutes a target for Ca(2+) sensitizer compounds, such as bepridil, known to increase its apparent Ca(2+) affinity.	Bepridil	168-176	tenascin C	Rattus norvegicus	26-36
11090126-2	2000	The Ca(2+)-sensor protein troponin C (TnC) exerts a key role in the regulation of muscle contraction, and constitutes a target for Ca(2+) sensitizer compounds, such as bepridil, known to increase its apparent Ca(2+) affinity.	Bepridil	168-176	tenascin C	Rattus norvegicus	38-41
11090126-3	2000	Moreover, bepridil has been reported to exert a differential effect in slow and fast skeletal muscle fibres, which express the slow/cardiac and fast TnC isoform, respectively.	Bepridil	10-18	tenascin C	Rattus norvegicus	149-152
11090126-9	2000	These results indicated that the differential effect of bepridil in slow and fast fibres is related to the TnC isoform predominantly expressed in a fibre.	Bepridil	56-64	tenascin C	Rattus norvegicus	107-110
11090126-13	2000	Moreover, the amplitude of the reinforcement in the Ca(2+) affinity, induced by the binding of bepridil to the TnC molecule, is dependent on the number of functional regulatory sites, the larger affinity reinforcement being detected when only one regulatory site (either site I or II) is functional.	Bepridil	95-103	tenascin C	Rattus norvegicus	111-114
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.	Bepridil	19-27	potassium voltage-gated channel subfamily H member 2	Homo sapiens	0-4
10993480-9	2000	Both intracellular Ca2+ increase and induction of apoptosis were significantly inhibited by an extracellular Ca2+ chelator or Na+/Ca2+ exchanger blockers (bepridil and benzamil), whereas neither Ca2+ channel antagonists (verapamil and nifedipine) nor a nonselective cation channel blocker (flufenamic acid) had an effect.	Bepridil	155-163	solute carrier family 8 member A1	Homo sapiens	126-144
10737607-3	2000	These effects were counteracted by bepridil and by 5-(N-4-chlorobenzyl)-2",4"-dimethylbenzamil (CB-DMB), two specific inhibitors of the Na+-Ca2+ exchanger.	Bepridil	35-43	solute carrier family 8 member A1	Homo sapiens	136-154
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.	Bepridil	38-46	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.	Bepridil	38-46	potassium voltage-gated channel subfamily E regulatory subunit 1	Homo sapiens	18-21
10096910-7	1999	Thus bepridil increases the Ca2+ sensitivity through direct effects on TnC, whereas caffeine has significant effects on the cross-bridge interaction.	Bepridil	5-13	carbonic anhydrase 2	Rattus norvegicus	28-31
10516660-0	1999	Differential effects of bepridil on functional properties of troponin C in slow and fast skeletal muscles.	Bepridil	24-32	tenascin C	Homo sapiens	61-71
10516660-2	1999	Bepridil (BPD) is a pharmacological compound able to bind to the Ca2+ sensor protein troponin C (TnC), which triggers skeletal muscle contraction upon Ca2+-binding.	Bepridil	0-8	tenascin C	Homo sapiens	85-95
10516660-2	1999	Bepridil (BPD) is a pharmacological compound able to bind to the Ca2+ sensor protein troponin C (TnC), which triggers skeletal muscle contraction upon Ca2+-binding.	Bepridil	0-8	tenascin C	Homo sapiens	97-100
10516660-5	1999	The Ca2+-sensitizing action of bepridil was investigated on slow and fast isoforms of TnC from skinned slow and fast skeletal muscle fibres, activated by either Ca2+ or Sr2+ ions.	Bepridil	31-39	tenascin C	Homo sapiens	86-89
10516660-10	1999	However, in fast fibres, these lower Sr2+ maximal tensions could be reinforced by bepridil, suggesting an effect of bepridil on the function of site I of fast TnC.	Bepridil	116-124	tenascin C	Homo sapiens	159-162
10516660-12	1999	Under submaximal tension, bepridil induced an increase in Ca2+ affinity of TnC in both slow and fast fibres.	Bepridil	26-34	tenascin C	Homo sapiens	75-78
10096910-7	1999	Thus bepridil increases the Ca2+ sensitivity through direct effects on TnC, whereas caffeine has significant effects on the cross-bridge interaction.	Bepridil	5-13	tenascin C	Rattus norvegicus	71-74
9853105-0	1998	Blockade of bepridil on IA and IK in acutely isolated hippocampal CA1 neurons.	Bepridil	12-20	carbonic anhydrase 1	Rattus norvegicus	66-69
9853105-1	1998	The effects of bepridil, an antianginal agent with antiarrhythmic action, on voltage-dependent K+ currents in the CA1 pyramidal neurons acutely isolated from rat hippocampus were studied by means of whole-cell patch clamp techniques.	Bepridil	15-23	carbonic anhydrase 1	Rattus norvegicus	114-117
8839852-11	1996	3",4"-Dichlorobenzamil (DCB) and bepridil, relatively specific inhibitors of Na+/Ca2+ exchanger, also inhibited the chymotrypsin-induced alpha IIb beta 3 activation, and the IC50 values of these inhibitors for fibrinogen binding were 25 mumol/L and 52 mumol/L, respectively.	Bepridil	33-41	solute carrier family 8 member A1	Homo sapiens	77-95
9525919-0	1998	Identification of binding sites for bepridil and trifluoperazine on cardiac troponin C.	Bepridil	36-44	troponin C1, slow skeletal and cardiac type	Homo sapiens	68-86
9525919-7	1998	We report here the use of Met methyl groups as site-specific structural markers to identify drug binding sites for trifluoperazine and bepridil on cTnC.	Bepridil	135-143	troponin C1, slow skeletal and cardiac type	Homo sapiens	147-151
9525919-8	1998	Drug dependent changes in the NMR heteronuclear single-quantum coherence spectra of [methyl-13C]Met-labeled cTnC indicate that bepridil and trifluoperazine bind to similar sites but only in the presence of Ca2+.	Bepridil	127-135	troponin C1, slow skeletal and cardiac type	Homo sapiens	108-112
8957261-1	1996	The effects of bepridil, a potent antiarrhythmic agent, on the Na+ current (INa) of single guinea-pig ventricular myocytes were studied using the whole-cell patch-clamp technique.	Bepridil	15-23	alpha-internexin	Cavia porcellus	76-79
8957261-2	1996	Bepridil inhibited INa in a dose-dependent manner without causing any change in the I-V. relationship for INa.	Bepridil	0-8	alpha-internexin	Cavia porcellus	19-22
8957261-4	1996	10 microM bepridil shifted the steady-state inactivation curve for INa toward more negative potentials by 7.7 mV (n = 6).	Bepridil	10-18	alpha-internexin	Cavia porcellus	67-70
8957261-6	1996	Recovery of INa from inactivation was retarded (time constant 290 ms) at a holding potential of -140 mV in the presence of 10 microM bepridil.	Bepridil	133-141	alpha-internexin	Cavia porcellus	12-15
8957261-7	1996	When the onset of INa block was studied in experiments using a double-pulse protocol, bepridil blocked INa by 11.5% after a 4-ms pre-pulse, but significantly blocked it after pre-pulses longer than 16 ms.	Bepridil	86-94	alpha-internexin	Cavia porcellus	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.	Bepridil	92-100	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.	Bepridil	92-100	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.	Bepridil	96-104	potassium voltage-gated channel subfamily H member 2	Homo sapiens	41-45
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.	Bepridil	38-46	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.	Bepridil	38-46	potassium voltage-gated channel subfamily E regulatory subunit 1	Homo sapiens	18-21
9084984-6	1997	It is shown that bepridil blocks both cellular calcium entry as measured by Mn2+ quenching of fura-2 fluorescence and activation of the Na+/H(+)-exchanger following expression of the Ha-ras oncogene.	Bepridil	17-25	Harvey rat sarcoma virus oncogene	Mus musculus	183-189
8839852-11	1996	3",4"-Dichlorobenzamil (DCB) and bepridil, relatively specific inhibitors of Na+/Ca2+ exchanger, also inhibited the chymotrypsin-induced alpha IIb beta 3 activation, and the IC50 values of these inhibitors for fibrinogen binding were 25 mumol/L and 52 mumol/L, respectively.	Bepridil	33-41	fibrinogen beta chain	Homo sapiens	210-220
7790125-13	1995	The effect of bepridil on DNR and VCR accumulation and chemosensitivity in the XG cells was in accordance with the XG expression of mdr1/Pgp.	Bepridil	14-22	ATP binding cassette subfamily B member 1	Homo sapiens	132-136
7790125-13	1995	The effect of bepridil on DNR and VCR accumulation and chemosensitivity in the XG cells was in accordance with the XG expression of mdr1/Pgp.	Bepridil	14-22	ATP binding cassette subfamily B member 1	Homo sapiens	137-140
8229086-6	1993	Supplementation of normal medium with drugs modulating Ca2+, such as Bepridil which blocks the Na+Ca2+ exchanger or compound 48/80 which inhibits calmodulin, also prevent the expression of the nerve growth factor receptor gene during Wallerian degeneration in vitro.	Bepridil	69-77	nerve growth factor receptor	Rattus norvegicus	193-221
7906528-4	1994	An application of bepridil immediately after glutamate pulse when [Na+]i was greatly elevated, but not 14 min after glutamate removal when a basal [Na+]i was restored, evoked a [Ca2+]i increase accompanied by a decrease of [Na+]i, indicating a reverse mode of operation of the Na+/Ca2+ exchanger.	Bepridil	18-26	solute carrier family 8 member A1	Homo sapiens	277-295
7908691-1	1994	PURPOSE: To achieve an adequate plasma concentration of bepridil, a calcium channel blocker, which reverts multidrug resistance (MDR) in vitro, when administered in combination with vinblastine in patients with advanced colorectal cancer, a tumor characterized by high MDR1 gene expression.	Bepridil	56-64	ATP binding cassette subfamily B member 1	Homo sapiens	269-273
1397005-4	1992	The direct negative inotropic effect (NIE) of bepridil (IC50NIE = 10.96 microM) resulted in an VIC/NIE ratio of 5.19 for this drug.	Bepridil	46-54	endothelin 2	Rattus norvegicus	95-98
1423657-3	1992	In addition, we have found that certain Ca2+ channel entry blockers (e.g. nifedipine and bepridil) or calmodulin antagonists (e.g. W-7) specifically inhibit collagen-induced Ca2+ influx, myosin light chain phosphorylation and subsequent granule secretion.	Bepridil	89-97	carbonic anhydrase 2	Homo sapiens	40-43
1423657-3	1992	In addition, we have found that certain Ca2+ channel entry blockers (e.g. nifedipine and bepridil) or calmodulin antagonists (e.g. W-7) specifically inhibit collagen-induced Ca2+ influx, myosin light chain phosphorylation and subsequent granule secretion.	Bepridil	89-97	carbonic anhydrase 2	Homo sapiens	174-177
2663886-4	1989	The HVPGS-induced increase in insulin binding can be inhibited by bepridil, a specific Ca2+ channel blocker, suggesting that the Ca2+ influx is required for the exposure of additional insulin receptors on the cell surface.	Bepridil	66-74	insulin	Homo sapiens	30-37
1632105-10	1992	Oral plasma clearance (CLp) of Bp was very low in man (ca.	Bepridil	31-33	calmodulin like 3	Homo sapiens	23-26
2148481-8	1990	Our results suggest that verapamil, diltiazem and bepridil (0.01 to 0.3 mM), but not nifedipine (1 nM to 0.01 mM), in relatively high concentrations can antagonize the calmodulin-stimulated Ca2(+)-pump, i.e. the ATPase as well as the transport process.	Bepridil	50-58	carbonic anhydrase 2	Homo sapiens	190-193
2148481-8	1990	Our results suggest that verapamil, diltiazem and bepridil (0.01 to 0.3 mM), but not nifedipine (1 nM to 0.01 mM), in relatively high concentrations can antagonize the calmodulin-stimulated Ca2(+)-pump, i.e. the ATPase as well as the transport process.	Bepridil	50-58	dynein axonemal heavy chain 8	Homo sapiens	212-218
2172919-9	1990	All the CCEs blocked specific binding of [3H]-PCP to its binding site on the nAChR-channel complex, with bepridil and nicardipine being the most potent.	Bepridil	105-113	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	77-82
34430564-0	2021	Bepridil, a class IV antiarrhythmic agent, can block the TREK-1 potassium channel.	Bepridil	0-8	potassium two pore domain channel subfamily K member 2	Homo sapiens	57-63
34430564-3	2021	In the present study, the effect of bepridil on the TREK-1 currents is investigated.	Bepridil	36-44	potassium two pore domain channel subfamily K member 2	Homo sapiens	52-58
34430564-9	2021	However, bepridil decreased the baseline TREK-1 currents, with a concentration of half-maximal inhibition (IC50) 0.59 microM and a Hill coefficient of 1.1.	Bepridil	9-17	potassium two pore domain channel subfamily K member 2	Homo sapiens	41-47
34430564-10	2021	Also, bepridil inhibited BL1249-activated TREK-1 currents, with an IC50 4.08 microM and a Hill coefficient of 3.22.	Bepridil	6-14	potassium two pore domain channel subfamily K member 2	Homo sapiens	42-48
34430564-11	2021	The outside-out patch-clamp confirmed bepridil inhibited BL1249-activated TREK-1 currents.	Bepridil	38-46	potassium two pore domain channel subfamily K member 2	Homo sapiens	74-80
34430564-12	2021	In U251MG cells and myocytes, BL1249 activated outwardly rectifying endogenous TREK-1 currents, which could be inhibited by bepridil.	Bepridil	124-132	potassium two pore domain channel subfamily K member 2	Homo sapiens	79-85
34430564-16	2021	Conclusions: Bepridil may be a blocker for the TREK-1K+channel at a clinically therapeutic concentration, providing a new mechanism of TREK-1 regulation and bepridil"s antiarrhythmic effect.	Bepridil	13-21	potassium two pore domain channel subfamily K member 2	Homo sapiens	135-141
1372785-4	1992	However, in vascular smooth muscle where the calcium-calmodulin complex promotes muscle contraction by activating myosin light-chain kinase phosphorylation of contractile proteins, calmodulin antagonism, coupled with bepridil"s blockade of calcium influx, leads to vasorelaxation.	Bepridil	217-225	myosin light chain kinase	Homo sapiens	114-139
1311030-10	1992	Na(+)-Ca2+ exchanger blockers (bepridil, benzamil, dichlorobenzamil) significantly protected the optic nerve from anoxic injury.	Bepridil	31-39	solute carrier family 8 member A1	Homo sapiens	0-20
1290306-3	1992	2) compounds like trifluoperazine or bepridil, both known to interact with calmodulin, increase the Ca++ sensitivity of the contractile structures of the heart, in high concentrations, as expected from the high natural abundance of troponin C. 3) DPI 201-106 interacts with calmodulin (and presumably with the structurally closely related troponin C) in the microM concentration range.	Bepridil	37-45	calmodulin 1	Homo sapiens	75-85
1290306-3	1992	2) compounds like trifluoperazine or bepridil, both known to interact with calmodulin, increase the Ca++ sensitivity of the contractile structures of the heart, in high concentrations, as expected from the high natural abundance of troponin C. 3) DPI 201-106 interacts with calmodulin (and presumably with the structurally closely related troponin C) in the microM concentration range.	Bepridil	37-45	calmodulin 1	Homo sapiens	274-284
1952825-6	1991	Direct pharmacological blockade of the Na+,Ca2+ exchanger during anoxia with bepridil or benzamil also significantly improved recovery.	Bepridil	77-85	solute carrier family 8 member A1	Homo sapiens	39-57
2351672-0	1990	Binding of a calcium sensitizer, bepridil, to cardiac troponin C.	Bepridil	33-41	troponin C1, slow skeletal and cardiac type	Homo sapiens	46-64
2663886-4	1989	The HVPGS-induced increase in insulin binding can be inhibited by bepridil, a specific Ca2+ channel blocker, suggesting that the Ca2+ influx is required for the exposure of additional insulin receptors on the cell surface.	Bepridil	66-74	insulin	Homo sapiens	184-191
2663886-6	1989	All three of these insulin-dependent effects are also inhibited by bepridil.	Bepridil	67-75	insulin	Homo sapiens	19-26
2792192-7	1989	It is concluded that intracellular actions, possibly calmodulin inhibition, play a substantial role in the vasodilator action of bepridil, a conclusion supported by the relative lack of stereospecificity shown by the bepridil isomers.	Bepridil	129-137	calmodulin	Oryctolagus cuniculus	53-63
3207972-11	1988	Bepridil (10 microM), a Ca2+ and calmodulin antagonist, also significantly attenuated AH induced by PLA2.	Bepridil	0-8	phospholipase A2 group IB	Rattus norvegicus	100-104
2429097-2	1986	At drive cycle lengths of 400 and 333 ms, bepridil significantly increased relative (RRP) and effective (ERP) refractory periods in both normal ventricular tissue (mean increases, RRP 7-14%, ERP 5-6%, p less than 0.05-0.01) and in infarcted ventricular tissue (mean increases, RRP 12-15%, ERP 13-14%, p less than 0.01).	Bepridil	42-50	ribosomal RNA processing 12 homolog	Canis lupus familiaris	277-283
2951341-4	1987	The effect of bepridil might be related to an enhancement of mitochondrial ATPase activity whereas nicardipine would act on mitochondria by a different mechanism.	Bepridil	14-22	ATP synthase F1 subunit epsilon	Homo sapiens	61-81
2468847-3	1988	The hydrophobic calcium antagonists prenylamine and bepridil, however, interacted with [3H]diltiazem binding at concentrations up to 50 times lower than their calmodulin inhibiting concentrations.	Bepridil	52-60	calmodulin 1	Homo sapiens	159-169
2964559-1	1987	The Ca2+ channel blockers felodipine and bepridil are known to affect selectively functions of calmodulin.	Bepridil	41-49	calmodulin	Oryctolagus cuniculus	95-105
2448039-3	1987	CaM antagonism of cloxacepride, picumast, oxatomide, fendiline and bepridil correlated not only with the inhibition of exocytosis evoked by compound 48/80 but also with that induced by A23187, concanavalin A and antigen-IgE.	Bepridil	67-75	calmodulin 1	Homo sapiens	0-3
3036157-3	1987	Contrary to W-7, nicergoline, nicardipine and quercetin, which decreased the fluorescence of the two probes bound to calmodulin, bepridil only decreased 9AC fluorescence but increased the fluorescence intensity at the wavelength of the emission maximum of TNS.	Bepridil	129-137	calmodulin 1	Homo sapiens	117-127
3036157-4	1987	In spite of this difference, bepridil as well as W-7 and nicergoline competitively inhibited calmodulin activation of phosphodiesterase.	Bepridil	29-37	calmodulin 1	Homo sapiens	93-103
3032617-11	1987	Binding of [3H]bepridil to calmodulin under equilibrium conditions yielded one high-affinity site (apparent Kd 0.4 microM) and four low affinity sites (apparent Kd 44 microM).	Bepridil	15-23	calmodulin 1	Homo sapiens	27-37
2942677-0	1986	Stimulation of cardiac myofilament force, ATPase activity and troponin C Ca++ binding by bepridil.	Bepridil	89-97	tenascin C	Sus scrofa	62-72
2942677-1	1986	We report that bepridil, a Ca++ channel blocker and calmodulin antagonist, which has been shown to enter myocytes, stimulates the mechanical and biochemical activity of cardiac myofilaments.	Bepridil	15-23	calmodulin-3	Sus scrofa	52-62
2942677-5	1986	Associated with the stimulation of force and ATPase activity by bepridil was an increase in the amounts of Ca++ bound to troponin C (TnC).	Bepridil	64-72	tenascin C	Sus scrofa	121-131
2942677-5	1986	Associated with the stimulation of force and ATPase activity by bepridil was an increase in the amounts of Ca++ bound to troponin C (TnC).	Bepridil	64-72	tenascin C	Sus scrofa	133-136
2942677-6	1986	That bepridil stimulates TnC Ca++ binding was also shown in experiments using pure TnC labeled with 2-(4"-iodoacetamidoanilo)naphthalene-6-sulfonic acid, a fluorescent probe that reports Ca++ bound to the single "regulatory" site.	Bepridil	5-13	tenascin C	Sus scrofa	25-28
2942677-6	1986	That bepridil stimulates TnC Ca++ binding was also shown in experiments using pure TnC labeled with 2-(4"-iodoacetamidoanilo)naphthalene-6-sulfonic acid, a fluorescent probe that reports Ca++ bound to the single "regulatory" site.	Bepridil	5-13	tenascin C	Sus scrofa	83-86
2942677-7	1986	Effects of bepridil on the fluorescence of a felodipine-cardiac TnC complex indicate that bepridil binds to TnC over the same range of doses where it affects myofilament activity.	Bepridil	11-19	tenascin C	Sus scrofa	64-67
2942677-7	1986	Effects of bepridil on the fluorescence of a felodipine-cardiac TnC complex indicate that bepridil binds to TnC over the same range of doses where it affects myofilament activity.	Bepridil	90-98	tenascin C	Sus scrofa	64-67
2942677-7	1986	Effects of bepridil on the fluorescence of a felodipine-cardiac TnC complex indicate that bepridil binds to TnC over the same range of doses where it affects myofilament activity.	Bepridil	90-98	tenascin C	Sus scrofa	108-111
3019548-0	1986	Protective effects of the calmodulin antagonist bepridil on ischaemia induced in the rat myocardium.	Bepridil	48-56	calmodulin 1	Rattus norvegicus	26-36
3019548-4	1986	Bepridil effectively inhibited the activation of calmodulin dependent enzymes, such as calcium calmodulin dependent cyclic nucleotide phosphodiesterase and myosin light chain kinase.	Bepridil	0-8	calmodulin 1	Rattus norvegicus	49-59
3019548-4	1986	Bepridil effectively inhibited the activation of calmodulin dependent enzymes, such as calcium calmodulin dependent cyclic nucleotide phosphodiesterase and myosin light chain kinase.	Bepridil	0-8	calmodulin 1	Rattus norvegicus	95-105
3019548-4	1986	Bepridil effectively inhibited the activation of calmodulin dependent enzymes, such as calcium calmodulin dependent cyclic nucleotide phosphodiesterase and myosin light chain kinase.	Bepridil	0-8	myosin light chain kinase	Rattus norvegicus	156-181
3019548-6	1986	Since bepridil protects the myocardium and minimises ischaemia induced damage these events might be related to a calmodulin antagonistic action as well as a calcium channel blocking action.	Bepridil	6-14	calmodulin 1	Rattus norvegicus	113-123
3487326-0	1986	Investigations on calmodulin antagonistic effects of bepridil in intact and skinned fibres of smooth muscle.	Bepridil	53-61	calmodulin 1	Rattus norvegicus	18-28
3487326-11	1986	Thus the effects of bepridil on the contractile mechanism in vascular smooth muscle are at least partly mediated through an intracellular mechanism - most probably inhibition of calmodulin.	Bepridil	20-28	calmodulin 1	Rattus norvegicus	178-188
3484629-0	1986	The binding of the calcium channel blocker, bepridil, to calmodulin.	Bepridil	44-52	calmodulin 1	Homo sapiens	57-67
3484629-1	1986	Bepridil had the highest relative potency for inhibition of myosin light chain kinase (MLCK) activated by Ca2+-calmodulin of all the calcium channel blockers we examined.	Bepridil	0-8	myosin light chain kinase	Homo sapiens	60-85
3484629-1	1986	Bepridil had the highest relative potency for inhibition of myosin light chain kinase (MLCK) activated by Ca2+-calmodulin of all the calcium channel blockers we examined.	Bepridil	0-8	myosin light chain kinase	Homo sapiens	87-91
3484629-1	1986	Bepridil had the highest relative potency for inhibition of myosin light chain kinase (MLCK) activated by Ca2+-calmodulin of all the calcium channel blockers we examined.	Bepridil	0-8	calmodulin 1	Homo sapiens	111-121
3484629-2	1986	Kinetic analysis indicated that the primary effect of bepridil was mediated through a competitive inhibition of the enzyme activation by interaction with calmodulin and the apparent Ki value of this agent was 2.2 microM.	Bepridil	54-62	calmodulin 1	Homo sapiens	154-164
3484629-3	1986	We then examined the binding of bepridil to calmodulin, using the equilibrium column binding technique.	Bepridil	32-40	calmodulin 1	Homo sapiens	44-54
3484629-5	1986	Scatchard analysis of the binding of bepridil to calmodulin demonstrated that the dissociation constant was 6.2 microM and the calculated number of specific binding sites was about 5 sites per molecule of calmodulin.	Bepridil	37-45	calmodulin 1	Homo sapiens	49-59
3484629-5	1986	Scatchard analysis of the binding of bepridil to calmodulin demonstrated that the dissociation constant was 6.2 microM and the calculated number of specific binding sites was about 5 sites per molecule of calmodulin.	Bepridil	37-45	calmodulin 1	Homo sapiens	205-215
3484629-6	1986	The concentrations of unlabeled bepridil, W-7, prenylamine, verapamil and diltiazem producing 50% inhibition (IC50) of the binding of [3H]bepridil to calmodulin were 4 microM, 28 microM, 45 microM, 130 microM and 700 microM, respectively.	Bepridil	32-40	calmodulin 1	Homo sapiens	150-160
3484629-6	1986	The concentrations of unlabeled bepridil, W-7, prenylamine, verapamil and diltiazem producing 50% inhibition (IC50) of the binding of [3H]bepridil to calmodulin were 4 microM, 28 microM, 45 microM, 130 microM and 700 microM, respectively.	Bepridil	138-146	calmodulin 1	Homo sapiens	150-160
2933041-2	1985	The effect of four slow Ca2+ channel blockers (felodipine, nifedipine, prenylamine and bepridil) that possess the ability to bind to calmodulin (CaM) section and to inhibit myosin light chain kinase (MLCK) on CaM-regulated Ca2+ pumping ATPase of cardiac sarcolemma (SL) and brain cyclic AMP phosphodiesterase (PDE) was studied.	Bepridil	87-95	calmodulin 1	Homo sapiens	133-143
2933041-2	1985	The effect of four slow Ca2+ channel blockers (felodipine, nifedipine, prenylamine and bepridil) that possess the ability to bind to calmodulin (CaM) section and to inhibit myosin light chain kinase (MLCK) on CaM-regulated Ca2+ pumping ATPase of cardiac sarcolemma (SL) and brain cyclic AMP phosphodiesterase (PDE) was studied.	Bepridil	87-95	calmodulin 1	Homo sapiens	145-148
2933041-2	1985	The effect of four slow Ca2+ channel blockers (felodipine, nifedipine, prenylamine and bepridil) that possess the ability to bind to calmodulin (CaM) section and to inhibit myosin light chain kinase (MLCK) on CaM-regulated Ca2+ pumping ATPase of cardiac sarcolemma (SL) and brain cyclic AMP phosphodiesterase (PDE) was studied.	Bepridil	87-95	myosin light chain kinase	Homo sapiens	173-198
2933041-2	1985	The effect of four slow Ca2+ channel blockers (felodipine, nifedipine, prenylamine and bepridil) that possess the ability to bind to calmodulin (CaM) section and to inhibit myosin light chain kinase (MLCK) on CaM-regulated Ca2+ pumping ATPase of cardiac sarcolemma (SL) and brain cyclic AMP phosphodiesterase (PDE) was studied.	Bepridil	87-95	myosin light chain kinase	Homo sapiens	200-204
2933041-2	1985	The effect of four slow Ca2+ channel blockers (felodipine, nifedipine, prenylamine and bepridil) that possess the ability to bind to calmodulin (CaM) section and to inhibit myosin light chain kinase (MLCK) on CaM-regulated Ca2+ pumping ATPase of cardiac sarcolemma (SL) and brain cyclic AMP phosphodiesterase (PDE) was studied.	Bepridil	87-95	calmodulin 1	Homo sapiens	209-212
6092067-10	1984	(iv) A low-affinity binding site for verapamil and for some other Ca2+ channel blockers is detected by studies of dissociation kinetics of the [3H]verapamil receptor in the presence of high concentrations of verapamil, gallopamil, bepridil and diltiazem.	Bepridil	231-239	carbonic anhydrase 2	Oryctolagus cuniculus	66-69
3484629-9	1986	These results suggest that bepridil binds to calmodulin in the presence of calcium and potently inhibits the phosphorylation of myosin light chain.	Bepridil	27-35	calmodulin 1	Homo sapiens	45-55
6088585-2	1984	Two new vascular smooth muscle relaxants, bepridil and cetiedil, were found to possess specific CaM-inhibitory properties which resembled those of trifluoperazine.	Bepridil	42-50	calmodulin 1	Homo sapiens	96-99
6088585-3	1984	Trifluoperazine, bepridil, and cetiedil inhibited Ca2+-dependent 125I-CaM binding to erythrocyte membranes and CaM activation of membrane Ca2+-ATPase with IC50 values of approximately 12, approximately 17, and approximately 40 microM, respectively.	Bepridil	17-25	calmodulin 1	Homo sapiens	70-73
6088585-3	1984	Trifluoperazine, bepridil, and cetiedil inhibited Ca2+-dependent 125I-CaM binding to erythrocyte membranes and CaM activation of membrane Ca2+-ATPase with IC50 values of approximately 12, approximately 17, and approximately 40 microM, respectively.	Bepridil	17-25	calmodulin 1	Homo sapiens	111-114
31034096-7	2019	Blocking the forward NCX with bepridil, CB-DMB, or KB-R7943 elevated [Ca2+ ]i and killed glioblastoma cells.	Bepridil	30-38	carbonic anhydrase 2	Homo sapiens	70-73
31493248-10	2020	Also, RUNX2 and Osterix expression were suppressed significantly when the cells were treated with bepridil, a non-selective VGCC inhibitor, prior to loading.	Bepridil	98-106	runt related transcription factor 2	Mus musculus	6-11
31493248-10	2020	Also, RUNX2 and Osterix expression were suppressed significantly when the cells were treated with bepridil, a non-selective VGCC inhibitor, prior to loading.	Bepridil	98-106	Sp7 transcription factor 7	Mus musculus	16-23
31493248-11	2020	Significantly higher amounts of osteocalcin and mineralized nodules were synthesized by osteoblasts on diffuse damaged bone wafers, while bepridil treatment resulted in a significant decrease in osteocalcin production and mineralized nodule formation.	Bepridil	138-146	bone gamma-carboxyglutamate protein 2	Mus musculus	195-206
31664641-1	2019	We previously reviewed our study of the pharmacological properties of cardiac Na+/Ca2+ exchange (NCX1) inhibitors among cardioprotective drugs, such as amiodarone, bepridil, dronedarone, cibenzoline, azimilide, aprindine, and benzyl-oxyphenyl derivatives (Watanabe et al.	Bepridil	164-172	solute carrier family 8 member A1	Homo sapiens	97-101
33597253-3	2021	A live virus-based modified microneutralization assay revealed that bepridil possesses significant anti-SARS-CoV-2 activity in both Vero E6 and A459/ACE2 cells in a dose-dependent manner with low micromolar effective concentration, 50% (EC50) values.	Bepridil	68-76	angiotensin-converting enzyme 2	Chlorocebus sabaeus	149-153
31034096-8	2019	Bepridil and CB-DMB caused Ca2+ -dependent cell cycle arrest together with apoptosis, which were all attenuated by a Ca2+ chelator BAPTA-AM.	Bepridil	0-8	carbonic anhydrase 2	Homo sapiens	27-30
31034096-8	2019	Bepridil and CB-DMB caused Ca2+ -dependent cell cycle arrest together with apoptosis, which were all attenuated by a Ca2+ chelator BAPTA-AM.	Bepridil	0-8	carbonic anhydrase 2	Homo sapiens	117-120
30871913-8	2019	Finally, we validated via molecular docking analysis that two drugs with unknown effects in HNSCC: MG-262 and bepridil might perturb the development of HNSCC through targeting PCNA.	Bepridil	110-118	proliferating cell nuclear antigen	Homo sapiens	176-180
30721669-7	2019	The inhibitory order towards SJSA-1 cell line is nutlin-3a (IC50 = 0.8 muM) > bepridil (23 muM) > azelastine (25 muM).	Bepridil	81-89	latexin	Homo sapiens	94-97
30816547-10	2019	Further molecular docking simulation suggested a relatively stable binding selectivity between Bepridil and eight proteins (CRK, FGFR4, LAMB1, PIK3R2, CD47, ELANE, HPGD, and PRKCB).	Bepridil	95-103	fibroblast growth factor receptor 4	Homo sapiens	129-134
30816547-10	2019	Further molecular docking simulation suggested a relatively stable binding selectivity between Bepridil and eight proteins (CRK, FGFR4, LAMB1, PIK3R2, CD47, ELANE, HPGD, and PRKCB).	Bepridil	95-103	laminin subunit beta 1	Homo sapiens	136-141
30816547-10	2019	Further molecular docking simulation suggested a relatively stable binding selectivity between Bepridil and eight proteins (CRK, FGFR4, LAMB1, PIK3R2, CD47, ELANE, HPGD, and PRKCB).	Bepridil	95-103	phosphoinositide-3-kinase regulatory subunit 2	Homo sapiens	143-149
30816547-10	2019	Further molecular docking simulation suggested a relatively stable binding selectivity between Bepridil and eight proteins (CRK, FGFR4, LAMB1, PIK3R2, CD47, ELANE, HPGD, and PRKCB).	Bepridil	95-103	elastase, neutrophil expressed	Homo sapiens	157-162
30816547-10	2019	Further molecular docking simulation suggested a relatively stable binding selectivity between Bepridil and eight proteins (CRK, FGFR4, LAMB1, PIK3R2, CD47, ELANE, HPGD, and PRKCB).	Bepridil	95-103	carbonyl reductase 1	Homo sapiens	164-168
30816547-10	2019	Further molecular docking simulation suggested a relatively stable binding selectivity between Bepridil and eight proteins (CRK, FGFR4, LAMB1, PIK3R2, CD47, ELANE, HPGD, and PRKCB).	Bepridil	95-103	protein kinase C beta	Homo sapiens	174-179
30721669-7	2019	The inhibitory order towards SJSA-1 cell line is nutlin-3a (IC50 = 0.8 muM) > bepridil (23 muM) > azelastine (25 muM).	Bepridil	81-89	latexin	Homo sapiens	94-97
30721669-9	2019	The anti-proliferation effects of bepridil and azelastine on the cell lines with mutated and deleted p53 implied some p53-independent anti-proliferation effects.	Bepridil	34-42	tumor protein p53	Homo sapiens	101-104
30721669-9	2019	The anti-proliferation effects of bepridil and azelastine on the cell lines with mutated and deleted p53 implied some p53-independent anti-proliferation effects.	Bepridil	34-42	tumor protein p53	Homo sapiens	118-121
30778102-8	2019	Finally, avermectin B1a, gliquidone, nicardipine and bepridil significantly increased IBABP promoter activity in a luciferase reporter assay in a dose-dependent manner.	Bepridil	53-61	fatty acid binding protein 6	Homo sapiens	86-91
30138628-4	2018	We also treated wild-type murine muscle with bepridil, a cTnC-targeting Ca2+ sensitizer.	Bepridil	45-53	troponin C, cardiac/slow skeletal	Mus musculus	57-61
29804308-7	2018	For instance, reduction in intracellular acidification by bepridil increased Abeta production in parallel with decreased BACE activity.	Bepridil	58-66	amyloid beta precursor protein	Homo sapiens	77-82
30816547-10	2019	Further molecular docking simulation suggested a relatively stable binding selectivity between Bepridil and eight proteins (CRK, FGFR4, LAMB1, PIK3R2, CD47, ELANE, HPGD, and PRKCB).	Bepridil	95-103	CRK proto-oncogene, adaptor protein	Homo sapiens	124-127
29508386-3	2018	Using gene expression-based screening, we identified the calcium channel modulator bepridil as a new NOTCH1 pathway inhibitor.	Bepridil	83-91	notch receptor 1	Homo sapiens	101-107
29508386-6	2018	The antitumor efficacy of bepridil was associated with inhibition of NOTCH1 activity through a decrement in trans-membrane and activated NOTCH1 protein levels with unchanged NOTCH2 protein levels.	Bepridil	26-34	notch receptor 1	Homo sapiens	69-75
29508386-6	2018	The antitumor efficacy of bepridil was associated with inhibition of NOTCH1 activity through a decrement in trans-membrane and activated NOTCH1 protein levels with unchanged NOTCH2 protein levels.	Bepridil	26-34	notch receptor 1	Homo sapiens	137-143
29508386-9	2018	These data provide a rationale for the clinical development of bepridil as anti-NOTCH1 targeted therapy for CLL patients.	Bepridil	63-71	notch receptor 1	Homo sapiens	80-86
27283899-3	2016	Here, we show that bepridil (BPD) and trifluoperazine (TFP), which are FDA-approved drugs for treatment of schizophrenia and angina respectively, inhibit Akt-pS473 phosphorylation and promote FOXO3 nuclear localization and activation in TNBC cells.	Bepridil	19-27	AKT serine/threonine kinase 1	Homo sapiens	154-157
27283899-3	2016	Here, we show that bepridil (BPD) and trifluoperazine (TFP), which are FDA-approved drugs for treatment of schizophrenia and angina respectively, inhibit Akt-pS473 phosphorylation and promote FOXO3 nuclear localization and activation in TNBC cells.	Bepridil	19-27	forkhead box O3	Homo sapiens	192-197
27283899-3	2016	Here, we show that bepridil (BPD) and trifluoperazine (TFP), which are FDA-approved drugs for treatment of schizophrenia and angina respectively, inhibit Akt-pS473 phosphorylation and promote FOXO3 nuclear localization and activation in TNBC cells.	Bepridil	29-32	AKT serine/threonine kinase 1	Homo sapiens	154-157
27283899-3	2016	Here, we show that bepridil (BPD) and trifluoperazine (TFP), which are FDA-approved drugs for treatment of schizophrenia and angina respectively, inhibit Akt-pS473 phosphorylation and promote FOXO3 nuclear localization and activation in TNBC cells.	Bepridil	29-32	forkhead box O3	Homo sapiens	192-197
26498939-0	2016	Short- and long-term inhibition of cardiac inward-rectifier potassium channel current by an antiarrhythmic drug bepridil.	Bepridil	112-120	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	35-77
26915042-0	2016	Erratum to: Short- and long-term inhibition of cardiac inward-rectifier potassium channel current by an antiarrhythmic drug bepridil.	Bepridil	124-132	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	47-89
26784557-6	2016	Interestingly, the KCNT1 blockers quinidine (3-1000muM) and bepridil (0.03-10muM) inhibited both wild-type and mutant KCNT1 currents in a concentration-dependent manner, with mutant channels showing higher sensitivity to blockade.	Bepridil	60-68	potassium sodium-activated channel subfamily T member 1	Homo sapiens	19-24
26784557-6	2016	Interestingly, the KCNT1 blockers quinidine (3-1000muM) and bepridil (0.03-10muM) inhibited both wild-type and mutant KCNT1 currents in a concentration-dependent manner, with mutant channels showing higher sensitivity to blockade.	Bepridil	60-68	potassium sodium-activated channel subfamily T member 1	Homo sapiens	118-123
27076907-10	2016	Bepridil, dichlorobenzamil, and KB-R7943, which are NCX inhibitors, decreased resting [Ca(2+)]i and pHi only in hypoxic PASMCs and blocked the changes in pHi induced by altering [Ca(2+)]i.	Bepridil	0-8	solute carrier family 8 member A1	Rattus norvegicus	52-55
27076907-10	2016	Bepridil, dichlorobenzamil, and KB-R7943, which are NCX inhibitors, decreased resting [Ca(2+)]i and pHi only in hypoxic PASMCs and blocked the changes in pHi induced by altering [Ca(2+)]i.	Bepridil	0-8	glucose-6-phosphate isomerase	Rattus norvegicus	100-103
27076907-10	2016	Bepridil, dichlorobenzamil, and KB-R7943, which are NCX inhibitors, decreased resting [Ca(2+)]i and pHi only in hypoxic PASMCs and blocked the changes in pHi induced by altering [Ca(2+)]i.	Bepridil	0-8	glucose-6-phosphate isomerase	Rattus norvegicus	154-157
26375298-9	2016	Levosimendan, bepridil, and pimobendan were found to elevate the Ca(2+) -sensitivity of cTnT(T204E) containing samples in this context.	Bepridil	14-22	troponin T2, cardiac type	Homo sapiens	88-92
26195225-6	2015	The S/R ratio in patients with co-administration of bepridil, a potent CYP2D6 inhibitor, was lower than 0.99, regardless of the CYP2D6 genotype status.	Bepridil	52-60	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	71-77
26616666-8	2015	At clinically relevant concentrations, verapamil blocked hCav1.2 and hERG, as did vanoxerine and bepridil both of which also blocked hNav1.5.	Bepridil	97-105	sodium voltage-gated channel alpha subunit 5	Homo sapiens	133-140
26616666-10	2015	Of the MICE drugs only bepridil inhibited hERG trafficking following overnight exposure.	Bepridil	23-31	ETS transcription factor ERG	Homo sapiens	42-46
25729581-3	2015	Selected Pgp transport ligands include: Amiodarone, Bepridil, Diltiazem, Dipyridamole, Nicardipine, Nifedipine, Propranolol, and Quinidine.	Bepridil	52-60	phosphoglycolate phosphatase	Mus musculus	9-12