As Ohm points out Leronlimab should surpass CD24 Fc fusion protein drug from Oncoimmune.
Actually, there are studies similar to Dr. Sacha's in macaques where the results don't seem to be as good as the ones obtained with LL.
"CD24 and Fc fusion protein protects SIVmac239-infected Chinese rhesus
macaque against progression to AIDS"
https://www.researchgate.net/publication/3261...on_to_AIDS
Some important excerpts from this paper:
We are way beyond this.
The viral load copies did not even reach statistical significance. Of course, this does not mean that this will translate into COVID ineffectiveness, but it does tell that LL is more effective in HIV area.
What it is important, though, is the effect in the inflammatory cytokines:
Again, I am not saying that this means that SACCOVID does not work, I am saying that this is good news for Leronlimab as we seem to be more effective in controlling cytokines (at least macaques) when this is necessary and, in that both drugs seem to operate in the same area.
Clinical trials are there exactly to dispel/decide these theories.
Actually, there are studies similar to Dr. Sacha's in macaques where the results don't seem to be as good as the ones obtained with LL.
"CD24 and Fc fusion protein protects SIVmac239-infected Chinese rhesus
macaque against progression to AIDS"
https://www.researchgate.net/publication/3261...on_to_AIDS
Some important excerpts from this paper:
Quote:Furthermore, althoughCD24Fc did not restore CD4+ T cell number or significantly change T cell subsets or CD4+ T cell activation , it maintained low levels of plasma soluble CD14, CD8+ T cell activation, viral load and proviral load in the peripheral blood mononuclear cells and marrow. These results suggested that CD24Fc confers protection to SIV infected ChRMs against progression to AIDS. It was also implied that CD24Fc may be a potential therapeutic approach for the control of HIV-1/AIDS.
We are way beyond this.
The viral load copies did not even reach statistical significance. Of course, this does not mean that this will translate into COVID ineffectiveness, but it does tell that LL is more effective in HIV area.
What it is important, though, is the effect in the inflammatory cytokines:
Quote:Owing to the under-sensitive level of IL-6, TNF-α, IFN-α, and IL-1β in the Luminex and enzyme linked immunosorbent assay (R&D) assays, we measured inflammation based on the mRNA expression of inflammatory cytokines in SIV-infected monkeys. Unexpectedly, although significantly lower levels of IL-6 (P = 0.0020) and indoleamine 2, 3- dioxygenase-1 (IDO) (P = 0.0020) were identified from 0 to 22 weeks after treatment and higher levels of IL-1β (P = 0.0137) were identified from 0 to 14 weeks after treatment in PBMCs in a longitudinal analysis under similar viral load, we did not find comprehensive effects of CD24Fc on the inflammatory cytokines .
Quote:To address the impact of CD24Fc on the inflammatory response of internal organs, we initiated another round of CD24Fc treatment at 30 weeks after SIV infection and analyze the transcripts of inflammatory cytokines and pathology in the organs. We found no effect of CD24Fc on IFN-α, TNF-α, IL-6, IFN-γ, IDO, and IL-1β expression in the spleen, marrow, mesentery LN, inguinal LN or ileum lymphoid cells (data not shown), and also no significant effects on cytokines expression in PBMCs at same time
Again, I am not saying that this means that SACCOVID does not work, I am saying that this is good news for Leronlimab as we seem to be more effective in controlling cytokines (at least macaques) when this is necessary and, in that both drugs seem to operate in the same area.
Clinical trials are there exactly to dispel/decide these theories.
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