Electrophysiological characterization of the state-dependent inhibition of Kv7.1 and IKs by UCL2077

Scritto il 01/11/2025
da Daniel Sastre

In cardiomyocytes, Kv7.1 associates with the regulatory subunit KCNE1 to generate the delayed rectifier potassium current I(Ks), which plays a crucial role in cardiac repolarization at elevated heart rates. Gain-of-function mutations in either of these subunits are associated with short QT syndrome, a condition that increases the risk of cardiac arrhythmias including atrial fibrillation, syncope, and sudden death. Therefore, the study of pharmacological inhibitors of Kv7.1 and I(Ks) is of...

Mol Pharmacol. 2025 Nov;107(11):100076. doi: 10.1016/j.molpha.2025.100076. Epub 2025 Sep 25.

ABSTRACT

In cardiomyocytes, Kv7.1 associates with the regulatory subunit KCNE1 to generate the delayed rectifier potassium current I, which plays a crucial role in cardiac repolarization at elevated heart rates. Gain-of-function mutations in either of these subunits are associated with short QT syndrome, a condition that increases the risk of cardiac arrhythmias including atrial fibrillation, syncope, and sudden death. Therefore, the study of pharmacological inhibitors of Kv7.1 and I is of significant therapeutic interest. In this work, we used whole-cell patch clamp recordings to characterize the electrophysiological effects of the Kv7.1 blocker 3-(triphenylmethylaminomethyl)pyridine (UCL2077) in both Kv7.1 and I (Kv7.1 + KCNE1) channels. We found that UCL2077 inhibited both Kv7.1 and I channels with high affinity (IC in the picomolar range) and mild voltage dependence. The drug induced a biphasic time-dependent current decay and reduced current reactivation of Kv7.1, whereas the kinetics of I were unaffected. We examined state dependence using mutations that functionally stabilize Kv7.1/I in either the intermediate-open (E160R/R231E) or in the activated-open (E160R/R237E) state. In both channels, UCL2077 potency correlated with the strength of the electromechanical coupling. Our results are further supported by a kinetic Markov model simulating UCL2077 binding that closely resembles the experimental currents. Overall, our work provides an in-depth characterization of UCL2077's action on Kv7.1 and I channels, offering valuable insights for the development of Kv7.1/I inhibitors in the context of short QT syndrome and other cardiac arrhythmias. SIGNIFICANCE STATEMENT: This study characterizes UCL2077: a highly specific, high-affinity inhibitor of Kv7.1 and I channels with therapeutic implications for cardiac arrhythmia. Our work reveals a picomolar affinity, mild voltage dependence, and a kinetic modulation consistent with state-dependent open-channel block.

PMID:41175503 | PMC:PMC12799529 | DOI:10.1016/j.molpha.2025.100076