Denis - The COVID info guy -The off-patent drug that could protect us from future COVID-19 variants.
🔹Ursodeoxycholic acid (UDCA) may prevent SARS-CoV-2 infection or reduce COVID-19 severity.
agronobotPrácticas agronómicas para la conservación de suelos y agua ➡️https://bit.ly/2OjHT5k ⬅️ #conservacion #aulavirtual #suelo #agua #agronomia #clases #cursos pic.twitter.com/1PGR9Ooeif, #UDCA #Colombia
Administración de empresas agrícolas: Factor Trabajo, Capital, Tierra ➡️ https://bit.ly/3fkIhzT ⬅️ #economia #administracion #agronomia #inventario #Contabilidad #agricola #cienciasagrarias #fcagrarias pic.twitter.com/9e6tUT3EAr, #UDCA #Colombia
Thomas E. GladwinLooks hopeful, and impressive - a treatment to prevent COVID targeting a receptor, rather than the specific variant of the virus. https://www.cam.ac.uk/stories/UDCA-COVID19 #COVID #UDCA
Zoomers of the Sunshine Coast 🇨🇦Off-patent liver disease drug could prevent COVID-19 infection and protect against future variants.
Unique experiments involved 'mini-organs', animal research, donated human organs, volunteers and patients.
Ursodeoxycholic acid (UDCA), an off-patent drug used to treat a form of liver disease known as primary biliary cholangitis, 'turns down' FXR and closes the ACE2 doorway.
https://www.nature.com/articles/s41586-022-05594-0
#Covid19 #BlockInfection #VariantProof #UDCA #UrsodeoxycholicAcid
https://www.sciencedaily.com/releases/2022/12/221205121604.htm
FXR inhibition may protect from SARS-CoV-2 infection by reducing ACE2 - Nature
Prevention of SARS-CoV-2 infection through the modulation of viral host receptors, such as ACE21, could represent a new chemoprophylactic approach for COVID-19 complementing vaccination2,3. However, the mechanisms controlling ACE2 expression remain elusive. Here, we identify the farnesoid X receptor (FXR) as a direct regulator of ACE2 transcription in multiple COVID19-affected tissues, including the gastrointestinal and respiratory systems. We then use the over-the-counter compound z-guggulsterone (ZGG) and the off-patent drug ursodeoxycholic acid (UDCA) to reduce FXR signalling and downregulate ACE2 in human lung, cholangiocyte and intestinal organoids and in the corresponding tissues in mice and hamsters. We demonstrate that UDCA-mediated ACE2 downregulation reduces susceptibility to SARS-CoV-2 infection in vitro, in vivo and in human lungs and livers perfused ex situ. Furthermore, we illustrate that UDCA reduces ACE2 expression in the nasal epithelium in humans. Finally, we identify a correlation between UDCA treatment and positive clinical outcomes following SARS-CoV-2 infection using retrospective registry data, and confirm these findings in an independent validation cohort of liver transplant recipients. In conclusion, we identify a novel function of FXR in controlling ACE2 expression and provide evidence that modulation of this pathway could be beneficial for reducing SARS-CoV-2 infection, paving the road for future clinical trials.
Dr Ruth Ann Crystal12/5/22 Nature: FXR inhibition may protect from #SARSCoV2 infection by reducing ACE2 https://buff.ly/3UxyUzA
Ursodeoxycholic acid (#UDCA) , an FXR blocker, is a generic drug used for liver disease. It downregulates ACE2.
UDCA (aka Ursodiol or Actigall) has been used for cholestasis of pregnancy.
This study used UDCA in organoids, mouse/hamster models and in people and shows that UDCA may block or reduce the severity of #COVID infections.
FXR inhibition may protect from SARS-CoV-2 infection by reducing ACE2 - Nature
Prevention of SARS-CoV-2 infection through the modulation of viral host receptors, such as ACE21, could represent a new chemoprophylactic approach for COVID-19 complementing vaccination2,3. However, the mechanisms controlling ACE2 expression remain elusive. Here, we identify the farnesoid X receptor (FXR) as a direct regulator of ACE2 transcription in multiple COVID19-affected tissues, including the gastrointestinal and respiratory systems. We then use the over-the-counter compound z-guggulsterone (ZGG) and the off-patent drug ursodeoxycholic acid (UDCA) to reduce FXR signalling and downregulate ACE2 in human lung, cholangiocyte and intestinal organoids and in the corresponding tissues in mice and hamsters. We demonstrate that UDCA-mediated ACE2 downregulation reduces susceptibility to SARS-CoV-2 infection in vitro, in vivo and in human lungs and livers perfused ex situ. Furthermore, we illustrate that UDCA reduces ACE2 expression in the nasal epithelium in humans. Finally, we identify a correlation between UDCA treatment and positive clinical outcomes following SARS-CoV-2 infection using retrospective registry data, and confirm these findings in an independent validation cohort of liver transplant recipients. In conclusion, we identify a novel function of FXR in controlling ACE2 expression and provide evidence that modulation of this pathway could be beneficial for reducing SARS-CoV-2 infection, paving the road for future clinical trials.