The Science Behind Infensa Bioscience
Cardiovascular disease
Infensa Bioscience will develop therapeutics to treat two of the leading causes of death worldwide — stroke and heart attack. Together, these disorders account for almost one-third of all deaths worldwide every year.
During ischemic stroke and heart attack, the brain and heart are deprived of oxygen. This leads to irreparable organ damage, which causes substantial mortality and reduced quality of life for survivors. Despite this huge clinical burden, there are no drugs available to treat these disorders. Infensa Bioscience will develop first-in-class drugs to protect the heart and brain during stroke and heart attack. The total addressable market for these drugs comprises more than 25 million patients per year.
During ischemic stroke and heart attack, the brain and heart are deprived of oxygen. This leads to irreparable organ damage, which causes substantial mortality and reduced quality of life for survivors. Despite this huge clinical burden, there are no drugs available to treat these disorders. Infensa Bioscience will develop first-in-class drugs to protect the heart and brain during stroke and heart attack. The total addressable market for these drugs comprises more than 25 million patients per year.
Acid-sensing ion channel 1a
Acid-sensing ion channel 1a, or more simply ASIC1a, is an ion channel found on the surface of brain nerve cells (neurons) and heart muscle cells (cardiomyocytes). It has the unusual property of being activated by acid.
During ischemic stroke and heart attack, the interrupted blood supply to the brain and heart causes tissue acidosis. This activates ASIC1a, which in turn initiates downstream biochemical pathways that cause brain neurons or cardiomyocytes to commit suicide. Genetic knockout of ASIC1a in mice leads to greatly improved outcomes after stroke and heart attack, highlighting the critical role played by this ion channel in mediating tissue injury during these life-threatening events.
During ischemic stroke and heart attack, the interrupted blood supply to the brain and heart causes tissue acidosis. This activates ASIC1a, which in turn initiates downstream biochemical pathways that cause brain neurons or cardiomyocytes to commit suicide. Genetic knockout of ASIC1a in mice leads to greatly improved outcomes after stroke and heart attack, highlighting the critical role played by this ion channel in mediating tissue injury during these life-threatening events.
Proprietary inhibitors of ASIC1a
Infensa Bioscience has developed proprietary inhibitors of ASIC1a that are protected by worldwide patents. Our lead compound is a unique peptide known as IB001, which is an extraordinarily potent and selective inhibitor of human ASIC1a. IB001 is 50,000-fold more potent than the best small-molecule inhibitor of ASIC1a, and it has 60-fold higher potency than beta blocker drugs.
In preclinical models of ischemic stroke, IB001 reduced brain infarct size and dramatically improved post-stroke performance even when administered 8 hours after stroke onset. IB001also has the potential to be delivered by first responders — this would be game-changer, as 2 million neurons are lost every minute after stroke onset and therefore early treatment would save lives and reduce stroke-related morbidity.
In preclinical models of heart attack and cardiac surgery, IB001 reduced injury to the heart and greatly improved cardiac performance. In preclinical models of heart transplantation, IB001 was shown to greatly improve the viability of donor hearts.