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

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anorgasmia on ssri's: the relevant 5HT subtype responsible?

I'm confused, I've been reading for hours about how the main suspected culprit is 5HT1a increased activation caused by ssri's, which causes incresed prolactin synthesis, but then again I read that a good treatment for sexual dysfunction in ssri use are 5HT1a agonists!
Obviously both can't be true.
And if there really is (and probably is) a particular 5HT subtype that reduces sexual feelings and response when either: a) subject to serotonin reuptake inhibition or b) the subsequent downgrading or upgrading of receptor types in response to this, then:

can we design an antagonist at that receptor or even a reverse agonist? What subtype? Hmmmm.....and in normal people, would a reverse agonist at this subtype act as a pro-sexual aphrodesiac?
 
4-alpha 3-phenylbutyric acid(phenibut) into a salt

I got side tracked and ended up in the dusty old section of bluelight. One of the members gave an experience about having converted phenibut into a salt from an acid, thus decreasing some pain from intranasal administration and apparently strengthening the oral administration

I woke up on the street, at the time I didn't give it a second thought - it's a very good anxiolytic indeed!) - absolutely zero recollection of the events in between. I found by changing it from it's acidic form to a sodium salt you can increase oral bioavailability quite significantly, and it tastes much less nasty as a salt so it's easier to mix into a drink.
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The Phenibut Thread

It would be in my best interest to know how one would one go about doing this conversion?
 
Textbook acid neutralisation. Add 22.2% by weight of sodium hydroxide (1 molar equivalent to phenibut - preferably add the lye in solution) and mix it really well, then remove the water by evaporation.

Or use your favourite alkali to bring a solution of phenibut to neutrality (ph 6.0-8.0) where it exist as a zwitterionic, doubly-charged form and is very water soluble. One could use sodium bicarbonate if you were hurtin'.
 
isn't the theory that DMT is the immediate metabolic precursor to psilocybin in mushrooms? if so then is all the DMT very rapidly converted to 4-ho and 4-po?

my immediate thought was that there must not be much DMT, if any. but then i got to wondering and i think maybe there is more in there, and perhaps it accounts some what for the increased effects of "shroomahuasca".

hoping for a paper rather than guesses tho.
 
from the 25I-NBOMe wikipedia article:

It is also believed to be the drug that caused a fatal overdose of a teen in East Grand Forks, Minnesota in June 2012, after a "hobby chemist" friend had converted 2C-I that he had purchased online, into the much more potent 25I-NBOMe.
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that's not even possible, is it? here's the link given as a reference for that portion: http://www.inforum.com/event/article/id/365948/publisher_ID/1/
 
It's definitely possible, but the article doesn't mention 2C-I. I think it's more likely he was just buying 25I and laying sheets.
 
To what extent should we attribute d-amphetamine's propensity to increase synaptic dopamine to reversal of DAT versus activity at VMAT2? What about for norepinephrine?

ebola
 
ebola? said:
To what extent should we attribute d-amphetamine's propensity to increase synaptic dopamine to reversal of DAT versus activity at VMAT2? What about for norepinephrine?

ebola
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You need both for synaptic dopamine to increase significantly, VMAT2 reversal ups cystolic dopamine and DAT reversal results in an efflux of cystolic dopamine. The same should go for norepinepherine.
 
(±)-1-(1,2-Diphenylethyl)piperidine maleate (lefetamine analog and NMDA antagonist)

I just noticed [insert major biopharm company here] offers it on its site

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What immediately catched my eye is that this compound is a lefetamine analog (piperidine instead of dimethylamino-group) and next to that it is offered as a racemic mixture (lefetamine being the l-isomere of 1,2-Diphenyl-1-dimethylaminoethane is the active one, the d-isomere not being very active but about of similar toxicity).

My obvious question is, what is known about the activity of this compound?
Tocris states:
Biological Activity
High affinity antagonist at the ion channel on the NMDA receptor.
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but the only paper that mentions it is:

Ragawski (1993) Therapeutic potential of excitatory amino acid antagonists: channel blockers and 2,3-benzodiazepines. TiPS 14 325. PMID: 7504360.
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which I cannot immediately locate... maybe at the pharmaceutical departement of the local uni, let's hope.

EDIT: and there's this paper, should be easier available:

http://www.ncbi.nlm.nih.gov/pubmed/19345586

NMDA receptor affinities of 1,2-diphenylethylamine and 1-(1,2-diphenylethyl)piperidine enantiomers and of related compounds.

Bioorg Med Chem. 2009 May 1;17(9):3456-62. Epub 2009 Mar 19
Berger ML, Schweifer A, Rebernik P, Hammerschmidt F.

Source
Center for Brain Research, Medical University of Vienna, Spitalgasse 4, Vienna, Austria. [email protected]

Abstract
We resolved 1,2-diphenylethylamine (DPEA) into its (S)- and (R)-enantiomer and used them as precursors for synthesis of (S)- and (R)-1-(1,2-diphenylethyl)piperidine, flexible homeomorphs of the NMDA channel blocker MK-801. We also describe the synthesis of the dicyclohexyl analogues of DPEA. These and related compounds were tested as inhibitors of [(3)H]MK-801 binding to rat brain membranes. Stereospecificity ranged between factors of 0.5 and 50. Some blockers exhibited stereospecific sensitivity to the modulator spermine. Our results may help to elucidate in more detail the NMDA channel pharmacophore.
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It can be found online here:
http://cbr.meduniwien.ac.at/fileadmin/db_files/pub_art_185.pdf

Note on page 3458:
Incorporation of the nitrogen atom of the primary amino group of (S)-5a into a piperidine ring resulted in the highly potent NMDA receptor channel blocker (S)-6, five times more potent than (S)-5a, with comparable stereoselectivity (factor 49)
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You're not allowed to source or even discuss vendors on this site :\

You should delete the first part of your post.

Welcome to Bluelight <3
 
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