The Big & Dandy 25C-NBOMe Thread (part 2) ver. "My skin feels like lightning"

[Solipsis]

I have assayed a test dose of 100 ug of 25C, and later when a mild + could be felt I added about 400 ug. It was taken intranasally on a mannitol carrier. I must have still had general psychedelic tolerance or the benzo(s) I had taken within the 24 hours before administration had a large impact on the intensity. It was enough to get a feel for it, I think it has a great quality!! The relaxation distantly reminded me of 2C-C but it was a far less limited headspace than any 2C-X, even 2C-T-7. Instead it came closer to LSD and also what I think DOX compounds try to be, but at least DOB fails. Not sure about the other DOX. It was hard for me to sense when the plateau dropped, and how long the total duration was... especially because of the low dosage.

Another possibility I just thought of is that the 400 ug redose hardly worked because the NBOMe's have such pronounced tachyphylaxis.

The thread title is funny, it has a very peculiar tactile effect! It was very pleasant, sort of like I felt my skin glistening and shimmering rather than seeing it do that. Visually it was very mild at best. I did feel a very basic hint of stimulation, the kind that I would really rather not feel 50 times as intensely, and it felt like there was some effect on my blood vessels which I thought I could tell by the way my hand felt. It did not feel like a body hallucination, just more similar to getting cold from constriction.

Anyway to me this is a warning or reminder to take it slowly with all NBOMe's, I have reason to believe I may be sensitive to muscle cramping and similar stim vasoconstricting side-effects.

 

[jason7]

Cutting highly potent drugs with large amounts of inert powder... I don't really trust it. If one of the compounds is dissolved, it can be concentrated on the surface of the pile (as solvent evaporates, more replaces it at the surface via capillary action, concentrating the compound dissolved in it at the surface). If both are dissolved, they may crystalize separately (in fact, they likely will each form their own crystals, which you hope are well mixed) - and since the substances have different physical properties, could begin to separate mechanically (via brazil nut effect). These effects may not be significant with the specific compounds you're using, but you don't really know either way. That's why I recommend against measuring doses in that way.

Why not dissolve it in 20% alcohol (50:50 water/vodka mixture) and use a nasal spray bottle? You can buy empty nasal spray bottles online, and in a liquid solution, you KNOW that the solute is evenly distributed, or you can buy and repurpose nasal sprayers from your local pharmacy...

Well, I just find powders more convenient to handle than liquids and I also don't like the idea of spraying liquid in my nose. Probably works well but not my preferred method. Snorting a small amount of powder would probably stay up there better, then maybe snort a small amount of water up there to help dissolve it, just enough to wet it. If I find that the powder doesn't work well enough then I'll try the liquid.

In regard to cutting with inert powders, after you dry it you also have to triturate it, meaning mortar and pestle it. That way, both powders are intimately mixed. It's not crystals anymore because the crystals get crushed into fine powder. As long as you crush and mix it well it should be completely uniform potency. It's a lot easier to weigh out 5 mg of the mixture than 500 mcg of pure.

In regard to the fish oil capsules, they are coated with an "enteric" coating, which does not dissolve in stomach acid but does dissolve in the alkaline environment of the duodenum/small intestine. Elemi oil is inactive when swallowed but I read a post on another forum where a guy put some in an enteric capsule and it worked, elemi oil contains elemicin which is the non-amine form of TMA. He said it had a very clean effect and no nausea. Enteric coating protects things from stomach enzymes. I don't know for sure if it will work with NBOMe but theoretically it should. It would be roughly the same as plugging.

 

[tmdoca]

Whenever I drop a sin-bomb my skin feels like fluffy daydreams, not lightning!

 

[lysergication]

I also don't like the idea of spraying liquid in my nose.

with a 0.2ml/500µg concentration, it's literally 2 drops of liquid.

 

[Cyanoide]

500µg intranasally with liquid was blissful. The only problem was that even 0,1 ml was too much and some got down my throat. I had to take doses with 0,05 ml with my syringe. The solution was distilled water and vodka with a ratio of 1:1. Having the vodka was great. Every time it burned in my nose I knew it went where it should. When I felt a burn in my throat (with 0,1 ml) I knew it was partly wasted. 0,05 ml always stayed in my nose.

The interesting thing was that there was a quite strong physical stimulation the first 30-45 minutes. When the trip really kicked in, I didn't feel or notice the stimulation anymore. And the afterglow was wonderful, deep and euphoric.

 

[Jesusgreen]

This chemical sounds utterly wonderful, I can see it really taking off in popularity going by the reports here and elsewhere. I was wondering what anyone's experiences of rather high doses with this were like? I like to push things into high dose territory, and I'd like to know if it's going to have an uncomfortable bodyload or anything I should be aware of like that.

 

[Jakeperson]

Once it gets above 1mg the bodyload can get pretty uncomfortable. I can't see many people willing to go beyond 1mg though, it is pretty powerful.

 

[jason7]

NBOMe chemicals will be the next big thing in drugs. We are very lucky to be around at this time. It wasn't even commercially available until 2010. The quite unpleasant body load of the 2C-X's means that they will never achieve wide popularity. Now that NBOMe is here, those days are over. They are very selective 5-HT2a agonists. It's the greatest discovery ever. Now we don't have to do LSD and feel like we got kicked in the nutsack anymore, and then go nuts like Syd Barrett and have flashbacks and stuff. Acid did have some good points but it also had too many bad points. It's an ergot alkaloid, after all. Ergot has a lot of nasty effects. The CNS stimulation is excessive too. First you're high for 8 hours and then you're wide awake all night.

Thank goodness for NBOMe. Since the wheels of drug legislation grind slowly, we are in the fortunate position of still being able to order some up, like you could with acid from Sandoz before it was banned. Anyone can order enough NBOMe to last them the rest of their life, and their friends (for legitimate research purposes only of course). It's a candy store right now. This can't last forever though, and there is much research to be done.

 

[IamMe90]

NBOMe chemicals will be the next big thing in drugs. We are very lucky to be around at this time. It wasn't even commercially available until 2010. The quite unpleasant body load of the 2C-X's means that they will never achieve wide popularity. Now that NBOMe is here, those days are over. They are very selective 5-HT2a agonists. It's the greatest discovery ever. Now we don't have to do LSD and feel like we got kicked in the nutsack anymore, and then go nuts like Syd Barrett and have flashbacks and stuff. Acid did have some good points but it also had too many bad points. It's an ergot alkaloid, after all. Ergot has a lot of nasty effects. The CNS stimulation is excessive too. First you're high for 8 hours and then you're wide awake all night.

Thank goodness for NBOMe. Since the wheels of drug legislation grind slowly, we are in the fortunate position of still being able to order some up, like you could with acid from Sandoz before it was banned. Anyone can order enough NBOMe to last them the rest of their life, and their friends (for legitimate research purposes only of course). It's a candy store right now. This can't last forever though, and there is much research to be done.

What on earth are you talking about? The compounds in the 2c-x series are massively popular, probably the most purchased psychedelic RCs on the scene. I HIGHLY doubt something like nbome is going to get as popular due to the relatively high amount of effort required to dose them. If they do got popular, it is because people will overlook the proper precautions necessary to dose them safely and they will get banned.

I also don't like your characterization of LSD, it's not one that I think a lot of people here would agree with (at least relative to most other 5Ht2a psychs - they all cause muscle tension and CNS stimulation to a degree and LSD is one of the cleanest psychedelics I've ever taken physically).

 

[jason7]

Point taken. I assumed they weren't very popular. I tried both 2C-X's and both caused a constant unpleasant feeling in the digestive system, just enough to ruin the whole thing. They are more convenient to measure out and administer than NBOMe's though, so probably better suited to the average person. I agree that somebody will probably take way too much sometime, not knowing how potent it is. The RC companies don't include directions. Fortunately, it's inactive by mouth. Or maybe only as potent as 2C-X, after the benzyloxymethyl part gets cleaved off by enzymes.

In regard to LSD, I've never really been satisfied with it myself, don't like the tremors, anxiety and other side effects. I want a more perfect psychedelic. Whether NBOMe is it is a matter of personal opinion. I still have to try a full dose to see what the full effects are like. A very small test dose was nice. People specifically mention a lack of anxiety. I can't say that for LSD, which can be quite frightening at times. I often had a feeling of impending doom with LSD. Listening to Slayer on 4 hits of acid, not a great idea.

 

[jason7]

I tried the enteric capsule injecting yesterday. It didn't work at all. I don't know if it dissolved in my stomach or not, it's possible. It worked by sublingual/buccal though, mixed with 9x as much inositol. I took 5 mg of the 10% mixture and got a medium effect. I topped it up a few hours later with about another 3 mg. The redosing worked. I did get stronger effects. Still not really full effects though. I think 10 mg would do it, meaning 1 mg of 25C. It's pretty good. Not as good as acid though, I must admit. Not as euphoric. There is some minor body load, nothing like 2C-X though. Maybe 25I would be cleaner. I'll have a sample of that next week.

 

[Penthos]

I tried the enteric capsule injecting yesterday. It didn't work at all. I don't know if it dissolved in my stomach or not, it's possible. It worked by sublingual/buccal though, mixed with 9x as much inositol. I took 5 mg of the 10% mixture and got a medium effect. I topped it up a few hours later with about another 3 mg. The redosing worked. I did get stronger effects. Still not really full effects though. I think 10 mg would do it, meaning 1 mg of 25C. It's pretty good. Not as good as acid though, I must admit. Not as euphoric. There is some minor body load, nothing like 2C-X though. Maybe 25I would be cleaner. I'll have a sample of that next week.

Perhaps the tiny injection point in the capsule was enough to allow your stomach enzymes to penetrate and fully dissolve the pill from the inside out?

However I'm confused...I thought the metabolic action of the liver is what prevented the nBOMe's from being orally active...don't chemicals still pass through the liver if absorbed in the small intestine as well? That is where almost all of the nutrient absorption takes place, after all. Please correct me if I'm wrong

 

[MattPsy]

Correct, they are still metabolised if absorbed from small (or large for that matter) intestine.

It [first-pass-metabolism] simply can't be the only reason that 25C is almost inactive orally. In the 25I thread, I provided some math showing this, that even when around 30mg of a NBOMe compound is taken, no appreciable 2C-X (the product of debenzylation due to metabolism) trip takes place.

 

[tryp2fun]

Correct, they are still metabolised if absorbed from small (or large for that matter) intestine.

It [first-pass-metabolism] simply can't be the only reason that 25C is almost inactive orally. In the 25I thread, I provided some math showing this, that even when around 30mg of a NBOMe compound is taken, no appreciable 2C-X (the product of debenzylation due to metabolism) trip takes place.

How do you know that MAO catalyzes the oxidation of the benzyl of 25X? Maybe the product is 2-methoxybenzylamine and the phenylacetaldehyde?

 

[MattPsy]

Because the metabolic pathway for 25X should be predominated by debenzylation, with demethylation at both 'sides' as a additional pathway cf. DOI.

Look at benzphetamine (N-benzylmethamphetamine) and clobenzorex (N-(2-chloro)benzylamphetamine) - these are prodrugs for amphetamine. Seeing as both are readily debenzylated, I don't think it's at all speculative to say the same will happen for the 25Xs, especially so because the amphetamines are inherently harder to debenzylate due to steric hindrance from the a-methyl carbon, and clobenzorex is also ortho-substituted on the N-benzyl making it even more similar to the N-benzyl of the 25Xs, yet it too is also readily debenzylated. Benzphetamine is also N-methylated (so it metabolises to both methamphetamine and amphetamine), lending even more credence, since debenzylation takes place even on the tertiary amine form (fully substituted). Clearly, the enzyme responsible for this behaviour is pretty substrate-tolerant.

Now, it's true that with benzphetamine and clobenzorex that only a small fraction is metabolised to the parent amphetamines- however, this is due to para-hydroxylation of the amphetamine side of the molecule, with subsequent glucuronidation and excretion. If para-hydroxylation is blocked (because the para [4] position is already substituted in the 25Xs, say in 25I where it is iodo substituted), then this pathway won't take place and so debenzylation will predominate. p-hydroxylation was not observed on the N-benzyl side, interestingly, which means the same pathway (hydroxylation -> glucuronidation) won't instead happen on the N-benzyl side.


Refs:
B. Glasson, A. Benakis and M. Thomasset, Localisation, distribution, excretion et metabolisme d'un nouveau medicament anorexigene marque au C14, le chlorhydrate de clobenzorex. Arzneim.–Forsch., 21 (1971), pp. 1985–1992
T. Inoue and S. Suzuki, The metabolism of 1-phenyl-2-(N-methyl-N-benzylamino)propane (benzphetamine) and 1-phenyl-2-(N-methyl-N-furfurylamino)propane (furfenorex) in man. Xenobiotica, 16 (1986), pp. 691–698
K. Baden, S. Valtier, C. Sandra, and J.T. Cody, Metabolic Production of Amphetamine Following Multidose Administration of Clobenzorex. Journal of Analytical Toxicology, Volume 23, Number 6, October 1999 , pp. 511-517(7)

 

[Powerup]

Point taken. I assumed they weren't very popular. I tried both 2C-X's and both caused a constant unpleasant feeling in the digestive system, just enough to ruin the whole thing. They are more convenient to measure out and administer than NBOMe's though, so probably better suited to the average person. I agree that somebody will probably take way too much sometime, not knowing how potent it is. The RC companies don't include directions. Fortunately, it's inactive by mouth. Or maybe only as potent as 2C-X, after the benzyloxymethyl part gets cleaved off by enzymes.

In regard to LSD, I've never really been satisfied with it myself, don't like the tremors, anxiety and other side effects. I want a more perfect psychedelic. Whether NBOMe is it is a matter of personal opinion. I still have to try a full dose to see what the full effects are like. A very small test dose was nice. People specifically mention a lack of anxiety. I can't say that for LSD, which can be quite frightening at times. I often had a feeling of impending doom with LSD. Listening to Slayer on 4 hits of acid, not a great idea.

You need a higher dose of LSD I would rate it second in 'power' only to DMT.

 

[tryp2fun]

Because the metabolic pathway for 25X should be predominated by debenzylation, with demethylation at both 'sides' as a additional pathway cf. DOI.

Look at benzphetamine (N-benzylmethamphetamine) and clobenzorex (N-(2-chloro)benzylamphetamine) - these are prodrugs for amphetamine. Seeing as both are readily debenzylated, I don't think it's at all speculative to say the same will happen for the 25Xs, especially so because the amphetamines are inherently harder to debenzylate due to steric hindrance from the a-methyl carbon, and clobenzorex is also ortho-substituted on the N-benzyl making it even more similar to the N-benzyl of the 25Xs, yet it too is also readily debenzylated. Benzphetamine is also N-methylated (so it metabolises to both methamphetamine and amphetamine), lending even more credence, since debenzylation takes place even on the tertiary amine form (fully substituted). Clearly, the enzyme responsible for this behaviour is pretty substrate-tolerant.

Now, it's true that with benzphetamine and clobenzorex that only a small fraction is metabolised to the parent amphetamines- however, this is due to para-hydroxylation of the amphetamine side of the molecule, with subsequent glucuronidation and excretion. If para-hydroxylation is blocked (because the para [4] position is already substituted in the 25Xs, say in 25I where it is iodo substituted), then this pathway won't take place and so debenzylation will predominate. p-hydroxylation was not observed on the N-benzyl side, interestingly, which means the same pathway (hydroxylation -> glucuronidation) won't instead happen on the N-benzyl side.


Refs:
B. Glasson, A. Benakis and M. Thomasset, Localisation, distribution, excretion et metabolisme d'un nouveau medicament anorexigene marque au C14, le chlorhydrate de clobenzorex. Arzneim.–Forsch., 21 (1971), pp. 1985–1992
T. Inoue and S. Suzuki, The metabolism of 1-phenyl-2-(N-methyl-N-benzylamino)propane (benzphetamine) and 1-phenyl-2-(N-methyl-N-furfurylamino)propane (furfenorex) in man. Xenobiotica, 16 (1986), pp. 691–698
K. Baden, S. Valtier, C. Sandra, and J.T. Cody, Metabolic Production of Amphetamine Following Multidose Administration of Clobenzorex. Journal of Analytical Toxicology, Volume 23, Number 6, October 1999 , pp. 511-517(7)

Yes, I am quite familiar with this. Benzphetamine has to be debenzylated since the alpha-methyl keeps it from oxidation on the phenethylamine side. But, what happens to N-benzyl-2-phenylethylamine? I don't think that it has been studied, since I can't find anything on PubMed, so you are making an assumption that it will be metabolized like benzphetamine. Benzylamine is certainly an MAO substrate, and so is phenethylamine. However, based on this paper, phenethylamine is metabolized by human MAO-A with a kcat 25-fold faster than for benzylamine, while with MAO-B they react almost equally. So, at least for MAO-A, it is reasonable to predict N-benzyl-2-phenylethylamine will be metabolized mainly to benzylamine and phenylacetaldehyde.

http://www.ncbi.nlm.nih.gov/pubmed/20079438

 

[MattPsy]

^ Cool, I wasn't aware of that - perhaps this then explains a lot of the potency differences between individuals, as there are quite a few different isoforms of MAO enzymes due to genetic differentiation. You probably get a pretty complex mixture of metabolites.

Now, I want to see someone try 25C (or 25I, et al.) with a MAO inhibitor,or preferably a non-selective one and then on a separate time a selective MAO-B inhibitor like selegiline - and take the drug orally. That would really elucidate the metabolism pathway . I wonder how extensive first-pass metabolism is by MAO - debenzylation is actually carried out by cytochrome P450 enzymes instead of MAO, AFAIK. So if we get rid of MAO activity we can really see what its role is both quantitatively and qualitatively.

 

[tryp2fun]

^ Cool, I wasn't aware of that - perhaps this then explains a lot of the potency differences between individuals, as there are quite a few different isoforms of MAO enzymes due to genetic differentiation. You probably get a pretty complex mixture of metabolites.

Now, I want to see someone try 25C (or 25I, et al.) with a MAO inhibitor,or preferably a non-selective one and then on a separate time a selective MAO-B inhibitor like selegiline - and take the drug orally. That would really elucidate the metabolism pathway . I wonder how extensive first-pass metabolism is by MAO - debenzylation is actually carried out by cytochrome P450 enzymes instead of MAO, AFAIK. So if we get rid of MAO activity we can really see what its role is both quantitatively and qualitatively.

At least for the 2C-Xs, MAOs are primarily responsible for metabolism, and P-450s contribute little if anything. See the paper below. That suggests to me that P-450s probably do not play much of a role in metabolism of 25Xs, although they are responsible for benzphetamine metabolism.

Biochem Pharmacol. 2007 Jan 15;73(2):287-97. Epub 2006 Sep 24.
Identification of monoamine oxidase and cytochrome P450 isoenzymes involved in the deamination of phenethylamine-derived designer drugs (2C-series).
Theobald DS, Maurer HH.

Department of Experimental and Clinical Toxicology, Institute of Experimental and Clinical Pharmacology and Toxicology, University of Saarland, D-66421 Homburg (Saar), Germany.
Abstract

In recent years, several compounds of the phenethylamine-type (2C-series) have entered the illicit drug market as designer drugs. In former studies, the qualitative metabolism of frequently abused 2Cs (2C-B, 2C-I, 2C-D, 2C-E, 2C-T-2, 2C-T-7) was studied using a rat model. Major phase I metabolic steps were deamination and O-demethylation. Deamination to the corresponding aldehyde was the reaction, which was observed for all studied compounds. Such reactions could in principal be catalyzed by two enzyme systems: monoamine oxidase (MAO) and cytochrome P450 (CYP). The aim of this study was to determine the human MAO and CYP isoenzymes involved in this major metabolic step and to measure the Michaelis-Menten kinetics of the deamination reactions. For these studies, cDNA-expressed CYPs and MAOs were used. The formation of the aldehyde metabolite was measured using GC-MS after extraction. For all compounds studied, MAO-A and MAO-B were the major enzymes involved in the deamination. For 2C-D, 2C-E, 2C-T-2 and 2C-T-7, CYP2D6 was also involved, but only to a very small extent. Because of the isoenzymes involved, the 2Cs are likely to be susceptible for drug-drug interactions with MAO inhibitors.

 

[MattPsy]

Yes, that's for PEAs, which are primary amines - it's going to be different for these bulky N-substitutions, IMO. Like with benzphetamine. Can't look at the paper right now..