Key result
NIP-141 inhibited the transient outward current and the ultra-rapid delayed rectifier K current in human atrial myocytes with half-maximal inhibition concentrations of 16.3 microM and 5.3 microM.
Why the study?
Does NIP-141 inhibit K currents in isolated human atrial myocytes?
Population
Isolated human atrial myocytes (n=5)
Design
Preclinical
Authors
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Hypothesis-generating for NIP-141 in AF; in vivo studies needed before clinical consideration.
Does NIP-141 inhibit K currents in isolated human atrial myocytes?
Effect estimate: IC50 16.3 microM for I(to) and 5.3 microM for I(Kur)
NIP-141 inhibits transient outward and ultra-rapid delayed rectifier K currents in human atrial myocytes, suggesting a mechanism for terminating atrial fibrillation by prolonging action potential duration.
Seki et al. (2002) studied Atrial fibrillation (n=5). NIP-141 was evaluated on Inhibition of transient outward current (I(to)) and ultra-rapid delayed rectifier K current (I(Kur)) (IC50 16.3 microM for I(to) and 5.3 microM for I(Kur)). NIP-141 inhibited the transient outward current and the ultra-rapid delayed rectifier K current in human atrial myocytes with half-maximal inhibition concentrations of 16.3 microM and 5.3 microM.
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