Anyone who claims that 25I-NBOMe and other NBOMes were always seen as less worthwhile has no idea what they’re talking about.
@FuckinAcidMan says “surprisingly pleasant for some folks” but it’s not surprising at all if you were here, NBOMes were a massive hit when they first came out - before they had ever killed anybody - on a scale that actually has little comparison in the research chemical world. NBOMe fever was wild, and we’re not just talking about 25I-NBOMe, 25B-NBOMe, and 25C-NBOMe, but also 25D-NBOMe, 25E-NBOMe, 25P-NBOMe, 25iP-NBOMe, 25N-NBOMe, 25G-NBOMe, 25F-NBOMe, 25T7-NBOMe, mescaline-NBOMe, all of these things and more were being discussed, sought out, and either made available publicly or privately synthesized and traded at the time, with people trying to build up lifetime supplies of as many different ones as possible, and many saying things like that 25I-NBOMe would be the “next LSD” and that 25C-NBOMe was “better than mescaline” and other things like that that people like to say. It pretty much seemed like we were in a brand new and previously unexpected frontier of psychedelic research chemical exploration and people were definitely on board, until people started dying on the NBOMes… and then the public sentiment changed pretty fast.
I think this history should be accurately preserved rather than either pretending like or assuming that no one ever really liked them that much in the first place which many people do, but that being said, I am 100% behind the community’s movement to move away from and discourage use of NBOMes. They are objectively the most dangerous psychedelics in existence, there is no arguing this, and they exist among a practical sea of equally fascinating psychedelic molecules that carry literally none of the same danger whatsoever. I will never use NBOMes in my life and will actively tell other people not to use them. And yes, other drugs can kill you too and at a greater rate and they’re still widely used - but many drug users assume that other drug users take all the same risks they do, and that’s just not the case. I specifically avoid all kinds of drugs that have those risks, not just NBOMes, despite the fact that I still regularly get high and trip on many things like other psychedelics, safe dissociatives, cannabis, kratom, blue lotus, salvia, and amanitas, and yet if you were to recommend NBOMes to me, you would be recommending to me the most dangerous drugs I’d taken in many years at this point, and if I died as a result, that’s something that never possibly would have happened if you never made that recommendation to me.
In the worlds of psychedelics and safe drug use, NBOMes are bad. I’m sorry to anyone who wishes that wasn’t the case, but it is. I’d be much happier if they were safe drugs too, I miss the days when people basically didn’t think about death as a risk from taking psychedelics.
That all being said, the
actual reason I’m making this post… is to point out that 25I-NBOMe and other NBOMes are, in fact, not full agonists at 5-HT2A receptors. The studies that said they were used scientific setups that would be understood by other scientists and amateurs who struggled to understand what it all meant, but not by the average person not looking it themselves. The NBOMes reliably produced full agonism in brain slices with plenty of receptor reserve, which makes them useful test ligands, but it doesn’t mean they have maximum intrinsic efficacy; in fact, the vast majority of psychedelics in existence including things like LSD and psilocin generally register as full agonists in this kind of test. Later studies, such as
this one have actually found that the activation efficacy of NBOMes at 5-HT2A receptors is generally really low, around 25-35%, which is even lower than regular 2C-x molecules, considerably lower than DOx molecules, and in fact even lower than the vast majority of synthetic tryptamines, some of which, such as DiPT, actually do tend to register as full agonists in this specific kind of test.
Intriguingly, the same study linked above shows that NBOMes are generally also more potent than LSD at 5-HT2A receptors, with 25I-NBOMe for instance having seven times higher affinity there than LSD, and LSD actually having similar activation efficacy to the NBOMes at 28%. However, despite this, a “standard dosage” of LSD is 100 micrograms and blotters of 25I-NBOMe would usually contain something like 1000 micrograms or more. I’m not saying the comparison is going to be exact - drug science is more complicated than that - but based on these numbers alone, one might be left with no choice but to point out that that “standard dosage” of 25I-NBOMe could be as much as like seventy times stronger than the “standard dosage” of LSD, given that it’s seven times more potent at the receptor with similar levels of activity there and yet you take ten times as much by weight. So, here’s an interesting question for anyone still reading this post at this point: are the NBOMes actually genuinely more active than other psychedelics like LSD visually and energetically and stuff like they’re often claimed to be, or do people simply take them at ridiculously, hilariously high dosages in comparison to other psychedelics, without even realizing what they’re doing? Also, is it really that crazy that people have died from dosages like 2-4 mg of 25I-NBOMe when that’s theoretically equivalent to like 140-280 doses of LSD?
Basically I just wanted to point out that people think NBOMes are dangerous because they’re super strong psychedelics, but the scientific research I’ve seen suggests to me that the reality might be more like, they’re dangerous because they’re actually relatively weak psychedelics but being taken at ludicrously high dosages to overcome that weakness. By contrast, some of the actual strongest 5-HT2A receptor agonists, like DOx amphetamines and some synthetic tryptamines, actually seem safer and have been used regularly for much longer than NBOMes without the same issues.
/rant
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