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.

Optical voltage imaging of human iPSC-derived cardiomyocytes was used to assess electrophysiological effects of compounds beyond hERG inhibition. Action potential waveform analysis revealed compound-specific and concentration-dependent changes, enabling mechanistic differentiation of multichannel activity and demonstrating a human-relevant approach for translational cardiac safety assessment.

Nature Communications paper ‘The nucleobase guanine at the 3′-terminus of oligonucleotide RGLS4326 drives off-target AMPAR inhibition and CNS toxicity'

The presence of sensory neuron markers, excitability properties consistent with sensory neurons, and evidence of nociceptor ion channels (using both RNASeq and electrophysiology) provides strong evidence that iCell Sensory Neurons have a robust sensory neuron phenotype suitable for supporting pain discovery programs.

Using automated patch clamp technology, we evaluate the potency and selectivity of ten Nav1.7-selective arachnid peptide toxins, which have been fused to the C-terminus (Fc region) of human IgG1.