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{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7600245","sourcedb":"PMC","sourceid":"7600245","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7600245","text":"The drug is associated with several mechanisms. The anti-protozoal activity demonstrated by this drug is promoted by the inhibition of pyruvate:ferredoxin oxidoreductase enzyme-dependent electron transfer reaction [137]. However, in the case of influenza, nitazoxanide and its metabolite inhibit the viral hemagglutinin maturation at the post-translational phase with no effect on the M2 protein or on the neuraminidase glycoprotein [138]. Furthermore, nitazoxanide modulates other targets and pathways in vitro including glutamate-gated chloride ion channels and glutathione-S-transferase in nematodes, respiration and other pathways in bacterial and cancer cells, and viral and host transcriptional factors [134]. In fact, nitazoxanide was shown to in vitro inhibit the replication of coronaviruses, including MERS-CoV in cells and the expression of the viral N protein [136,139]. The drug was also reported as a non-competitive inhibitor of thiol oxidoreductase ERp57 and thus demonstrated anti-paramyxovirus activity [140]. Moreover, nitazoxanide was reported to inhibit the production of pro-inflammatory cytokines in peripheral blood mononuclear cells and animal models [136]. In peripheral blood mononuclear cells exposed to influenza virus, nitazoxanide potentiated the release of INF-α and INF-β by fibroblasts [135]. In addition, nitazoxanide appears also to act as a bronchodilator in testing models by blocking the calcium-activated chloride channel TMEM16A 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