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

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Well, 70 proof is only ~35% ethanol.
Still your freezer would have to be negative 25 C to freeze it solid... [ref]

Lucky for you thermodynamics says that you can partially freeze a solution to do a freeze distillation, or fractional crystallisation (good for defatting soup). You're probably just making a Slushie-type mix of ice suspended in higher-proof alcohol.
 
there's two types of captain morgan in my freezer... traditional caramel-colored captain morgan, and captain morgan "silver". the caramel colored stuff gets quite a bit slushier than the silver, but the silver does display a bit of crystallization.

as of yet i haven't had a sample that remained controlled for a long enough period to determine whether or not volume changes over time due to strictly environmental factors.
 
Solipsis said:
Exactly, synthesis is balanced - when S-only is made there is R-only as waste, which is not dumped. It merely follows black-market paths, together with illegally siphoned off ketamine of other forms. The demand for R is just much more unstable and lower.

The reason we are talking about ketamine is that it is special since both isomers have activity although different activity. With most other drugs there is only one active form, or there is only one form where the activity is beneficial. With amphetamine for example, the dextro form feels more cleanly mental while the levo isomer is more physical and disregarded in psychiatry. In rare cases there is one active isomer of a drug while the other is toxic in a sense e.g. thalidomide.

Isomers have different symmetric orientation which is important for the way the compound fits into receptors like a key into a lock.
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I wondered do isomeric values apply to the production of synthetic testosterone..?

I had read somewhere there will be a D and an L form - mirror images of each other. Which I believe only one of the forms will work in the human body (the D if I remember correctly).

If I understand correctly it depends how the testosterone is synthetically produced. Usually Cholesterol is used as the raw material. It's extracted from plants and purified, and then treated with chemical reactions in a series of steps to produce testosterone (and other hormones).

Only one form of Cholesterol is found in nature, so whichever enantiomer is in nature, will be the starting point for the synthetic production of testosterone.

Can anyone confirm this...

Cheers in advance...
 
Testosterone has 6 chiral centres, so there are in theory 64 possible isomers.

Realistically, only the one isomer of testosterone is biologically active I think, and that's the one derived from cholesterol.
(In your body, testosterone is derived from cholsetrol by enzymes.)

Many drugs have specific chirality or are specifically racemic... for instance, if you buy citalopram it will NEVER be 75% R-citalopram and 25% S-citalopram, always 50/50, unless explicitly compounded by a pharmacy that way.

Some natural drugs like e.g. morphine are also :always" one isomer. Nobody ever sees the "unnatural" enantiomer of morphine in prescribing usage.
 
sekio said:
Testosterone has 6 chiral centres, so there are in theory 64 possible isomers.

Realistically, only the one isomer of testosterone is biologically active I think, and that's the one derived from cholesterol.
(In your body, testosterone is derived from cholesterol by enzymes.)

Many drugs have specific chirality or are specifically racemic... for instance, if you buy citalopram it will NEVER be 75% R-citalopram and 25% S-citalopram, always 50/50, unless explicitly compounded by a pharmacy that way.

Some natural drugs like e.g. morphine are also :always" one isomer. Nobody ever sees the "unnatural" enantiomer of morphine in prescribing usage.
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Can I conclude the end product of synthetically produced testosterone would only contain the one biologically active isomer....
 
Yes, I don't think that people would waste their time making the "inactive" isomer.
 
Where does the water go after IVing?

Ideally the compound of choice passes the blood brain barrier, but where does the water go? Jerry Stahl writes of having swollen limbs due to excess fluid from shooting dope. Can this really happen?
 
The water goes into your bloodstream, almost as if you'd drank it.

You would have to inject a lot of fluid to get swollen limbs, as water is removed from your circulation via the kidneys into the urine almost continouously. More likely swelling is from severe histamine release (from acute administration of opioids) or blockage of small veins/arteries by particulate matter, or it may just be that his kidneys were fucked to the point where he retained fluids.
 
I have had saline drips at the hospital, constant drips for days at a time and my body gets rid of it normally. (distributes it where needed and the excess gets processed through the kidneys/bladder)
 
IV'ing doesn't get past the blood brain barrier, it gets past first pass metabolism however.
Merging with big and dandy thread.
 
I have a rather complicated series of questions.

So, I'm pretty sure a ligand's primary effects are determined by the weight and shape of the molecule fitting into the receptor (correct me if I'm wrong at any point in this por favor)

But what about the actual metabolism of the ligand? My (limited) understanding is that after it's rocked your brain for whatever period of time it obviously goes through some sort of chemical reaction and you end up peeing/pooping out all of the metabolites, except for when some of the ligand remains unchanged after traveling all the way back through your body/digestive tract-- is this the case or did the unchanged ligand not make it to your brain, meaning it ultimately didn't get you high?

I recently watched a video where shulgin talked about how DOB is metabolized and that after first pass metabolism it goes to the lungs for a period of time, THEN the brain. I am under the impression that there are a LOT of enzymes in your lungs that can potentially move around methyl groups and do all sorts of crazy stuff like that, is this true? AND is this because lots of ligands have parts that are oxidized/hydrolyzed off by enzymes in the lungs?

and do you think this has anything to do with the bronchodilating effects of some phenethylamine compounds?

I'm under the impression that the main reason MDA is more neurotoxic than MDMA is because MDA is easier metabolized into Alpha-methyl-dopamine because the N-methyl group doesn't need to be metabolized off. Does this mean that almost any amphetamine can metabolize into alpha-methyl-dopamine? and would that mean that normal alpha-methyl-phenethylamine is probably one of the worst because it's just one chemical reaction away?

even more questions... according to the history section of this wikipedia article there are proteolytic bacteria in the large bowel producing phenols, indoles, and ammonia which to my knowledge are very related to phenethylamine and tryptamine. Shulgin experimented in vitro with myristicin and ammonia and discovered that MDA could be synthesized in vitro by a culture of lamb's bowel cells IIRC. Seeing that there are soooo many strains of different bacteria (good and bad) possibly metabolizing things in slightly different ways is there a possibility that by ingesting these novel compounds with all these bulky/irregular substitutions that there are metabolites going through the bowels causing the synthesis of other compounds that we don't know about? and would these compounds be active or would they just be on their way out of the body meaning it doesn't matter anyways?

Obviously I could be wayy wayy off so I thought I'd come here for answers to all these elaborate questions.

I'm also very tired so i'll check back in the morning to see if any part of this post just doesn't make sense.
 
Most ligands are eventually metabolised, but usually to less active compounds. In this day and age we can do wonderful things like get mass spectra of metabolites from blood.
Generally psychoactive amphetamine/tryptamine type drugs are active and their metabolites are not.
 
so the likelihood of ammonia adding a really active methyl group onto the end of a metabolite is either very unlikely or entirely unknown?
 
reason MDA is more neurotoxic than MDMA is because MDA is easier metabolized into Alpha-methyl-dopamine
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Not sure about that. MDA is also more potent than MDMA as a monoamine transporter ligand. (more efficacious releaster of monoamines)

Does this mean that almost any amphetamine can metabolize into alpha-methyl-dopamine? and would that mean that normal alpha-methyl-phenethylamine is probably one of the worst because it's just one chemical reaction away?
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No, and no. Well, okay, the cheater answer is 'yes, if you find the right combination of enzymes'. Fortunately for us humans, only a small portion amphetamine is only converted to 4-hydroxyamphetamine, and there it stops. There are no common enzymes that add a pair of hydroxyl groups onto an aromatic ring at once, it is almost always done stepwise. In the synthesis of dopamine, phenylalanine is converted to tyrosine and finally then to L-DOPA by two seperate enzymes. (The latter enzyme does not work well on amphetamines, nor phenethylamine... only amino acids I believe)

so the likelihood of ammonia adding a really active methyl group onto the end of a metabolite is either very unlikely
Click to expand...

Ammonia can't add any methyl groups anywhere. It is nitrogen and hydrogen, a methyl group is carbon and hydrogen.

If you are talking about the metabolism of compounds like safrole and myrsticin to MDA/TMA, it has never been observed to any significant extent in man. Sure lamb bowel cells might do it but it's not going to be any more than a trace...
 
^lol yea I assumed I was wayyy off with at least one aspect of that. I've heard that Amphetamine is neurotoxic while Ritalin is not, could you elaborate on this a little for me?
 
Hey peeps, first time poster here. Here's a question that's been bothering me:

Is there a correlation between how painful a substance is to snort, and how corrosive/damaging it is to the lining of the nose? I was sniffing ethylphenidate all day yesterday and, as anyone who's tried it will attest, it stings like a mother (worse than meth even) and feels corrosive as f*ck - is it reasonable to assume that a given amount of ethylphen or meth will do more damage to the septum than the same amount of a drug that hardly stings at all, like ketamine or mdpv?

Or am I being oversimplistic? Any thoughts appreciated.

muchas gracias!
 
Generally pain is indicative of damage, but not always directly correlated.
 
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