Author Topic: 4-halo meth and the making of it  (Read 6917 times)

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  • Guest
4-halo meth and the making of it
« on: September 29, 2004, 06:39:00 AM »
wouldn't this be fairly easy? and more potent? 4-fluro is pretty good, but shit, how about 4-iodo?

would this

not work just find on meth?

and, just as a side, is there anything similar one can do to cocaine?


  • Guest
They are neurotoxins
« Reply #1 on: September 29, 2004, 02:33:00 PM »

Post 353424 (missing)

(Rhodium: "4-chloro, 4-bromo and 4-iodoamphetamine are all ...", Chemistry Discourse)

Post 483358

(Rhodium: "PFA is no "neurotoxic 4-haloamphetamine"", Methods Discourse)


  • Guest
DOI, dosage and 4-haloamphetamines
« Reply #2 on: September 30, 2004, 09:22:00 AM »
if 4-haloamphetamines follow they same path to potency that DOI does vs other PEAs then the evidence of neurotoxicity might be based on massive over doses. what if a dose of 4-Br meth is like 1mg?


  • Guest
still toxic
« Reply #3 on: September 30, 2004, 10:04:00 AM »
You can be sure that when something is referred to as being neurotoxic, that it is; no matter how little you ingest. In other cases, enough rats have left their life to prove the "neurotoxicity at higher doses", and for establishing an LD50...

In the case of 4-Br-amphetamine, the neurotoxicity is apparent even at low doses, if I remember right - in human trials, several subjects experienced parkinson-like tremors over the course of the following week after ingesting several milligrams under medical supervision!
(ugly stuff IMO!)

EDIT: Apparently my memory didn't serve me right; it was several miligrams per kilo of body weight, not overall dose....



  • Guest
« Reply #4 on: September 30, 2004, 10:12:00 AM »
Mono-substituted amphetamines does not have potencies in that range, 50-250mg are common in humans for 4-methylthio-, 4-methoxy-,  4-fluoro-, and 4-methyl-amphetamine.

As for the effects, here is an example:

Postural changes, tremor, and myoclonus in the rat immediately following injections of p-chloroamphetamine
JH Growdon, Neurology, Vol 27, Issue 11 1074-1077 (1977)

A single dose of p-chloroamphetamine, 10 mg per kilogram, produced postural abnormalities, tremor, myoclonus, and autonomic signs in rats 5 minutes after intraperitoneal injection. This syndrome lasted 60 to 90 minutes, and its intensity was directly proportional to the amount of p-chloroamphetamine given over a 2 to 10 mg per kilogram range. Whole-brain levels of serotonin and 5-hydroxyindoleacetic acid were not altered during this interval, although both were reduced significantly 1 day later. Pretreatment with drugs that interfere with the uptake of p-chloroamphetamine into terminals of serotonergic neurons (fluoxetine), depress brain serotonin levels (p-chlorophenylalanine), or block serotonin receptors (methiothepin or methergoline) suppressed this syndrome, whereas drugs that antagonize the effects of dopamine, norepinephrine, and acetylcholine did not. These observations implicate serotonergic mechanisms and provide behavioral evidence of p- chloroamphetamine's immediate actions on serotonergic neurons in the central nervous system.

Long-term effects of p-chloroamphetamine and related drugs on central serotonergic mechanisms
E Sanders-Bush, JA Bushing and F Sulser
Journal of Pharmacology and Experimental Therapeutics, Volume 192, Issue 1, pp. 33-41 (1975)

Earlier studies from our laboratory have demonstrated a marked reduction in the brain level of 5-hydroxytryptamine (5-HT) and in the activity of tryptophan hydroxylase which persists for several weeks after a single dose of 10 mg/kg of p-chloroamphetamine (PCA). In the present study, equally long-lasting decreases were found after the administration of 5 mg/kg of PCA. p-Chloromethamphetamine also caused long-lasting reductions in the level of 5-HT and the activity of tryptophan hydroxylase in brain, whereas the effects of fenfluramine had disappeared 2 weeks after injection. The ability of brain synaptosomes to take up 5-HT was markedly reduced following doses of 2, 5 and 10 mg/kg of PCA. The in vitro addition of PCA to synaptosomal fractions markedly reduced the uptake of dopamine and norepinephrine; however, only a 30% reduction in the uptake of these amines was found in synaptosomes prepared from brains of rats treated with PCA. The effects on catecholamine uptake disappeared within 1 day after injection. In contrast, the time course of recovery of the synaptosomal uptake capacity for 5-HT followed a pattern similar to that found for the recovery of the level of 5-HT and the activity of tryptophan hydroxylase, with a 50% reduction still present 3 months after the injection of 10 mg/kg of PCA. The greatest reductions of 5-HT, tryptophan hydroxylase activity and synaptosomal uptake were found in the midbrain, hippocampus and striatum with less pronounced effects in the hypothalamus, medulla-pons and spinal cord. At both 1 and 14 days after injection of 5 and 7.5 mg/kg of PCA, tryptophan hydroxylase activity in whole brain was reduced by 50% or more; however, 4 days after treatment the activity of the enzyme was reduced only slightly or not at all. The results indicate that different independent mechanisms are responsible for the initial, reversible and the prolonged, irreversible effects of PCA on serotonergic neurons.


  • Guest
thus a human trial with a 1mg dose, which...
« Reply #5 on: October 01, 2004, 06:12:00 AM »
thus a human trial with a 1mg dose, which would be sane, imho, has not been tried. btw, i tested mk-801 on myself, so this is not new territory for me.

considering what taking 1mg/kg of body weight of DOI would do to you....

the rats stuff is useless, and it might have been a massive overdose - didn't y'all even read shulgin?


  • Guest
So you think DOI is a good compound to make...
« Reply #6 on: October 01, 2004, 07:42:00 AM »
So you think DOI is a good compound to compare to just because it has a 4-halogen? Please consider that it has quite a different pharmacological profile and mechanism compared to 4-haloamphetamines, and you are talking about N-methyl amphetamines which are generally even further away from hallucinogenic phenethylamines. Arguments based on DOI have no merit in this realm.


  • Guest
i would agree with this about DOI and 4-Br-A.
« Reply #7 on: October 02, 2004, 10:21:00 AM »
i would agree with this about DOI and 4-Br-A. but still...

consider - why was there never a 2,4,5-BrPEA? what would this compound do?

 but consider:  i personally field tested mk-801, a notorious neurotoxin. in research, it is usually given to mice at 1-10mg/kg body weight, which causes SERIOUS NAN/brain damage. it turns out that for human, a "recreational" dose of mk-801 is about 3 MICROgrams/kg.

the "" are because mk-801 is not actually fun. it produces involutary unending telepathy and weird memory gaps. just fyi.


  • Guest
« Reply #8 on: October 09, 2004, 10:10:00 PM »
yeah ok telepathy you seem like a pretty smart guy (just a little stubern for trying to argue with rhodium :) ) and now your saying u belive in telepathy? ok byby