Myocardial infarction (MI) and stroke account for 27% of global mortality, yet we have no drugs to prevent the tissue injury they cause. The switch to fuel production via anaerobic glycolysis during MI and stroke leads to tissue acidosis. The drop in pH activates acid-sensing ion channel 1a (ASIC1a), which in turn promotes programmed cell death pathways. We recently isolated a spider-venom peptide (Hi1a) that inhibits ASIC1a with picomolar potency and exceptional selectivity. Hi1a dramatically reduced infarct size and improved behavioural outcomes when administered after ischemic stroke in rats. Genetic ablation of ASIC1a led to improved functional recovery in a mouse model of MI, and this effect was recapitulated by ASIC1a blockade using Hi1a. In addition, we observed dramatic therapeutic benefit in rodent and pig models of heart transplantation, where Hi1a radically improved donor heart viability. While Hi1a is an exciting lead compound for treating stroke and MI, it is a complex 76-residue peptide with six disulfide bonds. Thus, in collaboration with Hiroaki Suga at the University of Tokyo, we used the RaPID mRNA display platform to develop venom-inspired cyclic peptides that are equally good inhibitors of ASIC1a but are much easier to manufacture and may have better brain penetration for neurological applications.Collectively, our data provide compelling evidence that ASIC1a is a novel target for drugs to reduce the burden of MI and stroke. Thus, in 2022 we founded Infensa Bioscience to commercialise this technology, with an initial focus on ST-elevation myocardial infarction (STEMI), the most serious form of heart attack. Infensa aims to begin Phase I clinical trials in Q3 2025.