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    Levomethorphan molecular structure

    Levomethorphan Stats & Data

    Lvm Ro 1-5470/6 L-methorphan
    NPS DataHub
    MW271.4
    FormulaC18H25NO
    CAS125-70-2
    IUPAC(1''R'',9''R'',10''R'')-4-methoxy-17-methyl-17-azatetracyclo[7.5.3.0¹,¹⁰.0²,⁷]heptadeca-2(7),3,5-triene
    SMILESCOc1ccc2CC3N(C)CCC4(CCCCC34)c2c1
    InChIKeyMKXZASYAUGDDCJ-CGTJXYLNSA-N
    Chemical Class Opioid
    Psychoactive Class Depressant
    Half-Life Levomethorphan: not well characterized; active metabolite levorphanol ~11–16 hours.

    Pharmacology

    DrugBank

    Metabolism

    Hepatic. Rapidly and extensively metabolized to dextrorphan (active metabolite). One well known metabolic catalyst involved is a specific cytochrome P450 enzyme known as 2D6, or CYP2D6. Half Life: 3-6 hours

    Effect Profile

    Curated
    Opioid 7.0

    Strong euphoria, itching/nausea, and pain relief with low sedation

    Euphoria / Warmth×3
    10
    Analgesia×2
    8
    Sedation / Relaxation×1
    3
    Itching / Nausea×1
    10

    Tolerance & Pharmacokinetics

    drugs.wiki
    Half-Life
    Levomethorphan: not well characterized; active metabolite levorphanol ~11–16 hours.
    Addiction Potential
    High risk of dependency and addiction, similar to other opioids.

    Harm Reduction

    drugs.wiki

    Levomethorphan is the levorotatory isomer of methorphan and the methyl ether of levorphanol; levorphanol is a potent μ-opioid agonist with additional κ/δ activity, which explains the significant risk of respiratory depression and dependence seen with levomethorphan exposure. By chemical relationship and analogy to dextromethorphan, levomethorphan is plausibly O‑demethylated in humans (likely via CYP2D6) to levorphanol; this implies strong interindividual variability (UMs higher conversion/toxicity; PMs lower conversion/effect) and sensitivity to CYP2D6 inhibitors such as quinidine or certain SSRIs. Because levorphanol’s elimination half-life is long (≈11–16 h), sedation and respiratory depression may persist or re‑emerge (“renarcotization”) after apparent improvement; in overdose, multiple naloxone doses or an infusion and prolonged observation can be required. Combining levomethorphan with other CNS depressants (alcohol, benzodiazepines, barbiturates, Z-drugs, gabapentinoids, first‑generation antihistamines, GHB/GBL) markedly increases overdose risk due to additive respiratory depression; avoid such combinations and use smallest effective doses if medically required. Some opioids have serotonergic properties (tramadol, methadone, tapentadol, meperidine), so mixing levomethorphan with these agents increases the risk of serotonin toxicity and seizures; avoid or use only under medical supervision. Given inconsistent supply chains and frequent high‑potency adulterants in the unregulated opioid market (fentanyl, analogs, nitazenes; sometimes veterinary tranquilizers), use verified drug‑checking services where available and start with a very small test dose; be aware that higher-than-usual naloxone doses may be needed when multiple high‑potency opioids are present. Always keep naloxone available, educate peers on its use, and call emergency services immediately during suspected overdose; naloxone’s action is shorter than many opioids, so re-dosing at 2–5 minute intervals and observation for 6–12 hours may be necessary. Use a calibrated milligram scale for measurement; avoid non-oral routes (insufflation, injection, smoking) due to rapid onset and sharply increased overdose risk. People with sleep‑disordered breathing, COPD, hepatic impairment, or concurrent sedative prescriptions are at elevated risk for respiratory depression and should avoid nonmedical use and seek medical guidance if prescribed opioids.

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