The spider toxin Phα1β recombinant possesses strong analgesic activity

- Phα1β, a Voltage-Gated Calcium Channel blocker and the Recombinant Version were both tested in rodent pain models.
- Both peptides caused antinociception on pain models of chronic chonstriction injury, capsaicin and formalin injections.
- Phα1β and the Recombinant caused full reversion of the hyperalgesia induced by melanoma cancer pain model.
- The antinociceptive effects of the native Phα1β were fully mimicked by the Recombinant, without causing any side effects.

The native Phα1β - a Voltage-Gated Calcium Channel (VGCC) blocker - and its Recombinant Version - were both tested in rodent pain models with an intraplantar injections of capsaicin or formalin, a chronic constriction injury, and melanoma cancer related pain. The formalin nociceptive behaviour in the neurogenic phase was not affected by the toxin pre-treatments, while in the inflammatory phase, Phα1β and the Recombinant form caused a significant reduction. The nociception that was triggered by capsaicin, an agonist of the TRPV1 vanilloid receptor, was totally blocked by 100 pmol/site, i.t. of Phα1β or the recombinant version. For the neuropathic pain that was induced by a chronic constriction injury of the sciatic nerve, Phα1β and its Recombinant reduced the allodynia that was induced by the CCI procedure in the rats and the hypersensitivity lasted for 4 h. Fourteen days after the inoculation of the B16-F10 melanoma cells in the mice, a marked hyperalgesia was induced in the melanoma cancer pain model. Phα1β and the Recombinant form reduced the hyperalgesia with a full reversion at 100 pmol/site i.t. The inhibitory effects of the nociception that was induced by native Phα1β and the Recombinant in the studied pain models were not statistically different and they developed with no side effects.