Beta toxins modify sodium channel function in two ways: an excitatory effect (shifting the activation process to more negative potential) and/or a depressant effect (reducing the peak current). At concentration of 500 nM this toxin produces channel opening at more negative potentials in hNav1.2/SCN2A and hNav1.3/SCN3A, which shows the biggest effect. On the other hand the peak current is decreased in hNav1.4/SCN4A and hNav1.5/SCN5A channels, without apparent modification of the activation gate. This toxin is active against mammals. 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) is 28.5 ug/kg by intracranial injection into mice. Does not produce significant modification of hNav1.1/SCN1A and hNav1.6/SCN8A currents. This toxin is thought to be responsible for the intoxication symptoms caused by the sting of this species to humans. Belongs to the long (4 C-C) scorpion toxin superfamily. Sodium channel inhibitor family. Beta subfamily.