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

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It doesn't seem impossible, after all, when you smash a quartz crystal you're breaking covalent bonds. It is interesting, I look forward to hearing an informed response.
 
al-lad binding profile

I had a look but couldnt see this previously mentioned on ADD.

Can anyone point me towards any information regarding the selectivity of al-lad vs LSD?
 
buildersoftime said:
I had a look but couldnt see this previously mentioned on ADD.

Can anyone point me towards any information regarding the selectivity of al-lad vs LSD?
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Good luck with this one. This report discusses AL-LAD chemical characteristics compared to LSD:
Synthesis and LSD-like discriminative stimulus properties in a series of N(6)-alkyl norlysergic acid N,N-diethylamide derivatives.

In that paper they mention that "pharmacological assays" of other N-alkyl substituted N,N-diethylamide derivatives (not necessarily AL-LAD) was done by:
Hashimoto, H., et al., Eur. J. Pharmacol. 1977, 45, 341.
and
Hashimoto, H., et al., Arch. Int. Pharmacodyn. Ther. 1977, 228, 314.
 
I had a quick question that might deserve it's own thread but I'm just looking for some scholarly articles:

What exactly about the nBOMe series causes their increased toxicity (greater ratio of 5-HT2A?)?

23536 said:
This is a silly question, but when I cut a piece of paper or a plastic jug with scissors, am I splitting covalent bonds? If so, what happens to the severed polymer tips?
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Also yea for sure, they probably react with themselves, other polymer tips, the air. Aluminum foil is a good example of this, cut a big piece of it and it'll be initially shiny where unprotected aluminum is, and then dull as it is oxidized.
 
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Roger&Me said:
they are full agonists at 5-HT receptors, whereas most (safer) psychedelics are partial agonists.
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I guess my question is looking for a more in depth reason of why these full agonists may be causing seizures. Especially useful would be any scholarly articles on the topic as my searches came up with little.
 
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The nature of a novel grey market research chemical is that there is little solid data about it.
 
What exactly about the nBOMe series causes their increased toxicity (greater ratio of 5-HT2A?)?
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Honestly, we don't yet know. It could be that they're not as selective as once thought, and broad-spectrum 5ht2 full agonism poses cardiovascular and seizure risks. Or it might be something about extremely tight binding at 5ht2a.

ebola
 
there's probably a secondary signaling angle to the issue, too (there usually is, and its almost always poorly understood or outright ignored).

IIRC, partial agonist psychedelics actually elicit a different signaling cascade than full agonists.
 
ebola? said:
Honestly, we don't yet know. It could be that they're not as selective as once thought, and broad-spectrum 5ht2 full agonism poses cardiovascular and seizure risks. Or it might be something about extremely tight binding at 5ht2a.

ebola
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I thought I remembered seeing fairly complete binding data for 5-HT receptors somewhere? These compounds were developed to be 5-HT2A selective radioligands IIRC, so we must know something about their binding.
 
There are current conflicting data from multiple studies, one showing the compounds in the series to be highly selective for binding at 5ht2a over 5ht2c, the other showing them to be broad-spectrum 5ht2 agonists. I don't think that these discrepancies have yet been adjudicated.

ebola
 
One Question:

http://en.wikipedia.org/wiki/Sceletium_tortuosum

How do half of the active compounds in this not even have wikipedia pages?

each time I've tried this it's antidepressant effect has been noticeable enough to say it works, how has no scientist tried to research the earths only natural SSRI?

With the amount of people suffering from depression in the world this could truly change it for the better.

at least we know that Kanna is a PDE4 inhibitor and an SSRI, but then how did nobody care once that was discovered??
 
How do half of the active compounds in this not even have wikipedia pages?
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because al of the research is in the peer reviewed literature and not in easily digested formats on wikipedia

how has no scientist tried to research the earths only natural SSRI?
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you must have missed the multiple studies suggesting sceletium and its extracts are useful for depression and anxiety.
 
Is there a reason that methamphetamine synthesis didn't boom into a cottage industry in the states until the RI/P and Birch methods became widely used, when there are plenty of other reducing agents that spring to mind that are just as easy, if not easier, to acquire? Is it just a coincidence of history, those are the methods that were disseminated within a community of people who didn't have a lot of chemistry knowledge? I know I'd rather prepare an amalgam than steal anhydrous ammonia and dissolve lithium in it in a motel room, but that's not what a nation of meth cooks chose to do. If this is too much synthy talk then so be it, I was just wondering.
 
Binding affinities for tryptamines

Can anyone point me toward binding affinity data for 4-sub, 5-meo and unsubstituted tryptamines please? Google isn't delivering. I'm particularly interested in 5-HT1B and 5-HT1D agonism.

Edit: Glennon RA has written a bunch of papers on this but I cant find anything that isn't behind a paywall.
 
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Heh, to what extent do we believe the PLoS One study, and why?
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What is up with VMAT2? To what extent should we attribute releasers' effects as dependent on VMAT2? Are there available cross-substance comparisons that shed light on this question? And might VMAT2 substrate + 5ht2b agonist be sufficient alone for proper entactogenesis?

ebola
 
ebola? said:
What is up with VMAT2? To what extent should we attribute releasers' effects as dependent on VMAT2? Are there available cross-substance comparisons that shed light on this question? And might VMAT2 substrate + 5ht2b agonist be sufficient alone for proper entactogenesis?
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Most of the research related to VMAT2 seems to be on dopamine.

Interesting new paper out on VMAT2 and dopamine, seeming to point to VMAT2 downregulation being responsible for a lot amphetamines' negative long term effects: http://www.sciencedirect.com/science/article/pii/S0028390813003481

Apparently this is an issue with cocaine also, which is a bit surprising: http://www.ncbi.nlm.nih.gov/pubmed/22193525

Although earlier research claims reversing the dopamine transporter is still the main mechanism of action for amphetamines as dopamine releasers: http://www.ncbi.nlm.nih.gov/pubmed/9482784

I'd seen a paper before speculating that bupropion may be a VMAT2 enhancer, but I can't find anything on its interaction with amphetamines long term. I think looking at that interaction long term might really shed some light on it.

I'm still a bit in the dark on possible efficacy as an entactogen, but everything I've read on VMAT2 inhibitors and 5-HT2B agonists would sort of point me away from intentionally using them (at least for a drug taken remotely often). Wouldn't combining 5-HT1A agonists and OXTR agonists be a much safer route?
 
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