Sodium channel protein type 10 subunit alpha (SCN10A) (SCN10A)

Sodium channel protein type 10 subunit alpha (SCN10A), also known as Nav1.8, is a tetrodotoxin-resistant voltage-gated sodium channel primarily expressed in the peripheral nervous system, specifically within nociceptive neurons of the dorsal root ganglia [1, 2, 8]. It plays a fundamental role in the initiation and maintenance of action potentials in response to noxious stimuli, making it a key mediator of pain signaling [2, 6, 13]. Beyond its neuronal function, SCN10A is also expressed in the heart, where it influences cardiac conduction and has been linked to arrhythmias such as Brugada syndrome and atrial fibrillation [5, 9, 14]. In clinical contexts, gain-of-function mutations in SCN10A are associated with painful conditions like small fiber neuropathy and familial episodic pain syndromes [1, 4, 7]. Because of its restricted expression in peripheral nociceptors, SCN10A is a highly attractive therapeutic target for the development of non-opioid analgesics [6, 13]. Selective inhibitors, such as suzetrigine (VX-548), are designed to block sodium influx through Nav1.8 channels, thereby providing potent pain relief for acute and neuropathic pain while minimizing central nervous system side effects and the risk of addiction [6, 13].

Other names

Nav1.8 [1, 2]PN3 [1, 3]SNS [2, 3]hPN3 [1, 3]Peripheral nerve sodium channel 3 [1, 4]Sodium channel protein type X subunit alpha [1, 8]FEPS2 [3, 7]

Selective inhibition of the Nav1.8 voltage-gated sodium channel, which blocks the influx of sodium ions into nociceptive neurons, thereby preventing the generation and propagation of pain signals [6, 13].