• Curr. Pharm. Des. · Jan 2020

    Pentoxifylline and Oxypurinol: Potential Drugs to Prevent the "Cytokine Release (Storm) Syndrome" Caused by SARS-CoV-2?

    • Francisco J López-Iranzo, Ana M López-Rodas, Luis Franco, and Gerardo López-Rodas.
    • Department of Biochemistry and Molecular Biology, University of Valencia, Valencia, Spain
    • Curr. Pharm. Des. 2020 Jan 1; 26 (35): 4515-4521.

    BackgroundCOVID-19, caused by SARS-CoV-2, is a potentially lethal, rapidly-expanding pandemic and many efforts are being carried out worldwide to understand and control the disease. COVID-19 patients may display a cytokine release syndrome, which causes severe lung inflammation, leading, in many instances, to death.ObjectiveThis paper is intended to explore the possibilities of controlling the COVID-19-associated hyperinflammation by using licensed drugs with anti-inflammatory effects.HypothesisWe have previously described that pentoxifylline alone, or in combination with oxypurinol, reduces the systemic inflammation caused by experimentally-induced pancreatitis in rats. Pentoxifylline is an inhibitor of TNF-α production and oxypurinol inhibits xanthine oxidase. TNF-α, in turn, activates other inflammatory genes such as Nos2, Icam or IL-6, which regulate migration and infiltration of neutrophils into the pulmonary interstitial tissue, causing injury to the lung parenchyma. In acute pancreatitis, the anti-inflammatory action of pentoxifylline seems to be mediated by the prevention of the rapid and presumably transient loss of PP2A activity. This may also occur in the hyperinflammatory -cytokine releasing phase- of SARS-CoV-2 infection. Therefore, it may be hypothesized that early treatment of COVID-19 patients with pentoxifylline, alone or in combination with oxypurinol, would prevent the potentially lethal acute respiratory distress syndrome.ConclusionPentoxifylline and oxypurinol are licensed drugs used for diseases other than COVID-19 and, therefore, phase I clinical trials would not be necessary for the administration to SARS-CoV-2- infected people. It would be worth investigating their potential effects against the hyperinflammatory response to SARS-CoV-2 infection.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

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