PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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 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 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 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 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 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 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 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 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 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 22020101-5 2011 Like nifekalant, amiodarone, quinidine and carvedilol, but not by dofetilide, caused the current facilitation of hERG, suggesting that the facilitation is a common effect to a subset of hERG blockers. Quinidine 29-38 ETS transcription factor ERG Homo sapiens 113-117 22020101-5 2011 Like nifekalant, amiodarone, quinidine and carvedilol, but not by dofetilide, caused the current facilitation of hERG, suggesting that the facilitation is a common effect to a subset of hERG blockers. Quinidine 29-38 ETS transcription factor ERG Homo sapiens 186-190 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 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 17604185-5 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 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