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

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They both have 18 carbons, 21 hydrogens, 1 nitrogen, and 4 oxygens. That's the end of the similarities :)

Compare the structures:
Boc-3-(2-Naphthyl)-D-alanine
CAS%5CGIF%5C76985-10-9.gif


Oxycodone
155px-Oxycodone2DACS2.svg.png
 
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Nichols published a paper demonstrating the activity of benzofuran analogs of some tryptamine. I was wondering if this trend might extend to thianaphthene as well. Thianaphthene is quite different in terms of electronics and reactivity relative to indole and benzofuran. I'd imagine it would also be very different in terms of biochemistry as the sulfur is fairly easily oxidized, maybe it would be excreted much fast?

I am quite curious about this, but I don't have any real biochemistry/pharma experience. I've been searching around a bit but haven't found much. If anything I've found my organic experience makes it much more difficult for me to wrap my head around bio and pharma publications. It messes with my mind that what might be considered analogous in organic doesn't apply in the realm of biochemistry so much.
 
Just a quick question, why don't scopolamine and cocaine share (at least a few) pharmacological mechanisms, since the structures look so similar?

You'd expect they would if you compared the structure.
 
Just a quick question, why don't scopolamine and cocaine share (at least a few) pharmacological mechanisms, since the structures look so similar?

The arrangement of atoms in space matter more than the skeleton of the compound mapped to 2d. In atropine the tropine group has the hydroxyl pointing down (axial), while in cocaine the hydroxyl points "up" (equatorial).

Also, for stimulant efficacy you need to have that carbomethoxy group that cocaine and methylphenidate share. This is why stuff like lidocaine is just an anesthetic and stuff like tropacocaine (cocaine minus the carbomethoxy group) is basically not worth writing home about either.
 
Anyone know to what extent amp inhibits maoi, and if its a b or a inhibitor? comparisons with dose of phenelzine/tranylcypromine?
 
14 to 20 micromolar Kd at human placental MAO-A for D-amph (14,000-20,000 nM). (Moclobemide is 200-400 nM) And it's reversible. Essentially no activity at MAOB. Not worth worrying about I think.

http://link.springer.com/article/10.1163/156856003765764290#page-1

The discovery that MAO exists in two functionally distinct activities {MAO-A and MAO-B) was followed by studies showing AMPH to be a preferential MAO-A inhibitor. In vitro, (+)-AMPH is many times more active against MAO-A than against MAO-B. Also the (+)-isomer is at least 3 to 4 times more active against MAO-A than the (-)-forms”. However, AMPH is a reversible MAO inhibitor and as such it is difficult to show a direct inhibitory effect in vivo. [...]
http://www.sciencedirect.com/science/article/pii/0165614780900322
 
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Ho-chi,
I honestly thought for the last decade that you wouldn't deplete DA as long as you kept the dose low, had acceptable nutrition, and slept regularly.

I truly didn't know there was a concern about DA depletion at reasonable doses!
 
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^ i've heard that is a difficult one to salt for some reason. dunno details as to why.

It's not as simple as mixing a solution of the freebase with a solution of an acid? That would raise the question of what is the freebase soluble in?
 
Ho-chi,
I honestly thought for the last decade that you wouldn't deplete DA as long as you kept the dose low, had acceptable nutrition, and slept regularly.

I truly didn't know there was a concern about DA depletion at reasonable doses!

He said there's not depletion at therapeutic doses.
 
Tartaric acid is a solid? Do you mean make a solution first?

from TiHKAL LSD:

This base was dissolved in warm, dry MeOH, using 4 mL per g of product. There was then added dry d-tartaric acid (0.232 g per g of LSD base), and the clear warm solution treated with Et2O dropwise until the cloudiness did not dispel on continued stirring. This opaqueness set to a fine crystalline suspension (this is achieved more quickly with seeding) and the solution allowed to crystallize overnight in the refrigerator. Ambient light should be severely restricted during these procedures. The product was removed by filtration, washed sparingly with cold methanol, with a cold 1:1 MeOH/Et2O mixture, and then dried to constant weight. The white crystalline product was lysergic acid diethylamide tartrate with two molecules of methanol of crystallization, with a mp of about 200 °C with decomposition, and weighed 3.11 g (66% ). Repeated recrystallizations from methanol produced a product that became progressively less soluble, and eventually virtually insoluble, as the purity increased. A totally pure salt, when dry and when shaken in the dark, will emit small flashes of white light.
 
A totally pure salt, when dry and when shaken in the dark, will emit small flashes of white light.
lsd can emit flashes in the dark? how fitting :D
[edit: holy shit i just heard he died... RIP mr. shulgin :( ]
 
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^ yeah seems like it

i was looking at some other food colorings.... Blue #1 here looked like it could potentially have some active metabolites to me:

Brilliant_Blue_FCF.png
The article you are referring to must be this one: http://www.feingold.org/Research/PDFstudies/Stevenson2007.pdf

They were using a mix of various coloring agents and sodium benzoate. Yes, allura red ac was contained in one of those mixes, but there really is no strong evidence showing that allura red ac would exacerbate adhd symptoms or induce hyperactivity in healthy children. There is a shit ton of articles on this, most of them financed by the food industry. Good luck finding any conclusive information lol. One issue is that almost no one will let anyone perform tests on their children with excessive doses of food additives that are proven to be toxic, even if only at very high doses. I honestly don't know how they even pulled off that 2007 study, but I'm not too familiar with this field anyway.

Anyone have a guess as to how turn AL-LAD ( http://en.wikipedia.org/wiki/AL-LAD ) freebase into a salt?
You must have a shitload of AL-LAD... I wouldn't try this on just a few mg personally.

@sekio: Wouldn't the process suggested there fail to yield a racemate (for lack of a better word when 4 isomers are present) if d-tartaric acid was used? "d-lsd" is the right isomer for lsd (its d at both the 5th and 8th c), but is it the same for al-lad? (edit: i guess it should be since it has the same stereocenters. i guess its safe to assume that d-al-lad is also the active isomer of al-lad, so forget what i said, im not familiar with lsd chemistry. :D )
 
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14 to 20 micromolar Kd at human placental MAO-A for D-amph (14,000-20,000 nM). (Moclobemide is 200-400 nM) And it's reversible. Essentially no activity at MAOB. Not worth worrying about I think.

http://link.springer.com/article/10.1163/156856003765764290#page-1


http://www.sciencedirect.com/science/article/pii/0165614780900322

Any idea at what dose amp would significantly (in a statistical sense, meaning that it has antidepressant effects basically) inhibit maoi? My guess is it's higher than all but a few users would ingest. I wonder because I took a therapeutic dose of it and wanted to know whether the AD effect I experienced was sustainable or not. Thanks.
 
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Any idea at what dose amp would significantly (in a statistical sense, meaning that it has antidepressant effects basically) inhibit maoi? My guess is it's higher than all but a few users would ingest. I wonder because I took a therapeutic dose of it and wanted to know whether the AD effect I experienced was sustainable or not. Thanks.

Take a look at this article:

http://www.ncbi.nlm.nih.gov/pubmed/16343411

Group 4 ranged from 0.54 mg/l to 1.00 mg/l, corresponding to the Cmax after the intake of approximately 140–300 mg amphetamine.

Let's just assume the 1.00mg/l corresponds to the 300mg dose. That works out to 7.39uM concentration in the blood. So even with a 300mg dose you're not even approaching the Kd. That's at a maximal blood level as well, levels will be much lower for the majority of the experience. d-Amph as an MAOI is all but an in vitro experimental artifact - it doesn't happen in practice.
 
I'd imagine that has to do with a lack of patience combined with...never mind, the study wasn't done in the US. I was going to say combined with over-prescribing. n>1000, nice. The study does mention that since these were people who had been illicitly found to be taking it from drug testing, the dose was more like 50mg-300mg, 60mg being the maximum recommended amount in many countries. Some need a higher dose but I'd doubt you would find a lot of people taking 100mg or more, but I guess in some places (like America) people are fat as all hell. Some pertinent information on the matter: http://pro.psychcentral.com/prescribing-and-dosing-stimulants-practical-issues/004421.html#. (obviously if its abused you're kind of screwed)

Anyways I think evaluating amphetamine-induced cognitive deficits/benefits based on driving is a little bit forward seeing as driving involves things you wouldn't have to deal with when taking an IQ test, doing paperwork, or otherwise completing a more individualized cognitive task. Of course stimulants raise blood pressure, high blood pressure being a main contributor to road rage. We all know that getting too angry or excited leads to that animalistic feeling that impairs you overall. Thanks for the source though.
 
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