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    Etoxadrol molecular structure

    Etoxadrol Stats & Data

    Cl-1848c U-37862a
    NPS DataHub
    MW261.36
    FormulaC16H23NO2
    CAS28189-85-7
    IUPAC(2S)-2-[(2S,4S)-2-ethyl-2-phenyl-1,3-dioxolan-4-yl]piperidine
    SMILESCCC1(OCC(O1)C1CCCCN1)c1ccccc1
    InChIKeyINOYCBNLWYEPSB-XHSDSOJGSA-N
    Psychoactive Class Dissociative
    Half-Life Unknown in humans (clinical reports describe effect‑windows rather than PK half‑life).

    Effect Profile

    Curated
    Dissociative 6.4

    Strong dissociative depth with moderate motor impairment, low mania and insight

    Dissociative Depth×3
    10
    Mania / Compulsion×1
    2
    Insight / Novel Thought×2
    2
    Motor / Sensory Impairment×1
    7

    Tolerance & Pharmacokinetics

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    Half-Life
    Unknown in humans (clinical reports describe effect‑windows rather than PK half‑life).
    Addiction Potential
    Moderate: PCP‑like reinforcing properties demonstrated in non‑human primate self‑administration; dissociatives in this class carry abuse liability and redosing tendencies. Human non‑medical use data are extremely limited.

    Cross-Tolerances

    ketamine
    50% ●○○
    PCP analogues
    50% ●○○
    other uncompetitive NMDA antagonists
    50% ●○○

    Harm Reduction

    drugs.wiki

    Etoxadrol is a 1,3‑dioxolane piperidine NMDA channel blocker developed as a dissociative anesthetic. In a 28‑patient surgical series, 0.75 mg/kg IV produced profound analgesia/amnesia with active airway reflexes, modest increases in blood pressure/heart rate, and tachypnea; alternating nystagmus and vivid dreams were common, with ~20% reporting unpleasant dreams that could persist up to 24 h. One overdose (4.65 mg/kg IV) caused catalepsy, amnesia, and analgesia lasting 6 days. These findings underline that use outside monitored settings is hazardous due to immobility, emesis, and aspiration risk despite nominal preservation of airway reflexes. Combination with CNS depressants (alcohol, benzodiazepines, opioids, GHB/GBL) increases risk of unconsciousness and aspiration; stimulant or MAOI co‑use may exacerbate hypertension and tachyarrhythmias. Class‑typical tolerance and cross‑tolerance with other uncompetitive NMDA antagonists can emerge quickly; spacing exposures reduces cumulative cognitive disturbance. Identity/adulteration risk is high in any unregulated context; reagent kits are insufficient to confirm this scaffold—only instrumental analysis (e.g., GC‑MS/HR‑LC‑MS) can verify identity and detect potent adulterants. Psychological emergence reactions (agitation, dysphoria, nightmares) benefit from a quiet, low‑stimulation environment; in medical settings, sedatives or antipsychotics are used by clinicians when indicated. Due to lack of modern human pharmacokinetics, any non‑medical exposure warrants conservative observation for delayed confusion or ataxia and avoidance of hazardous activities for 24 h.

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