• N&PD Moderators: Skorpio | thegreenhand

25F-NBOMe

[etc...etc...] Now when you look at MDMA/MDA, you have that dimethoxy bridge focusing a giant chunk of the structures electronegativity to the benzene end of the molecule. I imagine the bridge as being a sort of 'knife' or more like a better fitting ligand to serotogenic receptors, and as a result, the star of the show is now the empathogenic character brought on about the increased affinity to those receptors responsible. [etc...etc...]

Not even trying to be rude at all, but your understanding of stimulant and entactogen SAR seems pretty half baked. Bridging the dimethoxy only serves to change the orientation of the m-oxygen's nonbonding electrons, so that they lie anti to the 4-pos. That, in turn, changes the binding profile from a 5-HT2A agonist (e.g. 3,4-DMA) to a substrate at SERT/DAT/NET (eg. MDA).
 
Did anyone even notice reformers bioassay? Anyway, thanks for the datapoint, reformer :)
People should spend less time theorising about pharmacology and/or chemistry and more time studying what's already known.
 
Wish I could wipe this thread clean of the irrelevant posts, Erny where are you at and do you have anything to say about this one?
 
reformer said:
I plan to revisit the 25F-NBOMe experiments when time permits, but it's hard to resist the other 25X-NBOMe species for long enough to reduce tolerance and give 25F-NBOMe a fair trial.

Intriguing data. Would you say that the effects, while subtle, proved clearly discernible from placebo or not?

ebola
 
Yes, but...

Would you say that the effects, while subtle, proved clearly discernible from placebo or not?

Yes, but my reason for saying so might sound odd. When it came down to it, I felt that there was a clear, although not very pronounced shift from baseline.

But what makes me pretty sure that "something happened" was more that I experienced that weird in-between state where it feels like your starting to take off, but then you never quite get there. It's surely not baseline, but it doesn't manifest into fully discernible qualitative effects, let alone quantitative effects capable of comparison to previous experiences with other research tools.

It just kept hanging around for a couple of hours, so I ended up deciding to give up on those experiments and add some 25C-NBOMe to the mix in order to properly "launch" and get out of the fugue that was keeping me in limbo.

Now I'm fully intrigued that there aren't more reports on this molecule, and I've resolved to give it a fair go. I haven't touched a 5HT2A agonist for a couple of months, so it should be pretty soon.
 
If the trend towards higher electronegativity and smaller atomic radius -> higher activity were to continue, this one should be the most potent out of the bunch. The precursor is also unsuspicious as it has no activity.
What? Are you saying 2C-C is more potent than 2C-B? I think you're misunderstanding the basic trend here.
 
Nah, that's not what he said.

What? Are you saying 2C-C is more potent than 2C-B? I think you're misunderstanding the basic trend here.

No, he's not misunderstanding, you're taking his post out of context of the overall discussion that was foementing at that point.

Nuke was referring to the 25X-NBOMe series, as the NBOMe series seems to have a reversed potency trend relative to the 2C-X series.

So 2C-I and 2C-E are more potent (and larger and less electronegative) than 2C-C, but for the NBOMe series it is the opposite. 25I-NBOMe and 25E-NBOMe are less potent than 25C-NBOMe.

So, by extending the trend toward fluorine, we might expect that 25F-NBOMe is even more potent than 25C-NBOMe, whereas 2C-F is nearly inactive at any reasonable dose.
 
Now I'm fully intrigued that there aren't more reports on this molecule, and I've resolved to give it a fair go. I haven't touched a 5HT2A agonist for a couple of months, so it should be pretty soon.

May the Schwartz be with you. I am very excited to hear about this so please don't forget about it, could be something very interesting that is overlooked due to 2C-F.
 
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