WIKIMEDIA, YASUNORI KOIDEAn alteration in a sodium ion channel can leave people completely indifferent to pain, making the channel an appealing target for analgesic development. In a report published in the Proceedings of the National Academy of Sciences this week (September 30), researchers characterize a newly discovered component of centipede venom that inhibits this particular sodium channel, NaV1.7, and works even better than morphine to dampen pain in rodents. “Centipedes worked out hundreds of millions of years ago the easiest way to catch prey was to paralyze them by blocking their NaV channel,” Glenn King, one of the authors of the study, told ABC. “We're just lucky that of the nine NaV channels in humans, it hit the one we were after.”
King, a researcher at the University of Queensland, said that other attempts to bind the NaV1.7 channel blocked other sodium channels and produced untoward effects. But King and his colleagues found that the venom-derived peptide was much more selective for 1.7 than for other sodium ion channels. And it showed no negative impacts on heart rate, blood pressure, or motor function. The centipede peptide was also more potent than morphine in a chemically induced pain assay in mice, and was just as effective as the narcotic in relieving pain induced by acid or heat.
Of course, a number of studies will have to validate the safety and efficacy of the drug before it could be used to treat pain in humans. Already, several venom-derived peptides ...
