In a COVID-19 infection, the SARS-coronavirus-2 enters the renin-angiotensin-aldosterone system (RAAS) and degrades ACE2 proteins in the lungs, driving overactivation of the AT1 receptor. Conventional activation of the AT1 receptor causes downstream acute lung injury, which can progress to acute respiratory distress syndrome (ARDS), a major complication leading to mortality. COVID-19-related ARDS is associated with a mortality rate of 66% - 94%.1*
Through a collaboration with Imperial College London, Trevena is developing TRV027, a novel AT1 receptor selective agonist, as a potential treatment for acute lung injury and ARDS for COVID-19 patients. The potential therapeutic benefit of TRV027 is two-fold: 1) TRV027 competitively binds to the AT1 receptor, which disrupts overactivation caused by the SARS-coronavirus-2 and rebalances activation levels within the RAAS. 2) The unique mechanism of action of TRV027 preferentially engages the signaling pathway that promotes downstream reparative effects on lung tissue, as well as reduces abnormal blood clotting associated with COVID-19.
|Program||Molecular Target||Therapeutic Target||Current Phase||PC||PH1||PH2||PH3||NDA||Now Approved|
|TRV027||AT1 receptor||ARDS / abnormal clotting (COVID-19)||PH1||Intravenous PC complete||PH1 in progress||PH2 not started||PH3 not started||NDA not started||Now Approved not started|