Gating-modifier toxin that inhibits voltage-gated sodium channel with a preference for hNav1.7/SCN9A (IC(50)=25.4 nM) over hNav1.1/SCN1A (IC(50)=4.1 uM), hNav1.2/SCN2A (IC(50)=813 nM), and hNav1.6/SCN8A (IC(50)=15.2 uM) (PubMed:24082113). Is an effective analgesic in rodent pain models, since it is several-fold more effective than morphine in a rodent model of formalin-induced pain and is equipotent with morphine in its ability to reduce thermal and acid-induced pain (PubMed:24082113). In addition, this peptide shows a high level of resistance to proteases and a high thermal stability that may be explained by its predominant composition of alpha-helices (PubMed:24082113). Expressed by the venom gland. Is exclusively composed of 4 tightly packed alpha helices (no beta strand is present). Does not show effects on sodium channels hNav1.3/SCN3A, hNav1.4/SCN4A, hNav1.5/SCN5A, hNav1.8/SCN10A and potassium channel hKv11.1/KCNH2 (PubMed:24082113). The synthetic peptide has been found to be inactive against Nav1.7/SCN9A at concentrations up to 1 uM, in contrast to the isolated natural peptide described in PubMed:24082113 (PubMed:25658507). Intraperitoneal injection of this toxin has no effect on blood pressure, heart rate, or motor function (as judged by a swim test) at doses up to 1-10 umol/kg (PubMed:24082113). Arose via modification of ancestral neuropeptide hormones (ion transport peptide/crustacean hyperglycemic hormones (ITP/CHH)). Belongs to the scoloptoxin-03 family.