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PEA-NBOMe

Anon0631

Anon0631

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I happened across a small quantity of n,(2,methoxy-benzyl)-phenethylamine (please correct me if I haven't named this compound correctly and I will edit accordingly).

Seeing as I have no idea if this compound is active (or how it's activity would be characterised if it was (stimulant maybe?)) and there are no reports of it being trialled before, I decided to act as experimental subject.

100mg of the phosphate salt was dissolved in 5ml dH2O to make a stock 20mg/ml solution. From this solution, 0.05ml was removed and diluted with water to make 1ml of 1ml/mg dosing solution. 0.1ml of this solution (100μg PEA-NBOMe) was administered via nasal spray with no observable result.

The next trial will be at 250μg.
 
Do you have any experience with other "nbome" phenethylamines for reference?
 
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I really wouldn't take this, for some reason I don't think that the very adrenergic quality that 25H-NBOMe apparently has is a good sign... maybe it is farfetched, but it is the closest compound to PEA-NBOMe that I can think of.
 
From the linked thread:

me said:
The NBOMe substitution should indeed preclude rapid catabolism, but it should also abolish PEA's stimulant activity.*
Click to expand...

This needs further qualification: the nBOMe substitution should preclude PEA-nBOMe from acting as a substrate for MAO, but other metabolic processes (in particular digestive processes) should readily cleave off the nBOMe substitution. Also, by "stimulant activity", I was referring to action at monoamine transporters, not direct adrenergic agonism.

ebola
 
ebola? said:
This needs further qualification: the nBOMe substitution should preclude PEA-nBOMe from acting as a substrate for MAO, but other metabolic processes (in particular digestive processes) should readily cleave off the nBOMe substitution.
Click to expand...

Yes, we know this from 25X-PEA-NBOMe's and parenteral routes of administration would need to apply likewise - or do you mean to say that it may be even more metabolically unstable?
 
Do we even know if NBOME-ization poses any benefits for transporter affinity? I thought it was a pretty exclusively 5ht-2a/c thing.
 
I'm happy to defer to greater knowledge than mine but doesn't the logic go something like this: PEA would be active if it wasn't broken down so thoroughly by MAO. The NBOMe addition stops it being metabolised so readily. Therefore it should show some activity.

Anyway. I will answer the question if whether its active or not the Shulgin way - by putting it into me.
 
sekio said:
Do we even know if NBOME-ization poses any benefits for transporter affinity? I thought it was a pretty exclusively 5ht-2a/c thing.
Click to expand...

Right. The pattern of activity of the nBOMe 2Cs, compared to the parent compounds lacking the amine substitution, suggests abolition of transporter affinity (not to say that this is the most definitive test, as the 2Cs are very hit-and-miss, mostly miss, at these sites).

ebola
 
I'm wondering...might it be useful to modify the Shulgin procedure to include randomized single-blind placebo trials (double blind trials are pretty impractical for amateurs working at home :P)?

ebola
 
Yes. It's surprisingly hard to differentiate threshold activity from placebo. On the other hand placebo control (ie getting my girlfriend to label two nasal sprays "a" and "b" and only she knows which one is placebo and which one isn't) means that the step by step assay takes twice as long.

I'm starting to understand Shulgin's problem. You want to be able to test a variety of compounds for activity, even if some of them have a low likelyhood of coming good. That's how new things are discovered after all. But it takes such a long time it's tempting to limit research to avenues that you already know have a high likelyhood of positive results. Otherwise you will be working stuff up for ever.

PiHKAL took 25 or so years for 179 compounds and Shulgin missed loads of stuff. If mescaline had been unknown and untasted, he would have missed it because he would have stopped looking for activity at 50-100mg.
 
Possible threshold effect/possible placebo at 1mg liquid insufflation. I needed to shit 5 minutes after dosing. It could have been a coincidence but it was a very amphetamine-like toilet experience.

Too much information? It's all in the name of science :-)

UPDATE: after about 40 minutes, I'm leaning more toward mild plus one than placebo. It's not definite enough to know the nature of the effect though.
 
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no, just the right amount of information. ;)
...
Possible threshold effect/possible placebo at 1mg liquid insufflation. I needed to shit 5 minutes after dosing. It could have been a coincidence but it was a very amphetamine-like toilet experience.
Click to expand...

FWIW, I found selegiline + PEA to induce this type of...phenomenon...more reliably and intensely than amphetamine.

ebola
 
So, the verdict is this stuff is... shitty?

*ba dum tish*

Given NBOMe-Mescaline's apparent lack of activity until the tens of mg, maybe this comppound is active but considerably less so than the 25x series.
 
I should point out that my sample is likely to be a fairly impure synthesis. If anyone in the future uses this thread for dosage information, they might want to half the quantities.
 
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