Background Ever-growing research into the Covid-19 pandemic has revealed a number of potential treatment options, yet a mysterious shroud still envelops the virus. From what is known at the moment, admitted patients in the late, often fatal, stages of infection express hyper-inflammatory and hyper-oxidative stress reactions. In addition, a fraction of infected individuals exhibit lung immunopathogenesis, best described as an out-of-control immune response, resulting in pulmonary tissue damage and decreased lung capacity. The NF-κB signaling pathway may be the primary link in triggering the hyperreactive immune response during infection, due to its ability to activate the proinflammatory cascade leading to a cytokine storm. The NF-kB signaling system may be an attractive drug target. The oxidative stress that accompanies a hyper-immune response suggests that the anti-oxidant Nrf2 signaling pathway also may be a drug target. Therefore, treatment options involving the proper suppression of immune-related signaling pathways, such as NF-kB, and/or activation of anti-oxidant pathways, such as Nrf2, could potentially alleviate the symptoms seen in late stages of Covid-19 (SARS CoV2) infection. Technology Description A researcher at the University of New Mexico has proposed the use of a resveratrol analog, designated LD55, as a suppressant of the hyper-inflammatory and hyper-oxidative stress reactions associated with late stage Covid-19 infections. Developed originally to slow chronic neurological diseases progression and treat skin conditions, LD55 has exhibited unique behavior by inhibiting pro-inflammatory NF-κB signaling whilst activating anti-oxidant Nrf2 signaling. This dual behavior enables the drug to potentially inhibit inflammation and oxidative stress simultaneously. Therefore, administering LD55 to target the lung cells of Covid-19 patients would dampen the heightened immune system response, reducing the likelihood of pulmonary tissue damage and decreased lung capacity. Gregg Banninger GBanninger@innovations.unm.edu 505-272-7908
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