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  • Diltiazem inhibits SARS-CoV-2 cell attachment and internalization and decreases the viral infection in mouse lung #MMPMID35176124
  • Wang X; Luo J; Wen Z; Shuai L; Wang C; Zhong G; He X; Cao H; Liu R; Ge J; Hua R; Sun Z; Wang X; Wang J; Bu Z
  • PLoS Pathog 2022[Feb]; 18 (2): e1010343 PMID35176124show ga
  • The continuous emergence of severe acute respiratory coronavirus 2 (SARS-CoV-2) variants and the increasing number of breakthrough infection cases among vaccinated people support the urgent need for research and development of antiviral drugs. Viral entry is an intriguing target for antiviral drug development. We found that diltiazem, a blocker of the L-type calcium channel Cav1.2 pore-forming subunit (Cav1.2 alpha1c) and an FDA-approved drug, inhibits the binding and internalization of SARS-CoV-2, and decreases SARS-CoV-2 infection in cells and mouse lung. Cav1.2 alpha1c interacts with SARS-CoV-2 spike protein and ACE2, and affects the attachment and internalization of SARS-CoV-2. Our finding suggests that diltiazem has potential as a drug against SARS-CoV-2 infection and that Cav1.2 alpha1c is a promising target for antiviral drug development for COVID-19.
  • |*COVID-19/drug therapy/pathology/virology[MESH]
  • |A549 Cells[MESH]
  • |Animals[MESH]
  • |Cells, Cultured[MESH]
  • |Chlorocebus aethiops[MESH]
  • |Diltiazem/*pharmacology/therapeutic use[MESH]
  • |Disease Models, Animal[MESH]
  • |Female[MESH]
  • |HEK293 Cells[MESH]
  • |HeLa Cells[MESH]
  • |Humans[MESH]
  • |Lung/*drug effects/pathology/virology[MESH]
  • |Mice[MESH]
  • |Mice, Inbred BALB C[MESH]
  • |Mice, Inbred C57BL[MESH]
  • |Mice, Transgenic[MESH]
  • |SARS-CoV-2/*drug effects/physiology[MESH]
  • |Vero Cells[MESH]
  • |Virus Attachment/drug effects[MESH]
  • |Virus Internalization/drug effects[MESH]

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  • suck abstract from ncbi

    e1010343 2.18 2022