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Thread: 4-bromomethcathinone (Brephedrone)

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    #26
    Binned. Hope the vendor realises what they are selling and ceases selling asap. It actually makes me feel sick thinking about the after effects of it. Thanks so much for the info and advice on this, I can be naive when it comes to this kind of stuff. Stick to what you know that's what I say, at least you know what you are getting and you know the effects/after effects so you can prepare for it. Can't imagine the effect that this stuff could have on you based on the information available. I have already spread the word to anyone I know who may come into contact with it. Thanks guys.
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    #27
    Damn i know of two places who sells this. Why do they not research a little before they just release a rc?
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    #28
    ^I know it's ridiculous, I didn't realise how bad the rc scene is getting until recently. There are going to be people who won't do any research on this chem and just take it, god knows the damage they are going to do. Am so glad I threw mine out.
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    #29
    http://onlinelibrary.wiley.com/doi/1...530.x/abstract

    This abstract suggests that the serotonergic neurotoxic damage (measured by 5-hydroxyindoleacetic acid depletion post use) produced in response to 4-haloamphetamines is irreversible, or if recovery occurs, it will be only partial.

    http://www.sciencedirect.com/science...28390875900994 This abstract states that depletion of serotonin levels and 5HIAA levels in response to 4-fluoroamphetamine lasts mere 4-6 hours, whereas 4-bromo, and para-chloroamphetamine lasts many months at the very least, and that in the case of administration of the haloamphetamines (well para-chloro and bromo, no mention is made of 4-iodoamphetamine, but it is known to be extremely neurotoxic, and the pharmacology in this case is likely not to be any different) the damage is irreversible by administration of a serotonin reuptake inhibitor such as an SSRI or tricyclic antidepressant after a certain period, but within 24-48 hours, it can be prevented.

    While this is an untested idea, it may be adviseable to take an SSRI, a day after this, if somebody has been naiive or stupid enough to try this damn idiotic cathinone product...taking it along with the drug is likely to produce a hideously painful, or potentially fatal case of serotonin syndrome, but after the drug has gone...I don't imagine it doing so.

    This is conjecture, and until some other well educated people chime in on this respecting likely half life and weather after a day (the longer the period before this may be done, the more potential for irreversible damage I would be very confident in saying) the drug may still be active, or the hugely elevated 5HT levels would still be present, or weather serotonin levels by this time may already start getting hammered on.

    5HT syndrome is and awful, awful, nasty thing to experience...I know from hearing it first hand from somebody who it happened to. The woman I love, it happened to her, she takes an SSRI daily, and suffers from migraines sometimes, sometimes very severe ones, and took sumatriptan without problems for a long period of time, until suddenly she had a reaction and it caused serotonin syndrome.

    She collapsed, in horrendous pain, stuck on the floor, thinking she was going to die that day, overheated, muscles stiff to the point of being unable to move to seek help, she would have done then, which says something, she normally won't see a doctor, or take medication of any sort, as she doesn't want to have to depend on anything, ever, for any reason, although if its something so critical her life is at risk, she will do so if it gets to the point her life is actually under threat though

    (she hates having to take any sort of meds and being tied to doing so, to the point where she even avoids taking corticosteroids above the absolute, maybe way too low, minimum she can get away with without being close to adrenal insufficiency even more severe than she already has), but when this happened, she couldn't even get to the phone to get help. I would in a heartbeat have traded places, and had that been me, rather than her, but of course, that isn't possible.

    She is one hell of a tough cookie, determined to the max to do things in life as she wants them done, to live life the way she wants to live her life, and have the things she needs, and have them her way. But would have gone to hospital if she could, and feared for her life. She is NOT a person who sways from her chosen path, or bends her will, or scares easily, yet in this case, like I say, thought her time had come.

    Bear that in mind, when considering the possibility of serotonin syndrome, and the use of a serotonin reuptake inhibiting drug to retard the development of severe, possible permanent neurotoxic damage, with accompanying pronounced deficits in memory and cognitive function, before the safety of this may be discussed and established either way.

    This suggestion may be useless, given the fact that anybody reading this thread, who has not yet taken 'brephedrone' yet has some in their possession or is about to purchase some or receive a free sample of some sort, is most unlikely, unless they are exceptionally fucking stupid, to take any.

    Serotonin syndrome is likely mediated by overstimulation of the 5HT2a subtype (primary target of serotonergic psychedelics that produces psychdelia in response to taking them), so taking a serotonin antagonist, especially one targeting 5H22a specifically, such as pizotifen, an antimigraine drug currently in clinical use as a preventative, and I believe as an anxiolytic, also a 5HT2c antagonist.

    Nefazadone and trazadone are also potent 5HT2a antagonists, and antagonists at 5HT2a, although in the case of trazadone at least, it is a partial 5HT1a antagonist, although not particularly efficacious, greater so than buspirone/buspar. The caveat here is that whilst they are, they release 3-chlorophenylpiperazine (yes the same stuff thats been sold as a shite MDxx alternative at times) which is a 5HT agonist, as a metabolite which may complicate things, probably wouldn't overpower the effect as an antagonist, given its use as such in clinical practise as an antidepressant.

    I am going to suggest aggressive action against the potential neurotoxicity here, and say get to hospital, and tell them the above, and suggest that a dose of a combination of pizotifen and an SSRI be given, they will have the capability to treat serotonin syndrome if it occurs due to the the SSRI, dantrolene is usually given, for emergency treatment of serotonin syndrome, but this should not be attempted at home. Unlike the use of pizotifen, which has no such SSRI or serotonergic agonist activity, I believe that safe if its available.

    But get to hospital and suggest they give pizotifen and an SSRI as soon as possible, why to do so, and to watch for serotonin syndrome, under close observation, or try, if pizotifen is not available by any means, trazadone or nefazadone, and do so very carefully, keeping under observation.

    I would act fast, and without reserve, I say hospital, going there without hesitation and suggesting such potentially risky treatment as a possible treatment (but NOT doing it at home, in case of the occurence of serotonin syndrome with the antidepressants mentioned, if the chlorophenylpiperazine metabolite is sufficient to cause it potentially, although given the time elapse and the fact that its a mere metabolite, slowly released, of a potent 5HT2a and 5HT2c antagonist, it is unlikely)

    I say hospital, because of the fact that damage from this drug, is both very likely indeed, to follow the pattern of the para-haloamphetamines and to be permanent quite possibly, and at the least, almost certain to last from 4-6 months to a year if it is not permanent.

    Bring the drug remainder with you, and print the links off.

    This article states that lengthening the sidechain coming off the phenyl ring to a phenisobutylamine abolishes the neurotoxic activity (at least, the pronounced and prolonged depletion of 5HTIAA and profound serotonin depletion) and shortening it to an alphamethylbenzylamine also prevents it being a neurotoxin like the 4-chloroamphetamine parent is. I hope that the increased bulk of the sidechain, I.e the beta-carbonyl group, and differences between the pharmacology of the cathinones vs amphetamines stop this being a vicious, longterm-damaging or permanently damaging potent neurotoxin, but that is whilst perhaps possible, unknown and absolutely by no means either certain, or known to be likely.

    Perhaps if so, it will save some people some really nasty consequences of taking this shite, but quite likely it will not.

    Although I have heard that para-chloroamphetamine was used as an antidepressant at one point, without causing this longterm memory and cognitive destruction, humans are not rats, and its quite possible that 4-Cl-amphetamine and the other haloamphetamines other than 4-fluoro may not do this instantly, after a single dose, as it seems to in the rat or mouse model. Also bear in mind that not all studies were done via normal injection or by forced oral gavage (I.E forcing it into the stomach with a tube...sick..sick shit...), but to lesion selectively, areas of the brain intended as a target via injection directly into the brain.

    But I am fairly sure some such studies have been done by forced oral administration, or intraperitoneal injection into the body cavity (disgusting and abhorrently cruel...but common as a method of administration to a lab animal) and produced such profound neurotoxic insult.

    All my suggestions and info given, now I say again-do NOT FUCKING TAKE THIS DRUG! FLUSH THE FUCKING STUFF AND HAVE NOTHING ELSE TO DO WITH IT! don't give it away like you might with something you just weren't satisfied with, don't sell it, save to somebody truly deserving of suffering, get the hell rid of it!
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    #30
    AFOAF took 1 g in 4 days, oral, smoked, and sniffed.
    Smoked is like dreamy state but siumlated.
    Sniffed is like cleaning yr nose with cleaning product.
    Oral is very weird but he took it after two days of sleep, take 300 mg 5htp everyday for 1 month and vitamin B,C,D and Magnesium annd few amine acides every day for few weeks.
    After having felt sleepy, today my man seemed to feel creative, fine, little hard to do any sport, i will wait, but mind is clear, with unable to focus on unknown task for more than one hour. and he on weak Methadone trastment and party last night was huge.
    DO u think my friend did a terrible bad judgment ?
    The 1g was only to test it...I think and its not a whole G, will stay safe i read here 6 month after fx its scarry labsmate ! what can i tell this friend.
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    #31
    Your friend is one stupid, stupid motherfucker. Bad judgement doesn't close to cover it.

    I think a post-use longterm observation report would be a good idea, if you can/he can.
    Its important to get human data out there, especially when something like this happens.

    I would pay specific attention to his working, short term memory, ability to consolidate memories into longterm, and ability to retrieve/make use of formed memories.

    As well as motivation, and ability to perform cognitive reasoning tasks requiring thought/higher logical functioning.

    These are the areas I imagine are most likely to be impaired. As well as possible presence of emotional lability, and any evident depression and/or anhedonia.

    Tell him not to use any further doses of the drug, to avoid MDxx, MDAI, etc, any serotonin releasers that carry the potential for 5HT depletion, and personally I would avoid any stimulants, just to be on the safe side, as well as any potentially excitotoxic drugs such as GHB. And to keep on with the 5HTP (tryptophan is likely to pass the blood-brain barrier easier than the more polar 5HTP, but MDxx produces a temporary depletion of tryptophan-5-hydroxylase, the enzyme that metabolises tryptophan to 5HTP, for further metabolic synthesis of serotonin, given the long lasting impact on serotonergic function it isn't entirely inconceivable that tryptophan-5-hydroxylase expression may be inhibited longterm by these halo-amphetamines and cathinones, although I don't know for sure)

    Piracetam is a safe drug, and is generally neuroprotective, and given its stimulation of the AMPA receptor, inducing more NMDA activity (NMDA receptor expression is governed by excitatory input, direct agonists are potent, highly dangerous epileptogenic excitotoxins, but the indirect stimulation of expression via piracetam, aniracetam etc. is not excitotoxic, antagonists like ket, MXE etc actually downregulate the NMDA glutamate receptor..its a sort of coincidence detector, registering what neuronal pathways are used heavily, and as such are important, this may help with inducing neurogenesis and repair of the damage to an extent, and is unlikely to be harmful, even if it is not beneficial to a great extent, take with choline as it enhances choline uptake for preduction of acetylcholine)

    I am not a doctor, but this course of action is not at all likely to be in any way harmful, even if significant benefit does not occur. My non-medical prescription is this, and only this: healthy living, a good diet, lots of excersise, keep the mind and body active. Excersise increases expression of a neuropeptide, BDNF (brain-derived neurotrophic factor) which is a potent inducer of neurological repair.

    Hope for the best for the poor bastard...this stuff is near certain to be seriously toxic. Its a little known compound, with nearly certainly no exploration in humans. The outcome of this cannot be predicted, especially with the reports of para-chloroamphetamine seeing bried clinical use as an antidepressant, without causing massive cognitive destruction.

    Who knows? nobody most likely, but it sure as hell isn't going to be a good thing.
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    #32
    Bluelight Crew Vader's Avatar
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    DO u think my friend did a terrible bad judgment ?
    Yes, your friend did a bad judgment and as well not good grammar. You can tell this friend (who definitely, definitely isn't you) that he ought to do some research before he tries a completely new chemical, and that he might want to think about leaving such pioneering experimentation to people with enough of an understanding of pharmacology to make informed choices.
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    #33
    One of the vendors selling brephedrone has suspended sales of it. Wise move, should have been done a lot sooner.
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    #34
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    ^Good stuff. Makes you feel like the shit you post here does actually make a difference.
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    #35
    well dont forget that it is only a theory that brephedrone has the same potency of killing neurons than br-amp has. Dont get me wrong it is extremly stupid to take this drug and irrensponsible to sell it but cathinones are metabolised way faster then amphetamines and have lower binding values and dont cross the bbb so easily, so the friend of Limpet_Chicken may have luck please report to us how he feels in the next days
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    #36
    WTF!? Looks like that same vendor has started selling it again, could be wrong but it would definitely seem that way. I do not understand some vendors at all, fair enough I have been known to use their services now and again but they can be so clueless and reckless at times, this being one of those times. I have no reason to use that vendor any more due to the availability of the same products elsewhere for cheaper so good riddance to you mr.reckless vendor! Try not to completely ruin the rc scene with your ignorance and stupidity. This reminds me of this time last year after the first legal high ban when a 'bath salt' called 'Whack' appeared on the shelves of Irish head shops. For those who don't know this bath salt appeared out of nowhere after meph and all those chems were banned, nobody had any idea what was in it, not even the head shop owners. People who bought it just treated it like meph, big lines, constant re-dosing. Turned out that it was deoxipipradol. Over one hundred people hospitalised with severe psychosis, abnormally high heart rates in a state of total and utter panic. That bath salt lead to a blanket ban on all chemicals not already banned. Just hope the vendors don't shoot themselves in the foot like the head shop owners in Ireland did.
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    #37
    Enough of the vendor discussion folks - even if you're not discussing specific sources/vendors, there's really no need to keep referencing vendors at all. It just invites further and often more specific vendor discussion and/or PM sourcing so please, no more.
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    #38
    ^Apologies, won't happen again.
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    #39
    ^ no worries, you certainly didn't violate any guidelines... its just easy for people reading that to start inquiring about the vendor, sharing their vendor stories, etc. so it can quickly devolve into problematic posting and I wanted to head it off before it got there.
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    #40
    Friend of mine? nobody I know took it...this was advice given to an anonymous fellow BLer, thats all...not somebody I know personally, just to clarify.
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    #41
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    Bromine substitution at the ring 3- or 4-position of methcathinone enhances potency at serotonin uptake transporters.

    Nicholas V. Cozzi and Kevin F. Foley


    Department of Pharmacology, East Carolina University School of Medicine, Greenville, NC 27834

    Abstract

    We previously reported that methcathinone, the aryl ketone analog of methamphetamine, was an inhibitor of monoamine uptake into human platelets and cultured cells (Cozzi et al., Soc. Neurosci. Abs., 24, 341.8, 199. Based upon our pharmacophore model for the amphetamine binding site in the plasma membrane serotonin (5-HT) uptake transporter, it was hypothesized that halogen substituents on the phenyl ring of methcathinone would have a favorable effect on binding affinity at the 5-HT transporter. To test this proposal, 3-bromomethcathinone and 4-bromomethcathinone were synthesized and evaluated for their abilities to inhibit [3H]5-HT uptake into human platelets in vitro. In support of our hypothesis, both of the bromine-substituted compounds were about 15-fold more potent than methcathinone as 5-HT uptake inhibitors: 3-bromomethcathinone inhibited [3H]5-HT uptake with an IC50 of 2.05 0.17mM while 4-bromomethcathinone had an IC50 of 1.83 0.5 mM These results lend support to our model of the substrate binding site in the 5-HT uptake transporter. The model predicts that there is a pocket within the substrate binding domain of the transporter that can accommodate substituents at the ring meta-or para-positions of arylalkylamine ligands. Occupation of this pocket by such substituents leads to increased stability of the ligand-protein complex.
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    #42
    Doesn't say much about the potential for neurotoxicity there.

    Just that it has stronger serotonergic activity as a reuptake inhibitor, and I would be pretty surprised if it wasn't a strong 5HT releaser also. Very surprised in fact.

    Buggered if I would try it though..no chance.
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    #43
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    i would definitely not trust it.. but its your choice... perhaps your funeral?
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    #44
    I doubt its likely to kill. 'Just' produce profound and long lasting cognitive, memory and sleep deficits.
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    #45
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    Is everyone here retarded?

    Or just loves hopping on band wagons of any sort?

    4-BMC simply isn't neurotoxic. Cathinones share a very different SAR profile from amphetamines, people! That beta-ketone makes a HUGE difference in some areas!

    Source: http://www.zoklet.net/bbs/showpost.p...0&postcount=22
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    #46
    Actually, the question is more: are YOU retarded? Is a short lasting shitty high worth the potential for serious, long lasting brain damage? Yes, the cathinones have different pharmacology. The risk with halo amphetamine derivatives is simply too high to make it worthwhile. When we say this is neurotoxic, we aren't talking MDMA-neurotoxic. We're talking about a derivative if a drug that is used in research to selectively destroy serotonergic neurons. Frankly, if that isn't enough to dissuade you, then there is no hope. Fry away your brain if you must but don't encourage other people to do so as well.

    It may well be that this stuff is actually non neurotoxic however I imagine an appreciable fraction of it is deoxygenated at the benzylic carbon to yield the parent non-cathinone amphetamine as a matter of course in it's metabolism. Then it WILL be neurotoxic.
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    #47
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    I don't like the idea of having a bunch of 4-bromoephedrine (a 1' metabolite...) floating around in my blood. Eugh.
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    #48
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    ^neither do i, thanks for that speculation/info matt. i wouldnt have touched the chem anyways but shit son.

    is there possibility of bromine impurity?
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    #49
    I think the term: "neurotoxic" needs to be better defined in this conversation...
    I'm sure all or most people know that a "Neurotoxic" substance is something that causes: temporary damage, permanent damage, or total (neural / brain) cell death. BUT, there is actually a 4th outcome, that the "Neurotoxic" drug does NOT cause any neural cell damage at all!
    Just b/c a drug is neurotoxic does not mean it will actually be neurotoxic when ingested, it just means that the drug has the POTENTIAL to cause cellular damage. The amount of drug taken, the ROA used, the unique physiology of each person, and I'm sure many other factors, all determine whether or not a "neurotoxic" drug will actually be neurotoxic, and just how neurotoxic it will be.


    I am NOT suggesting this drug, or any of the RC's / analogues, etc... are safe, infact I'd bet that this 4-Bromo substance is probably very dangerous. All I'm saying is that a distinction needs to be made between a substance having the potential for being neurotoxic, and a substance known to be neurotoxic when taken at xxmg's via yy ROA....
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    #50
    Bluelighter N0 W4RN1NG's Avatar
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    Quote Originally Posted by MattPsy View Post
    Actually, the question is more: are YOU retarded? Is a short lasting shitty high worth the potential for serious, long lasting brain damage? Yes, the cathinones have different pharmacology. The risk with halo amphetamine derivatives is simply too high to make it worthwhile. When we say this is neurotoxic, we aren't talking MDMA-neurotoxic. We're talking about a derivative if a drug that is used in research to selectively destroy serotonergic neurons. Frankly, if that isn't enough to dissuade you, then there is no hope. Fry away your brain if you must but don't encourage other people to do so as well.

    It may well be that this stuff is actually non neurotoxic however I imagine an appreciable fraction of it is deoxygenated at the benzylic carbon to yield the parent non-cathinone amphetamine as a matter of course in it's metabolism. Then it WILL be neurotoxic.
    Did you read the link I posted? Since having a beta ketone annihilates potential affinity for the VMAT2, which is required for monoamine release, which is required for PBA\PCA's neurotoxicity to manifest...it's almost impossible for what you're saying to be true in this light!

    And anyone who's tried both bk-MDMA and MDMA [or 4-FMC and 4-FMA] will be able to tell you, no appreciable amount of metabolites are formed from deoxygenation at the beta carbon...you realize it undergoes demethylation first into the beta-hydroxy?
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