WHAT WE HAVE DETERMINED IN OUR ARDS STUDIES
ARDS is a lung disorder where fluid collects in the air sacs of the lungs, depriving organs of oxygen. We have determined through our studies RP-323 significantly reduces the influx of inflammatory cells into the lungs thereby limiting damage to the lungs. In addition, RP-323 has shown the ability to block over-active/over-productive pro-inflammatory cytokines including the following interleukins: IL-1, IL-2, IL-9 and IL-15. These interleukins have been shown to be key effectors that comprise the “cytokine storm syndrome” (CSS) consistently observed in severe ARDS associated with COVID-19 and other respiratory infections, including influenza and bacterial pneumonia.
ARDS presents in a variety of ways including sudden acute respiratory syndrome (SARS). In severe and fatal ARDS, disease severity is directly associated with the extent of inflammatory cell (neutrophil and macrophage) infiltration into the lungs. When ARDS occurs, these inflammatory cells are profoundly elevated in the blood vessels, alveoli and other lung tissue. This results in congestion, hypoxia, vascular destruction and thrombosis (clotting), swelling, and is reflected in histology in ARDS tissue.
In our on-going studies, the results demonstrate that RP-323 safely and effectively reduces pulmonary inflammation. The ARDS animal system that we used is a validated model that is predictive of clinical drug efficacy and widely accepted in the industry. This study therefore represents a milestone advancement towards the Company’s goal of initiating human clinical trials of RP-323 for treating ARDS and COVID-19 related lung disorders.