PMC:7319919 / 4383-5591 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7319919","sourcedb":"PMC","sourceid":"7319919","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7319919","text":"Although developed targeting the oncogenic fusion protein BCR-ABL, imatinib is able to inhibit other tyrosine kinases such as c-KIT, platelet-derived growth factor receptor and Abelson kinases (ABL) type 1 and 2 [4]; therefore, it has been postulated that the biological activity of this drug is not restricted to anticancer effects. In this regard, immunomodulatory properties of imatinib have been reported. Murine models of sepsis and acute lung injury have suggested a protective role of this drug by reducing pulmonary edema, preventing histological damage and improving endothelial barrier dysfunction, probably through attenuation of proinflammatory cytokine release including interleukin-6 and tumor necrosis factor-alpha [4,5]. These effects over inflammatory activation might be mediated by the inhibition of transcription factor NF-κB according to previous evidence from both animal models and studies with human cells [[4], [5], [6]]. Since NF-κB represents a key element in several inflammatory pathways [7], imatinib could be helpful to modulate host immune response against SARS-CoV-2. This is particularly noteworthy given that hyperinflammation plays a central role in severe COVID-19 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