Drug induced cardiotoxicity remains an important challenge in drug development because a promising compound can fail when unexpected effects on cardiac ion channels appear during later stages of development. Computational cardiac safety assessment has traditionally focused heavily on hERG, but cardiac electrophysiology is controlled by several ion channels working together. In particular, hERG, Cav1.2, and Nav1.5 regulate different phases of the cardiac action potential. This means that evaluating only one channel can provide an incomplete picture of potential cardiac risk. This was the main motivation for developing Cardiosim Tox, a computational platform designed to predict both the risk of channel blockade and the potency of that blockade, represented by pIC50, across all three channels.

Arch. Toxicol.2026-08-18