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Tryptamines Norbaecystin, Tryptamine and Psilocybin

Q

Quimchin

Greenlighter
Joined
Jul 30, 2022
Messages
10
These are questions for our chemists. It appears to my untrained and ignorant eye that the only difference between Tryptamine and NN DMT is the radical NH2 versus N- - , as show in the attached structures. (Notice that psilocin, NN dmt and 4 aco dmt, all very active, have N - - .) Why is one (NN DMT) psychedelically active and the other, Tryptamine not? -- this is the only visible difference. Is the NH2 sufficient difference to stop activity? #2 - Then looking at Norbaeocystin: it is very similar to psilocybin but it has the same NH2 instead of N- -. Does this stop its psychactivity? I am hoping someone can shed some light on this for me, blue or otherwise (bad joke).

What is the fundamental psychoactive structure, versus those that are not active? Again Tryptamine and NN DMT are so similar, yet one is and the other not.

Does anyone have an experience with Norbaeocystin (NBC)? It looks very similar to Psilocybin (4 PO), even more than 4 aco dmt, which experientially feels and works just like psilocybin to me. One might think that NBC would be as good as 4 PO -- except that it has the NH2 as does Tryptamine which might cancel its psychoactive effect.

Why does NN DMT orally requiere a MAOI while Psilocybin, Psilocin, and 4 aco, not?

Does anyone have experience taking 5 MEO DMT orally with a MAOI?

Link to image:
Formulas.jpg
 
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Not entirely certain, but there are two important factors at play.

One is the enzyme MAO, monoamine oxidase, which breaks down many monoamine structures. Apparently the 4-OH group blocks this enzyme. I would guess science knows how this works exactly, but i don't.

The other factor is lipophilicity. The brain has a barrier called blood-brain barrier that makes it more selective for lipophilic compounds. Plant toxins are generally hydrophilic i suppose, and having a filter like that has been advantageous in protecting this most sensitive structure. Extra methyl groups on n,n-DMT confer greater lipophilicity.

So, oral drugs need to first avoid being destroyed by enzymes and then also need to pass the BBB to get into the brain (like any drug by any ROA)

It could also be about the way these compounds fit into the serotonin receptors.
 
Pretty recent paper studying norbaeocystin showed that it did not induce head twitching in mice and is likely inactive on it's own.

Possibly with an MAOI it could be active?
 
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