2c-t-7 toxicity

[Dondante]

Maybe some compounds have different affinities for 5-HT1B. Since all have relatively significant affinities (roughly corresponding to dosage) for 5-HT2A, it must be something else. I wonder if 2C-T-7 has an unusually high affinity for 1B?

mCPP and TFMPP both have significant affinity for 5-HT1B, which could be responsible for the increased cardiovascular effects. LSD does as well, but the dosage is much lower. DMT has very low affinity (Ki = 2200 nM) while 5-meo-dmt has possibly relevant affinity (Ki = 350 nM) ... that's for rats. I think both numbers are lower for humans.

 

[haribo1]

5-HT2A is the one responsible for serotonergic hallucinogens. I did find an interesting article that cites 5-HT1B as the culprit for acute cardiovascular effects, so perhaps MAOI is not the problem. Here it is:

5-hydroxytryptamine receptors in the human cardiovascular system.
Kaumann AJ, Levy FO.

Whoops, how stupid of me. Well asife for that, what thinks you of the SF5 at the end of the chain. SF5Cl onto an alkene yields -CH-CH2-SF5
!
Cl

The chlorine can be chopped off with NaBH4...

 

[funknsoul1]

this probably isn't intelligent, it's just my subjective experience but: 2c-t-7 is quite powerful and beautiful, but I personally won't do it again. Something about it feels incredibly toxic to me (not just weird, i'm used to phenethalymines/tryptamines).... I can't stand up on 2c-t-7 because my stomach is SO queezy about the whole time, it gives me headache, and when i do puke - i feel like i'm going to puke out internal organs. I know people react differently, but I would guess it's somewhat toxic... It wouldn't let me stop puking even once everything was gone (dry heaving - painful).

Is it any more toxic than something like cocaine though?... who knows, i wouldn't think so, but i don't know. If you really get something out of a chemical, it's worth a lil toxicity in my opinion... but DEFINITELY only dose oral.

 

[elfdancer]

^ funknsoul: What dosage(s) have you tried? You also suggest oral admin; have you tried both oral and nasal?

After vomiting & dry heaves, were you able to recover your trip? (And, youch! that's an unfortunate effect!) How'd you feel the next day/week?

 

[Loki Laufey]

so a combo of t7 and yohimbe would be bad?
i have used t7 a few times and am keen to use it again

youhimbine is an anxiety inducing agent, so combining yohimbine with any psychedelic is a bad idea, unless a panic attack is your idea of fun.

 

[tadfish]

saline

Ideally you would restrain them and then administer IV/IM benzodiazepines and IV saline (especially if there is vomitting) keeping close attention to their BP and heart rate. This is probably what the hospital would do, too. If they're going to die/become comatose, it will happen within 4-5 hours of administering the drug orally, 1 hour nasally, or 5-20 minutes IM most likely.

what does the saline do?

 

[tadfish]

piperazines

youhimbine is an anxiety inducing agent, so combining yohimbine with any psychedelic is a bad idea, unless a panic attack is your idea of fun.

I have heard alot of piperzines cause panic attacks
like mcpp and meopp?
hmmm

 

[nuke]

what does the saline do?

When you have constant, repeated vomitting there's a pretty heavy loss of fluid and sodium, the saline helps to restore that, as well as not requiring them to get up and drink water.

 

[clubberdude]

TRA

Hmm well now that i re-read that paper it doesn't look like 2CT7 is even in there, all of those compounds have R7= CH3 or CH2CH3 which means they are the amphetamine analogues, not the phenethylamines.

From Table 1 it looks like the two strongest MAO-A inhibitors are compounds #22b and #29, these being 2,6-dimethoxy-4-ethylthioamphetamine (so psi-ALEPH-2 if we extend Shulgins naming system) and 2,4-dimethoxy-6-chloroamphetamine.

So i was mistaken, there is no evidence from this paper showing whether 2CT7 is an MAO-A inhibitor, or how strongly it might produce this effect. However id say its pretty clear that many structurally related compounds are MAOIs, and i would still cite this as a likely cause for those deaths given that MDMA and/or other stimulants were involved in two of the cases.

EDIT:

Ah yes,



So the referance i should have given for 2CT7's MAO inhibition was their #11 from this paper;

Scorza, M. C.; Carrau, C.; Silveira, R.; Zapata-Torres, G.; Cassels,
B. K.; Reyes-Parada, M. Monoamine oxidase inhibitory properties
of some methoxylated and alkylthio amphetamine derivatives:
structure-activity relationships. Biochem. Pharmacol.
1997, 54, 1361-1369.

Thought id seen actual numbers for 2CT7 somewhere!

So from this paper, a positional isomer of DOC (2,4-dimethoxy-6-chloroamphetamine) is a MAOI? How does this relate to DOC (the 2,5-dimethoxy-4-chloroamphetamine variant)? Is that also exhibit powerful MAOI effects? (I suspect 2,5,4-DOC might have slight MAOI properties as it is an amphetamine, but could be completely wrong about that).

Unfortunately I cannot access the document as my internet connection (through a dongle) prevents the site from loading (seems to do this to a lot of sites...)

(Apologies for thread resurrection, just that the MAOI properties of psychedelics is a topic of great interest to me at the moment)

 

[tryp2fun]

Rather than being inhibitors, 2C-T2 and 2C-T7 are substrates for MAO A and B, as is shown in the paper below. The corresponding amphetamines are inhibitors, as expected since amphetamines are resistant to MAO oxidation.

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.

 

[specialspack]

Am I being completely stupid - I can't see 2C-T-7 mentioned in the Scorza paper...?

Is it possible to both be a substrate of and an inhibitor of MAO..?

 

[ebola?]

Is it possible to both be a substrate of and an inhibitor of MAO..?

Yes. To some degree, all substrates of catabolic enzymes are competitive (usually reversible) inhibitors.

ebola

 

[specialspack]

Yes. To some degree, all substrates of catabolic enzymes are competitive (usually reversible) inhibitors.

ebola

I suppose I mean inhibit by another mechanism rather that by being a substrate... is there another mechanism for reversible inhibition?

Or is it that the things we call inhibitors are simply just substrates with a stronger affinity than the endogenous substrates..?

 

[ebola?]

I suppose I mean inhibit by another mechanism rather that by being a substrate... is there another mechanism for reversible inhibition?

Yes, you can have non-competitive reversible inhibitors, whereby the inhibitor bonds to the enzyme somewhere other than its active site, but still distorting the enzyme's geometry, thereby preventing substrates from bonding with the active site. The enzyme inhibition will be reversible insofar as the chemical reaction flows easily in the opposite direction (eg, with hydrogen bonding).

ebola

 

[Morninggloryseed]

Perplexing, all these years later upon reflection. I took 2C-T-7 more than anyother '2C' besides maybe 2C-B...it always felt harmless to me. I intentionally overdosed on it (back in 2000 @ 70mg orally), before the deaths happened and odd dose/response curve was well known, and really before enough people had tried the 2Cs (beyond 2C-B) to know they are not like LSD, and that you can not take 10X your max dose and be guaranteed to be ok physically. At 70mg, it was very uncomfortable but only in that the body-buzz/energy outweighed the benefits of return. At 60mg (a dose I have taken at least 3 times) I always had a grand time, and never felt physically uncomfortable beyond the expected purge.

In 2000, I also took it mixed with MDA and MDMA and honestly never felt concern for my health. I am not suggesting that mixing MDMA and 2C-T-7 is a healthy thing to do. I have also taken AET, never felt any physical danger, but my research says even one dose can result in non-reversible changes in neurochemistry. The boat is still out on MDMA...the data which was presented to keep it illegal was bogus, but other subsequent studies are still suggestive of some neurotoxicity.

Like I said, perplexing. For a time (2000-2002) 2C-T-7 was pretty popular, enough to inspire Rolling Stone to do an article about it. However, the rate of deaths is still lower than SSRIs and alcohol-related deaths in any year. Prescription drugs, even outside of opiate/depressant over-dosages, still kill 1000s per year, whether due to inherent toxicity, or mistakes at the pharmacy/incompetent doctor.

Do we really know what this does in a human? Is the petri dish always representative of the complexity of brain chemistry in the live person? If the deaths (of which there were 3 or 4?) were only associated with high-dose 2C-T-7 snorted/MDMA mixture I would be less dismissive, but these deaths seem too varied and sporadic to make any final conclusions in my opinion. I would argue most people should not take 2C-T-7, but they still have human prescription drugs that ARE DEFINITIVELY more toxic than T7 (SSRIs come to mine) and probably in your medicine cabinet now. Most should just play it safe and stick with 2C-B, it has been used by far more people, for a much longer time, and I am unaware of any deaths associated with it.

I still plan on a 2C-T-7 trip sometime when I feel up to a trip that lasts longer than DMT and 4acoDMT (my go-to psychedelics of choice) but I am not the casual experimenter.

 

[Chemical Wizard]

I like 2C-T-7 a lot. But it's a really intense drug that lasts a long time. I'm not too sure when I'll do it again, but I would like to experiment again. I would never do more than 30 mgs though. 20-25 seems like a nice level for me with this one. The trip seems very cosmic, yet grounded, and there's a huge amount of euphoria. I've never vomited from it, but I feel very queasy on it, and usually get a headache while coming down. I thought it was one of the harshest 2C drugs. Even compared to 2C-E, 2C-T-7 just felt much more intense in the body. The day after a 2C-T-7 trip I always remember feeling pretty drained.

 

[Daisybabe]

Perplexing, all these years later upon reflection. I took 2C-T-7 more than anyother '2C' besides maybe 2C-B...it always felt harmless to me. I intentionally overdosed on it (back in 2000 @ 70mg orally), before the deaths happened and odd dose/response curve was well known, and really before enough people had tried the 2Cs (beyond 2C-B) to know they are not like LSD, and that you can not take 10X your max dose and be guaranteed to be ok physically. At 70mg, it was very uncomfortable but only in that the body-buzz/energy outweighed the benefits of return. At 60mg (a dose I have taken at least 3 times) I always had a grand time, and never felt physically uncomfortable beyond the expected purge.

In 2000, I also took it mixed with MDA and MDMA and honestly never felt concern for my health. I am not suggesting that mixing MDMA and 2C-T-7 is a healthy thing to do. I have also taken AET, never felt any physical danger, but my research says even one dose can result in non-reversible changes in neurochemistry. The boat is still out on MDMA...the data which was presented to keep it illegal was bogus, but other subsequent studies are still suggestive of some neurotoxicity.

Like I said, perplexing. For a time (2000-2002) 2C-T-7 was pretty popular, enough to inspire Rolling Stone to do an article about it. However, the rate of deaths is still lower than SSRIs and alcohol-related deaths in any year. Prescription drugs, even outside of opiate/depressant over-dosages, still kill 1000s per year, whether due to inherent toxicity, or mistakes at the pharmacy/incompetent doctor.

Do we really know what this does in a human? Is the petri dish always representative of the complexity of brain chemistry in the live person? If the deaths (of which there were 3 or 4?) were only associated with high-dose 2C-T-7 snorted/MDMA mixture I would be less dismissive, but these deaths seem too varied and sporadic to make any final conclusions in my opinion. I would argue most people should not take 2C-T-7, but they still have human prescription drugs that ARE DEFINITIVELY more toxic than T7 (SSRIs come to mine) and probably in your medicine cabinet now. Most should just play it safe and stick with 2C-B, it has been used by far more people, for a much longer time, and I am unaware of any deaths associated with it.

I still plan on a 2C-T-7 trip sometime when I feel up to a trip that lasts longer than DMT and 4acoDMT (my go-to psychedelics of choice) but I am not the casual experimenter.

MGS, I loved your 2-ct-7 reports on Erowid, you inspired me to write one of my own back then as well. I was just curious if you knew of any research on whether the synthesis remains stable or degrades over time. I have been saving a small amount from my original batch in 2002 (Holy crap can that really be 10 years ago now? Damn!) for the proverbial rainy day. Any idea on whether it is still viable, or more importantly, whether it might have devolved into something toxic?

 

[sekio]

The general consensus is that unless you're doing something silly like storing them under UV lights, 2c-x drugs do not degrade appreciably at all.

 

[Daisybabe]

^^Thank you for the reply!