Sodium channel protein type (unspecified, but standard nomenclature is "Voltage-gated sodium channel" followed by subtype and subunit, e.g., "Sodium channel protein type 10 subunit alpha") (VGSC, Nav (plus subtype, e.g., Nav1.1, Nav1.2, etc.))

Sodium channel proteins are integral membrane proteins forming ion channels highly selective for sodium ions. The most therapeutically relevant group are the voltage-gated sodium channels (VGSCs, also called Nav channels), which are vital for generating and propagating action potentials in excitable cells such as neurons, muscles, and some endocrine cells. The canonical structure consists of a large α-subunit, forming the pore, and smaller auxiliary β-subunits that modulate activity and trafficking. Nine main α-subunit isoforms (Nav1.1–Nav1.9), encoded by SCN genes, are recognized with distinct tissue distribution and physiological roles. Some subtypes (e.g., Nav1.7, Nav1.8, Nav1.9) are of primary interest as therapeutic targets in pain disorders, whereas others are crucial in muscle and cardiac physiology. Many drugs—including local anesthetics, antiarrhythmics, and antiepileptics—act by inhibiting sodium channel function. Clinical development now emphasizes subtype-selective modulators to maximize efficacy and minimize off-target safety concerns, as non-selective inhibitors can cause serious side effects such as arrhythmias and CNS toxicity. Because "Sodium channel protein type" is generic and not a unique protein, it should be replaced by the appropriate subtype name when seeking structured data or therapeutic context.

Other names

Voltage-gated sodium channelNav channelVGSCVoltage-sensitive sodium channel

Blockade of sodium influx (channel blockers); Stabilization of inactive state of channel; Modulation of channel gating or expression