A molecule based on the venom of a funnel-web spider could keep cells from dying after a heart attack, having been previously shown to have similar potential after strokes. On encountering a K'gari funnel web spider, many people might have a heart attack (or at least feel like one is imminent). Soon, however, that spider's venom could be the basis of a medication that, if applied quickly, could make such an attack far less dangerous, preventing lasting damage to heart cells usually associated with such events. In both heart attacks and strokes, long-term damage is caused by the death of cells that don't regenerate. Surprisingly, these cells don't die through lack of blood supply alone – the body actually sends a signal through an acid-sensing ion channel (ASIC1a), causing them to self-destruct before they need to. The evolutionary basis for this response is mysterious, but a method to block it effectively could greatly reduce the damage these events produce. University of Queensland scientists think they've found one in a drug candidate called IB001. In 2017, they provided evidence for IB001's potential against strokes. Last year they followed up with a paper in Circulation showing it does the same thing for heart cells in vitro and in mice. It usually takes years for promising drug candidates to go from animal studies to clinical trials, with a long search for funding in between. However, the University of Queensland has now announced the licensing of IB001 to a start-up Infensa Bioscience, which has raised AU$23 million (US$16 million) to develop it further. Clinical trials are planned for 2023. The company's name was chosen to honor the spider, Hadronyche infensa, in whose venom the Hi1a molecule, on which IB001 is based, was found. “IB001 blocks the signals that causes heart cells to die, and when given immediately to heart attack victims could reduce damage to the heart and significantly improve outcomes for people with heart disease, particularly in rural and remote regions,” said Infensa CEO Dr Mark Smythe in a statement. Co-author Dr Nathan Palpant of the University of Queensland told IFLScience the team has experimented with models of applying IB001 before heart damage is anticipated – for example, when someone is going into surgery – and when a patient arrives in emergency. Astonishingly, he said; “It seems equivalently effective in all scenarios.” That includes for a patient who might have had a heart attack hours before reaching the hospital. True confirmation, however, will have to wait for clinical trials. Palpant told IFLScience the importance of ASIC1a in strokes has been known for decades, and a blocking mechanism sought, with IB001 easily the most effective found. The importance of the same channel in heart injuries is new. However, clinical applications could come much more quickly for hearts than strokes. “Access to the brain is much more difficult than the heart,” Palpant said. Other organs could follow. “We're targeting hearts as the most significant clinical needs,” Palpant told IFLScience. “If we can develop these therapies we foresee there could be a wide range of applications for organs such as the kidney and the eye.” The discovery was remarkably fortuitous – the University of Queensland's Professor Glenn King was studying a tarantula venom molecule PcTx1, with the potential to prevent neuron death in stroke victims. One of his students noticed one of the molecules in the funnel web venom he was investigating looked like two PcTx1 joined together, despite the large evolutionary gap between tarantulas and funnel webs. The molecule in question turned out to be far more effective than PcTx1, and with refinements, turned into IB001. Source
