Hi. I'm on the lookout for a 5ht2b antagonist that does not cross the blood brain barrier. I believe this could be the key to using serotonergic drugs without causing heart valve overproliferation over time. Does anyone know of anything? Also, any comments about psychedelics with low 5ht2b agonism would be great. I recently learned that 25i-NBOME might have a low affinity for 5ht2b, and at the dosage level of 1mg or less, this could mean it has almost no adverse effects on heart valves even with heavy use. All comments, even those that do not directly relate to these questions, are welcome and appreciated.
5ht2b antagonist that does not cross blood brain barrier
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Jekyl Anhydride
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Solipsis
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If LSD binds to 5-HT2a and 5-HT2b for extremely long times, I wonder if a 5-HT2b antagonist will even usually be any competition since it would just be a matter of time before most receptors are occupied by LSD and related lysergamides possibly for hours.
I fear combining a psychedelic with a 5-HT2b antagonist may be unsafe for different reasons but unfortunately I am kinda out of practice in this subject and am not sure about the exact reason or mechanism. Maybe you should inquire in Neuroscience & Pharm about that.
Taking NBOMe's to try and make things safer does not make a lot of sense to me. Highly imbalanced and selective effects on these receptors can apparently have potentially dangerous cardiovascular effects, acute ones unrelated to chronic formation of cardiac fibrosis but more like severe local vasoconstriction which may even fuck with blood supply to vital organs, possibly affecting this before the extremities compared to DOX / Br-Dragonfly OD. At least iirc this was an analysis by a medical professional?
This may be a cop out but just moderate your use of psychedelics and if you are worried about something like microdosing you may just wanna wait until more research is done on what kind of pattern of activation of 5-HT2b causes most significant fibrosis. The pharmacodynamic pattern of lysergamides seems to be so much different than from most others, it's like apples and oranges. You/we would have to find out whether fibrosis is started forming even with strong acute activation of 5-HT2b or whether it requires chronic activation and what the functional selectivity of the weird long binding action of lysergamides even means for this etiological mechanism.
You gotta ask yourself whether it is really worth experimenting when taking e.g. shrooms with reasonable frequency doesn't seem like the most dangerous thing in the world.
I fear combining a psychedelic with a 5-HT2b antagonist may be unsafe for different reasons but unfortunately I am kinda out of practice in this subject and am not sure about the exact reason or mechanism. Maybe you should inquire in Neuroscience & Pharm about that.
Taking NBOMe's to try and make things safer does not make a lot of sense to me. Highly imbalanced and selective effects on these receptors can apparently have potentially dangerous cardiovascular effects, acute ones unrelated to chronic formation of cardiac fibrosis but more like severe local vasoconstriction which may even fuck with blood supply to vital organs, possibly affecting this before the extremities compared to DOX / Br-Dragonfly OD. At least iirc this was an analysis by a medical professional?
This may be a cop out but just moderate your use of psychedelics and if you are worried about something like microdosing you may just wanna wait until more research is done on what kind of pattern of activation of 5-HT2b causes most significant fibrosis. The pharmacodynamic pattern of lysergamides seems to be so much different than from most others, it's like apples and oranges. You/we would have to find out whether fibrosis is started forming even with strong acute activation of 5-HT2b or whether it requires chronic activation and what the functional selectivity of the weird long binding action of lysergamides even means for this etiological mechanism.
You gotta ask yourself whether it is really worth experimenting when taking e.g. shrooms with reasonable frequency doesn't seem like the most dangerous thing in the world.
perpetualdawn
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If it turns out that 5ht2a agonism really is the magic behind microdosing, and that chronic 5ht2a activation in LSD microdosing turns out to be damaging to the heart, it could be possible that nbomes are actually a safer microdose than LSD, ironically. That takes a couple of "what ifs..." so it's more than speculative, but I think we could be cautiously open to that possibility.
There could be dangers around the full-agonism of nbomes regardless of dosage too though, and anyways having nbome around for microdosing would still be an accident waiting to happen.
There could be dangers around the full-agonism of nbomes regardless of dosage too though, and anyways having nbome around for microdosing would still be an accident waiting to happen.