Potentially big news from Israel: Professor Yaakov Nahmias of Jerusalem’s Hebrew University believes that he may have discovered a breakthrough treatment for Covid-19. Remarkably, the potential cure is a common prescription drug, Fenofibrate, that is already known to be tolerated by adults without significant side effects. Fenofibrate is widely available in both branded and generic forms; many take it as a cholesterol-lowering medication.
Working with Dr. Benjamin tenOever of New York’s Mount Sinai Medical Center, Professor Nahmias was able to show that in lab tests on human lung tissue, Fenofibrate seriously impeded the coronavirus’ ability to reproduce itself, hugely reducing the severity of infection and its resulting damage. The team is enthusiastic, and told another media source that “within a few months, treatment with our drug could be turning Covid-19 into a type of common cold.”
The theory still needs to be confirmed in human trials, but there is hope that it can be evaluated as a treatment for Covid-19 very quickly. Because the drug is already safe and well-understood, researchers will be able to fast-track clinical trials. And retrospective data, which his lab is currently reviewing, should show whether Covid-19 patients that are already taking Fenofibrate have superior outcomes.
We have followed Professor Nahmias’ work for years through his diabetes research. When ASweetLife reached to him, he gladly agreed to explain his potential breakthrough.
Any virus needs to ‘hijack’ host cells in order to replicate itself, and Nahmias observed that the way the novel coronavirus does so appears to be “unique”: “We see a lot more lipid droplets in human lung cells as well as massive membrane complexes that the virus uses to replicate, essentially factories to produce new viruses.”
“The new corona virus enters lung cells and produces viral proteins that seem to stick to different parts of the cells. A few of those virus proteins shut down the mitochondria, the part of the cell that burns sugar into energy. This causes the cells to take up more sugar and start make new fatty acids and phospholipids.”
“Phospholipids turn into the membrane replication complexes and spread throughout the cells. New viruses start being produced and packaged inside the lung cells, then released to infect other lung cells.”
The bottom line is that the virus causes an unusual amount of fat to build up on the inside of lung cells, fat that it requires to reproduce.
This mechanism also may help explain why both diabetes and non-diabetic hyperglycemia appear to be such significant risk factors: “We see that virus-infected lung cells use much more glucose and convert it to lipids that the virus needs to propagate. It makes sense that patients with high glucose levels would be more prone to lung damage and higher viremia due to this mechanism.”
The virus, therefore, appears to feast on high blood sugar. And when a patient’s blood sugar rises in response to Covid-19, while it “looks like insulin resistance, it is actually mitochondrial dysfunction. Virus proteins seem to bind specific genetic elements that shut down the mitochondria. Without it, lung cells can’t burn glucose into energy.”
If a medication were able to interrupt the dysfunctional metabolic processes triggered by the virus, it could stop Covid-19 in its tracks. Professor Nahmias’ team experimented with several medications that could plausibly get the job done, including statins, but when they evaluated the results it was clear that there was “nothing like Fenofibrate.”
“The virus shuts down PPARA, blocking the cell’s ability to burn fat. Fenofibrate specifically activates PPARA, specifically reversing the virus’ effect.”
The team’s work was published yesterday in a preprint, and has not yet been peer reviewed.