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for educational and safety purposes
4-HO-DET and 4-AcO-DET both come up in the same conversations; they overlap on Serotonin. 4-HO-DET: 4-HO-DET (4-hydroxy-N,N-diethyltryptamine, ethocin, CEY-19) is a synthetic tryptamine, the diethyl homolog of psilocin first investigated by Albert Hofmann and colleagues at Sandoz. 4-AcO-DET: 4-AcO-DET (4-acetoxy-N,N-diethyltryptamine) is a synthetic tryptamine, the acetate ester of 4-HO-DET and the diethyl homolog of psilacetin.
4-HO-DET (4-hydroxy-N,N-diethyltryptamine, ethocin, CEY-19) is a synthetic tryptamine, the diethyl homolog of psilocin first investigated by Albert Hofmann and colleagues at Sandoz. It acts as an agonist at the 5-HT2A serotonin receptor, the principal molecular target of classic serotonergic psychedelics, producing psilocin-like effects of moderate duration. In rodent drug-discrimination testing it fully substitutes for the hallucinogen DOM, and structure-activity studies place it among the psilocybin-like 4-hydroxytryptamines with retained 5-HT2A efficacy. Historically it was explored, together with its phosphate ester CZ-74, as a shorter-acting alternative to psilocybin in psycholytic psychotherapy. Contemporary pharmacological documentation remains modest.
4-AcO-DET (4-acetoxy-N,N-diethyltryptamine) is a synthetic tryptamine, the acetate ester of 4-HO-DET and the diethyl homolog of psilacetin. It is generally regarded as a prodrug that is hydrolyzed in the body to the active phenol 4-HO-DET, an agonist at the 5-HT2A serotonin receptor; in rodent drug-discrimination testing it and its 4-hydroxy metabolite fully substitute for the classic hallucinogen DOM, consistent with a psilocybin-like mechanism. Structure-activity studies indicate that O-acetylation lowers intrinsic 5-HT2A potency while preserving efficacy, supporting the view that in vivo activity depends on deacetylation. In vitro toxicology has flagged potential cardiac liabilities, including hERG potassium-channel inhibition and QT prolongation, and the compound has been identified in forensic casework. Controlled human pharmacology remains sparsely documented.
both fingerprints on one instrument; where the marks line up the two compounds work the same lever, where a slot goes dark only one of them touches it. read straight from each entry's affinity table; nothing here is invented.
agonist
agonist (via active metabolite)
agonist
agonist
agonist
agonist
strengths are the entries' qualitative ratings (strong / moderate / weak); Ki and EC50 figures appear where an entry records them.