A team at the Institute for Molecular Bioscience (IMB)- studying a molecule found in spider venom- has shown promising results toward becoming a treatment for heart attacks and strokes. Previously, Associate Professor Nathan Palpant and Professor Glenn King demonstrated that the drug candidate Hi1a could protect cells from the damage caused by heart attacks and strokes.
Subsequent preclinical tests aimed at mimicking real-life treatment scenarios have now met critical benchmarks, indicating the potential for further developing this spider venom molecule as a therapeutic option.
These tests provide valuable insights into how Hi1a might function as a treatment, including identifying the stage of a heart attack at which it could be practical and determining appropriate dosage levels.
Dr Palpant said, “We established that Hi1a is as effective at protecting the heart as the only cardioprotective drug to reach Phase 3 clinical trials, a drug that was ultimately shelved due to side effects. Importantly, we found that Hi1a only interacts with cells in the injured zone of the heart during an attack and doesn’t bind to healthy regions of the heart – reducing the chance of side effects.”
Prof. King discovered Hi1a in the venom of the K’gari funnel web spider.
Prof King said, “Hi1a could reduce damage to the heart and brain during heart attacks and strokes by preventing cell death caused by lack of oxygen. Our testing and safety studies from independent contract research organizations have provided evidence that Hi1a could be an effective and safe therapeutic.”
Infensa CEO and UQ researcher Associate Professor Mark Smythe said, “Most deaths from cardiovascular disease are caused by heart attacks and strokes, yet there are no drugs on the market that prevent the damage they cause. An effective drug to treat heart attacks would have a worldwide impact, providing a breakthrough to improve the lives of millions of individuals living with heart disease.”
Journal Reference:
- Meredith A Redd, Yusuke Yoshikawa, Nemat Khan et al. Acid-sensing ion channel 1a blockade reduces myocardial injury in rodent models of myocardial infarction. European Heart Journal, DOI: 10.1093/eurheartj/ehad793