3-MeO-PCE and 3-HO-PCE both come up in the same conversations; they overlap on Glutamate. 3-MeO-PCE: 3-MeO-PCE (3-methoxyeticyclidine) is a methoxylated analog of eticyclidine (PCE) in the arylcyclohexylamine class that acts as an NMDA receptor antagonist, reportedly with higher NMDA receptor binding affinity than phencyclidine itself. 3-HO-PCE: 3-HO-PCE (3-hydroxyeticyclidine) is an arylcyclohexylamine of the eticyclidine (PCE) family that produces dissociative, hallucinogenic, and euphoric effects and is presumed to act as an NMDA receptor antagonist.
3-MeO-PCE (3-methoxyeticyclidine) is a methoxylated analog of eticyclidine (PCE) in the arylcyclohexylamine class that acts as an NMDA receptor antagonist, reportedly with higher NMDA receptor binding affinity than phencyclidine itself. Positioned within the PCP/PCE family, it tends to be more stimulating and disinhibiting than ketamine and has been implicated in fatal intoxications, typically in combination with other substances. Its in vitro and in vivo metabolism has been mapped in human liver microsomes, a zebrafish model, and authentic urine samples, proceeding through hydroxylation, O-demethylation, and N-dealkylation, with a hydroxylated metabolite proposed as a biomarker of use. It remains an obscure research chemical with limited controlled human data.
3-HO-PCE (3-hydroxyeticyclidine) is an arylcyclohexylamine of the eticyclidine (PCE) family that produces dissociative, hallucinogenic, and euphoric effects and is presumed to act as an NMDA receptor antagonist. As with other 3-hydroxy arylcyclohexylamines, the phenolic substituent is associated with added opioid-receptor activity, which may contribute sedative properties on top of dissociation. Its metabolism has been characterized in human liver microsomes and authentic urine and hair samples, proceeding through N-dealkylation, deamination, oxidation, and glucuronidation, and paralleling that of the related designer ketamine O-PCE. In silico profiling of PCE and PCP analogs suggests moderate acute toxicity with cardiotoxicity signals, while robust human pharmacological data remain scarce.
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.
Antagonist
Antagonist
Agonist
strengths are the entries' qualitative ratings (strong / moderate / weak); Ki and EC50 figures appear where an entry records them.