Relief Therapeutics Holding AG (RLFTF)

[changes_iv]

I do recall that sad case because of the similarities/symptoms COVID-19 has with Ebola virus. >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
“... binds to uninfected dendritic cells (DCs) and macrophages, in a process dependent on the glycosylation pattern of shed GP and on cellular Toll-like receptor 4 (TLR4). The binding of shed GP resulted in the activation of DCs and macrophages, and induced the release of cytokines, which were sufficient to increase the permeability of endothelial barriers. These data suggest that the release of shed GP from infected cells leads to the dysregulation of the host immune response and the modulation of remote target cells, such as endothelial cells, resulting in increased inflammation and vascular permeability, which are two characteristics of fatal EBOV infection. https://www.nature.com/articles/nrmicro3412

Is RLF-100 the drug to cover all bases (ace2)? >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>> “Since identifying the possible route of infection has major implications for understanding the pathogenesis and future treatment strategies for SARS, the present study investigated the localization of ACE2 protein in various human organs (oral and nasal mucosa, nasopharynx, lung, stomach, small intestine, colon, skin, lymph nodes, thymus, bone marrow, spleen, liver, kidney, and brain). The most remarkable finding was the surface expression of ACE2 protein on lung alveolar epithelial cells and enterocytes of the small intestine. Furthermore, ACE2 was present in arterial and venous endothelial cells and arterial smooth muscle cells in all organs studied. In conclusion, ACE2 is abundantly present in humans in the epithelia of the lung and small intestine, which might provide possible routes of entry for the SARS-CoV. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7167720/
We’ll soon find out but not soon enough for the 28 y/o doctor.