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Tuesday, May 5, 2020

CohBar Agent Targets Covid-19 Linked Acute Respiratory Distress Syndrome

CohBar, Inc. (NASDAQ: CWBR), a clinical stage biotechnology company developing mitochondria based therapeutics to treat chronic diseases and extend healthy lifespan, announced today that it has initiated testing of its CB5064 analogs in preclinical models of ARDS, to assess their potential as therapeutics for coronavirus disease 2019 (COVID-19) associated ARDS. In preclinical studies to date, these peptides have demonstrated the ability to activate the apelin receptor, a cell signaling pathway that published preclinical studies have shown can reduce the severity of acute lung injury by reducing lung fluid accumulation, hypoxemia, and cytokine secretion, which occur in COVID-19 associated ARDS, and lead to downstream injury to the kidney, heart, and other organs.
“CohBar’s novel CB5064 analogs are agonists of the apelin receptor in vitro and also improve metabolic dysfunction in vivo in obese mice, a known apelin effect,” said Kenneth C. Cundy, PhD, CohBar’s Chief Scientific Officer. “In published preclinical studies, apelin signaling demonstrates a key role in protecting animals from acute lung injury and restoring metabolic homeostasis. Our peptides could potentially block many of the acute effects of COVID-19 associated ARDS, and their beneficial effects could extend to protecting other organs from the cytokine storm and reducing mortality in COVID-19 and other forms of acute lung injury.”
COVID-19 associated ARDS is a new target for the company’s ongoing program of CB5064 analogs. These analogs previously demonstrated efficacy in diet induced obese or DIO mice, a widely used model of type 2 diabetes, leading to significant reduction in body weight, adiposity, and improvement in insulin sensitivity, as presented by CohBar at the American Diabetes Association national meeting in 2019.i Published clinical reports show that obesity and diabetes are major underlying risk factors in severe COVID-19, and are associated with significantly increased mortality.
“Preventing ARDS in COVID-19 patients, including the damaging effects of fluid accumulation in the lungs, hypoxemia, and cytokine storm, is critical to reducing mortality,” stated Professor Toby Maher, British Lung Foundation Chair in Respiratory Research, Professor of Interstitial Lung Disease and head of the Fibrosis Research Group at the National Heart and Lung Institute, Imperial College, London, and Director of Respiratory Research at Royal Brompton Hospital, London. “Obesity and metabolic dysfunction are also major risk factors for development of severe COVID-19.  Targeting the apelin receptor to reduce lung injury while improving metabolic homeostasis is a promising strategy for treating both ARDS associated with COVID-19 and other forms of ARDS.”

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