• Akari’s complement and leukotriene inhibitor, nomacopan, demonstrated improved survival (80% vs. 30%) in a preclinical model of trauma
• A follow-on program relevant to both military and civilian trauma is planned as the next steps toward a clinical study
• Project was funded by the DoD U.S. Army Medical Research and Development Command

NEW YORK and LONDON, Feb. 28, 2022 (GLOBE NEWSWIRE) -- Akari Therapeutics, Plc (Nasdaq: AKTX), a late-stage biopharmaceutical company focused on innovative therapeutics to treat orphan autoimmune and inflammatory diseases where complement (C5) and/or leukotriene (LTB4) systems are implicated, today announced new data showing that clinical outcomes in U.S. Army trauma patients correlate with complement activation, and that nomacopan significantly improves survival from 30% to 80% in a clinically relevant preclinical model of traumatic hemorrhage. A full data set is available at https://doi.org/10.22541/au.164423459.98723938/v1

Clive Richardson, Chief Executive Officer of Akari Therapeutics, commented: “This very exciting data generated from our collaboration with the U.S. Army supports the development of nomacopan as an organ protective drug for treatment of severe trauma patients that has the potential to significantly reduce mortality in both a military and civilian setting. There is now a planned pathway to the clinic, and we look forward to leveraging nomacopan’s dual inhibition of the pro-inflammatory complement C5 and leukotriene LTB4 as a potential treatment for traumatic injury.”

Traumatic hemorrhage (TH) is the leading cause of potentially preventable deaths that occur during the pre-hospital phase of care. Current treatments still largely rely on organ/tissue supportive approaches and fluid resuscitation, and no effective pharmacological therapeutics are available. Identifying new life-supporting treatment focused on the interval between point of injury to hospital is a key objective. Military blast injury accounted for 70%-80% of U.S. casualties in Iraq and Afghanistan, while in the U.S. there are approximately 500,000 civilian trauma hospital discharges a year which are defined as severe and could benefit from early drug intervention to reduce multi-organ dysfunction. Annual inpatient trauma-related hospital costs in the U.S. are approximately $30 billion a year1.

An analysis of 54 military trauma patients in Baghdad with blast and gunshot injury showed that three key markers of complement activation – C5a, C5b9 and Bb – were elevated 300%-600% in the first eight hours after the traumatic event, compared to healthy controls. In addition, pro-inflammatory C5a and C5b9 plasma levels correlated with trauma severity, and complement activation correlated with clinical outcomes.

Nomacopan’s mode of action may be particularly suited for treatment of TH as critically it inhibits terminal complement activation (C5a, C5b9) via all three complement pathways (classical, lectin and alternative) and additionally inhibits leukotriene B4 (LTB4) which is also implicated in exacerbation of TH.

To test the anticipated efficacy of nomacopan, a clinically relevant pre-clinical model of blast injury and hemorrhagic shock was undertaken by the United States Army Institute of Surgical Research (USAISR). The addition of nomacopan to damage control resuscitation protocol, significantly inhibited terminal complement activity, decreased local and systemic inflammatory responses, improved hemodynamics and metabolism, attenuated tissue and organ damage and increased survival (80% vs 30%; p