Acute respiratory distress syndrome (ARDS) is a serious inflammatory edema of the lungs. In ARDS, direct or indirect injury to the lung triggers an intense inflammatory response in the pulmonary tissues, causing the alveoli to collapse or fill with fluid and hence to lose their ability to exchange oxygen and carbon dioxide with the blood. ARDS typically develops within 12-24 hours of the predisposing event, but can occur up to one week later.
Pulmonary or systemic inflammation is both triggered by and prompts the further systemic release of proinflammatory cytokines. Alveolar macrophages release cytokines (IL-1, IL-6, IL-8, IL-10 and TNF-alpha), which recruit and activating neutrophils in the lungs, leading to further release of leukotrienes, antioxidants, platelet-activating factor (PAF) and neutrophil elastase. All of these substances have harmful effects on the capillary endothelium and alveolar epithelium. As a result, the airspaces and interstitium are flooded with edema fluid, causing hypoxemia.
Approximately 190,600 Americans suffer ARDS/ALI each year, resulting in 3.6 million hospital days (Herridge, M.S. et al (2016)). This represents approximately 5% of all hospitalized, mechanically ventilated patients. The Orphan Drug Designation program provides orphan status to drugs and biologics which are defined as those intended for the treatment, prevention or diagnosis of a rare disease or condition, which is one that affects less than 200,000 persons in the US.
Making a biologic drug that addresses the inflammatory cascade in the orphan indication of ARDS is one of the largest unmet needs in hospitalizations for COVID and other causes of ARDS.
We have developed a suite of monoclonal antibodies targeting CD11d which plays a role in immune and inflammatory responses. CD11d is an important component of the CD11d/CD18 integrin expressed on the majority of circulating human neutrophils and monocytes/macrophages, NK, B and γδ T cells but not on αβT cells. Early treatment in animal (rat and mouse) models prevents neuroinflammatory damage by neutrophils and macrophages resulting in improved neurological recovery. It is believed that these antibodies target CD11d expressed on the first wave of pro-inflammatory cells entering the wound site whereby neutrophil and macrophage accumulation is reduced, overall secondary injury-associated cell death is decreased and more neuronal tissue is spared further injury leading to better functional recovery.
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