When you think of animals such as spiders and cone snails, you imagine the pain and harm they can cause. But did you know that some of the world’s deadliest creatures may hold the key to the next generation of painkillers and treatments for other diseases?
At UQ’s Institute for Molecular Bioscience (IMB), Professor Glenn King and Associate Professor Irina Vetter are exploring the chemical cocktails present in the venom of animals such as spiders and cone snails to uncover new treatments for pain, stroke and epilepsy.
At this Global Leadership Series event, Professor King and Professor Vetter discussed how these dangerous venoms can be developed into medicines, the exciting discoveries at IMB and what the next steps are for progressing new treatments into clinical trials. Here’s what they had to say.
Venom is complex (no, we’re not talking about the Marvel fictional character)
Venoms have evolved over millions of years into a cocktail of complex chemical compounds. For example, the funnel web spider has more than 1,000 different toxins, but only one of those toxins are lethal to humans - allowing us to put to good use the other 999 toxins.
Are there any drugs currently available that are derived from venom?
Absolutely. The first venom-derived drug, Captopril, is derived from the venom of the South American Pit Viper and it was the world’s first anti-hypertensive drug. Those bitten by the viper experienced a sudden drop in blood pressure. Pharmacologists studied the venom to discover which compound was causing the lowered blood pressure. They then used this peptide to create Captopril.
A more recently developed drug called Ziconotide, derived from the venom of a marine cone snail, is an analgesic used to treat chronic pain.
There are other drugs which are currently going through clinical trials including a peptide from the sea anemone for treating autoimmune disease and compounds from scorpions that binds to tumours, allowing surgeons to easily identify the margin of tumours.
What can venoms tell us about understanding and treating pain?
Venoms are used to not only capture prey but also to deter predators by rapidly inducing severe pain. For example, a sting from a bullet ant isn’t enough to kill but the pain caused by a sting from this ant lasts for up to five hours and has been described as being “like walking over flaming charcoal with a three-inch nail embedded in your heel” (Justin Schmidt, entomologist).
Pain is transmitted by specialised nerve cells called sensory neurons that extend to almost every tissue in the human body; some of these neurons are the body’s longest cells. When we encounter noxious stimuli, our sensory neurons send a signal to the brain, via the spinal cord, which the brain interprets as pain. By tracing the effect of venoms on sensory neurons, we can understand how venoms activate pain pathways.
Some venoms, such as that from the bullet ant, stimulate all sensory neurons, whereas others, such as venom from the Togo Starburst Tarantula, only activate a subset of neurons. Molecules from these venoms are particularly interesting as they can lead to the identification of new analgesic targets.
What exciting discoveries are happening at IMB?
Professor Glenn King and his team at IMB are using a compound from the venom of the Togo Starburst Tarantula to develop a treatment for Dravet Syndrome, a severe paediatric epilepsy that is worsened by some frontline anti-epileptic drugs.
Associate Professor Irina Vetter and her IMB group have found a molecule in the venom of the Blue Bloom Birdeater, a beautiful blue/purple tarantula, which blocks a pain signalling channel without causing the debilitating side effects associated with opioid analgesics.
What are the next steps?
Drug discovery is a slow process. Together, pre-clinical and clinical studies can cost hundreds of millions of dollars. This important work can be advanced by the support of our community. Together we can drive breakthroughs and discoveries into new medications. Find out more.
Research with real impact.
Find out how spider venom could also help address a devastating form of childhood epilepsy that is resistant to traditional drugs.