Spider venom compounds can relieve chronic pain

Melbourne

Chronic pain that cannot be controlled can ruin people’s lives. Not any more. New research shows that seven compounds found in spider venom block a key step in the body’s ability to pass pain signals to the brain.

Of the seven promising compounds, the team has discovered one that was particularly potent.

It had a chemical structure that suggested it would have high levels of chemical, thermal and biological stability that would be essential for administering a new medicine.

People sense that part of their body is hurting when nerves from the affected area send signals to the brain through what is called the pain pathway.

“Previous research shows indifference to pain among people who lack Nav1.7 channels due to a naturally-occurring genetic mutation - so blocking these channels has the potential of turning off pain in people with normal pain pathways,” explained lead researcher Glenn King from the University of Queensland’s Institute for Molecular Bioscience in Australia.

A conservative estimate indicates that there are nine million spider-venom peptides (protein molecules) and only 0.01 percent of this vast pharmacological landscape has been explored so far.

The challenge was to build a research method that could search through this huge number of peptides, looking for the ones that could be useful.

Taking up this challenge, the research team built a system that could rapidly analyse the compounds in spider venoms.

Using their novel approach, venoms from 206 species of spider were screened, revealing that 40 percent of the venoms contained at least one compound that blocked human Nav1.7 channels.

“Together, these properties make it particularly exciting as a potential painkiller,” added co-researcher Julie Kaae Klint.

“Untapping this natural source of new medicines brings a distinct hope of accelerating the development of a new class of painkillers that can help people who suffer from chronic pain that cannot be treated with current treatment options,” Klint pointed out.

The paper was published in the British Journal of Pharmacology. — IANS