@article{fdi:010082717,
  title = {{P}reclinical evaluation of {I}matinib does not support its use as an antiviral drug against {SARS}-{C}o{V}-2},
  author = {{T}ouret, {F}. and {D}riouich, {J}. {S}. and {C}ochin, {M}. and {P}etit, {P}. {R}. and {G}illes, {M}agali and {B}arthelemy, {K}. and {M}oureau, {G}. and {M}ahon, {F}. {X}. and {M}alvy, {D}. and {S}olas, {C}. and {L}amballerie, {X}. de and {N}ougairede, {A}.},
  editor = {},
  language = {{ENG}},
  abstract = {{F}ollowing the emergence of {SARS}-{C}o{V}-2, the search for an effective and rapidly available treatment was initiated worldwide based on repurposing of available drugs. {P}revious reports described the antiviral activity of certain tyrosine kinase inhibitors ({TKI}s) targeting the {A}belson kinase 2 against pathogenic coronaviruses. {I}matinib, one of them, has more than twenty years of safe utilization for the treatment of hematological malignancies. {I}n this context, {I}matinib was rapidly evaluated in clinical trials against {C}ovid-19. {H}ere, we present the pre-clinical evaluation of imatinib in multiple models. {O}ur results indicated that imatinib and another {TKI}, the masitinib, exhibit an antiviral activity in {V}ero{E}6 cells. {H}owever, imatinib was inactive in a reconstructed bronchial human airway epithelium model. {I}n vivo, imatinib therapy failed to impair {SARS}-{C}o{V}-2 replication in a golden {S}yrian hamster model despite high concentrations in plasma and in the lung. {O}verall, these results do not support the use of imatinib and similar {TKI}s as antivirals in the treatment of {C}ovid-19.},
  keywords = {{SARS}-{C}o{V}-2 ; {C}ovid-19 ; {C}oronavirus ; {A}ntivirals ; {T}yrosine kinase inhibitor ; {I}matinib},
  booktitle = {},
  journal = {{A}ntiviral {R}esearch},
  volume = {193},
  numero = {},
  pages = {105137 [8 ]},
  ISSN = {0166-3542},
  year = {2021},
  DOI = {10.1016/j.antiviral.2021.105137},
  URL = {https://www.documentation.ird.fr/hor/fdi:010082717},
}