Gating-modifier toxin that both inhibits the peak current of human Nav1.1/SCN1A, rat Nav1.2/SCN2A, human Nav1.6/SCN8A, and human Nav1.7/SCN9A and concurrently inhibits fast inactivation of human Nav1.1 and rat Nav1.3/SCN3A. The relative rank order potency for Nav modulation is Nav1.3 (inactivation EC(50)=45 nM) > Nav1.7 > Nav1.2 > Nav1.1 (inactivation) > Nav1.1 > Nav1.6 > Nav1.3 (IC(50)=8 uM). The DII and DIV S3-S4 loops of Nav channel voltage sensors are important for the interaction of this toxin with Nav channels but cannot account for its unique subtype selectivity. It is the variability of the S1-S2 loops between NaV channels which contributes substantially to the selectivity profile observed for this toxin, particularly with regards to fast inactivation. This toxin may bind the channel in the resting state (Probable). Expressed by the venom gland. The presence of a 'disulfide through disulfide knot' structurally defines this protein as a knottin. Monoisotopic mass. NMR structure determination (PDB 5I1X) is done on a mutant of 36 residues with an additional Ser at first position and an Ala residue replacing the Phe-7. Functional information is not known on this mutant. Belongs to the neurotoxin 10 (Hwtx-1) family.