xdrc
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I wouldn't push my luck too far. Plugging 100 mg will lead to big peak plasma concentrations, and it can be anyone's guess if that doesn't lead to neurotoxicity or carcinogenic activity.
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PD Moderators: Esperighanto | JackARoe |
Phenethylamines 2C-B, worth trying on its own?
- Thread starter chris_p
- Start date
I wouldn't push my luck too far. Plugging 100 mg will lead to big peak plasma concentrations, and it can be anyone's guess if that doesn't lead to neurotoxicity or carcinogenic activity.
That's interesting, it's the first case study I've seen of toxicity from 2C-B. I'm wondering if impure 2C-B could've contained synthesis byproducts, or if the alcohol in his system contributed to the damage at hand. I also have no idea what the dose or RoA was for this kid but damn, he seemed to sustain an amount of damage I've never seen even remotely occur in numerous people taking hundreds of milligrams daily. There were also people who used to take tenstrips of 25I-NBOMe numerous times a week back in the day though, which we now know if severely unwise.
xdrc
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I was also surprised when I stumbled upon this case study a couple weeks ago, I hadn't seen it previously. It is hard to tell what really happened there. I've also heard about (trustworthy) reports of people insufflating absolutely ridiculous doses I don't even want to mention here.
While I do enjoy reading about your crazy stories, I wouldn't like too careless handling being popularised. If too many people push their luck too far, eventually there will be the first case where too much is too much. I hold 2C-B very dear and it would hurt to see the first person losing their life from it. I do agree that it probably has a very broad therapeutic window, but I don't agree with gambling. @chris_p has straight up plugged relatively high doses (without running a titration, without having a tripsitter) in combination with MDMA for their first trial. I don't want to be the fun police, nor criticise them for their behaviour, but I don't want to encourage it either.
Do you think you can find that case with the suicide attempt, please? I would venture to guess that if anything, the benzodiazepine was helpful.
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I try to often mention in my recountings that I'm specifically notoriously hardheaded towards these drugs, and never use them alone. @chris_p Has exhibited pretty risky behaviors, mixing MDMA and MAOIs, binging huge amounts of MDMA, admittedly having addiction problems with alprazolam, etc. and I think it's important that we keep echoing around the posts that these things are unsafe and that even though one person survives it, it doesn't mean others will.
It was brought up by a guy on reddit and I found a link to it maybe 1.5-2 years ago, I'll search for it and see if I can find the case report, I think it was an NIH case study but I may not be correct.
As far as compounds people hold dear, LSD, mescaline and psilocybin I also hold very dear but they've been illegal for over twice my lifetime where I live. Hasn't stopped access or use for me, at least.
chris_p
Bluelighter
Yeah, my decision making was fairly impaired and I didnt go in expecting to use everything i had in one go it just kinda happens when you take something that feels great and want more. I've ordered another 150mg 2cb but will be more careful this time around. Though there is a good chance I might end up using it all fairly quickly, dont think its enough to cause harm. I've done much worse things like MAOI and MDMA combinations as @Esperighanto mentioned mostly out of desire for a more extreme experience.. I think I might have found a good replacement drug for MDMA and reading cases of people using a lot of it often without serious side effects has me hopeful I could use it as a crutch for now. Might try it with MAOIs at some point but in small doses but not sure that's a great idea.
Also yes, have suffered consequences from my use and well aware of the danger of what I am doing... my last 'break' after ten grams of syrian rue and a gram of MDMA taught me that lesson quite well for a good few weeks. I'm often under the belief I can handle things that other people can't but the more likely answer is I have just been very lucky so far. Still quite young and inexperienced so learning a lot, but don't want to kill myself in the process. Feel like every time I do these things I learn something new about myself and the world. I feel like an answer is very close in reach...
Viraldrome
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I just took 30 mg 2-CB (empty stomach) waited a bit and then 400 micrograms LSD in the gums and damn I loved this combo I take a lot of LSD so that amount of LSD maybe normal people should half dose but i recommend 30 mg of 2-cb . I like 2-cb i don't love it This made the visuals a lot more fluid, kind of a look hard to explain I dont get much in way of visuals on just 2-cb low doses anyway but with LSD the visuals were better than just LSD visuals alone . I may never try large dose of 2-cb but damn im trying this combo again maybe even more with more lsd
Only other thing I tried this with was ketamine and thats a great combo IMO
Only other thing I tried this with was ketamine and thats a great combo IMO
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Shinji Ikari
Bluelighter
Preloading with 2cb before LSD is great it makes the comeup feel so much smoother and rather surprisingly I think it's makes the LSD feel slightly less intense at the peak.
I remember reading a theory that 2cb may be mild 5ht2a antagonist which might explain that but I don't know how substantial the claim is, I think it was coming from one study cited on psychonaut wiki.
I remember reading a theory that 2cb may be mild 5ht2a antagonist which might explain that but I don't know how substantial the claim is, I think it was coming from one study cited on psychonaut wiki.
perpetualdawn
Bluelighter
It would make more sense to me that 2C-B could be a weaker agonist on 5ht2a than LSD, but have a higher affinity for the receptor. That would be a simple explanation for what you've noticed. I think it's unlikely that it would be a 5ht2a antagonist given its psychedelic character.
chris_p
Bluelighter
Finally, a boof tube big enough for my 2C-B
Shinji Ikari
Bluelighter
Maybe, and if so my followup question is if 2cb is a mild 2a agonist why don't we see any lasting tolerance from 2cb at any dose. If it was a mild 2a agonist I'd expect a higher dose or consecutive dosing to create a compounding tolerance, but it doesn't seem to and even when I've binged on 2cb for days I've been able to end the binge with an acid trip and no noticeable tolerance being observed.
The antagonist theory is lent credibility for me because I've only noticed blunting of the effects from the LSD when I've taken the LSD within a few hours of the 2cb and the 2cb is still active in my system.
Pure speculation on my end though most of this pharmacology stuff is over my head
xdrc
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Without searching the references, iirc those studies declaring 2C-B as an antagonist were not even conducted on human 5-HT2AR... As for the tolerance, I think there were some advances in understanding of receptor bias which may explain that. No pharmacology nerd though!
Shinji Ikari
Bluelighter
4-Bromo-2,5-dimethoxyphenethylamine (2C-B) and structurally related phenylethylamines are potent 5-HT2A receptor antagonists in Xenopus laevis oocytes - PMC
We recently described that several 2-(2,5-dimethoxy-4-substituted phenyl)ethylamines (PEAs), including 4-I=2C-I, 4-Br=2C-B, and 4-CH3=2C-D analogs, are partial agonists at 5-HT2C receptors, and show low or even negligible intrinsic efficacy at ...
pmc.ncbi.nlm.nih.gov
There's the study in question. Maybe one of the pharmacology nerds can poke some holes in it for us
chris_p
Bluelighter
I just boofed 25mg as a starter dose and lets just say I won't be needing MDMA anymore, this shit is fan fucking tastic, somehow it makes me even more ecstatic and happy than MDMA
It's a more "real" feeling happiness to me, less meth-ily pushed like MDMA feels. Do you relate 2C-B more to psychedelics like mescaline or LSD, or to empathogens like MDMA?
chris_p
Bluelighter
Very hard to compare to either honestly. Yea, it feels far more organic, and not orientated towards 'others' like MDMA but feels more self directed or general contentment. With MDMA im often frustrated if I dont have someone in the immediately vicinity to speak to or the euphoria needs to originate from a sense or a source like music, 2C-B just radiated happiness from every part of my being. Very comparable to mescaline but far more intense and different. There is some mild nausea and discomfort which I did not feel previously as I was rolling too, but it's almost unnoticeable
chris_p
Bluelighter
Feels a bit shroomy at times.. waves of sedation then back to stimulation, but primarily stimulatory euphoria. Classical psychedelics all have some very shared undertones and you can almost innately feel the shared action it has on the nervous system. Of course i haven't gone to my intended dose yet. I'm well aware of where going there entails, but I'll give it a few hours to enjoy this first before that happens
4-Bromo-2,5-dimethoxyphenethylamine (2C-B) and structurally related phenylethylamines are potent 5-HT2A receptor antagonists in Xenopus laevis oocytes - PMC
We recently described that several 2-(2,5-dimethoxy-4-substituted phenyl)ethylamines (PEAs), including 4-I=2C-I, 4-Br=2C-B, and 4-CH3=2C-D analogs, are partial agonists at 5-HT2C receptors, and show low or even negligible intrinsic efficacy at ...
There's the study in question. Maybe one of the pharmacology nerds can poke some holes in it for us
I'm far from being a pharmacology expert, but I do take a lot of interest in these things. These kinds of studies tend to be very problematic for a number of reasons. Right off the bat, I see that they are testing rat receptors, and my understanding is that rat serotonin receptors are a poor model of the human receptors. I believe mouse receptors are much closer but still quite a bit different such that this kind of work should be done with human receptors as much as possible. Even then, there are many many problems: differences in chemical environments (which is always a problem because the receptors themselves exist in different chemical environments in different parts of the body and brain and may respond differently to the same drug); the multi-functionality of the receptors which is a critical concept for understanding psychedelic action; and even problems with the data analysis itself including the use of non-linear regressions and improper propagation of uncertainties from the data to the key results (uncertainties which can be extremely high).
Generally speaking, I think it's a bad idea to assume any quantitative results from these assays are more accurate than say in order of magnitude. Because each receptor type requires a different assay, it's fundamentally difficult to compare affinities between receptor types for any given drug unless they are dramatically different from one another. Comparing affinities and efficacies for a particular receptor between multiple drugs is perhaps more tractable, but should only be done if they were subject to the exact same assay, like if they were tested as part of the same study. Even then though, a lot of results of this kind in the literature are inconsistent between studies, likely for reasons I just discussed.
If I had to guess from the studies I've seen, I would say that both LSD and 2C-B are relatively weak in terms of serotonin-like effect. For this reason, some people might describe these drugs as "almost antagonists", but IMO this is very wrong because in all likelihood, the baseline activity at the 5-HT2A receptor is quite low relative to the action of the drug at an effective dose. So, even though LSD or 2C-B may induce serotonin-like effects only weakly upon binding to the receptor, there's still enough drug present at an effective dose to induce far more serotonin-like action than occurs at baseline. Comparing the two, I believe that LSD actually has less serotonin-like than 2C-B even.
Of course, serotonin-like action represents only one possible dimension of action at 5-HT2A. Receptor multi-functionality was actually discovered in part because scientists were trying to understand why LSD makes people trip but many other 5-HT2A (partial-)agonists with serotonin-like action do not. It turns out that LSD and other psychedelics act on the receptors in a way that many other ligands including (probably) serotonin do not. This means that even if LSD or 2C-B had literally zero serotonin-like action at 5-HT2A, it would still be incorrect to conclude that they are antagonists because they are actually acting very effectively on the receptor in a more "LSD-like" way.
As to why taking 2C-B first may "smooth out" an LSD trip, the reason may be mostly to do with pharmacokinetic consequences. It's often assumed that pharmacokinetics only impact intensity versus time, but this assumes that the result of activating the receptor is exactly the same regardless of the recent history of activations. In reality, I think that the results of activating 5-HT2A and other receptors vary a lot depending on the recent history of activity at those and other receptors. If I may explain. Two different doses and administration methods might bind and activate 5-HT2A the same number of times, but the effects may be very different if all those activations occur within a short period of time versus being spread out over a long period of time. On the basis of this reasoning, we should expect different effects from administering the same drug using different ROAs, regardless of whether an attempt is made to find "equivalent" doses. Similar modifications of qualitative effect can be achieved by simply splitting up an oral dose over time, like taking half and then waiting 30 minutes to take the other half. This last point of mine is the one that many pharmacologists would probably push back on because a lack of evidence, but in my view, the only reason evidence is lacking is that the necessary experiments haven't been done yet. I have strong philosophical priors that lead me to believe this is likely true.
Oh---one other possibility re 2C-B softening and weakening an LSD trip is that in the brain at least, action at the 5-HT2B receptor enhances serotonin release in a major way, and any enhancement of serotonin release induced by 2C-B could lead to more competition versus LSD at the 5-HT2A receptor.
All these points should illustrate that the pharmacology of these things is very complicated leading to results that can be surprising and unintuitive when interpreted using overly simple models. Personally, I think it's time for pharmacology as a field to move on from the whole agonist/antagonist/partial-agonist paradigm which just causes unnecessary confusion.
Pfafffed
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My nose would never be the same again.
chris_p
Bluelighter
Jesus that was bad. Never doing that again. I overdosed very severely yesterday, Boofed 125mg heart started beating out of my chest like a jackhammer and I started throwing out all my drawers searching everywhere for my xanax while I was entering a very severe ego death. Started getting so confused didnt know what to do tried to climb into my bed but started forgetting basic concepts so I just ended up lying or falling on the floor dont quite remember. Dont know how long I was in that position for but I managed to stand up at like 2 AM. I was conscious and aware during the whole experience everything was just this overwhelming static that infiltrated every part of my mind that kept looping on repeat like an information bombardment so bad I was basically seizing. There were no shapes anymore everything was so dense it was just infinite static of every sense combined. Only other thing I remember is the sound of my cat purring very loudly and the feeling of her rubbing her face against me while I was lying face first on the ground. Be warned that 2cb is a drug that can cause DEFINITE overdoses and I am glad to be alive still.
chris_p
Bluelighter
At work now basically got zero sleep took 10mg more 2cb just to stay fucking awake. Very ashamed of myself currently. Gonna quit for a while again