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| Pronunciation | /kərˌaɪsʌˈproʊdɒl/ kər-EYE-suh-PROH-dol |
| Trade names | Soma, others[1] |
| AHFS/Drugs.com | Monograph |
| MedlinePlus | a682578 |
| License data | |
| Addiction liability | Moderate[2][failed verification] |
| Routes of administration | By mouth[3] |
| Drug class | Muscle relaxant[3] |
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| Pharmacokinetic data | |
| Protein binding | 60% |
| Metabolism | Liver (CYP2C19-mediated) |
| Metabolites | Meprobamate |
| Onset of action | Rapid (30 minutes[6][failed verification]) |
| Eliminationhalf-life | 2.5 hours [12 hours[nb 1]] |
| Excretion | Kidney |
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| CompTox Dashboard(EPA) | |
| ECHA InfoCard | 100.001.017 |
| Chemical and physical data | |
| Formula | C12H24N2O4 |
| Molar mass | 260.334 g·mol−1 |
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Carisoprodol, sold under the brand nameSoma among others, is an oral medication used formusculoskeletal pain.[7] Effects generally begin within half an hour and last for up to six hours.[7]
Common side effects include headache, dizziness, and sleepiness.[7] Serious side effect may includeaddiction,allergic reactions, andseizures.[7] In people with asulfa allergy certain formulations may result in problems.[7] Safety duringpregnancy andbreastfeeding is not clear.[7][8] How it works is not clear.[7] Some of its effects are believed to occur following metabolic conversion intomeprobamate, carisoprodol's main active metabolite.[7]
Carisoprodol was approved for medical use in the United States in 1959.[7] Its approval in the European Union was withdrawn in 2008.[9] It is available as ageneric medication.[7] In 2019, it was the 343rd most commonly prescribed medication in the United States, with more than 800 thousand prescriptions.[10] In the United States, it is aSchedule IV controlled substance.[7]
Carisoprodol is meant to be used along with rest,physical therapy and other measures to relax muscles afterstrains,sprains and muscle injuries.[11] It comes in tablet format and is taken by the mouth three times a day and before bed.[11]
The usual dose of 350 mg is unlikely to engender prominent side effects other thansomnolence, and mild to significanteuphoria ordysphoria, but the euphoria is generally short-lived due to the fast metabolism of carisoprodol into meprobamate and other metabolites; the euphoria derived is, according to new research,[12] most likely due to carisoprodol's inherent, potent anxiolytic effects that are far stronger than those produced by its primary metabolite, meprobamate, which is often misblamed for the drug-seeking associated with carisoprodol, as carisoprodol itself is responsible for the significantly more intense central nervous system effects than meprobamate alone. Carisoprodol has a qualitatively different set of effects to that of meprobamate (Miltown). The medication is well tolerated and without adverse effects in the majority of patients for whom it is indicated. In some patients, however, and/or early in therapy, carisoprodol can have the full spectrum of sedative side effects and can impair the patient's ability to operate a firearm, motor vehicles, and other machinery of various types, especially when taken with medications containingalcohol, in which case an alternative medication would be considered. The intensity of the side effects of carisoprodol tends to lessen as therapy continues, as is the case with many other drugs. Other side effects include:dizziness,clumsiness,headache, fastheart rate,upset stomach,vomiting andskin rash.[11]
There are 368 drugs known to interact with carisoprodol including 28 major drug interactions.[13] The interaction of carisoprodol with essentially all opioids, and other centrally acting analgesics, but especially codeine, those of the codeine-derived subgroup of the semisynthetic class (ethylmorphine, dihydrocodeine, hydrocodone, oxycodone, nicocodeine, benzylmorphine, the various acetylated codeine derivatives including acetyldihydrocodeine, dihydroisocodeine, nicodicodeine and others) which allows the use of a smaller dose of the opioid to have a given effect, is useful in general and especially where skeletal muscle injury and/or spasm is a large part of the problem. The potentiation effect is also useful in other pain situations and is also especially useful with opioids of the open-chain class, such as methadone, levomethadone, ketobemidone, phenadoxone and others. In recreational drug users, deaths have resulted from combining doses of hydrocodone and carisoprodol. Another danger of misuse of carisoprodol and opiates is the potential to asphyxiate while unconscious.[citation needed]
Meprobamate and other muscle-relaxing drugs often were subjects of misuse in the 1950s and 60s.[14][15] Overdose cases were reported as early as 1957, and have been reported on several occasions since then.[16][17][18][19][20][21][22]
Carisoprodol is metabolized by the liver and excreted by the kidneys, so this drug must be used with caution with patients that have impaired hepatic orrenal function.[23] Because of potential for more severe side effects, this drug is on the list to avoid for elderly people.[24]
Carisoprodol, meprobamate, and related drugs such astybamate, have the potential to produce physical dependence of the barbiturate type following periods of prolonged use. Withdrawal of the drug after extensive use may require hospitalization in medically compromised patients. In severe cases the withdrawal can mimic the symptoms ofalcohol withdrawal including the potentially lethalstatus epilepticus.
Psychological dependence has also been linked to carisoprodol use[25] although this is much less severe than with meprobamate itself (presumably due to the slower onset of effects). Psychological dependence is more common in those who use carisoprodol non-medically and those who have a history of substance use (particularlysedatives or alcohol). It may reach clinical significance before physiological tolerance and dependence have occurred and (as withbenzodiazepines) has been demonstrated to persist to varying degrees of severity for months or years after discontinuation.
Discontinuation of carisoprodol, as with all GABA-ergics, can result in cognitive changes which persist for weeks, months, or rarely even years including greatly increased anxiety and depression,social withdrawal, hair-trigger agitation/aggression, chronicinsomnia, new or aggravated (often illogical)phobias, reduced IQ, short term and long-term memory loss, and dozens of other sequelae.[26] The effects, severity, and duration appear to be slightly dose-dependent but are mainly determined by the patient's pattern of use (taken as prescribed, taken in bulk doses, mixed with other drugs, a combination of the above, etc.), genetic predisposition to substance use, and a history of substance use all increase the patients risk of persistent discontinuation syndrome symptoms.
Treatment for physical withdrawal generally involves switching the patient to a long-acting benzodiazepine such asdiazepam orclonazepam then slowly titrating them off the replacement drug completely at a rate which is both reasonably comfortable for the patient but rapid enough for the managing physician to consider the rate of progress acceptable (overly rapid dose reduction greatly increases the risk of patient non-compliance such as the use of illicitly obtained alternative sedatives and/or alcohol).Psychotherapy andcognitive behavioral therapy have demonstrated moderate success in reducing the rebound anxiety which results upon carisoprodol discontinuation but only when combined with regular and active attendance to a substance use support group.[27]
Carisoprodol withdrawal can be life-threatening (especially in high dose users and those who attempt to quit "cold turkey"). Medical supervision is recommended, with gradual reduction of dose of carisoprodol or a substituted medication, typical of other depressant drugs.
Combining a muscle relaxant like carisoprodol with opioids and benzodiazepines is referred to as "The Holy Trinity" as it has been reported to increase the power of the "high".[28]
Recreational users of carisoprodol usually seek its potentially heavy sedating, relaxant, andanxiolytic effects.[29] Because of itspotentiating effects onnarcotics, it is often used in conjunction with manyopioid drugs. Carisoprodol is not tested for on standarddrug testing screens, although tests for it do exist.
On 26 March 2010 the DEA issued aNotice of Hearing on a proposal for the placement of carisoprodol in schedule IV of theControlled Substances Act, later confirming its classification under schedule IV.[30][31]
Carisoprodol is sometimes mixed withdate rape drugs.[32]
As with other GABAergic drugs, combination with other drugs that depress the respiratory system, such as alcohol, sedatives and opioids possess a significant risk to the user in the form of overdose.[33] Overdose symptoms are similar to those of other GABAergics including excessive sedation and unresponsiveness to stimuli, severeataxia,amnesia,confusion,agitation,intoxication and inappropriate (potentially violent) behavior. Severe overdoses may present withrespiratory depression (and subsequentpulmonary aspiration),coma, anddeath.[34]
Carisoprodol is not detected on all toxicology tests which may delay diagnosis of overdose. Overdose symptoms in combination with opiates are similar but are distinguished by the presentation of normal orpinpoint pupils, which are generally unresponsive to light. Carisoprodol (as with its metabolite meprobamate) is particularly dangerous in combination with alcohol.Flumazenil (the benzodiazepine antidote) is not effective in the management of carisoprodol overdose as carisoprodol acts at the barbiturate binding site. Treatment mirrors that ofbarbiturate overdoses and is generally supportive, including the administration ofmechanical respiration andpressors as indicated and, in rare cases,bemegride. Total amnesia of the experience is not uncommon following recovery.[citation needed]
In 2014 actressSkye McCole Bartusiak died of an overdose due to the combined effects of carisoprodol,hydrocodone anddifluoroethane.[35]
In 1999 actressDana Plato died after taking carisoprodol (Soma) along with a few doses of ahydrocodone / acetaminophen painkiller (Lortab), in an overdose that was ruled a suicide.[36]
Carisoprodol, has a chemical structure similar toglutamate, a neurotransmitter, and dimethylglycine.
Carisoprodol's structural similarity tomeprobamate indicates GABAergic activity, including GABAA agonism, similar to the mechanism ofbenzodiazepines but distinct; benzodiazepines are positive allosteric modulators of the GABA A receptor, and which have no direct agonist activity but rather increase the potency of the endogenous agonist GABA at this receptor.[37] Similar to benzodiazepines, this allows carisoprodol to not only work as a muscle relaxant, but also help with anxiety.[38] However unlike benzodiazepines, carisoprodol does not treat or prevent seizures.[39] In fact it increases the risk of seizures, with the risk being even higher when discontinuing the drug after long-term use, especially if the drug is stopped suddenly, precipitating withdrawal.[40]
Carisoprodol has a rapid, 30-minute onset of action, with effects lasting around two to six hours. It is metabolized in the liver via thecytochrome P450 oxidaseisozymeCYP2C19, excreted by the kidneys and has about an eight-hour half-life. In patients with low levels of CYP2C19 (poor metabolizers), standard doses can lead to increased concentrations of carisoprodol (up-to a four-fold increase).[38] A considerable proportion of carisoprodol is metabolized tomeprobamate, which is a known addictive substance; this could account for the addictive potential of carisoprodol (meprobamate levels reach higher peak plasma levels than carisoprodol itself following administration).
It is slightlysoluble inwater and freely soluble inethanol,chloroform andacetone. The drug's solubility is practically independent ofpH.
In June 1959, several American pharmacologists convened atWayne State University inDetroit, Michigan to discuss a newly discoveredstructural analogue ofmeprobamate. The substitution of onehydrogen atom with anisopropyl group on one of thecarbamylnitrogens was intended to yield a drug with new pharmacological properties. It had been developed byFrank Berger atWallace Laboratories and was named carisoprodol.[41]
Building onmeprobamate's pharmacological effects, carisoprodol was intended to have better muscle relaxing properties, less potential for addiction, and a lower risk of overdose. Carisoprodol's effect profile did indeed turn out to differ significantly with respect to meprobamate, with carisoprodol possessing stronger muscle relaxant andanalgesic effects.[42]
Reports from Norway have shown carisoprodol has addictive potential[43] as a prodrug ofmeprobamate and/orpotentiator ofhydrocodone,oxycodone,codeine, and similar drugs. In May 2008 it was taken off the market in Norway.[44]
In the EU, the European Medicines Agency issued a release recommending member states suspend marketing authorization for this product in the treatment of acute (not chronic) back pain.[45]
As of November 2007, carisoprodol has been taken off the market in Sweden due to problems with dependence and side effects. The agency overseeing pharmaceuticals considered other drugs used with the same indications as carisoprodol to have the same or better effects without the risks of the drug.[46]
In December 2011, theDrug Enforcement Administration (DEA) issued the final ruling placing carisoprodol on Schedule IV of theControlled Substances Act (CSA). The placement of carisoprodol on Schedule IV was effective in January 2012.[47]
Federally, carisoprodol is a prescription drug.[48] Provincial regulations vary.[49] As of April 14, 2025 there are no forms of carisoprodol being marketed in Canada, and the drug was removed from the Prescription Drug List and reclassified as aSchedule V Controlled Substance.[50]
Carisoprodol is no longer included in theAustralian Register of Theraputic Goods, but can still be accessed through the Special Access Scheme.[51]
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