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4-AcO-DMT pharmacology

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Psilocity

Greenlighter
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Jan 13, 2010
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Is 4-AcO-DMT an active subsance? Does it affect any receptors in the brain?

I know that 4-AcO-DMT is deacetylated into psilocin, but does 4-AcO-DMT have any pharmacodynamic properties?

I'm asking because I've heard that 4-AcO-DMT is slightly more potent than psilocin itself, and I don't understand how that can be.

(Sry my crappy english, I'm from Sweden :\)
 
Welcome to BL.

Take a look at The Big and Dandy 4-AcO-DMT thread - New incarnation

But to quickly answer your question:
It is active.
It is a partial agonist at the 5-HT2A serotonin receptor in the brain where it mimics the effects of serotonin (5-HT). Psilacetin is an 5-HT1A and 5-HT2A/2C agonist.
(taken from the psilocin wiki)
Ive never had experience with pure 4 ho dmt, only had mushrooms, but if my memory is correct the doses for psilocin reported here were around the same if not slightly lower as those for psilacetin (4 aco dmt).
But it is a very potent substance, showing definite activity at 10mg. I just think 10mg of psilocin may be more powerful.
 
Thanks

Yes, I know that psilocin is active, but I was wondering about 4-AcO-DMT itself. Does it ever reach to the brain before getting deacetylated into psilocin, and if so, does it affect any receptors?
 
Yes 4 aco dmt is active in its own right.
Apparently it does reach the brain before being desacetylated because its effects are different than those of 4 ho dmt..
It probably effects the same receptors as psilocin because its pharmocology is so close, and beause 5ht2 (seratonin receptors) are the culprits of most psychedelic tryptamines psychopharmocology.
 
I still don't see what evidence there is that it doesn't just function as a prodrug. Yes I have experienced first-hand how different it feels, but is it not possible this is due to different pharmacokinetics ?
 
I dont believe there is any actual scientific data to prove its not a pro-drug, but experiences show they are pretty different from each other.
As im sure you know, there are diffferences in all the 4ho tryptamines and their acetoxy esters.
But in particular 4 ho dipt vs 4 aco dipt. The difference between those 2 are pretty drastic and im having a hard time believing its all due to pharmacokinetics.
 
a post by nuke thats sort of related to my above post...

nuke said:
It might, esters are non-polar enough to make their way through the BBB in reasonable amounts, but I am more curious as to whether that would interfere with 5HT2 binding or not. In fact the propionyl analogue probably has greater lipophilicity than the acetyl. The further up you go with the size of the carbon chain of esters, the greater the LogD and theoretical BBB permeation, however you also run the risk of the compound being too large to effectively fit into the 5HT2 receptor, as well as the compound being unable to be metabolized into the indolol. That would make for a drug that got into the brain very well, but did shit all once it got there.

4-AcO-DiPT was a weird one for me in that it took me damned near forever after taking it to sleep, despite the fact that I wasn't very much intoxicated, indicating to me that the 4-AcO group may have prolonged the action of the parent compound (either through metabolism or avoiding clearance or both).
Click to expand...
 
Alrighty then, not that I don't agree with that Delsyd - was just checking on (f)actual confirmation.

What about merging this thread with the one on 4-AcO-tryp to 4-HO-tryp biotransformation? I can see how this one is about only the (neuro)pharmacology of psilacetin but the only thing I think develops this is receptor affinities, quotes from studies and papers and the subsequent interpretation of them for the not so scientifically founded. (I mean I can understand enough of it but sometimes these research results are a linguistic maze :D )
 
Solipsis said:
I still don't see what evidence there is that it doesn't just function as a prodrug. Yes I have experienced first-hand how different it feels, but is it not possible this is due to different pharmacokinetics ?
Click to expand...
Reports of IV use indicate powerful and nearly immediate DMT-like effects. Unless there is enough of whatever it is exactly in the blood to convert 4-Ac0 to 4-ho that rapidly then indications are that 4-AcO is active on its own. This is the best evidence I know of for 4-AcO being more than a prodrug (though I don't doubt conversion also occurs), but I'm curious about any alternative explanations for the rapidity of its IV effects. I assume by now you must have come across the IV argument?
 
I've often wondered this myself, and I've heard anecdotal evidence of people being able to discriminate between the two in "blind taste tests," but i've yet to see anything definite as to it not being only a pro-drug. However, whether or not its active on its own, i'm pretty sure it is also a prodrug for psilocin
 
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