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Question concerning 4-Methylaminorex

Dysphoric

Dysphoric

Bluelighter
Joined
Feb 3, 2010
Messages
392
Why isn't this used as a prescription? It has all that prescription Meth/Amphetamines have to offer, along with a much longer duration.

Main reason I'm curious is beacause of this;

There have been three studies studying possible neurotoxicity of 4-methylaminorex. First study[12] using quite high doses (highest dose caused clonic seizures and some rats died) in rats and studying short term effects (rats were killed 30 min to 18 h after injection of 5, 10 or 20 mg/kg of racemic cis-4-methylaminorex) suggested reduction in tryptophan hydroxylase (TPH) activity (a possible marker for serotonin neurotoxicity) but citing study: "No change in TPH activity was observed 30 min after injection; by 8 h the activity of this enzyme appeared to be recovering." and "this agent is significantly less neurotoxic than methamphetamine or MDMA."
Study[13] published 2 years later than first one also suggested reduction in tryptophan hydroxylase activity, they used quite high dose too (10 mg/kg of cis-4-methylaminorex) and studied also long term effects (rats were killed 3 h, 18 h or 7 days after injection), they found reduction of 20-40% of tryptophan hydroxylase (TPH) activity and "recovery of TPH activity occurred 18 h after treatment, but was significantly decreased again by 7 days." but "It is noteworthy that, unlike the other analogs, the striatal levels of 5-HT did not decline with TPH activity following multiple 4-methylaminorex treatment"
Latest study[14] (using mice) was not able to find any long term effects suggesting neurotoxicity and they found instead increase in serotonin levels, they used quite high doses too(15 mg/kg of each isomers studied) "The dosages used in the present experiments are about 6-10 times than the effective doses of aminorex and stereoisomers inhibition of food intake." Doses were repeated 3 times a day and mice were killed 7 days after last dose. "Since a long-lasting depletion of dopamine or 5-HT appears to be a good predictor of dopamine or 5-HT neurotoxicity (Wagner et al. 1980; Ricaurte et al. 1985), the results suggest that the aminorex compounds except 4S,SS-dimethylaminorex, unlike MDMA or fenfluramine, are not toxic to either dopamine or 5-HT neurotransmitter systems in CBA[disambiguation needed ] mice. It was reported that although multiple doses of 4-methylaminorex caused long-term (7 days) declines in striatal tryptophan hydroxylase activity in SD rats, no changes were found in 5-HT and 5-HIAA levels (Hanson et al. 1992).[11]
That first study [11] also suggested reduced dopamine (DA) levels (a possible marker for dopamine neurotoxicity), but citing study: "However, 8 h after drug administration no differences from control values were seen in DA, DOPAC or HVA levels." and again later studies [12-13] didn't find any long term reduction.
Click to expand...

Significantly less neurotoxic, and from what I got, it seemed to actually raise Serotonin levels?

This stuff seems a hell of a lot cleaner, and beneficial.

Am I correct?
 
Hmmm... seems promising although it lasts a very long time. They probably don't want another methamphetamine on their hands. I could see the abuse potential being pretty high for this one, especially given its reported MDMA-like effects of an extremely long duration.

Pulmonary hypertension caused Aminorex to be taken off the market as well. Maybe there is a similar concern with 4-Methylaminorex?

Also note that the trans-4-methylaminorex appears to be something in the grey area.
 
Because of concerns for heart valve defects, same reason SRA's aren't used as antidepressants. Stuff would probably lead to heart problems and a lot of the same issues as AMT.
 
these compounds have a very small difference between pleasureable dosage and overdose. It's very easy to overdose on these compounds. When we look at methamfetamine we realize that it is illegal to posses and use with out script. Script being the key here as the drug still is used for medicine. if we look at aminorex it was withdrawn and never put back onto the RX listings in 1968 due to its adverse and dangerous side effects.

"During its use, an unacceptably high incidence of pulmonary hypertension was reported, which led to the deaths of several individuals" which means of course that it does indeed lead to heart problems"
(http://www.erowid.org/archive/rhodium/chemistry/aminorex.html#refs)
Please remeber that these deaths were not street related but rather from the prescribed use of aminorex.

aminorex and its sister methyl aminorex have durations of over 30 hours. Fallen in the wrong hands it could lead to very adverse effects and you'll be up longer then you'd expect;

http://www.ncbi.nlm.nih.gov/pubmed/11083709
Recreational use of aminorex and pulmonary hypertension.

http://www.ncbi.nlm.nih.gov/pubmed/3928246
Aminorex and pulmonary hypertension. A review.
http://www.ncbi.nlm.nih.gov/pubmed/3738463
[Prolonged survey of cases of pulmonary hypertension in relation to consumption of aminorex. Histological, quantitative and morphometric study of 9 cases].
http://www.ncbi.nlm.nih.gov/pubmed/389330
Pulmonary hypertension, "plexogenic pulmonary arteriopathy" and the appetite depressant drug aminorex: post or propter?
http://www.ncbi.nlm.nih.gov/pubmed/3816924
Polymorphic debrisoquine and mephenytoin hydroxylation in patients with pulmonary hypertension of vascular origin after aminorex fumarate.
http://www.ncbi.nlm.nih.gov/pubmed/7901949
[Aminorex-induced, plexogenic pulmonary arteriopathy: 25 years later!].
http://www.ncbi.nlm.nih.gov/pubmed/2399244
[Long-term follow-up of pulmonary hypertension of unknown etiology].
http://www.ncbi.nlm.nih.gov/pubmed/10458725
Aminorex, fenfluramine, and chlorphentermine are serotonin transporter substrates. Implications for primary pulmonary hypertension.
http://www.ncbi.nlm.nih.gov/pubmed/10458725
Aminorex, fenfluramine, and chlorphentermine are serotonin transporter substrates. Implications for primary pulmonary hypertension.
http://www.ncbi.nlm.nih.gov/pubmed/12163129
Therapeutic and adverse actions of serotonin transporter substrates.
http://www.ncbi.nlm.nih.gov/pubmed/20204739
The serotonin hypothesis of pulmonary hypertension revisited.
http://www.ncbi.nlm.nih.gov/pubmed/19112110
Review paper: Current strategies in the development of anti-obesity drugs and their safety concerns.
http://www.ncbi.nlm.nih.gov/pubmed/18536742
Pulmonary hypertension: therapeutic targets within the serotonin system.
http://www.ncbi.nlm.nih.gov/pubmed/15194172
Primary pulmonary arterial hypertension: a look back.
http://www.ncbi.nlm.nih.gov/pubmed/12457145
Anorexigen-related cardiopulmonary toxicity.


Conclusion
-Short term use at ordinary therapeutic doses does not appear to cause harm.
-Prolonged or high-dose use can cause significant harm.
-Patients harmed by prolonged therapeutic use may have genetically determined differences in drug metabolism. So check your genotype before deciding if aminorex is too risky for you .
-Patients harmed by aminorex use rarely recover fully.

Potency and potential abuse factors vs . other stimulants:
http://www.ncbi.nlm.nih.gov/pubmed/7889809
Evaluation of the abuse liability of aminorex.
http://www.ncbi.nlm.nih.gov/pubmed/1356272
Aminorex produces stimulus effects similar to amphetamine and unlike those of fenfluramine.
http://www.ncbi.nlm.nih.gov/pubmed/8516363
Cocaine-stimulus generalization to two new designer drugs: methcathinone and 4-methylaminorex.
http://www.ncbi.nlm.nih.gov/pubmed/9877004
Discriminative stimulus effects of S(-)-methcathinone (CAT): a potent stimulant drug of abuse.

Added note for paper one:

"Patient 1 is a 39-year-old man who owns a farm in rural
Pennsylvania. He presented in February 1993 with an 8-month
history of exertional dyspnea and syncope, and he was found to
have a pulmonary artery pressure of 56/20 mm Hg (mean, 34 mm
Hg) at cardiac catheterization. The pulmonary capillary wedge
pressure was normal, but left ventricular ejection fraction was
reduced to 40%. Patient 2, the 32-year-old wife of patient 1,
developed exertional dyspnea and syncope in November 1993.
Cardiac catheterization in August 1994 disclosed a pulmonary
artery pressure of 60/38 mm Hg (mean, 48 mm Hg).

Patient 3,
the nephew of patient 1, age 28 years, presented in January 1993
with dyspnea and light-headedness; at cardiac catheterization in
July 1993, he had a pulmonary artery pressure of 75/30 mm Hg
(mean, 50 mm Hg). No underlying cause for pulmonary hyper-
tension was found in any case, and all patients initially denied
ingestion of potentially toxic substances. Left ventricular function
was mildly and globally depressed in patients 1 and 2, although
left-heart filling pressures were normal. Pulmonary hypertension
has been persistent in all three patients, although echocardiog-
raphy in patient 1 suggested that pressures may have improved.
An investigation by federal Drug Enforcement Administration
agents resulted in indictment of patient 1 following the discovery
of a chemistry laboratory and > 20 lb of 4-methyl-aminorex, an
amphetamine analog, in a barn that was sublet on the farm.
Patient 3, who was not indicted, subsequently confirmed prior
4-methyl-aminorex ingestion."

-The pulmonary hypertension effect is genetically linked but rare, and these 3 just got unlucky.
-The pulmonary hypertension effect is genetically linked but common, so it is unsurprising that all 3 suffered.
-The pulmonary hypertension effect manifests regardless of genotype when someone has effectively unlimited (more than 20 pounds of 4-MAR!) ability to use aminorex compounds at recreational dose levels.
(speculations)

Information mostly derived from nk40ouvm

Cheers
 
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Epsilon Alpha said:
Because of concerns for heart valve defects, same reason SRA's aren't used as antidepressants. Stuff would probably lead to heart problems and a lot of the same issues as AMT.
Click to expand...

AMT? Do you have citations for that? First thing I have heard about heart problems with AMT - AET, on the other hand, I am aware of the agranulocytosis risk.

I used AMT pretty much daily, WELL BEYOND what is the "recommended" recreational dose, let alone what the prescription dose was and I had no serious issues. In fact at higher levels it had less of a body load than it did at lower ones, probably due to the absence of the amphetamine-like first 3 hours of the drug being completely eliminated by the massive flood of higher doses.

I took it daily at high doses for about 3 months and suffered no ill-effects. Not that I am recommending that to anyone.

And it appears that I was right about the pulmonary hypertension theory. Thanks for that post, rakketakke. I would honestly imagine 4-MAR to be worse than Aminorex simply because of the known correlation with 4-position amphetamines and cardiac issues (see 4-MTA for a good example of this as well as PMA, PMMA as well as the cathinones such as mephedrone and methedrone. I am sure there are others but I have yet to sleep and my brain is quite out of it.)
 
MagickalKat777 said:
I would honestly imagine 4-MAR to be worse than Aminorex simply because of the known correlation with 4-position amphetamines and cardiac issues (see 4-MTA for a good example of this as well as PMA, PMMA as well as the cathinones such as mephedrone and methedrone. I am sure there are others but I have yet to sleep and my brain is quite out of it.)
Click to expand...
The 4-position of amphetamines refers to the benzene ring, where as the 4-position in 4-MAR refers to the oxazoline ring. There is no substitution on the 4-MAR benzene ring.
 
rakketakke said:
these compounds have a very small difference between pleasureable dosage and overdose. It's very easy to overdose on these compounds. When we look at methamfetamine we realize that it is illegal to posses and use with out script. Script being the key here as the drug still is used for medicine. if we look at aminorex it was withdrawn and never put back onto the RX listings in 1968 due to its adverse and dangerous side effects.

"During its use, an unacceptably high incidence of pulmonary hypertension was reported, which led to the deaths of several individuals" which means of course that it does indeed lead to heart problems"
(http://www.erowid.org/archive/rhodium/chemistry/aminorex.html#refs)
Please remeber that these deaths were not street related but rather from the prescribed use of aminorex.

aminorex and its sister methyl aminorex have durations of over 30 hours. Fallen in the wrong hands it could lead to very adverse effects and you'll be up longer then you'd expect;
Click to expand...
This part of the post is copied not from nk4 but from another poster. Take it with a grain of salt. I should have deleted that post before it got spread
 
MagickalKat777 said:
AMT? Do you have citations for that? First thing I have heard about heart problems with AMT - AET, on the other hand, I am aware of the agranulocytosis risk.

I used AMT pretty much daily, WELL BEYOND what is the "recommended" recreational dose, let alone what the prescription dose was and I had no serious issues. In fact at higher levels it had less of a body load than it did at lower ones, probably due to the absence of the amphetamine-like first 3 hours of the drug being completely eliminated by the massive flood of higher doses.

I took it daily at high doses for about 3 months and suffered no ill-effects. Not that I am recommending that to anyone.

And it appears that I was right about the pulmonary hypertension theory. Thanks for that post, rakketakke. I would honestly imagine 4-MAR to be worse than Aminorex simply because of the known correlation with 4-position amphetamines and cardiac issues (see 4-MTA for a good example of this as well as PMA, PMMA as well as the cathinones such as mephedrone and methedrone. I am sure there are others but I have yet to sleep and my brain is quite out of it.)
Click to expand...

http://www.sciencedirect.com/science/article/pii/S016372581100074X
http://www.sciencedirect.com/science/article/pii/S0091305701006694

Its not a very solid link for AMT specifically, but it is enough to prevent it from being marketed for daily use. Its more of a 5HT2B mediated process, than a general 5HT mediated process so its hard to directly figure out the cause for various agents.

Not to mention that there are a few other pathways which 5HT releasers can cause issues, none of them are too well researched in respects to chronic use in humans however.

Sorry for being brief but I'm on call right now.
 
Enkidu said:
This part of the post is copied not from nk4 but from another poster. Take it with a grain of salt. I should have deleted that post before it got spread
Click to expand...

Why is that?

Ofcourse I do take it with a grain of salt but the evidence is rather clear... Mostly I prefer to keep the information there but this seemed relevant enough to Bluelight to share anyhow.
 
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Well I have no experience with cis-4-MAR, but I did go through 2g of trans-4-mar in just a few days time span many years ago. (and had a couple more grams I took my time with)

Speaking for trans-4-mar... this drug is extremely forgiving compared to any form of amphetamine, except maybe something like propyl-amphetamine. Yes I believe for ADHD and the likes it would be much more ideal than Adderal.

Then again something like Piracetam or a stronger nootropic might be a safer, although less immediately effective long-term solution.
 
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