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Stimulants of the Future III

Ah yeah, do I? Who said that?

To be honest, I do not consider a university's degree the deciding qualification. I've seen some Bluelighters, who admitted to not have a degree, but still impressed me immensely with their autodidactically aquired skills. Obviously, Opie_OC ain't one of them.

Opie_OC said:
How about Diactel-amphetamine-propyl-glycol-amine-MD-codone?
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It's spelled "diacetyl" you dishonourable imbecile!

Or maybe I'm the idiot, lol.
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Now you've got it. Saved myself to name it.


- Murphy
 
For no good reason, obviously. Since MMDA-2 doesn't produce amphetamine-appropriate responding and very weakly serotonin or dopamine (I dunno about reuptake inhibiting effects), it's really unlikely that bk-MMDA-2 and these N-methyl and N-ethyl derivatives are going to be wonderful.

MMDA-2 is a 5HT2a agonist, but we know that these cathinones are awful 5HT2a agonists, so I can't possibly fathom why anyone would suggest these.

Probably very weak stimulants (if at all) and probably very weak 5HT2a agonism. Maybe they'd be active at MDMA-like doses, but I'd put my money on mescaline-like. By that point, though, who knows what sort of peripheral effects would be killing you.
 
Chloramphenicol has side-effects listed like:
- (reversible) damage to the bone marrow; independent from the dose can up tto 2-8 weeks after application an irreversible aplasia of the bone arrow occur*
- Grey-syndrome*
- neurotoxicity
- sensitization upon topical contact
- allergic reactions, including anaphylactic reactions* and generalized urticaria upon systemic administration
- Herxheimer-reaction
- in rare cases: irreversible form of aplastic anemia*​
* potentially resp. certainly lethal!

With clonazepam (as well as with other nitro-containing benzodiazepines like nitrazepam), the usual therapeutic dose is 10-15 1.0-1.5 mg. That's almost nothing...

Not the best examples, I'd say. :\

When talking about stimulants, consumers notoriously tend to use larger doses, repeat dosing and go on binges. In such cases, when the liver is already under considerable stress, the toxicity of nitro-aromatics can unfold easily:
The reductive metabolism of aromatic nitro-compounds goes to the corresponding amine, -NH2, a pathway that passes through the corresponding nitroso-derivative, followed by the hydroxylamines. That was shown to happen with clonazepam, too (Fundam Clin Pharmacol 1993, 7, p.69). All mentioned intermediates, as well as the final anilines are not exactly healthy. The lack of serious and frequent side-effects for the benzodiazepines containing a nitro-group can be easily attributed to their low dosage.

Concluding, I'd still say with certainty that even if there may be exceptions, nitroaromatics are not the first choice in medicinal chemistry due to the frequently occuring toxicological problems associated with them.


Peace! - Murphy
 
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...which are supposed to tell me what exactly?

1. 4-nitromethcathinone does not equal DON. Dosage for 4-NO2-methcathinone is probably much larger than for DON.

2. 2,5-dimethoxy-4-nitroamphetamine (DON) is active in the one-digit mg-range. That's the dosage that applies for the benzos, too... Therefore, same reasoning as before: Very low dose, hence not very likely to see toxic side-effects.

3. Experience reports usually contain information about the quality of the 'high'. The toxic side-effects have nothing to do with the psychoactive effects. So what?


- Murphy
 
reports about one chemical that's taken occasionally are meaningless. but you should know that if you're literate.


I disagree with murphy though. The sort of toxicity usually claimed with these things is hepatic --> but that's not apparently an issue with nitro aromatics, and additionally, if the toxicity were associated with the nitro aromatic group, you'd expect there to be consistent toxicity across a wide range of of drugs. Instead there's different toxicity across a wide range of things. That seems way more likely to be the result of the class of drug than the presence of a potentially reactive group.

aromatic amines, OTOH, are indeed known to be hepatotoxic --> and that's consistent across a wide range of unrelated compounds. Yes, the nitro aromatics can be reduced to aromatic amines, but apparently it doesn't happen in the liver or it doesn't happen enough or else you'd be seeing liver issues with these drugs too.
 
"Toxicity of nitrobenzene compounds towards isolated hepatocytes: dependence on reduction potential"
Xenobiotica 1990, 20(9) , p.945
DOI: 10.3109/00498259009046910)
1. The cytotoxicity of ρ-substituted nitrobenzenes towards isolated hepatocytes under aerobic or hypoxic conditions has been determined. The nitrobenzene concentration required to cause 50% cytoxicity in 2h was a function of the one-electron reduction potential of the nitrobenzene, with the more cytotoxic compounds having the strongest electron-withdrawing substituents.

2. The effectiveness of the nitrobenzenes at causing cytotoxicity under aerobic but not hypoxic conditions was markedly increased if hepatocyte catalase was inhibited with azide.

3. Nitrobenzenes at cytotoxic concentrations induced cyanide-resistant respiration in isolated hepatocytes. Their effectiveness correlated with their cytotoxicity.

4. The rate of oxygen activation of these nitrobenzenes by ascorbate was also a function of the one-electron reduction potential. The nitro compounds with the strongest electron-withdrawing substituents were the most rapidly reduced.

5. Most nitrobenzenes were more cytotoxic under aerobic than hypoxic conditions. Ascorbate enhanced hypoxic, but not aerobic, cytotoxicity.

6. It was concluded that the cytotoxicity of different nitrobenzenes is related to their ease of reduction to nitro radical anions and nitrosobenzenes. Aerobic cytotoxicity is probably initiated by redox cycling and oxygen activation by the nitro radical anions whereas hypoxic cytotoxicity is probably initiated by the alkylation of macromolecules by nitrosobenzene metabolites.
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More later.

- Murphy
 
Yah I guessed so too...if not many benzodiazepines would show to be quite hepatotoxic. Or maybe they could be but the normal dose is relatively small to show signs of toxicity.

BTW could someone remind me at what place does the nitro substitution stand in the electronegativity scale?
 
Onandoff said:
Anybody have experience with Troparil yet? Looks as good as coke or better.
I will be testing the sample I'm getting very soon.
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How exactly does it look "as good or better" as coke?

To me, it looks like a pretty run-of-the-mill DNRI.

Troparil is documented to be a few times more potent than cocaine as a dopamine reuptake inhibitor,[1] but is less potent as a serotonin reuptake inhibitor,[2] and has a duration spanning a few times longer
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Troparil is the only regular phenyltropane having a NET affinity that exceeds the DAT affinity.
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Isn't that exactly what coke is? Is the serotonin reuptake inhibiting effect that important? it doesn't seem that people especially enjoy SSRIs.

effect at NET is important too. I've seen more than one study that found NE being most related to euphoriant properties, and DA being most related to addictiveness (not that they're exactly seperable.)
 
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