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beta-methylene n-methyl phenethylamine

wungchow

wungchow

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I wonder if this compound will have a nicer effects profile versus b-methyl phenethylamine (reducing the steric bulk at the beta position and increasing lipophilicity). Thoughts?
 

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the b-methyl group slows degradation via MAO, so it has stimulant effects, however it's mostly noradrenergic
 
LuxEtVeritas said:
b-Me-PEA is of no notable effect as I am aware
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Back to this issue; I agree with L et V. So: About what kinda effects are we talking?
 
If only someone, somewhere could figure out where to stick a methyl on this molecule to make a decent recreational drug.
 
Is there any report of CNS effect from any people from beta methyl?
I am just interesting in this as some people do get effect only from high dose PEA.

Anyway, if it is methylene, the conformation would change quite a lot (sp3 to sp2 making the angle between phenyl and alkyl change)

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Edit: Look like I was wrong, the methylene isnt that flat as I think, as i forgot about eclipsing hydrogen, in result it comes

j03p1.jpg
1e8p2.jpg


A fast overlay and MM2 of (S)-isomer of betamethyl and the betamethyllene(displayed in yellow)
shows quite a bit similarity about angle
w6rp3.jpg
 
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NeuronalPerception said:
I would stick with straight PEA.
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Why it's the same thing unless you eat a load of MAOI woith it, which isn't what's been asked (no ne of the PEA stuff you've mentioned in other threads without peer reviewed evidence of the evidence. I don't care hw many anecdotal things you say you have, it needs to be peer reviewed)
 
The related compound without the N-methyl group is part of a group of VMAT-2 (vesicular monamine transporter 2 ) inhibitors, the 3-amino-2-phenylpropenes. These should work to prevent VMAT-2 from taking cytosolic monoamines up into vesicles. They may even with appropriate substitution reverse VMAT-2. Both Methamphetamine and MDMA are known to alter VMAT activity and the ability of the vesicles to suck monoamines back into the vesicles. this combined with monoamine transport reversal pups monoamines out into the synapse.

I do not know whether they cause dumping of the vesicle contents by this mechanism alone rather than by the weak amine mechanism or some other mechanism as yet unknown

I was quite interested in these for a while, in particular the 3,4-methylenedioxyphenyl analog along with the potentially psychedelic 4-something 2,5-dimethoxy analogs I would expect that the methoxy substituted compounds would not retain VMAT activity whereas the 3,4-methylenedioxy would. If they do not have significant VMAT activity the potential psychedelic betamethylene compounds might have a future. this is pharmacological terra incognita and not somewhere I would want to go without animal tox testing.

The evidence as to the desirability of inhibiting VMAT and therefore increasing intracellular monoamine concentration is mixed. short term it probably does limited harm and it does seem to be part of the reason for the effects of MDMA/
the bad news:

1) Reserpine which is known to inhibit VMAT causing depletion of monamines in vesicles and is linked to severe depression, approximately 1 in 5 when it was widely used. Tetrabenazine another VMAT inhibitor is also linked to suicide and depression

2) The increased concentration of cytosolic monamines appears to be important in the neurotoxic effects of METH and MDMA.

3) Reduction in measurable VMAT is linked to depression and appears to play a part in the craving in cocaine addiction



for those interested:
the Bovine chromaffin transporter used in the study below is very similar to VMAT-2.

Perera R, Wimalasena DS, Kandatege W. Characterization of a series of 3-amino-2-phenylpropene derivatives as novel bovine chromaffin vesicular monoamine transporter inhibitors. J Med Chem. 2003;46: 2599-2605.
 
If they do not have significant VMAT activity the potential psychedelic betamethylene compounds might have a future. this is pharmacological terra incognita and not somewhere I would want to go without animal tox testing.
Click to expand...

When I started whittering on about the SAR of 5HT2a agonists in 'Dragonflies, acid & the 5HT2a receptor', it was partly in the hope that someone might think it a reasonable suggestion & investigate their activity in a lab. Appears I'll just have to wait (possibly a bloody long time) to find out as my post grad days are long behind me now.

It'd be nice to find my hunch was right as I can talk shite for Britain sometimes!
 
the Betamethylene analog of 2-cb has been made and from what I understand assayed from very low doses up to the dose where if it was equipotent or more potent than 2-cb threshold psychedelic effects would have been seen, but they weren't.
these compounds are pretty accessible through the related acetophenone. But there is a complete lack of safety info even for distantly related compounds.
 
I'm sure that they are active at some dose, just that they don't seem to be greater potency than their parent compounds. it would be interesting to see what shape the betamethylenes form in solution sort of real world conditions, rather than in silico modelling. COSY NMR anyone?
 
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