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Thread: 25B-NB (n-Benzyl-2C-B)

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    25B-NB (n-Benzyl-2C-B) 
    #1
    SWIM has been given a small sample of this compound, and after reading the following publications, it seems like this compound is active and potent.

    Molecular interaction of serotonin 5 HT2A receptor residues Phe339(6.51) and Phe340(6.52) with super-potent N-benzyl phenethylamine agonists
    Braden MR, Parrish JC, Naylor JC, Nichols DE
    Mol. Pharmacol., 2006

    Influence of amine substituents on 5-HT2A versus 5-HT2C binding of phenylalkyl- and indolylalkylamines
    Glennon RA, Dukat M, el-Bermawy M, Law H, De los Angeles J, Teitler M, King A, Herrick-Davis K
    J. Med. Chem, 1994, 37(13), 1929-1935

    Is it possible that this compound (and the analogues with ortho-substituted benzyl groups) would be subjected to debenzylation?

    Could anyone comment about an estimated dosage and duration of this compound?

    Thank you.
     

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    #2
    The N-benzyl compounds are inactive, because of their low intrinsic activity. They are only low activity partial agonists.
     

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    #3
    So they have high binding affinity but low efficacy? Would still be interested to hear results from a human trial, in vitro studies can only tell you so much...
     

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    #4
    Benzphetamine metabolism:
    1. The metabolism of 1-phenyl-2-(N-methyl-N-benzyl-amino)propane (benzphetamine) in vitro was studied using rat-liver microsomes.

    2. Five metabolites were isolated from the incubation mixture and identified as 1-phenyl-2-(N-benzylamino)propane (benzylamphetamine), 1-(p-hydroxyphenyl)-2-(N-methyl-N-benzylamino)propane, 1-(p-hydroxyphenyl)-2-(N-benzylamino)propane, methamphetamine and amphetamine. This metabolism in vitro was compared with that in vivo which was reported previously.

    3. The formation of all five metabolites were catalysed by liver microsomes supplemented with NADPH and O2, and inhibited by either SKF 525-A or CO.

    4. N-Demethylation was inhibited by either 2-methyl-1,2-bis-(3-pyridyl)-1-propanone (metyrapone) or n-octylamine, while aromatic hydroxylation was inhibited by 7,8-benzoflavone and N-debenzylation was depressed by all these inhibitors.

    5. N-Demethylation was enhanced by pretreatment of rats with phenobarbitone, while aromatic hydroxylation was induced by pretreatment with 3-methylcholanthrene, and N-debenzylation was induced by pretreatment with either phenobarbitone or 3-methylcholanthrene.

    6. These data suggested that the metabolism of benzphetamine was mediated by three slightly different enzyme systems.
    http://www.informaworld.com/smpp/con...all~order=page

    So, yes, the there will probably be n-debenzylation. My guess is that the duration of action (whatever action that may be) is longer than 2c-b, perhaps much longer (benzphetamine's half life is 16 to 31 hours). If the compound is not instrinsically active, it may be active through the metabolite 2c-b, in which case it could work as a sustained release 2c-b through metabolism, but that's more speculation.
     

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    #5
    Bluelight Crew ebola?'s Avatar
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    >>(benzphetamine's half life is 16 to 31 hours).>>

    IIRC, benzphetamine is a prodrug, extending the effective half-life.
     

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    #6
    Quote Originally Posted by nuke
    If the compound is not instrinsically active, it may be active through the metabolite 2c-b, in which case it could work as a sustained release 2c-b through metabolism, but that's more speculation.
    SWIM has have the same thoughts...

    But any idea what a safe trial-dosage would be for initial tasting?
     

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    #7
    I'd start at 50mcg and start doubling every week until I found activity.
     

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    #8
    Quote Originally Posted by Dextrose
    SWIM has have the same thoughts...

    But any idea what a safe trial-dosage would be for initial tasting?
    Don't use "SWIM" here, it's moronic and does't protect you- this has been said dozens of times, here and elsewhere- it's been almost universally dropped.

    Agreed with above, I'd start with a sub-1mg dose and then double, double, double. Be careful in the 10-30mg range though, you may find that 10mg isn't enough, but 20 is way too much. 4-HO-DiPT is a good example of something that does little at 12mg, but 15 can be quite intense.

    'fer instance...
     

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    #9
    even recommended to start twice with 50 micrograms (with a few days in between)
    Seemed to have read sometimes an allergic reaction might not show the first time
    but does mostly the second time.

    your ex.
     

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    #10
    Hello,

    I know the people who performed the experiments in the cited paper. It should be noted that not all the N-benzyls had low intrinsic activity for the phosphoinositide release assay. At rat 5HT2A receptors, 25I-NBOMe (the compound with the highest affinity) had an intrinsic activity of 78%. DOI had an intrinsic activity of 77% at the same assay. 25I-NB did have a lower intrinsic activity of 37%. All the human intrinsic activity values were higher, however this may be reflective of the higher expression of the h5HT2A receptors in the heterologous expression system.

    Finally, it should be noted that there is not a very good correlation between efficacy/potency at the phosphoinositide release assay ("IP3 release"; the most common functional assay reported for 5HT2A ligands) and activity in humans. There could be other issues involved, such as metabolism and pharmacokinetics. I am fairly confident, however, that the phosphoinositide release assay is a poor measure of "hallucinogenesis".

    Please be careful with so-called research chemicals. Who knows what the N-benzyls are metabolized into. Stay safe.

    aloha
    psilo
     

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    #11
    *bump*

    Any news on the "friend" who was going to try this compound? I'm very interested to hear any reported effects.

    aloha
    psilo
     

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    #12
    Yeah, me too. I really would love to read a bio-assay, if he did taste it...
     

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    #13
    Bluelighter Erny's Avatar
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    This one is the first bomamine ever mentioned here, am I correct? Be prepared to take it intranasally, intramuscularly or sublingually, it is likely to be without any oral activity at all, just like the 2-MeO-benzyls. The dose may be in the 5-20 mg range, as I suspect. But start low, perhaps with 1 mg. It is very lipophilic and you will be fully into it in about an hour. No 5-HT2C activity is great, but still not completely safe.
     

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    #14
    Quote Originally Posted by Erny
    This one is the first bomamine ever mentioned here, am I correct? Be prepared to take it intranasally, intramuscularly or sublingually, it is likely to be without any oral activity at all, just like the 2-MeO-benzyls. The dose may be in the 5-20 mg range, as I suspect. But start low, perhaps with 1 mg. It is very lipophilic and you will be fully into it in about an hour. No 5-HT2C activity is great, but still not completely safe.
    what is a bomamine?
     

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    #15
    Maybe he means a bromamine, like n-bromotaurine or something. I still can't make sense of that, though.
     

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    #16
    Bluelighter Erny's Avatar
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    Bomamine is BOM amine or NBOMe amine. Basically N-(2-MeO-benzyl)-phenylethylamine, but also any other N-benzylated amine. As their pharmacology call for a distinct individuality, and a special name.
     

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    #17
    Quote Originally Posted by Erny
    Bomamine is BOM amine or NBOMe amine. Basically N-(2-MeO-benzyl)-phenylethylamine, but also any other N-benzylated amine. As their pharmacology call for a distinct individuality, and a special name.
    OK. thanks for clearing it up

    but I don't buy it, they are not distinct as far as I am aware, and so not deserving of some special name. A few of the tryptamines with the N-benzyl substitution have been tasted in man and are totally inactive, and have been mentioned here.

    Additionally BOM is already widely used scientifically to refer to the benzyloxymethyl not N-benzyl.
     

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    #18
    Quote Originally Posted by Erny
    Bomamine is BOM amine or NBOMe amine. Basically N-(2-MeO-benzyl)-phenylethylamine, but also any other N-benzylated amine. As their pharmacology call for a distinct individuality, and a special name.
    Have you tried these compounds? If so, tell everything.
     

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    #19
    Bluelighter Erny's Avatar
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    Quote Originally Posted by vecktor
    Additionally BOM is already widely used scientifically to refer to the benzyloxymethyl not N-benzyl.
    Who cares?

    OK.

    As you may have seen in Nichols writing mentioned in the firt post of the topic, and probably in some older papers, phenylethylamines carrying a behzyl substituent on their nitrogen atom are very selective towards 5-HT2A serotonin receptor. This means we should at least feel less side effects resulting from the activation of a few more pharmacological targets with such a chemical, than there are with just any phenylethylamine from PIHKAL.

    Bomamines give almost no side effects in a reasonable dose. Even the appetite is normal. Though to say "none at all" would be unfair, since there is a rise of body temperature and a mild vasoconstriction present. So, you don't feel sick when coming up and throughout the trip. They doesn't drag you towards the earth as PEAs can do, you actually feel lightweighted. Combined with a light motor coordination loss and body scheme disturbance this gives a feeling like howering in zero gravity.

    Such structures may also possess sigma activity (see Glennon R. A. Pharmacophore identification for sigma-1 receptor binding: application of the "deconstruction-reconstruction-elaboration" approach. Mini Rev Med Chem. 2005 Oct;5(10):927-40., but this is just a speculation.

    It is still fun to raise the dose to the intensities you would not desire with a simple PEA, mostly due to the above mentioned side effects of the latter. But not too far. The ratio of a normal dose to a lethal one probably doesn't differ much if we compare NBOMe and simple PEAs.

    Chemicals we are speaking about develop a remarkable tolerance to their and any other psychedelic drugs effects, that may sometimes need about two weeks to trail off. And they are totally inactive when taken orally.

    N-(2-methoxybenzyl)-tryptamines and N-methyl-N-(2-methoxybenzyl)-tryptamines are inactive. Most of the 3,4,5-substituted PEAs are also inactive with the exception for NBOMe-mescaline, that require a 50-100 mg dose for a trip. NBOMe-2C-H is active at 5-10 mg. NBOMe amphetamines are about ten times weaker than their phenylethylamine counterparts.

    NBOMe-2,5-dimethoxy-4-something-phenylethylamines are so far the most remarkable substances in the group. Some of them are still much like Sasha's PEAs, while others differ in a very surprising ways. To name a few, David's NBOMe-2C-I is a true gem. Basically it resembles PEAs, but is much like acid in some of it's effects, especially in the emotional area. It is full with the deep glowing LSD-like empathy that is uncommon within phenylethylamines. Not all of the bomamines are like that, NBOMe-2C-C is more like DOI and is also a gem, NBOMe-2C-B is much like plain 2C-B, and NBOH-2C-B is simply uninteresting.

    The activity of bomamines in humans are sometimes inverted: NBOMe-2C-I requires 500-1000 mkg for a trip, NBOMe-2C-B - 500-800, NBOMe-2C-N - 400-700. The most active one I know about is NBOMe-2C-C with 200-500 mkg. Still, NBOMe-2C-D is less active than all theese, NBOMe-2,4,5-trimethoxy-PEA is many times less active, though I don't know the exact dose. Such SARs are likely a result of combination (if we try to simplify it a little) of the affinity to the receptor and weird pharmacokinetics. NBOMe-2C-C, B and I lasts 8 hours, NBOMe-2C-N - 5 hours, just like their ancestors from PIHKAL. When insufflated or injected i/m, they need a full hour to come up, even 1,5 hours in the case of NBOMe-2C-I. Like DOB and DOI. Thus, they are metabolised very rapidly, and it is clearly not MAO that does that. Looks like in the close series like C, B and I, the faster they get to the brain, the stronger they are.


    This nice picture is darkened by the lack of safety when handling such chemicals. No oral activity means it is very tricky to dose them without good scales. And if you remember the bromo-dragonfly story w w w . erowid.org/chemicals/bromo_dragonfly/bromo_dragonfly_death.shtml , you will see that if they will ever become popular, we will undoubtedly hear about accidental deaths associated with their consumption.

    BOM!
    Last edited by Erny; 13-09-2008 at 02:57.
     

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    #20
    Quote Originally Posted by Erny

    The activity of bomamines in humans are sometimes inverted: NBOMe-2C-I requires 500-1000 mkg for a trip, NBOMe-2C-B - 500-800, NBOMe-2C-N - 400-700. The most active one I know about is NBOMe-2C-C with 200-500 mkg. Still, NBOMe-2C-D is less active than all theese, NBOMe-2,4,5-trimethoxy-PEA is many times less active, though I don't know the exact dose. Such SARs are likely a result of combination (if we try to simplify it a little) of the affinity to the receptor and weird pharmacokinetics. NBOMe-2C-C, B and I lasts 8 hours, NBOMe-2C-N - 5 hours, just like their ancestors from PIHKAL. When insufflated or injected i/m, they need a full hour to come up, even 1,5 hours in the case of NBOMe-2C-I. Like DOB and DOI. Thus, they are metabolised very rapidly, and it is clearly not MAO that does that. Looks like in the close series like C, B and I, the faster they get to the brain, the stronger they are.
    I assume that mkg = µg or mcg, microgram,
    can you provide a link to a trip report or similar. I would also be very interested to see the physical data on the compounds.

    also your statements seem to indicate a lot of interesting inconsistancies between the properties of these materials in man and those of the pihkal parents. Also with the published in vitro data with respect to affinity intrinsic activity. in particular I have difficulty understanding

    When insufflated or injected i/m, they need a full hour to come up, even 1,5 hours in the case of NBOMe-2C-I. Like DOB and DOI. Thus, they are metabolised very rapidly, and it is clearly not MAO that does that. Looks like in the close series like C, B and I, the faster they get to the brain, the stronger they are.
    if they are being metabolised rapidly why do they take a long time to come up?
    I can't see the logic at all.
     

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    #21
    Bluelighter Erny's Avatar
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    Quote Originally Posted by vecktor
    I assume that mkg = µg or mcg, microgram,
    can you provide a link to a trip report or similar. I would also be very interested to see the physical data on the compounds.

    also your statements seem to indicate a lot of interesting inconsistancies between the properties of these materials in man and those of the pihkal parents. Also with the published in vitro data with respect to affinity intrinsic activity. in particular I have difficulty understanding
    I haven't seen any mention of human trials in english so far. What physycal data do you want to see? Hydrochlorides are white crystalline powders melting between 120 and 200 oC. 1H NMR and mass spectra are available for some of them.

    if they are being metabolised rapidly why do they take a long time to come up?
    I can't see the logic at all.
    Lipophilicity directly influences the duration of onset, as well as the full duration of effects. While some enzyme or enzymes does not allow it neither to last forever like DOB, nor to be orally active.
     

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    #22
    Quote Originally Posted by Erny
    I haven't seen any mention of human trials in english so far. What physycal data do you want to see? Hydrochlorides are white crystalline powders melting between 120 and 200 oC. 1H NMR and mass spectra are available for some of them.


    Lipophilicity directly influences the duration of onset, as well as the full duration of effects. While some enzyme or enzymes does not allow it neither to last forever like DOB, nor to be orally active.
    thanks so most of the HCl salts are active around say 0.5 - 1mg insufflated, what doses were tried orally before everyone gave up? I assume the Hydrochlorides are reasonably soluble in water?

    it would be very interesting to see if these metabolise in vivo to the parent amines, a la benzphetamine or whether the active species is the N-benzyl amine.

    I would suggest that the reason the I is less potent than the Br is because with the added bulk of the N benzyl there is not enough room in the receptor pocket to allow a very bulky 4-substituent as well.
     

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    #23
    Bluelighter Erny's Avatar
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    HCl salts have a relatively good solubility in water. And it is interesting that their solubility in methanol and ethanol is sometimes higher, than in water. They also dissolve in CHCl3, like phase transfer catalysts do, also having an amino group surrounded by bulky organic substituents.
     

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    #24
    Quote Originally Posted by Erny
    HCl salts have a relatively good solubility in water. And it is interesting that their solubility in methanol and ethanol is sometimes higher, than in water. They also dissolve in CHCl3, like phase transfer catalysts do, also having an amino group surrounded by bulky organic substituents.
    perhaps that is the reason for the lack of oral activity, they end up being locked up in lipids?

    a couple of phenethylamine hydrochlorides with bulky 4 positions also dissolve in chloroform and DCM, which if not known about causes problems with purification.

    all very interesting.
    would you mind translating the reports?

    vecktor
     

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    #25
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    The largest per os assay was with 30 mg NBOMe-2C-B. It gave a light +1/2 by Shulgin scale, only little stronger than 3 mg per os that can also be felt as a +/- threshold. And it could have been the adsorption through the mucous membrane. There are very few literary reports. The most detailed are about overdoses.
     

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