As a result of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, a clinical complication can arise that is characterized by a hyperinflammatory cytokine profile, often termed a ‘cytokine storm’. A protein complex (nuclear factor kappa-light-chain-enhancer of activated B cells; NF-κB) is intricately involved in regulating inflammation and the immune response following viral infections, with a reduction in cytokine production often observed following a decrease in NF-κB activity. An approved asthma drug, montelukast, has been found to modulate the activity of NF-κB, and result in a corresponding decrease in proinflammatory mediators. Herein, we hypothesize that repurposing montelukast to suppress NF-κB activation will result in an attenuation of proinflammatory mediators and a decrease in cytokine production, thereby leading to a reduction in symptom severity and to improved clinical outcomes in patients with Coronavirus 2019 (COVID-19).

严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 感染可能会出现临床并发症，其特征是细胞因子过度炎症，通常称为“细胞因子风暴”。蛋白质复合物（活化 B 细胞的核因子 kappa-轻链增强子；NF-κB）与调节炎症和病毒感染后的免疫反应密切相关，随着 NF-κB 的减少，细胞因子的产生通常会减少。 κB 活性。一种已批准的哮喘药物孟鲁司特被发现可以调节 NF-κB 的活性，并导致促炎介质相应减少。在此，我们假设重新利用孟鲁司特来抑制 NF-κB 激活将导致促炎介质减弱和细胞因子产生减少，从而减轻 2019 冠状病毒（COVID-19）患者的症状严重程度并改善临床结果）。