The voltage-gated sodium channels Nav1.7, Nav1.8, and Nav1.9 drive action potentials in nociceptors, with Nav1.9 regulating firing thresholds. There is a significant need for new chronic pain treatments due to the limitations of existing analgesics. While Nav1.7 and Nav1.8 have been widely explored, Nav1.9 is an attractive pain target due to its nociceptor-specific expression and genetic link to pain insensitivity. However, its prosecution has been challenging due to expression difficulties in heterologous systems.
Metrion has developed a monoclonal CHO cell line expressing hNav1.9, validated via manual and automated patch clamp techniques. Using Qube384, we established a high-throughput Nav1.9 assay, recording stable currents with GTPγS and multi-hole acquisition. The sodium channel inhibitor TC-N 1752 showed concentration-dependent inhibition (IC50 0.45 µM). Our robust high-throughput electrophysiology assay provides a reliable platform for Nav1.9 drug discovery.
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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.