I found this in the 25D thread thought it was interesting
Psoodonym
"I thought 25C and 25D were both highly selective for 5HT2a, so I don't understand why there should be more adrenergic effects with them than other psychedelics. I thought 25C and 25D were both highly selective for 5HT2a, so I don't understand why there should be more adrenergic effects with them than other psychedelics. 5HT2a 5HT2a agonism causes vasoconstriction on its own, meaning all 5HT psychs cause it, at least in certain areas - they actually vasodilate in others). So for a selective 5HT2a agonist agonism causes vasoconstriction on its own, meaning all 5HT psychs cause it, at least in certain areas - they actually vasodilate in others). So for a selective 5HT2a agonist shouldn't the degree of vasoconstriction theoretically rise in constant proportion with the degree of psychedelic effects? If so, a selective agonist's vasoconstrictive effects shouldn't the degree of vasoconstriction theoretically rise in constant proportion with the degree of psychedelic effects? If so, a selective agonist's vasoconstrictive effects should be less than say, a 2C-Xs, because there is evidence many 2C-Xs do have andrenergic effects IN ADDITION TO their 5HT2a agonism (in the form of reuptake inhibition should be less than say, a 2C-Xs, because there is evidence many 2C-Xs do have andrenergic effects IN ADDITION TO their 5HT2a agonism (in the form of reuptake inhibition and mild release). So, given some quantitative subjective intensity level of psychedelia for both a selective NBOMe and a non-selective 2C-X, say a plus 2.5 on Shulgin's scale, and mild release). So, given some quantitative subjective intensity level of psychedelia for both a selective NBOMe and a non-selective 2C-X, say a plus 2.5 on Shulgin's scale, the vasoconstrictive effects of the NBOMe should theoretically be less, correct?
So assuming 25D is similarly selective as 25C, it seems like the worry about the vasoconstriction is justified in so far as the doses are so small it's easy to overdose overdose, but Assuming 25D is similarly selective as 25C, it seems like the worry about the vasoconstriction is justified in so far as the doses are so small it's easy to overdose overdose, but seemingly not for any theoretical implications of the properties of the chemical itself. Of course, many more reports of blood pressure readings during use would be much more seemingly not for any theoretical implications of the properties of the chemical itself. Of course, many more reports of blood pressure readings during use would be much more helpful. helpful.
For what it's worth, I've used 25C up to 3.5 mg intramuscularly in one day (just to test the ridiculous strength of the rapid tolerance development with 25C), and never For what it's worth, I've used 25C up to 3.5 mg intramuscularly in one day (just to test the ridiculous strength of the rapid tolerance development with 25C), and never experienced any worrying symptoms of vasoconstrition or high blood pressure (granted I did not take my blood pressure). If it had vasoconstricting effects not mediated by experienced any worrying symptoms of vasoconstrition or high blood pressure (granted I did not take my blood pressure). If it had vasoconstricting effects not mediated by 5HT2a, and those other mediating channels (like adrenergic ones) are in fact what the spikes in blood pressure reported above are owed to, I imagine I would have definitely had 5HT2a, and those other mediating channels (like adrenergic ones) are in fact what the spikes in blood pressure reported above are owed to, I imagine I would have definitely had overt symptoms at such a high level (I know what to look for from mephedrone use and a few experiments with selegiline and PEA). LSD is the most vasoconstricting psych for overt symptoms at such a high level (I know what to look for from mephedrone use and a few experiments with selegiline and PEA). LSD is the most vasoconstricting psych for me, and I've never gotten any of the sore-back type symptoms I get from it sometimes with 25C."
So it seems like the vasoconstrictive properties are not as much an issue with selective 5-HT2A agonism as the 2C's are, also bearing in mind its only a partial agonist, it shouldnt be much of a problem as say 25D which is a full agonist
I think the potential killer brand is a little harsh on this potential gateway, however I do think an OH or MeO bond would be more effective in both places, maybe add an MeO on the 7 position?