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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We developed a high-throughput, electrophysiological assay of TREK-1 function to identify novel modulators. The assay was optimized to identify both activators and inhibitors, providing comprehensive mechanistic data for high value, limited supply screening libraries, such as the venom fraction library used in this study (Targeted Venom Discovery Array, T-VDA, Venomtech, UK).
We developed a high-throughput, electrophysiological assay of TREK-1 function to identify novel modulators. The assay was optimized to identify both activators and inhibitors, providing comprehensive mechanistic data for high value, limited supply screening libraries, such as the venom fraction library used in this study (Targeted Venom Discovery Array, T-VDA, Venomtech, UK).