Alpha toxins bind voltage-independently at site-3 of sodium channels (Nav) and inhibit the inactivation of the activated channels, thereby blocking neuronal transmission. The toxin principally slows the inactivation process of TTX-sensitive sodium channels (PubMed:23685008). It is active on rat brain Nav1.2/SCN2A sodium channel (EC(50)=2.6 nM) and on rat skeletal muscle Nav1.4/SCN4A sodium channel (EC(50)=2.2 nM) (PubMed:12911331), as well as on human neuronal Nav1.7/SCN9A (EC(50)=6.8 nM) (PubMed:23685008). This toxin is active against mammals. In vivo, intraplantar injection into mice induces spontaneous pain responses (PubMed:23685008). Expressed by the venom gland. Has the structural arrangement of an alpha-helix connected to antiparallel beta-sheets by disulfide bonds (CS-alpha/beta). The amidation of His-83 is not necessary for toxicity. LD(50) is 25 ng/kg by intracerebroventricular injection into mice, and LD(50) is 11 ug/kg by subcutaneous injection. Does not act on Nav1.8/SCN10A and Nav1.9/SCN11A when tested on TTX-resistant sodium channels. Belongs to the long (4 C-C) scorpion toxin superfamily. Sodium channel inhibitor family. Alpha subfamily.