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☛ Official ☚ The Big & Dandy RH-34 Thread

blueberries

Bluelighter
Joined
Jan 13, 2011
Messages
339
i had a bit of a look around and found next to nothing on it
its supposed to be a selective partial 5-HT2A receptor agonist
does anyone have any experience with this compound?
if not would we see notable activity or would it be an anti-depressant?
it looks quite interesting, especially as we'll get to see the quinoline side of psychedelics

RH-34_structure.png
 
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I noticed the name Ralf Heim at the Wikipedia article who's work the 25x-NBOMe compounds are based on. So, this may be something to keep an eye on. I also noticed this:

http://en.wikipedia.org/wiki/5-MeO-NBpBrT

Can someone here with the knowledge take a look at this molecule? Does this suggest something like an NBOMe version of a tryptamine?
 
This substance is covered in the same german dissertation as the 25X-NBOMe-compounds are. According to this publication it is a relatively selective partial agonist at 5-HT2A but is an antagonist (no intrinsic activity) at several other targets, e.g. 5-HT1B, 5-HT3, alpha1D, beta1, H1,2 and muscarinic receptors.
Take into consideration that several compounds exhibit 5-HT2A partial agonism but no psychedelic effect in humans.

It may be interesting as a novelty but I wouldn't really want to toy around with that one, I think.
 
This is pretty insane, new chemicals of every kind are just going to keep appearing on the market. Also, it does look like an NBOMe version of a tryptamine except instead of the methoxy ground present in the NBOMe it is instead a bromine (though I am no professional source) which is pretty radical that this many variations of psychedelics have been made.
 
People were discussing 5-MeO-NBpBrT. If you can't understand the properties of a 5HT2a antagonist you shouldn't be trying superpotent psychedelics.

RH-34 won't be psychedelic. I may have read this, but I can't remember. Call it a hunch but its simply too different from conventional agonists. There are plenty of non-psychedelic 2A agonists. Its all about phospholipase ratios.
 
It should act as a psychedelic - but whether it's a good one or not will require a bioassay.
 
RH-34 Could be psychedelic, its hard to say for sure. I seem to recall hearing some second or third hand info saying the tryptamines using the nbome pharmacore either weren't effective or as effective. Can't really recall. May have to brush up on my German & look through the Heim thesis again.

My question would be as to whether its oral bioavailability would be high enough for that to be an effective ROA
 
Yeah it sounds familiar to me as well, especially the structural formula.

Just like the more bulky NBOMe's e.g. 25iP-NBOMe there is a possibility that it could act in paradoxical ways, antagonizing 5-HT2A like ketanserin or as an inverse agonist or fuck if I know. I'm not sure if it would be similar to an antipsychotic, it could be even more messy. The activity sounds controversial, this warning was already given in a previous post. Better stay away. What is mentioned in the wiki page is theory and speculation, the compound is based on ketanserin which apparently has some affinity for adrenergic receptors and histaminergic receptors, if that action is docking and blocking / antagonizing - and the NBOMe moiety reverses this... you could expect adrenergic and histaminergic agonism.
Remember the vasoconstriction potential of something like 25D-NBOMe? Imagine that but even much worse. Potential killer.

No fucking way I would take this no matter what money you would offer.
 
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?
 
That compound may not be as selective for 5-HT receptors as 25x-NBOMes. That publication says it binds about 10 times stronger to 5-HT than to H1/2, M3 and alpha 1D/ beta 1, thats not so much difference (25x-NBOMes show a ratio of ca. 1000-10000) and psychedelic effects are certainly not guaranteed. To me it sounds like a potentially dangerous gamble. Keep that possibility in mind and be very careful, if you really must try it.
 
Yeh. I'm all for taking drugs but this shit is stupid. The same people who bitch about SSRIs are willing to take any potential 2A agonist that comes along.
 
This compound is even less potent than serotonin itself and selectivity is mediocre at best and the counterscreening is not exactly comprehensive. Bulk sellers will sell everything labelled as a 5-HT2A agonists on Wikipedia. Compounds show up there before they are even known in the literature. Somebody make a fake entry with a fake molecule and two weeks later we will have chinese bulk sellers offering it for sale.
 
Seen retailers offer this at a very high price cut down to 10%. Worthless crap usually has prices that are suggestive of the substance being worthless crap. Such fine deductive skills I have, eh? I'm imagining some sort of stoning psychedelic, but only time will tell. I sure the hell ain't gonna try it. Same vendor is also NOT offering this in bulk, which they usually do whenever they want to get rid of a shitty product.
 
Watch it with the source & price discussion tendencies, people.
 
Wow there's a shit storm over there at 420chan. Better shy away from this one folks.
 
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