A drug derived from funnel-web spider venom that could prevent damage from heart attacks and extend the life of donor hearts during organ transplants is set to begin human trials.
The new drug, currently referred to as Hi1a, has been developed by a team from the Victor Chang Cardiac Research Institute and the University of Queensland.
The team found that the drug works by blocking the acid-sensing ion channels in the heart that are activated by the build-up of lactic acid after a heart attack.
The lactic acid build-up triggers a “suicide message” that causes additional heart cells to die, causing irreversible tissue damage.
The new drug blocks that message, and the progressive expansion of tissue damage is averted.
The team is hoping that human trials involving 100 healthy people will start in the middle of 2025.
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According to the Victor Chang Institute, 2,300 West Australians die from heart disease each year. Nationally, 57,000 people are hospitalised for heart attacks every year.
Head of the Molecular Cardiology Laboratory at the Victor Change Institute Professor Bob Graham said Hi1a is a protein made up of 50 amino acids and was larger than insulin.
However, it is difficult and expensive to make and purify so the team has produced a peptide to make the drug.
“(The peptide) is about one sixth the size of Hi1a but retains its potency and specificity for blocking the ion channel, acid sensing ion channel-1a, which is how it works to limit damage after a heart attack or stroke, and to limit deterioration of donor hearts for transplantation,” he said.
“It is this lead peptide that will be tested in first-in-human clinical safety trials.”
Professor Graham added that the findings of the human trials will be used to inform further efficacy studies.
The drug’s development has been supported by $17.8 million funding from the Medical Research Future Fund and will be taken to market by Infensa Bioscience, a company that includes members of the Victor Chang Institute and University of Queensland.
Professor Glenn King from UQ’s Institute for Molecular Bioscience said they had shown in animal models that Hi1a protected the heart from damage caused by lack of oxygen during a heart attack or during donor heart retrieval.
“This funding will enable us to undertake human clinical trials to test a miniaturised version of Hi1a as a drug to treat heart attack and protect donor hearts during the retrieval process,” he said.
“If successful it will improve patient survival and quality of life, dramatically expand the pool of donor hearts available for transplantation and significantly reduce healthcare costs.”