Relief isn’t a term commonly associated with spiders, but Glenn King has found promising molecules in tarantula venom that he hopes will bring respite to the one in five Australian adults suffering from chronic pain.
He and his team at The University of Queensland’s Institute for Molecular Bioscience have found a molecule in tarantula venom that stops the pain signal travelling to the brain.
The team is also studying the venom of other mini-beasts including scorpions, centipedes, ants and assassin bugs.
We have nine sodium channels involved in nerve impulses, named NaV1.1 through to NaV1.9. The tarantula venom molecule targets NaV1.7, which is located in our pain-sensing nerves and is the ‘amplifier’ of pain signals to the brain.
“The cool thing about spiders is that they developed molecules that target the ‘switch’ on the side of these sodium channels, which turns them on or off, and these switches are all quite different,” Glenn says.
Many of the drugs currently on the market target the ‘hole’ in these channels, which are all similar, making it difficult to selectively target just one channel. No-one has developed a drug that exclusively targets NaV1.7.
“Our premise was that spider venoms have lots of different molecules that target these channels. So we took 205 venoms from spiders all around the world, screened their venoms against this human channel and, amazingly, 40 per cent of the venoms completely block that channel. So we had a huge pool of molecules to choose from,” Glenn says.
The next step will be to test the molecules in rodents, which have similar channels to humans, with the hope of isolating a lead molecule within three years to take to clinical trials.