Η fenofibrate φαίνεται να μειώνει την Α και Β μετάλλαξη του Covid-19

Study finds fenofibrate’s ability to reduce Covid-19 infection

09 Aug 2021

Fenofibrate[1] also demonstrated efficacy against the newly emergent alpha and beta variants of SARS-CoV-2 in the study.

A research team led by the University of Birmingham and Keele University in the UK has found that a licensed oral drug, fenofibrate, and its active form, fenofibric acid, can substantially reduce SARS-CoV-2 infection in human cells in the laboratory.

Approved in various countries, fenofibrate is being used for the treatment of conditions such as increased cholesterol and fatty substance levels in the blood.

Fenofibrate decreased Covid-19 infection by up to 70% at concentrations that are safe and attainable with its standard clinical dose, the University of Birmingham noted.

Led by the San Raffaele Scientific Institute in Italy, the research was conducted in partnership with the University of Copenhagen in Denmark and the University of Liverpool, UK.

In the study, researchers analysed a panel of presently licensed drugs, including fenofibrate, to detect candidates that can interrupt angiotensin-converting enzyme 2 (ACE2) and Spike interactions.

Fenofibrate was selected and assessed for efficacy in reducing infection in cells in the laboratory with the use of the SARS-CoV-2 original strains isolated last year.

Furthermore, additional unpublished findings showed that the drug worked against the newly emergent SARS-CoV-2 variants such as the Alpha and Beta variants.

The university added that further research is underway to analyse the drug’s efficacy against the Delta variant.

Πηγή:https://www.clinicaltrialsarena.com/news/study-fenofibrate-covid-infection/

[1]Η φαινοφιβράτη (fenofibrate) είναι ένα παράγωγο του ινικού οξέος, του οποίου η δράση να μεταβάλλει τα επίπεδα των λιπιδίων στον άνθρωπο μεσολαβείται με ενεργοποίηση του υποδοχέα PPARα. Μέσω της ενεργοποίησης του PPARα, η φαινοφιβράτη αυξάνει τη λιπόλυση και την αποβολή των αθηρογόνων πλούσιων σε τριγλυκερίδια σωματίων από το πλάσμα ενεργοποιώντας τη λιποπρωτεϊνική λιπάση και μειώνοντας την παραγωγή της αποπρωτεΐνης C-III.

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