Professor Yaakov Nahmias' team at the Hebrew University of Jerusalem (HU) reported that the new coronavirus causes abnormal accumulation of lipids, which are known to initiate severe inflammation in a process called lipotoxicity. The team identified the lipid-lowering drug TriCor (fenofibrate) as an effective antiviral last year, showing it both reduced lung cell damage and blocked virus replication in the laboratory.
A joint study was done by Prof Nahmias & Dr. Benjamin tenOever, a Professor of Medicine and Microbiology -also the Director of the Virus Engineering Center for Therapeutics and Research at Mount Sinai Medical Center’s Icahn School of Medicine in New York.
A clinical study with COVID-19 patients at Israel's Barzilai Medical Center with support from Abbott Laboratories was carried out. A dosage of 145 mg/day of TriCor (fenofibrate) for 10 days and continuously monitored for disease progression and outcomes.
"The results were astounding", shared Nahmias. "Progressive inflammation markers, that are the hallmark of deteriorative COVID-19, dropped within 48 hours of treatment. Moreover, 14 of the 15 severe patients didn't require oxygen support within a week of treatment.
Prof Nahmias also says that fenofibrate is far safer than other drugs proposed to date, and its mechanism of action makes is less likely to be variant-specific.
PS: TriCor is the same drug marketed as Lipidil - also some other alternate names as well.
Find below the abstract of their recent paper - still in Preprint.
"Viruses are efficient metabolic engineers that actively rewire host metabolic pathways to support their lifecycle, presenting attractive metabolic targets for intervention. Here we chart the metabolic response of lung epithelial cells to SARS-CoV-2 infection in primary cultures and COVID-19 patient samples. Bulk and single-cell analyses show that viral replication induces endoplasmic stress and lipid accumulation. Protein expression screen suggests a role for viral proteins in mediating this metabolic response even in the absence of replication. Metabolism-focused drug screen showed that fenofibrate reversed lipid accumulation and blocked SARS-CoV-2 replication. Analysis of 3,233 Israeli patients hospitalized due to COVID-19 supported in vitro findings. Patients taking fibrates showed significantly lower markers of immunoinflammation and faster recovery. Additional corroboration was received by comparative epidemiological analysis from cohorts in Europe and the United States. A subsequent prospective interventional open-label study was carried out in 15 patients hospitalized with severe COVID-19. The patients were treated with 145 mg/day of nanocrystallized fenofibrate (TriCor®) in addition to standard-of-care. Patients receiving fenofibrate demonstrated a rapid reduction in inflammation and a significantly faster recovery compared to control patients admitted during the same period and treated with the standard-of-care. Taken together, our data show that elevated lipid metabolism underlies critical aspects of COVID-19 pathogenesis, suggesting that pharmacological modulation of lipid metabolism should be strongly considered for the treatment of coronavirus infection."
A joint study was done by Prof Nahmias & Dr. Benjamin tenOever, a Professor of Medicine and Microbiology -also the Director of the Virus Engineering Center for Therapeutics and Research at Mount Sinai Medical Center’s Icahn School of Medicine in New York.
A clinical study with COVID-19 patients at Israel's Barzilai Medical Center with support from Abbott Laboratories was carried out. A dosage of 145 mg/day of TriCor (fenofibrate) for 10 days and continuously monitored for disease progression and outcomes.
"The results were astounding", shared Nahmias. "Progressive inflammation markers, that are the hallmark of deteriorative COVID-19, dropped within 48 hours of treatment. Moreover, 14 of the 15 severe patients didn't require oxygen support within a week of treatment.
Prof Nahmias also says that fenofibrate is far safer than other drugs proposed to date, and its mechanism of action makes is less likely to be variant-specific.
PS: TriCor is the same drug marketed as Lipidil - also some other alternate names as well.
Find below the abstract of their recent paper - still in Preprint.
"Viruses are efficient metabolic engineers that actively rewire host metabolic pathways to support their lifecycle, presenting attractive metabolic targets for intervention. Here we chart the metabolic response of lung epithelial cells to SARS-CoV-2 infection in primary cultures and COVID-19 patient samples. Bulk and single-cell analyses show that viral replication induces endoplasmic stress and lipid accumulation. Protein expression screen suggests a role for viral proteins in mediating this metabolic response even in the absence of replication. Metabolism-focused drug screen showed that fenofibrate reversed lipid accumulation and blocked SARS-CoV-2 replication. Analysis of 3,233 Israeli patients hospitalized due to COVID-19 supported in vitro findings. Patients taking fibrates showed significantly lower markers of immunoinflammation and faster recovery. Additional corroboration was received by comparative epidemiological analysis from cohorts in Europe and the United States. A subsequent prospective interventional open-label study was carried out in 15 patients hospitalized with severe COVID-19. The patients were treated with 145 mg/day of nanocrystallized fenofibrate (TriCor®) in addition to standard-of-care. Patients receiving fenofibrate demonstrated a rapid reduction in inflammation and a significantly faster recovery compared to control patients admitted during the same period and treated with the standard-of-care. Taken together, our data show that elevated lipid metabolism underlies critical aspects of COVID-19 pathogenesis, suggesting that pharmacological modulation of lipid metabolism should be strongly considered for the treatment of coronavirus infection."
