Cardiovascular disease stands as the leading global cause of mortality, accounting for 27% of deaths, primarily attributed to myocardial infarction (MI) and stroke. It's alarming that, despite this immense toll, there are currently no available drugs to safeguard the heart and brain from the harm inflicted by MI and stroke.

During these critical events, both MI and stroke, there is a reduction in oxygen supply to the heart and brain, triggering a metabolic shift towards anaerobic glycolysis and lactic acidosis. This metabolic alteration activates acid-sensing ion channel 1a (ASIC1a), intensifying cellular and tissue. Recent breakthroughs in the laboratory of Glenn King at the University of Queensland have led to the discovery of Hi1a, a peptide derived from the venom of the K'gari funnel-web spider. Hi1a exhibits potent and selective inhibition of ASIC1a. Administering Hi1a during ischemic stroke has shown substantial reductions in infarct size and improved patient outcomes. Additionally, when ASIC1a was genetically removed in mouse models of MI, it resulted in enhanced functional recovery. These significant findings underscore ASIC1a as a promising target for the development of neuroprotective and cardioprotective medications.

In this presentation, I will elucidate preclinical data concerning the translation of peptides into clinical applications, with a particular emphasis on blocking ASIC1a function. I will also provide context within the framework of prior experience in translating an additional six peptides into clinical trials.