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I Like to Draw Pictures of Random Molecules

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Nitropane. DRI, opioid, or tool compound?

nitropane.png


Naphthyladamancaine:
naphthyladamancaine.png
 
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This chemical has an IC50 of 780 nM for the mu receptor and 610 nM for the delta receptor, probably an agonist for both.

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Could also be a monoamine releaser because of the similarity to BZP...

Edit: And to increase the mu affinity, you could try to add a methyl group on that piperazine ring (akin to 3-methylfentanyl), or change one of those benzylic N-substituents to a 2-phenylethyl type substituent.
 
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Anyone know whether the N-demethylated derivative of cyclizine binds significantly to muscarine receptors? It could be a dopamine reuptake inhibitor because of the similarity to benzylpiperazine, and if it doesn't have anticholinergic effects it could even be interesting. There seem to be some new methods to N-demethylate amines with oxidizers and metal ion catalysts, but that of course can't be discussed here in detail.

Edit: You could possibly also make norcyclizine build up in your system by somehow making your urine alkaline (slowing down the renal excretion) and then taking small repeated doses of cyclizine, but a slow buildup isn't really the way how stimulants are used.
 
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I was thinking 'ebati-'aryl SNDRIs or releasers. Where the arene has a nitrogen heteroarom. Wonder how those'd go over.

Also, there's got to be some affinity with those Prozac / Effexor analogs where both rings are just plain cyclohexanes.
 
polymath said:
Anyone know whether the N-demethylated derivative of cyclizine binds significantly to muscarine receptors? It could be a dopamine reuptake inhibitor because of the similarity to benzylpiperazine, and if it doesn't have anticholinergic effects it could even be interesting. There seem to be some new methods to N-demethylate amines with oxidizers and metal ion catalysts, but that of course can't be discussed here in detail.

Edit: You could possibly also make norcyclizine build up in your system by somehow making your urine alkaline (slowing down the renal excretion) and then taking small repeated doses of cyclizine, but a slow buildup isn't really the way how stimulants are used.
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Are you talking about forming the N-oxide with hydrogen peroxide and then using iron sulfate to remove the alkyl group?
 
draculic acid69 said:
Are you talking about forming the N-oxide with hydrogen peroxide and then using iron sulfate to remove the alkyl group?
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Yes, the same thing as in the article that talks about that. In a similar paper the same is done to morphine or codeine and atmospheric oxygen is used as one possible oxidant. The problem is that the demethylated compound can't be separated from the reaction products with simple acid-base extraction, and it will possibly even require chromatography unless there's a significant difference in the boiling points at some reduced pressure.
 
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Here it is, no phenyl shortening so everything is optimum in dimension. "God Of 'Caine" I call it. The ortho-acetoxy gives the enhanced stimulation of the phenyltropanes, the styrene is optimum for the length of the benzoyloxy, the nitrogen tail is about twice cocaine, and the C-1 addition ten times it at DAT and even has SERT & DAT at the expense of NET. I could have used the vinylogous 2beta but went with the more compact isoxazole, which gives a modest boost over the carbmethoxy.
 
The N-sulfonylisocyanate screams reactivity (covalent inhibition anyone) to me, I wouldn't put anything like that in my body. Spoilers: if your substrate binds permanently, Ki doesn't matter much any more, it's just a matter of time before all the enzyme gets inhibited because the rate of reaction between the substrate and enzyme greatly outpaces how fast your body can reform new active enzyme.

I've worked with isocyanates as precursors to polyurethanes. They are nasty sensitizers and also stink - the same things that make them useful to make urethane rubber via reactions with polyols also permit reaction with amines and thiols of protiens, covalently linking bulky groups onto reactive sites of enzymes, crippling activity in general.

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One of the most potent piperidine analogs, note that apparently the potency goes N-phenylpropyl >> N-phenylbutyl > N-phenethyl > N-methyl > N-benzyl. This also suggests N-cinnamyl would be active, similar to bucinnazine. Also, esters of tertiary alcohols (MPPP-type) are more potent than 4-carboxypiperidines.

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I considered that, and now that you bring it up I figure that the assay of improved activity may be off. Everything else gimps activity at the nitrogen though, so either plan old methyl or desmethyl.
 
Nothing seems to be easily found about the derivatives of fentanyl with an N-(3-phenylpropyl) substituent or longer. Maybe it only increases affinity with meperidine-like compounds.

The desmethylcyclizine is also difficult to find information about, but it seemed that in repeated administration of cyclizine the blood levels of norcyclizine remain much lower than of cyclizine itself. The strange, almost fully aromatic DAT inhibitor 4-diphenylmethylpyridine becomes much less active if one of the phenyls is removed, but I'm not sure if there is the same trend with N-benzylpiperazines where there's an aliphatic ring with two nitrogens.
 
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