NaV1.8 is a voltage-gated sodium channel, encoded by the gene, that is primarily located in peripheral sensory neurons and plays a major role in transmitting pain signals.
Voltage-gated sodium channel subtype encoded by **SCN10A**, expressed selectively in peripheral sensory neurons and notably absent from CNS and cardiac tissue at therapeutically relevant levels.
It is the primary driver of nociceptor action potential propagation
Because Nav1.8 is peripherally restricted and not expressed in cardiac myocytes (unlike Nav1.5), selective blockade offers analgesia without CNS side effects or cardiac risk— the fundamental limitation of non-selective sodium channel blockers (lidocaine, mexiletine, carbamazepine).
Because it is found outside the central nervous system, blocking it offers a way to treat pain without the addiction risks tied to opioids.
Nervous system: Found mostly in peripheral nerve fibers and dorsal root ganglia.
Signal control: Regulates how sodium enters cells to start and send pain messages to the body.
Drug target: Targeted by non-addictive pain medicines like suzetrigine (Journavx).
Gain-of-function SCN10A mutations found in ~3% of painful neuropathy patients → establishes direct pathogenic role.
Suzetrigine (Journavx) is the first selective Nav1.8 blocker to reach market.