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The Big and Bangin' Pseudo-Advanced Drug Chemistry, Pharmacology and More Thread, V.2

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The way I'd do it. (I'm sure this is how labs do it too)

0. Decarboxylate the weed in an oven.
1. Take some dry weed, weigh it.
2. Pulverise it and extract with warm hexanes.
3. Dry the hexanes w/MgSO4 and evaporate them. Weigh how much hash oil you get (% Oil)
4. Take a measured amount of the oil, redissolve in a known amount of solvent. and shoot it into a GC. Compare it against a chromatogram of 1mg/ml THC (or really 1mg/ml of any suitable organic compound if you have a MS and can easily ID the THC peak). This gives you a figure of %THC in oil.
4a. [% oil in flowers] x [% THC in oil] = % THC in buds.

If I smoke a gram of 30% THC weed, am I ingesting 300 mg of THC?
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Not quite. Clarke's sez the BA of smoked THC is 20-50%. Ingested is 6-20%. I have a feeling the BA of vaporised THC is much higher, 60-90%. So if you smoke a gram of 30% THC weed, there's at best 300mg of THC in there and you deliver about 75-150mg. However a gram of 30% weed is probably massive overkill... anything above about 15% is a one hitter quitter.

Some labs use a different procedure that keeps the carboxylates seperate, in this case you get 2 sets of numbers, % free THC and % THC-COOH. (THC-COOH needs to be cooked or othwerwise decarb'd before it's active)

ed.note. I Fucking Love Clarke's Handbook.
 
sekio said:
4a. [% oil in flowers] x [% THC in oil] = % THC in buds.
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I suspect they're using a different formula than that. Like I said in another thread, I took a 10 mg marinol once and the effect was perfectly adequate.

If it's just the media and the industry making these claims, they might largely be bullshit.
 
THC is a partial agonist - quite a potent one though. So 100mg of THC may not neccesarily produce effects much different from 10mg, esp if you have a certain level of tolerance.

I suspect they're using a different formula than that.
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How would you measure it then?
 
sekio said:
THC is a partial agonist - quite a potent one though. So 100mg of THC may not neccesarily produce effects much different from 10mg, esp if you have a certain level of tolerance.
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That's a really good point.

How would you measure it then?
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You could measure it as a fraction of the weight of the oil or the resin. According to this source, resin is 2-10% THC by weight, and oil is 10-30% THC.

Obviously, it is impossible for THC to be 10% of the weight of the resin and 30% of the weight of the bud.
 
I think that source uses "resin" as a synonym for "hashish" (which is how that term is commonly understood in the UK), and is referring to traditional hashish produced in the Old World, which is made from cannabis that isn't particularly potent and contains water and leaf material and so on and so forth. I am sure that hash made using modern Western techniques from high-quality sensimilla is much more concentrated in THC than that.
 
Why does it seem as if only gabaergic agents which operate on the mesolimbic pathway are useful in acute psychotic features of mental disorders whereas lithium, valproic, carbamazepine, hell, even l-theanine and valerianic acid aren't?

Thats the justification for your d2 anti-psychotic over a typical mood stabilizer.
 
agonist, releaser, reuptake inhibiting agent

this is confusing to me and i have tried google as many people would first of all suggest and i got thousand of conflicting confusing results so i have to ask, what is such huge difference between an agent that is either releaser, agonist and/or inhibitor ? i know what antagonist is, and im sure any kid will figure it out. its blocking the uptake of neuro signals. so agonist should promote releasing of neurochemicals right ? but if agonist does that, i have never felt anything from agonist drugs. compare it to actual releaser or inhibiting reuptake. which to me seem to be actually potent when it comes to drugs. so what does agonist actually do ? its not a releaser or reuptake. and what is the difference between releaser and reuptake inhibitor since both of those increase the content of a specific neurochemical within the membrane. how do you differentiate between all three ?? :|
 
An agonist directly activates a receptor eliciting a receptor subtype specific response. A reuptake inhibitor prevents the reuptake of a transmitter resulting in more of it being able to activate receptors, thus indirectly resulting in non-specific receptor activation. A releasing agent has the activity of a reuptake inhibitor in addition to causing the release of the transmitter often by causing reversal of the transporters.

Potency for indirect agonists is better measured by "effective concentration 50" or EC50, rather than binding affinities as the response is more due to the amount of transmitter in the synaptic cleft than the amount of drug present.

As for subjective effects direct agonists likely lack the combination of receptor activation or other mechanisms that are typically associated with subjective liking.

Hope that made sense. Feel free to ask any further questions
 
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i dont understand why agonists do not create similar euphoria as reuptake or releasing agent. can you explain this better plz like if you take high doses of agonists dont they bombard the receptors to such extent that reuptake and releasing agents do and thus cause whatever effect they might be causing in excess such as euphoria one example ?
 
agonists of which receptors? some dopamine D1/D5 agonists (e.g. skf-81297) cause self administration (in rats and chimps) but they are not medically used in humans

some people would argue 5ht2a agonism is euphoric
 
I would certainly argue that 5ht2a agonism is euphoric especially in the case of a drug naive person.

However one time I saw data on how DMT, 5-Meo-dmt, and a few other drugs do indeed release some serotonin as well as being an agonist, and that 5-Meo released more which could be why it's slightly less safe, and it could also be why a lot of high dose psychedelic trips have periods of effects tht resemble serotonin syndrome, at least that's my guess. Any thoughts? Also if anyone happens to have the link to said data it would be much appreciated.
 
asecin said:
i dont understand why agonists do not create similar euphoria as reuptake or releasing agent. can you explain this better plz like if you take high doses of agonists dont they bombard the receptors to such extent that reuptake and releasing agents do and thus cause whatever effect they might be causing in excess such as euphoria one example ?
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Agonists are FAR more selective in effects, for all the hate it gets noradrenalin is pretty integral to any kind of enjoyment as are all the various receptor subtypes. Also you're probably going to have less... Writhy, side effects. Then there's pharmacokinetics which generally link rapid onset with liking. Most agonists are designed to be long lasting
 
sekio said:
some people would argue 5ht2a agonism is euphoric
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I used to think that LSD intoxication was intrinsically euphoric. But, with more experience, I realized that this was a fallacious assumption - LSD seemed euphoric only because it taught me things about myself, and there is pleasure associated with learning. To me, saying that psychedelics are pleasurable is akin to saying that books are pleasurable. Just opening a book and staring at the text is not good enough; you have to actually make an effort to read and absorb the information therein.


What do we know so far about MXE pharmacology? I remember there seemed to be some dispute as to whether or not it was a DARI, or something along those lines?
 
Binding data for popular arylcyclohexamines.

arzXb9M.png

M9xPB5N.png


So no, it's not a DRI.
 
also throws a big old wrench in the old claim that "methoxetamine/3-meo-pcp has a 3-methoxy group for opioid effects" because none of those arylcyclohexylamines actually have affinity for opioid receptors at all. and i guess the claim that ketamine has affinity for 5ht2a and dopamine receptors

i trust the ecmd guys more than the studies from the 70s/80s
 
Bunches of questions and statements. Please affirm/laugh at.

LSD is a receptor whore, psilocybin is much more selective, though I doubt totally. LSD is said to have pro-cognitive capacities at low doses similar to hydergine? Makes sense, no?

Are selective 5-ht2a agonists psychedelic?

And why is there no information on the pharmacology of mescaline beyond 5-ht2a agonism? Beyond that does it reverse transport as other phenethylamines? Let's see, its 3,4,5 tri-methoxyphenethylamine? Popularly thought to be the least likely psychedelic to induce a bad trip?

Is the stimulant model of endogenous psychoses still standard?
 
LSD is a receptor whore
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this keeps getting said all the time... but psilocin is not exactly selective for 5ht2a... LSD actually binds fewer types of receptors than psilocin does at "normal" dose levels.
although lsd does have affinity for lots of receptors it's pretty tightly selective for only a few receptors at typical dose levels. smaller molecules like psilocin, dmt etc are less complex (closer to serotonin) and therefore "dirtier".

refs:
psilocin affinity table (11 receptors w/significant binding) (scale reversed - pKi = -log Ki)
lsd affinity table (6 or maybe 7 receptors w/ significant binding)

Are selective 5-ht2a agonists psychedelic?
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functional selectivity is important (c.f. lisuride) but yes, in general... see for instance people using NBOMe compounds as psychedelics!

And why is there no information on the pharmacology of mescaline beyond 5-ht2a agonism?
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how hard are you looking? i thought that mescaline was mentioned in the big plos one psychedelics paper and i know there was a wealth of information on its effects in the 50s-60s.
i seem to recall mescaline & friends are broad spectrum serotonin agonists w/ affinity for a2a/a2c adrenergic receptors, 5ht1a and (to a lesser extent) 5ht2a/c.
psychedelics research is not exactly easy to do anymore.

Is the stimulant model of endogenous psychoses still standard?
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i dont think there is one canonical model of psychosis considered to be "the standard".
 
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Ok, so I've got a question.

I frequently take etizolam in doses of 1-5mg on any given day, usually not sequentially.

The most prominent behavioral change I notice, though, besides anxiolysis and perhaps motor impairment is that it causes me to compulsively clean, reorganize, and optimize things.

Doing a cursory search of The Google it seems that I am not alone in experiencing this phenomenon.

I am baffled, though, as to why taking a benzo-like would make me rearrange my friend's entire living room to the optimal configuration in terms of television visibility and coffee table accessibility. Similarly, I find myself organizing my various manila folders containing medical records, financial documents, academic transcripts etc.

I sometimes even feel compelled to optimize my social life by critically evaluating facebook friends and deleting or blocking them as appropriate based on anticipated future interactions, which I usually wouldn't otherwise bother with. I do trivial chores I've been putting off for weeks. I do other people's dishes and sweep the kitchen.

The list goes on.

But why? It's etizolam not dextroamphetamine.
 
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