The site does not allow crossposting. There are a lot of oversimplifications in this thread, but I suppose that's par for the course (not to be too disrespectrful; this site serves a different purpose). Empathogens based on the N-benzyl extensions of the PEA skeleton are very unlikely to be successful, for the simple reasons that there remains to be a high potency (on the order of milligrams, or even low tens of milligrams) empathogen developed, and hence the level of empathogenic activity will be be wildly unbalanced with the psychedelic activity, and empathogenic activity as we currently define it (MDMA-esque) depends on a wide range of simultaneous target activation that a ligand designed for specific activation of a specific target is going to be unable to accomplish (almost by definition - don't try to get a monogamous drug to be polygamous/promiscuous!), and finally because the N-benzyl moiety will interfere with the currently understood pharmacophore of empathogens (bits all hanging around in the wrong places).
Oh, I should probably confirm the dosages involved, since this stuff is about to hit primetime it would seem, for better or for worse (probably worse, people can't seem to use the existing 2Cxs and DOxs responsibly!) ...
Insufflated: threshold ~ 100ug, +2 @ 250ug, +3 @ >400ug
Vapourised, as HCl salt (freebase sometimes shows signs of decomposition if vapourising): threshold ~ 30ug, +2 @ 50ug, +3 @ 150ug. Reduced duration. Favourite method for author.
Oral: no appreciable activity past 1mg, 'ceiling' level is reached, probably pharmacokinetic in origin.
Repeated dosing past the 1hr mark seems to only increase duration and return intensity to first dose levels, not beyond, probably a function of very rapid receptor downregulation.
