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  • PD Moderators: Esperighanto | JackARoe |

Phenethylamines 2C-B, worth trying on its own?

4DQSAR said:
More costly? Yes? More potent? Likely yes
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Synthing the Indole precursor wouldn't be that tough compared to the annulation required to make something like a 2C-X-FLY or DRAGONFLY type of drug at least. It sure doesn't seem to be within the realms of clandestine reach without some precursor assistance, but I wouldn't be shocked to see Chinese pharma labs putting things like this out.
 
Esperighanto said:
Synthing the Indole precursor wouldn't be that tough compared to the annulation required to make something like a 2C-X-FLY or DRAGONFLY type of drug at least. It sure doesn't seem to be within the realms of clandestine reach without some precursor assistance, but I wouldn't be shocked to see Chinese pharma labs putting things like this out.
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Oh yeah - those are FAR more costly to produce.

But as I said, if someone can ONLY go through the 2,5-dimethoxy-4-<something> series both with the 2 carbon and 3 carbon tryptamines, that's still a LOT of compounds,

I've already pointed out that 7-methyl AMT overlays MMA, the latter mentioned in Pihkal as having been seized in Italy (?) where it was being sold AS MDMA.

Now I've never got on with the 5-MeO tryptamines but AET was also sold as MDMA (mentioned in Tihkal) and if you check out the Uphohn patents, you will notice that the addition of that 7 methyl increased it's monoamine release/reuptake by an order of magnitude, Now why 7-methyl AET but not 7-methyl AMT I do not know, but I found out, With the raecemate there is a window between inactive and psychedelic where is behaved as an entactogen, Sadly, cost at the time was too high at the scales we were considering,

I hasten to add that the cohort size was small so we really do not know when the stuff becomes toxic but along with a couple of other MDMA alternatives, it was just shelved. So what I'm saying is it worked... but I cannot assert it's at least as safe as MDMA.
 
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^ Damn and I thought the US laws were hard to interpret. I will understand that post when I do 4dqsar -- someone needs to take what you say and "Jon Stewart" it for stupi---- cognitively deficient individuals such as myself.
 
4DQSAR said:
Oh yeah - those are FAR more costly to produce.

But as I said, if someone can ONLY go through the 2,5-dimethoxy-4-<something> series both with the 2 carbon and 3 carbon tryptamines, that's still a LOT of compounds,

I've already pointed out that 7-methyl AMT overlays MMA, the latter mentioned in Pihkal as having been seized in Italy (?) where it was being sold AS MDMA.

Now I've never got on with the 5-MeO tryptamines but AET was also sold as MDMA (mentioned in Tihkal) and if you check out the Uphohn patents, you will notice that the addition of that 7 methyl increased it's monoamine release/reuptake by an order of magnitude, Now why 7-methyl AET but not 7-methyl AMT I do not know, but I found out, With the raecemate there is a window between inactive and psychedelic where is behaved as an entactogen, Sadly, cost at the time was too high at the scales we were considering,

I hasten to add that the cohort size was small so we really do not know when the stuff becomes toxic but along with a couple of other MDMA alternatives, it was just shelved. So what I'm saying is it worked... but I cannot assert it's at least as safe as MDMA.
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This is quite fascinating, I wonder if other variants of the phenethylamine skeleton as explored by Trachsel could be extrapolated to the tryptamine scaffold. Makes me wonder if there's any equivalent of say, Bromo-DRAGONFLY, MMDA, mescaline, 2C-T-4, or ARIADNE in the tryptamine world. I've always marveled over how diverse phenethylamines seem relative to tryptamines, but maybe we've just been working with a limited scope of tryptamines so far.
 
My guess is that these "equivalent" tryptamines aren't really equivalent. At the very least, pharmacokinetics may be very different, and IMO pharmacokinetics don't just affect the timeline but can also strongly influence qualitative effects. To give an (overly simplified) example, the drug must be absorbed into the blood stream first (facilitated by whatever ROA), and only then can it begin to cross the blood-brain barrier, which could affect the ratio of "mental" to "body" effects over the course of the experience. More generally, different drugs (with different chemistries) may partition in different proportions between receptor sites including within the brain itself due to different chemical properties. IMO, it's a serious mistake to assume any sort of equivalence, even if the part of the chemical that fits into the receptor were chemically identical. (It's not---only "close".)

That doesn't mean they aren't worth exploring, and there may be gems among them, even if they aren't necessarily the analogs of the Magical Half-Dozen (phenethylamines). Perhaps someone with more expertise than I could speculate as to what sort of duration of action to expect with these various tryptamines analogs. I mean, 2C-P might have been one of the "magical" ones if it weren't so long. A problem with many of the good common tryptamines is that they are metabolized too fast to be used orally and have relatively short trips.

BTW, I have read of at least one endogenous partial 5-HT2A agonist (produced by the skin it turns out) which is a peptide, so that pretty much rules out the whole notion that only small things can get into the receptor.
 
iom said:
A problem with many of the good common tryptamines is that they are metabolized too fast to be used orally and have relatively short trips.
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This depends on the activity of the enzyme that metabolises tryptamines intermediate aldehyde produced by MAO.
If this enzyme is inhibited due to alcohol or drug/food-based ALDH inhibitor this allows the aldehyde to react elsewhere and potentially form active substances.
This was shown possible (anecdotal experiments) using phenethylamine and tryptamine which led to psychoactive effects unlike what you'd expect from plain PEA or tryptamine.
This should also work for plain DMT which acts as a pro-drug in this scenario.

Back OT, this should also apply to 2C-X. Everyone knows not to combine 2C-X with MAOIs but ALDHIs are never mentioned.
 
iom said:
My guess is that these "equivalent" tryptamines aren't really equivalent.
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Maybe, maybe not, but aren't there niw sort of NOMBes of the tryptamines? 5-MeO-T-NBOMe for example? So that does rather suggest that at least the indole N: does approximate a methoxy O: moiety (I only dreaw one one-pair for oxygen since it can only be one, that it must be the one that approximates the N: and if I try to add a colon before and after that O, the software of the site drawes an emoji which isn't perfect for chemists),

I'm not in a position to study further byt why not look at those? I only bothered to remember one because itt's of no practical value to speclate on what you can no longer legally research.

If I had to take a guess, it would be because in a paper from the 60s (?) it was shown that while a methyl moiety WOULD fit (and would be the obvious place to start looking), but a bromine would not. No mention of other halogens. So that MAY have made researchers trust that no larger moiety is active. But nobody has tried it with the 5-methoxy tryptamines which does alter the conformation a LOT.
 
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xdrc said:
Those tryptamine NBOMe aren't new, they very much appeared in the original Heim thesis. I don't remember the details without looking up, but if I remember correctly the N-3-iodobenzyltryptamines were more potent. https://pmc.ncbi.nlm.nih.gov/articles/PMC4505863/
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Cheers for that,

I never said that the QSAR of the tryptamines would ALWAYS be the same as the PEAs but of the compounds in RHs thesis do have one nice detail - they are achiral. That's why I explicitly stated that although 7-methyl AMT appeared to be much like MDA i.e. it goes from stimulant to entactogen to hallucinogen. If resolved you can go for an entacotgen OR a hallucinogen i.e. nothing gets wasted. But I also explicitly stated that we did not have a large enough cohort to assert safety to my satisfaction.

So I'm not even saying they are safe - only that from the limited datasets known it appears that the two scaffolds act in a similar manner,

Why the meta I? No idea, I suppose it might be orientation of the space-filling aromatic, Is I a reasonable HBA?

BTW 7-methyl DMT was tested and in animal models was shown to demonstrate similar behaviors to those of DMT. I wish they had use a discrimination/reward model to see if the two are subjectively similar, but sadly... not.
 
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Esperighanto said:
That's definitely a huge fucking dose of 2C-B. I've taken similar doses and have had similar experiences where it resembles a DMT breakthrough, except my mind was taken to the place that mescaline or allylescaline take me in high enough doses, seeing precognizant visions of my future and the sort. 2C-B Habituation is rarely spoken of, but I've witnessed it myself, it's prone to attracting those who specifically need a mania inducer to combat depression in my personal experience.
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How large of mesca/ally doses are you talking about?

What are your thoughts on mescaline vs Methallylescaline? Is ally a near identical substitute?
 
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jveiojajoivioedsac said:
What are your thoughts on mescaline vs allyescaline? Is ally a near identical substitute?
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FWIW, mescaline has potential for so much more than people realise.
If you use the right combo and diet, one dose of mescaline can be cycled (meaning recycled) for days and the dose is potentiated significantly. Roughly speaking, a reasonable dose of 100mg can be as potent as 500-800mg+.
 
Allylbenzene said:
FWIW, mescaline has potential for so much more than people realise.
If you use the right combo and diet, one dose of mescaline can be cycled (meaning recycled) for days and the dose is potentiated significantly. Roughly speaking, a reasonable dose of 100mg can be as potent as 500-800mg+.
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Can you elaborate? What do you mean recycled for days? How?
 
In brief, SSAO/MAO enzymes metabolise mescaline into it's aldehyde. The theory is that this aldehyde can react with naturally occuring amines and form active products. Secondary amines seem preferable, but phenethylamine and methylamine are also present endogenously.
The specifics of this haven't been scientifically explored afaik, only mentioned indirectly in trouts notes on mescaline and reported anecdotally.
The key requirement is to inhibit ALDH and leave SSAO/MAO active. Keeping ALDH inhibited seems to cycle the aldehyde.

The same approach works for plain phenethylamine.
It's likely the ultimate potentiation method that nobody knows. Zero MAOIs used.
 
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Allylbenzene said:
In brief, SSAO/MAO enzymes metabolise mescaline into it's aldehyde. The theory is that this aldehyde can react with naturally occuring amines and form active products. Secondary amines seem preferable, but phenethylamine and methylamine are also present endogenosly.
The specifics of this haven't been scientifically explored afaik, only mentioned indirectly in trouts notes on mescaline and reported anecdotally.
The key requirement is to inhibit ALDH and leave SSAO/MAO active. Keeping ALDH inhibited seems to cycle the aldehyde.

The same approach works for plain phenethylamine and tryptamine (or tryptophan which the body turns into tryptamine).
It's likely the ultimate potentiation method that nobody knows. Zero MAOIs used.
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Ok but do you have a way to actually do this?
 
Use a food/plant-based extract ALDH inhibitor before taking mescaline.
Avoid sulforaphane foods because sulforaphane increases ALDH activity.
CAUTION: Don't drink alcohol if you choose to try this.
 
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Allylbenzene said:
Use a food/plant-based extract ALDH inhibitor before taking mescaline/phenethylamine/tryptamine.
Avoid sulforaphane foods because sulforaphane increases ALDH activity.
CAUTION: Don't drink alcohol if you choose to try this.
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Have you done this / do people do this successfully? Eat these foods and or take disulfiram?

Or is this your hypothesis?
 
jveiojajoivioedsac said:
Have you done this / do people do this successfully? Eat these foods and or take disulfiram?

Or is this your hypothesis?
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Do not use disulfiram. I can't encourage that since it affects many other things which make it unsuitable for this.
The best food-based inhibitors are durian, pomegranate, starfruit and garlic extract. Do not drink alcohol, use vingear or eat fermented products if you use these.
If you are using any medications, drugs, hormones or supplements of any kind do not attempt this. If you've used SSRIs in the past year, do not attempt this.

The metabolism of alcohol within the human body primarily relies on two key enzymes: alcohol dehydrogenase (ADH) and ALDH. Alcohol is initially converted into acetaldehyde by ADH. Subsequently, acetaldehyde is further metabolized into acetic acid by ALDH. Finally, acetic acid is metabolized into water and carbon dioxide. If food containing ALDH inhibitors is eaten, this prevents the metabolism of acetaldehyde to acetic acid, leading to the accumulation of toxic acetaldehyde in the body. The accumulation of acetaldehyde can cause symptoms such as palpitation, nausea, facial flushing and headache.
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These amino acids lysine and arginine are found in many foods; gut bacteria convert them into piperidine and pyrrolidine respectively.
The idea is to predose lysine/arginine foods for several days then use a safe ALDH inhibitor with mescaline.
It helps to avoid sulforaphane-containing foods/supplements since sulforaphane increases ALDH activity.
 
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Allylbenzene said:
Do not use disulfiram. I can't encourage that since it affects many other things which make it unsuitable for this.
The best food-based inhibitors are durian, pomegranate, starfruit and garlic extract. Do not drink alcohol, use vingear or eat fermented products if you use these.
If you are using any medications, drugs, hormones or supplements of any kind do not attempt this. If you've used SSRIs in the past year, do not attempt this.



These amino acids lysine and arginine are found in many foods; gut bacteria convert them into piperidine and pyrrolidine respectively.
The idea is to predose lysine/arginine foods for several days then use a safe ALDH inhibitor with mescaline or a low dose of phenethylamine.
It helps to avoid sulforaphane-containing foods/supplements since sulforaphane increases ALDH activity.
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Thanks.

But does anyone actually do this? Successfully? What are the results?
 
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