Gating-modifier toxin that targets voltage-gated sodium channels with a preferential activity on Nav1.7/SCN9A. On Nav1.7/SCN9A, the toxin acts by shifting the voltage-dependence of activation to more depolarized potentials, whereas it does not cause significant effect on the voltage-dependence of activation on other sodium channels. Minor effects are observed on the voltage-dependence of steady-state fast inactivation for all sodium channels tested (Nav1.1/SCN1A-Nav1.8/SCN10A). By testing the toxin on channel chimera, it has been shown to interact with the S3-S4 linkers in DII and DIV domains of Nav1.7/SCN9A. In vivo, the toxin dose-dependently reduces OD1-induced spontaneous pain behaviors. Expressed by the venom gland. The presence of a 'disulfide through disulfide knot' structurally defines this protein as a knottin. Monoisotopic mass. Shows no or weak effect on hNav1.8/SCN10A, rKv2.1/KCNB1 and hCav1.2/CACNA1C, hCav2.2/CACNA1B, alpha-7/SCN9A nAChR, alpha-3/SCN3A nAChR. Belongs to the neurotoxin 10 (Hwtx-1) family. 28 (Jztx-11) subfamily.