A team of scientists from Australia and China has found a molecule in centipede venom that could form the basis of a new drug to kill pain as effectively as morphine. The discovery brings new hope to millions of people whose lives are blighted because of chronic pain.
Their findings are published in this week’s online issue of the Proceedings of the National Academy of Sciences, PNAS.
One in five people is thought to suffer from chronic pain, defined as pain that lasts for more than 6 months.
Chronic pain ranges in severity from mild to excruciating, from inconvenient to totally incapacitating. It can be continuous or come and go, and pain signals can linger in the nervous system for years.
There are not many drugs available for treating chronic pain, and many that are have limited effects and cannot be taken in large doses because of side effects.
Some humans are born with gene mutations that make them indifferent to all types of pain. The mutated genes affect a mechanism that the nervous system uses to conduct electrical signals – the NaV1.7 sodium ion channel.
A sodium ion channel is a highly specialized protein that acts like a chemical gateway in the membrane of the nerve cell to only allow entry to sodium ions.
The researchers behind this new study started with the idea that there may be compounds that block the NaV1.7 sodium channel, which could be developed into new drugs for treating pain conditions.
Professor Glenn King, senior investigator from the Institute for Molecular Bioscience at Australia’s University of Queensland, says:
“People without a functioning Nav1.7 channel cannot feel pain, so it’s likely molecules that can block this channel will be powerful painkillers.”
The team focused their attention on centipedes because they paralyze their prey by blocking their Nav sodium channels.
They had already shown in another recent study that the venom of the Chinese red-headed centipede was rich in molecules that can alter the function of nerve channels.
In this latest study, they identified Ssm6a, a peptide from centipede venom that potently and selectively blocks the human NaV1.7 channel.
It was important to show that the compound blocks only the NaV1.7 channel and no other, because closely related channels play key roles in controlling the heart and muscles, says Prof. King.
He and his co-authors write how they found Ssm6a has a “150-fold selectivity for NaV1.7 over all other human NaV subtypes, with the exception of NaV1.2, for which the selectivity is 32-fold.”
Using mice, the team then showed how Ssm6a proved to have a stronger analgesic effect against pain than morphine and did not cause any side effects.
Prof. King says:
“There are a number of FDA-approved drugs derived from venom components currently on the market, with several more in clinical trials or various stages of preclinical development.”
“Our study suggests that centipede venoms, which to date have been largely unstudied, might provide a new source of potential drugs for treating chronic pain and other conditions.”