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The Large and Nifty Not-quite-advanced Drug Chemistry, Pharmacology and More Thread

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Ahh.. thanks for that info. Amphetamines are really calm and relaxed.. mephedrone is also (but prob from the serotonin), MDPV and methylphenidate cause too much "sketchyness" and anxiety. I wish there was a real good cheap research chem stimulant that was as relaxed as amphetamine.

http://en.wikipedia.org/wiki/1-Phenyl-2-methylaminobutan-1-one

It's out in the wild right now, and the feedback suggests it's a very vanilla 'd-amp feeling' stimulant, which is exactly what you (and I) are looking for.

This isn't remotely advanced, but I don't think I'll get good info in OD:
what can I do with GABA powder? My original plan turned out to be a tad beyond my means (*cough*).

If I were to take some GABA, would it potentiate a GABA agonist active in the CNS by displacing the drug from somatic receptors, making said drug more likely to end up in the brain?

I can't answer your last question, although it's an interesting idea. As to what to do with all that GABA...sandmeyer!
 
I'm a sociologist. Like I said, beyond my means. :)

Dude, I'm certainly no chemist, I'm a 20 year old psych major, if I can pull it off anyone can haha.

Just out of curiosity, it's not the BN GABA, is it? I've heard from a few sources now that that powder is too impure to be used as a precursor...
 
We can't really talk about this

The short of it is, I lack the knowledge and equipment to reliably extract the product. I would also never manufacture a scheduled compound.

And it is not that brand.
 
New question: What kind of idiot first claimed JWH is supercarcinogenic? Napthol/Napthalene/their burning products are on the same level of carcinogenicity as Benzene and it's friends. And people have been smoking phenyl compounds for how long? Napthalenoyl or whatever is not an epoxide super-carcinogen as some paranoid people might have you to believe.

What kind of idiot refuses to accept the facts?

http://www.bluelight.ru/vb/showthread.php?t=474536
 
I have a funny question. How do you guys know so much about this shit? I thought I had a good understanding of Neuroscience but it's nothing compared to some people here.

After I take General Chem 1+ 2, Organic chem 1 + 2, and Biochem, will that get me a little caught up some of the people here in ADD?
 
i have a question about the metabolism of lys-amp, i understand that the lysine is cleaved by trypsin enzymes but why does this result in the delayed onset of the drug? is it that there is not enough trypsin to do the conversion all at once, so that some of the lys-amp is effectively 'waiting' while the rest is being converted?

this makes me wonder about the potential of lys-PEA which could (at the very least) take care of the need for constant redosing, and since (short) duration is correlated with habituation perhaps this could lessen the abuse potential of the drug.
 
I have a funny question. How do you guys know so much about this shit? I thought I had a good understanding of Neuroscience but it's nothing compared to some people here.

After I take General Chem 1+ 2, Organic chem 1 + 2, and Biochem, will that get me a little caught up some of the people here in ADD?

Well, it'll help. Most students just ingest stuff as quickly as possible to try to regurgitate it on exams and then forget about it. Unfortunately a bunch of the theory is kind of useless anyway, compared to actual lab experience. There are probably lots of texts at your university library to look into if you are bored and want to get ahead.
 
i have a question about the metabolism of lys-amp, i understand that the lysine is cleaved by trypsin enzymes but why does this result in the delayed onset of the drug? is it that there is not enough trypsin to do the conversion all at once, so that some of the lys-amp is effectively 'waiting' while the rest is being converted?

this makes me wonder about the potential of lys-PEA which could (at the very least) take care of the need for constant redosing, and since (short) duration is correlated with habituation perhaps this could lessen the abuse potential of the drug.

The acylation step of catalysis is rate limiting in trypsin, so probably the substrate saturates the available enzymes and the remaining lysdexamphetamine has to wait for substrate pocket availability.
 
Nope, trypsin is found in digestive system, and assuming you bypassed MAO in digestive system, it still wouldn't be more effective then let's say injected PEA.

Right. But lis-dexamp, especially in high doses, releases d-amp *LONG* after 3-4 hours in (one time I took close to 300mg and I was feeling rushes like 9 hours in), which means that at least a significant portion of lis-dexamp is making it into the bloodstream.


lis-PEA would probably not be degraded by MAO, and although a fair bit would probably be destroyed in the stomach, once you initially clog the trypsin enzymes you'd probably be able to absorb all that lis-PEA into your blood stream for a slow and steady release...

I think it's a great idea.
 
What databases and journals do you guys use for drug chemistry, pharmacology, etc? I'm getting more and more into pharmacology and drug chemistry, and I've realized once again that I have access via my university to many different resources. One in particular I know is useful is pubmed, which I do have access to. What others do you guys recommend?
 
Excellent point, but are you suggesting that lis-PEA itself is active, and not just the metabolite PEA? Because as soon as Lis-PEA is turned to PEA, it would be very prone to oxidation anywhere (even in the blood stream) by MAO-B which is present in blood cells and in the brain, if lis-PEA can even cross BBB. Injected into the blood stream, PEA is found ineffective (in Pihkal).

I am not suggesting that lis-PEA is active, especially since lis-dexamp isn't.

However, PEA is active even when taken orally. It is well documented that people can take 2-3g of PEA straight up and get a pretty intense 10 minute rush. Since MAO is more concentrated in the GI tract than in the blood, I would assume that if you could sneak the PEA past your stomach you would get, at the very least, better effects than you would orally.

Taking several grams of lis-PEA would, in fact, be very similar to having a PEA IV drip.

(someone correct me if I'm wrong here)
 
Excellent point, but are you suggesting that lis-PEA itself is active, and not just the metabolite PEA? Because as soon as Lis-PEA is turned to PEA, it would be very prone to oxidation anywhere (even in the blood stream) by MAO-B

Some of us have destroyed our endogenous MAOB. ;)
 
without getting into specifics would lys PEA be something one could synth from PEA? i have always had the impression that binding lysene to a given molecule was difficult because the only RC i have seen with such a structure is lys-MDA.
 
without getting into specifics would lys PEA be something one could synth from PEA? i have always had the impression that binding lysene to a given molecule was difficult because the only RC i have seen with such a structure is lys-MDA.

very easy.

the reason as far as I can see that lys RC's are not more commonplace is that like in the case of Lys-MDA the highly illegal amine is required for synthesis.
 
why not these phenylethylamines

2,3-methylenedioxy 4-methoxy 5,6-methylenedioxy phenylethylamine

2,5-methoxy 3,4-methylenedioxy phenylethylamine

2,3-methylenedioxy 4,5-methylenedioxy phenylethylamine


I found 2,5-methoxy 3,4-methylenedioxy amphetamine in Shulgin.

(with 75 mg) This was equal to somewhere between 75 and 100 micrograms of LSD. I was caught up with the imagery, and there was an overriding religious aspect to the day. The experience had an esthetic value. I liked it.

I wonder why he didnt try a mescaline like dose.
 
Probably because the phenethylamines with a 3,4-dimethoxy group are so readily metabolized, or maybe the chemistry is hard.

You're welcome to make them yourself and taste them. I mean, the synthesis for the 2 carbon analogue of DMMDA is right there in PiHKAL if you just change one chemical.
 
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