Key result
Famotidine at concentrations up to 100 μM did not affect action potential parameters in guinea-pig papillary muscles or inhibit hERG K+ currents in CHO-K1 cells.
Why the study?
Does famotidine affect cardiac repolarization parameters in vitro?
Does famotidine affect cardiac repolarization parameters in vitro?
Famotidine lacks direct electrophysiological effects on cardiac repolarization in vitro, suggesting clinical cases of famotidine-associated long QT syndrome may involve other patient-specific factors.
Answers are grounded in this paper and cite their sources.
Famotidine shows no direct repolarization effects in vitro; leaves open patient-specific factors in clinical QT prolongation cases.
The direct effects of famotidine, a selective histamine H(2) receptor antagonist, on the cardiac repolarization process were assessed using two in vitro test systems. Neither famotidine (0.1 and 1 microM), nor its solvent, dimethylsulfoxide (0.1%), affected any of the action potential parameters of guinea-pig papillary muscles, whereas the positive control, dl-sotalol (30 microM), significantly prolonged the action potential duration. Moreover, neither famotidine (0.1, 1 and 10 microM) nor dimethylsulfoxide affected the human ether-a-go-go-related gene (hERG) K(+) current expressed in Chinese hamster ovary-K1 cells, whereas the positive control, E-4031 (0.1 microM), significantly decreased the current. These results indicate famotidine does not directly affect the cardiac repolarization process.
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Nakamura et al. (2009) studied Long QT syndrome (in vitro model). Famotidine vs. 0.1% DMSO (solvent) was evaluated on Action potential parameters and hERG K+ tail current. Famotidine at concentrations up to 100 μM did not affect action potential parameters in guinea-pig papillary muscles or inhibit hERG K+ currents in CHO-K1 cells.
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