We have developed a robust high-throughput automated electrophysiology assay using a monoclonal CHO-hNav1.9 cellular reagent suitable for fully supporting a Nav1.9 discovery program.
The TTX-resistant sodium channel Nav1.8 is expressed in peripheral sensory nociceptors and is implicated in a range of inflammatory and visceral pain conditions such as irritable bowel syndrome (IBS)1. Nav1.8 channel function in sensory neurons changes after injury or inflammation, with a redistribution from the soma to axons and upregulated activity through inflammatory mediators and signalling pathways. This is thought to underlie increased neuronal excitability and a greater role of Nav1.8 currents in persistent, repetitive and ectopic action potential firing in inflammatory and visceral pain. Several gain-of-function mutations in Nav1.8 have also been detected in human patients suffering from small fibre neuropathy (SFN), offering similar genetic target validation and clinical population for personalised medicine approaches seen with Nav1.7 mutations in primary erythmelalgia, paroxysmal extreme pain and SFN patients.
We have developed a robust high-throughput automated electrophysiology assay using a monoclonal CHO-hNav1.9 cellular reagent suitable for fully supporting a Nav1.9 discovery program.
Metrion and Sophion present findings that determine whether other insoluble salts can act as seal enhancers and how these solution pairs affect the biophysical properties and pharmacology of the investigated ion channels.