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beta-isopropylaminonaphathalene, aka Naphthylaminopropane

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Bluelighter
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Oct 20, 2008
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This one is supposed to release NE, 5-HT, and DA. Anyone tried it yet? If so, what were the subjective effects?
 
Am I parsing the non-IUPAC name correctly when i say it's structure is "Amphetamine with a napthyl group in place of the phenyl group, with the second ring where the 3 and 4 positions would be in amphetamine"?

If so, that'd be an interesting compound. The shape is similar to MDA, but with a completely different ring structure. Also, the metabolic fate of it could be a bit scary, for the same reason that we're worried about the JWH's. I have no information on it, but i'd be curious to know what it did when dumped into someone - just not me!
 
http://en.wikipedia.org/wiki/Napthylaminopropane

Naphthylaminopropane (NAP; PAL-287), also known as naphthylisopropylamine or alpha-methylnaphthylethylamine, is psychoactive drug currently under investigation for the treatment of alcohol and stimulant addiction.[1] It acts as a non-neurotoxic releasing agent of serotonin, norepinephrine, and dopamine, with EC50 values of 3.4 nM, 11.1 nM, and 12.6 nM, respectively
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A possible limitation of naphthylaminopropane is that it also has high affinity for the 5-HT2C receptor,[3] which is suggestive that it may have significant anorectic effects.
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So it's a monoamine releaser, leaning on 5ht release over DA and NE, with 5HT2C agonism... Sounds nifty otherwise but that 5ht2c sounds a bit iffy...
 
this one with 2-thienyl would have strong vasoconstrictor properties, i remember someone assayed it on hyperlab.info and said that stimulation was better than amphetamine but those damn vasoconstrictor properties are bad.
 
fastandbulbous said:
^ What like another panicogen (a la phenylpiperazines)


If you want a better aromatic group, replace the phenyl of amphetamine with a 2-thienyl group
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Hm, on what grounds do you think it would be piperazine-like garbage?

The structure is not really similar to the phenyl-pipes (more similar structurally to MDA/etc), and you can't tell from the release activity of the phenylpiperazines that they suck... Are you aware of human tests of it that indicate that it sucks?
 
Hm, on what grounds do you think it would be piperazine-like garbage?
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It was made clear already. It's a 5HT2c Agonist. 5HT2c Agonists are known as panicogens for a reason: they cause anxiety and panic, increase the risk of suicide and depression, and are downright nasty.

Phenylpiperazines are 5HT2c Agonists.
This is a 5HT2c Agonist.

5HT2c Agonists are known to promote anxiety and depression.

What's so hard to understand about this?
 
Wouldn't everything depend on the strength of monoaminergic release, the ratios of the monoamines released, and then the strength of 5ht2c agonism? IIRC, the former is rather weak in 'NAP', suggesting that it wouldn't make a good recreational drug. I wish it did though, as the slang would be top notch:

"Dude, you wanna take a nap?"

ebola
 
Yeah, of course. If the 5HT2c agonism were weak, then the fairly potent SE, NE and DA release would come to the fore, of course. In this case, though, that doesn't seem likely.
 
Ah, the 5HT2C agonism causing panic/anxiety was something i was not aware of.

I wonder about the non-neurotoxic bit too. Someone else posted this big blob of articles about MDMA metabolites and neurotoxicity, which i havn't had a chance to study: http://www.neurotransmitter.net/mdmametabolites.html
since we're concerned about MDMA-style neurotoxicity (i assume), it's relevant to know if it's inherant to the monoamine release (as is the prevailing theory here), or a result of metabolites of MDMA-like drugs that causes the neurotoxicity of MDMA.
 
Non-neurotoxic because it's generally a crappy releaser of monoamines and basal levels of DA don't go sky high like they do with METH. Duration is supposedly long so I doubt there's a lot of abuse potential. Also has the naphthalene ring which puts its toxicity to other organs into question.
 
boohigh said:
this one with 2-thienyl would have strong vasoconstrictor properties, i remember someone assayed it on hyperlab.info and said that stimulation was better than amphetamine but those damn vasoconstrictor properties are bad.
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Yo Boohigh, could you please post a copy of that assay or a link? I would really appreciate any further data on this compound.

Thanks a lot! - Murphy
 
What degree of 5ht2c agonism engenders moderate to severe anxiety? How do mcpp's other fx affect those of its agonism there?
 
Another intriguing triple-releaser - Napthylaminopropane

I am new to bluelight (obviously) but was wandering across the fora and wikipedia when I stumbled across this chem which I am curious why it has been overlooked in the search for intriguing new empathogens that don't end up producing that awful nasty alpha-methyldopamine et al. http://en.wikipedia.org/wiki/Napthylaminopropane is the substance I'm curious about. It would seem to follow from what we know of MDA that s-NAP would avoid the 5HT-2C agonism, so perhaps that's a way to avoid the unwanted anorectic effects? Anyhow, I'm following all the new research as best as I can and catching up on what I don't know as I go on these new triple-releasers, as they're something I think that there is a significant potential in, for the future of humanity to be honest. Imagine if you could have the empathic connection of mdma without the toxicity, wouldn't that be a wonderful thing? We really need to work on finding the right substance or substances to produce this effect, I really believe it will do a lot to help everyone. Of course I could just be an idealistic tripper but whatever. Anyhow, anyone have any info on NAP? I'm curious, and can't find much about it.
 
At what dose has this stuff been checked for neurotoxiticy? 5-IAI probably doesnt have the same toxic metabolites as MDMA and is therefor only very slightly neurotoxic, but its still neurotoxic. It seems to that both strong serotonin/dopamine release causes some neurotoxiticy.

Now my next question, has the releasing ability of this compound been screened with reserpine? It maye just be a poor releaser compared to the reuptake inhibition.
 
Re: neurotoxicity, this article (full text) reports the following:

"The ability of PAL-287 [naphthylaminopropane] to induce long-term depletion of brain 5-HT (i.e., neurotoxicity) was determined by administration of three sequential doses (18 mg/kg i.p.) every 2 h. As positive controls, other rats received (+)-methamphetamine (6.0 mg/kg i.p.) or (+/-)-MDMA (7.5 mg/kg i.p.) administered according to the same schedule. Rats were sacrificed 2 weeks later and cortical 5-HT levels determined...The results indicated that whereas both (+)-methamphetamine and MDMA decreased cortical 5-HT, PAL-287 did not. None of the treatments depleted cortical DA."

Re: releasing potency vs. reuptake inhibition potency, there's only one mention of reserpine in the article, in the methodology section for in vitro release assays. I don't know enough about the subject to interpret what exactly is happening, but there don't seem to be data tables of the sort found in rocknroll714's 5-IAI thread.

However, on page five there are some nice graphs of extracellular dopamine and serotonin in the rat prefrontal cortex, plotted vs. time, for both this compound and (+)-amphetamine. Both of them were able to raise extracellular dopamine levels to 500% of baseline (it took a total of 1.3 mg/kg injected for amphetamine, and 4 mg/kg injected for this stuff), but while amphetamine barely affected serotonin levels at all, the 4 mg/kg total dose of naphthylaminopropane raised extracellular serotonin levels to 900% of baseline. Fascinating stuff - apparently these concentrations were determined by microdialysis of the rats' cerebrospinal fluid at 20 minute intervals! Unfortunately I don't know what this means for releasing vs. reuptake inhibition potency; both of those would increase extracellular monoamine levels. I'd appreciate it if someone more knowledgeable could weigh in here...!
 
utfse gives the above thread, and it's already been discussed as to why it probably wouldn't make a good drug of abuse.
 
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