Noopept self-experiment: no effects

I suspect you can't and if you try, the blinding index will show blinding failed and the subject learned to distinguish even with whatever you add to try to mask the flavor.

Well I will consider you the expert on flavoring noopept solutions, then. It's not like I have made thousands of bottles, with all manner of methods for hiding the flavor.

I'm not sure why you are so hostile right now. You're either projecting some annoyance on me, or you are wound up tighter than a girdle on a Baptist minister's wife, at an all-you-can-eat pancake breakfast. I apologize for wasting your time... Next time I'll just ignore it, and move on with my day.

As you may or may not know, there is evidence that noopept is a prodrug for a few active metabolites. This makes sense, seeing as how the effects last a lot longer than the peptide itself does in the body. This is very similar to Selank and Semax, and is actually one of the reasons they were developed. The Russians saw the evidence that noopet was a prodrug for other substances, and decided to see if they could do similar modifcations to ACTH and Tuftsin. Two of the supposed active metabolites that noopept create, are phenylacetylproline and phenylacetic acid. Those two metabolites are not found if the substance passes through first pass metabolism, which oral does. This is because noopept is preferably hydrolyzed by plasma peptidase when administered in a manner that bypasses the GI tract and liver. When taken orally, the first pass through the GI tract and the liver subjects the peptide to different enzymes, and attacks the peptide bonds first. That breaks the two amino acids apart, and prevents the other metabolites from being created. It can and does still allow the noopept molecule to enter the bloodstream in some amounts. As I have shown you studies for, it is about 10% through oral.

There is another metabolite, cyclo-L-prolylglycine, which many feel is what causes the main nootropic actions of noopept. Unfortunately the only studies that I can find measuring cyclo-L-prolylglycine are after injecting noopept, not taking it orally. If you look at the structure of cyclo-L-prolylglycine, there is really only one way for it to form from noopept. That happens when phenylacetic acid deacetylates in plasma. Remember what I said about phenylacetic acid? It is NOT found after oral administration. That is because the enzymes in the GI tract and liver break apart the peptide at different parts. The only time cyclo-L-prolylglycine has been detected is in the presence of plasma and brain enzymes. So if the theory that cyclo-L-prolylglycine is responsible for the main nootropic effects, and the only way it can form is deacetylation by plasma and brain enzymes of phenylacetic acid, which is not detectable after oral administration, then it is safe to say that oral administration is never going to lead to the same effects as other routes of administration that bypass the GI tract and liver.

So now we get to the heart of the issue. Does sublingual lead to elevated levels of phenylacetylproline, phenylacetic acid, and consequently cyclo-L-prolylglycine? Well when you can figure out how to drip some noopept solution under the tongue of a rat, then that testing should be easy. But I do not know of a way to test sublingual administration in animal models. That leaves us with human studies. Those have not been run yet. So we are left with educated guessing. We know sublingual bypasses the GI tract and first pass metabolism through the liver. We know that the GI tract and liver are responsible for preventing the metabolites from occurring after oral administration of noopept. So it is not an unreasonable jump to say that sublingual is going to lead to much greater amounts of the active metabolites than oral would. Can I tell you how that compares to injection? No, I cannot give you hard numbers. I know you keep trying to use the excuse that I cannot give you those numbers as an argument against my case. However, that is silly. The reasoning behind my theory is sound, even though I cannot give you hard numbers. I hope that one day I can give you those numbers. But it is clear to me that sublingual is going to lead to much greater amounts of the known active metabolites than oral will.

So do with that information what you will. But noopept is one of the only peptides that people try and take orally. That is for good reason. Peptides do not like the GI tract and liver. Because noopept is a small dipeptide, and has more lipophillicity, it does get through oral much better than a lot of other peptides like Semax. But there is evidence that there is a breakdown of the active parts of the noopept structure after oral administration, and I think you should account for it in your studies.