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first-pass metabolism of NBoMes? - what enzyme destroys it orally?

gladiolus

Bluelighter
Joined
Dec 29, 2007
Messages
59
Hi, I'm writing a paper on NBoMes and I was wondering if anyone could speculate, or actually knows, of why these aren't active orally? What enzyme is responsible? - I'm assuming that whatever enzyme it is cleaves the BoMe off the phenethylamine structure, leaving trace amounts of 25x - too small to be active.
 
Maybe either some CYP or a MAO enzzyme.

Nobody has studied the pharmacokinetics and metabolites of 25x I don't think
 
I recently tried some syrian rue with 2c-t-2 the other day, a surprisingly good combo. but what you're suggesting? scary as fuck.

Shit, that combo sounds like a recipe for SS. IIRC, the thio 2c-x's have mao activity, like their alpha methylated cousins. Combining any of the t's, let alone 2c-x's in general with harmala's just sounds scary as fuck.
 
Shit, that combo sounds like a recipe for SS. IIRC, the thio 2c-x's have mao activity, like their alpha methylated cousins. Combining any of the t's, let alone 2c-x's in general with harmala's just sounds scary as fuck.

There's been reports of successful potentiation with no side effects on erowid with this combo.

I would never try it with and nbome because of their already fickle and wildly variant dosing for different people, and then you have the effect of the maoi which is also fickle and wildly variant in how much it potentiates a psychedelic. I propose we save combining MAOI and nbomes for the labs and try some better combos.

On a semi-related (and dangerous) note: Combos that have been known to be at risk serotonin syndrome have given me the most powerful and enjoyable trips.
 
I recently tried some syrian rue with 2c-t-2 the other day, a surprisingly good combo.

aye, that does sound scary. 2C-T-2 and 2C-T-7 are known for causing hypertensive crises even just on their own.

if anyone sees this and gets the idea to try the combination on their own, pleaseeeeeee start out with very small doses. probably best to leave this combo alone tho.
 
Hi, I'm writing a paper on NBoMes and I was wondering if anyone could speculate, or actually knows, of why these aren't active orally? What enzyme is responsible? - I'm assuming that whatever enzyme it is cleaves the BoMe off the phenethylamine structure, leaving trace amounts of 25x - too small to be active.
Would have thought some one would have had a theory about this. I do remember some speculation in the 25I/25C threads about the NBOMes getting caught in body fat or some such whatever I can't remember.....leaving them inactive orally.

I don't think taking a MAOI will make NBOMe's orally active, some one surely must have tried that already.

And the second B, just for putting things straight, cleaving the NBOMe of 25I-NBOMe won't give you 25I, it'll give you 2C-I. But that's probably what you meant.

interesting topic :)
 
And the second B, just for putting things straight, cleaving the NBOMe of 25I-NBOMe won't give you 25I, it'll give you 2C-I. But that's probably what you meant.

Actually, since phenethylamines are about 25-fold better substrates than benzylamines for MAO, it is much more likely that 25X-NBOMes will react to give the phenylacetaldehyde and 2-methoxybenzylamine.
 
^^ I see.

Actually I wasn't talking about how it metabolizes because I have no clue about that, I just ment theoretically if you removed the 2-methoxybenzyl part of 25I-NBOMe, you would have 2C-I.
 
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