We describe a remarkable benefit of IV NAC in severe COVID-19 infection. As expected, IV NAC initially mitigated the hemolysis in a G6PD-deficient, COVID-19-infected patient treated with hydroxychloroquine for a single day. We also observed an obvious drop in inflammatory markers following initial NAC administration. This was followed by rebound rises of CRP and ferritin upon discontinuation of NAC. Re-started IV NAC for two additional intervals resulted in repeated drops in CRP and ferritin levels (Fig. 1B). NAC administration allowed the discontinuation of ECMO and eventual discharge of the patient to his home.
NAC mechanism of action may involve the blockade of viral infection and the ensuing cytokine storm that warrant follow-up confirmatory studies in the setting of controlled clinical trials.
Preclinical and clinical studies have demonstrated that reactive oxygen species contribute to the destruction and programmed cell death of pulmonary epithelial cells.1 N-acetyl-cysteine (NAC) has been shown to significantly attenuate clinical symptoms in respiratory viral infections in animals and humans, primarily via donation of thiols to increase antioxidant activity of cellular glutathione2,3,4,5. Bucillamine (N-(mercapto-2-methylpropionyl)-l-cysteine) has a well-known safety profile and is prescribed in the treatment of rheumatoid arthritis in Japan and South Korea for over 30 years. Bucillamine, a cysteine derivative with two thiol groups, has been shown to be 16 times more potent as a thiol donor in vivo than NAC 6. The drug is non-toxic with high cellular permeability. The basis of the clinical study will analyze if Bucillamine has the potential, via increasing glutathione activity and other anti-inflammatory activity, to lessen the destructive consequences of SARS-CoV2 infection in the lungs and attenuate the clinical course of COVID-19.
News 
Market Data 
Discover 
