Drug could potentially prevent respiratory and cardiovascular damage in Covid-19 patients
A mutation in all SARS-CoV-2 variants results in significant damage to the lung tissue and blood vessels, RCSI research
DUBLIN, July 13, 2021 – Scientists have identified a drug that can prevent the virus that causes COVID-19 from binding to human cells, potentially preventing damage to the lung, clot formation and the development of sepsis.
The study, led by researchers from RCSI University of Medicine and Health Sciences, is published in PLOS ONE.
The researchers identified that a mutation, present in all the variants of the virus to date, creates an additional binding site in the virus’ spike protein. This additional binding site increases viral impact in the body, including damage to the lung tissue that causes breathing problems in COVID-19 patients.
The significant damage to the lung tissue allows the virus to spread from the lungs to the bloodstream, where it can cause clots and vascular damage.
In pre-clinical testing, a drug called cilengitide successfully prevented the virus from causing the tissue damage associated with COVID-19 by stopping the virus from sticking to the cell types that line the lungs and blood vessels.
“More pre-clinical and clinical testing is needed before this treatment can be used on patients, but the results are very promising,” said Professor Steve Kerrigan, the study’s senior author and Deputy Head of the RCSI School of Pharmacy and Biomolecular Sciences.
“It is imperative that we continue to develop treatments for COVID-19 for the many people who will not have access to vaccines and for patients with breakthrough infections. Our research in the lab has shown that cilengitide has the potential to significantly reduce the deaths associated with COVID-19.”
RCSI spin-out company Inthelia Therapeutics has recently been formed to commercialise this and other findings relating to the treatment of sepsis from Professor Kerrigan’s research group.
Ms Danielle Nader, PhD candidate in Professor Kerrigan’s group, carried out the work. The research was funded by an Enterprise Ireland Commercialisation Fund, an EMBARK fund award from Enterprise Ireland and Knowledge Transfer Ireland as well as a philanthropic donation from the 3M Foundation and GlobalGiving.
ENDS
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