COX2 inhibition in the treatment of COVID-19: Review of literature to propose repositioning of celecoxib for randomized controlled studies

•Coronavirus-triggered pulmonary and systemic disease has an unpredictable clinical course in different subsets of patients.•COX2, p38 MAPK, IL-1b, IL-6 and TGF-β play pivotal roles in coronavirus-related cell death, cytokine storm and pulmonary interstitial fibrosis.•Discussion is ongoing on refining immunomodulation in COVID-19 without COX2 inhibition.•We searched the literature to show a potential target (COX2) and a weapon (celecoxib). Coronavirus-triggered pulmonary and systemic disease, i.e. systemic inflammatory response to virally triggered lung injury, named COVID-19, and ongoing discussions on refining immunomodulation in COVID-19 without COX2 inhibition prompted us to search the related literature to show a potential target (COX2) and a weapon (celecoxib). The concept of selectively targeting COX2 and closely related cascades might be worth trying in the treatment of COVID-19 given the substantial amount of data showing that COX2, p38 MAPK, IL-1b, IL-6 and TGF-β play pivotal roles in coronavirus-related cell death, cytokine storm and pulmonary interstitial fibrosis. Considering the lack of definitive treatment and importance of immunomodulation in COVID-19, COX2 inhibition might be a valuable adjunct to still-evolving treatment strategies. Celecoxib has properties that should be evaluated in randomized controlled studies and is also available for off-label use.