Toxin that is known to potentiate erectile function (PubMed:18397797). It binds voltage-dependently to sodium channels (Nav), inhibits the inactivation of the activated channels and decreases the peak inward current (PubMed:19231838, PubMed:26119670). The toxin delays inactivation of Nav1.2/SCN2A, Nav1.3/SCN3A, Nav1.4/SCN4A and Nav1.8/SCN10A, slows the inactivation process and decreases the sodium peak amplitude of Nav1.5/SCN5A and Nav1.6/SCN8A (PubMed:26119670). In vivo, it enhances erectile function by inducing the release of nictric oxide (NO): it slows the sodium current, leading to depolarization, which leads to an increase in calcium influx (probably via activation of N-type calcium channels) which in turn activates neuronal NO synthase (nNOS/NOS1), inducing nitric oxide (NO) production (PubMed:20722794, PubMed:21975567). In a final step, NO activates soluble guanylate cyclase (GUCY1A1/GUCY1B1) which in turn increases cGMP formation, resulting in penile erection (PubMed:23583324). It is noteworthy that the toxin does not provoke erection by inhibiting phosphodiesterase type 5 (PDE5A), an enzyme that hydrolysis cGMP (PubMed:23583324). In vivo, it also causes scratching, lacrimation, hypersalivation, sweating and agitation followed by spastic paralysis of the anterior and posterior extremities and death at dose levels of 0.79 mg/mouse (PubMed:1397265, PubMed:16278100). It is insecticidal to the larval and adult forms of the house fly (PubMed:1397265). The toxin also improves cavernosal relaxation in different models where erectile dysfonction is observed, such as deoxycorticosterone-acetate (DOCA)-salt hypertensive rats, mice models for type-1 diabetes, as well as elderly rats (PubMed:18397797, PubMed:21975567, PubMed:22925420). Expressed by the venom gland. The presence of a 'disulfide through disulfide knot' structurally defines this protein as a knottin. PnPP-19, a 19 AA-peptide that is N-terminally acetylated and C-terminally amidated, has been suggested to be a promising drug candidate for the treatment of erectile dysfunction (PubMed:26119670). The peptide potentiates erection through an increase in nitric oxide (NO)/cGMP production (PubMed:26119670). It has no apparent toxicity (when tested on brain, heart, lung, liver and kidney) and low immunogenicity in mice (PubMed:26119670). It acts by a different mechanism than the native toxin, since it does not affect sodium channels, has no effect on the rat heart, and is independent of extracellular calcium influx through N-type calcium channels (PubMed:26119670). In addition, it has a long half-life since its potentiating effect is observed 15 minutes after injection and lasts about one hour (PubMed:26119670). PnPP-19, a 19 AA-peptide that is N-terminally acetylated and C-terminally amidated, has been suggested to be a promising drug candidate for the treatment of pain (PubMed:29342943). The peptide induces both peripheral and central antinociception (PubMed:28031732, PubMed:28087360). This antinociceptive effect involves the activation of opioid and cannabinoid receptors along with the activation of the NO/cGMP/KATP pathway (PubMed:28031732, PubMed:28087360, PubMed:29342943). Belongs to the neurotoxin 03 (Tx2) family. 06 subfamily.