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http://schema.org/dateModified 2025-03-05 00:47:51.014292+00:00 https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/ http://schema.org/datePublished 2021-12-10 10:05:51.703731+00:00 https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/ http://schema.org/description COVID-19 is a disease with unique characteristics that include lung thrombosis(1), frequent diarrhoea(2), abnormal activation of the inflammatory response(3) and rapid deterioration of lung function consistent with alveolar oedema(4). The pathological substrate for these findings remains unknown. Here we show that the lungs of patients with COVID-19 contain infected pneumocytes with abnormal morphology and frequent multinucleation. The generation of these syncytia results from activation of the SARS-CoV-2 spike protein at the cell plasma membrane level. On the basis of these observations, we performed two high-content microscopy-based screenings with more than 3,000 approved drugs to search for inhibitors of spike-driven syncytia. We converged on the identification of 83 drugs that inhibited spike-mediated cell fusion, several of which belonged to defined pharmacological classes. We focused our attention on effective drugs that also protected against virus replication and associated cytopathicity. One of the most effective molecules was the antihelminthic drug niclosamide, which markedly blunted calcium oscillations and membrane conductance in spike-expressing cells by suppressing the activity of TMEM16F (also known as anoctamin 6), a calcium-activated ion channel and scramblase that is responsible for exposure of phosphatidylserine on the cell surface. These findings suggest a potential mechanism for COVID-19 disease pathogenesis and support the repurposing of niclosamide for therapy. https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/ http://schema.org/encodingFormat application/ld+json https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/ http://schema.org/hasPart https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/resources/05b54af3-ce56-4474-9603-9d49e56e97c6 https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/ http://schema.org/identifier https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7 https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/ http://schema.org/license https://choosealicense.com/no-permission/ https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/ http://schema.org/name Drugs that inhibit TMEM16 proteins block SARS-CoV-2 spike-induced syncytia https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/ http://w3id.org/ro-id/rohub/model#creation_mode MANUAL https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/ http://www.w3.org/1999/02/22-rdf-syntax-ns#type http://purl.org/wf4ever/ro#ResearchObject https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/ http://www.w3.org/1999/02/22-rdf-syntax-ns#type http://purl.org/wf4ever/roevo#LiveRO https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/ http://www.w3.org/1999/02/22-rdf-syntax-ns#type http://schema.org/Dataset https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/ http://www.w3.org/1999/02/22-rdf-syntax-ns#type http://w3id.org/ro/earth-science#BibliographyResearchObject https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/ http://www.w3.org/1999/02/22-rdf-syntax-ns#type https://w3id.org/ro/terms/earth-science#BibliographyResearchObject https://w3id.org/ro-id/53cb4ba4-7529-4924-9e30-46d4bf7d55f7/ https://www.w3.org/ns/iana/link-relations/relation#cite-as Foglini, Federica. "Drugs that inhibit TMEM16 proteins block SARS-CoV-2 spike-induced syncytia." ROHub. 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The pathological substrate for these findings remains unknown. Here we show that the lungs of patients with COVID-19 contain infected pneumocytes with abnormal morphology and frequent multinucleation. The generation of these syncytia results from activation of the SARS-CoV-2 spike protein at the cell plasma membrane level. On the basis of these observations, we performed two high-content microscopy-based screenings with more than 3,000 approved drugs to search for inhibitors of spike-driven syncytia. We converged on the identification of 83 drugs that inhibited spike-mediated cell fusion, several of which belonged to defined pharmacological classes. We focused our attention on effective drugs that also protected against virus replication and associated cytopathicity. One of the most effective molecules was the antihelminthic drug niclosamide, which markedly blunted calcium oscillations and membrane conductance in spike-expressing cells by suppressing the activity of TMEM16F (also known as anoctamin 6), a calcium-activated ion channel and scramblase that is responsible for exposure of phosphatidylserine on the cell surface. 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