PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
8654202-9	1995	Other selective CYP inhibitors for CYP1A1/2 (alpha-naphthoflavone), CYP2C8-10 (sulfaphenazole), CYP2D6 (quinidine), and CYP2E1 (diallylsulfone) showed minor or no effects on both reactions.	Quinidine	104-113	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	16-19
8528270-10	1995	Similar Ki values (within a factor of three) were observed for perhexiline and (R,S)-propranolol while quinidine and dextromethorphan were 8.5-fold and 21-fold more effective inhibitors of CYP2D6-Val relative to CYP2D6-Met.	Quinidine	103-112	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	189-195
7593709-6	1995	Pretreatment of these subjects with 100 mg of quinidine, a selective inhibitor of CYP2D6, significantly suppressed the formation of dextrorphan and elevated the concentrations of dextromethorphan (t1/2, 16.4 hours).	Quinidine	46-55	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	82-88
7643631-4	1995	Downmodulation of Pgp function in these cell lines could be demonstrated with different substances (verapamil, vinblastine, trifluoperazine, cyclosporin A, progesterone and quinidine) and was proven to be consistently higher in the vinblastine selected cells than in their non-selected drug sensitive counterparts.	Quinidine	173-182	ATP binding cassette subfamily B member 1	Homo sapiens	18-21
7547962-7	1995	P-glycoprotein modulators generally demonstrated significantly greater potency (EC50; microM): SDZ PSC 833, 0.08; cyclosporin A, 1.3; verapamil, 4.1; quinidine, 6.4; prazosin, > 300.	Quinidine	150-159	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
7547962-10	1995	Scatchard analysis showed quinidine to be a noncompetitive inhibitor of P-glycoprotein-mediated Tc-SESTAMIBI transport, indicating allosteric effector sites on P-glycoprotein.	Quinidine	26-35	ATP binding cassette subfamily B member 1	Homo sapiens	72-86
7547962-10	1995	Scatchard analysis showed quinidine to be a noncompetitive inhibitor of P-glycoprotein-mediated Tc-SESTAMIBI transport, indicating allosteric effector sites on P-glycoprotein.	Quinidine	26-35	ATP binding cassette subfamily B member 1	Homo sapiens	160-174
7641327-3	1995	We recently reported that block of the human cardiac hKv1.5 channel by quinidine displayed similarity with internal quaternary ammonium block of squid and Shaker potassium channels.	Quinidine	71-80	potassium voltage-gated channel subfamily A member 5	Homo sapiens	53-59
8528270-10	1995	Similar Ki values (within a factor of three) were observed for perhexiline and (R,S)-propranolol while quinidine and dextromethorphan were 8.5-fold and 21-fold more effective inhibitors of CYP2D6-Val relative to CYP2D6-Met.	Quinidine	103-112	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	212-218
8586645-6	1995	Quinine and quinidine showed 400 and 80 times, respectively, higher affinity for MBP than for debrisoquine 4-hydroxylase.	Quinidine	12-21	myelin basic protein	Rattus norvegicus	81-84
7747708-2	1995	Quinidine is known to inhibit p-glycoprotein and enhance the activity of vinblastine against cultured renal carcinoma cells.	Quinidine	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	30-44
8586645-6	1995	Quinine and quinidine showed 400 and 80 times, respectively, higher affinity for MBP than for debrisoquine 4-hydroxylase.	Quinidine	12-21	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	94-120
7532036-0	1995	The glycoprotein Ib-IX complex-specific monoclonal antibody SZ1 binds to a conformation-sensitive epitope on glycoprotein IX: implications for the target antigen of quinine/quinidine-dependent autoantibodies.	Quinidine	173-182	DLG2 antisense RNA 1	Homo sapiens	60-63
7890608-5	1995	The rate of CO binding to the total mixture of P450 3A4 conformers was increased in the presence of nifedipine and erythromycin, decreased by quinidine, testosterone, and warfarin, and unaffected by cimetidine and 17 alpha-ethynylestradiol.	Quinidine	142-151	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	47-51
7640150-4	1995	alpha-Naphthoflavone and 7-ethoxyresorufin (selective inhibitors of CYP1A1/2) inhibited the N-desisopropylation of R- and S-propranolol by human liver microsomes by 20 and 40%, respectively, while quinidine (a selective inhibitor of CYP2D6) abolished the 4-hydroxylation of both propranolol enantiomers almost completely.	Quinidine	197-206	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	68-74
7532036-1	1995	The monoclonal antibody SZ1 is of interest for two reasons: it was used to define complex formation between glycoprotein (GP) Ib and GP IX, and its epitope is likely to be identical to that recognized by most quinine- and quinidine-dependent autoantibodies that cause thrombocytopenia.	Quinidine	222-231	DLG2 antisense RNA 1	Homo sapiens	24-27
7532036-8	1995	Because of the ability of SZ1 to block the binding of many quinine- and quinidine-dependent antibodies, these data strongly suggest that GP IX is the component of the GP Ib-IX complex recognized by those antibodies.	Quinidine	72-81	DLG2 antisense RNA 1	Homo sapiens	26-29
7532036-8	1995	Because of the ability of SZ1 to block the binding of many quinine- and quinidine-dependent antibodies, these data strongly suggest that GP IX is the component of the GP Ib-IX complex recognized by those antibodies.	Quinidine	72-81	glycoprotein IX platelet	Homo sapiens	137-142
7720517-7	1995	Substances known to interact with CYP2C (sulfaphenazole, mephenytoin, and tolbutamide) and with CYP2D6 (bufuralol and quinidine) did not specifically inhibit the metabolism of budesonide.	Quinidine	118-127	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	96-102
7850926-6	1995	Quinidine, an antiarrythmic agent, has been demonstrated to circumvent multidrug resistance in cell lines, possibly by interfering with Pgp function.	Quinidine	0-9	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	136-139
7850926-12	1995	The present data confirm that intestinal Pgp mediates the efflux of etoposide and that the use of Pgp-inhibiting agents such as quinidine may increase the bioavailability of etoposide.	Quinidine	128-137	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	98-101
7720520-5	1995	The probes sulfaphenazole (CYP2C9) and quinidine (CYP2D6) selectively inhibited tolbutamide methylhydroxylation and bufuralol 1"-hydroxylation, respectively.	Quinidine	39-48	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	50-56
8083699-1	1994	PURPOSE: To evaluate the effect of quinidine, a putative modulator of P-glycoprotein-mediated drug resistance, on the response rate and toxicity profile of epirubicin in patients with advanced breast cancer.	Quinidine	35-44	ATP binding cassette subfamily B member 1	Homo sapiens	70-84
7883281-0	1995	Prevention of ischaemia-induced biochemical changes by curcumin & quinidine in the cat heart.	Quinidine	70-79	catalase	Homo sapiens	87-90
7983045-9	1994	In support of this conclusion, both binding and transport were inhibited by verapamil, quinidine, and reserpine, all known to be inhibitors of photoaffinity labeling of P-gp, but only transport was inhibited by C219 anti-P-gp antibody or orthovanadate.	Quinidine	87-96	phosphoglycolate phosphatase	Mus musculus	169-173
7983045-9	1994	In support of this conclusion, both binding and transport were inhibited by verapamil, quinidine, and reserpine, all known to be inhibitors of photoaffinity labeling of P-gp, but only transport was inhibited by C219 anti-P-gp antibody or orthovanadate.	Quinidine	87-96	phosphoglycolate phosphatase	Mus musculus	221-225
7895609-8	1994	Quinidine, a specific inhibitor of CYP2D6, inhibited propranolol 4- and 5-hydroxylase activities selectively and in a concentration-dependent manner.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	35-41
7943358-3	1994	We confirmed the previously reported intermediate-conductance K+ channel (72 pS), which is inhibited by millimolar cell ATP, acidic pH, Ba2+, and quinidine (4).	Quinidine	146-155	potassium calcium-activated channel subfamily N member 4	Rattus norvegicus	37-72
7931489-10	1994	In 10 of 11 samples, the multi-drug resistance (Mdr) modulator quinidine altered nuclear daunorubicin (DNR) accumulation and whole-cell TPT accumulation by less than 15%, which suggests that Pgp-mediated effects on drug efflux are insufficient to explain the fourfold range of TPT sensitivities in the colony-forming assays.	Quinidine	63-72	ATP binding cassette subfamily B member 1	Homo sapiens	191-194
7808368-4	1994	The existence of drugs (calcium blockers, cyclosporine, tamoxifen, reserpine, quinidine) able to bind themselves to gp170 and to paralyze its activity in vitro is well known.	Quinidine	78-87	ATP binding cassette subfamily B member 1	Homo sapiens	116-121
8582470-1	1995	Quinidine is a very potent inhibitor of CYP2D6, but the role of the enzyme in the biotransformation of quinidine has only been investigated in a single in vitro study and in two small in vivo experiments, with contradictory results.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	40-46
8582470-2	1995	The present investigation was designed to present definite evaluation of whether quinidine is metabolised by CYP2D6.	Quinidine	81-90	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	109-115
7815332-11	1995	Quinidine"s blocking actions on IKur were similar to those previously reported for block of a cardiac K+ channel clone of the Shaker family (Kv1.5), for which IKur is believed to be the equivalent native current.	Quinidine	0-9	potassium voltage-gated channel subfamily A member 5	Homo sapiens	141-146
7517207-6	1994	Our findings indicate that DDAb induced by SMX and SIX, in contrast to those induced by quinidine and quinine, are mainly specific for GPIIb/IIIa and react preferentially with calcium-dependent epitopes present only on the intact GPIIb/IIIa heterodimer.	Quinidine	88-97	integrin subunit alpha 2b	Homo sapiens	135-140
7935340-7	1994	However, at low substrate concentrations bufuralol 1"-hydroxylation was shown to be catalyzed principally by P450 2D6, based on the inhibitory effects of anti-rat P450 2D1 antibody and quinidine, in both human samples HL-18 and HL-67.	Quinidine	185-194	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	109-113
8080088-5	1994	Furthermore, the O-demethylase activity in a panel of microsomes prepared from a series of human livers was significantly correlated with the immunochemically determined levels of CYP2D6 protein (r = 0.925, p < 0.001), and was inhibited (> 89%) by quinidine and lobeline.	Quinidine	254-263	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	180-186
7951142-4	1994	The bunitrolol 4-hydroxylase activity was significantly inhibited by quinidine, a selective inhibitor for CYP2D6.	Quinidine	69-78	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	106-112
8039662-3	1994	The largest complementation group has been designated QDS1, for increased quinidine-sensitivity.	Quinidine	74-83	kexin KEX2	Saccharomyces cerevisiae S288C	54-58
8039662-4	1994	Exposure of qds1 cells to lethal concentrations of quinidine results in a novel small-budded terminal morphology in about 70% of the cells in the culture.	Quinidine	51-60	kexin KEX2	Saccharomyces cerevisiae S288C	12-16
8039662-9	1994	Loss of QDS1/KEX2 function results in quinidine sensitivity.	Quinidine	38-47	kexin KEX2	Saccharomyces cerevisiae S288C	8-12
8039662-9	1994	Loss of QDS1/KEX2 function results in quinidine sensitivity.	Quinidine	38-47	kexin KEX2	Saccharomyces cerevisiae S288C	13-17
7908989-11	1994	Verapamil and quinidine lowered the IC50 values of doxorubicin for MDR1-positive cell lines.	Quinidine	14-23	ATP binding cassette subfamily B member 1	Homo sapiens	67-71
8138941-5	1994	Quinidine was a highly potent inhibitor of 2-OH-DMI formation (mean Ki = 0.053 microM), consistent with the presumed role of Cytochrome P450-2D6 in mediating this reaction.	Quinidine	0-9	cytochrome P450 2D6	Homo sapiens	125-144
8013282-3	1994	The cytochrome P-450 (CYP) 2D6 inhibitor quinidine (1 microM) reduced the hydroxylation of tropisetron (67%) and ondansetron (18%).	Quinidine	41-50	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	4-30
7909523-5	1994	ATP-dependent transport of the permanently charged amphiphilic cations was inhibited by the P-glycoprotein inhibitors and substrates quinidine, verapamil, and daunorubicin.	Quinidine	133-142	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	92-106
7909523-6	1994	The data demonstrate that N-alkylation of quinidine and ajmaline results in most efficient substrates for mdr1 P-glycoprotein-mediated ATP-dependent transport.	Quinidine	42-51	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	106-110
7909523-6	1994	The data demonstrate that N-alkylation of quinidine and ajmaline results in most efficient substrates for mdr1 P-glycoprotein-mediated ATP-dependent transport.	Quinidine	42-51	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	111-125
8301569-0	1994	Albumin decreases myocardial permeability of unbound quinidine in perfused rat heart.	Quinidine	53-62	albumin	Rattus norvegicus	0-7
8301569-3	1994	Compared with 0% albumin perfusate, the equilibrium rate of quinidine perfusate output concentration (Cout) was slower with 0.1% albumin but faster with 1% and 6% albumin.	Quinidine	60-69	albumin	Rattus norvegicus	17-24
12959268-10	1993	Formation of 5-O-desmethylomeprazole was inhibited by both R, S-mephenytoin and quinidine, indicating that both S-mephenytoin hydroxylase and CYP2D6 may mediate this reaction in human liver microsomes and in vivo.	Quinidine	80-89	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	142-148
8301569-3	1994	Compared with 0% albumin perfusate, the equilibrium rate of quinidine perfusate output concentration (Cout) was slower with 0.1% albumin but faster with 1% and 6% albumin.	Quinidine	60-69	albumin	Rattus norvegicus	129-136
8301569-3	1994	Compared with 0% albumin perfusate, the equilibrium rate of quinidine perfusate output concentration (Cout) was slower with 0.1% albumin but faster with 1% and 6% albumin.	Quinidine	60-69	albumin	Rattus norvegicus	129-136
8250956-0	1993	Effect of alpha 1-acidglycoprotein on myocardial uptake and pharmacodynamics of quinidine in perfused rat heart.	Quinidine	80-89	orosomucoid 1	Rattus norvegicus	10-34
8242617-12	1993	By contrast, the CYP2D6-selective inhibitor quinidine did not affect either microsomal activity, while anti-CYP2A antibodies had only a modest inhibitory effect.	Quinidine	44-53	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	17-23
8272795-3	1993	The influence of naloxone and quinidine (a selective P450DB1 or CAP2D6 inhibitor) on tramadol effect was investigated crossover and double-blind vs placebo in healthy subjects.	Quinidine	30-39	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	53-60
8272795-13	1993	Quinidine blockade of tramadol myosis suggests that the mu agonist component of tramadol effect results from its O-demethylation by the polymorphic P450DB1 enzyme.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	148-155
8006952-12	1994	P2-receptor-stimulated mucin and Isc release was strongly inhibited by a 30 min preincubation with the classical K+ channel blockers quinine (1 mM), quinidine (1 mM), and Ba2+ (3 mM).	Quinidine	149-158	LOC100508689	Homo sapiens	23-28
8250956-3	1993	The equilibration rate constant for the quinidine output concentration increased with increasing AAG concentration, but not as much as predicted by the conventional pharmacokinetic uptake model, which assumes constant capillary permeability among the phases.	Quinidine	40-49	orosomucoid 1	Rattus norvegicus	97-100
8300799-2	1993	By using a large-pore (300 A) Selectosil C18 column, developed for the analysis of macromolecules, we have shown that quinidine in plasma and protein solutions can be assayed accurately and rapidly by directly injecting 2 microliters plasma or protein solution onto the column.	Quinidine	118-127	Bardet-Biedl syndrome 9	Homo sapiens	41-44
8238476-7	1993	Blocking of the Kv1.5 channel by 60 microM quinidine negated the effects of Kv1.5 expression on intracellular volume, Na(+)-K(+)-ATPase, and Na(+)-dependent alanine transport.	Quinidine	43-52	potassium voltage-gated channel subfamily A member 5	Homo sapiens	16-21
8238476-7	1993	Blocking of the Kv1.5 channel by 60 microM quinidine negated the effects of Kv1.5 expression on intracellular volume, Na(+)-K(+)-ATPase, and Na(+)-dependent alanine transport.	Quinidine	43-52	potassium voltage-gated channel subfamily A member 5	Homo sapiens	76-81
7693389-7	1993	However, over the first hour after dosing, the extensive metabolizers reported more "good opiate effects" and fewer "bad opiate effects" than poor metabolizers and extensive metabolizers in whom CYP2D6 was inhibited by quinidine.	Quinidine	219-228	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	195-201
7911345-11	1993	Reversal compounds specifically inhibiting Pgp were found, such as verapamil, cyclosporin or quinidine.	Quinidine	93-102	ATP binding cassette subfamily B member 1	Homo sapiens	43-46
8408733-1	1993	Quinidine and nifedipine appear to be subject to metabolism by the same isozyme of cytochrome P-450.	Quinidine	0-9	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	83-99
8272570-6	1993	Prior administration of quinidine produced a large reduction in the metabolic oxidation of trimipramine with CYP2D6 while prior administration of quinine had no effect.	Quinidine	24-33	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	109-115
8371133-6	1993	As reported previously, RS-mexiletine disposition was altered by a genetically determined (PM) or drug-induced (quinidine) decrease in CYP2D6 activity.	Quinidine	112-121	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	135-141
8323546-4	1993	Quinidine, a selective inhibitor of CYP2D6, suppressed the ring-hydroxylase activities of CZ and FZ.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	36-42
8485585-7	1993	h2D6v2 microsomes were capable of metabolizing NNK and NNK metabolism and mutagenicity were markedly inhibited by the addition of quinidine, a CYP2D6 inhibitor.	Quinidine	130-139	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	143-149
8103798-10	1993	The findings obtained here support the hypothesis that digoxin is secreted by P-glycoprotein located on the luminal membrane of renal tubular epithelial cells, and that clinically important interactions with quinidine and verapamil are caused by the inhibition of P-glycoprotein.	Quinidine	208-217	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	264-278
8100167-0	1993	Quinidine inhibition of debrisoquine S(+)-4- and 7-hydroxylations in Chinese of different CYP2D6 genotypes.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	90-96
8100167-5	1993	The inhibition of CYP2D6 by quinidine was also investigated.	Quinidine	28-37	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	18-24
8100167-12	1993	This study shows that the cytochrome P450 catalysing the 4- and 7-hydroxylations of debrisoquine in Chinese EM has the same properties (product stereoselectivity and inhibition by quinidine) as the CYP2D6 in Caucasian EM.	Quinidine	180-189	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	198-204
1359120-2	1992	In this study, it was demonstrated that digoxin is a substrate of P-glycoprotein, and the mechanism of a clinically important drug interaction, such as digoxin-quinidine, was elucidated.	Quinidine	160-169	ATP binding cassette subfamily B member 1	Homo sapiens	66-80
8099844-5	1993	P-Glycoprotein inhibitors such as quinidine, verapamil, vincristine, and cyclosporine increased the net A-B flux and inhibited the total B-A flux without affecting the nonspecific flux significantly.	Quinidine	34-43	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
8276051-5	1993	The enzyme catalysing bupranolol metabolism was CYP2D6: microsomes from a liver with the genetic enzyme deficiency did not metabolize bupranolol; in microsomes from livers containing the enzyme and 10 microM bupranolol, 5 microM quinidine caused a 72% inhibition of bupranolol metabolism.	Quinidine	229-238	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	48-54
1337728-3	1992	The channel state dependent blocking effects on cardiac sodium current (INa) of quinidine and disopyramide were studied under the whole cell variation of the patch clamp technique.	Quinidine	80-89	alpha-internexin	Cavia porcellus	72-75
1337728-10	1992	CONCLUSIONS: Quinidine produces more potent tonic and use dependent block of INa by binding to sodium channels at both rested and inactivated states, while disopyramide has a higher affinity for activated state.	Quinidine	13-22	alpha-internexin	Cavia porcellus	77-80
1359120-11	1992	These findings demonstrate that digoxin is transported by human P-glycoprotein, which is a previously undiscovered drug transport system in the kidney other than organic cation and anion transport systems, and suggest a molecular mechanism for the renal tubular secretion of digoxin as well as clinically important digoxin-quinidine interaction via P-glycoprotein.	Quinidine	323-332	ATP binding cassette subfamily B member 1	Homo sapiens	64-78
1611804-7	1992	Based on the brain/plasma ratio for dextromethorphan in rats, it is estimated that brain dextromethorphan concentrations of 1.0 to 10 micrograms/gm may be attainable in humans by inhibition of cytochrome P4502D6 activity with quinidine.	Quinidine	226-235	cytochrome P450 2D6	Homo sapiens	193-211
1334137-6	1992	DDF and ine mutations each potentiated the effects of quinidine on synaptic transmission, but neither had any observable effects in the absence of quinidine.	Quinidine	54-63	inebriated	Drosophila melanogaster	8-11
1642641-2	1992	The clearance of quinidine, midazolam, triazolam, erythromycin, and lidocaine declines with age; these drugs are metabolized by the isoform, CYP3A.	Quinidine	17-26	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	141-146
1618918-3	1992	K-current blockers tested (quinidine, 4-aminopyridine, barium, and tetraethylammonium) exhibited similar rank order potency for K-current block and inhibition of prolactin-induced proliferation of malignant lymphocytes.	Quinidine	27-36	prolactin	Homo sapiens	162-171
1378852-4	1992	Fab fragments purified from the IgG of two quinidine-induced lupus patients and patients with isoniazid- and procainamide-induced lupus retained 39% +/- 8% of their original IgG reactivity compared to 34 +/- 28% of the original anti-tetanus toxoid activity of Fab fragments in two of the same sera and two normal sera.	Quinidine	43-52	FA complementation group B	Homo sapiens	0-3
1632813-7	1992	Propranolol and quinidine, specific inhibitors of debrisoquine 4-hydroxylase, markedly inhibited lidocaine 3-hydroxylase activity of Wistar male rats, but not N-deethylase activity.	Quinidine	16-25	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	50-76
1611804-0	1992	Dextromethorphan: enhancing its systemic availability by way of low-dose quinidine-mediated inhibition of cytochrome P4502D6.	Quinidine	73-82	cytochrome P450 2D6	Homo sapiens	106-124
1611804-3	1992	The purpose of this research was to determine whether quinidine (a selective inhibitor of cytochrome P4502D6) could improve dextromethorphan systemic delivery in patients with amyotrophic lateral sclerosis (a neurodegenerative disease).	Quinidine	54-63	cytochrome P450 2D6	Homo sapiens	90-108
1348448-9	1992	Cytotoxicity measurements performed by counting the number of surviving cells (MCF-7/Adriar) or employing a modified, highly stable tetrazolium dye reduction assay (leukemia cell lines) revealed that quinidine diminished the IC50 for TPT in the Pgp-overexpressing cell lines but not in the control lines.	Quinidine	200-209	ATP binding cassette subfamily B member 1	Homo sapiens	245-248
1451729-7	1992	These findings suggest that quinidine inhibits the first step of flecainide metabolism, although it may also reduce its renal clearance, but to a lesser extent (3.5 vs 2.9 ml.min-1 x kg-1).	Quinidine	28-37	CD59 molecule (CD59 blood group)	Homo sapiens	175-180
1494979-1	1992	The disposition of quinidine was investigated in rats with experimental hepatic disease caused by an intraperitoneal injection of CCl4.	Quinidine	19-28	C-C motif chemokine ligand 4	Rattus norvegicus	130-134
1494979-4	1992	In the CCl4-intoxicated rats, plasma total body clearance (CLtot), elimination rate constant of the central compartment (kel) and the volume of distribution (Vdss) of quinidine were decreased by 73, 51 and 36%, respectively, compared to those in the control rats.	Quinidine	167-176	C-C motif chemokine ligand 4	Rattus norvegicus	7-11
1494979-9	1992	Metabolic activity in the liver, the hepatic extraction ratio for quinidine, and the hepatic blood flow in the CCl4-intoxicated rats were decreased by 84, 57 and 47%, respectively, compared to those in the control rats.	Quinidine	66-75	C-C motif chemokine ligand 4	Rattus norvegicus	111-115
1559547-4	1992	The RVD primarily reflects loss of cell KCl since: (1) the K(+)-channel blockers quinidine and Ba2+ both inhibit the RVD; and (2) replacement of external Cl- with gluconate or addition of the Cl- channel blocker NPPB also inhibits the RVD.	Quinidine	81-90	natriuretic peptide B	Homo sapiens	212-216
1538710-1	1992	The interaction of quinidine with a cloned human cardiac potassium channel (HK2) expressed in a stable mouse L cell line was studied using the whole-cell tight-seal voltage-clamp technique.	Quinidine	19-28	hexokinase 2	Homo sapiens	76-79
1538710-10	1992	These data indicate that 1) the charged form of quinidine blocks the HK2 channel after it opens, 2) binding occurs within the transmembrane electrical field (probably in or near the ion permeation pathway), and 3) unbinding is required before the channel can close.	Quinidine	48-57	hexokinase 2	Homo sapiens	69-72
1623898-1	1992	We have studied the hypoalgesic effect of codeine (100 mg) after blocking the hepatic O-demethylation of codeine to morphine via the sparteine oxygenase (CYP2D6) by quinidine (200 mg).	Quinidine	165-174	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	154-160
1763518-0	1991	Quinine is a more potent inhibitor than quinidine in rat of the oxidative metabolic routes of methoxyphenamine which involve debrisoquine 4-hydroxylase.	Quinidine	40-49	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	125-151
1299135-6	1992	Lien and Qui 12 mg/kg lowered LVP, +dp/dtmax and SAP by 33%, 37%, 29% and 9%, 12%, 9% respectively.	Quinidine	9-12	amyloid P component, serum	Rattus norvegicus	49-52
1806288-1	1991	Plasma protein binding of weakly basic drugs such as propranolol and quinidine was determined in rats with carbon tetrachloride (CCl4)-induced hepatic disease.	Quinidine	69-78	C-C motif chemokine ligand 4	Rattus norvegicus	129-133
1658339-1	1991	To determine if the fast sodium current inactivation process is necessary for sodium current (INa) blockade by quinidine, we studied the effects of quinidine on INa in guinea-pig ventricular myocytes treated with chloramine-T, which removes the fast inactivation process of INa.	Quinidine	111-120	alpha-internexin	Cavia porcellus	94-97
1806288-2	1991	Free fractions of propranolol and quinidine in the plasma of rats at 24 h after CCl4-intoxication were decreased by 41 and 30%, respectively, compared to those of control rats.	Quinidine	34-43	C-C motif chemokine ligand 4	Rattus norvegicus	80-84
1658339-3	1991	Quinidine (10 microM) produced resting block of INa of 36 +/- 2% (n = 5) at the peak potential of -30 mV in chloramine-T treated myocytes.	Quinidine	0-9	alpha-internexin	Cavia porcellus	48-51
1658339-4	1991	Quinidine decreased INa in a dose-dependent manner.	Quinidine	0-9	alpha-internexin	Cavia porcellus	20-23
1658339-7	1991	Even after removal of the fast inactivation process of INa, use-dependent block was observed in the presence of quinidine when various depolarizing pulse durations (5 ms approximately 200 ms) were applied repetitively at intervals of 300 ms approximately 2 s. Longer depolarizing pulses and higher frequency pulse trains produced greater use-dependent block.	Quinidine	112-121	alpha-internexin	Cavia porcellus	55-58
1671173-6	1991	The resistance conferred by the MDR1 gene can be circumvented in a dose-dependent manner by simultaneous administration of agents previously shown to be inhibitors of the multidrug transporter in vitro, including verapamil isomers, quinidine, and quinine.	Quinidine	232-241	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	32-36
1674435-4	1991	The potential therefore exists for new therapeutic studies aimed at circumventing resistance which develops through this mechanism, by using modulators, such as verapamil, quinidine and several others, which prevent cellular drug efflux by competitive binding to P-glycoprotein.	Quinidine	172-181	ATP binding cassette subfamily B member 1	Homo sapiens	263-277
1899114-0	1991	Quinidine inhibits prolactin secretion induced by thyrotropin-releasing hormone, high medium potassium or hyposmolarity in GH4C1 cells.	Quinidine	0-9	prolactin	Rattus norvegicus	19-28
1709374-11	1991	The binding domain(s) on GPIIb/IIIa for the quinine/quinidine-dependent antibodies appear to be sterically close to the epitopes for 22C4 and SZ22.	Quinidine	52-61	integrin subunit alpha 2b	Homo sapiens	25-30
1761076-0	1991	Quinidine but not quinine inhibits in man the oxidative metabolic routes of methoxyphenamine which involve debrisoquine 4-hydroxylase.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	107-133
1761076-3	1991	The oxidative routes of methoxyphenamine metabolisms which had been previously shown to involve debrisoquine 4-hydroxylase, namely O-demethylation and 5-hydroxylation were both significantly inhibited by quinidine in the 12 extensive metabolizers.	Quinidine	204-213	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	96-122
1899114-0	1991	Quinidine inhibits prolactin secretion induced by thyrotropin-releasing hormone, high medium potassium or hyposmolarity in GH4C1 cells.	Quinidine	0-9	thyrotropin releasing hormone	Rattus norvegicus	50-79
1899114-1	1991	In cultured GH4C1 cells quinidine inhibited basal prolactin (PRL) secretion and that induced by 0.1 to 10 nM thyrotropin-releasing hormone (TRH), 30 mM medium K+ or 30% medium hyposmolarity but did not inhibit secretion induced by 100 nM 12-O-tetradecanoylphorbol 13-acetate.	Quinidine	24-33	prolactin	Rattus norvegicus	50-59
1899114-1	1991	In cultured GH4C1 cells quinidine inhibited basal prolactin (PRL) secretion and that induced by 0.1 to 10 nM thyrotropin-releasing hormone (TRH), 30 mM medium K+ or 30% medium hyposmolarity but did not inhibit secretion induced by 100 nM 12-O-tetradecanoylphorbol 13-acetate.	Quinidine	24-33	thyrotropin releasing hormone	Rattus norvegicus	109-138
1899114-1	1991	In cultured GH4C1 cells quinidine inhibited basal prolactin (PRL) secretion and that induced by 0.1 to 10 nM thyrotropin-releasing hormone (TRH), 30 mM medium K+ or 30% medium hyposmolarity but did not inhibit secretion induced by 100 nM 12-O-tetradecanoylphorbol 13-acetate.	Quinidine	24-33	thyrotropin releasing hormone	Rattus norvegicus	140-143
1899114-2	1991	Inhibition of basal PRL secretion was highly correlated with the drug concentration between 30 microM to 1 mM quinidine; 50% inhibition of basal secretion occurred at 300 microM and at this concentration quinidine completely blocked PRL secretion stimulated by TRH, K+ and hyposmolarity.	Quinidine	204-213	thyrotropin releasing hormone	Rattus norvegicus	261-264
1899114-3	1991	Significant inhibition of TRH-induced PRL secretion was produced by 15 microM quinidine, a concentration equivalent to that in plasma during standard antiarrhythmic therapy with quinidine in humans.	Quinidine	78-87	thyrotropin releasing hormone	Homo sapiens	26-29
1899114-3	1991	Significant inhibition of TRH-induced PRL secretion was produced by 15 microM quinidine, a concentration equivalent to that in plasma during standard antiarrhythmic therapy with quinidine in humans.	Quinidine	178-187	thyrotropin releasing hormone	Homo sapiens	26-29
2240575-5	1990	In this work, OH-, H+, and quinidine have been used to stop the enzymes LDH (EC 1.1.1.27) (with H+ and OH-) and cholinesterase (EC 3.1.1.8) (with quinidine).	Quinidine	27-36	butyrylcholinesterase	Homo sapiens	96-126
2269307-13	1990	Microsomal suspensions containing P450 NF25 were also able to catalyze several oxidation reactions that were expected from the activities of the protein isolated from human liver, including nifedipine 1,4-oxidation, quinidine 3-hydroxylation and N-oxygenation, and N-demethylation of the macrolide antibiotics erythromycin and troleandomycin.	Quinidine	216-225	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	39-43
2240575-5	1990	In this work, OH-, H+, and quinidine have been used to stop the enzymes LDH (EC 1.1.1.27) (with H+ and OH-) and cholinesterase (EC 3.1.1.8) (with quinidine).	Quinidine	146-155	butyrylcholinesterase	Homo sapiens	96-126
2263067-10	1990	These data show that quinidine inhibits in vivo metabolism of amphetamine in rats and suggest that amphetamine metabolism may, in part, be mediated by an isozyme of P450 which displays genetic polymorphism.	Quinidine	21-30	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	165-169
2357863-1	1990	Because both quinidine and propranolol bind to the cytochrome P-450 responsible for the oxidation of debrisoquin, six healthy male subjects were studied to determine whether an interaction occurred between the two drugs and the pharmacodynamic consequences of that interaction.	Quinidine	13-22	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	51-67
7835228-7	1994	MP metabolism studies were also conducted with CYP2D6 microsomes in the presence of quinidine and quinine.	Quinidine	84-93	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	47-53
1967551-7	1990	Modulators of Pgp-MDR also compete with LU-49888 for binding to Pgp: verapamil (82%), diltiazem (73%), quinidine (91%), reserpine (91%), rescinnamine (88%), and trimethoxybenzoylyohimbine (89%).	Quinidine	103-112	ATP binding cassette subfamily B member 1	Homo sapiens	14-17
2306418-4	1990	Otherwise, no significant phenotypic differences in total or metabolic clearance were found and it is concluded that the metabolism of quinidine is largely carried out by P450 isoenzymes different from P450db1.	Quinidine	135-144	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	171-175
1979534-11	1990	Io(ATP) was completely abolished by removal of external Ca2+, treatment with an intracellular Ca2+ chelator, the acetoxymethyl ester of 1,2-bis (2-aminophenoxy) ethane-N,N,N",N"-tetra acetic acid (BAPTA-AM) and bath applied quinidine but not tetraethylammonium (TEA) or apamin.	Quinidine	224-233	carbonic anhydrase 2	Mus musculus	94-97
2312782-1	1990	Quinidine has been reported to be a potent inhibitor of a specific isozyme of cytochrome P-450 (P-450db 1) that is responsible for the metabolism of a select group of drugs.	Quinidine	0-9	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	78-94
2312782-1	1990	Quinidine has been reported to be a potent inhibitor of a specific isozyme of cytochrome P-450 (P-450db 1) that is responsible for the metabolism of a select group of drugs.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	96-105
2312782-2	1990	In order to investigate the potential for quinidine to inhibit other isozymes of cytochrome P-450 and to assess whether or not P-450db 1 plays any role in antipyrine metabolism, we studied the effects of quinidine pretreatment on the pharmacokinetics and metabolism of antipyrine in six healthy, male volunteers.	Quinidine	42-51	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	81-97
34903590-4	2022	The resulting ISEF values for CYP3A4 were substrate-dependent and ranged 8-fold, with the highest value generated from intrinsic clearance of midazolam depletion (0.36) and the lowest from quinidine depletion (0.044).	Quinidine	189-198	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	30-36
34668334-2	2022	This study aimed to investigate an IVIVE for intestinal P-glycoprotein (Pgp, ABCB1)-mediated DDIs between three Pgp substrates, digoxin, dabigatran etexilate and quinidine, and two Pgp inhibitors, itraconazole and verapamil, via PBPK modeling.	Quinidine	162-171	ATP binding cassette subfamily B member 1	Homo sapiens	56-70
34668334-2	2022	This study aimed to investigate an IVIVE for intestinal P-glycoprotein (Pgp, ABCB1)-mediated DDIs between three Pgp substrates, digoxin, dabigatran etexilate and quinidine, and two Pgp inhibitors, itraconazole and verapamil, via PBPK modeling.	Quinidine	162-171	ATP binding cassette subfamily B member 1	Homo sapiens	72-75
34668334-2	2022	This study aimed to investigate an IVIVE for intestinal P-glycoprotein (Pgp, ABCB1)-mediated DDIs between three Pgp substrates, digoxin, dabigatran etexilate and quinidine, and two Pgp inhibitors, itraconazole and verapamil, via PBPK modeling.	Quinidine	162-171	ATP binding cassette subfamily B member 1	Homo sapiens	77-82
34668334-2	2022	This study aimed to investigate an IVIVE for intestinal P-glycoprotein (Pgp, ABCB1)-mediated DDIs between three Pgp substrates, digoxin, dabigatran etexilate and quinidine, and two Pgp inhibitors, itraconazole and verapamil, via PBPK modeling.	Quinidine	162-171	ATP binding cassette subfamily B member 1	Homo sapiens	112-115
34948226-6	2021	The data obtained demonstrate that cinchonidine and quinidine are potent inducers of gamma-globin mRNA and HbF in erythroid progenitor cells isolated from nine beta-thalassemia patients.	Quinidine	52-61	hemoglobin subunit gamma 1	Homo sapiens	85-97
34903589-6	2022	Reported digoxin concentrations in a drug-drug interaction study with MDR1 inhibitors quinidine and verapamil were consistent with the profiles simulated by our model incorporating inhibition of efflux transporter at the BM in addition to MVM.	Quinidine	86-95	ATP binding cassette subfamily B member 1	Homo sapiens	70-74
34122071-0	2021	Case Report of Novel Genetic Variant in KCNT1 Channel and Pharmacological Treatment With Quinidine.	Quinidine	89-98	potassium sodium-activated channel subfamily T member 1	Homo sapiens	40-45
34096834-4	2021	In addition, the GSH and NAC conjugates were also found in bile and urine of rats given ZOL, respectively.ZOL-derived GSH conjugate M1 was also observed in ZOL-treated rat primary hepatocytes, and the formation of M1 was inhibited by pre-cultured with quinidine (a selective inhibitor of CYP2D6).	Quinidine	252-261	cytochrome P450, family 2, subfamily d, polypeptide 3	Rattus norvegicus	288-294
34530005-4	2021	The inhibition study with quinidine clearly indicated that the decrease in secretory clearance of R-123 by adrenaline or the increase by DBcAMP would be attributed to the decrease or increase in P-gp activity, respectively.	Quinidine	26-35	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	195-199
34268580-6	2021	For digoxin, verapamil and quinidine, in vitro kinetic data on their transport by Pgp were derived from literature and used to scale to in vivo parameters.	Quinidine	27-36	ATP binding cassette subfamily B member 1	Homo sapiens	82-85
34373326-10	2021	We also show that both phosphorylation and patient mutations can impact Nav1.5 sensitivity toward the clinically used antiarrhythmic drugs quinidine and ranolazine, but not flecainide.	Quinidine	139-148	sodium voltage-gated channel alpha subunit 5	Homo sapiens	72-78
34122071-4	2021	Aim: To present the pharmacological response and therapeutic drug monitoring of a paediatric patient with a severe encephalopathy carrying a genetic variant in KCNT1 gene, whose identification led to include quinidine (QND) in the treatment regimen as an antiepileptic drug.	Quinidine	208-217	potassium sodium-activated channel subfamily T member 1	Homo sapiens	160-165
35616006-7	2022	The AUC of asciminib was marginally decreased by concomitant administration with the strong CYP3A inducer rifampicin (by ~13-15%) and the strong P-gp inhibitor quinidine (by ~13-16%).	Quinidine	160-169	ATP binding cassette subfamily B member 1	Homo sapiens	145-149
35599345-5	2022	Selective CYP inhibitor studies showed FFA metabolism partially inhibited by quinidine (CYP2D6, 48%), phencyclidine (CYP2B6, 42%), and furafylline (CYP1A2, 32%) and, to a lesser extent (<15%), by tienilic acid (CYP2C9), esomeprazole (CYP2C19), and troleandomycin (CYP3A4/5).	Quinidine	77-86	peptidylprolyl isomerase G	Homo sapiens	10-13
35599345-5	2022	Selective CYP inhibitor studies showed FFA metabolism partially inhibited by quinidine (CYP2D6, 48%), phencyclidine (CYP2B6, 42%), and furafylline (CYP1A2, 32%) and, to a lesser extent (<15%), by tienilic acid (CYP2C9), esomeprazole (CYP2C19), and troleandomycin (CYP3A4/5).	Quinidine	77-86	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	88-94
35442037-10	2022	Quinidine, a selective inhibitor of CYP2D6, attenuated the susceptibility of hepatocytes to the cytotoxicity of PPF.	Quinidine	0-9	cytochrome P450, family 2, subfamily d, polypeptide 3	Rattus norvegicus	36-42
35570332-4	2022	The constructed rifampicin model was verified using the remaining 5 DDI cases with digoxin and 5 DDI cases with other P-gp substrates (talinolol and quinidine).	Quinidine	149-158	ATP binding cassette subfamily B member 1	Homo sapiens	118-122
35570332-8	2022	For quinidine, predicted intestinal P-gp/CYP3A-mediated DDIs were slightly underestimated due to the complexity of non-linearity and transporter-enzyme interplay.	Quinidine	4-13	ATP binding cassette subfamily B member 1	Homo sapiens	36-40
35570332-8	2022	For quinidine, predicted intestinal P-gp/CYP3A-mediated DDIs were slightly underestimated due to the complexity of non-linearity and transporter-enzyme interplay.	Quinidine	4-13	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	41-46
35369761-3	2022	Quinidine is an anti-arrhythmic drug that functions as a moderately potent inhibitor of Slack channels; however, quinidine use is limited by its poor selectivity, safety and pharmacokinetic profile.	Quinidine	0-9	potassium sodium-activated channel subfamily T member 1	Homo sapiens	88-93
35388935-0	2022	Early Repolarization Syndrome, Epilepsy and Atrial Fibrillation in a young girl with novel KCND3 mutation managed with quinidine.	Quinidine	119-128	potassium voltage-gated channel subfamily D member 3	Homo sapiens	91-96
35246464-5	2022	The current study also demonstrated that selective inhibition sufficient for fm calculation was achieved by inhibitors of CYP1A2 (20 microM furafylline), CYP2C8 (40 microM montelukast), CYP2C9 (40 microM sulfaphenazole), CYP2C19 (3 microM (-)N-3-benzyl-phenobarbital) and CYP2D6 (5 microM quinidine).	Quinidine	289-298	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	122-128
35246464-5	2022	The current study also demonstrated that selective inhibition sufficient for fm calculation was achieved by inhibitors of CYP1A2 (20 microM furafylline), CYP2C8 (40 microM montelukast), CYP2C9 (40 microM sulfaphenazole), CYP2C19 (3 microM (-)N-3-benzyl-phenobarbital) and CYP2D6 (5 microM quinidine).	Quinidine	289-298	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	186-192
35389533-7	2022	In inhibitor experiments, quinidine and erythromycin inhibited ITZ hydroxylation in CYP2D15 and CYP3A12, respectively, in an isoform-specific manner.	Quinidine	26-35	cytochrome P450 2D15	Canis lupus familiaris	84-91
35389533-7	2022	In inhibitor experiments, quinidine and erythromycin inhibited ITZ hydroxylation in CYP2D15 and CYP3A12, respectively, in an isoform-specific manner.	Quinidine	26-35	cytochrome P450 3A12	Canis lupus familiaris	96-103
35369761-3	2022	Quinidine is an anti-arrhythmic drug that functions as a moderately potent inhibitor of Slack channels; however, quinidine use is limited by its poor selectivity, safety and pharmacokinetic profile.	Quinidine	113-122	potassium sodium-activated channel subfamily T member 1	Homo sapiens	88-93
2775304-0	1989	The specificity of inhibition of debrisoquine 4-hydroxylase activity by quinidine and quinine in the rat is the inverse of that in man.	Quinidine	72-81	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	33-59
35378899-9	2022	Through connectivity map, we also identified eight compounds that may be used as targeted therapeutic agents for ACBD4 gene in HBV-related HCC; these compounds were scopoletin, alfaxalone, bephenium hydroxynaphthoate, apramycin, 4,5-dianilinophthalimide, DL-thiorphan, aminohippuric acid and quinidine.	Quinidine	292-301	acyl-CoA binding domain containing 4	Homo sapiens	113-118
2775304-1	1989	The kinetics of inhibition of debrisoquine 4-hydroxylase activity by quinidine and quinine in rat and human liver microsomes have been compared.	Quinidine	69-78	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	30-56
2775304-2	1989	Quinidine is a potent inhibitor of debrisoquine 4-hydroxylase activity of human liver (IC50: 3.6 microM).	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	35-61
2775304-7	1989	Inhibition of debrisoquine 4-hydroxylase activity by both quinine and quinidine in human and rat liver is competitive.	Quinidine	70-79	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	14-40
2775304-10	1989	Although both quinidine and quinine are competitive inhibitors of debrisoquine 4-hydroxylase activity in rat and man, their potency is reversed.	Quinidine	14-23	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	66-92
2548389-10	1989	However, when AVP was applied during high K+ depolarization or in the presence of quinidine (1 mM), the initial hyperpolarizing response was practically abolished.	Quinidine	82-91	arginine vasopressin	Rattus norvegicus	14-17
2753156-4	1989	Na+-dependent Mg2+ efflux was inhibited by quinidine.	Quinidine	43-52	mucin 7, secreted	Homo sapiens	14-17
2561249-14	1989	The latter efflux activity is thought to be mediated by a membrane glycoprotein (p170) which is also sensitive to several of the various inhibitors (reserpine, verapamil, and quinidine) which reduce the efflux of methotrexate and cholate.	Quinidine	175-184	Ral GTPase activating protein, beta subunit (non-catalytic)	Mus musculus	81-85
2724349-0	1989	MDR1 RNA levels in human renal cell carcinomas: correlation with grade and prediction of reversal of doxorubicin resistance by quinidine in tumor explants.	Quinidine	127-136	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
2724349-6	1989	The enhancing effect of quinidine (7.5 micrograms/mL) on sensitivity to ADR was statistically significant only in the group with high MDR1 RNA levels.	Quinidine	24-33	ATP binding cassette subfamily B member 1	Homo sapiens	134-138
2724349-7	1989	Similar enhancement by quinidine of sensitivity to ADR was also observed in the established RCC cell lines in which MDR1 RNA levels were high.	Quinidine	23-32	ATP binding cassette subfamily B member 1	Homo sapiens	116-120
2538064-0	1989	Inhibition of ICa in single frog cardiac cells by quinidine, flecainide, ethmozin, and ethacizin.	Quinidine	50-59	calcium voltage-gated channel subunit alpha1 C	Canis lupus familiaris	14-17
2713218-0	1989	Lack of effect of treatment with human recombinant-tumour necrosis factor (HrTNF) on the binding of quinidine to alpha 1-acid glycoprotein (AGP).	Quinidine	100-109	orosomucoid 1	Rattus norvegicus	140-143
2713218-4	1989	It was observed that the quinidine binding ratio (the quotient of bound and free concentration in plasma) was highly correlated with the plasma concentration of AGP (r = 0.818) and that the mean pretreatment AGP concentration in the patients was about three times that found in normal subjects.	Quinidine	25-34	orosomucoid 1	Rattus norvegicus	161-164
2713218-4	1989	It was observed that the quinidine binding ratio (the quotient of bound and free concentration in plasma) was highly correlated with the plasma concentration of AGP (r = 0.818) and that the mean pretreatment AGP concentration in the patients was about three times that found in normal subjects.	Quinidine	25-34	orosomucoid 1	Rattus norvegicus	208-211
2816228-8	1989	The finding of red blood cells coated with IgG and C3d in this as well as in other cases adds further evidence to the hypothesis that a quinidine type mechanism of haemolysis might be responsible for Coombs positive haemolytic anaemia associated with solid tumours.	Quinidine	136-145	endogenous retrovirus group K member 13	Homo sapiens	51-54
2744218-5	1989	The inhibiting effect of amiodarone and propranolol on follicular production of cAMP, Tg and FT3 appears to result from several factors: (1) inhibition of thyroid 5"-deiodinase; (2) amiodarone high iodine content; (3) a quinidine-like effect of propranolol involving a membrane-stabilizing mechanism.	Quinidine	220-229	cathelicidin antimicrobial peptide	Homo sapiens	80-84
3689440-8	1987	Our data suggest that the debrisoquine/sparteine type of oxidation polymorphism is caused by an almost complete loss of a minor cytochrome P-450 isozyme which has a high affinity and stereoselectivity for (+)-bufuralol and a high sensitivity to inhibition by quinidine.	Quinidine	259-268	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	128-144
2773544-2	1989	In connection with other AChE-determination methods for blood quinidine sulphate in a concentration of 2.10(-5) mol/l is used as an inhibitor for the serum-cholinesterase (ChE).	Quinidine	62-80	acetylcholinesterase (Cartwright blood group)	Homo sapiens	25-29
2894945-1	1988	Competitive inhibition studies using human liver microsomes have shown that quinidine (QD) has an exceptionally high affinity (60 nM) for the genetically variable cytochrome P-450 that catalyzes the formation of 4-hydroxydebrisoquine and dehydrosparteines from debrisoquine and sparteine.	Quinidine	76-85	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	163-179
3681376-3	1987	Two criteria suggest that primary multidrug resistance in human adenocarcinomas of the kidney results, at least in part, from expression of the mdr1 gene: (1) mdr1 mRNA levels are elevated in four unselected kidney adenocarcinoma cell lines that show a multidrug-resistant phenotype; and (2) multidrug resistance in these kidney cancer cell lines is reversed by verapamil and quinidine, agents known to reverse mdr1-associated drug resistance in cell lines selected for multidrug resistance in vitro.	Quinidine	376-385	ATP binding cassette subfamily B member 1	Homo sapiens	144-148
3130251-1	1987	The activity of hepatic aldehyde oxidase from rabbit, guinea pig, rat, marmoset, dog, baboon and man was investigated in vitro with charged and uncharged N-heterocyclic substrates: Km and Vmax values were determined for phthalazine, 6,7-dimethoxy-1-[-4-(ethylcarbamoyloxy)piperidino]phthalazine (carbazeran), quinine and quinidine.	Quinidine	321-330	aldehyde oxidase 1	Homo sapiens	24-40
3674164-0	1987	Inhibitory effect of quinidine on plasma pseudocholinesterase activity in pregnant women.	Quinidine	21-30	butyrylcholinesterase	Homo sapiens	41-61
3674164-1	1987	The effect of quinidine at therapeutic and subtherapeutic concentrations on pseudocholinesterase activity in the plasma of 16 normal pregnant women was studied.	Quinidine	14-23	butyrylcholinesterase	Homo sapiens	76-96
3674164-2	1987	The mean plasma pseudocholinesterase activity in the absence of quinidine (control) was 0.67 +/- 0.11 U/ml.	Quinidine	64-73	butyrylcholinesterase	Homo sapiens	16-36
3674164-3	1987	The mean pseudocholinesterase activity in the presence of quinidine at concentrations of 0.5, 1.0, 2.0, and 5.0 micrograms/ml 0.48 +/- 0.09, 0.38 +/- 0.09, 0.29 +/- 0.10, and 0.19 +/- 0.09 U/ml, respectively.	Quinidine	58-67	butyrylcholinesterase	Homo sapiens	9-29
3674164-4	1987	At therapeutic concentrations needed to treat cardiac arrhythmias (2 to 5 micrograms/ml), quinidine inhibited pseudocholinesterase activity by 60% to 70%.	Quinidine	90-99	butyrylcholinesterase	Homo sapiens	110-130
3678237-9	1987	In 3 patients with sinus rate less than 50 beats min-1 and an abnormal intrinsic heart rate, quinidine induced marked depression of sinus automaticity.	Quinidine	93-102	CD59 molecule (CD59 blood group)	Homo sapiens	49-54
3330586-2	1987	From these findings and a review of 10 case reports, we propose that disopyramide causes hypoglycaemia by stimulation of insulin release as described for the antimalarial drugs quinine and quinidine.	Quinidine	189-198	insulin	Homo sapiens	121-128
2452453-8	1987	Membrane current through the inward rectifier (IK1) was slightly increased by lidocaine, but significantly inhibited by quinidine.	Quinidine	120-129	IKAROS family zinc finger 1	Homo sapiens	47-50
3035942-2	1987	Exposure of isolated toad bladders to quinidine, calcium ionophores (A23187, X537A), or low-sodium or potassium-free serosal solutions resulted in a dose-dependent decrease in the hydrosmotic response to vasopressin or exogenous adenosine 3",5"-cyclic monophosphate (cAMP).	Quinidine	38-47	arginine vasopressin	Homo sapiens	204-215
3035943-0	1987	Quinidine effect on hydrosmotic response of collecting tubules to vasopressin and cAMP.	Quinidine	0-9	arginine vasopressin	Homo sapiens	66-77
3035943-1	1987	Quinidine, a compound thought to increase cytosolic calcium ion activity, has been found to inhibit the hydrosmotic response to vasopressin (VP) and adenosine 3",5"-cyclic monophosphate (cAMP) in the toad urinary bladder.	Quinidine	0-9	arginine vasopressin	Homo sapiens	128-139
3818954-0	1987	Binding of quinine- and quinidine-dependent drug antibodies to platelets is mediated by the Fab domain of the immunoglobulin G and is not Fc dependent.	Quinidine	24-33	FA complementation group B	Homo sapiens	92-95
3030751-6	1987	The accumulation of c-fos mRNA and the transcriptional activation of c-fos induced by PDD or A23187 were inhibited by the protein kinase inhibitor H-7 and by quinidine and amiloride.	Quinidine	158-167	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	20-25
3030751-6	1987	The accumulation of c-fos mRNA and the transcriptional activation of c-fos induced by PDD or A23187 were inhibited by the protein kinase inhibitor H-7 and by quinidine and amiloride.	Quinidine	158-167	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	69-74
2438320-5	1987	Both NAPA and quinidine immediately prolonged the atrial flutter cycle length in all dogs, from 118 +/- 15 to 141 +/- 18 ms and from 119 +/- 17 to 153 +/- 21 ms, respectively (both p less than 0.001), and then terminated atrial flutter in 11 of the 12 NAPA studies and in 6 of the 10 quinidine studies.	Quinidine	14-23	NSF attachment protein alpha	Canis lupus familiaris	252-256
2438320-5	1987	Both NAPA and quinidine immediately prolonged the atrial flutter cycle length in all dogs, from 118 +/- 15 to 141 +/- 18 ms and from 119 +/- 17 to 153 +/- 21 ms, respectively (both p less than 0.001), and then terminated atrial flutter in 11 of the 12 NAPA studies and in 6 of the 10 quinidine studies.	Quinidine	284-293	NSF attachment protein alpha	Canis lupus familiaris	5-9
3013024-1	1986	The influence of quinidine, a putative K+ channel blocker, on Cl- secretion induced by vasoactive intestinal polypeptide (VIP) was investigated.	Quinidine	17-26	vasoactive intestinal peptide	Homo sapiens	87-120
3755602-4	1986	In mouse macrophages, PAF-acether stimulated a quinidine-sensitive K+ efflux.	Quinidine	47-56	patchy fur	Mus musculus	22-25
3767290-4	1986	We adapted the same technique for the determination of erythrocyte cholinesterase using whole blood as sample and quinidine sulphate as inhibitor of pseudocholinesterase.	Quinidine	114-132	butyrylcholinesterase	Homo sapiens	149-169
3748010-0	1986	Oxidation of quinidine by human liver cytochrome P-450.	Quinidine	13-22	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	38-54
3013024-1	1986	The influence of quinidine, a putative K+ channel blocker, on Cl- secretion induced by vasoactive intestinal polypeptide (VIP) was investigated.	Quinidine	17-26	vasoactive intestinal peptide	Homo sapiens	122-125
3013024-2	1986	Quinidine inhibited Cl- secretion induced by VIP in T84 cell monolayers.	Quinidine	0-9	vasoactive intestinal peptide	Homo sapiens	45-48
3945161-0	1986	Protection from quinidine or physostigmine against in vitro inhibition by sarin of acetylcholinesterase activity.	Quinidine	16-25	acetylcholinesterase	Canis lupus familiaris	83-103
3085830-2	1986	In volunteers given a fixed dose of 500 mg base and patients with malaria given a quinidine loading dose (15 mg base/kg) mean (SEM) plasma insulin concentrations rose from 6.1 (1.5) mU/l to 10.9 (4.4) mU/l (p less than 0.02) and 10.4 (2.0) mU/l to 18.5 (5.3) mU/l (p less than 0.04), respectively.	Quinidine	82-91	insulin	Homo sapiens	139-146
3945161-5	1986	Quinidine partially protected AChE from the inhibitory effects of sarin in vitro possibly by altering the sarin binding sites.	Quinidine	0-9	acetylcholinesterase	Canis lupus familiaris	30-34
3945161-1	1986	We have studied the relative effectiveness of quinidine and physostigmine in protecting against the inhibition of acetylcholinesterase (AChE) by sarin, an organophosphate (OP) compound.	Quinidine	46-55	acetylcholinesterase	Canis lupus familiaris	114-134
3945161-1	1986	We have studied the relative effectiveness of quinidine and physostigmine in protecting against the inhibition of acetylcholinesterase (AChE) by sarin, an organophosphate (OP) compound.	Quinidine	46-55	acetylcholinesterase	Canis lupus familiaris	136-140
6177320-8	1982	Inhibition of cyclic AMP of cyclic GMP phosphodiesterase activity by 1-methyl-3-isobutylxanthine, quinidine, or compound SQ 20,009 was not affected appreciably by calcium or EGTA.	Quinidine	98-107	5'-nucleotidase, cytosolic II	Homo sapiens	35-38
3920247-8	1985	(f) Quinidine, which releases Ca2+ from intracellular stores, produced a large inhibition of the action of ADH but not that of cAMP; the inhibition was greatly reduced if serosal Ca2+ was deleted.	Quinidine	4-13	arginine vasopressin	Homo sapiens	107-110
6238641-8	1984	The sera of two patients with quinidine-induced thrombocytopenia precipitated a 138,000-dalton band (glycoprotein Ib-alpha) in the presence of quinidine.	Quinidine	30-39	glycoprotein Ib platelet subunit alpha	Homo sapiens	101-122
6238641-8	1984	The sera of two patients with quinidine-induced thrombocytopenia precipitated a 138,000-dalton band (glycoprotein Ib-alpha) in the presence of quinidine.	Quinidine	143-152	glycoprotein Ib platelet subunit alpha	Homo sapiens	101-122
6206104-1	1984	N-Acetylprocainamide (NAPA), a class III antiarrhythmic drug, caused torsade de pointes in a 72 year old woman who had this arrhythmia on two previous occasions while being treated with quinidine and disopyramide.	Quinidine	186-195	NSF attachment protein alpha	Homo sapiens	22-26
6372564-2	1984	Quinidine-induced antinuclear autoantibodies were of the IgM and IgG classes and were directed mainly to nuclear histones, predominantly histones H1 and H2B.	Quinidine	0-9	H2B clustered histone 21	Homo sapiens	153-156
2997198-5	1985	VIP- or A23187-stimulated efflux was inhibited by 5 mM Ba2+ or 1 mM quinidine, but not by 20 mM tetraethylammonium, 4 mM 4-aminopyridine, or 1 microM apamin.	Quinidine	68-77	vasoactive intestinal peptide	Homo sapiens	0-3
3988396-1	1985	The elimination half-life of high polar metabolites pool of quinidine (t1/2 beta = 6.1 h) has been determined in a quinidine phenobarbiturate intoxicated patient after the complete elimination of quinidine (its precursor) from blood.	Quinidine	60-69	interleukin 1 receptor like 1	Homo sapiens	71-80
3988396-1	1985	The elimination half-life of high polar metabolites pool of quinidine (t1/2 beta = 6.1 h) has been determined in a quinidine phenobarbiturate intoxicated patient after the complete elimination of quinidine (its precursor) from blood.	Quinidine	115-124	interleukin 1 receptor like 1	Homo sapiens	71-80
3988396-1	1985	The elimination half-life of high polar metabolites pool of quinidine (t1/2 beta = 6.1 h) has been determined in a quinidine phenobarbiturate intoxicated patient after the complete elimination of quinidine (its precursor) from blood.	Quinidine	115-124	interleukin 1 receptor like 1	Homo sapiens	71-80
3988396-2	1985	It is equivalent to the generally accepted t1/2 beta of quinidine (6.1 +/- 1.8 h) but substantially different from the t1/2 beta "hybrid" of 3-hydroxyquinidine (10.0 h) determined in therapeutic conditions in which 3-hydroxyquinidine coexists with quinidine in blood.	Quinidine	56-65	interleukin 1 receptor like 1	Homo sapiens	43-52
6616988-6	1983	Conversely, during atrial stimulation the STA interval increased significantly under the effect of quinidine, while verapamil had no further influence.	Quinidine	99-108	GCY	Homo sapiens	42-45
7237776-2	1981	Quinidine sulfate is used as an inhibitor of plasma cholinesterase during the measurement of erythrocyte acetylcholinesterase activity, obviating the need for washing the erythrocytes before lysis.	Quinidine	0-17	butyrylcholinesterase	Homo sapiens	52-66
6287317-2	1982	When applied externally quinidine (5.10(-5) M) suppresses both INa and IK.	Quinidine	24-33	internexin neuronal intermediate filament protein alpha	Homo sapiens	63-73
6277664-7	1982	In contrast atenolol, a beta-antagonist devoid of "quinidine-like" activity was ineffective at 4 degree C. Furthermore, procaine, and quinidine itself were potent competitors of [3H]dihydroalprenolol binding at 4 degree C. Thus the specificity of [3H]dihydroalprenolol binding to rat heart membranes at 4 degree C appears to be directed non-stereoselectively at that portion of the competing molecule which recognized "quinidine-like" as opposed to adrenergic activity.	Quinidine	51-60	amyloid beta precursor protein	Rattus norvegicus	22-28
6277664-7	1982	In contrast atenolol, a beta-antagonist devoid of "quinidine-like" activity was ineffective at 4 degree C. Furthermore, procaine, and quinidine itself were potent competitors of [3H]dihydroalprenolol binding at 4 degree C. Thus the specificity of [3H]dihydroalprenolol binding to rat heart membranes at 4 degree C appears to be directed non-stereoselectively at that portion of the competing molecule which recognized "quinidine-like" as opposed to adrenergic activity.	Quinidine	134-143	amyloid beta precursor protein	Rattus norvegicus	22-28
6277664-7	1982	In contrast atenolol, a beta-antagonist devoid of "quinidine-like" activity was ineffective at 4 degree C. Furthermore, procaine, and quinidine itself were potent competitors of [3H]dihydroalprenolol binding at 4 degree C. Thus the specificity of [3H]dihydroalprenolol binding to rat heart membranes at 4 degree C appears to be directed non-stereoselectively at that portion of the competing molecule which recognized "quinidine-like" as opposed to adrenergic activity.	Quinidine	134-143	amyloid beta precursor protein	Rattus norvegicus	22-28
34009624-3	2021	The previous UWL resistance model was well fitted to Papp of static and flow condition by assuming UWL including and negligible condition, while P-gp substrates of higher passive permeability (quinidine) was apart from the fitting curve.	Quinidine	193-202	ATP binding cassette subfamily B member 1	Homo sapiens	145-149
7463324-3	1980	A significant difference between quinidine and 6"-hydroxycinchonine was observed for the following parameters: t1/2 alpha, beta, t1/w beta, k12, Vd beta, and the intercompartmental distribution ratio, k12/k21.	Quinidine	33-42	vitamin D-binding protein	Oryctolagus cuniculus	145-152
7463324-5	1980	The Vd beta value for 6"-hydroxycinchonine was approximately one-half of the value observed for quinidine, and its k12/k21 ration was about one-fourth of the quinidine value.	Quinidine	96-105	vitamin D-binding protein	Oryctolagus cuniculus	4-11
6251223-7	1980	Quinidine also inhibited vasopressin and cyclic AMP stimulated water flow in the toad bladder.	Quinidine	0-9	arginine vasopressin	Homo sapiens	25-36
356577-4	1978	Mean kinetic values for total quinidine in the young subjects were: elimination half-life (t 1/2 beta), 7.3 hours; total volume of distribution (Vd), 2.39 liters/kg; total clearance, 4.04 ml/min per kg; renal clearance 1.43 ml/min per kg; and percent unbound, 24.6 In the elderly subjects, the values for Vd (2.18 liters/kg) and percent unbound (28.2) did not differ significantly from these values in the young subjects.	Quinidine	30-39	interleukin 1 receptor like 1	Homo sapiens	91-101
856605-1	1977	The plasma protein binding of a representative acidic drug, salicylate, and a representative basic drug, quinidine, has been studied in patients with several diseases that are sometimes associated with uraemia or a change in serum albumin level.	Quinidine	105-114	albumin	Homo sapiens	231-238
5463-2	1976	A 2-ml volume of serum with 350 ng of quinidine as internal standard was extracted at pH 10, the solvent was evaporated off and the residue was dissolved in 50 mul of methanol.	Quinidine	38-47	ATPase H+ transporting V0 subunit a2	Homo sapiens	0-3
1245091-8	1976	Quinidine distribution was quite rapid (t1/2alpha = 7.19 +/- 0.70 min), while the apparent elimination half-life (t1/2beta) was considerably longer, 6.333 +/- 0.47 hr.	Quinidine	0-9	interleukin 1 receptor like 1	Homo sapiens	40-49
1188181-1	1975	Quinidine is bound at two sets of sites on serum albumin.	Quinidine	0-9	albumin	Homo sapiens	43-56
33979803-0	2021	The Organic Cation Transporter 2 Inhibitor Quinidine Modulates the Neuroprotective Effect of Nerve Growth Factor and Memantine on Cholinergic Neurons of the Basal Nucleus of Meynert in Organotypic Brain Slices.	Quinidine	43-52	solute carrier family 22 member 2	Homo sapiens	4-32
33979803-0	2021	The Organic Cation Transporter 2 Inhibitor Quinidine Modulates the Neuroprotective Effect of Nerve Growth Factor and Memantine on Cholinergic Neurons of the Basal Nucleus of Meynert in Organotypic Brain Slices.	Quinidine	43-52	nerve growth factor	Homo sapiens	93-112
33979803-3	2021	Quinidine is an inhibitor of organic cation transporter 2 (OCT2).	Quinidine	0-9	solute carrier family 22 member 2	Homo sapiens	29-57
33979803-3	2021	Quinidine is an inhibitor of organic cation transporter 2 (OCT2).	Quinidine	0-9	solute carrier family 22 member 2	Homo sapiens	59-63
33979803-5	2021	We hypothesize that quinidine can modulate the protective effects of NGF and memantine on cholinergic neurons in organotypic brain slices of the nucleus basalis of Meynert (nBM).	Quinidine	20-29	nerve growth factor	Homo sapiens	69-72
33979803-9	2021	Quinidine alone had no toxic effect on cholinergic neurons but inhibited the protective effect of NGF and memantine when applied simultaneously.	Quinidine	0-9	nerve growth factor	Homo sapiens	98-101
33979803-10	2021	DISCUSSION/CONCLUSION: Our data provide evidence that quinidine modulates the survival of cholinergic nBM neurons via OCT2.	Quinidine	54-63	solute carrier family 22 member 2	Homo sapiens	118-122
34025432-8	2021	Conclusion: The window current-reducing and deactivation-slowing effects may be important for the antiarrhythmic effect of ajmaline, ivabradine, quinidine and mexiletine in SQT1-cells.	Quinidine	145-154	potassium voltage-gated channel subfamily H member 2	Homo sapiens	173-177
34048814-12	2021	Thus, our data provide, for the first time, a detailed biophysical characterization of dysfunctional Na+ channels linked to compound heterozygosity in BrS as well as the benefits of the pharmacological treatment using quinidine on the biophysical properties of Nav1.5.	Quinidine	218-227	sodium voltage-gated channel alpha subunit 5	Homo sapiens	261-267
33684260-2	2021	Here we present the cryo-EM structure of full-length human Na v 1.5 bound to quinidine, a class Ia antiarrhythmic drug, at 3.3 A resolution.	Quinidine	77-86	sodium voltage-gated channel alpha subunit 5	Homo sapiens	59-67
34025432-4	2021	Results: Ajmaline, amiodarone, ivabradine, flecainide, quinidine, mexiletine and ranolazine inhibited the hERG channel current (IKr) less strongly in hiPSC-CMs from the SQTS1-patient (SQT1-hiPSC-CMs) comparing with cells from the healthy donor (donor-hiPSC-CMs).	Quinidine	55-64	ETS transcription factor ERG	Homo sapiens	106-110
34009624-4	2021	The concentration dependent non-linear kinetics of P-gp substrates, quinidine and talinolol, was more analyzed in detail, and apparent Vmax discrepancy between static and flow assay condition in the quinidine assay was observed, while that was not observed in talinolol, the lower permeable substrate.	Quinidine	68-77	ATP binding cassette subfamily B member 1	Homo sapiens	51-55
34009624-4	2021	The concentration dependent non-linear kinetics of P-gp substrates, quinidine and talinolol, was more analyzed in detail, and apparent Vmax discrepancy between static and flow assay condition in the quinidine assay was observed, while that was not observed in talinolol, the lower permeable substrate.	Quinidine	199-208	ATP binding cassette subfamily B member 1	Homo sapiens	51-55
33641805-7	2021	In canine and feline microsomes, the formation rate of demethyl-cimicoxib, a phase 1 metabolite, was decreased in presence of quinidine, a specific human cytochrome P450 (CYP)2D6 inhibitor.	Quinidine	126-135	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	154-178
33499241-7	2021	The molecular docking results showed that, among natural SGLT2 inhibitors, formononetin, (+)-pteryxin, and quinidine have a strong interaction with FimH proteins, with binding energy ( G) and inhibition constant (ki) values of -5.65 kcal/mol and 71.95 microM, -5.50 kcal/mol and 92.97 microM, and -5.70 kcal/mol and 66.40 microM, respectively.	Quinidine	107-116	solute carrier family 5 member 2	Homo sapiens	57-62
33712541-5	2021	The structure is nearly identical to that of the wild-type human Nav1.5 bound to quinidine.	Quinidine	81-90	sodium voltage-gated channel alpha subunit 5	Homo sapiens	65-71
33499241-11	2021	Therefore, formononetin, (+)-pteryxin, and quinidine can be proposed as promising SGLT2 inhibitors drugs, with add-on FimH inhibition potential that might reduce the probability of uropathogenic side effects.	Quinidine	43-52	solute carrier family 5 member 2	Homo sapiens	82-87
33084224-0	2020	A combination of quinidine/mexiletine reduces arrhythmia in dilated cardiomyopathy in two patients with R814W SCN5A mutation.	Quinidine	17-26	sodium voltage-gated channel alpha subunit 5	Homo sapiens	110-115
33514068-3	2021	The purpose of this study was to assess the efficacy of the AADs disopyramide, quinidine, and propafenone on human atrial arrhythmias mediated by Pitx2-induced remodelling, from a single cell to the tissue level, using drug binding models with multi-channel pharmacology.	Quinidine	79-88	paired like homeodomain 2	Homo sapiens	146-151
32723846-8	2020	Studies using primary neonatal rat cardiomyocytes showed that OCT1/3 inhibitors (quinidine, decynium-22, and levo-tetrahydropalmatine) prevented the accumulation of DHC, while OCTN2 inhibitors (mildronate and l-carnitine) did not affect its accumulation.	Quinidine	81-90	solute carrier family 22 member 1	Rattus norvegicus	62-68
32344126-0	2020	Modulation of nose-to-brain delivery of a P-glycoprotein (MDR1) substrate model drug (quinidine) in rats.	Quinidine	86-95	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	42-56
32505479-0	2020	KCNT1-positive epilepsy of infancy with migrating focal seizures successfully treated with nonnarcotic antitussive drugs after treatment failure with quinidine: A case report.	Quinidine	150-159	potassium sodium-activated channel subfamily T member 1	Homo sapiens	0-5
32505479-3	2020	Since gain of function is the only type of mutation identified in patients with EIMFS, quinidine, a partial antagonist of KCa4.1 channel, is considered as a potential candidate for targeted treatment of EIMFS.	Quinidine	87-96	potassium sodium-activated channel subfamily T member 1	Homo sapiens	122-128
32344126-0	2020	Modulation of nose-to-brain delivery of a P-glycoprotein (MDR1) substrate model drug (quinidine) in rats.	Quinidine	86-95	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	58-62
32344126-6	2020	Therefore, a P-gp substrate model drug, quinidine was tested by intranasal (IN) administration in presence of PSC-833 (specific P-gp inhibitor) given intravenously (IV) or IN and adrenaline (IN) at low (50 ng) or high (20 mug) dose.	Quinidine	40-49	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	13-17
32344126-8	2020	These results indicate that P-gp has an important role in drug absorption and efflux at nasal cavity, while adrenaline is also able to modify the penetration profile of the P-gp substrate model drug at nasal application as it decreases nose-to-blood absorption, letting more quinidine to reach the brain along with the nasal nerves.	Quinidine	275-284	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	28-32
32344126-8	2020	These results indicate that P-gp has an important role in drug absorption and efflux at nasal cavity, while adrenaline is also able to modify the penetration profile of the P-gp substrate model drug at nasal application as it decreases nose-to-blood absorption, letting more quinidine to reach the brain along with the nasal nerves.	Quinidine	275-284	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	173-177
31173922-10	2019	Extracellular application of quinidine significantly restored the inactivation time course in mutant Kv4.3.	Quinidine	29-38	potassium voltage-gated channel subfamily D member 3	Homo sapiens	101-106
32645615-10	2020	Ventricular arrhythmia incidence was significantly greater in gstm3 knockout zebrafish at baseline and after flecainide, but was reduced after quinidine, consistent with clinical observations.	Quinidine	143-152	glutathione S-transferase mu tandem duplicate 3	Danio rerio	62-67
31770573-0	2020	Enabling P-glycoprotein inhibition in multidrug resistant cancer through the reverse targeting of a quinidine-PEG conjugate.	Quinidine	100-113	phosphoglycolate phosphatase	Mus musculus	9-23
31770573-3	2020	Here, we explore the FDA-approved drug quinidine as a P-gp inhibitor.	Quinidine	39-48	phosphoglycolate phosphatase	Mus musculus	54-58
31770573-4	2020	Although used clinically for the treatment of malaria, arrhythmia, and pseudobulbar effect, quinidine can induce acquired long QT syndrome and torsade de pointes through its interaction with the Purkinje fibers, which hinders its clinical application as a P-gp inhibitor.	Quinidine	92-101	phosphoglycolate phosphatase	Mus musculus	256-260
31730751-9	2019	The use of potent pan-CYP4 inhibitor HET0016, the specific CYP2D6 inhibitor quinidine, or both confirmed major contributions of CYP4- and CYP2D6-mediated metabolism in the microsomal disappearance of BACs.	Quinidine	76-85	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	59-65
32198085-10	2020	Quinidine, a competitive CYP2D6 inhibitor, demonstrated protection on enzymes against the NOT-induced inactivation, but such protection was not found in incubation systems fortified with glutathione or catalase/superoxide dismutase.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	25-31
31925778-7	2020	The model was further challenged with simulations of oxycodone DDI with CYP3A4 inhibitors ketoconazole and itraconazole, CYP3A4 inducer rifampicin and CYP2D6 inhibitor quinidine.	Quinidine	168-177	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	151-157
31770573-5	2020	We hypothesize that the conjugation of quinidine to a polymer will permit its use as a P-gp inhibitor through mitigation of its distribution into the myocardium.	Quinidine	39-48	phosphoglycolate phosphatase	Mus musculus	87-91
31770573-7	2020	The mPEG-glycine-quinidine conjugate retained its ability to inhibit the function of P-gp (log IC50 of 4.20 nM for quinidine and 4.61 nM for the mPEG-glycine-quinidine conjugate).	Quinidine	17-26	phosphoglycolate phosphatase	Mus musculus	85-89
31770573-7	2020	The mPEG-glycine-quinidine conjugate retained its ability to inhibit the function of P-gp (log IC50 of 4.20 nM for quinidine and 4.61 nM for the mPEG-glycine-quinidine conjugate).	Quinidine	115-124	phosphoglycolate phosphatase	Mus musculus	85-89
31770573-7	2020	The mPEG-glycine-quinidine conjugate retained its ability to inhibit the function of P-gp (log IC50 of 4.20 nM for quinidine and 4.61 nM for the mPEG-glycine-quinidine conjugate).	Quinidine	115-124	phosphoglycolate phosphatase	Mus musculus	85-89
32242774-9	2020	Since Cyp2d22/CYP2D6 inhibitor (ketoconazole/quinidine) per se reduced Cyp2d22/CYP2D6 activity and dopamine content, it was found to substantially increase the pesticides-induced reduction in Cyp2d22/CYP2D6 activity and dopamine content.	Quinidine	45-54	cytochrome P450, family 2, subfamily d, polypeptide 22	Mus musculus	6-13
32242774-9	2020	Since Cyp2d22/CYP2D6 inhibitor (ketoconazole/quinidine) per se reduced Cyp2d22/CYP2D6 activity and dopamine content, it was found to substantially increase the pesticides-induced reduction in Cyp2d22/CYP2D6 activity and dopamine content.	Quinidine	45-54	cytochrome P450, family 2, subfamily d, polypeptide 22	Mus musculus	71-78
32242774-9	2020	Since Cyp2d22/CYP2D6 inhibitor (ketoconazole/quinidine) per se reduced Cyp2d22/CYP2D6 activity and dopamine content, it was found to substantially increase the pesticides-induced reduction in Cyp2d22/CYP2D6 activity and dopamine content.	Quinidine	45-54	cytochrome P450, family 2, subfamily d, polypeptide 22	Mus musculus	71-78
31147315-5	2019	Using the differential inhibition of the human enzymes by quinidine, we developed a method to distinguish the relative contribution of CYP1A1 or CYP1A2 in the metabolism of drugs and foreign compounds.	Quinidine	58-67	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	135-141
31208268-11	2019	Our data suggest that alternative therapies to quinidine should be considered as a therapeutic option for patients with KCNT1-related epilepsy.	Quinidine	47-56	potassium sodium-activated channel subfamily T member 1	Homo sapiens	120-125
31483500-17	2019	Low-certainty evidence from six RCTs suggested that risk of mortality may be higher in people taking quinidine (RR 2.01, 95% CI 0.84 to 4.77; participants = 1646).	Quinidine	101-110	ribonucleotide reductase regulatory subunit M2	Homo sapiens	112-116
31483500-20	2019	Certainty of the evidence for this outcome was low for disopyramide, amiodarone, dofetilide and flecainide; moderate to high for the remaining drugs.ProarrhythmiaVirtually all studied antiarrhythmics showed increased proarrhythmic effects (counting both tachyarrhythmias and bradyarrhythmias attributable to treatment) (quinidine: RR 2.05, 95% CI 0.95 to 4.41; disopyramide: no data; flecainide: RR 4.80, 95% CI 1.30 to 17.77; metoprolol: RR 18.14, 95% CI 2.42 to 135.66; amiodarone: RR 2.22, 95% CI 0.71 to 6.96; dofetilide: RR 5.50, 95% CI 1.33 to 22.76; dronedarone: RR 1.95, 95% CI 0.77 to 4.98; sotalol: RR 3.55, 95% CI 2.16 to 5.83); with the exception of propafenone (RR 1.32, 95% CI 0.39 to 4.47) for which the certainty of evidence was very low and we were uncertain about the effect.	Quinidine	320-329	ribonucleotide reductase regulatory subunit M2	Homo sapiens	331-335
31483500-20	2019	Certainty of the evidence for this outcome was low for disopyramide, amiodarone, dofetilide and flecainide; moderate to high for the remaining drugs.ProarrhythmiaVirtually all studied antiarrhythmics showed increased proarrhythmic effects (counting both tachyarrhythmias and bradyarrhythmias attributable to treatment) (quinidine: RR 2.05, 95% CI 0.95 to 4.41; disopyramide: no data; flecainide: RR 4.80, 95% CI 1.30 to 17.77; metoprolol: RR 18.14, 95% CI 2.42 to 135.66; amiodarone: RR 2.22, 95% CI 0.71 to 6.96; dofetilide: RR 5.50, 95% CI 1.33 to 22.76; dronedarone: RR 1.95, 95% CI 0.77 to 4.98; sotalol: RR 3.55, 95% CI 2.16 to 5.83); with the exception of propafenone (RR 1.32, 95% CI 0.39 to 4.47) for which the certainty of evidence was very low and we were uncertain about the effect.	Quinidine	320-329	ribonucleotide reductase regulatory subunit M2	Homo sapiens	484-488
31483500-20	2019	Certainty of the evidence for this outcome was low for disopyramide, amiodarone, dofetilide and flecainide; moderate to high for the remaining drugs.ProarrhythmiaVirtually all studied antiarrhythmics showed increased proarrhythmic effects (counting both tachyarrhythmias and bradyarrhythmias attributable to treatment) (quinidine: RR 2.05, 95% CI 0.95 to 4.41; disopyramide: no data; flecainide: RR 4.80, 95% CI 1.30 to 17.77; metoprolol: RR 18.14, 95% CI 2.42 to 135.66; amiodarone: RR 2.22, 95% CI 0.71 to 6.96; dofetilide: RR 5.50, 95% CI 1.33 to 22.76; dronedarone: RR 1.95, 95% CI 0.77 to 4.98; sotalol: RR 3.55, 95% CI 2.16 to 5.83); with the exception of propafenone (RR 1.32, 95% CI 0.39 to 4.47) for which the certainty of evidence was very low and we were uncertain about the effect.	Quinidine	320-329	ribonucleotide reductase catalytic subunit M1	Homo sapiens	439-443
31483500-20	2019	Certainty of the evidence for this outcome was low for disopyramide, amiodarone, dofetilide and flecainide; moderate to high for the remaining drugs.ProarrhythmiaVirtually all studied antiarrhythmics showed increased proarrhythmic effects (counting both tachyarrhythmias and bradyarrhythmias attributable to treatment) (quinidine: RR 2.05, 95% CI 0.95 to 4.41; disopyramide: no data; flecainide: RR 4.80, 95% CI 1.30 to 17.77; metoprolol: RR 18.14, 95% CI 2.42 to 135.66; amiodarone: RR 2.22, 95% CI 0.71 to 6.96; dofetilide: RR 5.50, 95% CI 1.33 to 22.76; dronedarone: RR 1.95, 95% CI 0.77 to 4.98; sotalol: RR 3.55, 95% CI 2.16 to 5.83); with the exception of propafenone (RR 1.32, 95% CI 0.39 to 4.47) for which the certainty of evidence was very low and we were uncertain about the effect.	Quinidine	320-329	ribonucleotide reductase catalytic subunit M1	Homo sapiens	570-574
31335150-8	2019	Three of five drugs (verapamil, ketoconazole, and quinidine) known to interact clinically with dabigatran, as P-gp inhibitors, presented as MATE inhibitors in vitro (IC50 = 1.0 to 25.2 muM).	Quinidine	50-59	PGP	Canis lupus familiaris	110-114
31147315-5	2019	Using the differential inhibition of the human enzymes by quinidine, we developed a method to distinguish the relative contribution of CYP1A1 or CYP1A2 in the metabolism of drugs and foreign compounds.	Quinidine	58-67	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	145-151
31946488-4	2019	In this study, computational modelling was used to investigate pharmacotherapeutic effects of selected class I drug quinidine on SQT1, SQT2 and SQT3 variants.	Quinidine	116-125	potassium voltage-gated channel subfamily H member 2	Homo sapiens	129-133
31359944-0	2019	Two South Indian Children with KCNT1-Related Malignant Migrating Focal Seizures of Infancy - Clinical Characteristics and Outcome of Targeted Treatment with Quinidine.	Quinidine	157-166	potassium sodium-activated channel subfamily T member 1	Homo sapiens	31-36
31359944-9	2019	A critical review on the current status of targeted treatment of KCNT1-related epileptic encephalopathies with quinidine is attempted.	Quinidine	111-120	potassium sodium-activated channel subfamily T member 1	Homo sapiens	65-70
31946488-4	2019	In this study, computational modelling was used to investigate pharmacotherapeutic effects of selected class I drug quinidine on SQT1, SQT2 and SQT3 variants.	Quinidine	116-125	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	135-139
31946488-4	2019	In this study, computational modelling was used to investigate pharmacotherapeutic effects of selected class I drug quinidine on SQT1, SQT2 and SQT3 variants.	Quinidine	116-125	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	144-148
31946488-10	2019	At the 10 muM concentration tested in this study, quinidine effectively prolonged the action potential duration (APD) under all the SQT1, SQT2 and SQT3 conditions.	Quinidine	50-59	potassium voltage-gated channel subfamily H member 2	Homo sapiens	132-136
31946488-10	2019	At the 10 muM concentration tested in this study, quinidine effectively prolonged the action potential duration (APD) under all the SQT1, SQT2 and SQT3 conditions.	Quinidine	50-59	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	138-142
31946488-10	2019	At the 10 muM concentration tested in this study, quinidine effectively prolonged the action potential duration (APD) under all the SQT1, SQT2 and SQT3 conditions.	Quinidine	50-59	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	147-151
30975793-5	2019	Further, hepatitis B virus myristoylated-preS1 peptide (0.1 microM), quinidine (100 microM), and ketoprofen (100-300 microM) are relatively selective against NTCP, OCT1, and OAT2, respectively.	Quinidine	69-78	solute carrier family 10 member 1	Homo sapiens	158-162
30975793-5	2019	Further, hepatitis B virus myristoylated-preS1 peptide (0.1 microM), quinidine (100 microM), and ketoprofen (100-300 microM) are relatively selective against NTCP, OCT1, and OAT2, respectively.	Quinidine	69-78	solute carrier family 22 member 1	Homo sapiens	164-168
30975793-5	2019	Further, hepatitis B virus myristoylated-preS1 peptide (0.1 microM), quinidine (100 microM), and ketoprofen (100-300 microM) are relatively selective against NTCP, OCT1, and OAT2, respectively.	Quinidine	69-78	solute carrier family 22 member 7	Homo sapiens	174-178
31072785-0	2019	Corrigendum to "Does age affect response to quinidine in patients with KCNT1 mutations?	Quinidine	44-53	potassium sodium-activated channel subfamily T member 1	Homo sapiens	71-76
31113867-5	2019	Our results reveal that activity and respiration in mouse brain mitochondrial complex I are significantly affected by these toxins in WT mice but remain unchanged in Cyp2d6 locus knockout mice, indicating a possible role of CYP2D6 in the metabolism of these compounds both in vivo and in vitro These metabolic effects were minimized in the presence of two CYP2D6 inhibitors, quinidine and ajmalicine.	Quinidine	375-384	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	224-230
30880181-0	2019	Comparative study of carvedilol and quinidine for inhibiting hKv4.3 channel stably expressed in HEK 293 cells.	Quinidine	36-45	potassium voltage-gated channel subfamily D member 3	Homo sapiens	61-67
30880181-3	2019	It was found that carvedilol and quinidine inhibited hKv4.3 current in a concentration-dependent manner.	Quinidine	33-42	potassium voltage-gated channel subfamily D member 3	Homo sapiens	53-59
30880181-5	2019	Both carvedilol and quinidine showed typical open channel blocking properties (i.e. decreasing the time to peak of activation and increasing the inactivation of hKv4.3), negatively shifted the V1/2 of activation and inactivation, and slowed the recovery from inactivation of the channel.	Quinidine	20-29	potassium voltage-gated channel subfamily D member 3	Homo sapiens	161-167
30880181-8	2019	These results provide the novel information that carvedilol, like quinidine, significantly inhibits hKv4.3 and action potential notch, suggesting that carvedilol is likely an alternative drug for preventing malignant ventricular arrhythmias in patients with Brugada syndrome in countries where quinidine is unavailable.	Quinidine	66-75	potassium voltage-gated channel subfamily D member 3	Homo sapiens	100-106
31054119-11	2019	More favorable response to quinidine in patients with KCNT1 variants distal to the NADP domain within the RCK2 domain may suggest a variant-specific response.	Quinidine	27-36	potassium sodium-activated channel subfamily T member 1	Homo sapiens	54-59
31388363-0	2019	Concurrent Quinidine and Phenobarbital in the Treatment of a Patient with 2 KCNT1 Mutations.	Quinidine	11-20	potassium sodium-activated channel subfamily T member 1	Homo sapiens	76-81
31049424-9	2019	Under AP voltage clamp the inhibitory effect of 1 muM quinidine was largely retained for I560T hERG and the timing of peak I560T IhERG was altered towards that of the WT channel.	Quinidine	54-63	ETS transcription factor ERG	Homo sapiens	95-99
31388363-4	2019	We report the case of an infant with 2 KCNT1 mutations who experienced minor relief with quinidine and discuss the drug"s important interaction with phenobarbital.	Quinidine	89-98	potassium sodium-activated channel subfamily T member 1	Homo sapiens	39-44
30687112-8	2018	At the concentrations tested in this study, quinidine most effectively prolonged the APD and ERP in the setting of SQT1, followed by disopyramide and propafenone.	Quinidine	44-53	potassium voltage-gated channel subfamily H member 2	Homo sapiens	115-119
30804880-0	2019	Quinidine Therapy for Lennox-Gastaut Syndrome With KCNT1 Mutation.	Quinidine	0-9	potassium sodium-activated channel subfamily T member 1	Homo sapiens	51-56
30804880-9	2019	Previous studies revealed that quinidine could block the KCNT1 channel.	Quinidine	31-40	potassium sodium-activated channel subfamily T member 1	Homo sapiens	57-62
30804880-13	2019	In conclusion, quinidine therapy may offer a new choice for the treatment of Lennox-Gastaut syndrome with KCNT1 mutations.	Quinidine	15-24	potassium sodium-activated channel subfamily T member 1	Homo sapiens	106-111
30782581-0	2019	Quinidine therapy and therapeutic drug monitoring in four patients with KCNT1 mutations.	Quinidine	0-9	potassium sodium-activated channel subfamily T member 1	Homo sapiens	72-77
30782581-1	2019	Several recent studies have reported potassium sodium-activated channel subfamily T member 1 (KCNT1) mutations in epilepsy patients on quinidine therapy.	Quinidine	135-144	potassium sodium-activated channel subfamily T member 1	Homo sapiens	94-99
30782581-3	2019	We herein report the cases of four patients with KCNT1 mutations treated with quinidine.	Quinidine	78-87	potassium sodium-activated channel subfamily T member 1	Homo sapiens	49-54
30782581-10	2019	Based on a review of previous reports and our experience with this case, quinidine should be considered as a promising drug for patients with EIMFS harbouring KCNT1 mutations, however, its efficacy remains controversial due to the limited number of cases, and more information on optimal serum concentrations and appropriate titration methods is required.	Quinidine	73-82	potassium sodium-activated channel subfamily T member 1	Homo sapiens	159-164
30368994-8	2019	Quinidine, a competitive inhibitor of CYP2D6, attenuated the CHE-mediated enzyme inactivation, while glutathione and catalase/superoxide dismutase did not markedly ameliorate the inhibitory effect.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	38-44
30431448-0	2019	Probable drug-drug interaction between dabigatran and quinidine resulting in thrombin time rebound despite multiple idarucizumab doses.	Quinidine	54-63	coagulation factor II, thrombin	Homo sapiens	77-85
30582453-10	2019	Moreover, QTc of SQT patient and action potential durations of SQT iPSC-CMs were both normalized by quinidine, indicating that quinidine is beneficial to KCNH2 T618I of SQT.	Quinidine	100-109	potassium voltage-gated channel subfamily H member 2	Homo sapiens	154-159
30582453-10	2019	Moreover, QTc of SQT patient and action potential durations of SQT iPSC-CMs were both normalized by quinidine, indicating that quinidine is beneficial to KCNH2 T618I of SQT.	Quinidine	127-136	potassium voltage-gated channel subfamily H member 2	Homo sapiens	154-159
30182418-0	2018	Lack of response to quinidine in KCNT1-related neonatal epilepsy.	Quinidine	20-29	potassium sodium-activated channel subfamily T member 1	Homo sapiens	33-38
30113702-8	2018	(+)-M5 formation from (+)-M1 in DLMs was potently inhibited by quinidine (CYP2D inhibitor) but had only a minor impact from all CYP inducers tested.	Quinidine	63-72	cytochrome P450 2D15	Canis lupus familiaris	74-79
31257298-5	2019	Uptake transporter substrate assay revealed that flecainide (1 microM) showed 1.11-fold accumulation though the hMATE1-related active transport was significantly decreased in the presence of quinidine (42.0 +- 23.9 vs. 11.8 +- 4.1 pmol/mg in transfected cells; p < 0.05).	Quinidine	191-200	solute carrier family 47 member 1	Homo sapiens	112-118
30058787-4	2018	The cytochrome P450 (human hepatic cytochrome [CYP]) 2D6 inhibitor quinidine reduced in vitro hydroxylation of ondansetron, which indicates the important role of CYP2D6 in ondansetron metabolism.	Quinidine	67-76	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	162-168
30219715-3	2018	In human liver microsomes (HLMs), a concentration-dependent inhibition of celecoxib hydroxylation by quinidine was observed after CYP2C9 and CYP3A4 were inhibited.	Quinidine	101-110	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	130-136
30219715-3	2018	In human liver microsomes (HLMs), a concentration-dependent inhibition of celecoxib hydroxylation by quinidine was observed after CYP2C9 and CYP3A4 were inhibited.	Quinidine	101-110	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	141-147
30182418-1	2018	OBJECTIVE: To evaluate the clinical efficacy and safety of quinidine in patients with KCNT1-related epilepsy of infancy with migrating focal seizures (EIMFS) in the infantile period and to compare with the effect of quinidine on mutant channels in vitro.	Quinidine	59-68	potassium sodium-activated channel subfamily T member 1	Homo sapiens	86-91
30175559-9	2018	Quinidine is thus likely to be effective in reducing excessively fast repolarization in SQTS resulting from the S631A hERG mutation.	Quinidine	0-9	ETS transcription factor ERG	Homo sapiens	118-122
30008082-6	2018	K2P17.1 channels expressed in Xenopus laevis oocytes were screened for sensitivity to antiarrhythmic drugs, revealing significant activation by propafenone (+ 296%; 100 muM), quinidine (+ 58%; 100 muM), mexiletine (+ 21%; 100 muM), propranolol (+ 139%; 100 muM), and metoprolol (+ 17%; 100 muM) within 60 min.	Quinidine	175-184	potassium two pore domain channel subfamily K member 17	Homo sapiens	0-7
30441852-11	2018	Transduction efficiency was enhanced by increasing extracellular potassium concentration, and with Quinidine, a Kcnh5 inhibitor, that blocks the channel in an open position.	Quinidine	99-108	potassium voltage-gated channel subfamily H member 5	Homo sapiens	112-117
30441852-15	2018	Cardiac targeting peptide appears to utilize Kcnh5 to gain cell entry, a phenomenon that is affected by pre-treatment with Quinidine and changes in potassium levels.	Quinidine	123-132	potassium voltage-gated channel subfamily H member 5	Homo sapiens	45-50
30112700-0	2018	Early Treatment with Quinidine in 2 Patients with Epilepsy of Infancy with Migrating Focal Seizures (EIMFS) Due to Gain-of-Function KCNT1 Mutations: Functional Studies, Clinical Responses, and Critical Issues for Personalized Therapy.	Quinidine	21-30	potassium sodium-activated channel subfamily T member 1	Homo sapiens	132-137
30112700-2	2018	The most common cause for EIMFS is a gain-of-function mutation in the KCNT1 potassium channel gene, and treatment with the KCNT1 blocker quinidine has been suggested as a rational approach for seizure control in EIMFS patients.	Quinidine	137-146	potassium sodium-activated channel subfamily T member 1	Homo sapiens	70-75
30112700-2	2018	The most common cause for EIMFS is a gain-of-function mutation in the KCNT1 potassium channel gene, and treatment with the KCNT1 blocker quinidine has been suggested as a rational approach for seizure control in EIMFS patients.	Quinidine	137-146	potassium sodium-activated channel subfamily T member 1	Homo sapiens	123-128
30112700-4	2018	In the present study, we provide a detailed description of the clinical, genetic, in vitro, and in vivo electrophysiological profile and pharmacological responses to quinidine of 2 EIMFS unrelated patients with a heterozygous de novo KCNT1 mutation: c.2849G&gt;A (p.R950Q) in patient 1 and c.2677G&gt;A (p.E893K) in patient 2.	Quinidine	166-175	potassium sodium-activated channel subfamily T member 1	Homo sapiens	234-239
30112700-5	2018	When expressed heterologously in CHO cells, KCNT1 channels carrying each variant showed gain-of-function effects, and were more effectively blocked by quinidine when compared to wild-type KCNT1 channels.	Quinidine	151-160	potassium channel subfamily T member 1	Cricetulus griseus	44-49
30112700-5	2018	When expressed heterologously in CHO cells, KCNT1 channels carrying each variant showed gain-of-function effects, and were more effectively blocked by quinidine when compared to wild-type KCNT1 channels.	Quinidine	151-160	potassium channel subfamily T member 1	Cricetulus griseus	188-193
30112700-8	2018	Based on the present experience, early quinidine intervention associated with heart monitoring and control of blood levels is among the critical factors for therapy effectiveness in EIMFS patients with KCNT1 gain-of-function mutations.	Quinidine	39-48	potassium sodium-activated channel subfamily T member 1	Homo sapiens	202-207
29806615-4	2018	Model cells were cultured on a membrane in the secretion component, and active transport mediated by P-glycoprotein (P-gp) was confirmed using the P-gp substrate rhodamine 123 with or without the P-gp inhibitor quinidine sulfate.	Quinidine	211-228	ATP binding cassette subfamily B member 1	Homo sapiens	101-115
29806615-4	2018	Model cells were cultured on a membrane in the secretion component, and active transport mediated by P-glycoprotein (P-gp) was confirmed using the P-gp substrate rhodamine 123 with or without the P-gp inhibitor quinidine sulfate.	Quinidine	211-228	ATP binding cassette subfamily B member 1	Homo sapiens	117-121
29773554-8	2018	Quinidine as a competitive inhibitor of CYP2D6 slowed down the inactivation by NC.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	40-46
29871609-0	2018	Rapid and effective response of the R222Q SCN5A to quinidine treatment in a patient with Purkinje-related ventricular arrhythmia and familial dilated cardiomyopathy: a case report.	Quinidine	51-60	sodium voltage-gated channel alpha subunit 5	Homo sapiens	42-47
29871609-10	2018	The quinidine treatment for the SCN5A R222Q mutation can be life saving for patients.	Quinidine	4-13	sodium voltage-gated channel alpha subunit 5	Homo sapiens	32-37
28010169-0	2018	Consequences of daily corticosteroid dosing with or without pre-treatment with quinidine on the in vivo cytochrome P450 2D (CYP2D) enzyme in rats: effect on O-demethylation activity of dextromethorphan and expression levels of CYP2D1 mRNA.	Quinidine	79-88	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	227-233
29866938-0	2018	Reader response: Quinidine-associated skin discoloration in KCNT1-associated pediatric epilepsy.	Quinidine	17-26	potassium sodium-activated channel subfamily T member 1	Homo sapiens	60-65
29866939-0	2018	Author response: Quinidine-associated skin discoloration in KCNT1-associated pediatric epilepsy.	Quinidine	17-26	potassium sodium-activated channel subfamily T member 1	Homo sapiens	60-65
29866940-0	2018	Quinidine-associated skin discoloration in KCNT1-associated pediatric epilepsy.	Quinidine	0-9	potassium sodium-activated channel subfamily T member 1	Homo sapiens	43-48
29291456-0	2018	Does age affect response to quinidine in patients with KCNT1 mutations?	Quinidine	28-37	potassium sodium-activated channel subfamily T member 1	Homo sapiens	55-60
29291456-4	2018	Here we report 3 additional children, with such KCNT1 mutations and refractory seizures, who received quinidine therapy.	Quinidine	102-111	potassium sodium-activated channel subfamily T member 1	Homo sapiens	48-53
29291456-11	2018	CONCLUSION: The above-mentioned findings support performance of prospective controlled studies of quinidine efficacy in children with KCNT1 gain-of-function mutations that control for age as a possible variable affecting response.	Quinidine	98-107	potassium sodium-activated channel subfamily T member 1	Homo sapiens	134-139
29196578-1	2018	OBJECTIVE: To evaluate quinidine as a precision therapy for severe epilepsy due to gain of function mutations in the potassium channel gene KCNT1.	Quinidine	23-32	potassium sodium-activated channel subfamily T member 1	Homo sapiens	140-145
29196578-14	2018	CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that for persons with severe epilepsy due to gain of function mutations in the potassium channel gene KCNT1, quinidine does not significantly reduce seizure frequency.	Quinidine	175-184	potassium sodium-activated channel subfamily T member 1	Homo sapiens	168-173
29196579-11	2018	All evaluated KCNT1 variants resulted in marked gain of function with significantly increased channel amplitude and variable blockade by quinidine.	Quinidine	137-146	potassium sodium-activated channel subfamily T member 1	Homo sapiens	14-19
29037447-0	2018	A quinidine non responsive novel KCNT1 mutation in an Indian infant with epilepsy of infancy with migrating focal seizures.	Quinidine	2-11	potassium sodium-activated channel subfamily T member 1	Homo sapiens	33-38
29037447-5	2018	Antagonist of KCNT1 coded ion channel like Quinidine has shown promising results in MMPSI.	Quinidine	43-52	potassium sodium-activated channel subfamily T member 1	Homo sapiens	14-19
30481776-10	2018	The hERG channel blockers tested inhibited K801T-hERG channel in concentration response, and the potencies of these drugs can be rank-ordered as follows: quinidine&gt; disopyramide&gt; sotalol&gt; flecainide.	Quinidine	154-163	ETS transcription factor ERG	Homo sapiens	4-8
30481776-10	2018	The hERG channel blockers tested inhibited K801T-hERG channel in concentration response, and the potencies of these drugs can be rank-ordered as follows: quinidine&gt; disopyramide&gt; sotalol&gt; flecainide.	Quinidine	154-163	ETS transcription factor ERG	Homo sapiens	49-53
30481776-12	2018	Quinidine and disopyramide could improve the function of K801T-hERG mutant channel, and may be therapeutic options for patients with the K801T hERG mutation.	Quinidine	0-9	ETS transcription factor ERG	Homo sapiens	63-67
30481776-12	2018	Quinidine and disopyramide could improve the function of K801T-hERG mutant channel, and may be therapeutic options for patients with the K801T hERG mutation.	Quinidine	0-9	ETS transcription factor ERG	Homo sapiens	143-147
28010169-2	2018	Present investigation was carried out in rats to study influence of corticosteroids after repeated dosing with/without pre-treatment with CYP2D inhibitor quinidine on the CYP2D1 mRNA levels and CYP2D enzyme activity using dextromethorphan as probe substrate.	Quinidine	154-163	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	171-177
28010169-4	2018	CYP2D1 mRNA was measured in liver homogenate using quantitative real-time polymerase chain reaction [qRT-PCR] and enzymatic reaction was studied ex vivo in liver S-9 fractions of rats treated with oral 10 mg/kg dexamethasone or prednisolone for five days or pre-treated with quinidine and followed by treatment with oral 10 mg/kg corticosteroids for five days.	Quinidine	275-284	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	0-6
28812984-11	2017	Furthermore, quinidine increased ERP and reduced temporal vulnerability and increased spatial vulnerability, resulting in a reduced susceptibility to arrhythmogenesis in SQT3.	Quinidine	13-22	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	170-174
29131436-7	2017	Consistent with the idea that GABAB receptors are coupled to two-pore domain potassium channels, the non-specific blockers quinidine and bupivacaine partially blocked GABAB responses in both layer 5 and CA1 neurons.	Quinidine	123-132	carbonic anhydrase 1	Rattus norvegicus	203-206
29158296-0	2017	Quinidine-associated skin discoloration in KCNT1-associated pediatric epilepsy.	Quinidine	0-9	potassium sodium-activated channel subfamily T member 1	Homo sapiens	43-48
29085299-0	2017	Computational Analysis of the Mode of Action of Disopyramide and Quinidine on hERG-Linked Short QT Syndrome in Human Ventricles.	Quinidine	65-74	ETS transcription factor ERG	Homo sapiens	78-82
28812984-13	2017	Quinidine exhibited significantly better therapeutic effects on SQT3 than disopyramide and E-4031.	Quinidine	0-9	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	64-68
28812984-14	2017	SIGNIFICANCE: This study substantiates a causal link between quinidine and QT interval prolongation in SQT3 Kir2.1 mutations and highlights possible pharmacological agent quinidine for treating SQT3 patients.	Quinidine	61-70	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	103-107
28812984-14	2017	SIGNIFICANCE: This study substantiates a causal link between quinidine and QT interval prolongation in SQT3 Kir2.1 mutations and highlights possible pharmacological agent quinidine for treating SQT3 patients.	Quinidine	61-70	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	108-114
28812984-14	2017	SIGNIFICANCE: This study substantiates a causal link between quinidine and QT interval prolongation in SQT3 Kir2.1 mutations and highlights possible pharmacological agent quinidine for treating SQT3 patients.	Quinidine	61-70	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	194-198
28812984-14	2017	SIGNIFICANCE: This study substantiates a causal link between quinidine and QT interval prolongation in SQT3 Kir2.1 mutations and highlights possible pharmacological agent quinidine for treating SQT3 patients.	Quinidine	171-180	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	103-107
28812984-14	2017	SIGNIFICANCE: This study substantiates a causal link between quinidine and QT interval prolongation in SQT3 Kir2.1 mutations and highlights possible pharmacological agent quinidine for treating SQT3 patients.	Quinidine	171-180	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	108-114
28812984-14	2017	SIGNIFICANCE: This study substantiates a causal link between quinidine and QT interval prolongation in SQT3 Kir2.1 mutations and highlights possible pharmacological agent quinidine for treating SQT3 patients.	Quinidine	171-180	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	194-198
28347660-4	2017	Quinidine exhibited stronger inhibition than quinine; however, these two compounds inhibited the CYP2D6.10-mediated reaction more weakly than the CYP2D6.1 and CYP2D6.2 reactions.	Quinidine	0-9	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	97-103
28478356-3	2017	METHODS: The current study is a phase IIa open label clinical trial examining the efficacy and tolerability of a combination of dextromethorphan (DM) and the CYP2D6 enzyme inhibitor quinidine (Q) in patients with TRD.	Quinidine	182-191	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	158-164
28811548-8	2017	Next, the ggTas2r1 structural model was successfully used to identify three quinine analogues (epiquinidine, ethylhydrocupreine, quinidine) as new ggTas2r1 agonists.	Quinidine	98-107	taste 2 receptor member 40	Gallus gallus	10-18
28811548-8	2017	Next, the ggTas2r1 structural model was successfully used to identify three quinine analogues (epiquinidine, ethylhydrocupreine, quinidine) as new ggTas2r1 agonists.	Quinidine	98-107	taste 2 receptor member 40	Gallus gallus	147-155
28632743-4	2017	Therefore, this study aimed to assess the potential effects of E-4031, disopyramide and quinidine on SQT1 using a mathematical model of human ventricular electrophysiology.	Quinidine	88-97	potassium voltage-gated channel subfamily H member 2	Homo sapiens	101-105
28632743-15	2017	Quinidine exhibited significantly better therapeutic effects on SQT1 than E-4031 and disopyramide.	Quinidine	0-9	potassium voltage-gated channel subfamily H member 2	Homo sapiens	64-68
28632743-16	2017	CONCLUSIONS: The simulated pharmacological actions of quinidine exhibited antiarrhythmic effects on SQT1.	Quinidine	54-63	potassium voltage-gated channel subfamily H member 2	Homo sapiens	100-104
28632743-17	2017	This study substantiates a causal link between quinidine and QT interval prolongation in SQT1 and suggests that quinidine may be a potential pharmacological agent for treating SQT1 patients.	Quinidine	47-56	potassium voltage-gated channel subfamily H member 2	Homo sapiens	89-93
28632743-17	2017	This study substantiates a causal link between quinidine and QT interval prolongation in SQT1 and suggests that quinidine may be a potential pharmacological agent for treating SQT1 patients.	Quinidine	47-56	potassium voltage-gated channel subfamily H member 2	Homo sapiens	176-180
28632743-17	2017	This study substantiates a causal link between quinidine and QT interval prolongation in SQT1 and suggests that quinidine may be a potential pharmacological agent for treating SQT1 patients.	Quinidine	112-121	potassium voltage-gated channel subfamily H member 2	Homo sapiens	89-93
28632743-17	2017	This study substantiates a causal link between quinidine and QT interval prolongation in SQT1 and suggests that quinidine may be a potential pharmacological agent for treating SQT1 patients.	Quinidine	112-121	potassium voltage-gated channel subfamily H member 2	Homo sapiens	176-180
28347660-4	2017	Quinidine exhibited stronger inhibition than quinine; however, these two compounds inhibited the CYP2D6.10-mediated reaction more weakly than the CYP2D6.1 and CYP2D6.2 reactions.	Quinidine	0-9	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	146-152
28347660-4	2017	Quinidine exhibited stronger inhibition than quinine; however, these two compounds inhibited the CYP2D6.10-mediated reaction more weakly than the CYP2D6.1 and CYP2D6.2 reactions.	Quinidine	0-9	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	146-152
27939799-4	2017	The selective P-gp inhibitors (CP100356 and PSC833) enhanced 3-hydroxy-quinidine (3OH-Qi) in jejunum and ileum, while dual inhibitors of P-gp and CYP3A4 (verapamil and ketoconazole) decreased the 3OH-Qi production, despite of the increased intracellular Qi concentration, due to inhibition of CYP3A4.	Quinidine	86-88	phosphoglycolate phosphatase	Rattus norvegicus	14-18
28520381-5	2012	In addition, a number of drugs inhibit CYP2D6 activity, such as quinidine, fluoxetine, paroxetine, and propafenone.	Quinidine	64-73	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	39-45
28340451-7	2017	Enzalutamide may decrease plasma levels of CYP3A4, 2C9 and 2C19 substrates including disopiramide, quetiapine, quinidine and warfarin.	Quinidine	111-120	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	43-49
29521222-4	2017	RESULTS: We observed that quinidine, a substrate for MDR1 transporter, showed efflux ratio (Papp B-A/ Papp A-B) of 838 in MDCKII-MDR1 cells which plummeted to 14 in presence of verapamil, a known inhibitor of MDR1.	Quinidine	26-35	ATP binding cassette subfamily B member 1	Homo sapiens	53-57
27578169-1	2017	The KCNT1 gene encodes the sodium-dependent potassium channel, with quinidine being a partial antagonist of the KCNT1 channel.	Quinidine	68-77	potassium sodium-activated channel subfamily T member 1	Homo sapiens	4-9
27578169-1	2017	The KCNT1 gene encodes the sodium-dependent potassium channel, with quinidine being a partial antagonist of the KCNT1 channel.	Quinidine	68-77	potassium sodium-activated channel subfamily T member 1	Homo sapiens	112-117
27578169-13	2017	Thus, quinidine therapy should be attempted in patients with West syndrome caused by KCNT1 mutations, as reported for MPSI.	Quinidine	6-15	potassium sodium-activated channel subfamily T member 1	Homo sapiens	85-90
28188270-3	2017	Although a low-affinity block of quinidine on Kir2.1 has already been described, a comparative analysis of effects on other Kir2.x channels has not been performed to date.	Quinidine	33-42	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	46-52
28188270-5	2017	Quinidine exerted differential inhibitory effects on Kir2.x channels with the highest affinity toward Kir2.3 subunits.	Quinidine	0-9	potassium inwardly rectifying channel subfamily J member 4	Homo sapiens	102-108
28188270-8	2017	By means of comparative Ala-scanning mutagenesis, we further found that residues E224, F254, D259, and E299 are essential for quinidine block in Kir2.1 subunits.	Quinidine	126-135	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	145-151
28188270-9	2017	Analogously, quinidine mediated Kir2.3 inhibition by binding corresponding residues E216, D247, D251, and E291.	Quinidine	13-22	potassium inwardly rectifying channel subfamily J member 4	Homo sapiens	32-38
28188270-11	2017	Using channel mutants with altered (phosphatidylinositol 4,5-bisphosphate PIP2) affinities, we were able to demonstrate that high PIP2 affinities (i.e., Kir2.3 I214L) correlate with low quinidine sensitivity.	Quinidine	186-195	potassium inwardly rectifying channel subfamily J member 4	Homo sapiens	153-159
29521222-4	2017	RESULTS: We observed that quinidine, a substrate for MDR1 transporter, showed efflux ratio (Papp B-A/ Papp A-B) of 838 in MDCKII-MDR1 cells which plummeted to 14 in presence of verapamil, a known inhibitor of MDR1.	Quinidine	26-35	ATP binding cassette subfamily B member 1	Homo sapiens	129-133
29521222-4	2017	RESULTS: We observed that quinidine, a substrate for MDR1 transporter, showed efflux ratio (Papp B-A/ Papp A-B) of 838 in MDCKII-MDR1 cells which plummeted to 14 in presence of verapamil, a known inhibitor of MDR1.	Quinidine	26-35	ATP binding cassette subfamily B member 1	Homo sapiens	129-133
27756789-6	2017	Coincubation with quinidine, a CYP2D6 inhibitor, ablated endoxifen generation by hCYP2D6 MLMs.	Quinidine	18-27	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	31-37
27756789-6	2017	Coincubation with quinidine, a CYP2D6 inhibitor, ablated endoxifen generation by hCYP2D6 MLMs.	Quinidine	18-27	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	81-88
29648732-4	2016	Expected domperidone-quinidine interactions could have its origin both in the ability of quinidine to inhibit P-glycoprotein (P-gp) activity as well as cytochrome P450-mediated metabolism of both compounds.	Quinidine	21-30	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	110-124
27643409-12	2016	Inhibition of CYP2D6 by quinidine and cimetidine increased the cytotoxicity of both trazodone and m-CPP.	Quinidine	24-33	cytochrome P450, family 2, subfamily d, polypeptide 3	Rattus norvegicus	14-20
27690007-0	2016	Stereoselective Blockage of Quinidine and Quinine in the hERG Channel and the Effect of Their Rescue Potency on Drug-Induced hERG Trafficking Defect.	Quinidine	28-37	ETS transcription factor ERG	Homo sapiens	57-61
27690007-4	2016	The aim of our research is to study and compare the impacts of quinidine and quinine on hERG.	Quinidine	63-72	ETS transcription factor ERG	Homo sapiens	88-92
27690007-5	2016	Results show that both drugs block the hERG channel, with quinine 14-fold less potent than quinidine.	Quinidine	91-100	ETS transcription factor ERG	Homo sapiens	39-43
27690007-9	2016	The mutation decreases affinity of the two drugs with hERG, and quinine was more potent than quinidine in F656C-hERG blockage.	Quinidine	93-102	ETS transcription factor ERG	Homo sapiens	54-58
27690007-9	2016	The mutation decreases affinity of the two drugs with hERG, and quinine was more potent than quinidine in F656C-hERG blockage.	Quinidine	93-102	ETS transcription factor ERG	Homo sapiens	112-116
27690007-12	2016	In rescue experiments, we found that they exert no reverse effect on pentamidine- or desipramine-induced hERG trafficking defect, although quinidine has been reported to rescue trafficking-deficient pore mutation hERG G601S based on the interaction with F656.	Quinidine	139-148	ETS transcription factor ERG	Homo sapiens	213-217
27690007-13	2016	Our research demonstrated stereoselective effects of quinidine and quinine on the hERG channel, and this is the first study to explore their reversal potency on drug-induced hERG deficiency.	Quinidine	53-62	ETS transcription factor ERG	Homo sapiens	82-86
27690007-13	2016	Our research demonstrated stereoselective effects of quinidine and quinine on the hERG channel, and this is the first study to explore their reversal potency on drug-induced hERG deficiency.	Quinidine	53-62	ETS transcription factor ERG	Homo sapiens	174-178
27652191-3	2016	In this study, we have evaluated the inhibitory effects of natural bioflavonoids (quercetin and silymarin) on P-gp by using digoxin and quinidine as model P-gp model substrate drugs.	Quinidine	136-145	ATP binding cassette subfamily B member 1	Homo sapiens	110-114
27262425-0	2016	Structure-activity relationships of dibenzoylhydrazines for the inhibition of P-glycoprotein-mediated quinidine transport.	Quinidine	102-111	ATP binding cassette subfamily B member 1	Homo sapiens	78-92
27262425-2	2016	In the present study, we evaluated the inhibition of P-gp-mediated quinidine transport by two series of DBHs and performed a classical QSAR analysis and docking simulation in order to investigate the mechanisms underlying P-gp substrate/inhibitor recognition.	Quinidine	67-76	ATP binding cassette subfamily B member 1	Homo sapiens	53-57
27262425-2	2016	In the present study, we evaluated the inhibition of P-gp-mediated quinidine transport by two series of DBHs and performed a classical QSAR analysis and docking simulation in order to investigate the mechanisms underlying P-gp substrate/inhibitor recognition.	Quinidine	67-76	ATP binding cassette subfamily B member 1	Homo sapiens	222-226
29648732-4	2016	Expected domperidone-quinidine interactions could have its origin both in the ability of quinidine to inhibit P-glycoprotein (P-gp) activity as well as cytochrome P450-mediated metabolism of both compounds.	Quinidine	21-30	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	126-130
29648732-4	2016	Expected domperidone-quinidine interactions could have its origin both in the ability of quinidine to inhibit P-glycoprotein (P-gp) activity as well as cytochrome P450-mediated metabolism of both compounds.	Quinidine	89-98	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	110-124
29648732-4	2016	Expected domperidone-quinidine interactions could have its origin both in the ability of quinidine to inhibit P-glycoprotein (P-gp) activity as well as cytochrome P450-mediated metabolism of both compounds.	Quinidine	89-98	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	126-130
26856397-4	2016	RESULTS: Furafylline (a CYP1A2 inhibitor), quinidine (a CYP2D6 inhibitor), and heat treatment (inactivates FMO3) suppressed liver microsomal metabolic clearance of olanzapine by approximately 30%.	Quinidine	43-52	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	56-62
27376043-7	2016	Verapamil (P-glycoprotein inhibitor), nelfinavir (OATP1B1 inhibitor), quinidine (OCT1 inhibitor) were used to differentiate the inhibitory properties of these agents to the transporter expressions in HepG2 and Huh-7 cells.	Quinidine	70-79	solute carrier family 22 member 1	Homo sapiens	81-85
27376043-9	2016	Verapamil reduces the expressions of P-glycoprotein in HepG2 and Huh-7; nelfinavir reduces the expression of OATP1B1 in HepG2 and Huh-7; while quinidine reduces the OCT1 gene expressions in HepG2, but not in Huh-7 cells.	Quinidine	143-152	solute carrier family 22 member 1	Homo sapiens	165-169
27063220-5	2016	Direct CYP inhibition was validated using 7 inhibitors (alpha-naphthoflavone, tranylcypromine, ticlopidine, fluconazole, quinidine, ketoconazole and 1-ABT).	Quinidine	121-130	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	7-10
26780675-8	2016	AZD1305, flecainide and quinidine induced QRS widening with 4.2, 10 and 5.6% muM(-1) unbound drug.	Quinidine	24-33	PWWP domain containing 3A, DNA repair factor	Canis lupus familiaris	77-83
26995013-8	2016	We also examined the inhibitory effects of DBHs on quinidine (a P-gp substrate) transport by P-gp in order to ascertain whether these derivatives are inhibitors of P-gp.	Quinidine	51-60	ATP binding cassette subfamily B member 1	Homo sapiens	64-68
26995013-8	2016	We also examined the inhibitory effects of DBHs on quinidine (a P-gp substrate) transport by P-gp in order to ascertain whether these derivatives are inhibitors of P-gp.	Quinidine	51-60	ATP binding cassette subfamily B member 1	Homo sapiens	93-97
26995013-8	2016	We also examined the inhibitory effects of DBHs on quinidine (a P-gp substrate) transport by P-gp in order to ascertain whether these derivatives are inhibitors of P-gp.	Quinidine	51-60	ATP binding cassette subfamily B member 1	Homo sapiens	93-97
27038701-6	2016	It is worth noting that this chiral stationary phase (CSP) containing quinidine with a tert-butyl carbamate residue as chiral selector exhibits much higher enantioselectivity and diastereoselectivity than the previously developed O-9-[2-(methacryloyloxy)-ethylcarbamoyl]-10,11-dihydroquinidine (MQD) based CSP for N-derivatized amino acids and dipeptides.	Quinidine	70-79	immunoglobulin kappa variable 1D-32 (pseudogene)	Homo sapiens	230-233
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.	Quinidine	34-43	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.	Quinidine	34-43	potassium sodium-activated channel subfamily T member 1	Homo sapiens	118-123
26748457-0	2016	Ineffective quinidine therapy in early onset epileptic encephalopathy with KCNT1 mutation.	Quinidine	12-21	potassium sodium-activated channel subfamily T member 1	Homo sapiens	75-80
26657265-8	2016	CYP3A4 and CYP2D6 inhibitory effect of SC and ursolic acid (IC50: 197.49+-2.68, 211.45+-3.54 and IC50: 229.25+-2.52, 212.66+-1.26 microg/mL) was less as compared to that known inhibitors, ketoconazole and quinidine respectively.	Quinidine	205-214	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	11-17
25417051-7	2016	All MDD showed inhibition against CYP2D6 activity and most of them in the range of the clinically relevant CYP2D6 inhibitors quinidine and fluoxetine.	Quinidine	125-134	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	34-40
25417051-7	2016	All MDD showed inhibition against CYP2D6 activity and most of them in the range of the clinically relevant CYP2D6 inhibitors quinidine and fluoxetine.	Quinidine	125-134	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	107-113
26932816-6	2016	Dual inhibitors of both P-gp and Cyp3a (verapamil and ketoconazole) increased the concentration of Qi in the jejunum and ileum, but less 3-hydroxy-quinidine was produced due to inhibition of Cyp3a.	Quinidine	99-101	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	24-28
26932816-6	2016	Dual inhibitors of both P-gp and Cyp3a (verapamil and ketoconazole) increased the concentration of Qi in the jejunum and ileum, but less 3-hydroxy-quinidine was produced due to inhibition of Cyp3a.	Quinidine	99-101	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	33-38
26932816-6	2016	Dual inhibitors of both P-gp and Cyp3a (verapamil and ketoconazole) increased the concentration of Qi in the jejunum and ileum, but less 3-hydroxy-quinidine was produced due to inhibition of Cyp3a.	Quinidine	99-101	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	191-196
26248047-0	2016	The effect of quinidine, a strong P-glycoprotein inhibitor, on the pharmacokinetics and central nervous system distribution of naloxegol.	Quinidine	14-23	ATP binding cassette subfamily B member 1	Homo sapiens	34-48
26248047-3	2016	This double-blind, randomized, 2-part, crossover study in healthy volunteers evaluated the effect of quinidine (600 mg PO), a CYP3A/PGP transporter inhibitor, on the pharmacokinetics and CNS distribution of naloxegol (25 mg PO).	Quinidine	101-110	ATP binding cassette subfamily B member 1	Homo sapiens	132-135
26248047-5	2016	Coadministration of quinidine and naloxegol increased naloxegol"s AUC 1.4-fold and Cmax 2.5-fold but did not antagonize morphine-induced miosis, suggesting that PGP inhibition does not increase the CNS penetration of naloxegol.	Quinidine	20-29	ATP binding cassette subfamily B member 1	Homo sapiens	161-164
26294260-9	2016	The formation of M1 and M2 in DLM was significantly abrogated in the presence of the specific CYP2D inhibitor, quinidine, and to a lesser extent by the CYP3A inhibitor, ketoconazole, corroborating data from human recombinant isozymes.	Quinidine	111-120	cytochrome P450 family 2 subfamily D member 7 (gene/pseudogene)	Homo sapiens	94-99
26892731-13	2016	In addition, quinidine inhibits both cynomolgus monkey CYP2D17 and Japanese monkey 2D29.	Quinidine	13-22	cytochrome P450 family 2 subfamily D member 6	Macaca fascicularis	55-62
26452722-11	2016	Similarly, quinidine-mediated CYP2D6 inhibition reduced clearance of dextromethorphan and desipramine by 71 and 22%, respectively.	Quinidine	11-20	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	30-36
26505474-6	2015	In contrast, Kv6.4 currents were potentiated by 4-AP while displaying moderately increased affinities for the channel pore blockers quinidine and flecainide.	Quinidine	132-141	potassium voltage-gated channel modifier subfamily G member 4	Homo sapiens	13-18
26354948-6	2015	At clinically relevant quinidine plasma concentrations, P-gp inhibition resulted in a 60% increase in (11)C-radioactivity distribution across the human BBB as measured by the brain extraction ratio (ER) of (11)C-radioactivity.	Quinidine	23-32	phosphoglycolate phosphatase	Homo sapiens	56-60
26354948-7	2015	Furthermore, the magnitude of BBB P-gp inhibition by quinidine was successfully predicted by a combination of in vitro and macaque data, but not by rat data.	Quinidine	53-62	phosphoglycolate phosphatase	Rattus norvegicus	34-38
26354948-8	2015	Although our findings demonstrated that quinidine did not completely inhibit P-gp at the human BBB, it has the potential to produce clinically significant CNS drug interactions with P-gp substrate drugs that exhibit a narrow therapeutic window and are significantly excluded from the brain by P-gp.	Quinidine	40-49	phosphoglycolate phosphatase	Homo sapiens	182-186
26354948-8	2015	Although our findings demonstrated that quinidine did not completely inhibit P-gp at the human BBB, it has the potential to produce clinically significant CNS drug interactions with P-gp substrate drugs that exhibit a narrow therapeutic window and are significantly excluded from the brain by P-gp.	Quinidine	40-49	phosphoglycolate phosphatase	Homo sapiens	182-186
26325084-9	2015	Quinidine, a known inhibitor of CYP2D6, was used as a reference.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	32-38
26325084-12	2015	Inhibition of CYP2D6 enzyme with Quinidine increased in a linear dose-related fashion from -7.07% at 2.06  nM to 84.05% at 500  nM.	Quinidine	33-42	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	14-20
25719307-3	2015	The phenomenon of phenocopy with regard to CYP2D6 was first described when Danish patients changed phenotype from extensive to poor metabolizers during treatment with quinidine.	Quinidine	167-176	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	43-49
26600643-7	2015	Fluorescence study revealed that the extract and the biomarker had some inhibition on CYP450 isozymes e.g. CYP3A4 and CYP2D6 (IC50 values of the extract: 102.65 +- 2.63-142.23 +- 2.61 microg/ml and TG: 168.73 +- 4.03-180.90 +- 2.49 microg/ml) which was very less compared to positive controls ketoconazole and quinidine.	Quinidine	310-319	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	118-124
25790957-6	2015	Experiments using the KCNH2-pore blocking agent quinidine supported these findings.	Quinidine	48-57	potassium voltage-gated channel subfamily H member 2	Homo sapiens	22-27
26369628-0	2015	Quinidine in the treatment of KCNT1-positive epilepsies.	Quinidine	0-9	potassium sodium-activated channel subfamily T member 1	Homo sapiens	30-35
26369628-1	2015	We report 2 patients with drug-resistant epilepsy caused by KCNT1 mutations who were treated with quinidine.	Quinidine	98-107	potassium sodium-activated channel subfamily T member 1	Homo sapiens	60-65
26381170-6	2015	Whole-cell patch-clamp recordings showed that hSlo3 currents are inhibited: significantly by progesterone, Ba(2+) and quinidine; partially by Penitrem A and Charybdotoxin; and poorly by Iberiotoxin and Slotoxin.	Quinidine	118-127	potassium calcium-activated channel subfamily U member 1	Homo sapiens	46-51
26045093-0	2015	Mechanism of inhibition of mouse Slo3 (KCa 5.1) potassium channels by quinine, quinidine and barium.	Quinidine	79-88	potassium channel, subfamily U, member 1	Mus musculus	33-37
26045093-0	2015	Mechanism of inhibition of mouse Slo3 (KCa 5.1) potassium channels by quinine, quinidine and barium.	Quinidine	79-88	potassium calcium-activated channel subfamily U member 1	Homo sapiens	39-46
26045093-5	2015	The interaction between quinidine and mSlo3 channels was modelled by in silico docking.	Quinidine	24-33	potassium channel, subfamily U, member 1	Mus musculus	38-43
26045093-10	2015	CONCLUSIONS AND IMPLICATIONS: Block of mSlo3 channels by quinine, quinidine and barium is not state-dependent.	Quinidine	66-75	potassium channel, subfamily U, member 1	Mus musculus	39-44
25883089-8	2015	Only a very modest saturable MPP+ uptake is measurable in NCl-H441 cells and the inhibitory effect of quinidine points to OCT1 as the subtype functionally involved in this model.	Quinidine	102-111	solute carrier family 22 member 1	Homo sapiens	122-126
25901027-7	2015	Furthermore, the intestinal absorption of P-gp substrates (quinidine and etoposide) was substantially suppressed by administering the drugs at the times of day when P-gp levels were abundant.	Quinidine	59-68	ATP binding cassette subfamily B member 1	Homo sapiens	42-46
25901027-7	2015	Furthermore, the intestinal absorption of P-gp substrates (quinidine and etoposide) was substantially suppressed by administering the drugs at the times of day when P-gp levels were abundant.	Quinidine	59-68	ATP binding cassette subfamily B member 1	Homo sapiens	165-169
25681130-10	2015	Preincubation of HLMs and rCYP2D6 resulted in the inactivation of the enzyme, which was attenuated by GFA or quinidine.	Quinidine	109-118	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	26-33
25410756-8	2015	Notably, the brain uptake clearance for [(3) H]amantadine was significantly decreased with the co-perfusion of quinidine or verapamil, which are cationic P-gp inhibitors, while MPP(+) did not have a significant effect.	Quinidine	111-120	phosphoglycolate phosphatase	Rattus norvegicus	154-158
26022171-3	2015	Examples of that include the need to avoid specific drugs in Dravet syndrome and the ongoing investigations of the potential use of new directed therapies such as retigabine in KCNQ2-related epilepsies, quinidine in KCNT1-related epilepsies, and memantine in GRIN2A-related epilepsies.	Quinidine	203-212	potassium sodium-activated channel subfamily T member 1	Homo sapiens	216-221
25735838-8	2015	Rates of PTP formation by MPTP N-demethylation in marmoset liver microsomes were correlated with bufuralol 1"-hydroxylation rates (r = 0.77, P &lt; 0.01) and were suppressed by quinidine (1 muM), thereby indicating the importance of marmoset CYP2D6 in PTP formation.	Quinidine	177-186	cytochrome P450 2D19	Callithrix jacchus	242-248
25857234-5	2015	The uptake was strongly inhibited by quinidine, pyrilamine and verapamil, and was moderately inhibited by TEA (substrate of OCTs and OCTNs) and l-carnitine (substrate of OCTN2), but was not inhibited by MPP(+) (substrate of OCTs and PMAT) or ergothioneine (substrate of OCTN1).	Quinidine	37-46	solute carrier family 22 member 5	Homo sapiens	170-175
25434721-9	2015	Furthermore, a pharmacokinetic assay using quinidine and amlodipine showed that CYP3A4 enzyme activity per mg of microsomal protein was also decreased in the group overexpressing CYP3A5 compared with the dexamethasone-induced control group.	Quinidine	43-52	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	80-86
25434721-9	2015	Furthermore, a pharmacokinetic assay using quinidine and amlodipine showed that CYP3A4 enzyme activity per mg of microsomal protein was also decreased in the group overexpressing CYP3A5 compared with the dexamethasone-induced control group.	Quinidine	43-52	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	179-185
25319098-0	2015	Vitamin D receptor activation induces P-glycoprotein and increases brain efflux of quinidine: an intracerebral microdialysis study in conscious rats.	Quinidine	83-92	vitamin D (1,25-dihydroxyvitamin D3) receptor	Mus musculus	0-18
25319098-1	2015	PURPOSE: Since the vitamin D receptor (VDR) was found to up-regulate cerebral P-glycoprotein expression in vitro and in mice, we extend our findings to rats by assessing the effect of rat Vdr activation on brain efflux of quinidine, a P-gp substrate that is eliminated primarily by cytochrome P450 3a.	Quinidine	222-231	vitamin D (1,25-dihydroxyvitamin D3) receptor	Mus musculus	19-37
25729581-3	2015	Selected Pgp transport ligands include: Amiodarone, Bepridil, Diltiazem, Dipyridamole, Nicardipine, Nifedipine, Propranolol, and Quinidine.	Quinidine	129-138	phosphoglycolate phosphatase	Mus musculus	9-12
25319098-1	2015	PURPOSE: Since the vitamin D receptor (VDR) was found to up-regulate cerebral P-glycoprotein expression in vitro and in mice, we extend our findings to rats by assessing the effect of rat Vdr activation on brain efflux of quinidine, a P-gp substrate that is eliminated primarily by cytochrome P450 3a.	Quinidine	222-231	vitamin D (1,25-dihydroxyvitamin D3) receptor	Mus musculus	39-42
25420507-0	2015	Voltage-gated K+ channel blocker quinidine inhibits proliferation and induces apoptosis by regulating expression of microRNAs in human glioma U87-MG cells.	Quinidine	33-42	potassium voltage-gated channel subfamily D member 3	Homo sapiens	0-24
25420507-3	2015	In the present study, we investigated the effect and mechanisms of quinidine, a commonly used voltage-gated K+ channel blocker, on cell proliferation and apoptosis of human glioma U87-MG cells.	Quinidine	67-76	potassium voltage-gated channel subfamily D member 3	Homo sapiens	94-118
25420507-6	2015	Furthermore, the concentration range of quinidine, which inhibited voltage-gated K+ channel currents in electrophysiological assay, was consistent with that of quinidine inhibiting cell proliferation and inducing cell apoptosis.	Quinidine	40-49	potassium voltage-gated channel subfamily D member 3	Homo sapiens	67-91
25420507-6	2015	Furthermore, the concentration range of quinidine, which inhibited voltage-gated K+ channel currents in electrophysiological assay, was consistent with that of quinidine inhibiting cell proliferation and inducing cell apoptosis.	Quinidine	160-169	potassium voltage-gated channel subfamily D member 3	Homo sapiens	67-91
25420507-8	2015	The upregulation of miR-149-3p and downregulation of miR-424-5p by quinidine treatment were further verified by using quantitative real-time PCR.	Quinidine	67-76	microRNA 424	Homo sapiens	53-60
25420507-10	2015	Taken together, these data suggested that the anti-proliferative and pro-apoptosis effect of voltage-gated K+ channel blocker quinidine in human glioma cells was mediated at least partly through regulating expression of miRNAs, and provided further support for the mechanisms of voltage-gated K+ channels in mediating cell proliferation and apoptosis.	Quinidine	126-135	potassium voltage-gated channel subfamily D member 3	Homo sapiens	93-117
26867116-5	2015	Four compounds, namely dextromethorphan, ketoconazole, terfenadine, and quinidine were screened for hERG inhibition with an automated patch clamp apparatus (CytoPatch(TM)2).	Quinidine	72-81	ETS transcription factor ERG	Homo sapiens	100-104
25619394-7	2015	The metabolism of TEST and DEM in HepG2 cells was dose-dependently inhibited by the specific CYP3A4 inhibitor ketoconazole and CYP2D6 inhibitor quinidine.	Quinidine	144-153	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	127-133
24839994-5	2014	In mdr1a (-/-) rats, however, quinidine pretreatment caused a dose-dependent decrease in the AUC.	Quinidine	30-39	ATP binding cassette subfamily B member 1A	Rattus norvegicus	3-8
25475885-8	2015	Mirtazapine clearance in pooled human liver microsomes was inhibited by quinidine (a CYP2D6 inhibitor), ketoconazole (a CYP3A inhibitor), and in combination with risperidone and duloxetine, possible coadministered medicines.	Quinidine	72-81	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	85-91
25263961-4	2014	Our results showed that quinidine, a prototypical inhibitor of Na(+)/Mg(2+) exchanger, inhibited Ang II-induced cardiac fibrosis via attenuating the overexpression of vital biomarkers of fibrosis, including connective tissue growth factor (CTGF), fibronectin (FN) and alpha-smooth muscle actin (alpha-SMA).	Quinidine	24-33	angiogenin	Homo sapiens	97-100
25263961-4	2014	Our results showed that quinidine, a prototypical inhibitor of Na(+)/Mg(2+) exchanger, inhibited Ang II-induced cardiac fibrosis via attenuating the overexpression of vital biomarkers of fibrosis, including connective tissue growth factor (CTGF), fibronectin (FN) and alpha-smooth muscle actin (alpha-SMA).	Quinidine	24-33	cellular communication network factor 2	Homo sapiens	207-238
25263961-4	2014	Our results showed that quinidine, a prototypical inhibitor of Na(+)/Mg(2+) exchanger, inhibited Ang II-induced cardiac fibrosis via attenuating the overexpression of vital biomarkers of fibrosis, including connective tissue growth factor (CTGF), fibronectin (FN) and alpha-smooth muscle actin (alpha-SMA).	Quinidine	24-33	cellular communication network factor 2	Homo sapiens	240-244
25263961-4	2014	Our results showed that quinidine, a prototypical inhibitor of Na(+)/Mg(2+) exchanger, inhibited Ang II-induced cardiac fibrosis via attenuating the overexpression of vital biomarkers of fibrosis, including connective tissue growth factor (CTGF), fibronectin (FN) and alpha-smooth muscle actin (alpha-SMA).	Quinidine	24-33	fibronectin 1	Homo sapiens	247-258
25263961-4	2014	Our results showed that quinidine, a prototypical inhibitor of Na(+)/Mg(2+) exchanger, inhibited Ang II-induced cardiac fibrosis via attenuating the overexpression of vital biomarkers of fibrosis, including connective tissue growth factor (CTGF), fibronectin (FN) and alpha-smooth muscle actin (alpha-SMA).	Quinidine	24-33	fibronectin 1	Homo sapiens	260-262
25263961-5	2014	In addition, quinidine also decreased the Ang II-mediated elevation of concentration of intracellular Ca(2+) ([Ca(2+)]i) and extrusion of intracellular Mg(2+).	Quinidine	13-22	angiogenin	Homo sapiens	42-45
24946104-1	2014	BACKGROUND AND PURPOSE: The Kv beta1.3 subunit modifies the gating and pharmacology of Kv 1.5 channels in a PKC-dependent manner, decreasing channel sensitivity to bupivacaine- and quinidine-mediated blockade.	Quinidine	181-190	potassium voltage-gated channel subfamily A regulatory beta subunit 1	Homo sapiens	28-38
24946104-1	2014	BACKGROUND AND PURPOSE: The Kv beta1.3 subunit modifies the gating and pharmacology of Kv 1.5 channels in a PKC-dependent manner, decreasing channel sensitivity to bupivacaine- and quinidine-mediated blockade.	Quinidine	181-190	potassium voltage-gated channel subfamily A member 5	Homo sapiens	87-93
24946104-3	2014	The aim of the present study was to investigate the effects of PKC inhibition on bupivacaine and quinidine block of Kv 1.5 + Kv beta1.3 channels.	Quinidine	97-106	potassium voltage-gated channel subfamily A member 5	Homo sapiens	116-122
24946104-3	2014	The aim of the present study was to investigate the effects of PKC inhibition on bupivacaine and quinidine block of Kv 1.5 + Kv beta1.3 channels.	Quinidine	97-106	potassium voltage-gated channel subfamily A regulatory beta subunit 1	Homo sapiens	125-133
25168620-7	2014	With IV dosing of edoxaban, co-administration of the P-gp inhibitor quinidine decreased both edoxaban clearance (CL) and V 2, resulting in an increase of 32 % in AUC and 66 % in C 24.	Quinidine	68-77	ATP binding cassette subfamily B member 1	Homo sapiens	53-57
24602137-3	2014	METHODS: Eighteen healthy male subjects were administered loperamide alone (period 1) or with loperamide plus quinidine or HM30181 in period 2 or 3, respectively.	Quinidine	110-119	period circadian regulator 2	Homo sapiens	134-142
24947467-2	2014	For five P-gp substrates (indinavir, quinidine, loperamide, paclitaxel, and verapamil) and one nonsubstrate (diazepam), in vitro P-gp transport activities were determined by measuring transcellular transport across monolayers of cynomolgus monkey P-gp-transfected LLC-PK1 and parental cells.	Quinidine	37-46	phosphoglycolate phosphatase	Homo sapiens	129-133
24947467-2	2014	For five P-gp substrates (indinavir, quinidine, loperamide, paclitaxel, and verapamil) and one nonsubstrate (diazepam), in vitro P-gp transport activities were determined by measuring transcellular transport across monolayers of cynomolgus monkey P-gp-transfected LLC-PK1 and parental cells.	Quinidine	37-46	phosphoglycolate phosphatase	Homo sapiens	129-133
24947867-7	2014	The OATP1A2-, OATP2B1-, and OCT1-mediated quercetin uptake was inhibited by known inhibitors such as naringin, cyclosporin A, and quinidine, respectively.	Quinidine	130-139	solute carrier organic anion transporter family member 1A2	Homo sapiens	4-11
24947867-7	2014	The OATP1A2-, OATP2B1-, and OCT1-mediated quercetin uptake was inhibited by known inhibitors such as naringin, cyclosporin A, and quinidine, respectively.	Quinidine	130-139	solute carrier organic anion transporter family member 2B1	Homo sapiens	14-21
24947867-7	2014	The OATP1A2-, OATP2B1-, and OCT1-mediated quercetin uptake was inhibited by known inhibitors such as naringin, cyclosporin A, and quinidine, respectively.	Quinidine	130-139	solute carrier family 22 member 1	Homo sapiens	28-32
25222611-6	2014	The inhibition effect of quinidine on CYP2D6 catalyze-cycle was also investigated.	Quinidine	25-34	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	38-44
24917180-5	2014	To this end, the exposure to the P-gp substrate quinidine was determined in the plasma and brain tissue after intravenous administration in rats at six different time points over the 24-h period.	Quinidine	48-57	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	33-37
24917180-7	2014	Upon inhibition of P-gp, exposure to quinidine in brain tissue is constant over the 24-h period.	Quinidine	37-46	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	19-23
25042079-3	2014	The antiarrhythmic drug quinidine is a partial antagonist of KCNT1 and hence may be a candidate drug for treatment of this condition.	Quinidine	24-33	potassium sodium-activated channel subfamily T member 1	Homo sapiens	61-66
25042079-4	2014	We report the case of a child with migrating partial seizures of infancy secondary to an activating mutation in KCNT1 treated with quinidine.	Quinidine	131-140	potassium sodium-activated channel subfamily T member 1	Homo sapiens	112-117
24778366-6	2014	Quinidine and (+)-tetrahydropalmatine [(+)-THP], OCT1 and OCT3 inhibitors, significantly reduced the uptake of NC in MDCK-hOCT1 cells, MDCK-hOCT3 cells, and rat primary hepatocytes, but only (+)-THP markedly attenuated the NC-induced toxicity.	Quinidine	0-9	solute carrier family 22 member 1	Homo sapiens	122-127
24778366-6	2014	Quinidine and (+)-tetrahydropalmatine [(+)-THP], OCT1 and OCT3 inhibitors, significantly reduced the uptake of NC in MDCK-hOCT1 cells, MDCK-hOCT3 cells, and rat primary hepatocytes, but only (+)-THP markedly attenuated the NC-induced toxicity.	Quinidine	0-9	solute carrier family 22 member 3	Homo sapiens	140-145
24081450-4	2014	Among 25 additional modulators tested, bupivacaine (100 muM), quinidine (50 muM) and Ba(2+) (3 mM) and cold (10  C) were most effective inhibitors of THIK-1 current (&gt;50 % inhibition).	Quinidine	62-71	latexin	Homo sapiens	76-79
24985475-3	2014	RESULTS: In both rat strains, quinidine, digoxin, and verapamil were transported by P-gp across each barrier; however, the impact of P-gp on retinal uptake of quinidine and verapamil was less pronounced than that on brain uptake.	Quinidine	30-39	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	84-88
24985475-6	2014	In P-gp-deficient conditions, the RUI and AHUI of quinidine, digoxin, and verapamil, as well as the BUI of quinidine and digoxin, were decreased by P-gp inhibitors.	Quinidine	50-59	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	3-7
24985475-6	2014	In P-gp-deficient conditions, the RUI and AHUI of quinidine, digoxin, and verapamil, as well as the BUI of quinidine and digoxin, were decreased by P-gp inhibitors.	Quinidine	107-116	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	3-7
24985475-9	2014	CONCLUSIONS: In both rat strains, P-gp operates in the blood-ocular barriers, and the impact of P-gp on BRB permeability to quinidine and verapamil is lower than that on BBB permeability.	Quinidine	124-133	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	96-100
24161619-5	2014	We found that the cinchona alkaloids quinidine and cinchonine, which have identical stereochemistry about carbons 8 and 9, exhibited the greatest inhibition of dSERT and hSERT transporter function whereas quinine and cinchonidine, enantiomers of quinidine and cinchonine, respectively, were weaker inhibitors of dSERT and hSERT.	Quinidine	37-46	Serotonin transporter	Drosophila melanogaster	160-165
24161619-5	2014	We found that the cinchona alkaloids quinidine and cinchonine, which have identical stereochemistry about carbons 8 and 9, exhibited the greatest inhibition of dSERT and hSERT transporter function whereas quinine and cinchonidine, enantiomers of quinidine and cinchonine, respectively, were weaker inhibitors of dSERT and hSERT.	Quinidine	37-46	solute carrier family 6 member 4	Homo sapiens	170-175
24161619-5	2014	We found that the cinchona alkaloids quinidine and cinchonine, which have identical stereochemistry about carbons 8 and 9, exhibited the greatest inhibition of dSERT and hSERT transporter function whereas quinine and cinchonidine, enantiomers of quinidine and cinchonine, respectively, were weaker inhibitors of dSERT and hSERT.	Quinidine	37-46	Serotonin transporter	Drosophila melanogaster	312-317
24161619-5	2014	We found that the cinchona alkaloids quinidine and cinchonine, which have identical stereochemistry about carbons 8 and 9, exhibited the greatest inhibition of dSERT and hSERT transporter function whereas quinine and cinchonidine, enantiomers of quinidine and cinchonine, respectively, were weaker inhibitors of dSERT and hSERT.	Quinidine	37-46	solute carrier family 6 member 4	Homo sapiens	322-327
24161619-6	2014	Furthermore, SERT mutations known to decrease the binding affinity of many antidepressants affected the cinchona alkaloids in a stereo-specific manner where the similar inhibitory profiles for quinine and cinchonidine (8S,9R) were distinct from quinidine and cinchonine (8R,9S).	Quinidine	245-254	solute carrier family 6 member 4	Homo sapiens	13-17
24161619-7	2014	Small molecule docking studies with hSERT homology models predict that quinine and cinchonidine bind to the central 5-HT binding site (S1) whereas quinidine and cinchonine bind to the S2 site.	Quinidine	147-156	solute carrier family 6 member 4	Homo sapiens	36-41
24081450-4	2014	Among 25 additional modulators tested, bupivacaine (100 muM), quinidine (50 muM) and Ba(2+) (3 mM) and cold (10  C) were most effective inhibitors of THIK-1 current (&gt;50 % inhibition).	Quinidine	62-71	potassium two pore domain channel subfamily K member 13	Homo sapiens	150-156
26000221-6	2014	To block DM hepatic metabolism, thereby increasing DM bioavailability, Quinidine, a cytochrome P450 2D6 inhibitor, is coadministered at a dosage well below those for treating cardiac arrhythmia.	Quinidine	71-80	cytochrome P450 2D6	Homo sapiens	84-103
25061302-4	2014	The quinidine component of DM/Q inhibits the cytochrome P450 2D6-mediated metabolic conversion of dextromethorphan to its active metabolite dextrorphan, thereby increasing dextromethorphan systemic bioavailability and driving the pharmacology toward that of the parent drug and away from adverse effects of the dextrorphan metabolite.	Quinidine	4-13	cytochrome P450 2D6	Homo sapiens	45-64
24440401-1	2014	In the present study, we investigated the effect of large neutral amino acid modification in overcoming P-gp mediated cellular efflux of quinidine.	Quinidine	137-146	PGP	Canis lupus familiaris	104-108
24440401-3	2014	[14C]-erythromycin was selected as a model substrate to study interaction of quinidine and Ile-quinidine with P-gp.	Quinidine	77-86	PGP	Canis lupus familiaris	110-114
24440401-13	2014	Based on these results, it was apparent that quinidine displayed higher substrate affinity toward P-gp relative to Ile-quinidine.	Quinidine	45-54	PGP	Canis lupus familiaris	98-102
24440401-16	2014	In conclusion, chemical modification of quinidine with neutral amino acids results in circumvention of P-gp mediated drug efflux.	Quinidine	40-49	PGP	Canis lupus familiaris	103-107
27957038-0	2014	Cytochrome P450-2D6 Genotype Definition May Improve Therapy for Paroxysmal Atrial Fibrillation A Case of Syncope Following "Pill-in-the-Pocket" Quinidine plus Propafenone.	Quinidine	144-153	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-19
24591078-0	2014	KCNT1 gain of function in 2 epilepsy phenotypes is reversed by quinidine.	Quinidine	63-72	potassium channel, subfamily T, member 1	Mus musculus	0-5
24524365-15	2014	TEA, amantadine, quinidine, and verapamil significantly inhibited ASP(+) uptake into NCl-H441 cells, whereas the effect of d- and l-carnitine and ergothioneine, two OCTN substrates, was less pronounced.	Quinidine	17-26	nucleolin	Homo sapiens	85-88
24269949-8	2014	Phosphomimetic and quinidine sensitivity studies suggest that I235N-Kv7.1 limits the conformational changes in Kv7.1 channels, which are necessary to upregulate IKs after PKA phosphorylation.	Quinidine	19-28	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	68-73
24269949-8	2014	Phosphomimetic and quinidine sensitivity studies suggest that I235N-Kv7.1 limits the conformational changes in Kv7.1 channels, which are necessary to upregulate IKs after PKA phosphorylation.	Quinidine	19-28	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	111-116
24212378-4	2014	From a set of potential P-gp inhibitors, clarithromycin, cyclosporin A, itraconazole, ketoconazole, quinidine, and ritonavir inhibited P-gp-mediated transport of dabigatran etexilate over a concentration range that may hypothetically occur in the intestine.	Quinidine	100-109	ATP binding cassette subfamily B member 1	Homo sapiens	24-28
24212378-4	2014	From a set of potential P-gp inhibitors, clarithromycin, cyclosporin A, itraconazole, ketoconazole, quinidine, and ritonavir inhibited P-gp-mediated transport of dabigatran etexilate over a concentration range that may hypothetically occur in the intestine.	Quinidine	100-109	ATP binding cassette subfamily B member 1	Homo sapiens	135-139
23777437-1	2013	Intracerebral microdialysis was utilized to investigate the effect of P-glycoprotein (a drug efflux transporter) induction at the mouse blood-brain barrier (BBB) on brain extracellular fluid concentrations of quinidine, an established substrate of P-glycoprotein.	Quinidine	209-218	phosphoglycolate phosphatase	Mus musculus	70-84
24027778-3	2013	Direct electron transfer (DET) between CYP3A4 and CNFs was observed at a formal potential of -0.302 V. The electrocatalytic reduction current increased with the addition of drugs including testosterone and quinidine.	Quinidine	206-215	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	39-45
24117377-6	2013	The oxygen reduction current at the polycrystalline ITO film electrodes had increased 3- to 4-fold, specifically coupled with the oxidation of drugs (testosterone and quinidine) by the monooxygenase activity of CYP.	Quinidine	167-176	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	211-214
24351551-9	2014	That is, morphine and quinidine significantly increased the bioavailability of etoposide believed to be due to competitive P-gp inhibition in the intestine.	Quinidine	22-31	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	123-127
24167220-4	2014	M-1 also markedly inhibited CYP2D6 activity; its inhibitory effect with an IC50 (Ki) value of 0.201 muM (0.120 muM) was more potent than that of sarpogrelate, and was similarly potent as quinidine (Ki, 0.129 muM), a well-known typical CYP2D6 inhibitor.	Quinidine	187-196	cholinergic receptor muscarinic 1	Homo sapiens	0-3
23777437-1	2013	Intracerebral microdialysis was utilized to investigate the effect of P-glycoprotein (a drug efflux transporter) induction at the mouse blood-brain barrier (BBB) on brain extracellular fluid concentrations of quinidine, an established substrate of P-glycoprotein.	Quinidine	209-218	phosphoglycolate phosphatase	Mus musculus	248-262
23777437-4	2013	P-glycoprotein, pregnane X receptor and Cyp3a11 (metabolizing enzyme for quinidine) protein expression in capillaries and brain homogenates was measured by immunoblot analysis.	Quinidine	73-82	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	40-47
23777437-8	2013	These data demonstrate that P-gp induction mediated by DEX at the BBB can significantly reduce quinidine brain extracellular fluid concentrations by decreasing its brain permeability and further suggest that drug-drug interactions as a result of P-gp induction at the BBB are possible.	Quinidine	95-104	phosphoglycolate phosphatase	Mus musculus	28-32
23777437-8	2013	These data demonstrate that P-gp induction mediated by DEX at the BBB can significantly reduce quinidine brain extracellular fluid concentrations by decreasing its brain permeability and further suggest that drug-drug interactions as a result of P-gp induction at the BBB are possible.	Quinidine	95-104	phosphoglycolate phosphatase	Mus musculus	246-250
23777437-9	2013	Applying microdialysis, distribution of quinidine, a P-gp substrate, in mouse brain extracellular fluid (ECF) was investigated following ligand-mediated P-glycoprotein (P-gp) induction at the blood-brain barrier (BBB).	Quinidine	40-49	phosphoglycolate phosphatase	Mus musculus	53-57
23777437-9	2013	Applying microdialysis, distribution of quinidine, a P-gp substrate, in mouse brain extracellular fluid (ECF) was investigated following ligand-mediated P-glycoprotein (P-gp) induction at the blood-brain barrier (BBB).	Quinidine	40-49	phosphoglycolate phosphatase	Mus musculus	153-167
23777437-9	2013	Applying microdialysis, distribution of quinidine, a P-gp substrate, in mouse brain extracellular fluid (ECF) was investigated following ligand-mediated P-glycoprotein (P-gp) induction at the blood-brain barrier (BBB).	Quinidine	40-49	phosphoglycolate phosphatase	Mus musculus	169-173
23777437-10	2013	We demonstrated that a PXR agonist (dexamethasone) significantly up-regulated P-gp in brain capillaries and reduced quinidine brain ECF concentrations.	Quinidine	116-125	nuclear receptor subfamily 1, group I, member 2	Mus musculus	23-26
24400172-7	2013	The I hERG blocking potency of the antiarrhythmic drug quinidine was similar between WT KCNE1 and the three KCNE1 variants.	Quinidine	55-64	ETS transcription factor ERG	Homo sapiens	6-10
24174816-7	2013	Positive inhibitors appropriate for CYP2C9, CYP2D6, and CYP3A4 which are sulfaphenazole, quinidine and ketoconazole were used respectively.	Quinidine	89-98	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	36-42
23784266-11	2013	CONCLUSION: Coadministration of the P-gp inhibitors quinidine, verapamil, and dronedarone increased edoxaban exposure.	Quinidine	52-61	ATP binding cassette subfamily B member 1	Homo sapiens	36-40
23190297-6	2013	The oxidase activity affording 5-OH-BP-3 was inhibited by SKF 525-A and ketoconazole, and partly by quinidine and sulfaphenazole.	Quinidine	100-109	Blood pressure QTL 3	Rattus norvegicus	36-40
23831208-6	2013	Moreover, the OCT1 inhibitors, such as quinidine, d-tetrahydropalmatine (d-THP), obviously inhibited the uptake of MCT in MDCK-hOCT1 cells and isolated rat primary hepatocytes, and attenuated the viability reduction and LDH release of the primary cultured rat hepatocytes caused by MCT.	Quinidine	39-48	solute carrier family 22 member 1	Rattus norvegicus	14-18
23831208-6	2013	Moreover, the OCT1 inhibitors, such as quinidine, d-tetrahydropalmatine (d-THP), obviously inhibited the uptake of MCT in MDCK-hOCT1 cells and isolated rat primary hepatocytes, and attenuated the viability reduction and LDH release of the primary cultured rat hepatocytes caused by MCT.	Quinidine	39-48	solute carrier family 22 member 1	Homo sapiens	127-132
24030418-6	2013	Torsadogenic hERG blockers, such as sotalol and quinidine, produced statistically and physiologically significant effects, consistent with patch-clamp studies, on human embryonic stem cell-derived cardiomyocytes hESC-CMs.	Quinidine	48-57	ETS transcription factor ERG	Homo sapiens	13-17
23836691-8	2013	Quinidine reduced maximum theta" in WT and caused earlier conduction failure in the RV of both Scn5a(+/-) and WT.	Quinidine	0-9	sodium channel, voltage-gated, type V, alpha	Mus musculus	95-100
23836691-13	2013	Flecainide or quinidine decreased the pacing rates at which this occurred, through reducing basic cycle distance, in the Scn5a(+/-) RV epicardium, directly predictive of its arrhythmic phenotype.	Quinidine	14-23	sodium channel, voltage-gated, type V, alpha	Mus musculus	121-126
23629708-7	2013	Interestingly, the functional heterologous expression of CgQDR2 in the model yeast Saccharomyces cerevisiae further confirmed the role of this gene as a multidrug resistance determinant: its expression was able to complement the susceptibility phenotype exhibited by its S. cerevisiae homologue, QDR2, in the presence of imidazoles and of the antimalarial and antiarrhythmic drug quinidine.	Quinidine	380-389	cation transporter	Saccharomyces cerevisiae S288C	59-63
23976943-12	2013	We also find that P-gp substrates with relatively low passive permeability such as digoxin, loperamide and vinblastine kinetically require basolateral uptake transport over that allowed by +GF120918 passive permeability, while highly permeable P-gp substrates such as amprenavir, quinidine, ketoconazole and verapamil do not, regardless of whether they actually use the basolateral transporter.	Quinidine	280-289	phosphoglycolate phosphatase	Homo sapiens	18-22
23827307-1	2013	INTRODUCTION: To analyse the impact of both epilepsy and pharmacological modulation of P-glycoprotein on brain uptake and kinetics of positron emission tomography (PET) radiotracers [(11)C]quinidine and [(11)C]laniquidar.	Quinidine	189-198	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	87-101
23827307-11	2013	CONCLUSIONS: We confirmed that both [(11)C]quinidine and [(11)C]laniquidar are P-glycoprotein substrates.	Quinidine	43-52	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	79-93
23435914-4	2013	Compared with MDCKII or MCF-7, intracellular distribution of [(3)H]-menadione was significantly lower in MDCKII/MDR1 or NCI/ADR-RES cells, which could be restored by the P-gp inhibitors, verapamil and quinidine.	Quinidine	201-210	ATP binding cassette subfamily B member 1	Homo sapiens	170-174
23116562-4	2013	The efflux activity of P-gp was assessed by performing in vitro uptake studies on isolated mitochondria with Rhodamine 123 (Rho-123) alone and in the presence of P-gp inhibitors (quinidine and cyclosporine A) using fluorimetry and flow cytometry analysis.	Quinidine	179-188	ATP-dependent translocase ABCB1	Oryctolagus cuniculus	23-27
23270998-12	2013	Significant increase in the uptake generated by Ile-quinidine relative to quinidine suggests that LAT1 can be utilized for enhancing the cellular permeation of poor cell permeable anticancer drugs.	Quinidine	52-61	solute carrier family 7 member 5	Homo sapiens	98-102
23204072-1	2013	An integrated assay system involving dual/triple-probe microdialysis techniques in rats was developed earlier for testing interactions with P-glycoprotein (P-gp) at the blood-brain barrier using quinidine/PSC-833 as a P-gp substrate/inhibitor combination.	Quinidine	195-204	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	140-154
23204072-1	2013	An integrated assay system involving dual/triple-probe microdialysis techniques in rats was developed earlier for testing interactions with P-glycoprotein (P-gp) at the blood-brain barrier using quinidine/PSC-833 as a P-gp substrate/inhibitor combination.	Quinidine	195-204	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	156-160
23204072-1	2013	An integrated assay system involving dual/triple-probe microdialysis techniques in rats was developed earlier for testing interactions with P-glycoprotein (P-gp) at the blood-brain barrier using quinidine/PSC-833 as a P-gp substrate/inhibitor combination.	Quinidine	195-204	phosphoglycolate phosphatase	Mus musculus	218-222
23204072-6	2013	The P-gp-mediated vectorial transport of quinidine was eliminated by PSC-833.	Quinidine	41-50	phosphoglycolate phosphatase	Mus musculus	4-8
23204072-7	2013	These results indicate that quinidine with PSC-833 is a good probe substrate-reference inhibitor combination for testing drug-drug interactions with P-gp in the in vivo and in vitro mouse systems.	Quinidine	28-37	phosphoglycolate phosphatase	Mus musculus	149-153
23258538-8	2013	These studies show for the first time that dopaminergic neurons expressing mitochondrial CYP2D6 are fully capable of activating the pro-neurotoxin MPTP and inducing neuronal damage, which is effectively prevented by the CYP2D6 inhibitor quinidine.	Quinidine	237-246	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	89-95
23258538-8	2013	These studies show for the first time that dopaminergic neurons expressing mitochondrial CYP2D6 are fully capable of activating the pro-neurotoxin MPTP and inducing neuronal damage, which is effectively prevented by the CYP2D6 inhibitor quinidine.	Quinidine	237-246	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	220-226
23106982-2	2013	Qdr2 is a multidrug transporter of the major facilitator superfamily, originally described for its ability to transport the antimalarial drug quinidine and the herbicide barban.	Quinidine	142-151	cation transporter	Saccharomyces cerevisiae S288C	0-4
24018691-3	2013	Vba2p was also responsible for quinidine sensitivity, and the addition of lysine improved cell growth on quinidine-containing media.	Quinidine	31-40	Vba2p	Saccharomyces cerevisiae S288C	0-5
24166670-5	2013	Inhibition of the CYP3A4-mediated metabolism of BI 11634 by quinidine was further evaluated.	Quinidine	60-69	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	18-24
24166670-6	2013	RESULTS: From the reaction phenotyping studies, it was shown that the metabolism of BI 11634 in HLM was inhibited by ketoconazole and quinidine, well-accepted specific inhibitors of CYP3A4 and CYP2D6, respectively.	Quinidine	134-143	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	182-188
24166670-6	2013	RESULTS: From the reaction phenotyping studies, it was shown that the metabolism of BI 11634 in HLM was inhibited by ketoconazole and quinidine, well-accepted specific inhibitors of CYP3A4 and CYP2D6, respectively.	Quinidine	134-143	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	193-199
24166670-8	2013	Additional studies confirmed that BI 11634 was metabolized by CYP3A4 to form one major metabolite and this reaction was inhibited by quinidine with a Ki of 7 microM.	Quinidine	133-142	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	62-68
24166670-12	2013	The specificity of quinidine as a CYP2D6 inhibitor is questionable as it can also significantly inhibit CYP3A4-mediated metabolism of some compounds.	Quinidine	19-28	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	34-40
24166670-12	2013	The specificity of quinidine as a CYP2D6 inhibitor is questionable as it can also significantly inhibit CYP3A4-mediated metabolism of some compounds.	Quinidine	19-28	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	104-110
22480862-2	2012	The present study reports on the first electrochemically-driven drug-drug interactions of human cytochrome P450 3A4 probed with erythromycin, ketoconazole, cimetidine, diclofenac and quinidine.	Quinidine	183-192	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	96-115
23340533-7	2013	RESULTS: Quinidine was effective in inhibiting CYP2D6 activity, with 2-fold reduction of DM to DOR biotransformation clearance, prolonged DM half-life, and increased DM systemic availability.	Quinidine	9-18	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	47-53
23340533-11	2013	CONCLUSION: CYP2D6 inhibition by quinidine influenced the pre-emptive analgesic effectiveness of DM confirming that CYP2D6 phenotypic switch increases the neuromodulatory effect of oral dextromethorphan.	Quinidine	33-42	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	12-18
23103595-11	2013	Astemizole, terfenadine and quinidine inhibited hERG currents with IC(50) values of 159nM, 224nM and 2muM, respectively (n=51, 10 and 18).	Quinidine	28-37	ETS transcription factor ERG	Homo sapiens	48-52
22688609-8	2012	Inhibition of CYP2D6 (by quinidine) reduced formation of 7-hydroxy-N-desalkylquetiapine by 81%, whereas the CYP3A4 inhibitor ketoconazole inhibited formation of N-desalkylquetiapine sulfoxide and M3 by 65 and 34%, respectively.	Quinidine	25-34	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	14-20
22480862-6	2012	In this case, diclofenac 5-hydroxylation was stimulated by the presence of quinidine resulting in doubling of the potency of this inhibitor i.e. lowering the measured IC(50) of diclofenac from 311 muM down to 157 muM.	Quinidine	75-84	latexin	Homo sapiens	197-200
22480862-6	2012	In this case, diclofenac 5-hydroxylation was stimulated by the presence of quinidine resulting in doubling of the potency of this inhibitor i.e. lowering the measured IC(50) of diclofenac from 311 muM down to 157 muM.	Quinidine	75-84	latexin	Homo sapiens	213-216
22459173-5	2012	While the unliganded CYP2D6 is compressible, quinidine binding significantly rigidifies the CYP2D6 active site.	Quinidine	45-54	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	92-98
22461438-7	2012	Scn5a(+/-) hearts showed greater frequencies of arrhythmic endpoints with increased incidences of ventricular tachycardia, diminished by quinidine, and earlier onsets of ventricular fibrillation, particularly following flecainide challenge.	Quinidine	137-146	sodium channel, voltage-gated, type V, alpha	Mus musculus	0-5
22764568-0	2012	Characterization of intestinal absorption of quinidine, a P-glycoprotein substrate, given as a powder in rats.	Quinidine	45-54	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	58-72
22764568-3	2012	Quinidine administered orally at a dose of 10 mg/kg was discharged from the stomach steadily with time and disappeared rapidly from the proximal intestine, where P-gp expression was low.	Quinidine	0-9	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	162-166
22764568-5	2012	The pretreatment with cyclosporine A, a P-gp inhibitor, greatly increased the intestinal absorption of quinidine given at a dose of 0.1 mg/kg.	Quinidine	103-112	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	40-44
22459173-0	2012	Binding of quinidine radically increases the stability and decreases the flexibility of the cytochrome P450 2D6 active site.	Quinidine	11-20	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	92-111
22459173-2	2012	Here, we present a combined experimental and computational study on the compressibility and flexibility of unliganded and quinidine-bound CYP2D6.	Quinidine	122-131	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	138-144
22459173-4	2012	We identified sharp differences between ligand-free and quinidine-bound CYP2D6 forms in compressibility, flexibility parameters and active site solvation.	Quinidine	56-65	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	72-78
22266842-7	2012	Furafylline, quinidine, and ketoconazole, selective inhibitors of CYP1A2, CYP2D6, and CYP3A4, respectively, inhibited 5-hydroxylorcaserin (IC(50) = 1.914 muM), 7-hydroxylorcaserin (IC(50) = 0.213 muM), and 1-hydroxylorcaserin formation (IC(50) = 0.281 muM), respectively.	Quinidine	13-22	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	66-72
22266842-7	2012	Furafylline, quinidine, and ketoconazole, selective inhibitors of CYP1A2, CYP2D6, and CYP3A4, respectively, inhibited 5-hydroxylorcaserin (IC(50) = 1.914 muM), 7-hydroxylorcaserin (IC(50) = 0.213 muM), and 1-hydroxylorcaserin formation (IC(50) = 0.281 muM), respectively.	Quinidine	13-22	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	74-80
22266842-7	2012	Furafylline, quinidine, and ketoconazole, selective inhibitors of CYP1A2, CYP2D6, and CYP3A4, respectively, inhibited 5-hydroxylorcaserin (IC(50) = 1.914 muM), 7-hydroxylorcaserin (IC(50) = 0.213 muM), and 1-hydroxylorcaserin formation (IC(50) = 0.281 muM), respectively.	Quinidine	13-22	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	86-92
22034916-9	2012	Isoproterenol (100 nM) or quinidine (10 muM) reversed the effects of amitriptyline aborting phase 2 reentry and VT (4/4).	Quinidine	26-35	latexin	Homo sapiens	40-43
22420660-9	2012	The greatest results were obtained for solid dispersions in the presence of P-gp inhibitors at their highest concentrations, with an absorption improvement of 3.41- and 3.91-fold for naringin (15mg/kg) and quinidine (200microm), respectively.	Quinidine	206-215	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	76-80
22215264-0	2012	Alteration in P-glycoprotein functionality affects intrabrain distribution of quinidine more than brain entry-a study in rats subjected to status epilepticus by kainate.	Quinidine	78-87	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	14-28
22215264-1	2012	This study aimed to investigate the use of quinidine microdialysis to study potential changes in brain P-glycoprotein functionality after induction of status epilepticus (SE) by kainate.	Quinidine	43-52	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	103-117
22215264-6	2012	The quinidine microdialysis assay clearly revealed differences in brain distribution upon changes in P-glycoprotein functionality by pre-administration of tariquidar, which resulted in a 7.2-fold increase in brain ECF and a 40-fold increase in total brain quinidine concentration.	Quinidine	4-13	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	101-115
22215264-6	2012	The quinidine microdialysis assay clearly revealed differences in brain distribution upon changes in P-glycoprotein functionality by pre-administration of tariquidar, which resulted in a 7.2-fold increase in brain ECF and a 40-fold increase in total brain quinidine concentration.	Quinidine	256-265	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	101-115
21842479-2	2012	Recombinant human CYP3A4 and CYP2D6 enzymes were used and the activities were expressed by the metabolism of testosterone and dextromethorphan with ketoconazole and quinidine as positive inhibitor controls, respectively.	Quinidine	165-174	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	18-24
21842479-2	2012	Recombinant human CYP3A4 and CYP2D6 enzymes were used and the activities were expressed by the metabolism of testosterone and dextromethorphan with ketoconazole and quinidine as positive inhibitor controls, respectively.	Quinidine	165-174	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	29-35
21508180-4	2012	Throughout the study (follow-up, 199 +- 155 days), quinidine successfully inhibited CYP2D6: propafenone concentrations were 3 times higher in patients receiving quinidine (1033 +- 611 ng/mL vs 328 +- 229 ng/mL; P &lt; .001).	Quinidine	51-60	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	84-90
21508180-7	2012	Thus, chronic inhibition of CYP2D6 is achievable with low-dose quinidine in humans.	Quinidine	63-72	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	28-34
21779762-6	2011	The pro- and anti-arrhythmic agents flecainide and quinidine increased regional VERPs despite respectively decreasing and increasing the corresponding APD(90)s particularly in Scn5a (+/-) RV epicardia.	Quinidine	51-60	sodium channel, voltage-gated, type V, alpha	Mus musculus	176-181
22031603-7	2012	Imipramine and quinidine, known unspecific Na(+)/Mg(2+) exchanger inhibitors, led to a strong 88% to 100% inhibition of hSLC41A1-related Mg(2+) extrusion.	Quinidine	15-24	solute carrier family 41 member 1	Homo sapiens	120-128
23300672-11	2012	Under conventional voltage clamp, half-maximal inhibitory concentrations (IC(50)) for inhibition of I(hERG) tails by quinidine, disopyramide, D-sotalol and flecainide for T618I hERG ranged between 1.4 and 3.2 fold that for WT hERG.	Quinidine	117-126	ETS transcription factor ERG	Homo sapiens	102-106
23300672-11	2012	Under conventional voltage clamp, half-maximal inhibitory concentrations (IC(50)) for inhibition of I(hERG) tails by quinidine, disopyramide, D-sotalol and flecainide for T618I hERG ranged between 1.4 and 3.2 fold that for WT hERG.	Quinidine	117-126	ETS transcription factor ERG	Homo sapiens	177-181
23300672-11	2012	Under conventional voltage clamp, half-maximal inhibitory concentrations (IC(50)) for inhibition of I(hERG) tails by quinidine, disopyramide, D-sotalol and flecainide for T618I hERG ranged between 1.4 and 3.2 fold that for WT hERG.	Quinidine	117-126	ETS transcription factor ERG	Homo sapiens	177-181
22675558-8	2012	Moreover, quinidine, a potent inhibitor of human CYP2D6, only inhibited the bufuralol 1"-hydroxylation activity of CYP2D49 to a negligible degree.	Quinidine	10-19	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	49-55
22675558-8	2012	Moreover, quinidine, a potent inhibitor of human CYP2D6, only inhibited the bufuralol 1"-hydroxylation activity of CYP2D49 to a negligible degree.	Quinidine	10-19	cytochrome P450 family 2 subfamily D member 6	Gallus gallus	115-122
21934030-5	2011	K(p,uu,CSF/brain) values of P-gp-specific (quinidine and verapamil) and Bcrp-specific (daidzein and genistein) substrates were significantly decreased in Mdr1a/1b(-/-) and Bcrp(-/-) mice, respectively.	Quinidine	43-52	phosphoglycolate phosphatase	Mus musculus	28-32
21934030-5	2011	K(p,uu,CSF/brain) values of P-gp-specific (quinidine and verapamil) and Bcrp-specific (daidzein and genistein) substrates were significantly decreased in Mdr1a/1b(-/-) and Bcrp(-/-) mice, respectively.	Quinidine	43-52	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	154-159
21934030-5	2011	K(p,uu,CSF/brain) values of P-gp-specific (quinidine and verapamil) and Bcrp-specific (daidzein and genistein) substrates were significantly decreased in Mdr1a/1b(-/-) and Bcrp(-/-) mice, respectively.	Quinidine	43-52	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	172-176
22033299-5	2011	Salicylate enhanced the quinidine-induced tonic and use-dependent block of both hH1 and hSkM1 currents at a holding potential (HP) of -100 mV but not at -140 mV.	Quinidine	24-33	H1.5 linker histone, cluster member	Homo sapiens	80-83
22033299-5	2011	Salicylate enhanced the quinidine-induced tonic and use-dependent block of both hH1 and hSkM1 currents at a holding potential (HP) of -100 mV but not at -140 mV.	Quinidine	24-33	sodium voltage-gated channel alpha subunit 4	Homo sapiens	88-93
22033299-6	2011	Salicylate decreased the IC50 value for the quinidine-induced tonic block of hH1 at an HP of -100 mV, and produced a negative shift in the steady-state inactivation curve of hH1 in the presence of quinidine.	Quinidine	44-53	H1.5 linker histone, cluster member	Homo sapiens	77-80
22033299-6	2011	Salicylate decreased the IC50 value for the quinidine-induced tonic block of hH1 at an HP of -100 mV, and produced a negative shift in the steady-state inactivation curve of hH1 in the presence of quinidine.	Quinidine	44-53	H1.5 linker histone, cluster member	Homo sapiens	174-177
22033299-6	2011	Salicylate decreased the IC50 value for the quinidine-induced tonic block of hH1 at an HP of -100 mV, and produced a negative shift in the steady-state inactivation curve of hH1 in the presence of quinidine.	Quinidine	197-206	H1.5 linker histone, cluster member	Homo sapiens	174-177
21964404-6	2012	Here, we demonstrate that bupivacaine and quinidine, blockers of four-transmembrane domain, two-pore potassium (K2P) channels, inhibit both amiloride-sensitive sodium absorption and forskolin-stimulated anion secretion in polarized, normal human bronchial epithelial cells at lower concentrations when applied to the mucosal surface than when applied to the serosal surface.	Quinidine	42-51	keratin 76	Homo sapiens	112-115
21976621-11	2012	Finally, the magnitude of in vivo CYP2D6 DDIs caused by quinidine was predicted using desipramine, dextromethorphan, and metoprolol.	Quinidine	56-65	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	34-40
22675558-9	2012	All these results indicated that CYP2D49 had functional characteristics similar to those of human CYP2D6 but measurably differed in the debrisoquine 4"-hydroxylation and quinidine inhibitory profile.	Quinidine	170-179	cytochrome P450 family 2 subfamily D member 6	Gallus gallus	33-40
22020101-5	2011	Like nifekalant, amiodarone, quinidine and carvedilol, but not by dofetilide, caused the current facilitation of hERG, suggesting that the facilitation is a common effect to a subset of hERG blockers.	Quinidine	29-38	ETS transcription factor ERG	Homo sapiens	113-117
22020101-5	2011	Like nifekalant, amiodarone, quinidine and carvedilol, but not by dofetilide, caused the current facilitation of hERG, suggesting that the facilitation is a common effect to a subset of hERG blockers.	Quinidine	29-38	ETS transcription factor ERG	Homo sapiens	186-190
21925601-4	2011	Oct1-mediated active uptake of 10 muM [(3)H]-1-methyl-4-phenylpyridinium (MPP+) into hepatocytes was assessed in the presence of quinidine (1 mM).	Quinidine	129-138	solute carrier family 22 member 1	Rattus norvegicus	0-4
21725799-6	2011	Overall, quinidine was found to be a good probe substrate for routine use to assess the in vitro inhibitory potency of NCEs on Pgp-mediated transport.	Quinidine	9-18	phosphoglycolate phosphatase	Homo sapiens	127-130
21832259-0	2011	Quinidine as an ABCB1 probe for testing drug interactions at the blood-brain barrier: an in vitro in vivo correlation study.	Quinidine	0-9	ATP binding cassette subfamily B member 1A	Rattus norvegicus	16-21
21832259-1	2011	This study provides evidence that quinidine can be used as a probe substrate for ABCB1 in multiple experimental systems both in vitro and in vivo relevant to the blood-brain barrier (BBB).	Quinidine	34-43	ATP binding cassette subfamily B member 1A	Rattus norvegicus	81-86
21832259-2	2011	The combination of quinidine and PSC-833 (valspodar) is an effective tool to assess investigational drugs for interactions on ABCB1.	Quinidine	19-28	ATP binding cassette subfamily B member 1A	Rattus norvegicus	126-131
21832259-4	2011	The authors compared quinidine and digoxin as ABCB1 probes in the in vitro assays and found that quinidine was more potent and at least as specific as digoxin in ATPase and monolayer efflux assays employing MDCKII-MDR1 and the rat brain microcapillary endothelial cell system.	Quinidine	97-106	ATP binding cassette subfamily B member 1A	Rattus norvegicus	46-51
21832259-4	2011	The authors compared quinidine and digoxin as ABCB1 probes in the in vitro assays and found that quinidine was more potent and at least as specific as digoxin in ATPase and monolayer efflux assays employing MDCKII-MDR1 and the rat brain microcapillary endothelial cell system.	Quinidine	97-106	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	207-218
21832259-6	2011	Comparing quinidine levels in dialysate samples from valspodar-treated and control animals, it is evident that systemic/local administration of the inhibitor diminishes the pumping function of ABCB1 at the BBB, resulting in an increased brain penetration of quinidine.	Quinidine	10-19	ATP binding cassette subfamily B member 1A	Rattus norvegicus	193-198
21832259-6	2011	Comparing quinidine levels in dialysate samples from valspodar-treated and control animals, it is evident that systemic/local administration of the inhibitor diminishes the pumping function of ABCB1 at the BBB, resulting in an increased brain penetration of quinidine.	Quinidine	258-267	ATP binding cassette subfamily B member 1A	Rattus norvegicus	193-198
21832259-7	2011	In sum, quinidine is a good probe to study ABCB1 function at the BBB.	Quinidine	8-17	ATP binding cassette subfamily B member 1A	Rattus norvegicus	43-48
21832259-8	2011	Moreover, quinidine/PSC-833 is an ABCB1-specific substrate/inhibitor combination applicable to many assay systems both in vitro and in vivo.	Quinidine	10-19	ATP binding cassette subfamily B member 1A	Rattus norvegicus	34-39
21679153-6	2011	Tyramine elimination rates were inhibited by quinidine and significantly correlated with bufuralol 1"-hydroxylation activities (a CYP2D6 marker).	Quinidine	45-54	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	130-136
21722088-10	2011	Impurities with potent CYP2D6 inhibition, such as quinidine, can significantly decrease the apparent IC(50) value for the mixture.	Quinidine	50-59	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	23-29
20196146-5	2011	Rhodamine assay also revealed that hydrocinchonine, cinchonine, and quinidine effectively enhanced the accumulation of a P-gp substrate, rhodamine in TAX-treated MES-SA/DX5 cells compared with TAX-treated control.	Quinidine	68-77	phosphoglycolate phosphatase	Homo sapiens	121-125
20196146-6	2011	In addition, hydrocinchonine, cinchonine, and quinidine effectively cleaved poly (ADP-ribose) polymerase (PARP), activated caspase-3, and downregulated P-gp expression as well as increased sub-G1 apoptotic portion in TAX-treated MES-SA/DX5 cells.	Quinidine	46-55	poly(ADP-ribose) polymerase 1	Homo sapiens	76-104
20196146-6	2011	In addition, hydrocinchonine, cinchonine, and quinidine effectively cleaved poly (ADP-ribose) polymerase (PARP), activated caspase-3, and downregulated P-gp expression as well as increased sub-G1 apoptotic portion in TAX-treated MES-SA/DX5 cells.	Quinidine	46-55	poly(ADP-ribose) polymerase 1	Homo sapiens	106-110
20196146-6	2011	In addition, hydrocinchonine, cinchonine, and quinidine effectively cleaved poly (ADP-ribose) polymerase (PARP), activated caspase-3, and downregulated P-gp expression as well as increased sub-G1 apoptotic portion in TAX-treated MES-SA/DX5 cells.	Quinidine	46-55	caspase 3	Homo sapiens	123-132
20196146-6	2011	In addition, hydrocinchonine, cinchonine, and quinidine effectively cleaved poly (ADP-ribose) polymerase (PARP), activated caspase-3, and downregulated P-gp expression as well as increased sub-G1 apoptotic portion in TAX-treated MES-SA/DX5 cells.	Quinidine	46-55	phosphoglycolate phosphatase	Homo sapiens	152-156
21484807-5	2011	The inhibition of P-gp-mediated efflux of these two fluorescent substrates by several drugs, including quinidine and itraconazole, was found to be substrate- and/or species-dependent.	Quinidine	103-112	ATP binding cassette subfamily B member 1	Homo sapiens	18-22
21725799-0	2011	Validation of quinidine as a probe substrate for the in vitro P-gp inhibition assay in Caco-2 cell monolayer.	Quinidine	14-23	phosphoglycolate phosphatase	Homo sapiens	62-66
21725799-1	2011	Although quinidine has been recommended as a probe substrate for the P-gp inhibition assay using Caco-2 cell monolayer, it has not been studied widely in the in vitro system.	Quinidine	9-18	phosphoglycolate phosphatase	Homo sapiens	69-73
21725799-2	2011	In the present investigation, in vitro permeability studies using Caco-2 cell monolayer were carried out in order to optimize and validate quinidine as a P-gp probe substrate.	Quinidine	139-148	phosphoglycolate phosphatase	Homo sapiens	154-158
21832258-4	2011	The non-CYP3A4 inhibitors diethyldithiocarbamate, quercetin, quinidine, sulfaphenazole, ticlopidine, and tranylcypromine were found to have substantially lower (maximum inhibition of &lt;50%) or no apparent inhibitory effects in the HTS assay.	Quinidine	61-70	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	8-14
21716273-3	2011	Verapamil and quinidine are good substrates of both the multidrug resistance 1 transporter (MDR1) and the cytochrome P450 (CYP) 3A4 enzyme (CYP3A4).	Quinidine	14-23	ATP binding cassette subfamily B member 1	Homo sapiens	56-78
21716273-3	2011	Verapamil and quinidine are good substrates of both the multidrug resistance 1 transporter (MDR1) and the cytochrome P450 (CYP) 3A4 enzyme (CYP3A4).	Quinidine	14-23	ATP binding cassette subfamily B member 1	Homo sapiens	92-96
21716273-3	2011	Verapamil and quinidine are good substrates of both the multidrug resistance 1 transporter (MDR1) and the cytochrome P450 (CYP) 3A4 enzyme (CYP3A4).	Quinidine	14-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	140-146
21471209-3	2011	Cholesterol inhibited the P450 3A4-catalyzed oxidations of nifedipine and quinidine, two prototypic substrates, in liver microsomes and a reconstituted enzyme system with K(i) ~ 10 muM in an apparently non-competitive manner.	Quinidine	74-83	latexin	Homo sapiens	181-184
20977453-4	2010	KEY RESULTS: Co-expression of OCTN1 significantly facilitated block by quinidine (10 microM), verapamil (20 microM), propafenone (5 microM) and clofilium (30 microM).	Quinidine	71-80	solute carrier family 22 member 1	Homo sapiens	30-35
21233253-3	2011	We tested the hypothesis that chloroquine"s mode of interaction with the vestibule of the cytoplasmic domain of the inward rectifier potassium channel Kir2.1 makes it a more effective I(K1) blocker and anti-fibrillatory agent than quinidine.	Quinidine	231-240	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	151-157
21233253-4	2011	METHODS AND RESULTS: We used comparative molecular modelling and ligand docking of the three-dimensional structures of quinidine and chloroquine in the intracellular domain of Kir2.1.	Quinidine	119-128	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	176-182
21233253-13	2011	Chloroquine binds at the centre of the ion permeation vestibule of Kir2.1, which makes it a more effective I(K1) blocker and anti-fibrillatory agent than quinidine.	Quinidine	154-163	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	67-73
21336516-7	2011	The most selective inhibitors available are furafylline (in co-incubation and pre-incubation conditions) for CYP1A2, 2-phenyl-2-(1-piperidinyl)propane (PPP) for CYP2B6, montelukast for CYP2C8, sulfaphenazole for CYP2C9, (-)-N-3-benzyl-phenobarbital for CYP2C19 and quinidine for CYP2D6.	Quinidine	265-274	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	161-167
22028871-7	2011	The proarrhythmic compounds E-4031, quinidine, procainamide, cisapride, and sertindole exerted robust, concentration-dependent and reversible decreases in relaxation velocity and irregular beating at concentrations that recapitulate findings in hERG channel assays.	Quinidine	36-45	ETS transcription factor ERG	Homo sapiens	245-249
21105702-3	2010	The electrochemical response of the P450-electrode in the microfluidic cell was tested using four drugs that are known substrates of P450 3A4: quinidine, nifedipine, alosetron and ondansetron.	Quinidine	143-152	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	36-40
21476614-4	2011	Dextromethorphan/quinidine 20 mg/10 mg twice daily was associated with a significantly greater decrease in the rate of pseudobulbar affect episodes per day (primary endpoint) than placebo in the 12-week, randomized, double-blind, placebo-controlled, multicentre STAR trial (Safety, Tolerability, And efficacy Results trial of AVP-923 in PBA [pseudobulbar affect]) involving patients with pseudobulbar affect and ALS or multiple sclerosis.	Quinidine	17-26	steroidogenic acute regulatory protein	Homo sapiens	262-266
21148207-1	2011	The yeast QDR3 gene encodes a plasma membrane drug : H(+) antiporter of the DHA1 family that was described as conferring resistance against the drugs quinidine, cisplatin and bleomycin and the herbicide barban, similar to its close homologue QDR2.	Quinidine	150-159	Qdr3p	Saccharomyces cerevisiae S288C	10-14
21148207-1	2011	The yeast QDR3 gene encodes a plasma membrane drug : H(+) antiporter of the DHA1 family that was described as conferring resistance against the drugs quinidine, cisplatin and bleomycin and the herbicide barban, similar to its close homologue QDR2.	Quinidine	150-159	cation transporter	Saccharomyces cerevisiae S288C	242-246
21130771-8	2011	Quinidine (5 muM) and sotalol (500 muM) had similar inhibitory effects on steady currents measured at +20 mV in WT and T618I but were less effective in inhibiting tail currents of mutant channels.	Quinidine	0-9	latexin	Homo sapiens	13-16
21130771-10	2011	Both quinidine and sotalol may be therapeutic options for patients with the T618I HERG mutation.	Quinidine	5-14	potassium voltage-gated channel subfamily H member 2	Homo sapiens	82-86
22028772-9	2011	The P-gp efflux rate constants for quinidine and digoxin were about 3-fold smaller than reported ATP hydrolysis rate constants from P-gp proteoliposomes.	Quinidine	35-44	phosphoglycolate phosphatase	Homo sapiens	4-8
22028772-9	2011	The P-gp efflux rate constants for quinidine and digoxin were about 3-fold smaller than reported ATP hydrolysis rate constants from P-gp proteoliposomes.	Quinidine	35-44	phosphoglycolate phosphatase	Homo sapiens	132-136
20924570-3	2010	Enzyme activities of CYP1A2 and CYP3A4 were determined as metabolic ratios of caffeine (CMR = (AFMU + 1MU + 1MX)/17DMU) and quinidine (QMR = 3-hydroxy-quinidine/quinidine) respectively before and 34 h after insertion of the suppository.	Quinidine	124-133	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	21-27
20924570-3	2010	Enzyme activities of CYP1A2 and CYP3A4 were determined as metabolic ratios of caffeine (CMR = (AFMU + 1MU + 1MX)/17DMU) and quinidine (QMR = 3-hydroxy-quinidine/quinidine) respectively before and 34 h after insertion of the suppository.	Quinidine	124-133	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	32-38
20924570-3	2010	Enzyme activities of CYP1A2 and CYP3A4 were determined as metabolic ratios of caffeine (CMR = (AFMU + 1MU + 1MX)/17DMU) and quinidine (QMR = 3-hydroxy-quinidine/quinidine) respectively before and 34 h after insertion of the suppository.	Quinidine	151-160	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	21-27
20924570-3	2010	Enzyme activities of CYP1A2 and CYP3A4 were determined as metabolic ratios of caffeine (CMR = (AFMU + 1MU + 1MX)/17DMU) and quinidine (QMR = 3-hydroxy-quinidine/quinidine) respectively before and 34 h after insertion of the suppository.	Quinidine	151-160	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	32-38
20388857-6	2010	MDMA metabolism by CYP2D6 significantly increased cytotoxicity, which was counteracted by CYP2D6 inhibition by quinidine.	Quinidine	111-120	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	19-25
20621962-9	2010	Both flecainide and quinidine then prevented both induced and spontaneous atrial arrhythmias in all the arrhythmic WT and Scn5a+/- hearts, in contrast to their differing ventricular effects.	Quinidine	20-29	sodium channel, voltage-gated, type V, alpha	Mus musculus	122-127
20621962-10	2010	However, flecainide prolonged APD(90) in WT but not Scn5a+/-, whereas quinidine prolonged APD(90) in both WT and Scn5a+/-.	Quinidine	70-79	sodium channel, voltage-gated, type V, alpha	Mus musculus	113-118
20697309-6	2010	RESULTS: POR A287P and R457H had low activity with all substrates; Q153R had 76-94% of wild-type (WT) activity with midazolam and erythromycin, but 129-150% activity with testosterone and quinidine.	Quinidine	188-197	cytochrome p450 oxidoreductase	Homo sapiens	9-12
20840389-3	2010	The P-gp substrates quinidine, loperamide, nelfinavir, cyclosporin and the control (non P-gp substrate) drug diazepam were individually administered intravenously and per os to ABCB1-1Delta dogs, which have a P-gp null phenotype and ABCB1 wildtype dogs.	Quinidine	20-29	PGP	Canis lupus familiaris	4-8
20132234-14	2010	It is concluded that both flecainide and quinidine exert anti-arrhythmogenic effects in Scn3b(-/-) hearts, doing so through modifying VERP rather than DeltaAPD, in contrast to their differing effects in Scn5a(+/-) and Scn5a(+/DeltaKPQ) hearts.	Quinidine	41-50	sodium channel, voltage-gated, type III, beta	Mus musculus	88-93
20132234-14	2010	It is concluded that both flecainide and quinidine exert anti-arrhythmogenic effects in Scn3b(-/-) hearts, doing so through modifying VERP rather than DeltaAPD, in contrast to their differing effects in Scn5a(+/-) and Scn5a(+/DeltaKPQ) hearts.	Quinidine	41-50	sodium channel, voltage-gated, type V, alpha	Mus musculus	218-223
20388857-6	2010	MDMA metabolism by CYP2D6 significantly increased cytotoxicity, which was counteracted by CYP2D6 inhibition by quinidine.	Quinidine	111-120	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	90-96
19816852-0	2010	Development and validation of RP-HPLC-fluorescence method for quantitative determination of quinidine, a probe substrate for P-glycoprotein inhibition assay using Caco-2 cell monolayer.	Quinidine	92-101	ATP binding cassette subfamily B member 1	Homo sapiens	125-139
19816852-2	2010	The method was applicable in the bi-directional transport assay for evaluation of the inhibitory effect of test compounds on P-glycoprotein-mediated quinidine transport; quinidine was used as a probe P-glycoprotein substrate.	Quinidine	149-158	ATP binding cassette subfamily B member 1	Homo sapiens	125-139
19816852-2	2010	The method was applicable in the bi-directional transport assay for evaluation of the inhibitory effect of test compounds on P-glycoprotein-mediated quinidine transport; quinidine was used as a probe P-glycoprotein substrate.	Quinidine	170-179	ATP binding cassette subfamily B member 1	Homo sapiens	125-139
19816852-2	2010	The method was applicable in the bi-directional transport assay for evaluation of the inhibitory effect of test compounds on P-glycoprotein-mediated quinidine transport; quinidine was used as a probe P-glycoprotein substrate.	Quinidine	170-179	ATP binding cassette subfamily B member 1	Homo sapiens	200-214
19816852-8	2010	The efflux ratio for quinidine (100 nm) alone was 10.8, which reduced to less than 2 in the presence of the classical P-gp inhibitors verapamil and ketoconazole (100 mum each).	Quinidine	21-30	phosphoglycolate phosphatase	Homo sapiens	118-122
20590587-11	2010	Blocking CYP2D6 (with quinidine) reduced oxymorphone and noroxymorphone C(max) by 40% and 80%, and increased noroxycodone AUC(infinity) by 70%.	Quinidine	22-31	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	9-15
20153443-7	2010	RESULTS: AP prolongation was observed upon exposure to hERG channel blockers (terfenadine, quinidine, cisapride, sotalol, E-4031 and verapamil), with significantly shorter latencies than in PF assays.	Quinidine	91-100	ETS transcription factor ERG	Homo sapiens	55-59
20614693-2	2010	In the present study, the effects of altered gastric emptying rates (GER) on intestinal absorption of quinidine (a substrate for P-glycoprotein, P-gp) and methotrexate (a substrate for multiple-transporters including proton-coupled folate transporter, PCFT) were examined to find their main absorption sites along the intestine employing rats.	Quinidine	102-111	phosphoglycolate phosphatase	Rattus norvegicus	145-149
20614693-3	2010	In untreated control rats, quinidine administered orally was rapidly absorbed from the proximal intestine, where P-gp is less expressed.	Quinidine	27-36	phosphoglycolate phosphatase	Rattus norvegicus	113-117
20332617-6	2010	This LPS-induced current exhibited KCNQ1 K+ channel characteristics, i.e. inhibition by quinidine, chromanol293B and low dose of HMR1556 (IC50&lt;1 microM) and insensitive to TEA and charybdotoxin.	Quinidine	88-97	potassium voltage-gated channel, subfamily Q, member 1	Mus musculus	35-40
20214407-4	2010	Digoxin, fexofenadine, talinolol and quinidine are commonly used probe drugs for P-gp phenotyping.	Quinidine	37-46	ATP binding cassette subfamily B member 1	Homo sapiens	81-85
20019330-5	2010	One is the amiloride-sensitive acid-sensing sodium channel (ASIC3), which is activated by low pH and the other is the 2-pore domain acid-sensing K(+) channel (TASK1), which is inhibited by low pH and blocked by quinidine.	Quinidine	211-220	acid sensing ion channel subunit 3	Rattus norvegicus	60-65
19874821-5	2010	Caspase-8 activity induced by exposure to UV-B at 150 mJ/cm(2) was significantly reduced when the cells were incubated in 0.3 microM BDS-I or 0.05-1 mM quinidine.	Quinidine	152-161	caspase 8	Homo sapiens	0-9
19874821-6	2010	Caspase-3 was also activated by UV-B and a reduction in activity was observed after incubation in 0.1-0.3 microM BDS-I and 0.1-1 mM quinidine.	Quinidine	132-141	caspase 3	Homo sapiens	0-9
20614693-2	2010	In the present study, the effects of altered gastric emptying rates (GER) on intestinal absorption of quinidine (a substrate for P-glycoprotein, P-gp) and methotrexate (a substrate for multiple-transporters including proton-coupled folate transporter, PCFT) were examined to find their main absorption sites along the intestine employing rats.	Quinidine	102-111	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	129-143
20163161-5	2010	In this study, the effects of the aqueous boundary layers, extracellular pH and cellular retention on the apparent saturation kinetics of P-glycoprotein mediated transport of quinidine in an in vitro cell permeation setting were explored.	Quinidine	175-184	ATP binding cassette subfamily B member 1	Homo sapiens	138-152
20163161-6	2010	The changes in the experimental conditions caused 1 order of magnitude variation in the apparent affinity to P-glycoprotein (K(m,app)) and a 5-fold difference in the maximum effective P-glycoprotein mediated transport rate of quinidine (V(max,app)).	Quinidine	226-235	ATP binding cassette subfamily B member 1	Homo sapiens	109-123
20163161-6	2010	The changes in the experimental conditions caused 1 order of magnitude variation in the apparent affinity to P-glycoprotein (K(m,app)) and a 5-fold difference in the maximum effective P-glycoprotein mediated transport rate of quinidine (V(max,app)).	Quinidine	226-235	ATP binding cassette subfamily B member 1	Homo sapiens	184-198
20345925-6	2010	CYP2D6 metabolized 3-[2-(N,N-diethyl-N-methylammonium)ethyl]-7-methoxy-4-methylcoumarin and the CYP2D6-specific inhibitor quinidine (1 microM) blocked 96 +/- 1% of this metabolism, indicating that CYP2D6 is functional in this cell line.	Quinidine	122-131	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-6
20345925-6	2010	CYP2D6 metabolized 3-[2-(N,N-diethyl-N-methylammonium)ethyl]-7-methoxy-4-methylcoumarin and the CYP2D6-specific inhibitor quinidine (1 microM) blocked 96 +/- 1% of this metabolism, indicating that CYP2D6 is functional in this cell line.	Quinidine	122-131	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	96-102
20345925-6	2010	CYP2D6 metabolized 3-[2-(N,N-diethyl-N-methylammonium)ethyl]-7-methoxy-4-methylcoumarin and the CYP2D6-specific inhibitor quinidine (1 microM) blocked 96 +/- 1% of this metabolism, indicating that CYP2D6 is functional in this cell line.	Quinidine	122-131	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	96-102
20345925-7	2010	Treatment of cells with CYP2D6 inhibitors (quinidine, propanolol, metoprolol or timolol) at varying concentrations significantly increased the neurotoxicity caused by 1-methyl-4-phenylpyridinium (MPP+) at 10 and 25 microM by between 9 +/- 1 and 22 +/- 5% (P &lt; 0.01).	Quinidine	43-52	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	24-30
20373255-3	2010	AVP-923 consists of a combination of the NMDA antagonist/sigma1 receptor agonist dextromethorphan hydrobromide (DM) and the cytochrome P450 2D6 (CYP2D6) enzyme inhibitor quinidine sulfate (Q).	Quinidine	170-187	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	145-151
20135207-4	2010	METHODS: The previously reported concentration-dependent permeability of verapamil, quinidine, and vinblastine in MDR1-MDCKII, P-gp-highly induced Caco-2, P-gp-induced Caco-2, normal Caco-2, and MDR1-knockdown Caco-2 cells data were analyzed using a model in which the Km value was defined for the intracellular substrate concentration.	Quinidine	84-93	ATP binding cassette subfamily B member 1	Homo sapiens	114-118
20135207-4	2010	METHODS: The previously reported concentration-dependent permeability of verapamil, quinidine, and vinblastine in MDR1-MDCKII, P-gp-highly induced Caco-2, P-gp-induced Caco-2, normal Caco-2, and MDR1-knockdown Caco-2 cells data were analyzed using a model in which the Km value was defined for the intracellular substrate concentration.	Quinidine	84-93	ATP binding cassette subfamily B member 1	Homo sapiens	127-131
20135207-4	2010	METHODS: The previously reported concentration-dependent permeability of verapamil, quinidine, and vinblastine in MDR1-MDCKII, P-gp-highly induced Caco-2, P-gp-induced Caco-2, normal Caco-2, and MDR1-knockdown Caco-2 cells data were analyzed using a model in which the Km value was defined for the intracellular substrate concentration.	Quinidine	84-93	ATP binding cassette subfamily B member 1	Homo sapiens	155-159
20135207-4	2010	METHODS: The previously reported concentration-dependent permeability of verapamil, quinidine, and vinblastine in MDR1-MDCKII, P-gp-highly induced Caco-2, P-gp-induced Caco-2, normal Caco-2, and MDR1-knockdown Caco-2 cells data were analyzed using a model in which the Km value was defined for the intracellular substrate concentration.	Quinidine	84-93	ATP binding cassette subfamily B member 1	Homo sapiens	195-199
19934650-0	2010	Block of mouse Slo1 and Slo3 K+ channels by CTX, IbTX, TEA, 4-AP and quinidine.	Quinidine	69-78	potassium channel, subfamily U, member 1	Mus musculus	24-28
19934650-8	2010	Quinidine was more effective in blocking Slo3 than Slo1.	Quinidine	0-9	potassium calcium-activated channel subfamily U member 1	Homo sapiens	41-45
19934650-10	2010	For Slo3, quinidine block was relieved by depolarization, irrespective of the side of application, with strong block by less than 10 microM quinidine at potentials near 0 mV.	Quinidine	10-19	potassium calcium-activated channel subfamily U member 1	Homo sapiens	4-8
19934650-11	2010	The unusual voltage-dependence of block of Slo3 by quinidine may result from preferential binding of quinidine to closed Slo3 channels.	Quinidine	51-60	potassium calcium-activated channel subfamily U member 1	Homo sapiens	43-47
19934650-11	2010	The unusual voltage-dependence of block of Slo3 by quinidine may result from preferential binding of quinidine to closed Slo3 channels.	Quinidine	51-60	potassium calcium-activated channel subfamily U member 1	Homo sapiens	121-125
19934650-11	2010	The unusual voltage-dependence of block of Slo3 by quinidine may result from preferential binding of quinidine to closed Slo3 channels.	Quinidine	101-110	potassium calcium-activated channel subfamily U member 1	Homo sapiens	43-47
19934650-11	2010	The unusual voltage-dependence of block of Slo3 by quinidine may result from preferential binding of quinidine to closed Slo3 channels.	Quinidine	101-110	potassium calcium-activated channel subfamily U member 1	Homo sapiens	121-125
19934650-12	2010	The quinidine concentrations effective in blocking Slo3 suggest, that in experiments that have examined quinidine effects on sperm, any Slo3 currents would be almost completely inhibited.	Quinidine	4-13	potassium calcium-activated channel subfamily U member 1	Homo sapiens	51-55
19934650-12	2010	The quinidine concentrations effective in blocking Slo3 suggest, that in experiments that have examined quinidine effects on sperm, any Slo3 currents would be almost completely inhibited.	Quinidine	4-13	potassium calcium-activated channel subfamily U member 1	Homo sapiens	136-140
19934650-12	2010	The quinidine concentrations effective in blocking Slo3 suggest, that in experiments that have examined quinidine effects on sperm, any Slo3 currents would be almost completely inhibited.	Quinidine	104-113	potassium calcium-activated channel subfamily U member 1	Homo sapiens	51-55
20041473-2	2010	This study examined whether pharmacological inhibition of CYP2D6 activity with quinidine would mimic the genetic mutation and thus also alter the psychoactive effects of DM.	Quinidine	79-88	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	58-64
19631272-5	2010	Quinidine and verapamil, known MDR1 substrates/inhibitors, showed trans-inhibition on MDR1-mediated [(3)H]vinblastine and [(3)H]digoxin efflux.	Quinidine	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	31-35
19631272-5	2010	Quinidine and verapamil, known MDR1 substrates/inhibitors, showed trans-inhibition on MDR1-mediated [(3)H]vinblastine and [(3)H]digoxin efflux.	Quinidine	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	86-90
19444798-7	2009	The method has been successfully applied for the in vitro inhibition of metabolism of dextromethorphan by CYP2D6 and CYP3A4 using known inhibitors of CYPs such as quinidine and verapamil.	Quinidine	163-172	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	106-112
19444798-7	2009	The method has been successfully applied for the in vitro inhibition of metabolism of dextromethorphan by CYP2D6 and CYP3A4 using known inhibitors of CYPs such as quinidine and verapamil.	Quinidine	163-172	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	117-123
19508886-9	2009	At the hepato-biliary interface, we showed the involvement of Abcb1, Abcc2 and Abcg2; indeed, AMI concentration was increased in liver and decreased in bile, where quinidine is the strongest inhibitor, followed by probenecid and novobiocin.	Quinidine	164-173	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	62-67
19508886-4	2009	5 mg/kg AMI+100 mg/kg quinidine (Abcb1 inhibitor).	Quinidine	22-31	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	33-38
19775284-8	2009	Tanshinone IIA restored the diminished I(K1) current density and Kir2.1 protein after MI in rat ventricular myocytes, while quinidine further inhibited I(K1)/Kir2.1.	Quinidine	124-133	potassium inwardly-rectifying channel, subfamily J, member 2	Rattus norvegicus	158-164
19508886-9	2009	At the hepato-biliary interface, we showed the involvement of Abcb1, Abcc2 and Abcg2; indeed, AMI concentration was increased in liver and decreased in bile, where quinidine is the strongest inhibitor, followed by probenecid and novobiocin.	Quinidine	164-173	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	79-84
19617705-0	2009	Extracellular potassium dependency of block of HERG by quinidine and cisapride is primarily determined by the permeant ion and not by inactivation.	Quinidine	55-64	potassium voltage-gated channel subfamily H member 2	Homo sapiens	47-51
19406953-0	2009	Vitreal kinetics of quinidine in rabbits in the presence of topically coadministered P-glycoprotein substrates/modulators.	Quinidine	20-29	ATP-dependent translocase ABCB1	Oryctolagus cuniculus	85-99
19406953-1	2009	The purpose of this study was to investigate whether topically administered P-glycoprotein (P-gp) substrates/modulators can alter vitreal kinetics of intravitreally administered quinidine.	Quinidine	178-187	ATP-dependent translocase ABCB1	Oryctolagus cuniculus	76-90
19406953-1	2009	The purpose of this study was to investigate whether topically administered P-glycoprotein (P-gp) substrates/modulators can alter vitreal kinetics of intravitreally administered quinidine.	Quinidine	178-187	ATP-dependent translocase ABCB1	Oryctolagus cuniculus	92-96
19451401-4	2009	Substantially lower inhibitory effects were observed for the non-CYP3A4 inhibitors diethyldithiocarbamate, furafylline, omeprazole, orphenadrine, sulfaphenazole, and quinidine.	Quinidine	166-175	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	65-71
19617705-6	2009	In this study, HERG block by quinidine and cisapride was assessed in extracellular solutions of calcium, potassium, rubidium, cesium and tetraethylammonium (TEA) using two-electrode voltage clamping of Xenopus oocytes.	Quinidine	29-38	potassium voltage-gated channel subfamily H member 2	Homo sapiens	15-19
19617705-7	2009	Consistent with previous reports we show that increases in extracellular potassium reduce HERG block by quinidine and cisapride.	Quinidine	104-113	potassium voltage-gated channel subfamily H member 2	Homo sapiens	90-94
19617705-8	2009	We also show that increasing extracellular rubidium and cesium reduced HERG block by quinidine and cisapride whereas increasing extracellular calcium and extracellular TEA did not alter HERG block by quinidine and cisapride.	Quinidine	85-94	potassium voltage-gated channel subfamily H member 2	Homo sapiens	71-75
19122284-6	2009	Upon addition of quinidine, a mixed P-gp and MRP1 inhibitor, the permeation of W2 from the apical side was significantly increased (P(app) 17.1+/-0.32x10(-6) cm/s) while the efflux was inhibited (P(app) 21.3+/-0.19x10(-6) cm/s).	Quinidine	17-26	ATP binding cassette subfamily B member 1	Homo sapiens	36-40
19528813-4	2009	METHODS AND RESULTS: Reverse transcriptase-polymerase chain reaction identified expression in the human atrium and ventricle of 14 of 31 candidate drug uptake and efflux transporters, including OCTN1 (SLC22A4), a known uptake transporter of the HERG channel blocker quinidine.	Quinidine	266-275	solute carrier family 22 member 4	Homo sapiens	194-199
19528813-6	2009	The IC50 for quinidine block of IKr in CHO cells transfected with HERG alone was significantly higher than cells transfected with HERG + OCTN1 (0.66 +/- 0.15 microM versus 0.14 +/- 0.06 microM [52% absolute increase in drug block; 95% confidence interval, 0.4-0.64 microM]), and this effect was further potentiated by a common genetic variant of OCTN1, L503F.	Quinidine	13-22	potassium voltage-gated channel subfamily H member 2	Homo sapiens	66-70
19528813-6	2009	The IC50 for quinidine block of IKr in CHO cells transfected with HERG alone was significantly higher than cells transfected with HERG + OCTN1 (0.66 +/- 0.15 microM versus 0.14 +/- 0.06 microM [52% absolute increase in drug block; 95% confidence interval, 0.4-0.64 microM]), and this effect was further potentiated by a common genetic variant of OCTN1, L503F.	Quinidine	13-22	solute carrier family 22 member 4	Homo sapiens	346-351
19528813-9	2009	CONCLUSIONS: Coexpression of the organic cation transporter, OCTN1, expressed in human cardiac myocytes, intensifies quinidine-induced HERG block.	Quinidine	117-126	solute carrier family 22 member 4	Homo sapiens	61-66
19428327-6	2009	In addition, inhibition studies towards MBDB biotransformation using the CYP2D6 selective inhibitor quinidine confirmed the dominant role of this polymorphic isozyme in total MBDB metabolism.	Quinidine	100-109	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	73-79
18855917-3	2009	The activities of P-gp in these models were characterized using a known substrate (quinidine) and known inhibitors [cyclosporine A (CyA), GF-120918, PSC-833] of P-gp.	Quinidine	83-92	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	18-22
18855917-8	2009	MDCK-MDR1 cells can predict the order of potencies of the investigated P-gp inhibitors to enhance the rat BBB permeation of quinidine and the cyclic prodrugs.	Quinidine	124-133	PGP	Canis lupus familiaris	71-75
19443837-4	2009	In this study, treatment of HL-1 atrial myocytes expressing Kv1.5-GFP with the class I antiarrhythmic agent quinidine resulted in a dose- and temperature-dependent internalization of Kv1.5, concomitant with channel block.	Quinidine	108-117	potassium voltage-gated channel subfamily A member 5	Homo sapiens	60-65
19443837-4	2009	In this study, treatment of HL-1 atrial myocytes expressing Kv1.5-GFP with the class I antiarrhythmic agent quinidine resulted in a dose- and temperature-dependent internalization of Kv1.5, concomitant with channel block.	Quinidine	108-117	potassium voltage-gated channel subfamily A member 5	Homo sapiens	183-188
18950609-12	2009	Results with the isoform-selective inhibitors suggest that the isoforms inhibited by ketoconazole (mainly CYP3A4) and diethyldithiocarbamate (mainly CYP2A6, and CYP2E1), but not the isoforms inhibited by furafylline (mainly CYP1A2), sulfaphenazole (mainly CYP2C9) and quinidine (mainly CYP2D6) are involved in the metabolic activation of AFB1.	Quinidine	268-277	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	106-112
18950609-12	2009	Results with the isoform-selective inhibitors suggest that the isoforms inhibited by ketoconazole (mainly CYP3A4) and diethyldithiocarbamate (mainly CYP2A6, and CYP2E1), but not the isoforms inhibited by furafylline (mainly CYP1A2), sulfaphenazole (mainly CYP2C9) and quinidine (mainly CYP2D6) are involved in the metabolic activation of AFB1.	Quinidine	268-277	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	149-155
19122284-6	2009	Upon addition of quinidine, a mixed P-gp and MRP1 inhibitor, the permeation of W2 from the apical side was significantly increased (P(app) 17.1+/-0.32x10(-6) cm/s) while the efflux was inhibited (P(app) 21.3+/-0.19x10(-6) cm/s).	Quinidine	17-26	ATP binding cassette subfamily C member 1	Homo sapiens	45-49
19053318-8	2009	The P-gp activity was absent in the cells since P-gp-mediated efflux of quinidine was not blocked by GF120918.	Quinidine	72-81	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	4-8
19053318-8	2009	The P-gp activity was absent in the cells since P-gp-mediated efflux of quinidine was not blocked by GF120918.	Quinidine	72-81	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	48-52
18945821-2	2009	In this work, rationally designed second-generation P-gp inhibitors are disclosed, based on dimerized versions of the substrates quinine and quinidine.	Quinidine	141-150	ATP binding cassette subfamily B member 1	Homo sapiens	52-56
19248230-8	2009	Concentration dependent decrease of this secretion was obtained by the P-gp inhibitors verapamil, erythromycin and quinidine, while no effect was evident by the MRP2 inhibitor MK-571 and the BCRP inhibitor FTC, indicating that P-gp is the transporter mediates the intestinal efflux of cimetidine and famotidine.	Quinidine	115-124	phosphoglycolate phosphatase	Homo sapiens	71-75
19000552-2	2008	The pharmacokinetics of pactimibe and its pharmacologically inactive plasma metabolite, R-125528, of which the main clearance pathway is CYP2D6, was affected by coadministration of quinidine.	Quinidine	181-190	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	137-143
18938231-6	2008	For comparison, the K(i) values for quinidine and fluoxetine were 0.0092 and 8.2microM using recombinant CYP2D6 and 0.019 and 0.93microM using HLM.	Quinidine	36-45	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	105-111
18724381-7	2008	KEY RESULTS: The N588K mutation attenuated I(hERG) inhibition in the following order: E-4031&gt;amiodarone&gt;quinidine&gt;propafenone&gt;disopyramide.	Quinidine	110-119	ETS transcription factor ERG	Homo sapiens	45-49
18448569-11	2008	Moreover, the f(m CYP2D6) of R-125528 estimated to be almost 1 would well explain the accumulation of R-125528 observed with the quinidine treatment.	Quinidine	129-138	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	18-24
19230594-5	2008	The formation of AS2036313-00, and YM-394111 or YM-394112 was inhibited by quinidine and ketoconazole with Ki values of 140 and 0.24 microM, respectively, which indicates that YM758 metabolism may be affected by coadministration of strong CYP2D6 and 3A4 inhibitors in vivo, given the clinical plasma concentrations of quinidine and ketoconazole.	Quinidine	75-84	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	239-245
18703021-7	2008	A number of Pgp substrates (quinidine, amprenavir, irinotecan, topotecan, atorvastatin and erythromycin) induced net digoxin secretion, as did the non-Pgp substrate artemisinin.	Quinidine	28-37	ATP binding cassette subfamily B member 1	Homo sapiens	12-15
18703021-9	2008	Of the compounds that increased Pgp secretion, quinidine, topotecan, atorvastatin and amprenavir pre-exposure also elevated MDR1 mRNA levels, whereas erythromycin, irinotecan and artemisinin displayed no change in transcript levels.	Quinidine	47-56	ATP binding cassette subfamily B member 1	Homo sapiens	124-128
18718123-4	2008	Treatment with transporter inhibitors MK571, quinidine or mitoxantrone, which inhibit MRP2, P-glycoprotein (P-gp) and BCRP, respectively, led to an increase in the accumulation of EC into Caco-2 cells and a decrease in the Papp ratio (Papp B--&gt;A/Papp A--&gt;B) for EC.	Quinidine	45-54	ATP binding cassette subfamily C member 2	Homo sapiens	86-90
18718123-4	2008	Treatment with transporter inhibitors MK571, quinidine or mitoxantrone, which inhibit MRP2, P-glycoprotein (P-gp) and BCRP, respectively, led to an increase in the accumulation of EC into Caco-2 cells and a decrease in the Papp ratio (Papp B--&gt;A/Papp A--&gt;B) for EC.	Quinidine	45-54	ATP binding cassette subfamily B member 1	Homo sapiens	92-106
18718123-4	2008	Treatment with transporter inhibitors MK571, quinidine or mitoxantrone, which inhibit MRP2, P-glycoprotein (P-gp) and BCRP, respectively, led to an increase in the accumulation of EC into Caco-2 cells and a decrease in the Papp ratio (Papp B--&gt;A/Papp A--&gt;B) for EC.	Quinidine	45-54	ATP binding cassette subfamily B member 1	Homo sapiens	108-112
18718123-4	2008	Treatment with transporter inhibitors MK571, quinidine or mitoxantrone, which inhibit MRP2, P-glycoprotein (P-gp) and BCRP, respectively, led to an increase in the accumulation of EC into Caco-2 cells and a decrease in the Papp ratio (Papp B--&gt;A/Papp A--&gt;B) for EC.	Quinidine	45-54	BCR pseudogene 1	Homo sapiens	118-122
18718123-4	2008	Treatment with transporter inhibitors MK571, quinidine or mitoxantrone, which inhibit MRP2, P-glycoprotein (P-gp) and BCRP, respectively, led to an increase in the accumulation of EC into Caco-2 cells and a decrease in the Papp ratio (Papp B--&gt;A/Papp A--&gt;B) for EC.	Quinidine	45-54	pappalysin 1	Homo sapiens	249-255
18686197-5	2008	As for hOCT2-mediated uptake, the IC(50) values of quinidine and the I(f) channel inhibitor for metformin uptake were lower than those for MPP uptake.	Quinidine	51-60	POU class 2 homeobox 2	Homo sapiens	7-12
18668443-9	2008	Additionally, the low IC(50) values determined for ketoconazole and quinidine indicated that these inhibitors were suitable to use to confirm the role of P-gp in the efflux of a test compound.	Quinidine	68-77	ATP binding cassette subfamily B member 1	Homo sapiens	154-158
18356267-2	2008	Significant differences in IC(50,u) values between enzyme sources were observed for quinidine (0.02 microM in recombinant CYP2D6 versus 0.5 microM in hepatocytes) and propafenone (0.02 versus 4.1 microM).	Quinidine	84-93	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	122-128
18276834-1	2008	In a previous study, the concentration-dependent permeability of P-glycoprotein (P-gp) substrate drugs, quinidine, verapamil, and vinblastine, in several cell monolayers with different levels of P-gp expression was analyzed kinetically to obtain fundamental parameters for P-gp-mediated transport, V(max) and K(m(app)) values.	Quinidine	104-113	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	65-79
18238857-8	2008	In contrast to CYP3A4-dependent bioactivation of trazodone itself, formation of M4 was mediated specifically by CYP2D6, as evidenced by cDNA-expressed CYP2D6-catalyzing formation of M4 from m-CPP, strong inhibition of formation of M4 by quinidine, a specific CYP2D6 inhibitor, in both incubations of trazodone and m-CPP with human liver microsomes, and concentration-dependent inhibition of M4 formation by quinidine.	Quinidine	237-246	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	112-118
18238857-8	2008	In contrast to CYP3A4-dependent bioactivation of trazodone itself, formation of M4 was mediated specifically by CYP2D6, as evidenced by cDNA-expressed CYP2D6-catalyzing formation of M4 from m-CPP, strong inhibition of formation of M4 by quinidine, a specific CYP2D6 inhibitor, in both incubations of trazodone and m-CPP with human liver microsomes, and concentration-dependent inhibition of M4 formation by quinidine.	Quinidine	237-246	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	151-157
18238857-8	2008	In contrast to CYP3A4-dependent bioactivation of trazodone itself, formation of M4 was mediated specifically by CYP2D6, as evidenced by cDNA-expressed CYP2D6-catalyzing formation of M4 from m-CPP, strong inhibition of formation of M4 by quinidine, a specific CYP2D6 inhibitor, in both incubations of trazodone and m-CPP with human liver microsomes, and concentration-dependent inhibition of M4 formation by quinidine.	Quinidine	237-246	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	151-157
18238857-8	2008	In contrast to CYP3A4-dependent bioactivation of trazodone itself, formation of M4 was mediated specifically by CYP2D6, as evidenced by cDNA-expressed CYP2D6-catalyzing formation of M4 from m-CPP, strong inhibition of formation of M4 by quinidine, a specific CYP2D6 inhibitor, in both incubations of trazodone and m-CPP with human liver microsomes, and concentration-dependent inhibition of M4 formation by quinidine.	Quinidine	407-416	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	112-118
18238857-8	2008	In contrast to CYP3A4-dependent bioactivation of trazodone itself, formation of M4 was mediated specifically by CYP2D6, as evidenced by cDNA-expressed CYP2D6-catalyzing formation of M4 from m-CPP, strong inhibition of formation of M4 by quinidine, a specific CYP2D6 inhibitor, in both incubations of trazodone and m-CPP with human liver microsomes, and concentration-dependent inhibition of M4 formation by quinidine.	Quinidine	407-416	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	151-157
18238857-8	2008	In contrast to CYP3A4-dependent bioactivation of trazodone itself, formation of M4 was mediated specifically by CYP2D6, as evidenced by cDNA-expressed CYP2D6-catalyzing formation of M4 from m-CPP, strong inhibition of formation of M4 by quinidine, a specific CYP2D6 inhibitor, in both incubations of trazodone and m-CPP with human liver microsomes, and concentration-dependent inhibition of M4 formation by quinidine.	Quinidine	407-416	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	151-157
18276834-1	2008	In a previous study, the concentration-dependent permeability of P-glycoprotein (P-gp) substrate drugs, quinidine, verapamil, and vinblastine, in several cell monolayers with different levels of P-gp expression was analyzed kinetically to obtain fundamental parameters for P-gp-mediated transport, V(max) and K(m(app)) values.	Quinidine	104-113	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	81-85
18248412-7	2008	In the presence of K+-channel blockers (Cs+, Ba2+ and quinidine), the growth advantage of rEAG1 Delta 190 expressing trk1,2 tok1 Delta cells disappeared, indicating its dependence on functional rEAG1 channels.	Quinidine	54-63	potassium voltage-gated channel subfamily H member 1	Rattus norvegicus	90-95
18248412-7	2008	In the presence of K+-channel blockers (Cs+, Ba2+ and quinidine), the growth advantage of rEAG1 Delta 190 expressing trk1,2 tok1 Delta cells disappeared, indicating its dependence on functional rEAG1 channels.	Quinidine	54-63	Trk1p	Saccharomyces cerevisiae S288C	117-128
18248412-7	2008	In the presence of K+-channel blockers (Cs+, Ba2+ and quinidine), the growth advantage of rEAG1 Delta 190 expressing trk1,2 tok1 Delta cells disappeared, indicating its dependence on functional rEAG1 channels.	Quinidine	54-63	potassium voltage-gated channel subfamily H member 1	Rattus norvegicus	194-199
17683917-3	2008	Studies using mice devoid of functional P-gp have revealed that P-gp at the blood-brain barrier (BBB) can exert a profound effect on the ability of some drugs to enter the brain, e.g. cardiovascular drugs (digoxin, quinidine), opioids (morphine, loperamide, methadone), HIV protease inhibitors, the new generation of antihistamines, and some antidepressants and antipsychotics.	Quinidine	215-224	phosphoglycolate phosphatase	Mus musculus	64-68
18346782-1	2008	3D-models were created and refined for CYP2D6 and for its complexes with ajmalicine and quinidine.	Quinidine	88-97	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	39-45
18346782-3	2008	The results suggested that the experimental binding values of ajmalicine- and quinidine-like inhibitors better fit with the energetic terms derived from their interaction with structures of CYP2D6 obtained by, respectively, optimizing the ajmalicine/CYP2D6 and the quinidine/CYP2D6 complexes, rather than exploiting the 3D-strucure of the enzyme not subjected to a ligand-induced conformational change.	Quinidine	78-87	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	190-196
18346782-3	2008	The results suggested that the experimental binding values of ajmalicine- and quinidine-like inhibitors better fit with the energetic terms derived from their interaction with structures of CYP2D6 obtained by, respectively, optimizing the ajmalicine/CYP2D6 and the quinidine/CYP2D6 complexes, rather than exploiting the 3D-strucure of the enzyme not subjected to a ligand-induced conformational change.	Quinidine	78-87	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	250-256
18346782-3	2008	The results suggested that the experimental binding values of ajmalicine- and quinidine-like inhibitors better fit with the energetic terms derived from their interaction with structures of CYP2D6 obtained by, respectively, optimizing the ajmalicine/CYP2D6 and the quinidine/CYP2D6 complexes, rather than exploiting the 3D-strucure of the enzyme not subjected to a ligand-induced conformational change.	Quinidine	78-87	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	250-256
18346782-3	2008	The results suggested that the experimental binding values of ajmalicine- and quinidine-like inhibitors better fit with the energetic terms derived from their interaction with structures of CYP2D6 obtained by, respectively, optimizing the ajmalicine/CYP2D6 and the quinidine/CYP2D6 complexes, rather than exploiting the 3D-strucure of the enzyme not subjected to a ligand-induced conformational change.	Quinidine	265-274	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	190-196
18346782-3	2008	The results suggested that the experimental binding values of ajmalicine- and quinidine-like inhibitors better fit with the energetic terms derived from their interaction with structures of CYP2D6 obtained by, respectively, optimizing the ajmalicine/CYP2D6 and the quinidine/CYP2D6 complexes, rather than exploiting the 3D-strucure of the enzyme not subjected to a ligand-induced conformational change.	Quinidine	265-274	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	250-256
18346782-3	2008	The results suggested that the experimental binding values of ajmalicine- and quinidine-like inhibitors better fit with the energetic terms derived from their interaction with structures of CYP2D6 obtained by, respectively, optimizing the ajmalicine/CYP2D6 and the quinidine/CYP2D6 complexes, rather than exploiting the 3D-strucure of the enzyme not subjected to a ligand-induced conformational change.	Quinidine	265-274	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	250-256
18026129-7	2008	This work has led directly to the successful design of CYP2D6 mutants with novel activity-including creating a testosterone hydroxylase, converting quinidine from inhibitor to substrate, creating a diclofenac hydroxylase and creating a dextromethorphan O-demethylase.	Quinidine	148-157	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	55-61
18057117-6	2008	Using this assay, quinine, quinidine, CsA, and amprenavir were predicted to be the most potent P-gp inhibitors in vivo at their respective therapeutic maximal unbound plasma concentrations.	Quinidine	27-36	ATP binding cassette subfamily B member 1	Homo sapiens	95-99
18332079-6	2008	This saturable uptake of YM758 into human hepatocytes was inhibited in the presence of quinidine (an inhibitor for OATP1B1) but not cimetidine (an inhibitor for the hOCT family).	Quinidine	87-96	solute carrier organic anion transporter family member 1B1	Homo sapiens	115-122
17967933-3	2008	Using a confluent monolayer of MDCKII-hMDR1 cells, we have determined the elementary rate constants for the P-gp efflux of amprenavir, digoxin, loperamide, and quinidine.	Quinidine	160-169	ATP binding cassette subfamily B member 1	Homo sapiens	108-112
18444515-0	2008	Fate of quinidine, a P-glycoprotein substrate, in the gastrointestinal tract after oral administration in rats.	Quinidine	8-17	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	21-35
18444515-2	2008	In this study, the fate of quinidine, a P-gp substrate, in the gastrointestinal tract after oral administration was examined in conscious rats.	Quinidine	27-36	phosphoglycolate phosphatase	Rattus norvegicus	40-44
18444515-7	2008	In conclusion, this study has demonstrated that compounds with high solubility and high permeability, such as quinidine, can be absorbed rapidly at the proximal intestine,escaping the barrier function of P-gp, because P-gp is mostly expressed in the distal intestine.	Quinidine	110-119	phosphoglycolate phosphatase	Rattus norvegicus	204-208
18444515-7	2008	In conclusion, this study has demonstrated that compounds with high solubility and high permeability, such as quinidine, can be absorbed rapidly at the proximal intestine,escaping the barrier function of P-gp, because P-gp is mostly expressed in the distal intestine.	Quinidine	110-119	phosphoglycolate phosphatase	Rattus norvegicus	218-222
17967933-4	2008	For amprenavir and quinidine, transport was fitted with just P-gp and passive permeability.	Quinidine	19-28	ATP binding cassette subfamily B member 1	Homo sapiens	61-65
17967933-8	2008	We propose that amprenavir and quinidine are robust probe substrates for assessing P-gp interactions using the MDCKII-hMDR1 confluent cell monolayer.	Quinidine	31-40	ATP binding cassette subfamily B member 1	Homo sapiens	83-87
17967933-8	2008	We propose that amprenavir and quinidine are robust probe substrates for assessing P-gp interactions using the MDCKII-hMDR1 confluent cell monolayer.	Quinidine	31-40	ATP binding cassette subfamily B member 1	Homo sapiens	118-123
18197559-11	2008	TSIIA was metabolized by rat CYP2C, 3A and 2D, as ticlopidine, ketoconazole and quinidine all inhibited TSIIA metabolism in rat liver microsomes.	Quinidine	80-89	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	29-45
17962373-5	2008	At 1 microM MPBP, the chemical inhibitors quinidine (CYP2D6), fluconazole (CYP2C19), and alpha-naphthoflavone (CYP1A2) reduced metabolite formation in pooled HLM by 83, 53, and 47%, respectively, and at 50 microM MPBP by 41, 47, and 45%, respectively.	Quinidine	42-51	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	53-59
18057887-2	2008	Our previous studies have shown that extracellular acidosis and hyperkalemia attenuate the HERG-inhibitory effect of proarrhythmic drugs, e.g. quinidine, but have little impact on the less-proarrhythmic drug amiodarone.	Quinidine	143-152	potassium voltage-gated channel subfamily H member 2	Homo sapiens	91-95
18574325-8	2008	Distribution of [3H]quinidine, another Octn2 substrate, to the heart was not reduced by L-carnitine, and [3H]quinidine uptake in heart slices was Na(-)-independent and inhibited by cationic drugs, but not carnitine analogs.	Quinidine	20-29	solute carrier family 22 (organic cation transporter), member 5	Mus musculus	39-44
18445989-9	2008	Quinidine (1 microM) completely inhibited the metabolism of enclomiphene by all the EM livers and by recombinant CYP2D6 (p&lt;0.001, one way ANOVA).	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	113-119
18974610-6	2008	In addition, the method was applied to the CYP2D6-mediated desipramine-quinidine interaction: the predicted 6.4-fold increase of desipramine AUC by quinidine was consistent with the observed 6.7-fold increase of AUC in the clinical drug-drug interaction study.	Quinidine	71-80	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	43-49
18974610-6	2008	In addition, the method was applied to the CYP2D6-mediated desipramine-quinidine interaction: the predicted 6.4-fold increase of desipramine AUC by quinidine was consistent with the observed 6.7-fold increase of AUC in the clinical drug-drug interaction study.	Quinidine	148-157	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	43-49
17849171-8	2008	In the presence of these membrane transport inhibitors, ACh still evoked a decrease in [Mg(2+)](i) but the response was less pronounced with either [Na(+)](o) removal or in the presence of either amiloride or quinidine.	Quinidine	209-218	acyl-CoA thioesterase 12	Rattus norvegicus	56-59
18574325-11	2008	Some mechanism(s) other than OCTN2 is involved in the distribution of quinidine to the heart.	Quinidine	70-79	solute carrier family 22 (organic cation transporter), member 5	Mus musculus	29-34
17962323-9	2007	Different responses to K(2P) channel regulators such as bupivacaine, extracellular protons and quinidine corroborated the finding that approximately 20% of IK(so) is carried by TRESK channels.	Quinidine	95-104	potassium channel, subfamily K, member 18	Mus musculus	177-182
17470526-4	2007	In vitro, CP-615,003 displayed quinidine-like efflux in MDR1-expressing Madin-Darby canine kidney II cells.	Quinidine	31-40	ATP binding cassette subfamily B member 1	Canis lupus familiaris	56-60
18229607-5	2007	Furthermore, the metabolism of neferine in rat liver microsomes showed that the percentage inhibition of the major metabolism (liensinine) formation was 80.5% by quinidine (10 micromol x L(-1), selective CYP2D1 inhibitor) and 25.7% by ketoconazole (1 micromol x L(-1), selective CYP3A1 inhibitor).	Quinidine	162-171	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	204-210
18229607-5	2007	Furthermore, the metabolism of neferine in rat liver microsomes showed that the percentage inhibition of the major metabolism (liensinine) formation was 80.5% by quinidine (10 micromol x L(-1), selective CYP2D1 inhibitor) and 25.7% by ketoconazole (1 micromol x L(-1), selective CYP3A1 inhibitor).	Quinidine	162-171	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	279-285
17604185-3	2007	METHODS: The effects of D,L-sotalol, flecainide and quinidine were investigated on potassium (hERG) and sodium (Na(V)1.5) currents transfected in HEK-293 cells to determine the repercussion of the blockade of these currents on rabbit Purkinje fibre (PF) and atrial action potentials.	Quinidine	52-61	ETS transcription factor ERG	Homo sapiens	94-98
17604185-3	2007	METHODS: The effects of D,L-sotalol, flecainide and quinidine were investigated on potassium (hERG) and sodium (Na(V)1.5) currents transfected in HEK-293 cells to determine the repercussion of the blockade of these currents on rabbit Purkinje fibre (PF) and atrial action potentials.	Quinidine	52-61	sodium voltage-gated channel alpha subunit 5	Homo sapiens	111-120
17604185-5	2007	RESULTS: hERG channels were blocked by D,L-sotalol, quinidine and flecainide (IC(50): 69, 0.33 and 0.74 micromol/L, respectively).	Quinidine	52-61	ETS transcription factor ERG	Homo sapiens	9-13
17881661-4	2007	Its formation was inhibited in human microsomes only by quinidine, a CYP2D6 inhibitor.	Quinidine	56-65	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	69-75
17711440-1	2007	INTRODUCTION: Quinidine has been evaluated in patients with a short QT-1 syndrome caused by an IKr gain-of-function mutation of HERG.	Quinidine	14-23	potassium voltage-gated channel subfamily H member 2	Homo sapiens	128-132
17548462-6	2007	The effect of increasing P-glycoprotein expression on apparent transport kinetics was studied using quinidine and digoxin as model compounds.	Quinidine	100-109	ATP binding cassette subfamily B member 1	Homo sapiens	25-39
17520698-6	2007	The MCF-7 cell proliferation induced by IGF-1 is inhibited pharmacologically by Astemizole or Quinidine or more specifically using siRNA against hEAG channel.	Quinidine	94-103	insulin like growth factor 1	Homo sapiens	40-45
17431033-8	2007	The CYP2D6 inhibitor quinidine proved a potent competitive inhibitor of timolol metabolism, with an in vitro K(i) value of 0.08 microM.	Quinidine	21-30	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	4-10
17303635-6	2007	Quinidine (10 microM) prevented VT in six out of six flecainide-treated WT and 13 out of the 16 arrhythmogenic Scn5a+/- hearts in parallel with its clinical effects.	Quinidine	0-9	sodium channel, voltage-gated, type V, alpha	Mus musculus	111-116
17094122-5	2007	On daunorubicin transport, the relative IC(50) value (quinidine IC(50)/verapamil IC(50)) of human P-gp was 5.25 and those from other species ranged from 0.89 to 10.70.	Quinidine	54-63	ATP binding cassette subfamily B member 1	Homo sapiens	98-102
17094122-3	2007	The purpose of the present study was to evaluate the species differences in the inhibitory effects of typical P-gp inhibitors, quinidine and verapamil, on P-gp-mediated drug transport using MDR1 transfected cell lines.	Quinidine	127-136	ATP binding cassette subfamily B member 1	Homo sapiens	110-114
17094122-3	2007	The purpose of the present study was to evaluate the species differences in the inhibitory effects of typical P-gp inhibitors, quinidine and verapamil, on P-gp-mediated drug transport using MDR1 transfected cell lines.	Quinidine	127-136	ATP binding cassette subfamily B member 1	Homo sapiens	155-159
17094122-3	2007	The purpose of the present study was to evaluate the species differences in the inhibitory effects of typical P-gp inhibitors, quinidine and verapamil, on P-gp-mediated drug transport using MDR1 transfected cell lines.	Quinidine	127-136	ATP binding cassette subfamily B member 1	Homo sapiens	190-194
17371284-12	2007	Our study indicates that the antiproliferative effect of quinidine is not due to a simple membrane depolarization but is caused by a block of ODC activity.	Quinidine	57-66	ornithine decarboxylase 1	Homo sapiens	142-145
17504222-5	2007	The P(blood), but not P(lumen), was significantly increased when co-perfused with verapamil, or quinidine (both P-gp inhibitors).	Quinidine	96-105	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	112-116
17466325-5	2007	Importantly, atorvastatin- and SVA-induced block was added to that produced by quinidine, a drug that blocks hKv1.5 channels by binding to their pore cavity.	Quinidine	79-88	potassium voltage-gated channel subfamily A member 5	Homo sapiens	109-115
16960444-9	2007	Amiodarone, azimilide, dofetilide, quinidine and sotalol all produced a dose-dependent inhibition of HERG current.	Quinidine	35-44	potassium voltage-gated channel subfamily H member 2	Homo sapiens	101-105
16960444-12	2007	Raising the extracellular potassium to 10 mmol/l, HERG block by azimilide, dofetilide, quinidine and sotalol was significantly decreased, while the block by amiodarone was unchanged.	Quinidine	87-96	potassium voltage-gated channel subfamily H member 2	Homo sapiens	50-54
17713975-2	2007	We therefore investigated whether inhibition of intestinal P-glycoprotein-mediated efflux by quinidine leads to increased absorption of the P-glycoprotein substrate digoxin.	Quinidine	93-102	ATP binding cassette subfamily B member 1	Homo sapiens	59-73
17713975-2	2007	We therefore investigated whether inhibition of intestinal P-glycoprotein-mediated efflux by quinidine leads to increased absorption of the P-glycoprotein substrate digoxin.	Quinidine	93-102	ATP binding cassette subfamily B member 1	Homo sapiens	140-154
17713975-6	2007	One of the segments was additionally perfused with the P-glycoprotein inhibitor quinidine.	Quinidine	80-89	ATP binding cassette subfamily B member 1	Homo sapiens	55-69
17364883-12	2007	After the treatment with quinidine, a specific inhibitor of human CYP2D6, the area under the curve (AUC) of a CYP2D6 metabolite, 4"-hydroxydebrisoquin, was significantly decreased in the chimeric mice but not in the control mice.	Quinidine	25-34	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	66-72
17364883-12	2007	After the treatment with quinidine, a specific inhibitor of human CYP2D6, the area under the curve (AUC) of a CYP2D6 metabolite, 4"-hydroxydebrisoquin, was significantly decreased in the chimeric mice but not in the control mice.	Quinidine	25-34	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	110-116
17515703-0	2007	The effects of quinidine and its chiral isolates on erg-1sm potassium current and correlation with gastrointestinal augmentation.	Quinidine	15-24	potassium voltage-gated channel subfamily H member 2	Rattus norvegicus	52-57
17515703-2	2007	Because quinidine inhibits cardiac potassium channel and as a result augments gastrointestinal contractility, it was thought that quinidine may affect erg1-sm.	Quinidine	8-17	potassium voltage-gated channel subfamily H member 2	Rattus norvegicus	151-155
17515703-2	2007	Because quinidine inhibits cardiac potassium channel and as a result augments gastrointestinal contractility, it was thought that quinidine may affect erg1-sm.	Quinidine	130-139	potassium voltage-gated channel subfamily H member 2	Rattus norvegicus	151-155
17515703-3	2007	Studies were undertaken to evaluate the effects of quinidine and its chiral isolates on gastrointestinal erg1-sm potassium current and correlate these effects with colon contractility.	Quinidine	51-60	potassium voltage-gated channel subfamily H member 2	Rattus norvegicus	105-109
17515703-10	2007	The inhibition of erg1-sm currents by quinidine was 19 +/- 4, 21 +/- 5, and 48 +/- 6 (P &lt; or = 0.05), respectively; that by isolate X was 20 +/- 4, 23 +/- 5, and 39 +/- 7 (P &lt; or = 0.05), and that by isolate Y was 22 +/- 4, 21 +/- 4, and 31 +/- 6.	Quinidine	38-47	potassium voltage-gated channel subfamily H member 2	Rattus norvegicus	18-22
17515703-11	2007	One chiral isolate and quinidine markedly augmented contractility, whereas quinidine and the two chiral isolates inhibited the erg1-sm potassium currents to a similar extent.	Quinidine	75-84	potassium voltage-gated channel subfamily H member 2	Rattus norvegicus	127-131
17374625-8	2007	DATA SYNTHESIS: Elevated plasma concentrations and toxicities have been reported for a number of CYP3A substrates including amiodarone, carbamazepine, quinidine, tacrolimus, and cyclosporine when administered with metronidazole.	Quinidine	151-160	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	97-102
17409567-4	2007	Quinidine, a CYP2D6 selective inhibitor, was applied to investigate its effect on biotransformation.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	13-19
17409567-5	2007	The concentration of quinidine was 4-folds higher than that of dextromethorphan and the yield of dextrorphan was reduced by 84%, which proved there was drug metabolism enzyme similar to CYP2D6 in C. blakesleeana AS 3.153.	Quinidine	21-30	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	186-192
17346248-4	2007	We performed a study in healthy volunteers to investigate the relative inductive effect of CBZ and OXCZ on CYP3A4 activity using the metabolism of quinidine as a biomarker reaction.	Quinidine	147-156	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	107-113
18072155-11	2007	Following in vitro inhibition of pseudo cholinesterase by quinidine sulfate, true cholinesterase activity was estimated in the plasma of the subjects.	Quinidine	58-75	butyrylcholinesterase	Homo sapiens	40-54
18072155-15	2007	Ten minutes after in vitro addition of quinidine sulfate to inhibit pseudo cholinesterase activity in the plasma, the estimated true cholinesterase activities in males and females were 0.08 and 0.07 DeltapH/20 min, respectively.	Quinidine	39-56	butyrylcholinesterase	Homo sapiens	75-89
18072155-15	2007	Ten minutes after in vitro addition of quinidine sulfate to inhibit pseudo cholinesterase activity in the plasma, the estimated true cholinesterase activities in males and females were 0.08 and 0.07 DeltapH/20 min, respectively.	Quinidine	39-56	butyrylcholinesterase	Homo sapiens	133-147
17189489-0	2007	Saccharomyces cerevisiae multidrug resistance transporter Qdr2 is implicated in potassium uptake, providing a physiological advantage to quinidine-stressed cells.	Quinidine	137-146	cation transporter	Saccharomyces cerevisiae S288C	58-62
17189489-1	2007	The QDR2 gene of Saccharomyces cerevisiae encodes a putative plasma membrane drug:H(+) antiporter that confers resistance against quinidine, barban, bleomycin, and cisplatin.	Quinidine	130-139	cation transporter	Saccharomyces cerevisiae S288C	4-8
17189489-4	2007	QDR2 expression confers a physiological advantage for the yeast cell during the onset of K(+) limited growth, due either to a limiting level of K(+) in the growth medium or to the presence of quinidine.	Quinidine	192-201	cation transporter	Saccharomyces cerevisiae S288C	0-4
17189489-6	2007	Qdr2p also helps to sustain the decrease of intracellular pH in quinidine-stressed cells in growth medium at pH 5.5 by indirectly promoting H(+) extrusion affected by the drug.	Quinidine	64-73	cation transporter	Saccharomyces cerevisiae S288C	0-5
17189489-7	2007	The results are consistent with the hypothesis that Qdr2p may also couple K(+) movement with substrate export, presumably with quinidine.	Quinidine	127-136	cation transporter	Saccharomyces cerevisiae S288C	52-57
17051594-5	2007	By pre-treatment with a typical CYP2D6 inhibitor, quinidine, the AUC0-8 value of 4-OH DB in High was decreased although such values in Low and uPA-/-/SCID mice did not change.	Quinidine	50-59	plasminogen activator, urokinase	Mus musculus	143-146
17484519-4	2007	The formation of fluvoxamino alcohol from fluvoxamine in pooled human liver microsomes was significantly inhibited by quinidine, a relatively specific CYP2D6 inhibitor, with a Ki value of 2.2 microM, whereas other several relatively specific CYP inhibitors did not inhibit the formation of fluvoxamino alcohol.	Quinidine	118-127	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	151-157
17484519-4	2007	The formation of fluvoxamino alcohol from fluvoxamine in pooled human liver microsomes was significantly inhibited by quinidine, a relatively specific CYP2D6 inhibitor, with a Ki value of 2.2 microM, whereas other several relatively specific CYP inhibitors did not inhibit the formation of fluvoxamino alcohol.	Quinidine	118-127	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	151-154
17079336-8	2007	Specific blockade of Shab I(K) by quinidine mimicked the Shab phenotypes and converted tonic firing to a damping pattern.	Quinidine	34-43	Shaker cognate b	Drosophila melanogaster	21-25
17079336-8	2007	Specific blockade of Shab I(K) by quinidine mimicked the Shab phenotypes and converted tonic firing to a damping pattern.	Quinidine	34-43	Shaker cognate b	Drosophila melanogaster	57-61
16942825-7	2006	Quinidine proved to be efficient in prolonging the QT interval and rendering ventricular tachyarrhythmias non-inducible in patients with a mutation in KCNH2 (HERG).	Quinidine	0-9	potassium voltage-gated channel subfamily H member 2	Homo sapiens	151-156
16926058-5	2006	Pre-administration of human receptor-associated protein, a low-density lipoprotein receptor-related protein (LRP) antagonist, reduced the elimination of [(125)I]hAbeta(1-40) by 20.3%, while quinidine or verapamil, P-glycoprotein (P-gp) inhibitors, did not significantly affect the elimination.	Quinidine	190-199	LDL receptor related protein 1	Homo sapiens	109-112
16842817-2	2006	The use of implantable cardioverter defibrillators helps to protect SQTS patients from ventricular fibrillation; however, pharmacological treatments to normalise the QT interval are limited: thus far only quinidine has been found to be effective in a subset of patients, with the SQT1 variant.	Quinidine	205-214	potassium voltage-gated channel subfamily H member 2	Homo sapiens	280-284
16842817-4	2006	We demonstrate here that the N588K-HERG mutation only slightly attenuates I(HERG) blockade by the Class Ia antiarrhythmic drug disopyramide (1.5-fold elevation of IC(50)), compared to quinidine (3.5-fold elevation of IC(50)) and the Class III antiarrhythmic drug E-4031 (11.5-fold elevation of IC(50)).	Quinidine	184-193	potassium voltage-gated channel subfamily H member 2	Homo sapiens	35-39
17172009-8	2006	Na+/Mg2+ antiport is inhibited by amiloride, quinidine and imipramine.	Quinidine	45-54	mucin 7, secreted	Homo sapiens	4-7
17172009-13	2006	Na+-independent Mg2+ efflux via the choline exchanger is also inhibited by amiloride, quinidine and imipramine, and can also be regulated by phosphorylation-dephosphorylation.	Quinidine	86-95	mucin 7, secreted	Homo sapiens	16-19
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.	Quinidine	49-58	potassium sodium-activated channel subfamily T member 1	Homo sapiens	70-75
17365275-2	2007	P-gp inhibitors, such as cyclosporin A, quinidine and verapamil, enhanced the apparent brain uptake of [3H]BNP by 1.5-fold.	Quinidine	40-49	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-4
16847696-0	2006	Adaptive downregulation of a quinidine-sensitive cation conductance in renal principal cells of TWIK-1 knockout mice.	Quinidine	29-38	potassium channel, subfamily K, member 1	Mus musculus	96-102
16931690-10	2006	Systemic ondansetron had a small but statistically significant pronociceptive effect after treatment of wild-type mice with the P-gp inhibitor quinidine but not with cyclosporine or verapamil.	Quinidine	143-152	phosphoglycolate phosphatase	Mus musculus	128-132
16763018-2	2006	The reliability of the selective CYP2D6 inhibitor quinidine was evaluated in a retrospective analysis using a standardized approach that avoids laboratory-to-laboratory variation.	Quinidine	50-59	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	33-39
16763018-6	2006	An estimate of the fraction metabolized by CYP2D6 in microsomes was derived from the rate constant determined with and without 1 microM quinidine for 11 substrates.	Quinidine	136-145	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	43-49
16807400-9	2006	Ammonium chloride-induced intracellular acidification significantly stimulated the hMATE2-K-dependent transport of organic cations such as TEA, MPP, procainamide, metformin, N1-methylnicotinamide, creatinine, guanidine, quinidine, quinine, thiamine, and verapamil.	Quinidine	220-229	solute carrier family 47 member 2	Homo sapiens	83-89
16942825-7	2006	Quinidine proved to be efficient in prolonging the QT interval and rendering ventricular tachyarrhythmias non-inducible in patients with a mutation in KCNH2 (HERG).	Quinidine	0-9	potassium voltage-gated channel subfamily H member 2	Homo sapiens	158-162
16772377-8	2006	Mefloquine, a close derivative of quinine and quinidine that exhibits antimalarial and antiarrhythmic properties, reduced conductance of cell-cell junctions and dye uptake through mCx30.2 hemichannels with approximately the same affinity (IC(50) = approximately 10 microM) and increased dependence of junctional conductance on transjunctional voltage.	Quinidine	46-55	gap junction protein, delta 3	Mus musculus	180-187
16647797-6	2006	Treatment with quinidine or cyclosporine A, which are P-gp inhibitors, decreased the P(app) of Rho-123 to the same degree in both monolayers.	Quinidine	15-24	ATP binding cassette subfamily B member 1	Homo sapiens	54-58
16595712-9	2006	Quinidine and ketoconazole, potent inhibitors to CYP2D6 and CYP3A4, respectively, did not show strong inhibition toward Cyp2d22-mediated dextromethorphan O- or N-demethylation.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	49-55
16595712-9	2006	Quinidine and ketoconazole, potent inhibitors to CYP2D6 and CYP3A4, respectively, did not show strong inhibition toward Cyp2d22-mediated dextromethorphan O- or N-demethylation.	Quinidine	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	60-66
16545584-12	2006	The cells demonstrated P-glycoprotein-mediated function by directional transport of dexamethasone, ritonavir, and vinblastine in a transwell assay that was inhibited in the presence of cyclosporin A, verapamil, or quinidine.	Quinidine	214-223	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	23-37
16406207-5	2006	The inhibitory potencies (apparent IC50) of known Pgp inhibitors astemizole, GF120918, ketoconazole, itraconazole, quinidine, verapamil and quinine were determined over at least a 1000-fold concentration range.	Quinidine	115-124	ATP binding cassette subfamily B member 1	Homo sapiens	50-53
16722797-1	2006	The aim of this study was to investigate the modulation of efflux mechanisms using transporter- targeted prodrug derivatization of a model P-gp substrate, quinidine.	Quinidine	155-164	ATP-dependent translocase ABCB1	Oryctolagus cuniculus	139-143
16722797-3	2006	[(14)C] erythromycin was chosen to delineate the affinity of quinidine (Q) toward P-gp.	Quinidine	61-70	ATP-dependent translocase ABCB1	Oryctolagus cuniculus	82-86
16722797-9	2006	Results from this study clearly indicate that prodrug derivatization of quinidine can modulate P-gp-mediated efflux.	Quinidine	72-81	ATP-dependent translocase ABCB1	Oryctolagus cuniculus	95-99
16307862-6	2006	The results from enzyme kinetic studies were confirmed by incubation of BVT.2938 in the presence of the chemical inhibitor of CYP2D6*1, quinidine.	Quinidine	136-145	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	126-132
16472104-8	2006	However, after co-administration of drugs such as quinidine, propafenone and thioridazine (potent inhibitors of CYP2D6), the NE-100 AUC(oral) ratios predicted from the dispersion model was much greater than those from well-stirred model.	Quinidine	50-59	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	112-118
16381668-9	2006	Inhibition of UGT2B7 by quinidine was also investigated further, because the effects of this compound on morphine pharmacokinetics (a known UGT2B7 substrate) have been ascribed to inhibition of P-glycoprotein.	Quinidine	24-33	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	14-20
16381668-10	2006	Quinidine inhibited human liver microsomal and recombinant UGT2B7, with respective Ki values of 335+/-128 microM and 186 microM.	Quinidine	0-9	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	59-65
16258992-0	2005	pH-dependent functional activity of P-glycoprotein in limiting intestinal absorption of protic drugs: kinetic analysis of quinidine efflux in situ.	Quinidine	122-131	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	36-50
16162505-0	2005	Why is quinidine an inhibitor of cytochrome P450 2D6?	Quinidine	7-16	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	33-52
16162505-7	2005	We have now examined the effect of mutations of these residues on interactions of the enzyme with the prototypical CYP2D6 inhibitor, quinidine.	Quinidine	133-142	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	115-121
16258992-7	2005	Further, apparent Michaelis-Menten constants (K(M), J(P-gp,max)) for the quinidine efflux in jejunum indicated that efflux activity was more at luminal pH 4.5 over pH 7.4.	Quinidine	73-82	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	54-58
16258992-8	2005	K(M) values for jejunum quinidine efflux at pH 4.5 and pH 7.4 were determined to be 77.63 +/- 10.90 and 22.86 +/- 5.22 microM, with J(P-gp,max) values of 1.47 +/- 0.08 and 0.62 +/- 0.04 nM/cm2/sec, respectively.	Quinidine	24-33	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	134-138
16099839-8	2005	Prototype OCT inhibitors, including cimetidine, and type II cations (e.g., quinidine, quinine, verapamil, and rhodamine123) are also PMAT inhibitors.	Quinidine	75-84	solute carrier family 29 member 4	Homo sapiens	133-137
15507542-6	2005	This catalytic activity was &gt;95% inhibited by quinidine, a CYP2D6 inhibitor.	Quinidine	49-58	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	62-68
16226079-11	2005	Furthermore, in patients with a mutation in HERG (SQT1), quinidine rendered ventricular tachyarrhythmias noninducible and restored the QT interval/heart rate relationship toward a reference range.	Quinidine	57-66	potassium voltage-gated channel subfamily H member 2	Homo sapiens	44-48
16226079-11	2005	Furthermore, in patients with a mutation in HERG (SQT1), quinidine rendered ventricular tachyarrhythmias noninducible and restored the QT interval/heart rate relationship toward a reference range.	Quinidine	57-66	potassium voltage-gated channel subfamily H member 2	Homo sapiens	50-54
15784650-3	2005	In addition to midazolam, testosterone, and nifedipine, quinidine was explored as a more "pragmatic" substrate due to its kinetic properties and specificity toward CYP3A4 in comparison with CYP3A5.	Quinidine	56-65	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	164-170
16192109-3	2005	The contributions of CYP2D6 to the primary metabolisms of the substrates were estimated from the quinidine-mediated inhibition of their depletion rate constants in human hepatocytes and liver microsomes.	Quinidine	97-106	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	21-27
15909533-12	2005	In addition, the AUC of ranitidine in bile decreased in the treatment of cyclosporine or quinidine, which suggests that the hepatobiliary excretion of ranitidine was partially regulated by P-glycoprotein or organic cation transporter.	Quinidine	89-98	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	189-203
15748622-4	2005	The I(K) present in these cells, the electrical properties of which resembled those for the Kv2.1-related K+ current, was sensitive to inhibition by quinidine or dendrotoxin, yet not by pandinotoxin-Kalpha, E-4031 or apamin.	Quinidine	149-158	potassium voltage-gated channel subfamily B member 1	Rattus norvegicus	92-97
15619261-2	2005	Quinidine (a specific inhibitor of CYP2D6) did not markedly affect the metabolism of perospirone, whereas quercetin (an inhibitor of CYP2C8) and ketoconazole (an inhibitor of CYP3A4) caused a decrease in the metabolism with human liver microsomes in a concentration dependent fashion.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	35-41
15821840-5	2005	RESULTS: Quinidine (10 microM) inhibited HERG tail current by 37% +/- 5% at pH7.4.	Quinidine	9-18	potassium voltage-gated channel subfamily H member 2	Homo sapiens	41-45
15649438-0	2005	The yeast multidrug transporter Qdr3 (Ybr043c): localization and role as a determinant of resistance to quinidine, barban, cisplatin, and bleomycin.	Quinidine	104-113	Qdr3p	Saccharomyces cerevisiae S288C	32-36
15649438-1	2005	Saccharomyces cerevisiae ORF YBR043c, predicted to code for a transporter of the major facilitator superfamily required for multiple drug resistance, encodes a plasma membrane protein that confers resistance to quinidine and barban, as observed before for its close homologues QDR1 and QDR2.	Quinidine	211-220	multidrug transporter	Saccharomyces cerevisiae S288C	277-281
15649438-1	2005	Saccharomyces cerevisiae ORF YBR043c, predicted to code for a transporter of the major facilitator superfamily required for multiple drug resistance, encodes a plasma membrane protein that confers resistance to quinidine and barban, as observed before for its close homologues QDR1 and QDR2.	Quinidine	211-220	cation transporter	Saccharomyces cerevisiae S288C	286-290
15649438-5	2005	Transport assays support the concept that Qdr3 is involved, even if opportunistically, in the active export of quinidine out of yeast cell.	Quinidine	111-120	Qdr3p	Saccharomyces cerevisiae S288C	42-46
15649438-6	2005	A correlation was established between the efficiency of quinidine active export mediated by Qdr3p, Qdr2p or Qdr1p, and the efficacy of the expression of the encoding genes in alleviating the deleterious action of quinidine, as well as of the other compounds (QDR2&gt;QDR3&gt;&gt;&gt;QDR1).	Quinidine	56-65	Qdr3p	Saccharomyces cerevisiae S288C	92-97
15649438-6	2005	A correlation was established between the efficiency of quinidine active export mediated by Qdr3p, Qdr2p or Qdr1p, and the efficacy of the expression of the encoding genes in alleviating the deleterious action of quinidine, as well as of the other compounds (QDR2&gt;QDR3&gt;&gt;&gt;QDR1).	Quinidine	56-65	cation transporter	Saccharomyces cerevisiae S288C	99-104
15649438-6	2005	A correlation was established between the efficiency of quinidine active export mediated by Qdr3p, Qdr2p or Qdr1p, and the efficacy of the expression of the encoding genes in alleviating the deleterious action of quinidine, as well as of the other compounds (QDR2&gt;QDR3&gt;&gt;&gt;QDR1).	Quinidine	56-65	multidrug transporter	Saccharomyces cerevisiae S288C	108-113
15649438-6	2005	A correlation was established between the efficiency of quinidine active export mediated by Qdr3p, Qdr2p or Qdr1p, and the efficacy of the expression of the encoding genes in alleviating the deleterious action of quinidine, as well as of the other compounds (QDR2&gt;QDR3&gt;&gt;&gt;QDR1).	Quinidine	56-65	cation transporter	Saccharomyces cerevisiae S288C	259-263
15649438-6	2005	A correlation was established between the efficiency of quinidine active export mediated by Qdr3p, Qdr2p or Qdr1p, and the efficacy of the expression of the encoding genes in alleviating the deleterious action of quinidine, as well as of the other compounds (QDR2&gt;QDR3&gt;&gt;&gt;QDR1).	Quinidine	56-65	Qdr3p	Saccharomyces cerevisiae S288C	267-271
15649438-6	2005	A correlation was established between the efficiency of quinidine active export mediated by Qdr3p, Qdr2p or Qdr1p, and the efficacy of the expression of the encoding genes in alleviating the deleterious action of quinidine, as well as of the other compounds (QDR2&gt;QDR3&gt;&gt;&gt;QDR1).	Quinidine	56-65	multidrug transporter	Saccharomyces cerevisiae S288C	283-287
15649438-6	2005	A correlation was established between the efficiency of quinidine active export mediated by Qdr3p, Qdr2p or Qdr1p, and the efficacy of the expression of the encoding genes in alleviating the deleterious action of quinidine, as well as of the other compounds (QDR2&gt;QDR3&gt;&gt;&gt;QDR1).	Quinidine	213-222	Qdr3p	Saccharomyces cerevisiae S288C	92-97
15649438-6	2005	A correlation was established between the efficiency of quinidine active export mediated by Qdr3p, Qdr2p or Qdr1p, and the efficacy of the expression of the encoding genes in alleviating the deleterious action of quinidine, as well as of the other compounds (QDR2&gt;QDR3&gt;&gt;&gt;QDR1).	Quinidine	213-222	cation transporter	Saccharomyces cerevisiae S288C	99-104
15649438-6	2005	A correlation was established between the efficiency of quinidine active export mediated by Qdr3p, Qdr2p or Qdr1p, and the efficacy of the expression of the encoding genes in alleviating the deleterious action of quinidine, as well as of the other compounds (QDR2&gt;QDR3&gt;&gt;&gt;QDR1).	Quinidine	213-222	multidrug transporter	Saccharomyces cerevisiae S288C	108-113
16041196-4	2005	Since the HERG gene encodes IKr, we studied quinidine"s effect on HERG expressed in Xenopus oocytes by the 2-electrode voltage clamp technique.	Quinidine	44-53	potassium voltage-gated channel subfamily H member 2	Homo sapiens	10-14
16041196-4	2005	Since the HERG gene encodes IKr, we studied quinidine"s effect on HERG expressed in Xenopus oocytes by the 2-electrode voltage clamp technique.	Quinidine	44-53	potassium voltage-gated channel subfamily H member 2	Homo sapiens	66-70
16041196-5	2005	When extracellular K+ was 5 mmol/L, quinidine blocked the HERG current dose dependently, with an IC50 of 6.3 +/- 0.2 micromol/L.	Quinidine	36-45	potassium voltage-gated channel subfamily H member 2	Homo sapiens	58-62
16041196-7	2005	The inhibition of HERG by quinidine was not use dependent.	Quinidine	26-35	potassium voltage-gated channel subfamily H member 2	Homo sapiens	18-22
15821840-9	2005	There were significant differences in the HERG inhibition by quinidine, dofetilide, and azimilide between pH 7.4 and pH 6.2 (P &lt; .01).	Quinidine	61-70	potassium voltage-gated channel subfamily H member 2	Homo sapiens	42-46
16019948-7	2005	The CYP2D6-specific chemical inhibitor quinidine (3 microM) significantly (p&lt;0.001) inhibited di-HO-PPP formation by 75.8%+/-1.7% (mean+/-standard error of the mean) in incubation mixtures with HLM and 2 microM MDPPP.	Quinidine	39-48	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	4-10
16019950-9	2005	Chemical-inhibition studies showed that quinidine (selective for CYP2D6) and ticlopidine (selective for CYP2C19) inhibited the formation of the hydroxy metabolite of DRF 4367, whereas potent inhibitors selective for other forms of CYP did not inhibit this oxidative reaction.	Quinidine	40-49	peptidyl-prolyl isomerase G (cyclophilin G)	Mus musculus	65-68
15664356-8	2005	The method was found to be reliable in permeability determination and to estimate pH-dependent P-glycoprotein (P-gp)-mediated efflux transport of quinidine.	Quinidine	146-155	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	95-109
15664356-8	2005	The method was found to be reliable in permeability determination and to estimate pH-dependent P-glycoprotein (P-gp)-mediated efflux transport of quinidine.	Quinidine	146-155	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	111-115
15664356-10	2005	Inhibition of P-gp by verapamil (200 microM) indicated that about 68% and only 35% of passive transport of quinidine was attenuated by P-gp-mediated efflux at pH 4.5 and 7.4, respectively.	Quinidine	107-116	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	14-18
15664356-10	2005	Inhibition of P-gp by verapamil (200 microM) indicated that about 68% and only 35% of passive transport of quinidine was attenuated by P-gp-mediated efflux at pH 4.5 and 7.4, respectively.	Quinidine	107-116	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	135-139
15501934-9	2005	For three P-gp substrates (amprenavir, loperamide, and quinidine), we have successfully fitted the elementary rate constants, i.e., drug association to P-gp from the apical membrane inner monolayer, drug dissociation back into the apical membrane inner monolayer, and drug efflux from P-gp into the apical chamber, as well as the density of efflux active P-gp.	Quinidine	55-64	phosphoglycolate phosphatase	Homo sapiens	10-14
15501934-9	2005	For three P-gp substrates (amprenavir, loperamide, and quinidine), we have successfully fitted the elementary rate constants, i.e., drug association to P-gp from the apical membrane inner monolayer, drug dissociation back into the apical membrane inner monolayer, and drug efflux from P-gp into the apical chamber, as well as the density of efflux active P-gp.	Quinidine	55-64	phosphoglycolate phosphatase	Homo sapiens	152-156
15501934-9	2005	For three P-gp substrates (amprenavir, loperamide, and quinidine), we have successfully fitted the elementary rate constants, i.e., drug association to P-gp from the apical membrane inner monolayer, drug dissociation back into the apical membrane inner monolayer, and drug efflux from P-gp into the apical chamber, as well as the density of efflux active P-gp.	Quinidine	55-64	phosphoglycolate phosphatase	Homo sapiens	152-156
15673388-0	2005	Further insights into the effect of quinidine in short QT syndrome caused by a mutation in HERG.	Quinidine	36-45	potassium voltage-gated channel subfamily H member 2	Homo sapiens	91-95
15673388-1	2005	INTRODUCTION: The principal aim of this study was to assess the efficacy of quinidine in suppressing IKr in vitro and in modulating the rate dependence of the QT interval in the "SQT1" form of the short QT syndrome.	Quinidine	76-85	potassium voltage-gated channel subfamily H member 2	Homo sapiens	179-183
15673388-6	2005	Data from heterologous expression of wild-type and mutant HERG genes indicate the mutation causes a 20-fold increase in IC50 of d-sotalol but only a 5.8-fold increase in IC50 of quinidine.	Quinidine	178-187	potassium voltage-gated channel subfamily H member 2	Homo sapiens	58-62
15673388-7	2005	CONCLUSION: Oral quinidine is effective in suppressing the gain of function in IKr responsible for some cases of short QT syndrome with a mutation in HERG and thus restoring normal rate dependence of the QT interval and rendering ventricular tachycardia/ventricular fibrillation noninducible.	Quinidine	17-26	potassium voltage-gated channel subfamily H member 2	Homo sapiens	150-154
15848954-6	2005	P-glycoprotein (P-gp) inhibitors (verapamil and quinidine) reduced the PTZ efflux transport.	Quinidine	48-57	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-14
15848954-6	2005	P-glycoprotein (P-gp) inhibitors (verapamil and quinidine) reduced the PTZ efflux transport.	Quinidine	48-57	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	16-20
15466248-1	2005	To investigate the role of serotonin (5-HT), an important neurotransmitter and hormone/paracrine agent in the small intestine, in the transport activity of P-glycoprotein (P-gp), the intestinal transport of quinidine, a P-gp substrate, was examined in 5-HT-depleted rats prepared by intraperitoneal administration of p-chlorophenylalanine, a specific inhibitor of tryptophan hydroxylase in 5-HT biosynthesis.	Quinidine	207-216	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	156-170
15466248-7	2005	These results indicate that the secretory transport of quinidine via P-gp was significantly enhanced under 5-HT-depleted conditions.	Quinidine	55-64	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	69-73
15059841-7	2004	Additional ABC transporter substrate inhibitors like quinidine, diltiazem, and ritonavir also enhanced transduction 2- to 3-fold, although ABC transporter inhibitors that are not substrates did not.	Quinidine	53-62	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	11-26
15501934-9	2005	For three P-gp substrates (amprenavir, loperamide, and quinidine), we have successfully fitted the elementary rate constants, i.e., drug association to P-gp from the apical membrane inner monolayer, drug dissociation back into the apical membrane inner monolayer, and drug efflux from P-gp into the apical chamber, as well as the density of efflux active P-gp.	Quinidine	55-64	phosphoglycolate phosphatase	Homo sapiens	152-156
15342614-2	2004	To find out whether quinidine (Q), a CYP2D6 inhibitor, could elevate and prolong DM plasma profiles, 2 multiple-dose studies identified the lowest oral dose of Q that could be used in a fixed combination with 3 doses of DM.	Quinidine	20-29	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	37-43
15363950-4	2004	Human-OCT3 mediated a time- and dose-dependent uptake of quinidine and lidocaine, with Km values of 216 and 139 microM, respectively.	Quinidine	57-66	solute carrier family 22 member 3	Homo sapiens	6-10
15363950-8	2004	Kinetic analysis revealed that disopyramide, lidocaine, procainamide and quinidine inhibited histamine uptake mediated by human-OCT3 in a competitive manner.	Quinidine	73-82	solute carrier family 22 member 3	Homo sapiens	128-132
15123670-9	2004	TRESK-2 was inhibited by 10 microm quinidine, 20 microm arachidonate and acid (pH 6.3) at 49, 43, and 23%, respectively.	Quinidine	35-44	potassium channel, subfamily K, member 18	Mus musculus	0-7
15266218-7	2004	These values were also comparable with the inhibitory effect of quinidine in Caco-2 cells, a well-known inhibitor of P-gp, on ritonavir efflux from Caco-2 cells.	Quinidine	64-73	phosphoglycolate phosphatase	Homo sapiens	117-121
15215105-0	2004	Saccharomyces cerevisiae multidrug transporter Qdr2p (Yil121wp): localization and function as a quinidine resistance determinant.	Quinidine	96-105	cation transporter	Saccharomyces cerevisiae S288C	47-52
15215105-2	2004	Like its close homologue Qdr1p, Yil121wp was localized at the plasma membrane, and its increased expression also led to increased tolerance to the antiarrhythmia and antimalarial drug quinidine.	Quinidine	184-193	multidrug transporter	Saccharomyces cerevisiae S288C	25-30
15215105-3	2004	The quinidine resistance phenotype was confirmed for different yeast strains and growth media, including a prototrophic strain, and YIL121w was named the QDR2 gene.	Quinidine	4-13	cation transporter	Saccharomyces cerevisiae S288C	154-158
15215105-7	2004	Although QDR2 transcription was not enhanced in response to quinidine, the results confirmed that Qdr2p is involved in the active export of quinidine out of the cell, thus conferring resistance to the drug.	Quinidine	140-149	cation transporter	Saccharomyces cerevisiae S288C	98-103
15183128-9	2004	A known inhibitor of CYP2D6, quinidine, effectively inhibited the BF 1"-hydroxylation activities in liver microsomal fractions prepared from KYU- and KAU-marmosets.	Quinidine	29-38	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	21-27
15229466-10	2004	Its extent is considerable and similar to the effect of other potent P-gp inhibitors on digoxin disposition such as quinidine.	Quinidine	116-125	ATP binding cassette subfamily B member 1	Homo sapiens	69-73
15537169-4	2004	Quinidine (a selective inhibitor of CYP2D6) inhibited the O-demethylation of DMAE in pooled human microsomes by 86%, while selective inhibitors for other forms of CYP did not show any appreciable effect.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	36-42
15537169-4	2004	Quinidine (a selective inhibitor of CYP2D6) inhibited the O-demethylation of DMAE in pooled human microsomes by 86%, while selective inhibitors for other forms of CYP did not show any appreciable effect.	Quinidine	0-9	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	36-39
15981588-0	2004	Circumventing P-glycoprotein-mediated cellular efflux of quinidine by prodrug derivatization.	Quinidine	57-66	ATP binding cassette subfamily B member 1	Homo sapiens	14-28
15981588-1	2004	The objective of this study is to investigate whether transporter-targeted prodrug derivatization of quinidine, a model P-glycoprotein (P-gp) substrate, can circumvent P-gp-mediated efflux.	Quinidine	101-110	ATP binding cassette subfamily B member 1	Homo sapiens	120-134
15981588-1	2004	The objective of this study is to investigate whether transporter-targeted prodrug derivatization of quinidine, a model P-glycoprotein (P-gp) substrate, can circumvent P-gp-mediated efflux.	Quinidine	101-110	ATP binding cassette subfamily B member 1	Homo sapiens	136-140
15981588-1	2004	The objective of this study is to investigate whether transporter-targeted prodrug derivatization of quinidine, a model P-glycoprotein (P-gp) substrate, can circumvent P-gp-mediated efflux.	Quinidine	101-110	ATP binding cassette subfamily B member 1	Homo sapiens	168-172
15981588-10	2004	Results from this study clearly indicate that prodrug derivatization of quinidine into val-quinidine can overcome P-gp-mediated efflux.	Quinidine	72-81	ATP binding cassette subfamily B member 1	Homo sapiens	114-118
15189761-0	2004	Comparison of kinetic properties of quinidine and dofetilide block of HERG channels.	Quinidine	36-45	potassium voltage-gated channel subfamily H member 2	Homo sapiens	70-74
15089813-13	2004	CONCLUSIONS: Quinidine increased the plasma concentrations of oral methadone in the absorptive phase and the miosis caused by methadone, suggesting that intestinal P-gp affects oral methadone absorption and hence its clinical effects.	Quinidine	13-22	ATP binding cassette subfamily B member 1	Homo sapiens	164-168
15125690-2	2004	The ether-a-go-go-related gene, HERG, is a primary target for blockade by many drugs including dofetilide, quinidine and azimilide.	Quinidine	107-116	potassium voltage-gated channel subfamily H member 2	Homo sapiens	32-36
15125690-10	2004	Acidification weakened the inhibitory effects of quinidine and azimilide on HERG channels.	Quinidine	49-58	potassium voltage-gated channel subfamily H member 2	Homo sapiens	76-80
15189761-2	2004	We examined the kinetic properties of quinidine block of HERG channels expressed in Xenopus oocytes in comparison with those of the block by a class III antiarrhythmic dofetilide.	Quinidine	38-47	potassium voltage-gated channel subfamily H member 2	Homo sapiens	57-61
14634033-1	2004	The disposition of digoxin and the influence of the organic anion transporting polypeptide (Oatp)2 inhibitor rifampicin and the P-glycoprotein (P-gp) inhibitor quinidine on its hepatic disposition were examined in the isolated perfused rat liver.	Quinidine	160-169	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	144-148
15039299-9	2004	Quinidine inhibition showed that CYP2D6 is the high affinity enzyme for O-demethylation with a mean K(m) of 130 +/- 33 microM and a V(max) that ranged from 89 to 356 pmol/mg/min.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	33-39
14998425-9	2004	Hydromorphone formation was inhibited by quinidine (a selective inhibitor of CYP2D6 activity), and monoclonal antibodies specific to CYP2D6.	Quinidine	41-50	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	77-83
14973303-0	2004	Quinidine as a probe for the role of p-glycoprotein in the intestinal absorption and clinical effects of fentanyl.	Quinidine	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	37-51
14973303-12	2004	Quinidine increased oral fentanyl plasma concentrations, suggesting that intestinal P-gp or some other quinidine-sensitive transporter affects the absorption, bioavailability, and hence clinical effects of oral fentanyl.	Quinidine	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	84-88
14973303-13	2004	Quinidine had less effect on fentanyl pharmacodynamics, suggesting that if quinidine is an effective inhibitor of brain P-gp, then P-gp appears to have less effect on brain access of fentanyl.	Quinidine	75-84	ATP binding cassette subfamily B member 1	Homo sapiens	120-124
15370963-9	2004	In incubations with CYP3A4 "freed" from its host membrane, the 5-hydroxylation of diclofenac increased with increasing quinidine concentrations, reaching a maximal eightfold elevation relative to controls.	Quinidine	119-128	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	20-26
15370963-12	2004	Kinetically, enhancement by quinidine of the 5-hydroxylation of diclofenac in incubations with solubilized CYP3A4 was characterized by increases in the rate of metabolism with little change in the substrate-binding affinity.	Quinidine	28-37	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	107-113
15370963-16	2004	The absence of cooperative drug interactions with quinidine when CYP3A4 was expressed in insect cells might be due to an absence of enzyme conformation changes on quinidine binding, or the inability of quinidine to gain access to a putative effector-binding domain.	Quinidine	163-172	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	65-71
15370963-16	2004	The absence of cooperative drug interactions with quinidine when CYP3A4 was expressed in insect cells might be due to an absence of enzyme conformation changes on quinidine binding, or the inability of quinidine to gain access to a putative effector-binding domain.	Quinidine	163-172	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	65-71
15039293-5	2004	Moreover, berberine was processed through hepatobiliary excretion against a concentration gradient based on the bile-to-blood distribution ratio (AUC(bile)/AUC(blood)); the active berberine efflux might be affected by P-gp and OCT since coadministration of berberine and CsA or quinidine at the same dosage of 10 mg kg(-1) significantly decreased the berberine amount in bile.	Quinidine	278-287	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	218-222
16680870-8	2004	Preincubation of human liver microsomes with cimetidine and NADPH did not increase the inhibitory potency of cimetidine; however, preincubation with recombinant CYP2D6 resulted in enzyme inactivation that could be attenuated by the CYP2D6 inhibitor quinidine.	Quinidine	249-258	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	161-167
14704918-0	2003	Effect of P-glycoprotein on the ocular disposition of a model substrate, quinidine.	Quinidine	73-82	ATP-dependent translocase ABCB1	Oryctolagus cuniculus	10-24
14634033-9	2004	It is concluded that rifampicin limits the hepatic entrance of digoxin and reduced the hepatic exposure of digoxin to CYP3A by inhibiting the basolateral Oatp2 uptake transport, whereas quinidine increased the hepatic exposure of digoxin to CYP3A by inhibiting the canalicular P-gp transport.	Quinidine	186-195	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	277-281
14563706-4	2004	In rat brain microsomes, these activities were not inhibited by anti-P450c21 antibodies, but they were effectively inhibited by the CYP2D-specific chemical inhibitor quinidine and by anti-CYP2D4 antibodies.	Quinidine	166-175	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	132-137
14563706-4	2004	In rat brain microsomes, these activities were not inhibited by anti-P450c21 antibodies, but they were effectively inhibited by the CYP2D-specific chemical inhibitor quinidine and by anti-CYP2D4 antibodies.	Quinidine	166-175	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	188-194
14985146-11	2004	The CYP2D6-specific chemical inhibitor quinidine (1 and 3 microM) significantly inhibited 4-HO-PP formation by 71.9 +/- 4.8% and by 98.5% +/- 0.5%, respectively, in incubation mixtures with pHLM and 200 microM MeOPP.	Quinidine	39-48	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	4-10
14663457-18	2003	DISCUSSION: Quinidine increased the absorption and plasma concentrations of oral morphine, suggesting that intestinal P-glycoprotein affected the absorption, bioavailability, and, hence, clinical effects of oral morphine.	Quinidine	12-21	ATP binding cassette subfamily B member 1	Homo sapiens	118-132
14729096-1	2004	Quinidine and Ba(2+), non-selective K(+)-channel blockers, have previously been shown to inhibit antigen-induced mediator (beta-hexosaminidase) release from RBL-2H3 cells, a mucosal-type mast cell line.	Quinidine	0-9	O-GlcNAcase	Rattus norvegicus	123-142
14729096-1	2004	Quinidine and Ba(2+), non-selective K(+)-channel blockers, have previously been shown to inhibit antigen-induced mediator (beta-hexosaminidase) release from RBL-2H3 cells, a mucosal-type mast cell line.	Quinidine	0-9	RB transcriptional corepressor like 2	Rattus norvegicus	157-162
14704918-1	2003	PURPOSE: The objective of this study was to determine the effect of the multi-drug efflux transport protein, P-glycoprotein (P-gp), on the ocular distribution of a model substrate, quinidine.	Quinidine	181-190	ATP-dependent translocase ABCB1	Oryctolagus cuniculus	109-123
14704918-1	2003	PURPOSE: The objective of this study was to determine the effect of the multi-drug efflux transport protein, P-glycoprotein (P-gp), on the ocular distribution of a model substrate, quinidine.	Quinidine	181-190	ATP-dependent translocase ABCB1	Oryctolagus cuniculus	125-129
14525819-0	2003	The P-glycoprotein inhibitor quinidine decreases the threshold for bupivacaine-induced, but not lidocaine-induced, convulsions in rats.	Quinidine	29-38	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	4-18
14652237-12	2003	In vitro, troleandomycin, an inhibitor of CYP3A4, inhibited the demethylation of tamoxifen to N-desmethyl-tamoxifen by 78% (95% CI = 65% to 91%), and quinidine, an inhibitor of CYP2D6, reduced the subsequent hydroxylation of N-desmethyl-tamoxifen to endoxifen by 79% (95% CI = 50% to 108%).	Quinidine	150-159	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-48
14525949-6	2003	Functionally, KCR1 reduces the sensitivity of HERG to classic proarrhythmic HERG blockers (sotalol, quinidine, dofetilide) in both cardiac and noncardiac cell lines.	Quinidine	100-109	ALG10 alpha-1,2-glucosyltransferase B	Homo sapiens	14-18
14525949-6	2003	Functionally, KCR1 reduces the sensitivity of HERG to classic proarrhythmic HERG blockers (sotalol, quinidine, dofetilide) in both cardiac and noncardiac cell lines.	Quinidine	100-109	potassium voltage-gated channel subfamily H member 2	Homo sapiens	46-50
14738594-7	2003	Secondly, we studied the inhibition of CYP2A6 with clinically used drugs of quinoline compounds, such as norfloxacin as an antibacterial agent, quinidine as an antiarrhythmic agent, quinine and chloroquine as antimalaria agents and rebamipide as an anti-ulcer agent.	Quinidine	144-153	cytochrome P450 2A13	Bos taurus	39-45
14738594-11	2003	These results also show that CYP2A6 discriminates the structure difference between the diastereoisomers quinidine and quinine.	Quinidine	104-113	cytochrome P450 2A13	Bos taurus	29-35
14583678-10	2003	The ABCB1 TT3435 genotype was associated with the most pronounced increase of the miotic effects of loperamide when quinidine was co-administered.	Quinidine	116-125	ATP binding cassette subfamily B member 1	Homo sapiens	4-9
14525819-1	2003	PURPOSE: To examine whether inhibition of P-glycoprotein (P-gp) activity by quinidine affects the central nervous system toxicity of lidocaine and racemic bupivacaine (bupivacaine).	Quinidine	76-85	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	42-56
14525819-1	2003	PURPOSE: To examine whether inhibition of P-glycoprotein (P-gp) activity by quinidine affects the central nervous system toxicity of lidocaine and racemic bupivacaine (bupivacaine).	Quinidine	76-85	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	58-62
14525819-10	2003	CONCLUSION: These results suggest that quinidine inhibited P-gp activity, resulting in increased brain/plasma concentration ratio of bupivacaine, but not of lidocaine, and decreased the threshold of plasma concentration for bupivacaine-induced convulsions.	Quinidine	39-48	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	59-63
12867484-10	2003	Incubation of 2 microM MPPP with 3 microM of the CYP2D6-specific inhibitor quinidine resulted in significant (p &lt; 0.01) turnover inhibition (11.8 +/- 1.6% of control).	Quinidine	75-84	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	49-55
14555336-11	2003	The CYP2D6 specific chemical inhibitor quinidine (3 microM) significantly (p&lt;0.0001) inhibited HO-PPP formation by 91.8 +/- 0.5% (mean +/- SEM) in incubation mixtures with HLM and 2 microM MOPPP.	Quinidine	39-48	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	4-10
12871048-6	2003	The 5-hydroxylation of diclofenac is subject to CYP3A4 cooperativity elicited by quinidine.	Quinidine	81-90	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	48-54
12871048-9	2003	Nevertheless, the in vivo significance of CYP3A cooperativity was demonstrated in a pharmacokinetic study in monkeys, wherein the hepatic clearance of diclofenac increased 2-fold when quinidine was co-administered.	Quinidine	184-193	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-47
14534517-0	2003	Respiratory and miotic effects of morphine in healthy volunteers when P-glycoprotein is blocked by quinidine.	Quinidine	99-108	ATP binding cassette subfamily B member 1	Homo sapiens	70-84
14534517-1	2003	AIM: Our objective was to evaluate whether P-glycoprotein inhibition after quinidine pretreatment results in modified central nervous effects of morphine.	Quinidine	75-84	ATP binding cassette subfamily B member 1	Homo sapiens	43-57
14534517-11	2003	CONCLUSIONS: Whereas morphine clearly produced miosis and respiratory depression, pretreatment with quinidine as an inhibitor of P-glycoprotein did not result in an enhancement of central nervous opioid effects in healthy volunteers.	Quinidine	100-109	ATP binding cassette subfamily B member 1	Homo sapiens	129-143
12725644-6	2003	Development of hypertension was attenuated in Ang II-infused rats treated with quinidine (173+/-6 mmHg) and imipramine (152+/-6 mmHg) (P &lt;0.01).	Quinidine	79-88	angiotensinogen	Rattus norvegicus	46-52
12725644-7	2003	Phosphorylation of ERK1/2, p38MAP kinase and JNK, which were increased 2-3-fold in arteries of the Ang II group, were reduced by quinidine and imipramine (P &lt;0.05).	Quinidine	129-138	mitogen activated protein kinase 3	Rattus norvegicus	19-25
12725644-7	2003	Phosphorylation of ERK1/2, p38MAP kinase and JNK, which were increased 2-3-fold in arteries of the Ang II group, were reduced by quinidine and imipramine (P &lt;0.05).	Quinidine	129-138	mitogen activated protein kinase 14	Rattus norvegicus	27-30
12725644-7	2003	Phosphorylation of ERK1/2, p38MAP kinase and JNK, which were increased 2-3-fold in arteries of the Ang II group, were reduced by quinidine and imipramine (P &lt;0.05).	Quinidine	129-138	mitogen-activated protein kinase 8	Rattus norvegicus	45-48
12725644-7	2003	Phosphorylation of ERK1/2, p38MAP kinase and JNK, which were increased 2-3-fold in arteries of the Ang II group, were reduced by quinidine and imipramine (P &lt;0.05).	Quinidine	129-138	angiotensinogen	Rattus norvegicus	99-105
12725644-9	2003	Quinidine and imipramine reduced the phosphorylation of renal ERK1/2, but did not modify renal p38MAP kinase or JNK.	Quinidine	0-9	mitogen activated protein kinase 3	Rattus norvegicus	62-68
12781333-5	2003	Addition of CYP3A4 substrates (verapamil, midazolam, quinidine, and progesterone) to the oxygenated solution caused a concentration-dependent increase in the reduction current in cyclic voltammetric and amperometric experiments.	Quinidine	53-62	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	12-18
12721332-6	2003	Maximum inhibition of P-gp-mediated efflux of verapamil by rifampin pretreatment in vivo (150 mg/kg) was approximately 55%, whereas there was only approximately 12% inhibition of P-gp-mediated efflux of quinidine at that rifampin dose.	Quinidine	203-212	phosphoglycolate phosphatase	Mus musculus	22-26
12721332-8	2003	However, only approximately 40% inhibition of P-gp-mediated efflux of quinidine was observed with coperfusion of rifampin, even at a 2-fold higher rifampin concentration (1000 microM).	Quinidine	70-79	phosphoglycolate phosphatase	Mus musculus	46-50
12948010-6	2003	Furthermore, a mixture of pH-dependent passive and active efflux was found for the P-glycoprotein (P-gp, MDR1, ABCB1) substrates, talinolol and quinidine, but not for the neutral drug, digoxin.	Quinidine	144-153	ATP binding cassette subfamily B member 1	Homo sapiens	83-97
12948010-8	2003	Hence, the degree of interaction depends on the amount of quinidine available at the binding site of the P-gp.	Quinidine	58-67	ATP binding cassette subfamily B member 1	Homo sapiens	105-109
12948013-5	2003	RESULTS: In situ experimental results revealed that the extent to which the intestinal absorption is affected by P-gp was in the following order: quinidine &gt; ritonavir &gt; loperamide, verapamil, daunomycin &gt; digoxin, cyclosporin A &gt; dexamethasone, and vinblastine.	Quinidine	146-155	ATP binding cassette subfamily B member 1	Homo sapiens	113-117
12754259-7	2003	Pharmacological analysis showed TRESK to be inhibited by previously reported K+ channel inhibitors Ba2+, propafenone, glyburide, lidocaine, quinine, quinidine, and triethanolamine.	Quinidine	149-158	potassium two pore domain channel subfamily K member 18	Homo sapiens	32-37
12893521-7	2003	Additionally, 7-benzyloxyresorufin O-debenzylation by recombinant CYP3A4 was increased by the addition of alpha-naphthoflavone, testosterone and progesterone but not by quinidine, whereas no chemicals tested could activate the O-debenzylation of 7-benzyloxyresorufin by CYP2B6.	Quinidine	169-178	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	66-72
12893521-10	2003	Quinidine and testosterone increased 7-benzyloxyresorufin O-debenzylase and nifedipine oxidase activities, respectively, in human liver microsomes, whereas activation was not observed in CYP3A4.	Quinidine	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	76-94
12695349-1	2003	The effects of microsomal concentration on the inhibitory potencies of four compounds--fluoxetine, quinidine, imipramine, and ezlopitant--on heterologously expressed recombinant CYP2D6-catalyzed bufuralol 1"-hydroxylase activity were determined.	Quinidine	99-108	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	178-184
12948018-11	2003	For structurally diverse P-gp substrates (acebutolol, colchicine, digoxin, etoposide, methylprednisolone, prednisolone, quinidine, and talinolol) apparent Km was approximately 3 to 8-fold greater in absorptive vs. secretory transport direction, whereas apparent J(max) was somewhat similar in both transport directions.	Quinidine	120-129	ATP binding cassette subfamily B member 1	Homo sapiens	25-29
12621387-8	2003	Enterocyte P-glycoprotein content correlated with the area under the plasma concentration-time curve of digoxin (Spearman nonparametric correlation coefficient [r(S)] = -0.73, P =.003) and digoxin nonrenal clearance (r(S) = 0.52, P =.056), as well as with intraluminal and plasma concentrations of quinidine (r(S) = 0.55, P =.041 and r(S) = -0.67, P =.009, respectively).	Quinidine	298-307	ATP binding cassette subfamily B member 1	Homo sapiens	11-25
12695533-2	2003	Here we investigate the molecular mechanisms of voltage-dependent block of human ether-a-go-go-related gene (HERG) delayed rectifier K(+) channels expressed in Xenopus laevis oocytes by quinidine, an antiarrhythmic drug, and vesnarinone, a cardiotonic drug.	Quinidine	186-195	potassium voltage-gated channel subfamily H member 2	Homo sapiens	109-113
12695533-4	2003	Block of HERG by quinidine (and its isomer quinine) was enhanced by progressive membrane depolarization and accompanied by a negative shift in the voltage dependence of channel activation.	Quinidine	17-26	potassium voltage-gated channel subfamily H member 2	Homo sapiens	9-13
12695533-5	2003	As reported previously for other HERG blockers (e.g., MK-499, cisapride, terfenadine, chloroquine), the potency of quinidine was reduced &gt;100-fold by the mutation of key aromatic residues (Y652, F656) located in the S6 domain.	Quinidine	115-124	potassium voltage-gated channel subfamily H member 2	Homo sapiens	33-37
12695533-6	2003	Mutations of Y652 eliminated (Y652F) or reversed (Y652A) the voltage dependence of HERG channel block by quinidine and quinine.	Quinidine	105-114	potassium voltage-gated channel subfamily H member 2	Homo sapiens	83-87
12673723-5	2003	The enhanced proliferation of merlin-deficient NF2 schwannoma cells could be reduced in the presence of quinidine, a K(+) channel blocker, whereas the proliferation of normal Schwann cells is not affected.	Quinidine	104-113	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	30-36
12673723-5	2003	The enhanced proliferation of merlin-deficient NF2 schwannoma cells could be reduced in the presence of quinidine, a K(+) channel blocker, whereas the proliferation of normal Schwann cells is not affected.	Quinidine	104-113	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	47-50
12673723-6	2003	The current study was undertaken to evaluate the effect of quinidine on the proliferation of HMM cell lines in relation to their NF2 status.	Quinidine	59-68	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	129-132
12673723-9	2003	The cytochrome P450 2D6 locus, known to be mutated at high frequencies in NF2 patients and to be specifically inhibited by quinidine, was screened for mutations by cycle sequencing.	Quinidine	123-132	cytochrome P450 2D6	Homo sapiens	4-23
12673723-10	2003	RESULTS: Quinidine selectively reduces the proliferation of merlin-deficient HMM cell lines by causing a G(0)/G(1) arrest, whereas the proliferation rates of merlin-expressing HMM cell lines remain unchanged.	Quinidine	9-18	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	60-66
12673723-11	2003	The effect of quinidine on the proliferation of HMM cell lines appears to be correlated with the NF2 gene status but not with the K(+) outward current.	Quinidine	14-23	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	97-100
12673723-13	2003	CONCLUSIONS: Quinidine or quinidine analogs are of potential therapeutic interest for the subset of merlin-deficient mesothelioma tumors.	Quinidine	13-22	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	100-106
12673723-13	2003	CONCLUSIONS: Quinidine or quinidine analogs are of potential therapeutic interest for the subset of merlin-deficient mesothelioma tumors.	Quinidine	26-35	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	100-106
12642457-6	2003	In their study, they have also demonstrated that quinidine inhibits both CYP2D6- and CYP1A1-mediated debrisoquine 4-hydroxylation.	Quinidine	49-58	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	73-79
12642457-6	2003	In their study, they have also demonstrated that quinidine inhibits both CYP2D6- and CYP1A1-mediated debrisoquine 4-hydroxylation.	Quinidine	49-58	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	85-91
12649369-5	2003	All antidepressants tested except O-desmethylvenlafaxine showed Pgp inhibitory activity with sertraline, desmethylsertraline, and paroxetine being the most potent, comparable with the well known Pgp inhibitor quinidine.	Quinidine	209-218	ATP binding cassette subfamily B member 1	Homo sapiens	195-198
12604693-7	2003	Oral coadministration of quinidine (10 and 30 mg/kg) increased both the extent and the first-order rate of absorption of MRK-1 (2 mg/kg) by approximately 40 to 50% and approximately 100 to 300%, respectively, in rats, thus further substantiating the role of P-gp in modulating the intestinal absorption of MRK-1 in this species.	Quinidine	25-34	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	258-262
12569264-6	2003	The magnitude of the increase was lower ( 0.01) in Ang II groups treated with imipramine (151 +/- 7.4 mmHg) or quinidine (163 +/- 4 mmHg) than in the Ang II only group (205 +/- 4 mmHg).	Quinidine	111-120	angiotensinogen	Rattus norvegicus	51-57
12527726-0	2003	Kv1.4 channel block by quinidine: evidence for a drug-induced allosteric effect.	Quinidine	23-32	potassium voltage-gated channel subfamily A member 4 S homeolog	Xenopus laevis	0-5
18968851-4	2002	Transport of Rho123 was scanned under various conditions (ATP-synthesis inhibition) and several inhibitors of P-glycoprotein transporter were tested (e.g. quinidine).	Quinidine	155-164	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	110-124
12502361-6	2003	MD studies on the binding mode of sparteine, quinidine, and quinine in CYP2D2 and CYP2D6 furthermore concurred well with experimentally determined IC(50) values and metabolic profiles.	Quinidine	45-54	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	82-88
12889657-6	2003	The high- and low-affinity human carnitine transporters, OCTN2 and OCTN1, are multifunctional polyspecific organic cation transporters; therefore, defects in these transporters may have widespread implications for the absorption and/or elimination of a number of key pharmacological agents such as cephalosporins, verapamil, quinidine and valproic acid.	Quinidine	325-334	solute carrier family 22 member 5	Homo sapiens	57-62
12889657-6	2003	The high- and low-affinity human carnitine transporters, OCTN2 and OCTN1, are multifunctional polyspecific organic cation transporters; therefore, defects in these transporters may have widespread implications for the absorption and/or elimination of a number of key pharmacological agents such as cephalosporins, verapamil, quinidine and valproic acid.	Quinidine	325-334	solute carrier family 22 member 4	Homo sapiens	67-72
12433827-0	2002	Quinidine and haloperidol as modifiers of CYP3A4 activity: multisite kinetic model approach.	Quinidine	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-48
12433806-6	2002	quinidine, a CYP2D6-specific inhibitor, inhibited (-)-OSU6162 N-depropylation, whereas other p450 enzyme-specific substrates/inhibitors did not significantly inhibit this activity; 3).	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	13-19
12435814-7	2002	Quinidine was also less potent to block Kvalpha1.5+Kvbeta1.3 channels than Kvalpha1.5 channels (IC(50) = 49.6 microM versus 6.2 microM, respectively).	Quinidine	0-9	potassium voltage-gated channel subfamily A regulatory beta subunit 1	Homo sapiens	40-60
12435814-8	2002	These results suggest that the Kvbeta1.3 subunit does not modify the affinity of the charged bupivacaine for its external receptor site but markedly reduces the affinity of bupivacaine and quinidine for their internal receptor site in hKv1.5 channels.	Quinidine	189-198	potassium voltage-gated channel subfamily A regulatory beta subunit 1	Homo sapiens	31-40
12435814-8	2002	These results suggest that the Kvbeta1.3 subunit does not modify the affinity of the charged bupivacaine for its external receptor site but markedly reduces the affinity of bupivacaine and quinidine for their internal receptor site in hKv1.5 channels.	Quinidine	189-198	potassium voltage-gated channel subfamily A member 5	Homo sapiens	235-241
12353235-0	2002	Myc protein is differentially sensitive to quinidine in tumor versus immortalized breast epithelial cell lines.	Quinidine	43-52	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	0-3
12353235-3	2002	Myc protein levels were suppressed in human breast tumor cell lines, but not in MCF-10A cells, an observation that supports the hypothesis that suppression of c-myc gene expression is involved in the preferential growth and differentiation response of breast tumor cells to quinidine.	Quinidine	274-283	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	0-3
12353235-3	2002	Myc protein levels were suppressed in human breast tumor cell lines, but not in MCF-10A cells, an observation that supports the hypothesis that suppression of c-myc gene expression is involved in the preferential growth and differentiation response of breast tumor cells to quinidine.	Quinidine	274-283	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	159-164
12353235-4	2002	Quinidine reduced c-myc mRNA levels in MCF-7 cells.	Quinidine	0-9	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	18-23
12353235-5	2002	Acute induction of c-myc mRNA by estradiol, as well as the c-myc response to sub-cultivation in fresh serum and H-ras driven elevations in c-myc mRNA were depressed by 50-60% in the presence of quinidine.	Quinidine	194-203	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	19-24
12353235-5	2002	Acute induction of c-myc mRNA by estradiol, as well as the c-myc response to sub-cultivation in fresh serum and H-ras driven elevations in c-myc mRNA were depressed by 50-60% in the presence of quinidine.	Quinidine	194-203	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	59-64
12353235-5	2002	Acute induction of c-myc mRNA by estradiol, as well as the c-myc response to sub-cultivation in fresh serum and H-ras driven elevations in c-myc mRNA were depressed by 50-60% in the presence of quinidine.	Quinidine	194-203	HRas proto-oncogene, GTPase	Homo sapiens	112-117
12353235-5	2002	Acute induction of c-myc mRNA by estradiol, as well as the c-myc response to sub-cultivation in fresh serum and H-ras driven elevations in c-myc mRNA were depressed by 50-60% in the presence of quinidine.	Quinidine	194-203	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	59-64
12353235-6	2002	Quinidine decreased c-myc promoter activity in MCF-7 cells in a transient reporter gene assay and a 168 bp region of human c-myc promoter (-100 to +68 with respect to the P1 promoter) was sufficient to confer responsiveness to quinidine.	Quinidine	0-9	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	20-25
12353235-6	2002	Quinidine decreased c-myc promoter activity in MCF-7 cells in a transient reporter gene assay and a 168 bp region of human c-myc promoter (-100 to +68 with respect to the P1 promoter) was sufficient to confer responsiveness to quinidine.	Quinidine	227-236	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	123-128
12353235-7	2002	Quinidine is a potential lead compound for developing pharmacological agents to regulate Myc.	Quinidine	0-9	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	89-92
12235248-5	2002	In inhibition studies, quinidine, a known CYP2D6 inhibitor, markedly inhibited BF 1"-hydroxylation in the fractions of human liver microsomes that showed the CYP2D6-type selectivity.	Quinidine	23-32	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	42-48
12228192-0	2002	Diclofenac-induced inactivation of CYP3A4 and its stimulation by quinidine.	Quinidine	65-74	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	35-41
12228192-5	2002	Quinidine, a stimulant of CYP3A4-mediated diclofenac 5-hydroxylation, did not affect the inactivation of CYP3A4 assessed by testosterone 6 beta-hydroxylation activity but accelerated the inactivation assessed by diazepam 3-hydroxylation activity.	Quinidine	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	26-32
12235248-5	2002	In inhibition studies, quinidine, a known CYP2D6 inhibitor, markedly inhibited BF 1"-hydroxylation in the fractions of human liver microsomes that showed the CYP2D6-type selectivity.	Quinidine	23-32	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	158-164
12086981-15	2002	Under similar recording conditions QUIN inhibited I(HERG) with an IC(50) of 0.41+/-0.04 microM and PROPAF inhibited I(HERG) with an IC(50) of 0.44+/-0.07 microM.	Quinidine	35-39	potassium voltage-gated channel subfamily H member 2	Homo sapiens	52-56
12167559-7	2002	In incubations with human liver microsomes, quinidine, an inhibitor of CYP2D6, demonstrated little inhibition of metabolite formation while ketoconazole, an inhibitor of CYP3A, demonstrated almost complete inhibition.	Quinidine	44-53	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	71-77
12208456-0	2002	Characterization of quinidine 3-hydroxylation as a probe for the CYP 3A enzyme using a novel capillary electrophoresis technique.	Quinidine	20-29	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	65-71
12086981-21	2002	The rank potency as HERG blockers of the Class I drugs tested in this study was QUIN=PROPAF&gt;FLEC&gt;&gt;LIG.	Quinidine	80-84	potassium voltage-gated channel subfamily H member 2	Homo sapiens	20-24
12006904-5	2002	Two weeks of baseline monitoring were followed by 8 weeks of daily treatment with fluoxetine or quinidine (two potent CYP2D6 inhibitors) or placebo.	Quinidine	96-105	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	118-124
12023534-0	2002	4-Hydroxylation of debrisoquine by human CYP1A1 and its inhibition by quinidine and quinine.	Quinidine	70-79	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	41-47
12023534-5	2002	Additionally and surprisingly, this reaction was also inhibited by quinidine and quinine, with respective IC(50) values of 1.38 +/- 0.10 and 3.31 +/- 0.14 microM, compared with those for CYP2D6 debrisoquine 4-hydroxylase of 0.018 +/- 0.05 and 3.75 +/- 2.07 microM, respectively.	Quinidine	67-76	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	187-193
12023534-5	2002	Additionally and surprisingly, this reaction was also inhibited by quinidine and quinine, with respective IC(50) values of 1.38 +/- 0.10 and 3.31 +/- 0.14 microM, compared with those for CYP2D6 debrisoquine 4-hydroxylase of 0.018 +/- 0.05 and 3.75 +/- 2.07 microM, respectively.	Quinidine	67-76	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	194-220
12006904-8	2002	Quinidine &gt; fluoxetine &gt; placebo inhibited CYP2D6 as reflected in the change of the O-demethylation of dextromethorphan, a specific CYP2D6 probe.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	49-55
12006904-8	2002	Quinidine &gt; fluoxetine &gt; placebo inhibited CYP2D6 as reflected in the change of the O-demethylation of dextromethorphan, a specific CYP2D6 probe.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	138-144
11922628-0	2002	AQR1 gene (ORF YNL065w) encodes a plasma membrane transporter of the major facilitator superfamily that confers resistance to short-chain monocarboxylic acids and quinidine in Saccharomyces cerevisiae.	Quinidine	163-172	Aqr1p	Saccharomyces cerevisiae S288C	0-4
11994058-7	2002	In CYP2D6 poor metabolizers, systemic exposure was greater after chlorpheniramine alone than in extensive metabolizers, and administration of quinidine resulted in a slight increase in CLoral.	Quinidine	142-151	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	3-9
11943152-5	2002	Upon expression in mammalian cells, quinidine blocked hEAG1 channels (IC(50) 1.4 microM) more potently than hEAG2 channels (IC(50) 152 microM), thus providing a useful tool for the functional distinction between hEAG1 and hEAG2 potassium channels.	Quinidine	36-45	potassium voltage-gated channel subfamily H member 1	Homo sapiens	54-59
11943152-5	2002	Upon expression in mammalian cells, quinidine blocked hEAG1 channels (IC(50) 1.4 microM) more potently than hEAG2 channels (IC(50) 152 microM), thus providing a useful tool for the functional distinction between hEAG1 and hEAG2 potassium channels.	Quinidine	36-45	potassium voltage-gated channel subfamily H member 1	Homo sapiens	212-217
11943152-5	2002	Upon expression in mammalian cells, quinidine blocked hEAG1 channels (IC(50) 1.4 microM) more potently than hEAG2 channels (IC(50) 152 microM), thus providing a useful tool for the functional distinction between hEAG1 and hEAG2 potassium channels.	Quinidine	36-45	potassium voltage-gated channel subfamily H member 5	Homo sapiens	222-227
11821009-9	2002	Moreover, the activation of P-gp ATPase by indinavir was inhibited by quinidine.	Quinidine	70-79	ATP binding cassette subfamily B member 1	Homo sapiens	28-32
11814462-0	2002	Influence of the ORM1 phenotypes on serum unbound concentration and protein binding of quinidine.	Quinidine	87-96	orosomucoid 1	Homo sapiens	17-21
11814462-9	2002	Unbound quinidine concentration in ORM1 F1 phenotype subjects was higher than that in ORM1 S and ORM1 F1S phenotype; the free drug percentage for the subjects with ORM1 F1 phenotype (19.79%) was twice as high as that with ORM1 S phenotype (10.96%) (P&lt;0.01) at 24 h after administration of oral quinidine when the state of disposition equilibrium occurred.	Quinidine	8-17	orosomucoid 1	Homo sapiens	35-39
11814462-11	2002	CONCLUSIONS: Different ORM1 phenotypes may affect the disposition of quinidine, a basic drug, rather than its hepatic metabolism and elimination.	Quinidine	69-78	orosomucoid 1	Homo sapiens	23-27
11814462-12	2002	The functional heterogeneity of ORM1 could be responsible for the differences in plasma binding of quinidine.	Quinidine	99-108	orosomucoid 1	Homo sapiens	32-36
11814462-13	2002	Therefore, monitoring of the unbound quinidine concentration would be important for the patients with different ORM1 phenotypes who are treated with quinidine.	Quinidine	37-46	orosomucoid 1	Homo sapiens	112-116
11814462-13	2002	Therefore, monitoring of the unbound quinidine concentration would be important for the patients with different ORM1 phenotypes who are treated with quinidine.	Quinidine	149-158	orosomucoid 1	Homo sapiens	112-116
11883641-7	2002	The Ki values of ibuprofen and quinidine were estimated to be 19 and 13 times lower for Oatpl compared with Oatp2, whereas the values for rifampicin, quinine, and digoxin were 13, 20, and 100&lt; times lower for Oatp2 compared with Oatpl.	Quinidine	31-40	solute carrier organic anion transporter family, member 1a4	Rattus norvegicus	108-113
11821009-6	2002	Pretreatment of the BBB model with the P-gp inhibitor, quinidine, significantly increased apical to basal transport.	Quinidine	55-64	ATP binding cassette subfamily B member 1	Homo sapiens	39-43
11816004-2	2002	3OHQ is the CYP 3A4 metabolite of quinidine sulfate (QS) and is therefore useful for metabolism screening studies.	Quinidine	34-51	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	12-19
11816004-2	2002	3OHQ is the CYP 3A4 metabolite of quinidine sulfate (QS) and is therefore useful for metabolism screening studies.	Quinidine	53-55	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	12-19
11684147-4	2001	I(K(DR)) present in these cells is sensitive to the inhibition by quinidine and dendrotoxin, yet not by E-4031.	Quinidine	66-75	kinase insert domain protein receptor	Mus musculus	2-7
11825096-8	2002	Lack of morphine formation from codeine as a result of CYP2D6 inhibition by quinidine results in an almost complete loss of the analgesic effects of codeine.	Quinidine	76-85	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	55-61
11560868-5	2001	The formation of (+)-9-hydroxyrisperidone was strongly inhibited by quinidine, a potent CYP2D6 inhibitor, whereas ketoconazole, a CYP3A4 inhibitor, strongly inhibited the formation of (-)-9-hydroxyrisperidone.	Quinidine	68-77	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	88-94
11765139-0	2001	Differential inhibition of human CYP1A1 and CYP1A2 by quinidine and quinine.	Quinidine	54-63	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	33-39
11765139-0	2001	Differential inhibition of human CYP1A1 and CYP1A2 by quinidine and quinine.	Quinidine	54-63	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	44-50
11765139-2	2001	The inhibition of recombinant CYP1A1 and CYP1A2 activity by quinidine and quinine was evluated using ethoxyresorutin O-deethylation, phenacetin O-deethylation and propranolol desisopropylation as probe catalytic pathways.	Quinidine	60-69	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	30-36
11765139-2	2001	The inhibition of recombinant CYP1A1 and CYP1A2 activity by quinidine and quinine was evluated using ethoxyresorutin O-deethylation, phenacetin O-deethylation and propranolol desisopropylation as probe catalytic pathways.	Quinidine	60-69	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	41-47
11765139-4	2001	With substrate concentrations near the Km of catalysis, both quinidine and quinine potently inhibited CYP1A1 activity with [I](0.5) approximately 1-3 microM, whereas in contrast, there was little inhibition of CYP1A2 activity.	Quinidine	61-70	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	102-108
11765139-7	2001	There was only trace metabolism of quinidine by recombinant CYP1A1, whereas rat liver microsomes as a control showed extensive consumption of quinidine and metabolite production.	Quinidine	35-44	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	60-66
11765139-9	2001	This work suggests that quinidine is a non-classical inhibitor of CYP1A1 and that it is not as highly specific at inhibiting CYP2D6 as previously thought.	Quinidine	24-33	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	66-72
11691539-9	2001	RESULTS: E-4031, 4-AP, tetra-ethylammonium and quinidine induced phosphorylation of ERK.	Quinidine	47-56	Eph receptor B1	Rattus norvegicus	84-87
11602243-1	2001	We did the experiments to search for amino acids that affect quinidine binding to the HERG channel, and have identified an amino acid whose change by mutation affects the binding of various drugs.	Quinidine	61-70	potassium voltage-gated channel subfamily H member 2	Homo sapiens	86-90
11703413-7	2001	In one patient, GP V-specific antibodies were associated with quinidine-induced thrombocytopenia.	Quinidine	62-71	glycoprotein V platelet	Homo sapiens	16-20
11560869-4	2001	This metabolite was also formed by cDNA expressed CYP2D6, and the reaction in human liver microsomes was inhibited by quinidine.	Quinidine	118-127	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	50-56
11504821-8	2001	The efflux of etoposide, a known substrate for both Pgp and MRP1, was shown to be mainly Pgp-mediated by using the multidrug-resistant inhibitors quinidine (mixed Pgp/MRP1), CsA (Pgp), and MK571 (MRP1).	Quinidine	146-155	ATP binding cassette subfamily B member 1	Homo sapiens	52-55
11504821-8	2001	The efflux of etoposide, a known substrate for both Pgp and MRP1, was shown to be mainly Pgp-mediated by using the multidrug-resistant inhibitors quinidine (mixed Pgp/MRP1), CsA (Pgp), and MK571 (MRP1).	Quinidine	146-155	ATP binding cassette subfamily C member 1	Homo sapiens	60-64
11504821-8	2001	The efflux of etoposide, a known substrate for both Pgp and MRP1, was shown to be mainly Pgp-mediated by using the multidrug-resistant inhibitors quinidine (mixed Pgp/MRP1), CsA (Pgp), and MK571 (MRP1).	Quinidine	146-155	ATP binding cassette subfamily B member 1	Homo sapiens	89-92
11504821-8	2001	The efflux of etoposide, a known substrate for both Pgp and MRP1, was shown to be mainly Pgp-mediated by using the multidrug-resistant inhibitors quinidine (mixed Pgp/MRP1), CsA (Pgp), and MK571 (MRP1).	Quinidine	146-155	ATP binding cassette subfamily B member 1	Homo sapiens	89-92
11504821-8	2001	The efflux of etoposide, a known substrate for both Pgp and MRP1, was shown to be mainly Pgp-mediated by using the multidrug-resistant inhibitors quinidine (mixed Pgp/MRP1), CsA (Pgp), and MK571 (MRP1).	Quinidine	146-155	ATP binding cassette subfamily C member 1	Homo sapiens	167-171
11504821-8	2001	The efflux of etoposide, a known substrate for both Pgp and MRP1, was shown to be mainly Pgp-mediated by using the multidrug-resistant inhibitors quinidine (mixed Pgp/MRP1), CsA (Pgp), and MK571 (MRP1).	Quinidine	146-155	ATP binding cassette subfamily B member 1	Homo sapiens	89-92
11504821-8	2001	The efflux of etoposide, a known substrate for both Pgp and MRP1, was shown to be mainly Pgp-mediated by using the multidrug-resistant inhibitors quinidine (mixed Pgp/MRP1), CsA (Pgp), and MK571 (MRP1).	Quinidine	146-155	ATP binding cassette subfamily C member 1	Homo sapiens	167-171
11489261-7	2001	In mice treated with MPTP and a P-GP inhibitor (quinidine, trans-flupentixol or cyclosporine A), the elimination of MPP(+) from the striatum was significantly delayed.	Quinidine	48-57	phosphoglycolate phosphatase	Mus musculus	32-36
11489261-11	2001	In other studies, we demonstrated that the VMAT2 inhibitors tetrabenazine and Ro 4-1284 inhibit P-GP and that the P-GP inhibitors trans-flupentixol and quinidine inhibit VMAT2.	Quinidine	152-161	phosphoglycolate phosphatase	Mus musculus	114-118
11489261-11	2001	In other studies, we demonstrated that the VMAT2 inhibitors tetrabenazine and Ro 4-1284 inhibit P-GP and that the P-GP inhibitors trans-flupentixol and quinidine inhibit VMAT2.	Quinidine	152-161	solute carrier family 18 (vesicular monoamine), member 2	Mus musculus	170-175
11454734-9	2001	Tramadol metabolism in human liver microsomes to M1 and M2 was markedly inhibited by the CYP2D6 inhibitor quinidine and the CYP3A4 inhibitor troleandomycin, respectively.	Quinidine	106-115	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	89-95
11689122-5	2001	In incubations containing either pooled microsomes or recombinant CYP2D6, [(14)C]dextromethorphan O-demethylase activity was inhibited in the presence of quinidine (IC(50) = 1.0 microM and 20 nM, respectively).	Quinidine	154-163	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	66-72
11519155-3	2001	The elimination of TCAs is impaired by CYP2D6 inhibitors such as quinidine.	Quinidine	65-74	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	39-45
11470516-0	2001	Novel target genes of the yeast regulator Pdr1p: a contribution of the TPO1 gene in resistance to quinidine and other drugs.	Quinidine	98-107	drug-responsive transcription factor PDR1	Saccharomyces cerevisiae S288C	42-47
11470516-0	2001	Novel target genes of the yeast regulator Pdr1p: a contribution of the TPO1 gene in resistance to quinidine and other drugs.	Quinidine	98-107	Tpo1p	Saccharomyces cerevisiae S288C	71-75
11470516-4	2001	The drug sensitivity of the strains deleted for these genes revealed that TPO1, a gene previously found to be involved in spermidine resistance and vacuolar polyamine transport, is a determinant of multidrug transporter since it also mediates growth resistance to cycloheximide and quinidine.	Quinidine	282-291	Tpo1p	Saccharomyces cerevisiae S288C	74-78
11408374-5	2001	In pooled human liver microsomes, formation of both metabolites was partially inhibited by both quinidine and ketoconazole, suggesting that CYP2D6 and CYP3A enzymes are involved in the metabolism of CJ-12,458.	Quinidine	96-105	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	140-146
11408374-5	2001	In pooled human liver microsomes, formation of both metabolites was partially inhibited by both quinidine and ketoconazole, suggesting that CYP2D6 and CYP3A enzymes are involved in the metabolism of CJ-12,458.	Quinidine	96-105	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	151-156
11377054-0	2001	A direct injection capillary electrophoretic technique for miniaturized high-throughput metabolic screening of the CYP 3A4 enzyme using quinidine as a probe.	Quinidine	136-145	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	115-122
11377054-2	2001	3-OHQ is the CYP 3A4 metabolite of QS and hence useful for metabolism screening studies.	Quinidine	35-37	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	13-20
11408531-6	2001	Finally, the data demonstrate that unmethylated quinidine is transported by rOCT1, hOCT1, and OATP-A at pH 6.0, but not at pH 7.5, indicating that quinidine requires a positive charge for carrier-mediated uptake into hepatocytes.	Quinidine	48-57	solute carrier family 22 member 1	Rattus norvegicus	76-81
11408531-6	2001	Finally, the data demonstrate that unmethylated quinidine is transported by rOCT1, hOCT1, and OATP-A at pH 6.0, but not at pH 7.5, indicating that quinidine requires a positive charge for carrier-mediated uptake into hepatocytes.	Quinidine	48-57	solute carrier family 22 member 1	Homo sapiens	83-88
11408531-6	2001	Finally, the data demonstrate that unmethylated quinidine is transported by rOCT1, hOCT1, and OATP-A at pH 6.0, but not at pH 7.5, indicating that quinidine requires a positive charge for carrier-mediated uptake into hepatocytes.	Quinidine	48-57	solute carrier organic anion transporter family member 1A2	Homo sapiens	94-100
11408531-6	2001	Finally, the data demonstrate that unmethylated quinidine is transported by rOCT1, hOCT1, and OATP-A at pH 6.0, but not at pH 7.5, indicating that quinidine requires a positive charge for carrier-mediated uptake into hepatocytes.	Quinidine	147-156	solute carrier family 22 member 1	Rattus norvegicus	76-81
11408531-6	2001	Finally, the data demonstrate that unmethylated quinidine is transported by rOCT1, hOCT1, and OATP-A at pH 6.0, but not at pH 7.5, indicating that quinidine requires a positive charge for carrier-mediated uptake into hepatocytes.	Quinidine	147-156	solute carrier family 22 member 1	Homo sapiens	83-88
11408531-6	2001	Finally, the data demonstrate that unmethylated quinidine is transported by rOCT1, hOCT1, and OATP-A at pH 6.0, but not at pH 7.5, indicating that quinidine requires a positive charge for carrier-mediated uptake into hepatocytes.	Quinidine	147-156	solute carrier organic anion transporter family member 1A2	Homo sapiens	94-100
11496955-5	2001	RESULTS: Genetic disruption of mdr1a P-gp resulted in 1.3-, 6.6- and 14-fold increases in Clup for morphine, verapamil and quinidine, respectively.	Quinidine	123-132	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	31-36
11496955-5	2001	RESULTS: Genetic disruption of mdr1a P-gp resulted in 1.3-, 6.6- and 14-fold increases in Clup for morphine, verapamil and quinidine, respectively.	Quinidine	123-132	phosphoglycolate phosphatase	Mus musculus	37-41
11496955-7	2001	Saturable transport of verapamil and quinidine was observed only in P-gp-competent mice, with apparent IC50 values for efflux of 8.6 +/- 2.3 microM and 36 +/- 2 microM, respectively.	Quinidine	37-46	phosphoglycolate phosphatase	Mus musculus	68-72
11496955-12	2001	CONCLUSIONS: P-gp decreases Clup of morphine, verapamil and quinidine in situ with little or no influence of gender, but this effect cannot fully account for the effects of P-gp in vivo.	Quinidine	60-69	phosphoglycolate phosphatase	Mus musculus	13-17
11496955-13	2001	P-gp is the only saturable transport mechanism for verapamil and quinidine at the murine blood-brain barrier.	Quinidine	65-74	phosphoglycolate phosphatase	Mus musculus	0-4
11469725-6	2001	Examples of in vivo CYP cooperativity are rare; representative cases include flavone-dependent stimulation of zoxazolamine metabolism in rats and enhancement of CYP3A-mediated hepatic clearance of diclofenac by quinidine in monkeys.	Quinidine	211-220	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	161-166
11302822-0	2001	Resistance and adaptation to quinidine in Saccharomyces cerevisiae: role of QDR1 (YIL120w), encoding a plasma membrane transporter of the major facilitator superfamily required for multidrug resistance.	Quinidine	29-38	multidrug transporter	Saccharomyces cerevisiae S288C	76-80
11353755-6	2001	Addition of quinidine, a reversible inhibitor of CYP2D6, to a preincubation mixture consisting of SCH 66712, HL microsomes, or Supersomes and NADPH partially protected CYP2D6 from inactivation.	Quinidine	12-21	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	49-55
11353755-6	2001	Addition of quinidine, a reversible inhibitor of CYP2D6, to a preincubation mixture consisting of SCH 66712, HL microsomes, or Supersomes and NADPH partially protected CYP2D6 from inactivation.	Quinidine	12-21	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	168-174
11353757-1	2001	It has been demonstrated that the activity of cytochrome P450 (CYP)3A4 in certain cases is stimulated by quinidine (positive heterotropic cooperativity).	Quinidine	105-114	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	46-70
11353757-5	2001	Stimulatory effects of quinidine also were observed with recombinant CYP3A4, suggesting that increases in warfarin metabolism were due to quinidine-mediated enhancement of CYP3A4 activity.	Quinidine	23-32	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	69-75
11353757-5	2001	Stimulatory effects of quinidine also were observed with recombinant CYP3A4, suggesting that increases in warfarin metabolism were due to quinidine-mediated enhancement of CYP3A4 activity.	Quinidine	23-32	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	172-178
11353757-5	2001	Stimulatory effects of quinidine also were observed with recombinant CYP3A4, suggesting that increases in warfarin metabolism were due to quinidine-mediated enhancement of CYP3A4 activity.	Quinidine	138-147	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	69-75
11353757-5	2001	Stimulatory effects of quinidine also were observed with recombinant CYP3A4, suggesting that increases in warfarin metabolism were due to quinidine-mediated enhancement of CYP3A4 activity.	Quinidine	138-147	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	172-178
11356921-4	2001	Fluorescein/probenecid and quinidine/LY-335979 were chosen as the substrate/inhibitor combinations for organic anion transport and P-glycoprotein-medicated transport, respectively.	Quinidine	27-36	ATP binding cassette subfamily B member 1	Homo sapiens	131-145
11302822-2	2001	Yil120wp was implicated in yeast resistance to ketoconazole and quinidine, but not to the stereoisomer quinine; the gene was thus named QDR1.	Quinidine	64-73	multidrug transporter	Saccharomyces cerevisiae S288C	136-140
11302822-3	2001	Qdr1p was proved to alleviate the deleterious effects of quinidine, revealed by the loss of cell viability following sudden exposure of the unadapted yeast population to the drug, and to allow the earlier eventual resumption of exponential growth under quinidine stress.	Quinidine	57-66	multidrug transporter	Saccharomyces cerevisiae S288C	0-5
11302822-3	2001	Qdr1p was proved to alleviate the deleterious effects of quinidine, revealed by the loss of cell viability following sudden exposure of the unadapted yeast population to the drug, and to allow the earlier eventual resumption of exponential growth under quinidine stress.	Quinidine	253-262	multidrug transporter	Saccharomyces cerevisiae S288C	0-5
11302822-8	2001	Results clearly suggest that there are other unidentified quinidine resistance mechanisms that can be used in the absence of QDR1.	Quinidine	58-67	multidrug transporter	Saccharomyces cerevisiae S288C	125-129
11556126-7	2001	(3-[m-(1-piperidinylmethyl)-phenoxy]propionic acid) and M-3 (m-(1-piperidinylmethyl) phenol) formation from M-5 were inhibited by quinidine and anti-CYP2D6 serum.	Quinidine	130-139	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	149-155
11278387-6	2001	Imipramine and quinidine (putative inhibitors of the Na(+)/Mg(2+) exchanger) and removal of extracellular Na(+) abrogated Ang II-mediated [Mg(2+)](i) effects.	Quinidine	15-24	ANG	Canis lupus familiaris	122-125
11334347-7	2001	The CYP2D6 inhibition assay has been validated using quinidine as a known selective inhibitor of the isoform.	Quinidine	53-62	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	4-10
11266079-9	2001	Quinidine inhibited bufuralol 1"-hydroxylation in liver microsomes, particularly at low substrate concentrations, in individuals with CYP2D6*1/*1, and 1/1*2, but not those with CYP2D6*4/*4 and very slightly in individuals with CYP2D6*10B/*10B.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	134-140
11336351-6	2001	The potency of inhibition of P-gp was cyclosporine &gt; tacrolimus &gt; quinidine &gt; verapamil &gt; vinblastine.	Quinidine	72-81	ATP binding cassette subfamily B member 1	Homo sapiens	29-33
11432537-8	2001	Quinidine is a potent inhibitor of CYP2D6, but it appears that this enzyme does not mediate the metabolism of any other antimalarial agent.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	35-41
11113407-3	2000	Low-dose quinidine may promote the efficacy of propafenone by inhibiting its degradation through the cytochrome P450 pathway (CYP2D6).	Quinidine	9-18	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	126-132
11061580-0	2000	In vivo modulation of CYP enzymes by quinidine and rifampin.	Quinidine	37-46	peptidylprolyl isomerase G	Homo sapiens	22-25
11061580-6	2000	RESULTS: Quinidine selectively and almost completely inhibited the activity of CYP2D6 from day 3 through day 28 without affecting any other enzymes.	Quinidine	9-18	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	79-85
11061580-8	2000	The quinidine/rifampin combination resulted in selective CYP2D6 inhibition and induction of all other enzymes evaluated over this time period, suggesting that predictable complex interactions occur with the drug combination.	Quinidine	4-13	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	57-63
10938272-5	2000	Hyperacetylated histone H4 appeared within 2 h of the addition of quinidine to the medium, and levels were maximal by 24 h. Quinidine-treated MCF-7 cells showed elevated p21(WAF1), hypophosphorylation and suppression of retinoblastoma protein, and down-regulation of cyclin D1, similar to the cell cycle response observed with cells induced to differentiate by histone deacetylase inhibitors, trichostatin A, and trapoxin.	Quinidine	124-133	cyclin dependent kinase inhibitor 1A	Homo sapiens	170-173
10938272-5	2000	Hyperacetylated histone H4 appeared within 2 h of the addition of quinidine to the medium, and levels were maximal by 24 h. Quinidine-treated MCF-7 cells showed elevated p21(WAF1), hypophosphorylation and suppression of retinoblastoma protein, and down-regulation of cyclin D1, similar to the cell cycle response observed with cells induced to differentiate by histone deacetylase inhibitors, trichostatin A, and trapoxin.	Quinidine	124-133	cyclin dependent kinase inhibitor 1A	Homo sapiens	174-178
10938272-5	2000	Hyperacetylated histone H4 appeared within 2 h of the addition of quinidine to the medium, and levels were maximal by 24 h. Quinidine-treated MCF-7 cells showed elevated p21(WAF1), hypophosphorylation and suppression of retinoblastoma protein, and down-regulation of cyclin D1, similar to the cell cycle response observed with cells induced to differentiate by histone deacetylase inhibitors, trichostatin A, and trapoxin.	Quinidine	124-133	cyclin D1	Homo sapiens	267-276
10938272-7	2000	HDAC1 was undetectable in MCF-7 cells 30 min after addition of quinidine to the growth medium.	Quinidine	63-72	histone deacetylase 1	Homo sapiens	0-5
10938272-8	2000	The proteasome inhibitors MG-132 and lactacystin completely protected HDAC1 from the action of quinidine.	Quinidine	95-104	histone deacetylase 1	Homo sapiens	70-75
10938272-9	2000	We conclude that quinidine is a breast tumor cell differentiating agent that causes the loss of HDAC1 via a proteasomal sensitive mechanism.	Quinidine	17-26	histone deacetylase 1	Homo sapiens	96-101
10924511-6	2000	Tolterodine inhibited the microsomal 25-hydroxylation, whereas quinidine, an inhibitor of CYP2D6, did not markedly inhibit the reaction.	Quinidine	63-72	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	90-96
10997938-7	2000	These data were corroborated with the examination of the effects of CYP-specific inhibitors quinidine (CYP2D6), sulfaphenazole (CYP2C9), and ketoconazole (CYP3A4) on fluoxetine N-demethylation in pooled human liver microsomes.	Quinidine	92-101	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	103-109
10950847-0	2000	Cytochrome P450 3A4-mediated interaction of diclofenac and quinidine.	Quinidine	59-68	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-19
11128045-5	2000	Production of desmethylranitidine by rat and human liver microsomes was inhibited by tranylcypromine, a-naphthoflavon and quinidine, which are known to inhibit CYP2C19, 1A2 and 2D6, repectively.	Quinidine	122-131	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	160-167
10950860-5	2000	The M1 formation from R(+)-cibenzoline was highly correlated with bufuralol 1"-hydroxylation and CYP2D6 content and was inhibited by quinidine, a potent inhibitor of CYP2D6.	Quinidine	133-142	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	97-103
10950860-5	2000	The M1 formation from R(+)-cibenzoline was highly correlated with bufuralol 1"-hydroxylation and CYP2D6 content and was inhibited by quinidine, a potent inhibitor of CYP2D6.	Quinidine	133-142	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	166-172
10950860-9	2000	Ketoconazole, which is a potent inhibitor of CYP3A4/5, had a strong inhibitory effect on their formation, and the M4 formation from R(+)-cibenzoline was inhibited by quinidine by 45%.	Quinidine	166-175	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	45-53
10887187-7	2000	In a physiological K(+) gradient, TWIK-2 is half inhibited by 0.1 mm Ba(2+), quinine, and quinidine.	Quinidine	90-99	potassium two pore domain channel subfamily K member 6	Homo sapiens	34-40
10976551-11	2000	CONCLUSION: The formation clearance of 3-hydroxyquinidine after a single oral dose of 200 mg quinidine sulfate may represent a useful index of CYP3A4 activity in vivo.	Quinidine	93-110	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	143-149
10942385-11	2000	Analysis of 20 sera from patients with quinidine-induced thrombocytopenia by MAIPA assay revealed evidence that DDAbs against PECAM-1 are involved in addition to anti-GPIb/IX and anti-GPIIb/IIIa.	Quinidine	39-48	platelet and endothelial cell adhesion molecule 1	Homo sapiens	126-133
10942385-11	2000	Analysis of 20 sera from patients with quinidine-induced thrombocytopenia by MAIPA assay revealed evidence that DDAbs against PECAM-1 are involved in addition to anti-GPIb/IX and anti-GPIIb/IIIa.	Quinidine	39-48	integrin subunit alpha 2b	Homo sapiens	184-189
10945865-5	2000	Significant correlations were noted between propranolol 4-hydroxylation and ethoxyresorufin-O-deethylation (marker of CYP1A2 activity), with marked improvement in the correlations when CYP2D6-mediated propranolol 4-hydroxylation was inhibited with quinidine.	Quinidine	248-257	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	185-191
10996483-4	2000	Compared to control incubations (no inhibitor) where cholinesterase activity was inhibited to between 1 and 4% of control levels, incorporation of the CYP2D6 inhibitor quinidine into the microsomal incubation resulted in cholinesterase activity of 50% for parathion, 38% for diazinon and 30% for chlorpyrifos.	Quinidine	168-177	butyrylcholinesterase	Homo sapiens	53-67
10996483-4	2000	Compared to control incubations (no inhibitor) where cholinesterase activity was inhibited to between 1 and 4% of control levels, incorporation of the CYP2D6 inhibitor quinidine into the microsomal incubation resulted in cholinesterase activity of 50% for parathion, 38% for diazinon and 30% for chlorpyrifos.	Quinidine	168-177	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	151-157
10996483-4	2000	Compared to control incubations (no inhibitor) where cholinesterase activity was inhibited to between 1 and 4% of control levels, incorporation of the CYP2D6 inhibitor quinidine into the microsomal incubation resulted in cholinesterase activity of 50% for parathion, 38% for diazinon and 30% for chlorpyrifos.	Quinidine	168-177	butyrylcholinesterase	Homo sapiens	221-235
11501186-8	2000	Inhibition experiments showed that troleandomycin (100 mumol.L-1) and diethyldithiocarbamate (100 mumol.L-1), as potent CYP3A4 and CYP2E1 inhibitors, respectively, reduced the formation rate of CG by 81.1% and 47.23%, while quinidine (10 mumol.L-1), furafylline (20 mumol.L-1), and sulfaphenazole (10 mumol.L-1), which were inhibitors towards CYP2D6, 1A2 and 2C9/10, respectively, did not display significant inhibition.	Quinidine	224-233	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	120-126
11501186-8	2000	Inhibition experiments showed that troleandomycin (100 mumol.L-1) and diethyldithiocarbamate (100 mumol.L-1), as potent CYP3A4 and CYP2E1 inhibitors, respectively, reduced the formation rate of CG by 81.1% and 47.23%, while quinidine (10 mumol.L-1), furafylline (20 mumol.L-1), and sulfaphenazole (10 mumol.L-1), which were inhibitors towards CYP2D6, 1A2 and 2C9/10, respectively, did not display significant inhibition.	Quinidine	224-233	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	131-137
10976551-0	2000	Quinidine as a probe for CYP3A4 activity: intrasubject variability and lack of correlation with probe-based assays for CYP1A2, CYP2C9, CYP2C19, and CYP2D6.	Quinidine	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	25-31
10976551-1	2000	BACKGROUND: In vitro studies have shown that the formation of 3-hydroxyquinidine from quinidine is catalyzed almost exclusively by CYP3A4.	Quinidine	71-80	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	131-137
10964617-0	2000	Enhanced proliferation and potassium conductance of Schwann cells isolated from NF2 schwannomas can be reduced by quinidine.	Quinidine	114-123	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	80-83
10964617-6	2000	Importantly, treatment with quinidine reduces proliferation of NF2 Schwann cells in a concentration dependent manner but did not reduce proliferation of normal Schwann cells.	Quinidine	28-37	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	63-66
10964617-7	2000	Therefore, the use of quinidine or quinidine-like components would possibly provide a novel adjuvant therapeutic option for NF2 patients to slow down or freeze growth of schwannomas.	Quinidine	22-31	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	124-127
10964617-7	2000	Therefore, the use of quinidine or quinidine-like components would possibly provide a novel adjuvant therapeutic option for NF2 patients to slow down or freeze growth of schwannomas.	Quinidine	35-44	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	124-127
10803680-6	2000	Treatment of blood cultures with 25 microM diethyldithiocarbamate (DDC), a specific CYP2E1 inhibitor, or 0.5 microM quinidine, a specific CYP2D6 inhibitor, simultaneously with NNK, significantly decreased NNK-induced chromosome aberration.	Quinidine	116-125	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	138-144
10806376-9	2000	The reaction was sensitive to inhibition by the CYP2D6-selective inhibitors quinidine, quinine, lobeline and norfluoxetine, whereas chemical inhibitors selective for other CYP isoforms failed to affect the reaction.	Quinidine	76-85	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	48-54
10806376-9	2000	The reaction was sensitive to inhibition by the CYP2D6-selective inhibitors quinidine, quinine, lobeline and norfluoxetine, whereas chemical inhibitors selective for other CYP isoforms failed to affect the reaction.	Quinidine	76-85	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	48-51
10838122-3	2000	Results showed that the accumulation of P-gp substrates calcein-AM and vinblastine by BeWo cells or primary cultures of human cytotrophoblasts was significantly enhanced in the presence of a typical P-gp inhibitor, cyclosporin-A, or other inhibitors such as quinidine, verapamil, and dipyridamole.	Quinidine	258-267	ATP binding cassette subfamily B member 1	Homo sapiens	40-44
10838122-3	2000	Results showed that the accumulation of P-gp substrates calcein-AM and vinblastine by BeWo cells or primary cultures of human cytotrophoblasts was significantly enhanced in the presence of a typical P-gp inhibitor, cyclosporin-A, or other inhibitors such as quinidine, verapamil, and dipyridamole.	Quinidine	258-267	ATP binding cassette subfamily B member 1	Homo sapiens	199-203
10736425-7	2000	Moreover, using IAAQ, we showed that molar excesses of chloroquine, quinine, quinidine, and MK-571 inhibit the photoaffinity labeling of MRP.	Quinidine	77-86	ATP binding cassette subfamily C member 3	Homo sapiens	137-140
10772630-5	2000	Known Pgp inhibitors, such as cyclosporin A, nicardipine, verapamil, quinidine, terfenadine, tamoxifen, and vinblastine were demonstrated to inhibit the Pgp-mediated efflux of daunorubicin.	Quinidine	69-78	ATP binding cassette subfamily B member 1	Homo sapiens	6-9
10772630-5	2000	Known Pgp inhibitors, such as cyclosporin A, nicardipine, verapamil, quinidine, terfenadine, tamoxifen, and vinblastine were demonstrated to inhibit the Pgp-mediated efflux of daunorubicin.	Quinidine	69-78	ATP binding cassette subfamily B member 1	Homo sapiens	153-156
10821163-3	2000	The results indicate that sulphaphenazole, quinidine and alpha-naphthoflavone are selective inhibitors of CYP2C9 (IC50 = 0.5-0.7 microM), CYP2D6 (0.3-0.4 microM) and CYP1A (0.05-5 microM) respectively on the basis of the IC50, which are much lower than those of other P450 isoforms (&gt; 10-fold).	Quinidine	43-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	106-112
10821163-3	2000	The results indicate that sulphaphenazole, quinidine and alpha-naphthoflavone are selective inhibitors of CYP2C9 (IC50 = 0.5-0.7 microM), CYP2D6 (0.3-0.4 microM) and CYP1A (0.05-5 microM) respectively on the basis of the IC50, which are much lower than those of other P450 isoforms (&gt; 10-fold).	Quinidine	43-52	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	138-144
10821163-3	2000	The results indicate that sulphaphenazole, quinidine and alpha-naphthoflavone are selective inhibitors of CYP2C9 (IC50 = 0.5-0.7 microM), CYP2D6 (0.3-0.4 microM) and CYP1A (0.05-5 microM) respectively on the basis of the IC50, which are much lower than those of other P450 isoforms (&gt; 10-fold).	Quinidine	43-52	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	268-272
10821163-10	2000	Furafylline, quinidine and alpha-naphthoflavone activated CYP3A4-catalysed phenanthrene metabolism by 1.7-, 2- and 15-fold respectively.	Quinidine	13-22	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-64
10671914-0	2000	Inhibition of debrisoquine hydroxylation with quinidine in subjects with three or more functional CYP2D6 genes.	Quinidine	46-55	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	98-104
10677595-4	2000	Inhibition studies using ketoconazole, furafylline, sulfaphenazole, omeprazole and quinidine suggested that CYP3A4 is the isoform responsible for this reaction whereas CYP1A2, CYP2C9, CYP2C19 and CYP2D6 do not seem to be involved.	Quinidine	83-92	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	108-114
10677595-4	2000	Inhibition studies using ketoconazole, furafylline, sulfaphenazole, omeprazole and quinidine suggested that CYP3A4 is the isoform responsible for this reaction whereas CYP1A2, CYP2C9, CYP2C19 and CYP2D6 do not seem to be involved.	Quinidine	83-92	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	184-191
10677595-4	2000	Inhibition studies using ketoconazole, furafylline, sulfaphenazole, omeprazole and quinidine suggested that CYP3A4 is the isoform responsible for this reaction whereas CYP1A2, CYP2C9, CYP2C19 and CYP2D6 do not seem to be involved.	Quinidine	83-92	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	196-202
10706193-5	2000	Human P-glycoprotein has been shown to transport a wide range of structurally unrelated drugs such as digoxin, quinidine, cyclosporine and HIV-1 protease inhibitors.	Quinidine	111-120	ATP binding cassette subfamily B member 1	Homo sapiens	6-20
10706193-7	2000	Moreover, P-glycoprotein knock-out mice were used to identify inhibition of P-glycoprotein-mediated transport as a mechanism for drug interactions such as the digoxin-quinidine interaction.	Quinidine	167-176	ATP binding cassette subfamily B member 1	Homo sapiens	10-24
10706193-7	2000	Moreover, P-glycoprotein knock-out mice were used to identify inhibition of P-glycoprotein-mediated transport as a mechanism for drug interactions such as the digoxin-quinidine interaction.	Quinidine	167-176	ATP binding cassette subfamily B member 1	Homo sapiens	76-90
10831384-1	2000	A multidrug-resistant strain of Plasmodium yoelii nigeriensis (MDR) showing a wide spectrum of resistance to chloroquine, amodiaquine, mepacrine, mefloquine, halofantrine, quinine, and quinidine was used in this study for in vivo evaluation of the blood schizontocidal activity of pyronaridine, a topoisomerase II inhibitor, in Swiss mice.	Quinidine	185-194	malic enzyme complex, mitochondrial	Mus musculus	63-66
10671914-1	2000	AIMS: To study whether the CYP2D6 capacity in ultrarapid metabolizers of debrisoquine due to duplication/multiduplication of a functional CYP2D6 gene, can be "normalised" by low doses of the CYP2D6 inhibitor quinidine and whether this is dose-dependent.	Quinidine	208-217	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	27-33
10671914-1	2000	AIMS: To study whether the CYP2D6 capacity in ultrarapid metabolizers of debrisoquine due to duplication/multiduplication of a functional CYP2D6 gene, can be "normalised" by low doses of the CYP2D6 inhibitor quinidine and whether this is dose-dependent.	Quinidine	208-217	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	138-144
10671914-1	2000	AIMS: To study whether the CYP2D6 capacity in ultrarapid metabolizers of debrisoquine due to duplication/multiduplication of a functional CYP2D6 gene, can be "normalised" by low doses of the CYP2D6 inhibitor quinidine and whether this is dose-dependent.	Quinidine	208-217	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	138-144
10671914-8	2000	A dose-effect relationship could be established for quinidine with regard to the inhibitory effect on CYP2D6 activity.	Quinidine	52-61	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	102-108
10671914-11	2000	CONCLUSIONS: A dose-effect relationship could be established for quinidine inhibition of CYP2D6 in ultrarapid metabolizers.	Quinidine	65-74	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	89-95
10671914-12	2000	The clinical use of low doses of quinidine as an inhibitor of CYP2D6 might be considered in ultrarapid metabolizers taking CYP2D6 metabolized drugs rather than giving increased doses of the drug.	Quinidine	33-42	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	62-68
10671914-12	2000	The clinical use of low doses of quinidine as an inhibitor of CYP2D6 might be considered in ultrarapid metabolizers taking CYP2D6 metabolized drugs rather than giving increased doses of the drug.	Quinidine	33-42	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	123-129
10671914-13	2000	Normalizing the metabolic capacity of CYP2D6, by giving a low dose of quinidine, may solve the problem of "treatment resistance" caused by ultrarapid metabolism.	Quinidine	70-79	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	38-44
10901285-5	2000	Quinidine (an inhibitor of CYP2D6) completely inhibited while alpha-naphthoflavone (an inhibitor of CYP1A2) marginally inhibited the chlorpromazine 7-hydroxylase activity in a human liver microsomal sample showing high CYP2D6 activity.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	27-33
10901285-5	2000	Quinidine (an inhibitor of CYP2D6) completely inhibited while alpha-naphthoflavone (an inhibitor of CYP1A2) marginally inhibited the chlorpromazine 7-hydroxylase activity in a human liver microsomal sample showing high CYP2D6 activity.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	219-225
10381752-9	1999	Meloxicam, in turn, decreased both Km and Vmax of quinidine metabolism by CYP 3A4, indicating an uncompetitive inhibition mechanism.	Quinidine	50-59	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	74-81
10556149-2	1999	In blood-free perfused and ventilated rat lungs, PAF increased lung weight by 0.59 +/- 0.18 g. The cyclooxygenase inhibitor aspirin (500 microM) blocked this response by one-third, and the quinolines quinine (330 microM), quinidine (100 microM), and chloroquine (100 microM) by two-thirds.	Quinidine	222-231	PCNA clamp associated factor	Rattus norvegicus	49-52
10556149-4	1999	In combination with aspirin, quinine or quinidine completely prevented PAF-induced weight gain and the concomitant increase of the capillary filtration coefficient (K(f,c)).	Quinidine	40-49	PCNA clamp associated factor	Rattus norvegicus	71-74
10525100-9	1999	Among these inhibitors, tetraethylammonium, pyrilamine, quinidine, verapamil, and valproate were found to be transported by hOCTN2.	Quinidine	56-65	solute carrier family 22 member 5	Homo sapiens	124-130
10484078-9	1999	Greater inhibition was produced by the less selective CYP3A inhibitors parathion, quinidine, and ketoconazole; CYP1A inhibitors were ineffective.	Quinidine	82-91	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	54-59
10497139-12	1999	Quinidine (a specific CYP2D inhibitor) prevented celecoxib metabolism in dog hepatic microsomes, providing evidence of a predominant role for the CYP2D subfamily in canine celecoxib metabolism.	Quinidine	0-9	cytochrome P450 2D15	Canis lupus familiaris	22-27
10497139-12	1999	Quinidine (a specific CYP2D inhibitor) prevented celecoxib metabolism in dog hepatic microsomes, providing evidence of a predominant role for the CYP2D subfamily in canine celecoxib metabolism.	Quinidine	0-9	cytochrome P450 2D15	Canis lupus familiaris	146-151
10510150-1	1999	AIMS: To test the hypothesis that inhibition of cytochrome P450 2D6 (CYP2D6) by quinidine increases the antitussive effect of dextromethorphan (DEX) in an induced cough model.	Quinidine	80-89	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	48-67
10510150-1	1999	AIMS: To test the hypothesis that inhibition of cytochrome P450 2D6 (CYP2D6) by quinidine increases the antitussive effect of dextromethorphan (DEX) in an induced cough model.	Quinidine	80-89	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	69-75
10510150-4	1999	RESULTS: Inhibition of CYP2D6 by quinidine caused a significant increase in the mean ratio of DEX to dextrorphan (DEX:DOR) plasma AUC(96) (0.04 vs 1.81, P&lt;0.001).	Quinidine	33-42	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	23-29
10455332-4	1999	In the presence of quinidine, verapamil and cyclosporin (substrates of the P-glycoprotein (P-gp)), plasma AUCs of ciprofloxacin were 1.5 - 2 fold increased, while biliary clearance (1.5 - 2 fold), intestinal overall and net clearances (2 - 4 fold and 1.5 - 8 fold respectively) decreased.	Quinidine	19-28	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	75-89
10455332-4	1999	In the presence of quinidine, verapamil and cyclosporin (substrates of the P-glycoprotein (P-gp)), plasma AUCs of ciprofloxacin were 1.5 - 2 fold increased, while biliary clearance (1.5 - 2 fold), intestinal overall and net clearances (2 - 4 fold and 1.5 - 8 fold respectively) decreased.	Quinidine	19-28	phosphoglycolate phosphatase	Rattus norvegicus	91-96
10455332-5	1999	The weak effect obtained with cyclosporin as compared to verapamil and especially quinidine, suggests, for ciprofloxacin, the existence of transport systems distinct from the P-gp, as the OCT1 transporter which could be inhibited by quinidine.	Quinidine	82-91	solute carrier family 22 member 1	Rattus norvegicus	188-192
10455332-5	1999	The weak effect obtained with cyclosporin as compared to verapamil and especially quinidine, suggests, for ciprofloxacin, the existence of transport systems distinct from the P-gp, as the OCT1 transporter which could be inhibited by quinidine.	Quinidine	233-242	solute carrier family 22 member 1	Rattus norvegicus	188-192
10421620-7	1999	The enzyme activity was significantly (p &lt;.01) and stereoselectively inhibited by CYP2D1 inhibitors quinine and quinidine (not by CYP2C or CYP3A inhibitors), and by anti-CYP2D6 peptide antiserum (not by anti-CYP2C, -CYP2B, or -CYP3A antibodies).	Quinidine	115-124	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	85-91
10421620-7	1999	The enzyme activity was significantly (p &lt;.01) and stereoselectively inhibited by CYP2D1 inhibitors quinine and quinidine (not by CYP2C or CYP3A inhibitors), and by anti-CYP2D6 peptide antiserum (not by anti-CYP2C, -CYP2B, or -CYP3A antibodies).	Quinidine	115-124	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	173-179
10492058-1	1999	OBJECTIVE: To investigate the possible involvement of cytochromes CYP1A2 and CYP2C19 in the in vivo oxidative metabolism of quinidine.	Quinidine	124-133	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	66-72
10492058-1	1999	OBJECTIVE: To investigate the possible involvement of cytochromes CYP1A2 and CYP2C19 in the in vivo oxidative metabolism of quinidine.	Quinidine	124-133	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	77-84
10383917-5	1999	At the substrate concentration of 20 microM, which approximated the apparent KM value, sulfaphenazole (CYP2C9 inhibitor) and triazolam (CYP3A substrate) reduced the N-demethylation activities by 20 to 35% in human liver microsomes, whereas the inhibition induced by mephenytoin (CYP2C19 substrate) or quinidine (CYP2D6 inhibitor) was marginal.	Quinidine	301-310	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	103-109
10381752-0	1999	Activation of human cytochrome P-450 3A4-catalyzed meloxicam 5"-methylhydroxylation by quinidine and hydroquinidine in vitro.	Quinidine	87-96	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	20-40
10381752-3	1999	Quinidine, a CYP 3A4 substrate commonly used as a selective in vitro inhibitor of CYP 2D6, was found to markedly increase the rate of meloxicam hydroxylation during in vitro experiments with human liver microsomes.	Quinidine	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	13-20
10381752-3	1999	Quinidine, a CYP 3A4 substrate commonly used as a selective in vitro inhibitor of CYP 2D6, was found to markedly increase the rate of meloxicam hydroxylation during in vitro experiments with human liver microsomes.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	82-89
10381752-6	1999	Using expressed cytochrome P-450 enzymes and selective chemical inhibitors of CYP 2C9 and CYP 3A4, it was found that quinidine markedly increased the rate of CYP 3A4-mediated meloxicam hydroxylation but was virtually without effect on CYP 2C9.	Quinidine	117-126	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	16-32
10381752-6	1999	Using expressed cytochrome P-450 enzymes and selective chemical inhibitors of CYP 2C9 and CYP 3A4, it was found that quinidine markedly increased the rate of CYP 3A4-mediated meloxicam hydroxylation but was virtually without effect on CYP 2C9.	Quinidine	117-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	78-85
10381752-6	1999	Using expressed cytochrome P-450 enzymes and selective chemical inhibitors of CYP 2C9 and CYP 3A4, it was found that quinidine markedly increased the rate of CYP 3A4-mediated meloxicam hydroxylation but was virtually without effect on CYP 2C9.	Quinidine	117-126	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	90-97
10381752-6	1999	Using expressed cytochrome P-450 enzymes and selective chemical inhibitors of CYP 2C9 and CYP 3A4, it was found that quinidine markedly increased the rate of CYP 3A4-mediated meloxicam hydroxylation but was virtually without effect on CYP 2C9.	Quinidine	117-126	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	158-165
10381752-6	1999	Using expressed cytochrome P-450 enzymes and selective chemical inhibitors of CYP 2C9 and CYP 3A4, it was found that quinidine markedly increased the rate of CYP 3A4-mediated meloxicam hydroxylation but was virtually without effect on CYP 2C9.	Quinidine	117-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	235-242
10381759-8	1999	The steady-state uptake of HSR-903 by a monolayer of primary cultured bovine brain capillary endothelial cells was increased in the presence of several quinolone antibacterial agents or anionic compounds, such as 4,4"-diisothiocyanatostilbene-2,2"-disulfonic acid, and in bicarbonate ion-free medium, as well as by P-gp inhibitors (cyclosporin A and quinidine).	Quinidine	350-359	HSR	Homo sapiens	27-30
10418968-11	1999	Furafylline, sulfaphenazole, quinidine, and ketoconazole were found to be specific inhibitors of CYP1A2, CYP2C9, CYP2D6, and CYP3A4, respectively.	Quinidine	29-38	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	97-103
10418968-11	1999	Furafylline, sulfaphenazole, quinidine, and ketoconazole were found to be specific inhibitors of CYP1A2, CYP2C9, CYP2D6, and CYP3A4, respectively.	Quinidine	29-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	105-111
10418968-11	1999	Furafylline, sulfaphenazole, quinidine, and ketoconazole were found to be specific inhibitors of CYP1A2, CYP2C9, CYP2D6, and CYP3A4, respectively.	Quinidine	29-38	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	113-119
10418968-11	1999	Furafylline, sulfaphenazole, quinidine, and ketoconazole were found to be specific inhibitors of CYP1A2, CYP2C9, CYP2D6, and CYP3A4, respectively.	Quinidine	29-38	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	125-131
10215651-8	1999	OCTN1-mediated [14C]TEA uptake was inhibited by various organic cations such as cimetidine, procainamide, pyrilamine, quinidine, quinine, and verapamil.	Quinidine	118-127	solute carrier family 22 member 4	Homo sapiens	0-5
10365641-5	1999	There was a marked decrease in the serum cholinesterase (CHE) activity as QUINID concentrations were increased to 154 micromol/L (19.8% decrease in CHE) and to 308 micromol/L (36.8% decrease in CHE).	Quinidine	74-80	butyrylcholinesterase	Homo sapiens	41-55
10365641-5	1999	There was a marked decrease in the serum cholinesterase (CHE) activity as QUINID concentrations were increased to 154 micromol/L (19.8% decrease in CHE) and to 308 micromol/L (36.8% decrease in CHE).	Quinidine	74-80	butyrylcholinesterase	Homo sapiens	57-60
10365641-6	1999	These data suggest that QUINID inhibits the hydrolysis of CE in human serum by suppressing CHE activity.	Quinidine	24-30	butyrylcholinesterase	Homo sapiens	91-94
10365641-8	1999	They also have important implications for individuals receiving QUINID together with other drugs whose hydrolysis may be catalyzed by CHE.	Quinidine	64-70	butyrylcholinesterase	Homo sapiens	134-137
10320683-3	1999	RESULTS: Salicylate enhanced quinidine-induced tonic and phasic block of INa at a holding potential of -100 mV but not at a holding potential of -140 mV; this enhancement was accompanied by a shift of the hinfinity curve in the presence of quinidine in a further hyperpolarized direction, although salicylate alone did not affect INa.	Quinidine	29-38	alpha-internexin	Cavia porcellus	73-76
10320683-3	1999	RESULTS: Salicylate enhanced quinidine-induced tonic and phasic block of INa at a holding potential of -100 mV but not at a holding potential of -140 mV; this enhancement was accompanied by a shift of the hinfinity curve in the presence of quinidine in a further hyperpolarized direction, although salicylate alone did not affect INa.	Quinidine	29-38	alpha-internexin	Cavia porcellus	330-333
10320683-3	1999	RESULTS: Salicylate enhanced quinidine-induced tonic and phasic block of INa at a holding potential of -100 mV but not at a holding potential of -140 mV; this enhancement was accompanied by a shift of the hinfinity curve in the presence of quinidine in a further hyperpolarized direction, although salicylate alone did not affect INa.	Quinidine	240-249	alpha-internexin	Cavia porcellus	73-76
10086984-11	1999	Hence, the (3S)-3-hydroxylation of quinidine is a specific probe for CYP3A4 activity in human liver microsome preparations, whereas the N-oxidation of quinidine is a somewhat less specific marker reaction for CYP3A4 activity, because the presence of a low affinity enzyme is demonstrated by different approaches.	Quinidine	151-160	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	209-215
10354960-4	1999	The high-affinity component (Km 1.3 +/- 0.4 microM, n = 11 livers) was selectively inhibited by the CYP 2D6 inhibitor quinidine, whereas the CYP3A4 inhibitor ketoconazole selectively inhibited the low-affinity component (K(m) 24.4 +/- 7 microM, n = 11 livers).	Quinidine	118-127	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	100-107
10342379-9	1999	Topical quinidine (a P-gp inhibitor) markedly increased the aqueous distribution of Rho-123, depending on the aqueous concentrations of quinidine, though it did not affect the aqueous distribution of Rho-B.	Quinidine	8-17	ATP-dependent translocase ABCB1	Oryctolagus cuniculus	21-25
10075682-8	1999	Pharmacologically, TWIK-2 channels are distinct from TWIK-1 channels in their response to quinidine, quinine, and barium.	Quinidine	90-99	potassium two pore domain channel subfamily K member 6	Homo sapiens	19-25
10075682-8	1999	Pharmacologically, TWIK-2 channels are distinct from TWIK-1 channels in their response to quinidine, quinine, and barium.	Quinidine	90-99	potassium channel, two pore domain subfamily K, member 1 L homeolog	Xenopus laevis	53-59
10342379-10	1999	CONCLUSIONS: The contribution of functional P-gp in blood-aqueous barrier was clearly demonstrated by analyzing the aqueous distribution of Rho-123 in the presence or absence of quinidine.	Quinidine	178-187	ATP-dependent translocase ABCB1	Oryctolagus cuniculus	44-48
9929520-8	1999	Quinidine almost completely inhibited the CYP2D6-mediated de-esterification at the concentration of 1 x 10(-6) M. Ketoconazole and troleandomycin inhibited the CYP3A4-mediated reaction in a dose-related manner.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	42-48
10230863-4	1999	I(ALK) was strongly suppressed with tetraethylammonium (TEA), 4-aminopyridine (4-AP) and streptomycin (SM), but was completely resistant to quinidine (QND).	Quinidine	140-149	anaplastic lymphoma kinase	Mus musculus	2-5
10230863-4	1999	I(ALK) was strongly suppressed with tetraethylammonium (TEA), 4-aminopyridine (4-AP) and streptomycin (SM), but was completely resistant to quinidine (QND).	Quinidine	151-154	anaplastic lymphoma kinase	Mus musculus	2-5
10219965-14	1999	Quinidine, an inhibitor of human CYP2D6, had little effect on these latter activities in human hepatic microsomes.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	33-39
9927403-7	1999	Because the in vitro data showed that quinidine itself is a P-glycoprotein substrate, quinidine doses were reduced in mdr1a(-/-) mice to produce plasma concentrations similar to those in wild-type control animals.	Quinidine	86-95	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	118-123
9929520-8	1999	Quinidine almost completely inhibited the CYP2D6-mediated de-esterification at the concentration of 1 x 10(-6) M. Ketoconazole and troleandomycin inhibited the CYP3A4-mediated reaction in a dose-related manner.	Quinidine	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	160-166
10456292-5	1999	The transport of methadone was increased in presence of P-gp inhibitors verapamil and quinidine.	Quinidine	86-95	phosphoglycolate phosphatase	Rattus norvegicus	56-60
10028924-10	1999	Quinidine (3 microM) inhibited HERG currents expressed in oocytes by 32.1 +/- 3.2% (n = 5), whereas 1 microM quinidine inhibited HERG currents in tsA201 cells by 75.8 +/- 2.4% (n = 12).	Quinidine	0-9	potassium voltage-gated channel subfamily H member 2	Homo sapiens	31-35
10028924-0	1999	Modulation of HERG potassium channels by extracellular magnesium and quinidine.	Quinidine	69-78	potassium voltage-gated channel subfamily H member 2	Homo sapiens	14-18
10028924-10	1999	Quinidine (3 microM) inhibited HERG currents expressed in oocytes by 32.1 +/- 3.2% (n = 5), whereas 1 microM quinidine inhibited HERG currents in tsA201 cells by 75.8 +/- 2.4% (n = 12).	Quinidine	109-118	potassium voltage-gated channel subfamily H member 2	Homo sapiens	129-133
10028924-14	1999	Potent suppression of HERG channel current by quinidine, compared with that of I(Ks) and I(Na), is a likely contributor to torsades de pointes arrhythmias.	Quinidine	46-55	potassium voltage-gated channel subfamily H member 2	Homo sapiens	22-26
10048600-8	1999	This observation is confirmed by the findings that both quinidine (inhibitor of CYP2D6) and ketoconazole (inhibitor of CYP3A4) can inhibit the formation of 9-hydroxyrisperidone.	Quinidine	56-65	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	80-86
10086984-1	1999	The aim of this study was to evaluate the (3S)-3-hydroxylation and the N-oxidation of quinidine as biomarkers for cytochrome P-450 (CYP)3A4 activity in human liver microsome preparations.	Quinidine	86-95	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	114-139
10086984-11	1999	Hence, the (3S)-3-hydroxylation of quinidine is a specific probe for CYP3A4 activity in human liver microsome preparations, whereas the N-oxidation of quinidine is a somewhat less specific marker reaction for CYP3A4 activity, because the presence of a low affinity enzyme is demonstrated by different approaches.	Quinidine	35-44	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	69-75
10078840-6	1999	Furafylline, sulphaphenazole, omeprazole, quinidine and ketoconazole were identified as specific markers for the respective CYP1A2 (IC50 = 6 microM), CYP2C9 (0.7 microM), CYP2C19 (6 microM), CYP2D6 (0.02 microM) and CYP3A4 (0.2 microM) inhibition screens.	Quinidine	42-51	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	124-130
10702886-0	1999	Inhibition of CYP2D6 by quinidine and its effects on the metabolism of cilostazol.	Quinidine	24-33	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	14-20
10702886-12	1999	Hence, quinidine effectively converted extensive metabolisers of CYP2D6 to poor metabolisers of CYP2D6.	Quinidine	7-16	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	65-71
10702886-12	1999	Hence, quinidine effectively converted extensive metabolisers of CYP2D6 to poor metabolisers of CYP2D6.	Quinidine	7-16	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	96-102
10702886-13	1999	The 21-day washout period was adequate to have complete recovery from quinidine inhibition of CYP2D6.	Quinidine	70-79	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	94-100
10702886-19	1999	CONCLUSIONS: Administration of quinidine sulfate 200 mg profoundly inhibited CYP2D6-mediated metabolism.	Quinidine	31-48	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	77-83
10702886-20	1999	The effects of quinidine inhibition of CYP2D6 metabolism were completely reversible during the 21-day washout period.	Quinidine	15-24	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	39-45
9851939-3	1998	We investigated the effects of postnatal development on quinidine"s interaction with major repolarizing currents (Ito, IKur, Ins, and IK1) in human atrial myocytes, using the whole-cell configuration of the voltage-clamp technique.	Quinidine	56-65	IKAROS family zinc finger 1	Homo sapiens	134-137
9851939-5	1998	In contrast, quinidine was found to inhibit both adult and pediatric IK1 and IKur in an age-independent manner, whereas the nonselective cation current (Ins), which contributes to the sustained outward current (Isus), was insensitive to quinidine.	Quinidine	13-22	IKAROS family zinc finger 1	Homo sapiens	69-72
9836023-7	1998	Finally, when the specific CYP2D6 inhibitor quinidine was preincubated with either human liver microsomes or cells expressing human CYP2D6, there was a concentration-dependent decrease in the production of OH-mCPP.	Quinidine	44-53	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	27-33
9836023-7	1998	Finally, when the specific CYP2D6 inhibitor quinidine was preincubated with either human liver microsomes or cells expressing human CYP2D6, there was a concentration-dependent decrease in the production of OH-mCPP.	Quinidine	44-53	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	132-138
9806111-15	1998	EMs, but not PMs, are susceptible to drug interactions between mexiletine and drugs that inhibit CYP2D6 (e.g. quinidine).	Quinidine	110-119	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	97-103
9871425-4	1998	The aim of this study was to evaluate the role of oxymorphone in mediating the opioid effects of oxycodone by means of blocking CYP2D6 with quinidine.	Quinidine	140-149	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	128-134
9808712-6	1998	Although various hydrophilic organic cations such as 1-methyl-4-phenylpyridinium, cimetidine, quinidine, nicotine, N1-methylnicotinamide and guanidine markedly inhibited TEA uptake by both MDCK-OCT1 and MDCK-OCT2 cells, there were no significant differences in the apparent inhibition constants (Ki) against these organic cations between both transfectants.	Quinidine	94-103	solute carrier family 22 member 1	Rattus norvegicus	189-198
9808712-6	1998	Although various hydrophilic organic cations such as 1-methyl-4-phenylpyridinium, cimetidine, quinidine, nicotine, N1-methylnicotinamide and guanidine markedly inhibited TEA uptake by both MDCK-OCT1 and MDCK-OCT2 cells, there were no significant differences in the apparent inhibition constants (Ki) against these organic cations between both transfectants.	Quinidine	94-103	POU class 2 homeobox 2	Rattus norvegicus	208-212
9746775-4	1998	From the pattern of monoclonal antibody (MoAb) inhibition and the reactions of antibody with Chinese hamster ovary (CHO) cells transfected with GPIX and GPIbbeta, we found that the patient"s antibody is specific for an epitope on GPIX close to, or identical with a site recognized by the MoAb SZ1 that is a common target for antibodies induced by quinine and quinidine, drugs structurally unrelated to ranitidine.	Quinidine	359-368	glycoprotein IX platelet	Homo sapiens	144-148
9744804-3	1998	In this report, we have investigated the transport properties of ORCTL2 and show that this protein can confer resistance to chloroquine and quinidine when overexpressed in bacteria.	Quinidine	140-149	solute carrier family 22 member 18	Homo sapiens	65-71
9765354-0	1998	Differential effects of S6 mutations on binding of quinidine and 4-aminopyridine to rat isoform of Kv1.4: common site but different factors in determining blockers" binding affinity.	Quinidine	51-60	potassium voltage-gated channel subfamily A member 4	Rattus norvegicus	99-104
9765354-6	1998	Our data show that mutations at a position in the S6 domain of rKv1.4 (position 529) can cause dramatic and often opposite effects on quinidine and 4AP binding.	Quinidine	134-143	potassium voltage-gated channel subfamily A member 4	Rattus norvegicus	63-69
9721180-9	1998	The human CYP2D6-specific inhibitor quinidine and the rat CYP2D1-specific inhibitor quinine were both shown to be inhibitors of bufuralol 1"-hydroxylase activity for dog liver microsomes, CYP2D15 WT2, and the CYP2D15 V1 variant with nearly equal potency.	Quinidine	36-45	cytochrome P450 2D15	Canis lupus familiaris	209-216
9721180-10	1998	Thus, the dog expresses a CYP2D ortholog possessing enzymatic activities similar to human CYP2D6, but is affected by the inhibitors quinine and quinidine in a manner closer to that of rat CYP2D1.	Quinidine	144-153	cytochrome P450 2D15	Canis lupus familiaris	26-31
9758674-0	1998	Inhibition of desipramine hydroxylation (Cytochrome P450-2D6) in vitro by quinidine and by viral protease inhibitors: relation to drug interactions in vivo.	Quinidine	74-83	cytochrome P450 2D6	Homo sapiens	41-60
9721180-9	1998	The human CYP2D6-specific inhibitor quinidine and the rat CYP2D1-specific inhibitor quinine were both shown to be inhibitors of bufuralol 1"-hydroxylase activity for dog liver microsomes, CYP2D15 WT2, and the CYP2D15 V1 variant with nearly equal potency.	Quinidine	36-45	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	10-16
9721180-9	1998	The human CYP2D6-specific inhibitor quinidine and the rat CYP2D1-specific inhibitor quinine were both shown to be inhibitors of bufuralol 1"-hydroxylase activity for dog liver microsomes, CYP2D15 WT2, and the CYP2D15 V1 variant with nearly equal potency.	Quinidine	36-45	cytochrome P450 2D15	Canis lupus familiaris	188-195
9744804-5	1998	These results suggest that ORCTL2 may play a role in the transport of chloroquine and quinidine related compounds in the kidney.	Quinidine	86-95	solute carrier family 22 member 18	Homo sapiens	27-33
9698290-9	1998	Quinidine, a CYP2D6-specific inhibitor, inhibited ibogaine O-demethylase (IC50 = 0.2 microM), whereas other P450 isoform-specific inhibitors did not inhibit this activity.	Quinidine	0-9	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	13-19
9721873-3	1998	Quinidine and GF120918 inhibit the transport of P-gp substrates, including doxorubicin.	Quinidine	0-9	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	48-52
9620113-8	1998	Quinidine unbound fraction (UF) was related to ORM phenotype.	Quinidine	0-9	orosomucoid 1	Homo sapiens	47-50
9731719-12	1998	They also suggest that the Ghanaians have an additional unidentified allele(s) with altered substrate specificity and quinidine sensitivity which is currently genotyped as CYP2D6*1.	Quinidine	118-127	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	172-178
9620113-12	1998	Quinidine binding showed significant relationships to specific ORM variants.	Quinidine	0-9	orosomucoid 1	Homo sapiens	63-66
9506530-6	1998	The P-glycoprotein-mediated multidrug resistance (MDR)-reversing agents verapamil, cyclosporin A, quinidine, sodium orthovanadate and tamoxifen significantly increased dox fluorescence at this depth, whereas genistein, indomethacin, probenecid and brefeldin A, which reverse multidrug-resistance-associated protein (MRP) function, exerted no effect.	Quinidine	98-107	ATP binding cassette subfamily B member 1	Homo sapiens	4-18
9524137-0	1998	On the mechanism by which 4-Aminopyridine occludes quinidine block of the cardiac K+ channel, hKv1.5.	Quinidine	51-60	potassium voltage-gated channel subfamily A member 5	Homo sapiens	94-100
9592721-4	1998	Quinidine (30 microM) and verapamil (0.1 microM) produced use-dependent depression of INa and ICa, respectively.	Quinidine	0-9	alpha-internexin	Cavia porcellus	86-97
9523981-0	1998	Role of P-glycoprotein as a secretory mechanism in quinidine absorption from rat small intestine.	Quinidine	51-60	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	8-22
9523981-5	1998	The secretion of quinidine, well-known as an inhibitor of P-glycoprotein, was inhibited significantly and its absorption was enhanced significantly by several substrates of P-glycoprotein including verapamil, diltiazem, and digitoxin in jejunum.	Quinidine	17-26	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	58-72
9523981-5	1998	The secretion of quinidine, well-known as an inhibitor of P-glycoprotein, was inhibited significantly and its absorption was enhanced significantly by several substrates of P-glycoprotein including verapamil, diltiazem, and digitoxin in jejunum.	Quinidine	17-26	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	173-187
9523981-9	1998	Quinidine was also recognized to inhibit the secretion and to promote the absorption of substrates of P-glycoprotein, chlorpromazine, and verapamil.	Quinidine	0-9	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	102-116
9523981-10	1998	These results strongly suggest that quinidine is not only an inhibitor but also a substrate of P-glycoprotein and that the P-glycoprotein-mediated secretory flux acts as a barrier to quinidine absorption in the small intestine, especially jejunum.	Quinidine	36-45	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	95-109
9523981-10	1998	These results strongly suggest that quinidine is not only an inhibitor but also a substrate of P-glycoprotein and that the P-glycoprotein-mediated secretory flux acts as a barrier to quinidine absorption in the small intestine, especially jejunum.	Quinidine	36-45	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	123-137
9523981-10	1998	These results strongly suggest that quinidine is not only an inhibitor but also a substrate of P-glycoprotein and that the P-glycoprotein-mediated secretory flux acts as a barrier to quinidine absorption in the small intestine, especially jejunum.	Quinidine	183-192	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	123-137
9506530-6	1998	The P-glycoprotein-mediated multidrug resistance (MDR)-reversing agents verapamil, cyclosporin A, quinidine, sodium orthovanadate and tamoxifen significantly increased dox fluorescence at this depth, whereas genistein, indomethacin, probenecid and brefeldin A, which reverse multidrug-resistance-associated protein (MRP) function, exerted no effect.	Quinidine	98-107	ATP binding cassette subfamily C member 3	Homo sapiens	275-314
9506530-6	1998	The P-glycoprotein-mediated multidrug resistance (MDR)-reversing agents verapamil, cyclosporin A, quinidine, sodium orthovanadate and tamoxifen significantly increased dox fluorescence at this depth, whereas genistein, indomethacin, probenecid and brefeldin A, which reverse multidrug-resistance-associated protein (MRP) function, exerted no effect.	Quinidine	98-107	ATP binding cassette subfamily C member 3	Homo sapiens	316-319
9488065-11	1998	Calcium-channel blockers (verapamil, quinidine) and protein kinase C inhibitors (tamoxifen) inhibited gp-170 activity and slowed the drug-efflux pump, with the acquired-MDR cells subsequently accumulating anticancer drugs.	Quinidine	37-46	ATP binding cassette subfamily B member 1	Homo sapiens	102-108
9528676-3	1998	The cardioactive drugs verapamil, quinidine, diltiazem, nifedipine, and a series of digitalis analogs, interacted directly with Pgp as shown on ATPase in both systems.	Quinidine	34-43	ATP binding cassette subfamily B member 1	Homo sapiens	128-131
9528676-3	1998	The cardioactive drugs verapamil, quinidine, diltiazem, nifedipine, and a series of digitalis analogs, interacted directly with Pgp as shown on ATPase in both systems.	Quinidine	34-43	dynein axonemal heavy chain 8	Homo sapiens	144-150
9482283-9	1998	When MCS were incubated with verapamil, cyclosporin A, orthovanadate, and quinidine, which are known to reverse P-glycoprotein (Pgp)-mediated multidrug resistance (MDR), Dox accumulated also in deeper cell layers.	Quinidine	74-83	ATP binding cassette subfamily B member 1	Homo sapiens	112-126
9635150-1	1998	The vasoconstrictors norepinephrine (NE) and angiotensin II (AII) mediate increases in oxygen uptake (VO2) by the constant flow perfused rat hind limb that are inhibited by quinidine-like membrane-stabilizing effects (involving the interruption of action potential) of (+/-)-propranolol with little effect on vasoconstriction.	Quinidine	173-182	angiotensinogen	Rattus norvegicus	45-59
9635150-1	1998	The vasoconstrictors norepinephrine (NE) and angiotensin II (AII) mediate increases in oxygen uptake (VO2) by the constant flow perfused rat hind limb that are inhibited by quinidine-like membrane-stabilizing effects (involving the interruption of action potential) of (+/-)-propranolol with little effect on vasoconstriction.	Quinidine	173-182	angiotensinogen	Rattus norvegicus	61-64
9482283-9	1998	When MCS were incubated with verapamil, cyclosporin A, orthovanadate, and quinidine, which are known to reverse P-glycoprotein (Pgp)-mediated multidrug resistance (MDR), Dox accumulated also in deeper cell layers.	Quinidine	74-83	ATP binding cassette subfamily B member 1	Homo sapiens	128-131
9452971-4	1998	In the presence of verapamil an quinidine, the retarded absorption of methylprednisolone was completely recovered, suggesting that P-glycoprotein is responsible for the unique features of methylprednisolone absorption.	Quinidine	32-41	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	131-145
9436627-8	1998	Furthermore, in the presence of quinidine, a blocker of Ca2+-dependent K+ conductance fMLP and PAF caused only prolonged depolarization while the effect of O2.- was reduced to a minimum.	Quinidine	32-41	patchy fur	Mus musculus	95-98
9262363-5	1997	The increased basolateral-to-apical transport in LLC-GA5-COL150 monolayers was completely inhibited by cyclosporin A and quinidine to the level observed in LLC-PK1 monolayers.	Quinidine	121-130	prokineticin 1	Homo sapiens	160-163
9405386-3	1997	Previous electrical measurements suggested that cations like quinine, quinidine, and cyanine 863, which have been classified as type 2 cations in the liver, are also transported by rOCT1, since they may induce inward currents in rOCT1 expressing Xenopus oocytes (Busch, A. E., Quester, S., Ulzheimer, J. C., Waldegger, S., Gorboulev, V., Arndt, P., Lang, F., and Koepsell, H. (1996) J. Biol.	Quinidine	70-79	solute carrier family 22 member 1	Rattus norvegicus	181-186
9405386-3	1997	Previous electrical measurements suggested that cations like quinine, quinidine, and cyanine 863, which have been classified as type 2 cations in the liver, are also transported by rOCT1, since they may induce inward currents in rOCT1 expressing Xenopus oocytes (Busch, A. E., Quester, S., Ulzheimer, J. C., Waldegger, S., Gorboulev, V., Arndt, P., Lang, F., and Koepsell, H. (1996) J. Biol.	Quinidine	70-79	solute carrier family 22 member 1	Rattus norvegicus	229-234
9405386-7	1997	The voltage dependence observed for the quinine- or quinidine-induced inward currents in rOCT1-expressing oocytes, and tracer efflux measurements indicate that the inward currents by type 2 cations are generated by the inhibition of electrogenic efflux of transported type 1 cations.	Quinidine	52-61	solute carrier family 22 member 1	Rattus norvegicus	89-94
9413916-8	1997	Quinine (Ki = 0.06 microM) and quinidine (Ki = 2.0 microM), selective inhibitors of CYP2D1, competitively inhibited 8-hydroxycarteolol formation.	Quinidine	31-40	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	84-90
9315521-6	1997	TNF-alpha production was inhibited by amiodarone but stimulated by quinidine in a concentration-dependent manner.	Quinidine	67-76	tumor necrosis factor	Homo sapiens	0-9
9431831-7	1997	Ketoconazole, an inhibitor of CYP3A4, inhibited competitively CPHP formation (Ki=0.1 microM), whereas sulphaphenazole (CYP2C9), furafylline (CYP1A2) and quinidine (CYP2D6) gave only little inhibition (IC50 &gt; 100 microM).	Quinidine	153-162	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	30-36
9390107-1	1997	BACKGROUND: Quinidine is eliminated mainly by CYP3A4-mediated metabolism.	Quinidine	12-21	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	46-52
9390107-12	1997	CONCLUSIONS: Itraconazole increases plasma concentrations of oral quinidine, probably by inhibiting the CYP3A4 isozyme during the first-pass and elimination phases of quinidine.	Quinidine	66-75	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	104-110
9390107-12	1997	CONCLUSIONS: Itraconazole increases plasma concentrations of oral quinidine, probably by inhibiting the CYP3A4 isozyme during the first-pass and elimination phases of quinidine.	Quinidine	167-176	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	104-110
9390107-14	1997	The concentrations of quinidine should be closely monitored if itraconazole or some other potent CYP3A inhibitors are used with quinidine.	Quinidine	22-31	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	97-102
9390107-14	1997	The concentrations of quinidine should be closely monitored if itraconazole or some other potent CYP3A inhibitors are used with quinidine.	Quinidine	128-137	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	97-102
9353372-0	1997	P-Glycoprotein mediates the efflux of quinidine across the blood-brain barrier.	Quinidine	38-47	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-14
9353372-2	1997	We examined the role of P-glycoprotein on the restricted entry of quinidine to the brain.	Quinidine	66-75	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	24-38
9353372-3	1997	Quinidine is a well known inhibitor of P-glycoprotein, although it is not yet clarified whether quinidine is the substrate for P-glycoprotein.	Quinidine	0-9	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	39-53
9353372-3	1997	Quinidine is a well known inhibitor of P-glycoprotein, although it is not yet clarified whether quinidine is the substrate for P-glycoprotein.	Quinidine	96-105	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	127-141
9353372-10	1997	These results suggest that P-glycoprotein mediates the efflux of quinidine across the blood-brain barrier, resulting in its restricted entry to the brain.	Quinidine	65-74	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	27-41
9352574-5	1997	Additional experiments demonstrated that the formation rate of N-hydroxyprocainamide by CYP2D6 enriched microsomes was decreased from 45 +/- 4% to 93 +/- 1% by quinidine at concentrations ranging from 30 nM to 100 microM (all p &lt; 0.05 vs control) and by approximately 75% by antibodies directed against CYP2D6.	Quinidine	160-169	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	88-94
9352574-5	1997	Additional experiments demonstrated that the formation rate of N-hydroxyprocainamide by CYP2D6 enriched microsomes was decreased from 45 +/- 4% to 93 +/- 1% by quinidine at concentrations ranging from 30 nM to 100 microM (all p &lt; 0.05 vs control) and by approximately 75% by antibodies directed against CYP2D6.	Quinidine	160-169	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	306-312
9315342-7	1997	Quinidine (260 microM) (an antiarrhythmic agent with membrane-stabilizing activity) inhibited only the increase in VO2, but neither nadolol (300 microM) nor atenolol (300 microM) (beta-blockers without membrane-stabilizing activity) inhibited VO2 or perfusion pressure increases produced by 5 nM angiotensin II.	Quinidine	0-9	angiotensinogen	Rattus norvegicus	296-310
9161979-4	1997	Addition of Ba2+ alone, quinidine alone, or both inhibitors together revealed two separate conductances, one of which was blocked by both Ba2+ and quinidine (GBa)1, the other being sensitive to quinidine alone (Gquin).	Quinidine	24-33	glucosylceramidase beta	Homo sapiens	158-163
9256169-6	1997	The binding of [3H]GBR-12935 to CYP2D6 was decreased partially by substrates or inhibitors of CYP2D isoforms (quinine, quinidine, propranolol, bufuralol, imipramine, and desipramine).	Quinidine	119-128	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	32-38
9256169-6	1997	The binding of [3H]GBR-12935 to CYP2D6 was decreased partially by substrates or inhibitors of CYP2D isoforms (quinine, quinidine, propranolol, bufuralol, imipramine, and desipramine).	Quinidine	119-128	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	32-37
9264312-8	1997	This reaction was negligible in CYP2D6-deficient liver microsomes, was inhibited stereoselectively by the quinidine/quinine enantiomer pair, and was cosegregated with dextromethorphan O-demethylation (r = 0.975).	Quinidine	106-115	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	32-38
9161979-4	1997	Addition of Ba2+ alone, quinidine alone, or both inhibitors together revealed two separate conductances, one of which was blocked by both Ba2+ and quinidine (GBa)1, the other being sensitive to quinidine alone (Gquin).	Quinidine	147-156	glucosylceramidase beta	Homo sapiens	158-163
9161979-4	1997	Addition of Ba2+ alone, quinidine alone, or both inhibitors together revealed two separate conductances, one of which was blocked by both Ba2+ and quinidine (GBa)1, the other being sensitive to quinidine alone (Gquin).	Quinidine	147-156	glucosylceramidase beta	Homo sapiens	158-163
9105395-0	1997	Drug-drug interactions: effect of quinidine on nifedipine binding to human cytochrome P450 3A4.	Quinidine	34-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	75-94
9103485-1	1997	Enzymatic conversion of hydrocodone to hydromorphone is catalyzed by cytochrome P450 2D6, which is inactive in about 7% of Caucasians [poor metabolizers (PMs)] and can be inhibited by quinidine pretreatment in the remainder [extensive metabolizers (EMs)].	Quinidine	184-193	cytochrome P450 2D6	Homo sapiens	69-88
9097932-10	1997	Quinidine inhibits Kv4.2 in L-cells and It in rat ventricular cells in a similar fashion.	Quinidine	0-9	potassium voltage-gated channel, Shal-related family, member 2	Mus musculus	19-24
9097932-11	1997	In L-cells quinidine reduced the amplitude of Kv4.2 and accelerated its time course of inactivation, suggesting that quinidine may act as an open channel blocker of Kv4.2, as has been described for It in rat ventricle.	Quinidine	11-20	potassium voltage-gated channel subfamily D member 2	Rattus norvegicus	46-51
9097932-11	1997	In L-cells quinidine reduced the amplitude of Kv4.2 and accelerated its time course of inactivation, suggesting that quinidine may act as an open channel blocker of Kv4.2, as has been described for It in rat ventricle.	Quinidine	11-20	potassium voltage-gated channel subfamily D member 2	Rattus norvegicus	165-170
9097932-11	1997	In L-cells quinidine reduced the amplitude of Kv4.2 and accelerated its time course of inactivation, suggesting that quinidine may act as an open channel blocker of Kv4.2, as has been described for It in rat ventricle.	Quinidine	117-126	potassium voltage-gated channel subfamily D member 2	Rattus norvegicus	46-51
9097932-11	1997	In L-cells quinidine reduced the amplitude of Kv4.2 and accelerated its time course of inactivation, suggesting that quinidine may act as an open channel blocker of Kv4.2, as has been described for It in rat ventricle.	Quinidine	117-126	potassium voltage-gated channel subfamily D member 2	Rattus norvegicus	165-170
9149373-4	1997	A number of typical CYP2D6 substrates are shown to fit the putative active site of the enzyme, as can the specific inhibitor quinidine.	Quinidine	125-134	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	20-26
9149377-0	1997	Major role of the CYP2C isozymes in deamination of amphetamine and benzphetamine: evidence for the quinidine-specific inhibition of the reactions catalysed by rabbit enzyme.	Quinidine	99-108	cytochrome P450 2C3	Oryctolagus cuniculus	18-23
9149377-10	1997	AP deamination with purified rabbit CYP2C3, which was previously identified as the major isozyme responsible for this metabolism, was extensively inhibited with quinidine, previously thought to be a specific inhibitor of CYP2D.	Quinidine	161-170	cytochrome P450 2C3	Oryctolagus cuniculus	36-42
9130163-0	1997	Gating charge and ionic currents associated with quinidine block of human Kv1.5 delayed rectifier channels.	Quinidine	49-58	potassium voltage-gated channel subfamily A member 5	Homo sapiens	74-79
9130163-2	1997	The mechanism of quinidine-induced ionic and gating current inhibition was studied in human Kv1.5 (hKv1.5) delayed rectifier channels expressed in human embryonic kidney cells.	Quinidine	17-26	potassium voltage-gated channel subfamily A member 5	Homo sapiens	92-97
9130163-2	1997	The mechanism of quinidine-induced ionic and gating current inhibition was studied in human Kv1.5 (hKv1.5) delayed rectifier channels expressed in human embryonic kidney cells.	Quinidine	17-26	potassium voltage-gated channel subfamily A member 5	Homo sapiens	99-105
9130163-19	1997	The gating current data confirm directly that ionic current block by quinidine occurs by binding at a site on the hKv1.5 channel that becomes accessible when the channel opens.	Quinidine	69-78	potassium voltage-gated channel subfamily A member 5	Homo sapiens	114-120
9085043-6	1997	However, pretreatment of the kidneys with verapamil and quinidine (inhibitors of both P-glycoprotein and organic cation transport) or cimetidine (organic cation transport inhibitor) resulted in a significantly reduced rhodamine 123 clearance, indicating that the renal organic cation carrier may be involved in active secretion.	Quinidine	56-65	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	86-100
9235086-9	1997	Chemicals such as verapamil, nifedine, quinidine and calmodulin inhibitors are joined to pgp inhibiting it.	Quinidine	39-48	ATP binding cassette subfamily B member 1	Homo sapiens	89-92
9105395-2	1997	The interactions of nifedipine and quinidine with human cytochrome P450 3A4, which metabolizes these drugs, were examined using the kinetics of CO binding to this P450 as a rapid kinetic probe of protein conformation and dynamics.	Quinidine	35-44	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	56-75
9037249-6	1997	Inhibition of activity by quinidine (1 microM), sulphaphenazole (20 microM) and ketoconazole (2 microM), selective inhibitors of CYPs 2D6, 2C9 and 3A4, respectively, was 0-80%, 0-80% and 12-57%.	Quinidine	26-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	129-142
9131945-6	1997	The addition of quinidine, a selective inhibitor of CYP2D6, along with triacetyloleandomycin and sulphaphenazole produced an additional decrease in the rate of NT formation in all but the PM liver, but did not completely eliminate the reaction.	Quinidine	16-25	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	52-58
9037249-7	1997	The proportion of activity inhibited by quinidine correlated positively with total microsomal tamoxifen 4-hydroxylation activity (rs = 0.89, P &lt; 0.01), indicating a major involvement of CYP2D6 in this reaction.	Quinidine	40-49	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	189-195
8960070-8	1997	Chemical inhibition of CYP3A4 by preincubation with gestodene (40 microM) or troleandomycin (40 microM) reduced the formation of 3DMC and 2DMC by 70 and 80%, respectively, whereas quinidine, diethyldithiocarbamate, and sulfaphenazole had no inhibitory effect.	Quinidine	180-189	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	23-29
9143866-6	1997	Quinidine and lignocaine, although they are substrates of CYP3A, showed preferential inhibition over the O-demethylation of codeine, suggesting a low affinity to the CYP3A.	Quinidine	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-63
9143866-6	1997	Quinidine and lignocaine, although they are substrates of CYP3A, showed preferential inhibition over the O-demethylation of codeine, suggesting a low affinity to the CYP3A.	Quinidine	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	166-171
9041677-4	1997	When the metabolism of AMI by CYP2D6 was repeated in the presence of quinidine, none of the metabolites, 10-hydroxy-AMI, NT and 10-hydroxy-NT, was formed.	Quinidine	69-78	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	30-36
8878593-10	1996	In addition, verapamil and quinidine, two P-glycoprotein blockers, significantly reduced the intestinal elimination of both ofloxacin isomers (with concomitant verapamil, intestinal clearances were 0.12 +/- 0.02 versus 0.18 +/- 0.03 ml/min for S-(-)- and R-(+)-ofloxacin, respectively, while with concomitant quinidine, values were 0.18 +/- 0.01 versus 0.23 +/- 0.01 ml/min without modifying their areas under the concentration-time curve in serum.	Quinidine	27-36	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	42-56
8930192-0	1996	Quinidine enhances and suppresses Kv1.2 from outside and inside the cell, respectively.	Quinidine	0-9	potassium channel, voltage gated shaker related subfamily A, member 2 L homeolog	Xenopus laevis	34-39
8930192-2	1996	Quinidine had an agonist (enhancement) and a blocker (suppression) action on Kv1.2, whereas only the blocker action was seen with Kv1.4.	Quinidine	0-9	potassium channel, voltage gated shaker related subfamily A, member 2 L homeolog	Xenopus laevis	77-82
8930192-10	1996	In oocytes coexpressing Kv1.2 and Kv1.4 at approximately a 1:1 ratio, the response to Q+1C was similar to that of oocytes expressing Kv1.2 alone, suggesting that heteromultimer channels of Kv1.2 and Kv1.4 subunits could respond to the agonist action of quinidine.	Quinidine	253-262	potassium voltage-gated channel subfamily A member 4 S homeolog	Xenopus laevis	34-39
8930193-1	1996	We examined the effects of quinidine on a slow delayed rectifier K current induced by a human IsK cDNA (hlsK) in Xenopus oocytes.	Quinidine	27-36	potassium voltage-gated channel subfamily E regulatory subunit 1	Homo sapiens	94-97
8946477-3	1996	The promethazine hydroxylase in human liver microsomes was inhibited by SKF-525A, propranolol, sparteine, quinidine and anti-CYP2D6 serum suggesting involvement of a P450 related to CYP2D6.	Quinidine	106-115	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	182-188
8806763-14	1996	Quinidine, a specific inhibitor of P450 2D6, was not an effective inhibitor of NNK metabolism.	Quinidine	0-9	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	35-39
8866916-6	1996	The 1"-hydroxylation of bufuralol, form selective for CYP2D6, was competitively inhibited by olanzapine (Ki = 89 microM), clozapine (Ki = 19 microM), and quinidine (Ki = 0.03 microM).	Quinidine	154-163	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	54-60
8877032-5	1996	N-desisopropylpropranolol formation inhibitable by quinidine was highly correlated with specific CYP2D6 activity, as measured by the alpha-hydroxylation of metoprolol (rs = 0.90; P &lt; 0.001).	Quinidine	51-60	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	97-103
8702418-4	1996	When expressed in Xenopus oocytes, rat OCT2 stimulated the uptake of tetraethylammonium, and the uptake was markedly inhibited by the presence of cimetidine, procainamide and quinidine.	Quinidine	175-184	POU class 2 homeobox 2	Rattus norvegicus	39-43
8650203-4	1996	Expression of mouse Mdr1 in the mutant confers cross-resistance to daunomycin, quinidine, chloroquine, rhodamine 6G, and puromycin.	Quinidine	79-88	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	20-24
8627546-6	1996	Yeast microsomes containing heterologously expressed CYP2D6 N-demethylated MPTP (Km = 39 microM), and there was a high correlation between the quinidine-inhibitable N-demethylation of MPTP (50 microM) (0.7-91%, mean 44%, of total activity) and the alpha-hydroxylation of metoprolol in microsomes from 11 human livers (rs = 0.92; P < .001).	Quinidine	143-152	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	53-59
8801060-13	1996	In contrast, amiodarone (IC50, 25 microM) and flecainide (49 microM) inhibited CYP2C9 and quinidine (0.26 microM), and flecainide (0.44 microM) inhibited CYP2D6.	Quinidine	90-99	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	154-160
8861656-4	1996	The involvement of CYP2D6 in drug metabolism was assessed by inhibition studies using quinidine (5 mu M), a specific inhibitor of human CYP2D6, as well as by incubating compounds with microsomes prepared from cells transfected with cDNA encoding human CYP2D6.	Quinidine	86-95	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	19-25
8819299-8	1996	Sulphaphenazole, 7,8-benzoflavone, quinidine and troleandomycin were selective inhibitors of the CYP2C subfamily (except CYP2C19), the CYP1A subfamily, CYP2D6 and the CYP3A subfamily respectively.	Quinidine	35-44	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	152-158
8635242-2	1996	The antiarrhythmic agent quinidine blocks the human cardiac hKv1.5 channel expressed in mammalian cells at therapeutically relevant concentrations (EC50, 6.2 mumol/L).	Quinidine	25-34	potassium voltage-gated channel subfamily A member 5	Homo sapiens	60-66
8605869-11	1996	TWIK-1 channel activity is blocked by Ba2+(IC50=100 microM), quinine (IC50=50 microM) and quinidine (IC50=95 microM).	Quinidine	90-99	potassium two pore domain channel subfamily K member 1	Homo sapiens	0-6
8820427-7	1996	During inhibition of CYP2D6-mediated metabolism with quinidine, S-metoprolol areas under the concentration vs. time curves were 2515 +/- 749 and 2719 +/- 742 in White and Black subjects, respectively.	Quinidine	53-62	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	21-27
8820420-8	1996	Quinidine competitively inhibited the formation of hydroxybupranolol, with Ki values of 5 nM in expressed CYP2D6 and 14.05 nM in human liver (L-1).	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	106-112
8820421-4	1996	Ketoconazole and troleandomycin, both selective inhibitors for cytochrome P450 3A4 (CYP3A4), markedly inhibited the formation of all oxidative metabolites of MK-639; whereas other inhibitors (furafylline, sulfaphenazole, quinidine, S-mephenytoin, and diethyldithiocarbamate) had little effect on MK-639 metabolism.	Quinidine	221-230	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	63-82
8820421-4	1996	Ketoconazole and troleandomycin, both selective inhibitors for cytochrome P450 3A4 (CYP3A4), markedly inhibited the formation of all oxidative metabolites of MK-639; whereas other inhibitors (furafylline, sulfaphenazole, quinidine, S-mephenytoin, and diethyldithiocarbamate) had little effect on MK-639 metabolism.	Quinidine	221-230	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	84-90
8742224-3	1996	Previously, it was shown that quinidine reduced digoxin secretion by inhibiting P-glycoprotein (Pgp) in the renal tubule.	Quinidine	30-39	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	80-94
8742224-3	1996	Previously, it was shown that quinidine reduced digoxin secretion by inhibiting P-glycoprotein (Pgp) in the renal tubule.	Quinidine	30-39	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	96-99
8742224-13	1996	This study suggests that Pgp is involved in the drug interaction between digoxin and quinidine in the small intestine.	Quinidine	85-94	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	25-28
8615885-9	1996	Quinidine (5 microm), a CYP2D6 inhibitor, inhibited the formation of DCL approximately 20% when added to microsomal incubations of loratadine at concentrations of 7-35 microM.	Quinidine	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	24-30
8548776-5	1996	The formation of hydroxydocetaxel was strongly reduced by CYP3A inhibitors such as ketoconazole, midazolam, erythromycin, testosterone, orphenadrine, and troleandomycin, whereas quinidine (CYP2D6), hexobarbital, tolbutamide, and mephenytoin (CYP2C) had no or little effect.	Quinidine	178-187	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-63
8706777-2	1996	We studied the ability of quinidine, which is a potent inhibitor of CYP2D6, to penetrate the blood brain barrier and its possible impact on codeine O-demethylation in CNS.	Quinidine	26-35	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	68-74
7498497-2	1995	The "strong" inward-rectifier K+ channel IRK1 was inhibited by quinidine with an EC50 of 0.7 mM, while the "weak" rectifier channel ROMK1 was only moderately inhibited.	Quinidine	63-72	potassium inwardly-rectifying channel, subfamily J, member 2	Rattus norvegicus	41-45
7498497-3	1995	ROMK1(N171D)-IRK1C-term chimeric channels, which carry both sites for strong rectification of IRK1 channels (the negatively charged D171 in the second transmembrane domain and the IRK1-C-terminus including E224), displayed strong rectification like IRK1, but showed weak sensitivity to quinidine-like ROMK1, suggesting independence of quinidine binding and rectification mechanisms.	Quinidine	286-295	potassium inwardly-rectifying channel, subfamily J, member 1	Rattus norvegicus	0-5
7498497-3	1995	ROMK1(N171D)-IRK1C-term chimeric channels, which carry both sites for strong rectification of IRK1 channels (the negatively charged D171 in the second transmembrane domain and the IRK1-C-terminus including E224), displayed strong rectification like IRK1, but showed weak sensitivity to quinidine-like ROMK1, suggesting independence of quinidine binding and rectification mechanisms.	Quinidine	286-295	potassium inwardly-rectifying channel, subfamily J, member 2	Rattus norvegicus	13-17
7498497-3	1995	ROMK1(N171D)-IRK1C-term chimeric channels, which carry both sites for strong rectification of IRK1 channels (the negatively charged D171 in the second transmembrane domain and the IRK1-C-terminus including E224), displayed strong rectification like IRK1, but showed weak sensitivity to quinidine-like ROMK1, suggesting independence of quinidine binding and rectification mechanisms.	Quinidine	335-344	potassium inwardly-rectifying channel, subfamily J, member 1	Rattus norvegicus	0-5
7498497-3	1995	ROMK1(N171D)-IRK1C-term chimeric channels, which carry both sites for strong rectification of IRK1 channels (the negatively charged D171 in the second transmembrane domain and the IRK1-C-terminus including E224), displayed strong rectification like IRK1, but showed weak sensitivity to quinidine-like ROMK1, suggesting independence of quinidine binding and rectification mechanisms.	Quinidine	335-344	potassium inwardly-rectifying channel, subfamily J, member 2	Rattus norvegicus	13-17
7498497-4	1995	Moreover, BIR10 and BIR11, two strong rectifier subunits originally cloned from rat brain, exerted subunit-specific sensitivity to quinidine, being much higher for BIR11.	Quinidine	131-140	potassium inwardly-rectifying channel, subfamily J, member 10	Rattus norvegicus	10-15
7498497-4	1995	Moreover, BIR10 and BIR11, two strong rectifier subunits originally cloned from rat brain, exerted subunit-specific sensitivity to quinidine, being much higher for BIR11.	Quinidine	131-140	potassium inwardly-rectifying channel, subfamily J, member 4	Rattus norvegicus	20-25
7498497-4	1995	Moreover, BIR10 and BIR11, two strong rectifier subunits originally cloned from rat brain, exerted subunit-specific sensitivity to quinidine, being much higher for BIR11.	Quinidine	131-140	potassium inwardly-rectifying channel, subfamily J, member 4	Rattus norvegicus	164-169
7498497-5	1995	Quinidine blockade of IRK1 was not voltage-dependent, but strongly dependent on the pH in the superfusate.	Quinidine	0-9	potassium inwardly-rectifying channel, subfamily J, member 2	Rattus norvegicus	22-26
8591723-4	1995	Studies with human hepatic microsomes and the specific inhibitors furafylene, quinidine, and ketoconazole confirmed the role of CYP1A2 and CYP2D6 and also demonstrated the involvement of the CYP3A subfamily.	Quinidine	78-87	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	128-134
8531125-7	1995	Similarly, CYP 2D6 inactivation also was prevented by quinidine, a specific competitive inhibitor of this isoform.	Quinidine	54-63	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	11-18
8845855-8	1995	Examples of potent inhibitors of CYP2D6 are quinidine, some selective serotonin reuptake inhibitors and some neuroleptics.	Quinidine	44-53	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	33-39
7503774-7	1995	The magnitude of inhibition was: PSC &gt; CsA &gt; quinidine &gt; vinblastine &gt; verapamil &lt; actinomycin D &gt; colchicine &gt; reserpine &gt; bilirubin &gt; doxorubicin &gt; progesterone.	Quinidine	51-60	PSC	Homo sapiens	33-36