Affects sodium-permeability in pituitary GH3 cells in culture. Inhibits the inactivation of sodium activated channels (Nav). Slightly delays the activation time course, and consequently the time to peak. Shifts the voltage dependence of the activation to more negative potentials. Does not reduce the peak sodium-current amplitude. Expressed by the venom gland. Has the structural arrangement of an alpha-helix connected to antiparallel beta-sheets by disulfide bonds (CS-alpha/beta). Belongs to the long (4 C-C) scorpion toxin superfamily. Sodium channel inhibitor family. Beta subfamily. This toxin does not seem to be a typical beta-scorpion toxin, but causes a rather alpha-scorpion toxin-like effect.