PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 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 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 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 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 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 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 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 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 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 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 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>A (p.R950Q) in patient 1 and c.2677G>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 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 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 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 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 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 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 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 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 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 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 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 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 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> disopyramide> sotalol> 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> disopyramide> sotalol> 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 28010169-0 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 81-88 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 < 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 (>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 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 (>50 % inhibition). Quinidine 62-71 potassium two pore domain channel subfamily K member 13 Homo sapiens 150-156 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 23836691-13 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 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 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 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 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 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 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 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 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 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 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 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 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 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 22459173-0 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 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 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 22459173-5 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 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 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 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 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 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 22215264-1 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 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 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 < .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 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 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 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 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 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 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 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 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 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 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 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 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 21725799-0 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 21725799-6 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 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 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 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 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 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 21832258-4 2011 The non-CYP3A4 inhibitors diethyldithiocarbamate, quercetin, quinidine, sulfaphenazole, ticlopidine, and tranylcypromine were found to have substantially lower (maximum inhibition of <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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 19816852-2 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 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 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 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 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 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 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 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 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 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 < 0.01). Quinidine 43-52 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 24-30 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 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 20332617-6 2010 This LPS-induced current exhibited KCNQ1 K+ channel characteristics, i.e. inhibition by quinidine, chromanol293B and low dose of HMR1556 (IC50<1 microM) and insensitive to TEA and charybdotoxin. Quinidine 88-97 potassium voltage-gated channel, subfamily Q, member 1 Mus musculus 35-40 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 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 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 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 3 subfamily A member 4 Homo sapiens 117-123 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, sub-family B (MDR/TAP), member 1B Mus musculus 62-67 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 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 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 19617705-0 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 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 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 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 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 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 B member 1 Homo sapiens 36-40 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 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 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 18724381-7 2008 KEY RESULTS: The N588K mutation attenuated I(hERG) inhibition in the following order: E-4031>amiodarone>quinidine>propafenone>disopyramide. Quinidine 110-119 ETS transcription factor ERG Homo sapiens 45-49 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 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 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 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 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-->A/Papp A-->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-->A/Papp A-->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-->A/Papp A-->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-->A/Papp A-->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-->A/Papp A-->B) for EC. Quinidine 45-54 pappalysin 1 Homo sapiens 249-255 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 18445989-9 2008 Quinidine (1 microM) completely inhibited the metabolism of enclomiphene by all the EM livers and by recombinant CYP2D6 (p<0.001, one way ANOVA). Quinidine 0-9 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 113-119 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 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 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 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 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 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 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 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 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 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 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 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 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 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 17094122-5 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 190-194 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 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 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 < or = 0.05), respectively; that by isolate X was 20 +/- 4, 23 +/- 5, and 39 +/- 7 (P < 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 17172009-8 2006 Na+/Mg2+ antiport is inhibited by amiloride, quinidine and imipramine. Quinidine 45-54 mucin 7, secreted Homo sapiens 4-7 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 17172009-13 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 15821840-5 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 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 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 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 < .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<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 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 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 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>QDR3>>>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>QDR3>>>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>QDR3>>>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>QDR3>>>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>QDR3>>>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>QDR3>>>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>QDR3>>>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>QDR3>>>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>QDR3>>>QDR1). Quinidine 213-222 multidrug transporter Saccharomyces cerevisiae S288C 108-113 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 15507542-6 2005 This catalytic activity was >95% inhibited by quinidine, a CYP2D6 inhibitor. Quinidine 49-58 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 62-68 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 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 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 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 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 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 15363950-8 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 14555336-11 2003 The CYP2D6 specific chemical inhibitor quinidine (3 microM) significantly (p<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 12867484-10 2003 Incubation of 2 microM MPPP with 3 microM of the CYP2D6-specific inhibitor quinidine resulted in significant (p < 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 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 <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 <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 <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 <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 <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 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 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 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 12948010-8 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 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 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 > ritonavir > loperamide, verapamil, daunomycin > digoxin, cyclosporin A > dexamethasone, and vinblastine. Quinidine 146-155 ATP binding cassette subfamily B member 1 Homo sapiens 113-117 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 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 12893521-10 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 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 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 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 >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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 12086981-21 2002 The rank potency as HERG blockers of the Class I drugs tested in this study was QUIN=PROPAF>FLEC>>LIG. Quinidine 80-84 potassium voltage-gated channel subfamily H member 2 Homo sapiens 20-24 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 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 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 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<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 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 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 12006904-8 2002 Quinidine > fluoxetine > 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 > fluoxetine > 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 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 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 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 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 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< times lower for Oatp2 compared with Oatpl. Quinidine 31-40 solute carrier organic anion transporter family, member 1a4 Rattus norvegicus 108-113 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 11336351-6 2001 The potency of inhibition of P-gp was cyclosporine > tacrolimus > quinidine > verapamil > vinblastine. Quinidine 72-81 ATP binding cassette subfamily B member 1 Homo sapiens 29-33 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 (> 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 (> 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 (> 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 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 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 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 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 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 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 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 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 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 10421620-7 1999 The enzyme activity was significantly (p <.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 <.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 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 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<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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 2 subfamily D member 6 Homo sapiens 42-48 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 3 subfamily A member 4 Homo sapiens 160-166 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 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 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 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 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 10702886-12 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 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 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 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 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 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 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 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 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 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 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 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 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 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 9620113-8 1998 Quinidine unbound fraction (UF) was related to ORM phenotype. Quinidine 0-9 orosomucoid 1 Homo sapiens 47-50 9620113-12 1998 Quinidine binding showed significant relationships to specific ORM variants. Quinidine 0-9 orosomucoid 1 Homo sapiens 63-66 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 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 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 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 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 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 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 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 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 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 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 > 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 9353372-2 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 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 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 < 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 < 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 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 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 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 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 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 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 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 24-33 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 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 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 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 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 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 9130163-2 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 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 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 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 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 9037249-7 1997 The proportion of activity inhibited by quinidine correlated positively with total microsomal tamoxifen 4-hydroxylation activity (rs = 0.89, P < 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 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 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 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 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 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 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 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 < 0.001). Quinidine 51-60 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 97-103 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 7503774-7 1995 The magnitude of inhibition was: PSC > CsA > quinidine > vinblastine > verapamil < actinomycin D > colchicine > reserpine > bilirubin > doxorubicin > progesterone. Quinidine 51-60 PSC Homo sapiens 33-36 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 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 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 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 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 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 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 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 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 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 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 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 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 7883281-0 1995 Prevention of ischaemia-induced biochemical changes by curcumin & quinidine in the cat heart. Quinidine 70-79 catalase Homo sapiens 87-90 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 8301569-0 1994 Albumin decreases myocardial permeability of unbound quinidine in perfused rat heart. Quinidine 53-62 albumin Rattus norvegicus 0-7 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 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 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 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 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 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 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 8272795-13 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 1611804-7 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 0-9 potassium sodium-activated channel subfamily T member 1 Homo sapiens 88-93 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 3755602-4 1986 In mouse macrophages, PAF-acether stimulated a quinidine-sensitive K+ efflux. Quinidine 47-56 patchy fur Mus musculus 22-25 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 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 3945161-1 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 3945161-5 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 136-140 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 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 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 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 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 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 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 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 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 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 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 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 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 1188181-1 1975 Quinidine is bound at two sets of sites on serum albumin. Quinidine 0-9 albumin Homo sapiens 43-56 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 31770573-7 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 31770573-3 2020 Here, we explore the FDA-approved drug quinidine as a P-gp inhibitor. Quinidine 39-48 phosphoglycolate phosphatase Mus musculus 54-58 31770573-7 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 31770573-4 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 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 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 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 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 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 31483500-17 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 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 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 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 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 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 H member 2 Homo sapiens 129-133 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 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 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 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 31388363-0 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 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 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 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