Alpha toxins bind voltage-independently at site-3 of sodium channels (Nav) and inhibit the inactivation of the activated channels, thereby blocking neuronal transmission. This toxin is active against mammals (Ref.1). The recombinant toxin selectively inhibits the fast inactivation of hNav1.7/SCN9A channel (EC(50)=136.7 nM) (PubMed:34379289). Is potent in inhibiting the fast inactivation of hNav1.7 and has little effect on the steady-state inactivation (PubMed:34379289). In vivo, intravenous injection into mice induces muscle contraction, leading to severe paralysis and death (Ref.1). Expressed by the venom gland. Has the structural arrangement of an alpha-helix connected to antiparallel beta-sheets by disulfide bonds (CS-alpha/beta). LD(50) of native toxin is 29.5 ug/kg by intravenous injection into mice. LD(100) is 39 ug/kg by intravenous injection into mice. LD(50) of recombinant toxin is 167 ug/kg by intravenous injection into mice. Has very weak activity on hNav1.5/SCN5A sodium channels (EC(50)=31.9 uM). Belongs to the long (4 C-C) scorpion toxin superfamily. Sodium channel inhibitor family. Alpha subfamily.