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NBOMe-2C-X compared to NBOH-2C-X

ungelesene_bettlek

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so since only a few years the psychedelic community has experience with the NBOMe-2C-X series of psychedelics, which is pose some quite special problems to the user because of their high potency, which makes the dosage difficult to measure, and their oral inactivity (it seems to me it is still widely undecided which parenteral ROA is the best for this group). yet, they have gained their fanbase, so I guess there must be something very unique about them (I haven't tried them myself yet, but I surely plan to do so one day). and now, only a few month ago, a new subgroup spread of, the NBOH-2C-X compounds lacking one methyl group. the reason for this new development is solely to get one step ahead in the law again (correct me if I'm wrong), and this argument is actually only valid in a handful of legislations - but for some reasons, the british one is one of those few, and our English fellowmen seem to be especially fond about their grey marked psychedelics.

when one looks at the structure-activity-relationship of 5HT2A-psychedelics, one of the most important rules one has to accept is that there are surprisingly few rules, and one has to expect the unexpected, for example, I still know of no rule of thumb to conclude from the properties of a psychedelic two-carbon-chain phenethylamine to the properties of the corresponding amphetamine. who could have e.g. guesses from the beginning that 2C-E is a much more powerful psychedelic than 2C-D, while with DOM and DOET it is just the other way round?

now you can surely already guess in what direction my question goes: how is the interrelationship between a NBOMe-2C-X compound to its corresponding NBOH-2C-X: I have already read that the latter ones are a bit less potent per weight, and a bit shorter-lived; but apart from that, how strong is the qualitative difference in the experience that this little missing methyl group makes? do we again get completely new compounds with a completely different headspace, or is this difference little enough that one can say that the two corresponding trips are pretty similar, at least if one doesn't look to close?
 
PD >> ADD

comment: I can this thread being kicked back to PD at some point, but right now this seems quite theoretical and asking about SAR and probing beyond the obvious (the more polar benzyl OH should speed up excretion hence the reduction in duration) is prrretty advanced
 
I just joined Bluelight because I really need to tell folks that
25I-NBOMe, and probably other relatives, are indeed orally active, but approximately twice as much is required. I will shortly know if this is also true of Cimbi-27 (25I-NBOH), and I will report back, all you psycho-nuts!
 
I just joined Bluelight because I really need to tell folks that
25I-NBOMe, and probably other relatives, are indeed orally active, but approximately twice as much is required. I will shortly know if this is also true of Cimbi-27 (25I-NBOH), and I will report back, all you psycho-nuts!

How did you come to this conclusion? When dosing did you capsulize the dose and swallow it or put it in water, alcohol, what?

Many people have tried to consume NBOMe's orally without success, myself included.

When they first came out, it wasn't really known that they were not orally active.
 
If the relationship between 25I-nbome and 25i-nbome holds more generally, then we should expect nbohs to exert activity pretty damn similar to their nbome counterparts.

ebola
 
OP You answer your own question about the missing methyl group: less potent per weight, shorter half life. This is usually the case with most substances but that is a generalization. I think the transfer of drug through the blood brain barrier and how it is effected by the addition or subtraction of a key methyl chain in any substance is really the question you should ask. With the addition of a methyl chain it usually crosses that barrier far more readily than some other chemical compositions.
 
OP You answer your own question about the missing methyl group: less potent per weight, shorter half life. This is usually the case with most substances but that is a generalization. I think the transfer of drug through the blood brain barrier and how it is effected by the addition or subtraction of a key methyl chain in any substance is really the question you should ask. With the addition of a methyl chain it usually crosses that barrier far more readily than some other chemical compositions.

This is not at all true in regards to most substances. It applies to a large cross-section of primary 2,5-desmethoxyamphetamines and N-monoalkyltryptamines in terms of N-methylation (or N-alkylation in regards to tryptamines), but that's where the trend stops. N-methylation of any of the psychedelic 2,5-dimethoxyphenethylamines spells an end to all psychedelic activity, same with N-methylation of alpha-alkyltryptamines. O-methylation of 4-hydroxytryptamines causes a huge reduction in potency. 3O-Methylation of morphinan opioids, for example morphine, oxymorphone, or hydromorphone, produces inferior compounds, codeine, oxycodone, and hydrocodone respectively. Also, a shorter halflife (I assume you are measuring 'halflife' in terms of duration of effects) and/or decreased potency from desmethylation does not even hold universally true in the world of amphetamines, which is where I think you're getting this idea from. Take MDA vs. MDMA for example: Shulgin states in PiHKAL that they are equipotent and have an identical duration of effects, whereas some others state that MDA lasts longer and requires a smaller dose...

Saying that sticking a methyl group somewhere will automatically increase potency compared to the desmethyl homologue is overgeneralizing to the extreme, and does not provide useful data. You can say, for example that methylating x position in y compound series will produce an increased potency, but not that methylating anything will produce a superior compound. Yes there are cases where this is the truth, but it is not even close to universal enough to make such a blanket statement.
 
It should be noted that with the n-benzoxy system's addition, these compounds' lipid solubility is affected less by a single hydroxyl substitution than with 'simpler' phenethylamine-based skeletons. Eg, bk-2cb seems to be way less potent than the parent compound, and this could be in part due to reduced BBB penetration (yes, and 5ht binding too, I'm sure).

ebola
 
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It should be noted that with the n-benzoxy system's addition, these compounds' lipid solubility is affected less by a single hydroxyl substitution than with 'simpler' phenethylamine-based skeletons. Eg, bk-2cb seems to be way less potent than the parent compound, and be in part due to reduced BBB penetration (yes, and 5ht binding too, I'm sure).

ebola

I wonder if this has something to do with hydrogen bonding between the hydroxl group and the amine nitrogen, a-la 4-HO-Dialkyltryptamines. It would make sense since they are in close proximity to one another...
 
I'm pretty sure everyone I've heard of trying both said that the effects were nearly identical yet nboh had a shorter duration except for maybe 1 of them had an abnormally long duration.
 
Can't speak for the nbome versions, but I've tried 25c-nboh and according to everything I've read about 25c-nbome, sean107 is correct, the effects are similar, the duration shorter and required dose a little higher. Pleasant enough with great visuals, mental space mostly lacking (especially if price is considered), but the dangers probably remain as does the lasting tolerance. Have some 25i-nboh on the way and will test in when the time's right. Would also love to see 25b and 25d nboh (even if the 25d and 25b nbome remain legal here - they only made 25i and 25c illegal + no analogue laws).
 
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