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    Naltrexone molecular structure

    Naltrexone Stats & Data

    Revia Depade Trexan Nalorex Vivitrol
    NPS DataHub
    MW341.41
    FormulaC20H23NO4
    CAS16590-41-3
    IUPAC(4R,4aS,7aR,12bS)-3-(cyclopropylmethyl)-4a,9-dihydroxy-2,4,5,6,7a,13-hexahydro-1H-4,12-methanobenzofuro[3,2-e]isoquinolin-7-one
    SMILESO=C1CCC2(O)C3Cc4ccc(O)c5OC1C2(CCN3CC1CC1)c45
    InChIKeyDQCKKXVULJGBQN-XFWGSAIBSA-N
    Chemical Class medicine
    Psychoactive Class Depressant

    Pharmacology

    DrugBank
    State Solid Vd * 1350 L intravenous administration Clearance * ~ 3.5 L/min after IV administration

    Description

    Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of naloxone. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence.

    Mechanism of Action

    Naltrexone is a pure opiate antagonist and has little or no agonist activity. The mechanism of action of naltrexone in alcoholism is not understood; however, involvement of the endogenous opioid system is suggested by preclinical data. Naltrexone is thought to act as a competitive antagonist at mc, κ, and δ receptors in the CNS, with the highest affintiy for the μ receptor. Naltrexone competitively binds to such receptors and may block the effects of endogenous opioids. This leads to the antagonization of most of the subjective and objective effects of opiates, including respiratory depression, miosis, euphoria, and drug craving. The major metabolite of naltrexone, 6-β-naltrexol, is also an opiate antagonist and may contribute to the antagonistic activity of the drug.

    Pharmacodynamics

    Naltrexone, a pure opioid antagonist, is a synthetic congener of oxymorphone with no opioid agonist properties. Naltrexone is indicated in the treatment of alcohol dependence and for the blockade of the effects of exogenously administered opioids. It markedly attenuates or completely blocks, reversibly, the subjective effects of intravenously administered opioids. When co-administered with morphine, on a chronic basis, naltrexone blocks the physical dependence to morphine, heroin and other opioids. In subjects physically dependent on opioids, naltrexone will precipitate withdrawal symptomatology.

    Metabolism

    Hepatic. When administered orally, naltrexone undergoes extensive biotransformation and is metabolized to 6 beta-naltrexol (which may contribute to the therapeutic effect) and other minor metabolites.

    Absorption

    Although well absorbed orally, naltrexone is subject to significant first pass metabolism with oral bioavailability estimates ranging from 5 to 40%.

    Toxicity

    In the mouse, rat and guinea pig, the oral LD50s were 1,100-1,550 mg/kg; 1,450 mg/kg; and 1,490 mg/kg; respectively. High doses of naltrexone (generally >1,000 mg/kg) produce salivation, depression/reduced activity, tremors, and convulsions.

    Indication

    Used as an adjunct to a medically supervised behaviour modification program in the maintenance of opiate cessation in individuals who were formerly physically dependent on opiates and who have successfully undergone detoxification. Also used for the management of alcohol dependence in conjunction with a behavioural modification program.

    Half-life

    4 hours for naltrexone and 13 hours for the active metabolite 6 beta-naltrexol.

    Protein Binding

    21% bound to plasma proteins over the therapeutic dose range.

    Elimination

    Both parent drug and metabolites are excreted primarily by the kidney (53% to 79% of the dose), however, urinary excretion of unchanged naltrexone accounts for less than 2% of an oral dose and fecal excretion is a minor elimination pathway. The renal clearance for naltrexone ranges from 30 to 127 mL/min and suggests that renal elimination is primarily by glomerular filtration.

    Effect Profile

    Curated + 15 Reports
    Opioid 5.1

    Strong euphoria with moderate itching/nausea, mild sedation

    Euphoria / Warmth×3
    9
    Analgesia×2
    0
    Sedation / Relaxation×1
    5
    Itching / Nausea×1
    6

    Tolerance & Pharmacokinetics

    drugs.wiki

    Tolerance Decay

    Full tolerance 1d Half tolerance 21d Baseline ~35d

    Experience Report Analysis

    Erowid
    15 Reports
    2005–2025 Date Range
    10 With Age Data
    9 Effects Detected

    Demographics

    Gender Distribution

    Age Distribution

    Reports Over Time

    Effect Analysis

    Erowid

    Effects aggregated from 15 experience reports (15 Erowid)

    15 Reports
    9 Effects Detected
    5 Positive
    3 Adverse
    1 Neutral

    Effect Sentiment Distribution

    Confidence Distribution

    Positive Effects 5

    Stimulation 53.3% 70%
    Anxiety Suppression 40.0% 70%
    Body High 20.0% 70%
    Empathy 20.0% 70%
    Tactile Enhancement 20.0% 70%

    Adverse Effects 3

    Nausea 53.3% 70%
    Sweating 26.7% 70%
    Confusion 20.0% 70%

    Real-World Dose Distribution

    62K Doses

    From 15 individual dose entries

    Oral (n=13)

    Median: 50.0mg 25th: 10.0mg 75th: 50.0mg 90th: 50.0mg
    mg/kg median: 0.551 mg/kg 75th: 0.648

    Common Combinations

    Most co-occurring substances in experience reports

    Form / Preparation

    Most common forms and preparations reported

    Body-Weight Dosing

    Dose relative to body weight from reports with weight data

    Median: 0.221 mg/kg IQR: 0.057–0.649 mg/kg n=9

    Redose Patterns

    Redosing behavior across 13 reports

    0.0% Redosed
    1.0 Avg Doses
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