Edesa Biotech's ARDS Drug Inhibits Inflammation from Influenza and Other Pathogens

• Positive Findings Support Potential Expanded Uses for Paridiprubart

TORONTO, ON / ACCESSWIRE / June 28, 2023 / Edesa Biotech, Inc. (NASDAQ:EDSA), a clinical-stage biopharmaceutical company focused on inflammatory and immune-related diseases, announced positive findings from an in vitro study of its monoclonal antibody candidate, paridiprubart, against a panel of respiratory pathogens. The study was completed by the University of Toronto in parallel to the company's ongoing clinical study of EB05 (paridiprubart) in hospitalized Covid-19 patients with Acute Respiratory Distress Syndrome (ARDS), a severe form of respiratory failure characterized by widespread inflammatory injury to the lungs. Approximately 10% of all ICU admissions are ARDS related.

The research results available today in preprint demonstrated that multiple pathogens, including Influenza A, coronavirus and a common bacterium (H. influenzae), can initiate an overactive immune response through Toll-like Receptor 4 (TLR4), a key component of the innate immune system. More importantly, the study determined that inflammation signaling from each of these pathogens was inhibited by Edesa's TLR4 antagonist, paridiprubart.

Paridiprubart represents a new class of emerging therapies called Host-Directed Therapeutics (HDTs) that are designed to modulate the body's own immune response when confronted with infectious diseases or even chemical agents. Importantly, these therapies are designed to work across multiple infectious diseases and threats, and could be stockpiled preemptively ahead of outbreaks.

"The inflammatory pathways associated with ARDS and paridiprubart's mechanism of action are well understood and these latest findings - in combination with clinical experience in more than 600 subjects - provide further support for our view that our drug candidate could provide a safe and effective treatment for ARDS caused by coronaviruses, pandemic influenza and harmful bacteria," said Par Nijhawan, MD, Chief Executive Officer of Edesa. He noted that in addition to the pathogens tested in this research, a number of other viral glycoproteins directly bind and activate TLR4, including those from Ebola virus, dengue virus, and respiratory syncytial virus (RSV).