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

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Greetings to all! I was just birthed(joined) and not 2 b rude or needy... But. Could someone please
Walk me thru the acetone wash? I'm on my iPod touch which appears to be faulty making it difficult to surf past threads. I apologize for barreling into your conversation
 
ok ADD gurus please do not flame - after all I am a college dropout teaching myself, but I assume adding a 3,4 methylenedioxy chain to nardil(Phenelzine) would essentially equal death?
 
Yeah. Organic hydrazines are really good irreversible inhibitors because of their instability.

Walk me thru the acetone wash? I'm on my iPod touch which appears to be faulty making it difficult to surf past threads. I apologize for barreling into your conversation
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Ok:
1. Put product in filter.
2. Chill acetone.
3. Dump cold acetone onto product.
4. Dry product.
5. Profit?
 
MDMA IC50 Values

Just out of curiosity I'm wondering if anybody could tell me the IC50 values for MDMA in relation to serotonin, dopamine and norepinephrine? I have tried Google but it didnt seem to help.

Apologies if this is in the wrong forum. Thanks.
 
UYI said:
Just out of curiosity I'm wondering if anybody could tell me the IC50 values for MDMA in relation to serotonin, dopamine and norepinephrine? I have tried Google but it didnt seem to help.

Apologies if this is in the wrong forum. Thanks.
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Go here: http://pdsp.med.unc.edu/pdsp.php

And select MDMA as the test ligand.

This will not tell you EC50s for monoamine release though,

The user rocknroll714 compiled a big list of IC50s/EC50s on his wiki too: http://en.wikipedia.org/wiki/User:El3ctr0nika/affinities

I suggest you read up on the methodology by which these tests are conducted too if you want to make a decent amount of sense out of them, it's important to know what the hot ligand (radioligand) was that the new ligand displaced because different ligands can occupy different places in the receptor.
 
Differences between 5-HT2a and HT 2c

I've rencentlly begun an attempt to gain a much deeper understanding of the pharmacology of Tryptamines and Phenethylamines. Out of this study I've come across 2 questions which I'm having trouble finding an answer two. Firstly can anyone explain to me the differences in the function of the 5-HT2a and 2c receptors. while i know both are G protein-coupled receptors i''m not sure of their individual functions. Second, What is the difference between partial and Full agonism/antagonism. Thanks for your responses.
 
Questions like this might be better suited in The Large and Nifty Not-quite-advanced Drug Chemistry, Pharmacology and More Thread for future note. Anyway, someone else may correct me but to my knowledge...

5-HT2C: As far as I know, it plays a role in anxiety naturally. The binding site is similar to 5-HT2A which why there is no 'solely 5-HT2A agonist' currently.

5-HT2A: Responsible for 'psychedelic effects' when activated by a drug. It's also plays a role in regulating intraoccular pressure (non-centrally).

Partial agonist v. full agonist: I believe when a drug activates the receptor with lower efficacy than neurotransmitter. On the other hand a full agonist will activate the site with equal (or greater) efficacy than the neurotransmitter.
 
^Thanks a lot, I had a feeling this was the wrong thread, im still learning what goes where. This was actually my first ever post. Your answer definitely helped, i appreciate it.
 
opiates suppress immune system
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Yes.

And after lurking/eavesdropping on multiple forums/conversations, there still appears to be an inordinate degree of uncertainty regarding the amphetamines' actual mechanism of action. Is this discrepancy still reflected in the literature? Because it seems like those with advanced pharmacological knowledge briskly brush past the topic like it's old news while the rest of the world wonders: HOW does amphetamine phosphorylate the transporter? An allosteric binding site? Some weird direct mechanism as a modifying substrate? Kinase modulation? And is the old 'weak base' theory of amphetamine-mediated monoamine release still viable, or has some academic consensus been reached of which I've been completely unaware? I got tired of scavenging Google Scholar a long time ago, and nothing I found appeared conclusive in the least.

EDIT: In other words, if amphetamine-elicited monoamine release is truly nothing more sophisticated than typical exchange diffusion, then why haven't the DAT, SERT, NET and others been reclassified as functional antiporters? And further, why would this dramatic aberration of basal neurotransmitter release be so highly dependent upon increased intracellular PKC and MAPK? And how would the transporter become/have to be phosphorylated by a kinase-dependant mechanism in the first place if it already exists as an antiporter capable of sucking up these exogenous releasing agents in exchange for the endogenous amines? Or are these researchers actually suggesting that each of the many, many structurally diverse releasing agents each happen to have three separate, essentially identical actions [one extra- and two intracellular] that mediate their effects? That just sounds way too unlikely and convoluted, but again, maybe I'm missing something big here.

Also, does anyone have the nanomolar affinities for dextrorphan at the SERT and nicotinic receptors? I tried extensively UTFSEing, but with no luck whatsoever. And to what extent is methorphan's pharmacology even relevant to its dissociative properties, given its comparatively low affinity for the PCP site? Is its 'recreational' role simply that of a practically inert prodrug, and if so, what's with all the cautionary tales regarding serotonin syndrome? Typical hysteria, or is there something of a biphasic metabolism here? Or is dextrorphan's affinity at the transporter comparable to that of the parent compound?
 
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What are the major differences between noradrenaline and adrenaline when they are currently activating their respective adrenergic receptors?

Edit: Another question, although rather off topic: What is the nomenclature behind using the commonly found pyr- prefix in chemistry? E.G. Pyrazole, Pyridine, Pyrocatechol. Does it simply mean its commonly a product of pyrolysis?
 
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What are the major differences between noradrenaline and adrenaline when they are currently activating their respective adrenergic receptors?
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As a rule, there are no 'respective' receptors for either sympathogen, as their highly analogous structures predicate similar binding profiles. Though this is explanation is highly simplistic, it's generally helpful to pair epinephrine (adrenaline) with the beta adrenoreceptors and norepinephrine (noradrenaline) with the alpha receptors. The former compound has higher affinity for the much more peripherally active and "drastic" and myocardically "potent" of the two subtypes [the beta adrenergic receptors] given its well-known function as a vasomotor pressor agent to be used by the body only in intermittent scenarios of emergency fight-or-flight. The comparatively more "regular" or "mild" adrenoreceptors [those of the alpha subtype] mediate basal ("normal") peripheral neurotransmission, allowing strictly for baseline maintenance of heart rate and blood pressure. In other words, though both ligands have affinity for both receptor subtypes, their differential effects on the peripheral nervous system are mediated by their proportionally selective affinities for one adrenergic receptor subtype over the other. So epinephrine=beta/alpha and norepinephrine=alpha/beta.

As for the central nervous system, adrenaline's structure denies it access to the brain via diffusion across the blood-brain barrier, making it effectively irrelevant as a central neurotransmitter. Noradrenaline, on the other hand, is the one of the three most prevalent monoamine transmitters in the mammalian brain, with significant effects on transmission reaching from the spine to the brainstem to the cerebral cortex. And while there are still beta receptors in the CNS, they essentially function as nothing more than special low-affinity receptor sites for noradrenaline and are much less widely expressed than their alpha counterparts. And in case you're wondering, noradrenaline is more prevalent due its presence within the presynaptic neurons that release it, both within selected nerve terminals in the periphery and the locus coeruleus within the brainstem. To my knowledge, adrenaline originates [and is released] solely from the adrenal medulla, a specialized gland mobilized only in extreme circumstances of physiological stress.
 
Thank you for the detailed response!

Edit: Also I noticed you said noradrenaline was one of the three most prevalent monoamine transmitters. Are the other two serotonin and dopamine?
 
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If you have a single isomer of a chemical, will it form larger crystals than the racemic counterpart?
 
How much amphetamine was in Benzedrine inhalers?

I have been reading On the Road: The Original Scroll and of course, one of the Beats most used drugs: Benzedrine is frequently mentioned. From what I have read so far, it appears that 1 strip was the optimal dose.

I am curious as to just how much racemic amphetamine was in one of those things. I have been able to find that the tablets contained 5 mg, but I have had no such luck in figuring out the total amount in the inhalers.

So if there is anyone here with knowledge of old school pharmaceuticals, or better yet someone that used these back in the day who could enlighten me it would be greatly appreciated. Thanks in advance-pld
 
Usually once was enough when we young shitheads broke open the Vicks Inhalers and scarfed down the cellulosic filler that contained the low rent, amphetamine load .
One could look forward to belching menthol laden stomach fumes and chattering on and on for hours upon hours--One time was a cure.
Greenwich Village prior to '63 was not a place where reason was struck.
 
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