Key result
Nav1.5 inhibitors evaluated for effects on intracellular sodium and electrophysiological properties in hiPSC-derived cardiomyocytes.
Why the study?
Existing methods either lack throughput or fail to mechanistically distinguish between sodium channel modulators, creating a need for improved cardiac safety screening.
A novel fluorescence-based sodium flux imaging method in hiPSC-CMs can mechanistically distinguish sodium channel modulators for early-phase cardiotoxicity screening.
Drug-induced cardiotoxicity remains a significant challenge in pharmaceutical development. While patch-clamp remains the gold standard for evaluating ion channel effects, its low throughput limits early-phase screening. Multi-electrode array (MEA) systems offer higher throughput but often fail to mechanistically distinguish between various sodium channel modulators, such as agonists versus antagonists. The purpose of this study was to develop a cardiac safety assessment method capable of mechanistically distinguishing sodium channel modulators. In this study, we developed a cardiac safety assessment method using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) combined with fluorescence-based intracellular Na
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Kim et al. (2026) studied this question. Nav1.5 inhibitors (Flecainide, Lidocaine, Ajmaline, Phenytoin) vs. Vehicle (0.1% DMSO, Nifedipine 0.1 μM) was evaluated.
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