Laboratory studies indicate that a cheap generic drug reduces SARS-CoV-2 infection in human cells by up to 70%.
The drug, called fenofibrate, regulates cholesterol levels but also destabilizes the spike protein on SARS-CoV-2 and inhibits binding to human cells.
It was effective against all the SARS-CoV-2 variants that the scientists tested in vitro.
An international effort — involving scientists from Keele University and the University of Birmingham, both in the United Kingdom, and the San Raffaele Scientific Institute in Milan — has found that a drug that people formerly used to control cholesterol levels could be an effective treatment against Covid-19.
The results of the study will appear in the journal Frontiers in Pharmacology.
Researchers first tested several licensed drugs. They were looking for any that disrupted interactions between the viral spike protein — that is, the part of the virus that binds to host cells — and the surface of human cells to see if it would be possible to repurpose the drugs as a Covid-19 treatment.
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Co-corresponding study author Dr. Alan Richardson, of Keele University, told Medical News Today: “We tested more than 100 drugs and found that fibric acidsTrusted Source had the most potential. Initially, clofibrate looked good, but it has adverse effects, so we then looked at fenofibrate.”
Scientists developed fenofibrate in the 1980sTrusted Source, and doctors used it widely to control people’s cholesterol levels.
It was popular until the discovery of statins, which have the added benefit of reducing the risk of heart disease.
Around 30 millionTrusted Source people worldwide now take statins. However, some people who cannot tolerate statins still take fenofibrate.
In laboratory experiments, the researchers found that fenofibrate destabilized the spike protein and inhibited binding to the ACE2Trusted Source membrane protein, through which the virus enters the cells.
The drug is effective against the Alpha and Beta variants of SARS-CoV-2, and the team is now investigating its effectiveness against the Delta variant.
“Because the drug affects multiple targets, not just the spike protein, it will be harder for resistance to develop, so new variants should not be able to escape the effect.”