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Naltrexone, sold under the brand names ReVia and Vivitrol among others, is a medication primarily used to manage alcohol or opioid dependence.
Side effects may include trouble sleeping, anxiety, nausea, and headaches.
Naltrexone was first made in 1965 and was approved for medical use in the United States in 1984.
1 Medical uses
1.2 Opioid use
1.4 Available forms
3 Side effects
4.1.1 Mechanism of action
7 Society and culture
7.1 Generic names
7.2 Brand names
8.4 Behavioral disorders
8.5 Interferon alpha
9 See also
Naltrexone has been best studied as a treatment for alcoholism.
Acamprosate may work better than naltrexone for eliminating drinking, while naltrexone may decrease the desire for alcohol to a greater extent.
The Sinclair method is a method of using opiate antagonists such as naltrexone to treat alcoholism. The person takes the medication about an hour (and only then) before drinking to avoid side effects that arise from chronic use.
Long-acting injectable naltrexone decreases heroin use more than placebo.
A 2011 review found insufficient evidence to determine the effect of naltrexone taken by mouth in opioid dependence.
Naltrexone is not useful for quitting smoking.
Naltrexone is available and most commonly used in the form of an oral tablet (50 mg).
Naltrexone should not be used by persons with acute hepatitis or liver failure, or those with recent opioid use (typically 7–10 days).
The most common side effects reported with naltrexone are gastrointestinal complaints such as diarrhea and abdominal cramping. These adverse effects are analogous to the symptoms of opioid withdrawal, as the mu receptor blockade will increase GI motility.
Naltrexone has been reported to cause liver damage (when given at doses higher than recommended). It carries an FDA boxed warning for this rare side effect. Due to these reports, some physicians may check liver function tests prior to starting naltrexone, and periodically thereafter. Concerns for liver toxicity initially arose from a study of nonaddicted obese patients receiving 300 mg of naltrexone. Subsequent studies have suggested limited toxicity in other patient populations.
Naltrexone should not be started until several (typically 7-10) days of abstinence from opioids have been achieved. This is due to the risk of acute opioid withdrawal if naltrexone is taken, as naltrexone will displace most opioids from their receptors. The time of abstinence may be shorter than 7 days, depending on the half-life of the specific opioid taken. Some physicians use a naloxone challenge to determine whether an individual has any opioids remaining. The challenge involves giving a test dose of naloxone and monitoring for opioid withdrawal. If withdrawal occurs, naltrexone should not be started.
Naltrexone at opioid receptors
Affinities ( K i )
1.0 nM 0.0825 nM
149 nM 8.02 nM
3.9 nM 0.509 nM
Naltrexone and its active metabolite 6β-naltrexol are competitive antagonists at the μ-opioid receptor (MOR), the κ-opioid receptor (KOR) to a lesser extent, and, to a far lesser extent, at the δ-opioid receptor (DOR).
Mechanism of action
The blockade of opioid receptors is the basis behind naltrexone’s action in the management of opioid dependence—it reversibly blocks or attenuates the effects of opioids. Its mechanism of action in alcohol dependence is not fully understood, but as an opioid receptor antagonist is likely to be due to the modulation of the dopaminergic mesolimbic pathway (one of the primary centers for risk-reward analysis in the brain, and a tertiary “pleasure center”) which is hypothesized to be a major center of the reward associated with addiction that all major drugs of abuse are believed to activate.
Naltrexone is metabolized in the liver mainly to 6β-naltrexol by the enzyme dihydrodiol dehydrogenase. Other metabolites include 2-hydroxy-3-methoxy-6β-naltrexol and 2-hydroxy-3-methoxy-naltrexone. These are then further metabolized by conjugation with glucuronide.
Tentative evidence suggests that family history and presence of the Asn40Asp polymorphism predicts naltrexone being effective.
Naltrexone can be described as a substituted oxymorphone – here the tertiary amine methyl -substituent is replaced with methylcyclopropane. Naltrexone is the N-cyclopropylmethyl derivative of oxymorphone.
The closely related medication, methylnaltrexone, is used to treat opioid-induced constipation, but does not treat addiction as it does not cross the blood–brain barrier. Nalmefene is similar to naltrexone and is used for the same purposes as naltrexone. Naltrexone should not be confused with naloxone, which is used in emergency cases of opioid overdose. Other related opioid antagonists include nalodeine and samidorphan.
Naltrexone was first synthesized in 1963 by Metossian at Endo Laboratories, a small pharmaceutical company in New York City.
Society and culture
Naltrexone is the generic name of the drug and its INN, USAN, BAN, DCF, and DCIT, while naltrexone hydrochloride is its USP and BANM.
Naltrexone is or has been marketed under a variety of brand names, including Adepend, Antaxone, Celupan, Depade, Nalorex, Narcoral, Nemexin, Revia/ReVia, Trexan, and Vivitrol.
The FDA authorized use of injectable naltrexone for opioid addiction using a single study
In May 2017, United States Secretary of Health and Human Services Tom Price, praised The experts pointed out that Vivitrol’s competitors, buprenorphine and methadone, are “less expensive”, “more widely used”, and have been “rigorously studied”.
Price had claimed that buprenorphine and methadone were “simply substitute[s]” for “illicit drugs”
According to a June 11, 2017, The New York Times article, Alkermes “has spent years coaxing, with a deft lobbying strategy that has targeted lawmakers and law enforcement officials. The company has spent millions of dollars on contributions to officials struggling to stem the epidemic of opioid abuse. It has also provided thousands of free doses to encourage the use of Vivitrol in jails and prisons, which have by default become major detox centers”.
Naltrexone is sometimes used in the treatment of dissociative symptoms such as depersonalization and derealization.
Main article: Low-dose naltrexone
“Low-dose naltrexone” (LDN) describes the ” off-label ” use of naltrexone at low doses for diseases not related to chemical dependency or intoxication, such as multiple sclerosis. More research needs to be done before it can be recommended for clinical use.
Although some scientific studies show its efficacy in some conditions such as fibromyalgia,
One study suggests that self-injurious behaviors present in persons with developmental disabilities (including autism) can sometimes be remedied with naltrexone.
In these cases, the self-injury is believed to be done to release beta-endorphin, which binds to the same receptors as heroin and morphine. If the “rush” generated by self-injury is removed, the behavior may stop.
Some indications exist that naltrexone might be beneficial in the treatment of impulse-control disorders such as kleptomania, compulsive gambling, or trichotillomania (compulsive hair pulling), but evidence of its effectiveness for gambling is conflicting.
Naltrexone is effective in suppressing the cytokine -mediated adverse neuropsychiatric effects of interferon alpha therapy.
Opioid antagonist § List of opioid antagonists
One Little Pill (2014 film) – documentary about using naltrexone to treat alcohol use disorder
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