Naltrexone
is a opioid antagonist used
in alcohol and opioid dependency treatment.
It 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 the user attempts to get high while
under its effects, he/she will experience little to no effect from the
opioid. It is much like an "insurance"
policy for addicts, protecting against the sudden urge to use heroin or
another narcotic. 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 Suboxone and Subutex.
Vivitrol, an extended-release formulation approved for alcohol dependency, 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, naltrexone has very defined peaks and drop-offs, whereas Vivitrol is designed to maintain a steady concentration of the drug in the bloodstream.[1]
Chemical Name. (5a)-17-(cyclopropylmethyl)-4,5-epoxy-3,14-dihydroxymorphinan-6-one
Classification. Opioid antagonist.
Primary Uses. Alcohol dependence, Blockades
effects of externally-administered opioids.
Other Names. Revia, Vivitrol, Depade, Trexan,
Nalorex.
Pharmacology and Pharmacokinetics
Naltrexone is an opioid
antagonist with an extremely high binding affinity for the µ-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 reached in about one hour. The average elimination half-life for naltrexone is 4 hours, and 13 hours for the metabolite, 6-(beta)-naltrexol.[2]
In
the United States, naltrexone 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 licence. Possession is not illegal for those without
a prescription.[3]
Difficulty sleeping
Loss of energy
Anxiety
Nausea/vomiting
Abdominal pain
Joint/muscle pain
Headache
Suicidal ideation*
*NOTE: Suicide attempts, and suicidal ideation have been reported by patients taking naltrexone. No casual relationship has been proven to date. It is hard 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 are not fully understood.
[1] Healthcare Professionals
Homepage :: Vivitrol. Alkermes: Vivitrol. 2006. [link]
Accessed: November 9, 2006.
[2] Revia (naltrexone): Clinical Pharmacology. RxList. 2006. [link]
Accessed: November 9, 2006.
[3] Pharms: Naltrexone: Legal Status. Erowid.org. July 8, 2006.
[link]
Accessed: November 9, 2006.