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

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Many people have had experiences where stimulants potentiate dissociatives in general. The precise mechanism is unknown. However, alcohol and tramadol should also exert such potentiation, exerting minor NMDA antagonism.

ebola
 
Br J Dermatol. 2011 Jun 28. doi: 10.1111/j.1365-2133.2011.10490.x.
Serotonin induces melanogenesis via serotonin receptor 2A.
Lee HJ, Park MK, Kim SY, Park Choo HY, Lee AY, Lee CH.

College of pharmacy, Dongguk University, Seoul 100-715, Korea Graduate School of East-West Medical Science, Kyung Hee University Global Campus, #1 Seocheon-dong, Giheung-gu, Yongin, Gyeonggi-do 446-701, Republic of Korea College of Pharmacy & Division of Life & Pharmaceutical Sciences, Ewha Womans University, Seoul 120-750, Republic of Korea Department of dermatology, College of medicine, Dongguk University, Ilsan Hospital, Goyang, Korea.

Background:  The serotonin levels were increased by light exposure but the role and mechanism of serotonin in the pigmentation of skin cells are unclear. Objectives:  To clarify the effect of serotonin on melanogenesis and to determine the serotonin receptor subtype involved. Methods:  B16F10, SK-MEL-2 and Melan-a cells were cultured DMEM with low FBS. Three cell lines were treated with various concentration of serotonin (5-HT), 5-HT receptor agonists, and antagonists. The involvement of the 5-HT receptor 2A (5-HTR2A) was examined by gene silencing and 5-HTR2A antagonists. Results:  5-HT and the 5-HTR2A agonist, DOI increased the melanogenesis in three cell lines. These increased events were suppressed by 5-HTR2A antagonists or gene silencing of the 5-HTR2A gene. Conclusions:  The serotonin receptor 5-HTR2A is involved in melanogenesis. These findings highlight the role of serotonin and suggest new ways of controlling melanogenesis.
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So not only will DOI make you trip balls, it'll help you get that California tan you always wanted too!
 
Can someone explain to me something about the structures of the 2C-X drugs? Basically, without getting into any synth details, I would like to know why when a halogen is bonded to 2C-H it ens up in the 4 position instead of the 1 or the 3. My hypothesis would be that it has to do with the electrostatic potential at that location (para, or 4 position) on the phenyl. The other available positions are closer to the mass of electrons that are part of the ethylamine carbon chain. Anything close to the actual answer or am I talking BS?
 
steric hindrance to electrophilic substitution at other positions on the ring?
 
6' bromination also happens in e.g. illicit production of 2cb if the conditions are not controlled, I thought.
 
Cool so it's really that there are a couple of different reasons all working in concert to make the 4-position the most friendly to halogen substitutions.
 
Both the methoxy groups and the aliphatic chain are ortho/para directing with regards to aromatic susbstitution. If bromination was to occur at the 3' position it would be meta to two ortho/para directing groups and therefore not as favorable as the 4' position. As seiko mentions bromination could also occur at the 6' position as it would be ortho to two groups and meta to one as the 4' position. However the 6' position is more sterically hindered due to the aliphatic chain. Also the amine is probably protonated under the reaction conditions. This destabilizes the partly charged transistion state at the 6' position. Its mostly about sterics and electronics :)
 
EDIT: Wikipedia was wrong saying dexamp is (R) so i changed it. Teaches me not to rely on wikipedia as much.
Spent a while trying to figure it out, ends up its just that somebody put the wrong IUPAC name for dextroamphetamine :(. So a lot of this below i get now.


I have a question regarding ChemBioDraw Ultra.

di-1Z9H.gif

i forgot how to imbed an image apparently so here's the link:
http://anony.ws/di-1Z9H.gif

I'm puzzled with (S) and (R), dextro and levo. Why when i simply select the molecule, and invert it vertically does the R change to an S or visa versa? Do I have a corrupt copy of ChemOffice?

I was trying to make a correct image of the dextro versions of N-hydroxy-amphetamine or N-hydroxy-N-ethylamphetamine etc. Also the wedged bond and hashed wedged bond is confusing. Sometimes it will put the chiral carbon towards the amine if i type something into "convert name to structure". I don't remember previous versions of chemdraw doing things like this..

Is (R)-amphetamine and (R)-methamphetamine both the dextro versions? Google turns up different results, some saying d-meth is (S) etc. Apparently both are (S). Never mind..ehh.
 
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when you flip it two-dimensionally you are in effect creating the original molecule's mirror image (its optical isomer if my terminology is correct... never taken orgo). if you wanted the oxygen to point downwards without changing which optical isomer you are looking at you would need to rotate the molecule so that the phenyl is on the right rather than flipping it.

look at the original and the flipped molecule... there's no way you could rotate them in 3D space so that they overlap, right? therefore they are optical isomers.
 
Wow, thanks for that! I'll fool around with it.

But this version sucks.. The useful tool "Convert name to structure" its like they went backwards, more like a downgrade. I used to be able to type in all sorts of stuff like d-amphetamine, levoamphetamine, now it doesn't understand that. I have to be very specific. Gonna try this chemsketch its free.
 
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I have a three-part question.

1. I am taking 200 mg of amisupride every morning. At this dosage it "preferentially block inhibitory pre-synaptic autoreceptors". What does that mean?

2. What will the effect of that dosage of amisulprider be with regards to various stimulants?

3. Somehow I seem to get more euphoria when I take amisulpride. Is that "right"? Or is it just placebo?
 
Hi guys,

Was hoping to get chemistry info about the pill-test kits. My understanding is limited. So (in the marquis) sulphuric acid acts as a catalyst and formaldehyde reacts with the compound to produce new compounds. These new compounds have colours? Can someone go into some detail?

Can someone think of an improved test kit? Would it be possible (theoretically) produce a test kit (or series of kits) that was able to make finer distinctions between compounds?
 
mukaki said:
I have a three-part question.

1. I am taking 200 mg of amisupride every morning. At this dosage it "preferentially block inhibitory pre-synaptic autoreceptors". What does that mean?

2. What will the effect of that dosage of amisulprider be with regards to various stimulants?

3. Somehow I seem to get more euphoria when I take amisulpride. Is that "right"? Or is it just placebo?
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1. The axon of the pre-synaptic neuron stores, produces(?) and releases neurotransmitters into the synaptic cleft where they bind to receptors on the post-synaptic neuron, transmitting a signal. Autoreceptors are located on the pre-synaptic neuron and bind the same neurotransmitter, but the effect is generally to reduce the amount of neurotransmitter produced/released by the neuron, so they provide negative-feedback to regulate neurotransmitter release. Blocking dopamine autoreceptors will increase dopamine release and, therefore, dopaminergic neurotransmission.

2. I guess it would potentiate the dopaminergic component of stimulants.

3. That's the effect I'd expect, though I tried 100mg amisulpride and maybe 5mg aripiprazole and noticed no effect. Were you told it should have that effect when you started taking it?

I have a related question, a doctor prescribed low dose (5mg) aripiprazole to try to counteract hyperprolactinemia caused by risperidone (8mg I think, amisulpride initially caused the problem, was switched to risperidone with no improvement.) Don't know if it's working yet, but is there any reason to think this would be any different to simply reducing the dose of risperidone slightly? I'd expect the overall effect to be the same, a slight increase in dopaminergic transmission, unless there's maybe selectivity for different brain areas between the two drugs?

lab slave said:
Hi guys,

Was hoping to get chemistry info about the pill-test kits. My understanding is limited. So (in the marquis) sulphuric acid acts as a catalyst and formaldehyde reacts with the compound to produce new compounds. These new compounds have colours? Can someone go into some detail?

Can someone think of an improved test kit? Would it be possible (theoretically) produce a test kit (or series of kits) that was able to make finer distinctions between compounds?
Click to expand...

There are several reagent tests you can use, see the wiki page.
 
There are several reagent tests yes, and using them in combination helps narrow the results, but there is only so narrow they can go. I'm mostly interested in understanding the reaction(s).
 
skillet said:
1. The axon of the pre-synaptic neuron stores, produces(?) and releases neurotransmitters into the synaptic cleft where they bind to receptors on the post-synaptic neuron, transmitting a signal. Autoreceptors are located on the pre-synaptic neuron and bind the same neurotransmitter, but the effect is generally to reduce the amount of neurotransmitter produced/released by the neuron, so they provide negative-feedback to regulate neurotransmitter release. Blocking dopamine autoreceptors will increase dopamine release and, therefore, dopaminergic neurotransmission.

2. I guess it would potentiate the dopaminergic component of stimulants.

3. That's the effect I'd expect, though I tried 100mg amisulpride and maybe 5mg aripiprazole and noticed no effect. Were you told it should have that effect when you started taking it?
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Thank you for the quick and precise answer. The stimulants I take are not prescribed, and my psychiatrist did not say anything about stimulants. I don't think she knows that's how amisulpride works....
 
lab slave said:
Hi guys,

Was hoping to get chemistry info about the pill-test kits. My understanding is limited. So (in the marquis) sulphuric acid acts as a catalyst and formaldehyde reacts with the compound to produce new compounds. These new compounds have colours? Can someone go into some detail?

Can someone think of an improved test kit? Would it be possible (theoretically) produce a test kit (or series of kits) that was able to make finer distinctions between compounds?
Click to expand...

Thin-layer chromatography would be the way to go. I doubt you'd get people signing up to buy a TLC kit, it's cheap but a bit complicated for the typical raver.

DanceSafe sells multiple reagent tests which is the best you'll likely do.
 
Well, you also need reference compounds of relatively high purity for a TLC analysis to work properly. I agree that TLC analysis would be a bit too complicated for the average raver.
 
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