Multimodal toxin that enhances nociceptor excitability mainly by the simultaneous stimulation of repetitive firing (through Nav1.8/SCN10A channel current enhancement) and impairment of repolarization (by inhibiting delayed rectifier current of Kv2.1/KCNB1), with a potential contribution from tetrodotoxin-sensitive voltage-gated sodium channels (Nav) modified excitability. Enhances Nav1.8/SCN10A currents (EC(50)=1.1 uM), modifies the channel gating by a right-shift in steady-state inactivation and delays open-state inactivation. Also decreases Kv2.1/KCNB1 currents (IC(50)=0.43 uM) and causes a depolarizing shift in the voltage dependence of activation without change in steady-state inactivation. In addition, inhibits peak currents of human sodium channels (Nav1.1 to Nav1.7, IC(50)=0.38-2.3 uM) and delays fast inactivation of Nav1.1/SCN1A, Nav1.3/SCN3A, Nav1.6/SCN8A, and Nav1.7/SCN9A. In small dorsal root ganglion neurons, induces hyperexcitability by enhancing tetrodotoxin-resistant sodium currents, impairing repolarization and lowering the threshold of action potential firing, consistent with the severe pain associated with envenomation. In vivo, elicits nocifensive behavior in mice after intraplantar injection. Expressed by the venom gland. The presence of a 'disulfide through disulfide knot' structurally defines this protein as a knottin. Monoisotopic mass. Belongs to the neurotoxin 10 (Hwtx-1) family.