Comment · Wed, April 13, 2016
Which universities is Ceretropic partnering with and what research is being pursued?
Original post in this thread
narlsnarly · 4 points
Which universities is Ceretropic partnering with and what research is being pursued?
What they were answering
rmcfar11 · 1 points
Just a follow-up, I've been doing some research and found the original article I mentioned in addition to a couple others. One actually looked at Semax and various derivatives at the N-Terminal AA. Apparently Semax nootropic properties are still retained if you use Lysine instead. I think they tested methionine, Lysine, Valine, and one other. Only one of those AA'S caused semax to lose the cognitive enhancement properties. If you are interested, lmk and I'll send you the links.
Also of note, I found one article that investigated the effects of acylation (like you've done with NAS/A.) and how long this increased the duration of action. Specifically they tried to do liposomal (can't recall spelling) encapsulation and found it wasn't viable with Max content being 8% encapped.... BUT, what they did investigate was the enzymes that are responsible for semax degradation (prolyl, neutral, ACE, etc). They messed around with various inhibitors of these enzymes to find out how long they could extend the duration of action. They managed to achieve a cognitive enhancement effect that lasted 24 hours, despite semax being lysed after only ~30 min if I recall correctly... Anyhow, my point is, they discovered that of the common enzymes that degrade peptides, there was only ONE that was mostly responsible! They quantified it to something like ¿70%? of semax degradation is caused by this one e…
u/MisterYouAreSoDumb
Can you upload that paper for me, or give me the DOI? I would love to read it.
Prolyl endopeptidase is certainly the enzyme that cleaves off the C-terminal end of Semax. That is what the amidation is protecting from. The PGP on the C-terminal end is the "nootropic" side of the peptide. That is what is increasing BDNF, and is what is similar to Noopept. The ACTH fragment is more the stimulation end of things. If we modify the N-terminal amino acid to a lysine, or to a D-form, then it will probably still retain the nootropic effect, but lose the stimulation effect. That's because we are altering the ACTH fragment. Many people like the stimulation effect. So I am not sure if that would improve things.