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

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Are the active principles of nutmeg, myristicin and elemicin, soluble in alcohol, water, acetone, or in any other solvent?
 
freemind said:
Are the active principles of nutmeg, myristicin and elemicin, soluble in alcohol, water, acetone, or in any other solvent?
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Solubility looks like this:
Diethyl ether = Hexane > Acetone > Ethanol > Water
 
However I read in wiki that SSREs (reuptake Enhancers) work as much as the SSRIs (reuptake inhibitors). How is that possible?
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Tianeptine's modest efficacy as an SSRE might not explain it's anti-depressant action (though coadministration with SSRIs reduces drastically T's effects on long-term potentiation). T also acts at AMPA and NMDA sites and causes downstream increase in intercellular monoamines.

ebola
 
MasterOfDeception said:
Thnx for the reply. However why antagonizing 2A and 2C results in increased activity to other serotonin receptors? It might seem kind of obvious but I would like to see it explained more analytically. Serotonin neurotransmitters can't use 2A and 2C so they use the remaining receptors? The exact same serotonin neurotransmitter can bind to any serotonin receptor?
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That's exactly how it is.
 
MasterOfDeception said:
SSRIs work by inhibiting the reuptake mechanism of a neuron, and that results in greater serotonin activity in the serotoninergic receptors.

A serotine antagonist does pretty much the opposite, it blocks serotonin activity in the receptors.

So, since SSRIs are supposed to be antidepressants, serotonin antagonists can cause depression ? I am asking cuz most/all 2nd generation antipsychotics are serotonin antagonists, amongst others.
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Some theories on SSRI efficacy regard postsynaptic 5-HT2 and presynaptic 5-HT1 family receptor desensitization and down-regulation due to increased synaptic 5-HT as the actual mechanism. The long term consequence of an SSRI or 5-HT2 antagonist would thus be similar.
 
hi all :) I wanted to take some promethazine to potentate some DHC but i have had 75mg of amytriptyline an hour or 2 ago and i read somewhere on the net there are 'a moderate interaction' between amytriptyline and promethazine. Can someone elaborate for me please, does this mean steer clear or preceed with caution? has any1else had a bad reaction mixing the two?
 
Do phenazone or its derivatives have any abuse potential?

Torizo Takahashi has some interesting papers.
 
How is thalidomide a sedative? What does it do up there?
 
I was under the impression that thalidomide was comparable to the barbiturates or glutethimide.
 
^That's not the kind of endearing attitude that makes other posters want to help you. Don't be a dick.
 
At first, I thought that he was calling himself worthless. :p

ebola
 
Hi,

I was thinking about mephedrone and...How fast will be converted to 4-methylephedrine? Is it possible that this metabolite plays an important role in its effect (stimulant part)?
I mean

Meth(strong stimulant) -> MDMA(milder stimulant)
Amphetamine(medium stimulant) -> 6-APB(milder psychedelic like stimulant)

Methcathinone(mild stimulant / entactogen?)-> 4-MMC(very strong and potent entactogenic drug and stimulant)

and even more important

Amphetamine(medium stimulant)->4-MA(potent serotonine releasing agent, not really stimulant)



4-N-Methyl is a magical group on methcathinone, or what? Why is meph so potent and fast?
 
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Mephedrone releases both serotonin and dopamine in large amounts. A large release of serotonin has a 'muting' effect on the stimulant effects dopamine releasers.
 
If you speak japanese, please PM me. This "translation job" is mostly reading.
 
Does anyone know if there are any major differences between catecholamine catabolism in the PFC vs the limbic system in regards to proportions broken down by COMT vs MAO?

I've been searching around but can't find anything definitive for humans.
 
Mechanism of potentiation of methoxetamine by methiopropamine

Several BLers have reported that the stimulant RC methiopropamine potentiates the dissociative methoxetamine. I myself have had an experience where a dose of methoxetamine which is well within my regular range, about 40mg, combined with an unknown but not huge quantity (perhaps 70mg) of methiopropamine resulted in me behaving erratically (trying to pee against a wall) and having to be put to bed several times - and I have no memory of these events.

Alcohol and o-desmethyltramadol were also involved, but they have been before without any such issue, the methiopropamine was the only novel factor.

Is the potentiation mechanism understood, and if so what is it? Is it something likely to be encountered with other stimulants and dissociatives?

I'm intrigued because I haven't previously noticed such a powerful effect of combinations in my drug taking experience, other than cannabis potentiating methoxetamine, and I'd be interested to understand that too (no amnesia/irrational behaviour there though, just extreme psychedelia and stimulation).

Thanks for any replies in advance.
 
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