SARS-2 coronavirus-induced respiratory system damage resulting in pernicious clinical disease and death represents a significant and growing cause for concern worldwide, and has already been estimated to have become a leading cause of death in SARS-2 coronavirus affected populations. Medical evidence suggests that clinically asymptomatic persons, not obviously ill, may progress to serious compromises of pulmonary function before the seriousness of the pathology becomes clinically evident to affected persons and others about them. 

In normal lung, Surfactant protects the alveoli (the tiny air sacs in the lungs) from collapsing and failing to inflate with inspiration.  In Covid-19, viral damage to alveolar cells lining the air sacs in lung reduces surfactant levels causing increased surface tension for the fluid lining the air sacs. Surfactant is a complex mixture of phospholipids and surfactant proteins that reduce alveolar surface tension and support lung inflation. Due to this often rapid and damaging tissue pathological progression, an intervention against the cascade of pathology is desperately needed.  

PhenT has been shown able to block cell dysfunction and death in cultured cells and in five animal models of head trauma, stroke, Alzheimer’s disease and nerve gas toxicity. In Covid-19 this protection or delay could extend alveolar cellular function and counter the reduction of Surfactant, and thus maintains Surfactant concentrations better able to prevent the increase in surface tension to levels required for alveoli to collapse. From the known pathology from SARS-Cov-2 virus infections the protection of alveoli from programmed cell death can be expected to raise the functioning capacity of the lung to both maintain O2 blood saturation and make available working alveoli sufficient to protect these alveoli and others from overstretching and succumbing to the damage cascade found in progressive SARS-Cov-2 virus infections.