Picture of Naltrexone molecule

Naltrexone

Chemical Name:
(5a)-17-(cyclopropylmethyl)-4,5-epoxy-3,14-dihydroxymorphinan-6-one
Classification:
Opioid antagonist
Primary Uses:
Alcohol addiction treatment, opiate addiction treatment
Brand Names:
ReVia, Vivitrol, Depade, Trexan, Nalorex
Slang:

General Information

Naltrexone is an opioid antagonist used in alcohol and opioid dependency treatment. Naltrexone blocks externally-administered opiates and opioids, which helps deter narcotic abuse. If a user can persistently take naltrexone, the odds of abstinence are greatly increased. If a patient taking naltrexone attempts to get high while under its effects, he or she will likely experience little to no effect from the opioid. It is much like an "insurance policy" for addicts, protecting against the sudden decision to use heroin or another opioid. Naltrexone is chemically related to oxymorphone, but possesses no opioid agonist properties. It is also related to another potent opioid antagonist, naloxone, one of the active ingredients in the popular ORT drug called Suboxone.

Vivitrol, an extended-release formulation of naloxone, was approved by the FDA on April 13, 2006 for the treatment of alcohol dependency. A single gluteal IM injection of Vivitrol delivers a steady dose of naltrexone for one month. The technology used in this formulation is called Medisorb®. The drug is stored in microspheres made of a biodegradable polymer called poly(d,l-lactide-co-glycolide) or PLG. As the body breaks down the PLG, naltrexone is steadily released into the body. When taken orally, naloxone has very defined peaks and drop-offs, whereas Vivitrol is designed to maintain a steady concentration of the drug in the bloodstream.1

Pharmacology & Pharmacokinetics

Naltrexone is an opioid antagonist with an extremely high binding affinity for the mu-opioid receptor. It reduces or completely blocks the subjective effects of opioids. Not only does the drug block the effects of exogenously administered opioids, but it may also inhibit those of endogenous opioids.

The activity of naltrexone is caused by the parent and 6-(beta)-naltrexol metabolite; minor metabolites include 2-hydroxy-3-methoxy-6-(beta)-naltrexol and 2-hydroxy-3-methyl-naltrexone. Oral bioavailability is estimated to be between 5% and 40%. About 96% of an oral dose is rapidly absorbed from the gastrointestinal tract, with peak plasma levels occurring in about one hour. The average elimination half-life for naltrexone is four hours, and 13 hours for the metabolite, 6-(beta)-naltrexol.2

Legal Status

In the United States, this drug is not currently controlled under the Controlled Substances Act (CSA). Because it is not controlled, there are no CSA regulations regarding distribution, manufacturing, or prescription of this chemical. According to FDA regulations, sales and distribution are only allowed by those with a valid license. Possession is not illegal for those without a prescription; however, law may differ from state-to-state.

Side Effects

  • Difficulty sleeping
  • Loss of energy
  • Anxiety
  • Nausea and vomiting
  • Abdominal pain
  • Joint and muscle pain
  • Headache
  • Suicidal ideation*

*Note: Suicide attempts and suicidal ideation have been reported by patients taking naltrexone. No casual relationship has been proven at this time (11/2006). It is difficult to distinguish the side effects of a withdrawal syndrome from those originating with naltrexone therapy. Naltrexone therapy has been associated with a change in levels from the norm for certain hormones (hypothalamic, pituitary, adrenal, or gonadal hormones). The significance of these changes is not fully understood.

Sources

[1] Healthcare Professionals Homepage :: Vivitrol. Alkermes: Vivitrol. 2006. Accessed: November 9, 2006.
[2] Revia (Naltrexone) Drug Information. RxList. 2006. Accessed: November 9, 2006.
[3] Pharms: Naltrexone: Legal Status. Erowid.org. July 8, 2006. Accessed: November 9, 2006.