Drug Index



none known

Naltrexone is a pure opioid antagonist (blocker). It markedly attenuates or completely blocks, reversibly, the subjective effects of opioids. Naltrexone blocks the effects of opioids by competitive binding (i.e., it occupies the receptors and "blocks" the effects of opioids) at opioid receptors. Naltrexone has few, if any, intrinsic actions besides its opioid blocking properties. However, it does produce some pupillary constriction, by an unknown mechanism. When co-administered with morphine, on a chronic basis, naltrexone blocks the physical dependence to morphine, heroin and other opioids. Naltrexone has also been shown to reduce alcohol consumption in individuals who have alcohol dependence. The administration of naltrexone is not associated with the development of tolerance or dependence. In subjects physically dependent on opioids, naltrexone will precipitate withdrawal symptoms. Naltrexone hydrochloride is a synthetic congener of oxymorphone, but with no opioid agonist properties. Naltrexone differs in structure from oxymorphone in that the methyl group on the nitrogen atom is replaced by a cyclopropylmethyl group. Naltrexone hydrochloride is also related to the potent opioid antagonist, naloxone (or n-allylnoroxymorphone, also known by the brand name Narcan). Naltrexone is well absorbed orally. Peak plasma levels of both naltrexone and 6-Beta-Naltrexone occur within one hour of dosing. Naltrexone is subject to significant first pass metabolism (passage through the liver). The activity of Naltrexone is believed to be due to both the parent drug (naltrexone) and the 6-Beta-naltrexol metabolite. Both parent drug and metabolites are excreted primarily by the kidney. The mean elimination half-life (the time it takes for the body to eliminate half of the drug from the blood stream) values for naltrexone and 6-Beta-naltrexol are 4 hours and 13 hours, respectively.

It is available as film coated tablets, containing 50 mg of Naltrexone hydrochloride. Naltrexone hydrochloride tablets are approved for use in the treatment of alcohol dependence and for the blockade of the effects of opioids. Naltrexone hydrochloride tablets have not been shown to provide any therapeutic benefit except as part of an appropriate plan of management for the addictions.


Naltrexone is not aversive therapy and does not cause a disulfiram-like reaction (i.e. does not cause very unpleasant physical symptoms when drinking alcohol as one would experience after taking disulfiram { Antabuse}) either as a result of opiate use or alcohol ingestion. The efficacy of naltrexone as an aid to the treatment of alcoholism was tested in placebo-controlled, outpatient, double blind trials. These studies used a dose of naltrexone hydrochloride 50 mg once daily for 12 weeks as an adjunct to social and psychotherapeutic methods when given under conditions that enhanced patient compliance. Patients with psychosis, dementia, and secondary psychiatric diagnoses were excluded from these studies. In one of these studies, 104 alcohol-dependent patients were randomized to receive either Naltrexone hydrochloride 50 mg once daily or placebo. In this study, Naltrexone proved superior to placebo in measures of drinking including abstention rates (51% vs. 23%), number of drinking days, and relapse (31% vs. 60%). In a second study with 82 alcohol-dependent patients, the group of patients receiving Naltrexone were shown to have lower relapse rates (21% vs. 41%), less alcohol craving, and fewer drinking days compared with patients who received placebo, but these results depended on the specific analysis used. The clinical use of naltrexone as adjunctive pharmacotherapy for the treatment of alcoholism was also evaluated in a multicenter safety study. This study of 865 individuals with alcoholism included patients with comorbid psychiatric conditions, concomitant medications, polysubstance abuse and HIV disease. Results of this study demonstrated that the side effect profile of Naltrexone appears to be similar in both alcoholic and opioid dependent populations, and that serious side effects are uncommon. In the clinical studies, treatment with naltrexone supported abstinence, helped prevent relapse and decreased alcohol consumption (in the subset of patients who respond to the beneficial effects of this medication). Naltrexone is not uniformly helpful to all patients, and the expected effect of the drug is a modest improvement in the outcome of conventional treatment. Use in treatment of opiate addiction: Naltrexone has been shown to produce complete blockade of the euphoric effects of opioids ("high") in both volunteer and addict populations. When administered by means that enforce compliance, it will produce an effective opioid blockade, but has not been shown to affect the use of cocaine or other non-opioid drugs of abuse. There are no data that demonstrate an unequivocally beneficial effect of naltrexone on rates of recidivism (relapse) among detoxified, formerly opioid-dependent individuals who self-administer the drug. The failure of the drug in this setting appears to be due to poor medication compliance. The drug is reported to be of greatest use in good prognosis opioid addicts who take the drug as part of a comprehensive occupational rehabilitative program, behavioral contract, or other compliance-enhancing protocol. Naltrexone, unlike methadone, does not reinforce medication compliance and is expected to have a therapeutic effect only when given under external conditions that support and enforced continued use of the medication.


There is limited clinical experience with Naltrexone overdosage in humans. In one study, subjects who received 800 mg daily Naltrexone hydrochloride for up to one week showed no evidence of toxicity.


Naltrexone has the capacity to cause hepatocellular (liver) injury when given in excessive doses. Naltrexone is contraindicated in acute hepatitis or liver failure, and its use in patients with active liver disease must be carefully considered in light of its hepatotoxic effects. Naltrexone and its primary metabolite are excreted primarily in the urine, and caution is recommended in administering the drug to patients with renal impairment (kidney disease). To prevent occurrence of an acute abstinence syndrome, or exacerbation of a pre-existing subclinical abstinence syndrome, patients must be opioid-free for a minimum of 7 to 10 days before starting naltrexone. Severe opioid withdrawal syndromes precipitated by the accidental ingestion of naltrexone have been reported in opioid-dependent individuals. Symptoms of withdrawal have usually appeared within five minutes of ingestion of naltrexone and have lasted for up to 48 hours. Mental status changes including confusion, somnolence and visual hallucinations have occurred. Significant fluid losses from vomiting and diarrhea have required intravenous fluid administration. In all cases patients were closely monitored and therapy with non-opioid medications was tailored to meet individual requirements. While Naltrexone is a potent antagonist with a prolonged pharmacologic effect (24 to 72 hours), the blockade produced by naltrexone is surmountable. This is useful in patients who may require analgesia, but poses a potential risk to individuals who attempt, on their own, to overcome the blockade by administering large amounts of exogenous opioids. Indeed, any attempt by a patient to overcome the antagonism by taking opioids is very dangerous and may lead to a fatal overdose.


Naltrexone has not been shown to cause significant increases in complaints in placebo-controlled trials in patients known to be free of opioids for more than 7 to 10 days. Studies in alcoholic populations and in volunteers in clinical pharmacology studies have suggested that a small fraction of patients may experience an opioid withdrawal-like symptom complex consisting of tearfulness, mild nausea, abdominal cramps, restlessness, bone or joint pain, myalgia (generalized body ache), and nasal symptoms. This may represent the unmasking of occult opioid use, or it may represent symptoms attributable to Naltrexone. A number of alternative dosing patterns have been recommended to try to reduce the frequency of these complaints.The following adverse reactions have been reported both at baseline and during the Naltrexone clinical trials in opioid addiction at an incidence rate of more than 10%: Difficulty sleeping, anxiety, nervousness, abdominal pain/cramps, nausea and/or vomiting, low energy, joint and muscle pain, and headache. The incidence was less than 10% for: Loss of appetite, diarrhea, constipation, increased thirst, increased energy, feeling down, irritability, dizziness, skin rash, delayed ejaculation, decreased potency, and chills. The following events occurred in less than 1% of subjects: Respiratory: nasal congestion, itching, rhinorrhea (runny nose), sneezing, sore throat, excess mucus or phlegm, sinus trouble, heavy breathing, hoarseness, cough, shortness of breath. Cardiovascular: nose bleeds, phlebitis, edema, increased blood pressure, non-specific ECG changes, palpitations, tachycardia. Gastrointestinal: excessive gas, hemorrhoids, diarrhea, ulcer. Musculoskeletal: painful shoulders, legs or knees; tremors, twitching. Genitourinary: increased frequency of, or discomfort during, urination; increased or decreased sexual interest. Dermatologic: oily skin, pruritus, acne, athlete's foot, cold sores, alopecia. Psychiatric: depression, paranoia, fatigue, restlessness, confusion, disorientation, hallucinations, nightmares, bad dreams. Special senses: eyes-blurred, burning, light sensitive, swollen, aching, strained; ears-“clogged”, aching, tinnitus. General: increased appetite, weight loss, weight gain, yawning, somnolence, fever, dry mouth, head “pounding”, inguinal pain, swollen glands, “side” pains, cold feet, “hot spells.”


*This is a condensed description of naltrexone. For more details check with your physician, pharmacist, or resources such as The Physicians' Desk Reference (PDR)




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