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Is this the right name? 4-F-MABP

tropics

Greenlighter
Joined
Apr 19, 2008
Messages
30
Location
Canada
I can't find anything on this, I think it's Buphedrone.

Please help with any info?
 
http://www.bluelight.ru/vb/showthread.php?t=531743

I will post the structure if it isn't in the thread I linked to.

edit: no need

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Probably 10-50mg dose, standard NDRI stimulant like Buphedrone or a stronger version of Fleph. Probably much closer to buphedrone than anythiong else. But I'm talking out my ass.
 
Could you explain from a SAR standpoint, what happens
- if you go from MCat to buphedrone or methylone to butylone ?
- What happens between amphetamine and 4-FMP or mephedrone and flephedrone?
- a beta-ketone addition shifts activity towards dopamine and away from serotonine somewhat? correct? what else is important

I wonder why you think this doesn't make sense, do you think a compound has to act on serotonine for a significant part to justify a para-fluor? Does it have to be monoamine release instead of inhibiting reuptake transporters (making 4-fluoro-MDPV useless) or doesn't it?

There is also the 4-methyl version of this compound, I presume you don't see why that is made either?
 
As I understand, 4-fluoro substitutions enhance serotonin release but also increase 5HT2b affinity. not a big deal for seldom use, but bad bad for much more than that.
 
Oh yes, that... cardiac valvular fibrosis. IIRC there are those who remarked that one would have to be a regular user of such compounds to do such notable damage but with these kinds of things it's just too hard (wanted to write heart) to make a sensible claim and drawing a line without giving the receptor affinity and frequency and duration of use of a compound.

In other words, must be exactly like you said: for an insignificant number of uses insignificant damage, but beware if things become significant.
 
hammilton said:
As I understand, 4-fluoro substitutions enhance serotonin release but also increase 5HT2b affinity. not a big deal for seldom use, but bad bad for much more than that.

This sounds right, but I should dig up the Nichols paper on 4-fluoro-amphetamine.

So basically we know that:
1. the 4-fluoro substitution increases serotonergic activity (but not to nearly the same degree as a methyl would) while enhancing selectivity for DA over NE (see amp-->4-fluoro).
2. the beta-ketone increases adrenergic activity (if mainly via metabolism to corresponding beta-hydroxy compounds), decreases serotonergic activity (see mdma-->m1), reduces overall potency, and likely skews activity a bit away from release and toward reuptake inhibition (the latter remains unclear, as many cathinones act as releasers) (see meth-->mcat).
3. extending the alpha-substitution to ethyl tends to yield a compound that acts as a reuptake inhibitor.

Another NDRI...greeeeaaatttt.... :P

(who knows if this would actually pan out though...)

ebola
 
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