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Benzydamine- NSAID, Stimulant, Psychedelic?

I'm not a chemist so I don't know about the molecular structure, but the experience reports sound primarily anticholergenic, but they didn't break through into full delirium. Perhaps, it is an anticholergenic but its effects are weak enough that users typically don't fully leave sub-delirium dose territory where perceptions are altered yet one still has insights into the fact that they have taken a drug and the hallucinations are caused by the drug rather then being real events. From my own experiences with anticholergenics (three of them, all were bad, three strikes and anticholergenics are out for me), low doses of datura and diphenhydramine (above recommended doses but below delirium doses) feel vaguely similar to the stimulation of psychedelia but with different overall effects and more of a negative, confused state that tends to bring out feelings of anger, confusion, and negativity rather than the oneness, creativity, insightful thought patterns, and expansion of the mind that I have had from LSD and mushrooms. Although, it is possible for a drug to bind to multiple receptor sites.

Therefore, perhaps it has some serotogenic effects along with a significant amount of anticholergenic effects. I would guess that it probably does have some serotogenic activity, but the experience reports indicate that for most users it probably is overshadowed by the anticholergenic effects. There does seem to be a synergy between serotogenic drugs and anticholergenics, in my experience anyways. One time, while I was on mushrooms, I took 50 milligrams of diphenhydramine (a low dose) and found that it changed the trip to become more "dreamlike" and at one point the whole world really began to feel like it was a dream. I can't describe the difference exactly, but it definitely influenced the trip in a significant way that I will admit probably would make it more difficult to handle for someone who was inexperienced with psychedelics due to the fact that it seemed to create an unusual confusion. Ayahuasca brews also contain anticholergenics in low doses, and it definitely plays a role in altering the ayahuasca experience.

So, perhaps if it binds to both receptors, it really is a unique drug most likely. However, generally speaking, it sounds like this stuff is anticholergenic enough that it probably could easily cause someone to cross over into delirium or end up having their trip turned in a strongly anticholergenic direction (e.g. anger, negativity, and delusional behavior). Plus, it apparently is a strain on the liver and kidneys. Thus, this stuff probably is best avoided honestly.
 
Honestly, that trip report sounds like it was written by a teenager that has probably never taken LSD.
 
If you are feeling melatonin and certizine i would strongly suggest you do not do this at any dose. Based on what ive read it doesnt clearly have a known mechanism (5ht2a cannabinoid mach who knows), has major side effects, and the evidence it increases mood is extremely poor compared to just about every other drug.
 
I thought it was established that benzydamine was a JWH-type cannabinoid agonist.
 
I could only find one paper on that (let me know if you're aware of others), but it does seem highly likely given its structural resemblance to other cannabinoids like pravadoline and AB-FUBINACA, not to mention the fact that the endogenous ligands of NSAID targets are very structurally similar to endocannabinoids.
 
Synthetic cannabinoids can produce deleriant-type effects but that's from CB1 full agonism, more accurately it's just super strong cannabinoid effects and not "normal" deleriant action through e.g. antimuscarinic effects like atropine.

Paracetamol does not metabolize to a CB1 full agonist but instead a FAAH inhibitor (much more mild) explaining why acetaminophen doesn't give a "high".
 
sekio said:
I thought it was established that benzydamine was a JWH-type cannabinoid agonist.
Click to expand...

I can relate that structurally very possible, but the reported effect seems very unlikely cannabinergic action and much more like antimuscarinic.
Is there any study or calculation of its CB-1 binding? I still have doubt in it.

PS. I have first hand experience on very strong CB1 full agonist of indolic/indazolic type, up to the point of admission to hospital before, and the experience is dissimilar to Benzydamine, even the "deliriant" aspect feels very different.
These agents are synthesized (not bought), and characterized using HNMR, CNMR and LCMS with very high purity. (some are MUCH stronger than 018 tho)
 
sekio said:
Paracetamol does not metabolize to a CB1 full agonist but instead a FAAH inhibitor (much more mild) explaining why acetaminophen doesn't give a "high".
Click to expand...

I realize this is getting really, really far from the topic of benzydamine, but I've always wondered if pure AM-404 would actually be able to give a "high" (or, perceptible subjective effects other than just reduced pain) in sufficiently high dosages.
 
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