In two recent studies at the University of Pennsylvania and elsewhere, researchers found that two anti-inflammatory compounds are capable of boost recovery from COVID-19.
They found the monoclonal antibody eculizumab and an experimental drug called AMY-101 had strong anti-inflammatory effects that led to a faster recovery by severe COVID-19 patients.
The study findings are published in Clinical Immunology. One author is Rodrigo Calado.
Many patients have the exacerbated inflammatory response to COVID-19 infection characterized by a systemic increase in pro-inflammatory cytokines and often referred to as a “cytokine storm.”
This process can result in inflammatory damage to the walls of blood vessels surrounding vital organs, potentially culminating in multiple organ failure.
In the study, the team compared the effects of eculizumab with that of the synthetic peptide AMY-101 in independent small groups of severe COVID-19 patients.
The two medications were administered separately.
The monoclonal antibody, routinely used to treat blood diseases, was tested on patients at the teaching hospital at the University of São Paulo.
Ten patients aged between 18 and 80 were undergoing treatment. Once a week while hospitalized, they were given 900 mg of eculizumab, which inhibits the complement protein C5.
AMY-101, a candidate drug developed by US-based pharmaceutical company Amynda, was given to patients at a hospital in Milan, Italy.
Three patients hospitalized Milan were given 5 mg of AMY-101, developed to inhibit complement protein C3, also once a week.
The team showed that eculizumab and AMY-101 elicited a robust anti-inflammatory process, a sharp fall in levels of C reactive protein (CRP) and interleukin-6 (IL-6), and a marked improvement in lung function.
Both drugs produced promising results, but because AMY-101 is cheaper and performed better in the clinical trial, the scientists envisage testing it on a larger number of patients in Brazil.
The team concluded that the therapeutic benefits of eculizumab and AMY-101 were due to inhibition of a bloodstream cascade of proteins involved in immune response and known as the complement system.
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