Gating-modifier toxin that potently and selectively acts on Nav1.1/SCN1A and Nav1.3/SCN3A (PubMed:32335140). It enhances hNav1.1/SCN1A currents and delays fast inactivation of the channel (EC(50)=11.6 nM), leading to a sustained current (PubMed:32335140). Similar effects are observed at Nav1.3/SCN3A (EC(50)=11.8 nM), but with less sustained currents (PubMed:32335140). When tested on Nav1.2/SCN2A, the native toxin decreases the peak current by 50% at saturating concentration, whereas the recombinant toxin only shows a weak decrease of peak current (PubMed:32335140). The native toxin specifically activates the voltage-gated sodium channel Nav1.1/SCN1A in somatosensory neurons to elicit acute pain and mechanical allodynia (PubMed:27281198). When tested on Nav1.1/SCN1A, the toxin induces a hyperpolarising shift of the voltage-dependence of steady-state activation, and induces a depolarizing shift in the voltage dependence of inactivation (PubMed:32335140). In addition, it does not modify the recovery from fast inactivation in Nav1.1/SCN1A (PubMed:32335140). The toxin hydrophobic face probably interacts with the domain IV voltage-sensor of Nav1.1/SCN1A and Nav1.3/SCN3A and may trap the voltage-sensing S4 helix in a partially activated state (PubMed:32335140). In vivo, intracerebroventricular injection into mice elicits convulsions, spasms, tremors and rapid death (By similarity). When injected into mouse hindpaw, the toxin elicits an immediate and robust response to pain (PubMed:27281198). However, intraplantar injection of toxin does not cause neurogenic inflammation or alter sensitivity to heat, indicative of a modality-specific effect on mechanosensitive neurons (PubMed:27281198). Expressed by the venom gland. The presence of a 'disulfide through disulfide knot' structurally defines this protein as a knottin. Monoisotopic mass. May be used to develop new agents to treat Nav1.1/SCN1A-associated epilepsies, such as the Dravet syndrome. Shows high stability in both cerebrospinal fluid and human serum (PubMed:32335140). Half-life of the recombinant toxin is >40 hours in human serum, and >70 hours in human cerebrospinal fluid (PubMed:32335140). Does not inhibit Nav1.4/SCN4A, Nav1.5/SCN5A, Nav1.6/SCN8A, and Nav1.7/SCN9A sodium channels. Belongs to the neurotoxin 10 (Hwtx-1) family. 09 (HaTx) subfamily.