Key result
RPR260243 enhances hERG1 current magnitude by shifting the voltage dependence of inactivation to more positive potentials and slows channel deactivation by interacting with S5 and S6 domains.
Why the study?
Does RPR260243 alter the gating mechanisms and current magnitude of hERG1 channels expressed in Xenopus laevis oocytes?
Population
Xenopus laevis oocytes heterologously expressing human ether-a-go-go-related gene 1 K channels and…
Design
Preclinical
Authors
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Advances hERG1 activation as potential LQTS therapy; leaves open clinical translation and safety data.
Does RPR260243 alter the gating mechanisms and current magnitude of hERG1 channels expressed in Xenopus laevis oocytes?
RPR260243 activates hERG1 channels by slowing deactivation and shifting inactivation voltage dependence, with specific binding determinants located in the S4-S5 linker and S6 domains.
Perry et al. (2007) studied Long QT syndrome (context). RPR260243 vs. Control (absence of drug) was evaluated on hERG1 channel deactivation rate and current magnitude (voltage dependence of inactivation). RPR260243 enhances hERG1 current magnitude by shifting the voltage dependence of inactivation to more positive potentials and slows channel deactivation by interacting with S5 and S6 domains.
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