Gating-modifier toxin that potently inhibits inactivation of the mammalian Nav1.1/SCN1A sodium channel (EC(50)=38 nM) (PubMed:27281198, PubMed:30076230). Also moderately inhibits inactivation of Nav1.2/SCN2A (EC(50)=236 nM) and Nav1.3/SCN3A (EC(50)=220 nM) when the channels are expressed in oocytes without the beta-1 auxiliary subunit (PubMed:27281198). Does not inhibit inactivation of Nav1.2/SCN2A when the channel is coexpressed with the beta-1 auxiliary subunit (PubMed:30076230). When tested on Nav1.1/SCN1A channel, it enhances peak current amplitude and potently delays channel inactivation in a dose-dependent manner, leading to a large sustained current (PubMed:30076230). It has no effect on the voltage-dependence of steady-state activation, and induces a depolarizing shift in the voltage dependence of inactivation (PubMed:30076230). In addition, it does not modify the recovery from fast inactivation in Nav1.1/SCN1A (PubMed:30076230). The binding affinity and subtype selectivity of the toxin towards Nav1.1/SCN1A channel is determined by residues within both the S1-S2 and S3-S4 loops of the domain IV voltage sensor of the channel (PubMed:27281198). This toxin also weakly inhibits several subtypes of voltage-gated potassium channels (PubMed:27281198). It moderately blocks Kv2.1/KCNB1 (23% inhibition at 100 nM), Kv2.2/KCNB2 (19.7% at 100 nM and 51% at 300 nM), Kv4.1/KCND1 (IC(50)=280 nM), Kv4.2/KCND2 (39% at 300 nM) and Kv4.3/KCND3 (43% at 300 nM) (PubMed:12065754). In vivo, intracerebroventricular injection into mice elicits convulsions, spasms, tremors and rapid death (PubMed:12065754). 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). In Dravet syndrome mice model, intracerebroventricular infusion of this peptide rescues mice from seizures and premature death (PubMed:30076230). 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. In Dravet syndrome mice model, by a selective activation of Nav1.1/SCN1A channels, this peptide restores the function of inhibitory interneurons without affecting the firing of excitatory neurons. Shows poor stability in cerebrospinal fluid and moderate stability in human serum (PubMed:32335140, PubMed:30076230). Half-life of the toxin is about 1.7 hour in cerebrospinal fluid (PubMed:30076230). Half-life of the native toxin is about 10 hours in human serum (PubMed:32335140). Does not inhibit Nav1.4/SCN4A, Nav1.5/SCN5A, Nav1.6/SCN8A, Nav1.7/SCN9A, and Nav1.8/SCN10A at concentrations up to 50 nM or 1 uM (PubMed:27281198, PubMed:30076230). Does not inhibit Nav1.2/SCN2A at concentrations up to 50 nM (PubMed:30076230). Has no or very weak effect on Kv1.1/KCNA1, Kv1.2/KCNA2, Kv1.3/KCNA3, Kv1.4/KCNA4, Kv1.5/KCNA5, Kv1.6/KCNA6 and Kv3.4/KCNC4 (PubMed:12065754). Does not show significant effects on Kv1.7/KCNQ1, Kv10.1/KCNH1/EAG1, Kv11.1/KCNH2/ERG1, KCa1.1/KCNMA1, KCa2.1/KCNN1 and KCa2.3/KCNN3 (PubMed:12065754). Belongs to the neurotoxin 10 (Hwtx-1) family. 09 (HaTx) subfamily.