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Re: None

Saturday, 12/26/2020 12:19:53 PM

Saturday, December 26, 2020 12:19:53 PM

Post# of 2221
Taming the adverse effects of excessive NF-kB

From the paper linked by power walker: "Anatabine ameliorates intestinal inflammation and reduces the production of pro-inflammatory factors in a dextran sulfate sodium mouse model of colitis"

https://journal-inflammation.biomedcentral.com/articles/10.1186/s12950-020-00260-6";

"Anatabine has been shown to inhibit lipopolysaccharide (LPS)-induced pro-inflammatory gene expression as well as NF-kB and STAT3 phosphorylation in human neuroblastoma SH-SY5Y, HEK293, human microglia, and human blood mononuclear cells [33] as well as in the brain and spleen of mouse models of autoimmune encephalomyelitis [31] and Alzheimer’s disease [33]. In SH-SY5Y cells, anatabine also reduced the expression of beta-secretase 1—the rate limiting enzyme for ß-amyloid peptide production, which is a major hallmark of Alzheimer’s disease—through inhibition of NF-kB activation [21].”

The more I learn about NF-kB the more important it seems. Akers may have something of great value, and that would explain a deal with MYMD that some have thought gave Akers too little.

The MYMD-1 molecule being brought into Akers, and it's successor company, MYMD, is also an alkaloid and if I understand correctly, is intended to have the same or similar effect on inflammation.