Current cardiac safety testing regimes have successfully prevented new drugs coming to market with unknown proarrhythmic risk. However, they are expensive and time-consuming, and an over-reliance on hERG liability as a marker for proarrhythmia has led to exclusion of useful chemical scaffolds from further drug development. In addition, the focus on hERG ignores the risk posed by potential drug interactions with multiple cardiac ion channels (MICE) that can alter cardiac action potentials.
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.