Antiviral activity of JS-K

Nitric oxide (NO) is an endothelium-derived relaxing factor that plays a key role in vascular signaling, regulation of blood flow, and host defense.1 NO can reduce the hemolysis and oxidative damage of red blood cells in patients with SARS-CoV-2 and suppress the hyper-inflammatory response causing acute respiratory distress syndrome (ARDS) and systemic organ failure.2ARDS and systemic organ failure are the leading causes of mortality in COVID-19 patients. Because SARS-CoV-2 infects endothelial cells, which are a major source of NO synthesis, NO is additionally well placed to respond to viral attack.2 Exogenous NO treatment by inhalation is currently clinically used for ARDS and is included in the emergency expanded access program by the U.S. Food and Drug Administration (FDA). Furthermore, it is reported that NO inhibits viral replication in SARS-CoV-1 infection by cytotoxic reactions through intermediates such as peroxynitrite.3 Based on these reports, it is evident that NO can potentially be a therapeutic option for the treatment of COVID-19. However, currently, there are no NO based treatment options that can be administered systemically in COVID-19 patients. Our compound JS-K is a NO donor and can spontaneously release NO upon contact with glutathione. JS-K, when administered systemically, can release NO spontaneously and can effectively suppress the inflammation cascade in SARS-CoV-2 infection and therefore reduce mortality in COVID-19 patients by halting the progression of ARDS and systemic organ failure. Due to the lack of vaccines and approved treatment options for COVID-19, there is a substantial unmet need to develop effective treatment options for COVID-19 to reduce the number of cases and deaths. Therefore, our molecule JS-K if proven effective against SARS-CoV-2, can potentially be developed into an effective treatment option for COVID-19.

1. Ignarro I.J, Nitric oxide: Biology and Pathobiology, Cambridge, MA, 2009. 2. Adusumilli, N. et al., Nitric Oxide 103 (2020) 4-8. 3. Akerstrom, S. J. Virol. 79 (2005) 1966-1969.