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

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You may like The Color Atlas of Pharmacology. The torrent is widely available.

Dude, thanks for the recommendation, this is a great book! :D

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Oh yes, I got a quick question. Would 4-AcO-DMT fumarate be soluble in water? I use liquid titration to get mostly accurate doses of RCs with this dose range as I only have a 0.01g scale (usually dissolve 100mg in 10ml water so 1ml = ~10mg), but am wondering if this will be a viable method with 4-AcO-DMT?
 
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^^^
yes its soluble

here is a question which is obviously hard to answer but i would appreciate any help. does anyone have a rough idea of how the profits of the black/grey market drug economy compare to that of mainstream pharmaceutical companies? more specifically how MDMA sales compare to those of something like prozac or another common SSRI?
 
What is the Binding Affinity Ratio (Ki) of THC to CB1:CB2?

I googled this but there are too many other conflicting searches with topics on similar terms. Does anyone happen to know or have a link handy that shows the Ki of THC's binding affinity of CB1:CB2?

I want to find a cannabinoid analog with as close as possible of a ratio of CB1:CB2 to THC. My theory is that it will provide the most similar experience as THC.

JWH-018, for example, has a Ki of 0.3:1 CB1:CB2

I love JWH-018, when I was on probation I smoked it every single day and did wonders, but of course nothing can compare to marijuana. My theory is that finding a cannabinoid with a similar ratio will be more suitable.
 
delta 9-THC CB1 7.1 nM (JPET August 1996 vol. 278 no. 2 871-878)

delta 9-THC CB1 54nM (Annu. Rev. Pharmacol. Toxicol. 1998. 38:179–200)
delta 9-THC CB2 76nM (Same as above)
 
Although, cannabis is not only THC. Shouldn't you calculate the average values of CBD and THC, then find a synthetic cannabinoid with affinities close to that?
 
suboxone question?

so here goes. im addicted to oxycodone have been for almost a year now. and for the past 4 months i plug my dose only. well the other day i thought id try an oral dose of half my plugging dose and i got blasted high. whoa sick. so i dont think anything of it except that maybe i just forgot what it feels like to take oral oxy. fast forward to today. im taking some sub to hold me over till i can get some more oxy. and as i plug my dose i get a slight buzz. and poof i remember reading in a "subplug" thread someone saying that the less bupe u take maybe the more norbupe can be recievd in ur mu receptors. well assuming that this is possible could it be possible if one wer inclined to get high off bupe to take a bupe dose orally which although has very low ba for bupe. the passs of 1st and 2nd metabolism would cause much more bupe to be converted to norbupe which would flood the brain since so little bupe would get thru???
 
you'd have to significantly increase your dose, and you'd end up wasting lots of bupe.

better alternatives, but those who've tried them agree, they're generally pointless too.
 
How come PEA's like 2C-B resemble dopamine chemically but work as 5-HT agonists? Wouldn't you expect something like DA agonism (though I've never even heard of that)?
 
Yes, 2,5-dimethyl-3,4-MDA *probably* is active, but there is some amount of pure speculation in predicting the properties of any drug before it has been tested.

Also, when you say, "2-methyl-MDA," I presume you mean 2-methyl-3,4-MDA and not 2-methyl-4,5-MDA, which is inactive. (The numbering of the ring gets prioritized to the closest substituent to the alkyl chain therefore making clarification necessary in such instances.)
 
My understanding is that the methoxy groups on the aromatic cycle give them 5ht affinity, being in correct positions for hydrogen bonding with the 5ht receptor. But I may be wrong about that, lately I seem to be wrong about lots of things...
 
How come PEA's like 2C-B resemble dopamine chemically but work as 5-HT agonists? Wouldn't you expect something like DA agonism (though I've never even heard of that)?

It's because of the substitutions on the aryl ring (phenyl ring). The ring makes for a planar configuration which is necessary for being a substrate for many receptors, while the ethers on the ring appear to provide hydrogen bonding for something inside the 5HT2A/C receptors that allows them to be agonists while also preventing their metabolism. The amine tail, normally associated with dopamine, appears to configure itself to interact as the amine tail of tryptamine does, probably hydrogen bonding with something acidic in 5HT2A/C receptors. It's thought that the orientation of the phenethylamines inside the receptors is slightly different than tryptamines on a 3D plane too. The basic answer is that all the substitutions cause it to have a very different shape and hydrogen bond capable structure that fits more "key-like" into the 5HT2A/C receptors than into the D1-D4 receptors.
 
2,5-dmo-3,4-mda has been made and tested, it's like another DOM analog but less potent. MDA is slightly trippy and a serotonin releaser, adding anything at the 2 and/or 5 positions is just going to make it a straight hallucinogen and not so much a serotogenic stimulant. Maybe at the 2 position it can take some sort of substitution without being too psychedelic but it's iffy.
 
How stable are these compounds?

I ask this question about a lot of drugs, but I'm no chemist and I like to know how long I could keep this stored... So how stable are 2C-X's and could there be a difference between various 2C-X's. How long could I keep it stored? The same question for etaqualone. Any extra info on etaqualone is also welcome. Thanks in advance.

Kind regards,

Gio
 
2cx compounds will be very stable as long as they are being stored as the hydrochloride/hydrobromide etc. salt. If your material is a solid powder, then it is going to be a salt, since most if not all the 2cx compounds I'm aware of are oils in the freebase state.

For compounds like 2cb, and 2ci you should keep them stored in a dark place. The carbon halide bonds in these materials are relatively strong (because the iodine/bromine are on the aromatic ring) but leaving them out in the sun for a prolonged period of time would not be advisable.

The other 2cx compounds with no halogens would probably be more stable by my guess.

If you wanted to store them for 10+ years, you could get a ziplock freezer bag with a good seal and a couple of those little pouches of sillica gel you find in OTC pill bottles to keep the 2cx's dry (taking them in/out of the freezer often will build up moisture and make them soggy/sticky).

If you keep them in a cool dark place, they will last a long time.
 
Fencamfamine mechanism

When they say that Fencamfamine is a partial DA releaser and a partial DRI, how exactly does that work? Does it reverse some DAT:s and inhibit others? Or does it bind to the DAT and then only reverse it occasionally? Or is there some completely different mechanism?

Wiki says it releases DA by the same mechanism as amphetamine, but does not say what mechanism it uses to inhibit the reuptake.
 
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Hello

Please identify this random substance. I have a non-saturated HPLC trace for you to look at. Its run on Acetonitrile / Water + 0.01% Trifluoroacetic acid. Told its Valium please confirm.
30237868.jpg


Thank you i can provide more info if needed. I need a response by friday if you would be so kind.
 
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