Cardiovascular disease ranks as the world's leading cause of death, with myocardial infarction (MI) and stroke responsible for 27% of global fatalities. Alarmingly, despite this staggering toll, there are currently no drugs available to protect the heart and brain from the damage inflicted by MI and stroke. During MI and stroke, oxygen supply to the heart and brain dwindles, prompting a metabolic shift to anaerobic glycolysis and lactic acidosis. This metabolic change activates acid-sensing ion channel 1a (ASIC1a), exacerbating cell damage and death. Recent advancements in Glenn Kings laboratory at the University of Queensland, have led to the discovery of Hi1a, a peptide from the K'gari funnel-web spider venom, which potently and selectively inhibits ASIC1a. Administering Hi1a during ischemic stroke significantly reduces infarct size and improves outcomes. Additionally, genetic removal of ASIC1a in mouse models of MI results in enhanced functional recovery. These findings demonstrate ASIC1a as a promising target for neuroprotective and cardioprotective drugs.
During this presentation, I will describe preclinical data concerning the translation of peptides to the clinic with a focus on blocking ASIC1a function. I will also contextualize this within the framework of previous experience in translating an additional six peptides to clinical trials.