SARS-Cov-2 virus is responsible for the global COVID-19 pandemic. Most patients with severe COVID-19 have substantially elevated serum levels of pro-inflammatory cytokines, which contribute to lung, heart, liver, and kidney injury that progresses to respiratory failure, multi-organ failure, shock, and death.
Acute respiratory distress syndrome (ARDS) is a frequent complication of severe COVID-19 and is present in nearly all fatal COVID-19 cases
AYX-101 consists of triciribine encapsulated in patients’ own red blood cells (RBCs).
Triciribine, an Akt inhibitor, has the potential to treat lung injury and inflammation-associated tissue damage with severe SARS-Cov-2 infection
Multiple mechanisms are thought to be responsible for reducing inflammation and associated tissue damage after triciribine administration:
· Suppression of inflammation directly by inhibition of macrophage and neutrophil activity
· Suppression of uncontrolled inflammation indirectly through inhibition of cytotoxic T-cells, natural killer (NK) cells, and neutrophils through activation and expansion of anti-inflammatory Regulatory T-cells (Tregs)
· Promotion of vascular regeneration in the injured lungs promoting resolution
Red blood cell encapsulation for administration of AYX-101 is expected to result in safer, efficient, long-lasting delivery of triciribine to lungs
Selected references: Artham S et al 2020, Abdalla M et al 2015; additional references available upon request
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