N&PD Moderators: Skorpio
Is bk-MBDB neurotoxic?
organicshroom
Bluelighter
I would like to hear your thoughts and comments on the neurotoxcity of bk-MBDB (Butylone) compared with MDMA or even MBDB itself. I have read that MBDB is relatively non toxic, so is safe to assume bk-MBDB may be too?
Thanks.
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ebola?
Bluelight Crew
my guess would be bk-MBDB is more neurotoxic than MBDB but less-so than MDMA. To the extent that something releases 5ht and DA simultaneously, it appears to be neurotoxic.
ebola
organicshroom
Bluelighter
^ What does the above study really mean to a moderate user? And would the cell death be significant? Even many pharmaceuticals cause hepatotoxicity and cytotoxicity right? One needs to put it into context in order to see if it's a concern or not.......
Rectify
Bluelighter
There's a report on erowid, or there was one there many years ago anyway, by a user who took 500 mg MBDB at one time and was fine. He didn't like it very much, but he's fine.
I just think you would have a better time spending your money on something like methylone or mdma (preferably mdma) or any number of a lot of other drugs--4-AcO-DMT, 2-AI, mephedrone, amp, meth, 2ce, 2ct2--than on bk-MBDB. The N,alpha-ethyl PEAs just really lack that joy d'vivre, that extra oomph, that mojo which makes the amphetamines so lovely and special in this world.
That being said, would I be afraid to sample bk-MBDB because of toxicity?
No, not at all; I just don't think it would be that good of a drug.
organicshroom
Bluelighter
^ I may agree but that's beside the point....... As I am concerned for people who will use it in the future.
Rectify
Bluelighter
I just read your recent bk-MBDB trip report on erowid, and to be honest it sounded rather lovely, actually!
I wouldn't be too concerned about bk-MBDB harming future generations of drug users. I wouldn't think it would be much more or less toxic than MDA, MDMA, MDE, MDC, methylone, ethylone, MBDB, BDB, amphetamine, methamphetamine, ethamphetamine, cathinone, methcathinone, or ethcathinone. These drugs have been used for years and have proven themselves to be quite safe as a whole.
In fact, the only PEAs/AMPs that I consider to be particularly dangerous at this point are pMA, pCA, fenfluramine, and 2ct7. Also, I try to avoid all DOx's, except for maybe DOET; in fact, I haven't done any DOx thus far, and that's perfectly fine with me. You see, I have some friends who had a long, sickening experience with DOC blotter which I watched first hand.
As for the four PEAs/AMPs that I listed above and which I consider to be dangerous at this point, half of them were available by prescription in the US for years before being pulled from the market. Fenfluramine caused heart valve defects, and I'm still not exactly what p-chloroamphetamine did wrong--that is, whether it was banned due to practical or theoretical considerations, though I suspect the latter.
To be quite honest, the reason for this gaping hole in my knowledge is that I have never been able yet to locate and talk to a 1970s drug user with any experience with pCA at all. I know a meta-aromatic chlorine seems to cause no problems for bupropion/Wellbutrin/Zyban, a popular prescription cathinone. It is possible that pCA was pulled from the market, whether openly or furtively, due to abuse potential concerns under the aegis of neurotoxicity; again, I really don't know.
I'd like to hear from someone who has tried
3,4-dichloromethamphetamine even more than that, though. From what I understand, aromatic chlorines are remarkably non-toxic. Solo
para-substituted amphetamines, on the other hand, are not always so forgiving.
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ebola?
Bluelight Crew
Quick side-question:
methylone doesn't really work for me.
Nor does any DARI that I've tasted.
Now, it's pretty clear that M1 releases 5ht rather than blocking reuptake (only lejunk will tell you that blocking 5ht uptake can be "fun" 
). Does m1 release DA or mainly block reuptake?
ebola
Rectify
Bluelighter
ebola?,
I'm not sure how methylone works exactly, only that for me it was a pleasant, mild trip no where near as good as ecstasy, speed, or a 1000 other drugs. At very high doses, to me, it didn't feel like it was releasing DA or 5HT; it felt like it was releasing NE. Just out of curiosity, what other DARIs have you tried?
Sturnam,
There's only so much that can be learned from giving drugs to mute rats. pCA was a prescription drug in the US in the 1970s before it was pulled off the market. What I want to do is to talk to someone who has had actual first or even second hand experience with it, for example, an ex-pCA user, a medical doctor who had experience with prescribing it, or a well-versed, well-experienced 1970s era drug geek.
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Hammilton
Bluelighter
I doubt it has much releasing effect on NE or DA; AFAIK, none of the cathinones are particularly good release promoting agents. However, they do tend to be decent DARIs; I doubt it's primarily a NARI as they tend not to be recreational at all (atomoxetine, reboxetine).
Sturnam
Bluelighter
Are you sure it was ever prescribed? And do you have a reference for this, other than you remembering it, or the fact that a buddy told you back in 'Nam that he had it? Cause the only things I can find on it are using it in scientific study specifically for its targeted neuronal destructive properties.
Hammilton
Bluelighter
I think it can be safely said that pCA was never, ever a prescription drug. It would never have passed animal testing, much less humans. I don't believe that it's even appeared as a human drug of abuse. Thank God.
Perhaps you're thinking of alpha-Ethyltryptamine? This was briefly marketed as the antidepressant Monase, but pulled due to unacceptable occurence of agranulocytosis
Even a single dose will cause significant damage.
It's not an issue of toxicity because of substitutent location that can be applied across drug classes, unlike aromatic amines and hepatotoxicity. It's a direct result of the effects that the drug has.
All of the 4-halo-amps are neurotoxic excepting 4-fluoro-amp. Probably because of it's small size ~60pm vs. chlorines 99pm) and very high electronegativity that sets it apart from the larger, less electronegative halogens.
Riemann Zeta
Bluelighter
If I recall correctly, 4-chloroamphetamine was investigated as a potential antidepressant in humans at the preclinical stage, but never made it past the initial phase. Soon after, it was discovered that higher doses of the compound cause severe serotonergic neurotoxicity in animals and it was obviously shelved for good!
organicshroom
Bluelighter
Bk-MBDB in my own subjective experience felt like it had mild DA activity but quite strong NE release or uptake inhibition, significantly more than MDMA. The compound kept me awake for 36hours from one 250mg oral dose, and my resting heart rate doubled from 50-60 to 110-120bpm for about 6-8 hours then dropped back to 80 for a following 12 hours. My heart rate didn't fully drop back to normal till the following day after a good sleep. Also I had some uneasy mild panic feelings for the first hour or two of the initial exposure, for me bk-mbdb was over stimulating, but still had enough SE and DA release to make it an empathetic warm experience.
Rectify
Bluelighter
This NE effect probably has more to do with methylone's (and bk-MBDB's) mimickry of epinephrine from a structural standpoint than any sort of catecholamine release.
As for PCA/4-chloroamphetamine, perhaps it was only investigated and tried on humans, not prescribed to them during the 70s. I'm not old enough to remember.
But if PCA is really so toxic (remember these people think MDMA is really toxic too or at least that's what they used to say), what then do you make of chlorphentermine? Chlorphentermine actually was prescribed; I know b/c I just looked it up.
The scariest amphetamine psychosis I ever had was from phentermine. I've never seen amphetamine do anything anywhere close to that. I seriously doubt PCA is more toxic than chlorphentermine. In fact, based on my experience, it's got to be the other way around.
More abusable? Sure.
More toxic? No.
Sturnam
Bluelighter
^ are you ACTUALLY disputing the claim the PCA is hideously toxic?
As for chlorphentermine, it's pretty different. It's like comparing the toxic effects of amphetamine to methamphetamine. Because of a slight change (one methyl group difference), methamphetamine is much more neurotoxic, whereas amphetamine itself is relatively benign in sane doses.
Hammilton
Bluelighter
1. "From a structural standpoint" it is not more similar. You and Ilostamadge would get along well. When it comes to binding a hydroxy and a ketone have nothing in common. One is an H-bond donor, the other an H-bond acceptor.
2. "Perhaps it was..." No, plain and simple, it was not. para-Chloroamphetamine has been used to selectively destroy serotonergic neurons since that time. It couldn't have passed animal trials, much less make it to human trial.
3. "Remember these people..." And that's what this is really about. Just like with MDMA, you've never looked at a single paper on the subject. You can't argue about the methodology, you just don't like the results. The Creationists feed on this anti-science mindset. "What you don't understand and makes you uncomfortable must be wrong." How about you go read a bit before making unfounded statements like pCA not being more neurotoxic than chlorphentermine.
4. "In my experience..." More antiscience nonsense. You seriously don't have any understanding of what qualifies as meaningful data, do you? Every time something doesn't agree with your personal opinion, then it must be wrong, as if the last 30 years of science decided to conspire against this one drug. Perhaps just to show science how wrong it is, you should take some pCA, 5,7-DHT, MPTP and 6-Hydroxydopamine.
I'm guessing PubMed and PubChem aren't sites you're familiar with?