The Endogenous Agonist (EA) of AT2 to Restore Lung Barrier Function in COVID-19 Patients with Acute Respiratory Distress Syndrome (ARDS)

University College Cork Background
ARDS represents a complex and devastating syndrome with considerable morbidity and mortality, for which there exists no targeted treatment strategies. Treatment is limited to supportive interventions like mechanical ventilation which is now in widespread use. There is an urgent, unmet need for effective pharmacotherapy to reduce disease burden and consumption of medical resources. ARDS develops when lungs become inflamed as a result of COVID-19 infection. As a result, the endothelial/epithelial barrier function within the lungs becomes compromised causing the air sacs to collapse and fluid to leak into the lungs. Older age and low immune response are major risk factors for ARDS and death associated with COVID-19. Mortality rates of up to 50% have now been reported.
Technology Overview
UCC researchers have discovered the endogenous agonist (EA) of the AT2 receptor (). The stimulation of the G protein-coupled receptor by EA could protect patients from COVID-19-mediated ARDS since activation of AT2 by the peptide protects lung endothelial cells from pathogen-driven disruption of inter-endothelial junctions and thus ARDS related death (). Prof. Walther’s team also discovered that epithelial barrier can be protected (). Restoration of barrier integrity will prevent invasion of neutrophils and inflammatory cells and thus prevent the progression of ARDS and reduce oedema. Since the formulation contains an endogenous human peptide, the implementation into the clinic could be realized with a partner within less than 5 months, which could save the life of ten-thousands of COVID-19 patients.
Stage of Development
Development objectives include:

Complete pre-clinical data package
Initiate Phase 1b clinical trial to evaluate the effect of EA in COVID-19 infected patients

Opportunity

Licensing
Venture creation
Research collaboration

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