After research and study, scientists have identified a potential new drug to intercept or mitigate the symptoms and consequences derived from infection by SARS-CoV-2, the virus responsible for Covid-19.
The research published in the journal Cytokine and Growth Factors Review suggested that the preliminary results of the study conducted on animal models showed that the drug 4-Phenylbutiric acid (4-PBA) fully curbs mortality caused by respiratory failure derived from cellular stress.
The inflammatory process, which has been identified in severe cases of coronavirus, causes an uncontrolled and excessive release of cytokines – molecules. These molecules are in charge of organizing the body’s defenses- which could even trigger vascular hyperpermeability and multi-organ failure.
Controlling such cytokine “storm”, through those controlling them, that is, the infected cells is precisely what these researchers proposed.
“When cells are stressed by infection, they call the cytokines, and the more stressed they are, the more persistent they become, provoking this uncontrolled inflammation. Hence, one possible treatment for Covid-19 is to reduce cellular stress,” explained one of the lead researchers Ivan Duran, Professor at the University of Malaga in Spain.
According to the researcher, repurposing the 4-PBA anti-stress drug could modulate such cellular stress, which is also present in pathologies like diabetes, aging, or carcinogenesis, which, in turn, are classified as risk factors for Covid-19.
The drug has already been approved for clinical use against other diseases and, hence, easy to apply clinically.
The study also identified the endoplasmic reticulum resident protein “BiP” (Binding Immunoglobulin Protein) – a stress blood marker — as an indicator of cellular stress situations, likely to be explored and measured in affected patients.
This way, BiP levels, apart from determining the efficacy of 4-PBA treatment, could serve as early indicators of Covid-19 risk groups, establishing a correlation between high levels and the inflammatory severity after the viral infection, Duran pointed out.