25P-NBOMe?

[icekila]

Does anyone have any info on 25p-nbome?

 

[Survived Abortion]

Woah - this has just hit the market. I guess we'll be seeing some reports in the coming weeks. Hopefully positive and glowing reports.

 

[Solipsis]

Remember that the analogy between compounds like 25P-NBOMe and 2C-P does not have to mean at all that they will be alike. They can actually be
opposite in effect, for example regarding potency.
25C is one the most potent 25X-NBOMe compounds yet 2C-C has low potency and needs a high dose.
Something similar is true for 25D and 2C-D.
Adding the NBOMe group changes steric hindrance: the key (drug) that fits into the serotonin receptor (lock) is bigger so there is less tolerance for bulky 4-sub groups because otherwise the key cannot cram into the lock properly.

I have tried 25D myself (one of the 4-alkyl 25X's, others being 25E, 25P and 25iP) and while the central effects reminded me in every way of descriptions of DOM, I did not find the vasoconstriction (adrenergic action?) tolerable even at a low dose.
25E is said to be lame and bland, though I never heard an elaborated explanation as to why. I guess some compounds are just 'meh'. It needs a higher dose than 25D does, IIRC. Which is the opposite for 2C-D compared to 2C-E.
So if 2C-P is even more potent and ferocious than 2C-E, we might expect 25P to be even less rewarding or needing a higher dose relative to other NBOMe's.
This is not ideal: it's possible that nasty side-effects start arising at lower doses than where the 'interesting' effects start. So it would be intrinsically harsh.
I guess part of 2C-N's problem has something to do with that: it needs extremely high doses for a 2C and is known for it's potential to be heavy on the body load and inpredictable in effects. But... it could also be something special about the nitro, I don't know.

I wonder if people feel that NBOMe compounds vary significantly in duration of action. I find the duration hard to pinpoint to begin with, because there are long and slowly dwindling after effects. That was the same for me with both 25C and 25D.
Apparently for example 25G does not act long as the parent 2C-G might indicate, so the hypothesis was made that maybe the duration is mostly dependent on (or at least limited by) the NBOMe group cleavage and not so much the properties of the parent. Although with metabolism there are almost always major and minor metabolism routes that have their own contribution to the half-life. The thing is: 2C-C itself acts quite short... so considering 25C acts so much longer would indicate that the NBOMe group not only limits the duration of action but can conversely help protecting the amine function from early metabolism the parent would normally succumb to.
If the NBOMe group is cleaved (cut off), there will be parent 2C-X drug as a result - if that was the very first metabolism step... but it's simply not nearly enough of a dose to have effect, especially with the developing tolerance.

With both 25C and 25D, I saw a sort of characteristic relationship that reminds only a little of 2C-C and 2C-D resp. (for example the unique 2C-C relaxation) but there is also some resemblance to the DOX counterparts I think. Made me think of my experiences with DOB and the fact that it felt a lot more crystal-clear mind-wide-open acid like than 2C-B ever would. Yet the NBOMe's I tried had less impact than I would expect from a DOX.

Maybe with small 4-substitutions that have proper electronegativity, it's like it makes the key fit better in the lock or at least isn't a problem. I think 25P is not promising. I don't have 25P but I do have 25iP. And also the 2C-iP to compare.

 

[Survived Abortion]

^I'm not sure your logic about requiring higher doses meaning more vasoconstriction/body load makes any sense. DOB and DOI are generally regarded to have a much worse body load than DOC, yet DOC doses are much greater. Similar thing with 2C-C; it's doses are far higher than 2C-E or 2C-P, yet it's body load is minimal. I don't think a compound's dosage range determines how vasoconstrictive it will be. Just look at mescaline and the doses that requires.

There was a lot of speculation from Erny about these compounds in the beginning, but his opinions have not always held up to be true. I would personally like to see this one assayed, as it may not be as simple as longer substitution chains decreasing the therapeautic margin. I'm sure that may be a factor in potency and binding affinity, but there may be more to whole experience than that.

 

[MattPsy]

2C-OCF3-NBOMe (or 2C-TFMeO-NBOMe if you prefer) might be interesting. N-(2'-methoxybenzyl)-2,5-dimethoxy-4-trifluoromethoxyphenethylamine.

Agreed that this will probably be crappy. Extending the chain to butyl, they might even become antagonists, actually becoming psychedelic antidotes. This same trend is noted with the parent compound family (the non-NBOMe compounds), but more pronounced. I wonder if 2C-pentyl was ever made..? If so,worthy of comparison, IMO.

 

[icekila]

Remember that the analogy between compounds like 25P-NBOMe and 2C-P does not have to mean at all that they will be alike. They can actually be
opposite in effect, for example regarding potency.
25C is one the most potent 25X-NBOMe compounds yet 2C-C has low potency and needs a high dose.
Something similar is true for 25D and 2C-D.
Adding the NBOMe group changes steric hindrance: the key (drug) that fits into the serotonin receptor (lock) is bigger so there is less tolerance for bulky 4-sub groups because otherwise the key cannot cram into the lock properly.

I have tried 25D myself (one of the 4-alkyl 25X's, others being 25E, 25P and 25iP) and while the central effects reminded me in every way of descriptions of DOM, I did not find the vasoconstriction (adrenergic action?) tolerable even at a low dose.
25E is said to be lame and bland, though I never heard an elaborated explanation as to why. I guess some compounds are just 'meh'. It needs a higher dose than 25D does, IIRC. Which is the opposite for 2C-D compared to 2C-E.
So if 2C-P is even more potent and ferocious than 2C-E, we might expect 25P to be even less rewarding or needing a higher dose relative to other NBOMe's.
This is not ideal: it's possible that nasty side-effects start arising at lower doses than where the 'interesting' effects start. So it would be intrinsically harsh.
I guess part of 2C-N's problem has something to do with that: it needs extremely high doses for a 2C and is known for it's potential to be heavy on the body load and inpredictable in effects. But... it could also be something special about the nitro, I don't know.

I wonder if people feel that NBOMe compounds vary significantly in duration of action. I find the duration hard to pinpoint to begin with, because there are long and slowly dwindling after effects. That was the same for me with both 25C and 25D.
Apparently for example 25G does not act long as the parent 2C-G might indicate, so the hypothesis was made that maybe the duration is mostly dependent on (or at least limited by) the NBOMe group cleavage and not so much the properties of the parent. Although with metabolism there are almost always major and minor metabolism routes that have their own contribution to the half-life. The thing is: 2C-C itself acts quite short... so considering 25C acts so much longer would indicate that the NBOMe group not only limits the duration of action but can conversely help protecting the amine function from early metabolism the parent would normally succumb to.
If the NBOMe group is cleaved (cut off), there will be parent 2C-X drug as a result - if that was the very first metabolism step... but it's simply not nearly enough of a dose to have effect, especially with the developing tolerance.

With both 25C and 25D, I saw a sort of characteristic relationship that reminds only a little of 2C-C and 2C-D resp. (for example the unique 2C-C relaxation) but there is also some resemblance to the DOX counterparts I think. Made me think of my experiences with DOB and the fact that it felt a lot more crystal-clear mind-wide-open acid like than 2C-B ever would. Yet the NBOMe's I tried had less impact than I would expect from a DOX.

Maybe with small 4-substitutions that have proper electronegativity, it's like it makes the key fit better in the lock or at least isn't a problem. I think 25P is not promising. I don't have 25P but I do have 25iP. And also the 2C-iP to compare.

Excellent post, keep it up

 

[Solipsis]

For the matter of the mescaline example: someone passed me info on high doses of mescaline like 600+ mg being harmful to the liver. *edit: correction, it seems I was right but instead of 600+ mg it is more like 1.2-1.5+ grams. Still, compared to one necessary dose to trip the therapeutic index isn't actually as wide. Anyway, mescaline is said to have a unique pharmacology*

And I didn't exactly mean to say that there would be a direct correlation between dosage range and body load. The only logic I used was that the adrenergic/stimmy effects don't have to be proportional to the psychoactive effects. If the dosage threshold for body load mechanisms is lower than the dosage
threshold for psychedelic or psychoactive effects... that would mean that in terms of body load a normal psychoactive dose can already be an overdose.
Such barely existent therapeutic indexes would apply to DOB, DPT (for me), and take stimulant RCs for example. They can really be terrible feeling at doses lower than when you get positive effects.

Of course this isn't solid logic, because there is also a good chance it's the other way around with 25P:
Good effects at modest to high doses higher doses ... but heavy nasty body load at even much higher doses. (possibly including hyperthermia, sweating, hypertension, stress, panic and more).

Yet lastly it does seem like psychoactive potency occurs in a certain range or spectrum unless there is a good reason for the chemical to be anomalous. Why should higher doses needed for a certain NBOMe to trip also mean that the adrenergic potential is diminished as well? Maybe there is something similar between for example an adrenergic or a dopaminergic or a norepinephrine receptor that results in somewhat similar criteria.
A bulky alkyl group like 2C-P an 25P likely causes steric hindrance in plenty of different types of receptors. Unless there is a hydrophobic pocket in the receptor right where you want it to be, then the bulky group increases efficacy instead of decreasing.

Compounds like 25I-NBMD also seem to be weaker in potency, an explanation can be that the N-benzyl substition group is even bigger than that of NBOMe's.

So I'm not talking about claims here, more like a theory and now that I think of it something I probably learned from someone here in a PD thread somewhere: The higher XXX-NBOMe doses get... the more risk there might be that the therapeutic index is completely messed up.

I do have to admit 25D showed vasoconstriction issues even at quite low levels for me. And 25H was said to be hellish. Those compounds had just about the smallest 4-position substitution (for 25H only a hydrogen which doesn't even count as a significant substitution since it instead the absence of any substitution , for 25D only a small methyl group)... So after all, if this SAR pattern were continued then 25E and 25P shouldn't be too bad. It would ease the suspicions about safe dosage trajectory a little but we still have to start as low as you would start with the most potent NBOMe or lower... then carefully check when changes are noted and if it feels wrong or right.

 

[icekila]

For the matter of the mescaline example: someone passed me info on high doses of mescaline like 600+ mg being harmful to the liver. *edit: correction, it seems I was right but instead of 600+ mg it is more like 1.2-1.5+ grams. Still, compared to one necessary dose to trip the therapeutic index isn't actually as wide. Anyway, mescaline is said to have a unique pharmacology*

And I didn't exactly mean to say that there would be a direct correlation between dosage range and body load. The only logic I used was that the adrenergic/stimmy effects don't have to be proportional to the psychoactive effects. If the dosage threshold for body load mechanisms is lower than the dosage
threshold for psychedelic or psychoactive effects... that would mean that in terms of body load a normal psychoactive dose can already be an overdose.
Such barely existent therapeutic indexes would apply to DOB, DPT (for me), and take stimulant RCs for example. They can really be terrible feeling at doses lower than when you get positive effects.

Of course this isn't solid logic, because there is also a good chance it's the other way around with 25P:
Good effects at modest to high doses higher doses ... but heavy nasty body load at even much higher doses. (possibly including hyperthermia, sweating, hypertension, stress, panic and more).

Yet lastly it does seem like psychoactive potency occurs in a certain range or spectrum unless there is a good reason for the chemical to be anomalous. Why should higher doses needed for a certain NBOMe to trip also mean that the adrenergic potential is diminished as well? Maybe there is something similar between for example an adrenergic or a dopaminergic or a norepinephrine receptor that results in somewhat similar criteria.
A bulky alkyl group like 2C-P an 25P likely causes steric hindrance in plenty of different types of receptors. Unless there is a hydrophobic pocket in the receptor right where you want it to be, then the bulky group increases efficacy instead of decreasing.

Compounds like 25I-NBMD also seem to be weaker in potency, an explanation can be that the N-benzyl substition group is even bigger than that of NBOMe's.

So I'm not talking about claims here, more like a theory and now that I think of it something I probably learned from someone here in a PD thread somewhere: The higher XXX-NBOMe doses get... the more risk there might be that the therapeutic index is completely messed up.

I do have to admit 25D showed vasoconstriction issues even at quite low levels for me. And 25H was said to be hellish. Those compounds had just about the smallest 4-position substitution (for 25H only a hydrogen which doesn't even count as a significant substitution since it instead the absence of any substitution , for 25D only a small methyl group)... So after all, if this SAR pattern were continued then 25E and 25P shouldn't be too bad. It would ease the suspicions about safe dosage trajectory a little but we still have to start as low as you would start with the most potent NBOMe or lower... then carefully check when changes are noted and if it feels wrong or right.

I see you have excellent knowledge on these rare compounds and was wandering do you have any comments regarding 25x-NBF's and 25x-NBOH's?