Action Potential Waveform Analysis in Human IPSC-Cardiomyocytes Enables Mechanistic Assessment of Multichannel Cardiac Effects

Cardiac toxicity remains the leading cause of new drug safety side-effects. Current preclinical cardiac safety assays rely on in vitro cell-based ion channel assays and ex vivo and in vivo animal models⁽¹⁾. These assays provide an indication of acute risk but they do not always predict the effect of chronic compound exposure, as recently seen with oncology drugs. Therefore, new assays are required to characterise chronic structural and functional effects in human cells earlier in drug discovery. Impedance-based technology can provide more accurate chronic cardiotoxicity measurements in an efficient manner using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs).

Automated patch clamp enables robust NaV1.9 screening, accelerating discovery of selective sodium channel modulators for pain research.

Automated patch clamp enables robust NaV1.9 screening, accelerating discovery of selective sodium channel modulators for pain research.

Using Qube 384, we profiled a panel of NaV inhibitors across species, providing valuable translational insight early in analgesic drug discovery.

We explore hNav1.9's unique fast and slow inactivation properties using Qube 384 and QPatch 48 platforms, helping to build more predictive screening assays for state-dependent inhibitors.

Development of a robust hNaV1.9 high-throughput screening assay on the Sophion Qube384 platform. This is complemented by a suite of ion channel selectivity assays and sensory neuron recordings to create a versatile screening cascade to support NaV1.9 drug discovery programmes.

Reliable, high-throughput KV7 assays paired with expert interpretation enable faster progression of pain and epilepsy drug discovery programmes.

By accurately defining the drug exposure levels that affect QRS duration, researchers can establish safety margins, prioritise lower-risk compounds, and reduce the chance of late-stage failures due to cardiac toxicity

NS5806, widely used as a Kv4-selective activator, also activates TREK-1 and TREK-2 potassium channels.