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Nav1.7 is a voltage-gated sodium channel that forms the pore-forming alpha subunit of the channel complex. It is critical for generation and conduction of action potentials, particularly in neurons involved in pain signaling (nociceptors). Mutations in SCN9A/Nav1.7 are associated with several human pain disorders, including congenital insensitivity to pain, primary erythromelalgia, and paroxysmal extreme pain disorder. It is a major target for analgesic drug development.
Sodium channel blockade
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