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I think as with 2ct-7 S dealkylation occurs, quick google search revealed that this happens, in a minor degree but it happens. Which liver enzyme is responsible I don’t know.
 
izo said:
I think as with 2ct-7 S dealkylation occurs, quick google search revealed that this happens, in a minor degree but it happens. Which liver enzyme is responsible I don’t know.
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So taking 2c-t-21 parenterally would eliminate this problem?
 
I don’t think there is a Problem when not dosed daily. And no, once the substance has left your receptors it should pass your liver.
 
Ok, thanks.

So hypothetically, if someone had access to the thio version of 2c-tfm (2c-t-tfm) this would generate what metabolite after the s-dealkylation?
 
CRYSTAL8 said:
Ok, thanks.

So hypothetically, if someone had access to the thio version of 2c-tfm (2c-t-tfm) this would generate what metabolite after the s-dealkylation?
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Do you mean the version with a S-CF3 substituent? I doubt S-dealkylation would occur, the main metabolites would probably be the the corresponding sulfoxide and sulfone.
 
4meSM said:
Do you mean the version with a S-CF3 substituent? I doubt S-dealkylation would occur, the main metabolites would probably be the the corresponding sulfoxide and sulfone.
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Yes, i just thought it might follow the same metabolism pathways as t-21 or t-7. Thanks for your answer
 
4meSM said:
I doubt S-dealkylation would occur,
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Do you mean That no s-dealkylation occurs with a CF3 ether or in general? If so, why? S-dealklyation occurs at least with 2c-7…
 
izo said:
Do you mean That no s-dealkylation occurs with a CF3 ether or in general? If so, why? S-dealklyation occurs at least with 2c-7…
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Because oxidative dealkylation typically involves the hydroxylation of the carbon adjacent to the heteroatom (either O, N or S) and that doesn't really happen when you have a CF3 group, at least as far as I know. Here's an example:
N-Dealkylation-mechanisms-of-b-blockers-by-CYP450-enzymes-and-by-electrochemical.png

In the case of 2c-t-7 dealkylation can occur but I don't think it's the main metabolic pathway, a thioether group is really easy to oxidize so I bet the sulfoxide is formed faster.
 
Ah, you’re right, didn’t think of it. The Enzyme needs at least on CH bond for attacking the thioether. Just read that with 2ct-7 dealkylation occurs but is not the main pathway of degradation.
 
izo said:
I think so, yes.
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But in @4meSM‘s example a tert-butanol group (or however that substitution is called) was N-desalkylated, no? Shouldn‘t that be similar to the t-Butyl or CF3 group?
 
In the case of 2CT-21, won't the S oxidize? I notice that Shulgin did not produce analogues with the S in +4 or +6 oxidation states. Yes, it's LogP will not be as good BUT I have often wondered if it's these oxidation products are the toxic species associated with 4MTA and such.
 
Why is especially midazolam so weak, judging from its structure it should be fully Active at 2mg, but its given up to 15mg. Is it the imidazole Ring, contrary to the usual triazolo ring?
 
It will readily form water-soluble addition salts so it can be injected. Other benzos are used IV using propylene glycol or an emulsion to dissolve them but both of those options may lead to complications.
 
does anybody know the structure of 8FA? its supposed to be a cannabinoid.
 
izo said:
does anybody know the structure of 8FA? its supposed to be a cannabinoid.
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It's sad that these RC vendors sell stuff like this without even showing a structure. I would be apprehensive that they even know what it is.
 
I'm prepared to bet 8FA is a JWH-021 with an -F at the end of the N-alkyl chain OR it's the indazole analogue of same. The -F was added so that it wouldn't be covered by the CsA,

I suggest that it's likely less potent than the analogues with shorter chains (N-pentyl seems the most active) BUT it will be more lipophilic and the -F will stop the body from metabolising that alkyl chain.

I have said it before, but one of these synthetics (of the thousands out there) is going to prove to have a serious toxicology issue. It's inevitable. I, for one, think that these drugs should be taken more seriously. It's just a matter of time before one of them is genotoxic, mutagenic and/or carcinogenic. Of course, that kind of toxicity can take years or even decades to show itself but I can imagine in 2040 a sudden spike in cancer cases and researchers will fists discover it's people who used these synthetics.... and then they will have to test each to find which one(s) are responsible.
 
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