Open Access Articles- Top Results for Carisoprodol


Systematic (IUPAC) name
(RS)-2-{[(aminocarbonyl)oxy]methyl}-2-methylpentyl isopropylcarbamate
Clinical data
Trade names Soma
AHFS/ monograph
MedlinePlus a682578
  • C
Pharmacokinetic data
Protein binding 60%
Metabolism Hepatic (CYP2C19-mediated)
Half-life 2 hours
Excretion Renal
78-44-4 7pxY
PubChem CID 2576
DrugBank DB00395 7pxY
ChemSpider 2478 7pxY
UNII 21925K482H 7pxY
KEGG D00768 7pxY
ChEBI CHEBI:3419 7pxY
Chemical data
Formula C12H24N2O4
260.33 g/mol
 14pxY (what is this?)  (verify)

Carisoprodol is a centrally acting skeletal muscle relaxant. It is slightly soluble in water and freely soluble in ethanol, chloroform and acetone. The drug's solubility is practically independent of pH. Carisoprodol is manufactured and marketed in the United States by Meda Pharmaceuticals[1] under the brand name Soma, and in the United Kingdom and other countries under the brand names Sanoma and Carisoma. The drug is available by itself or mixed with aspirin, and in one preparation with codeine and caffeine, as well. Although carisoprodol has significant pharmacological activity, its benefit in therapy is likely due mostly to the meprobamate metabolite as meprobamate remains in the system significantly longer and reaches a higher peak plasma concentration than the parent drug a few hours following administration. This is further evidenced by carisoprodol's ability to maintain relevant benefits when administered 3-4 times a day despite its short half-life of only two hours.


On June 1, 1959 several American pharmacologists convened at Wayne State University in Detroit, Michigan to discuss a new drug. The drug, originally thought to have antiseptic properties, was found to have central muscle-relaxing properties.[2] It had been developed by Frank M. Berger at Wallace Laboratories and was named carisoprodol.

Carisoprodol was a modification of meprobamate, intended to have better muscle relaxing properties, less potential for abuse, and less risk of overdose.[3] The substitution of one hydrogen atom with an isopropyl group on one of the carbamyl nitrogens was intended to yield a molecule with new pharmacological properties.

Usage and legal status

Abuse Potential first Noted in Norway Study

Reports from Norway have shown carisoprodol has abuse potential[4] as a prodrug of meprobamate and/or potentiator of hydrocodone, oxycodone, codeine and similar drugs. In May 2008 it was taken off the market in Norway.[5] It continues to be prescribed in North America alongside methocarbamol, cyclobenzaprine, metaxalone, tizanidine, orphenadrine, and chlorzoxazone. In the United States, carisopridol, while being recently scheduled as a controlled substance, is still as popular as cyclobenzaprine, tizanidine is almost as popular as methocarbamol, while chlorzoxazone is much less frequently prescribed at about the same frequency as orphenadrine. In Europe, doctors favor the safer cyclobenzaprine.


As of November 2007, carisoprodol (Somadril, Somadril comp.) 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.[6]

European Union

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.[7]

United States

Until December 12, 2011, when the Administrator of the Drug Enforcement Administration (DEA) issued the final ruling placing the substance carisoprodol into Schedule IV of the Controlled Substances Act (CSA), carisoprodol was not a controlled substance. The placement of carisoprodol into Schedule IV was effective January 11, 2012.[8]

Carisoprodol is available as a generic in 350 mg and, more recently, as 250 mg tablets. There is also a brand name formulation in 250 mg tablets.Compounded tablets with acetaminophen are also available. [9]


Federally, carisoprodol is a Prescription Drug (Schedule I, sub-schedule F1).[10] Provincial regulations may vary, e.g. for BC see It is no longer readily available.[11] Now unscheduled, available in powder base as a Research Chemical


In September 2013, carisoprodol has been taken off the market in Indonesia due to problems with diversion, dependence and side effects.


Side effects

The usual dose of 350 mg is unlikely to engender prominent side effects other than somnolence, and mild to significant euphoria or dysphoria, but the euphoria is generally short lived. 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 containing alcohol, 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.

The interaction of carisoprodol with essentially all opioids, and other centrally acting analgesics, but especially[citation needed] those of the codeine-derived subgroup of the semisynthetic class (codeine, ethylmorphine, dihydrocodeine, hydrocodone, oxycodone, nicocodeine, benzylmorphine, the various acetylated codeine derivatives including acetyldihydrocodeine, dihydroisocodeine, nicodicodeine and others)[citation needed] which allows the use of a smaller dose of the opioid to have a given effect[citation needed], 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 carelessly combining overdoses of hydrocodone and carisoprodol. Another danger of misuse of carisoprodol and opiates is the potential to aspirate while unconscious, which usually requires quick intervention and long hospital stays, if death can even be avoided.

Meprobamate and other muscle-relaxing drugs often were subjects of misuse in the 1950s and 1960s.[12][13] Overdose cases were reported as early as 1957, and have been reported on several occasions since then.[14][15][16][17][18][19][20]

Because of potential for more severe side effects, this drug is on the list to avoid in the elderly.[21]


Carisoprodol, meprobamate, and related drugs such as tybamate, 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 of alcohol withdrawal including the potentially lethal status epilepticus.

Psychological dependence has also been linked to carisoprodol use 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 abuse carisoprodol and those who have a history of drug abuse (particularly sedatives and/or alcohol). It may reach clinical significance before physiological tolerance and dependence have occurred and (as with benzodiazepines) has been demonstrated to persist to varying degrees of severity for months or years after discontinuation.

Withdrawal treatment

Discontinuation of carisoprodol, as with all GABA-ergics, can result in persistent cognitive changes which persist for weeks, months, or rarely even years including greatly increased anxiety and depression, social withdrawal, hair-trigger agitation/aggression, chronic insomnia, new or aggravated (often illogical) phobias, reduced IQ, short term and long term memory loss, and dozens of other sequela.[22] The effects, severity, and duration appear to be slightly dose-dependent but are mainly determined by the patients pattern of use (taken as prescribed, taken in bulk doses, mixed with other drugs, a combination of the above, etc.), genetic predisposition to drug abuse, and a history of substance abuse 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 as diazepam or clonazepam 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 abuse of illicitly obtained alternative sedatives and/or alcohol). Psychotherapy and cognitive behavior 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 abuse support group.

Anecdotal reports indicate that routine physical exercise speeds the recovery from dependence, with a long jog/swim/bike ride (etc.) effectively acting as a "rescue medication" for sudden/severe cravings and panic attacks. Claims for a wide range of many alternative medicine forms of reducing persistent psychological dependence have been made (meditation, yoga, acupuncture, chiropractic, martial arts, supplemental I.V. nutrition, etc.,), however such claims are promoted by the practitioners of such alternative medicines and appear to be mostly ineffective according to anecdotal reports (no formally conducted studies on the use of any of these alternative practices in the treatment of persistent post-withdrawal cravings).

Carisoprodol withdrawal can be life-threatening (especially in high dose users and those who attempt to quit "cold turkey"). A patient should always contact their doctor prior to attempting to discontinue carisoprodol use so that the physician and the patient can agree on a de-titration plan which is safe, affordable, comfortable, and effective for the patient in order to protect the patient and maximize program compliance.

Recreational use and abuse

Recreational users of carisoprodol usually seek its potentially heavy sedating, relaxant, and anxiolytic effects.[23] Also, because of its potentiating effects on narcotics, it is often abused in conjunction with many opioid drugs. Also it is not detected on standard drug testing screens. On March 26, 2010 the DEA issued a Notice of Hearing on proposed rule making in respect to the placement of carisoprodol in schedule IV of the Controlled Substances Act.[24] Carisoprodol is sometimes mixed with date rape drugs.[25]


As with other gabaminergic drugs, combination with other gabaminergic drugs, including alcohol, as well as with sedatives in general, possess a significant risk to the user in the form of overdose. Overdose symptoms are similar to those of other gabaminergics including excessive sedation, severe ataxia, amnesia, confusion, agitation, intoxication and inappropriate (potentially violent) behavior. Severe overdoses may present with respiratory depression, coma, and death. Carisoprodol is not detected on all toxicology tests which may delay diagnosis of overdose. Overdose symptoms in combination with opiates are similar but distinguished by miosis. Carisoprodol (as with its metabolite meprobamate) is particularly dangerous in combination with alcohol. Flumazenil may be used to counteract the effects of carisoprodol but its use is restricted by the potential for severe side effects and is contraindicated in mixed overdoses such as when it has been co-ingested with opiates.


Carisoprodol has a rapid, 30-minute onset of action, with the aforementioned effects lasting about two to six hours. It is metabolized in the liver via the cytochrome P450 oxidase isozyme CYP2C19, excreted by the kidneys and has about an eight-hour half-life. A considerable proportion of carisoprodol is metabolized to meprobamate, which is a known drug of abuse and dependence; this could account for the abuse potential of carisoprodol (meprobamate levels reach higher peak plasma levels than carisoprodol itself following administration).


Carisoprodol is a carbamic acid ester. It is a racemic mixture of two stereoisomers.

File:Carisoprodol synthesis.png
Carisoprodol synthesis: F.M. Berger, B.J. Ludwig, Carter Prod Inc; U.S. Patent 2,937,119 (1960).

Carisoprodol is synthesized by reacting 2-methyl-2-propylpropane-1,3-diol with 1 molar equivalent of phosgene, forming the chloroformate, from which carbamate is formed by reacting it with isopropylamine. Reacting this with either urethane or sodium cyanate gives carisoprodol.


  1. ^ Meda Pharmaceuticals Inc. of Somerset, New Jersey is the U.S. subsidiary of Meda AB of Solna, Sweden "Meda Pharmaceuticals Inc.". Retrieved June 22, 2010. 
  2. ^ Miller JG, ed. The pharmacology and clinical usefulness of carisoprodol. Detroit:Wayne State University; 1959.
  3. ^ Berger, F; Kletzkin, M; Ludwig, B; Margolin, S (1959). "The history, chemistry, and pharmacology of carisoprodol". Annals of the New York Academy of Sciences 86: 90–107. doi:10.1111/j.1749-6632.1960.tb42792.x. 
  4. ^ Bramness JG, Furu K, Engeland A, . (2007). "Carisoprodol use and abuse in Norway. A pharmacoepidemiological study". Br J Clin Pharmacol 64 (2): 210–218. PMC 2000626. PMID 17298482. doi:10.1111/j.1365-2125.2007.02847.x. 
  5. ^ "Somadril trekkes fra markedet". 20 April 2008. Retrieved 12 March 2010. 
  6. ^ "Marknadsföringen av Somadril och Somadril comp rekommenderas upphöra tillfälligt". 16 Nov 2007. Retrieved 9 May 2009. 
  7. ^ "Carisprodol press release" (PDF). EMEA. Retrieved 2008-05-12. 
  8. ^ US Department of Justice (2011). "Schedules of Controlled Substances: Placement of Carisoprodol into Schedule IV" (PDF). Federal Register 76 (238): 77330–77360. Retrieved 2012-02-01. 
  9. ^
  10. ^ "NAPRA - Search National Drug Schedule" (ASP). National Association of Pharmacy Regulatory Authorities. 2009. Retrieved 2014-01-07. 
  11. ^ Personal communication from a pharmacist
  12. ^ Kamin I, Shaskan D. (1959). "Death due to massive overdose of meprobamate". Am J Psychiatry 115 (12): 1123–1124. PMID 13649976. 
  13. ^ Hollister LE (1983). "The pre-benzodiazepine era". J Psychoactive Drugs 15 (1–2): 9–13. PMID 6350551. doi:10.1080/02791072.1983.10472117. 
  14. ^ Gaillard Y, Billault F, Pepin G (1997). "Meprobamate overdosage: a continuing problem. Sensitive GC-MS quantitation after solid phase extraction in 19 fatal cases". Forensic Sci.Int 86 (3): 173–180. PMID 9180026. doi:10.1016/S0379-0738(97)02128-2. 
  15. ^ Allen MD, Greenblatt DJ, Noel BJ (1977). "Meprobamate overdosage: a continuing problem". Clin Toxicol 11 (5): 501–515. PMID 608316. doi:10.3109/15563657708988216. 
  16. ^ Kintz P, Tracqui A, Mangin P, Lugnier AA (1988). "Fatal meprobamate self-poisoning". Am J Forensic Med Pathol 9 (2): 139–140. PMID 3381792. doi:10.1097/00000433-198806000-00009. 
  17. ^ Eeckhout E, Huyghens L, Loef B, Maes V, Sennesael J (1988). "Meprobamate poisoning, hypotension and the Swan-Ganz catheter". Intensive Care Med 14 (4): 437–438. PMID 3403779. doi:10.1007/BF00262904. 
  18. ^ Lhoste F, Lemaire F, Rapin M (1977). "Treatment of hypotension in meprobamate poisoning". N Engl J Med 296 (17): 1004. PMID 846530. doi:10.1056/NEJM197704282961717. 
  19. ^ Bedson H (1959). "Coma due to meprobamate intoxication. Report of a case confirmed by chemical analysis". Lancet 273 (1): 288–290. PMID 13632000. doi:10.1016/S0140-6736(59)90209-0. 
  20. ^ Blumberg A, Rosett H, Dobrow A (1959). "Severe hypotension reactions following meprobamate overdosage". Ann Intern Med 51 (3): 607–612. PMID 13801701. doi:10.7326/0003-4819-51-3-607. 
  21. ^ NCQA’s HEDIS Measure: Use of High Risk Medications in the Elderly
  22. ^ Melinda J Barker, Kenneth M Greenwood, Martin Jackson, Simon F Crowe. "Persistence of cognitive effects after withdrawal from long-term Archives of Clinical Neuropsychology". Archives of Clinical Neuropsychology 19: 437–454. doi:10.1016/S0887-6177(03)00096-9. 
  23. ^ "DEA Drugs & Chemicals of Concern "Carisoprodol"". Retrieved 29 April 2011. 
  24. ^
  25. ^ Knock-Out Drugs: Their Prevalence, Modes of Action, and Means of Detection Burkhard Madea, Prof. Dr. med.*1 and Frank Mußhoff, Prof. Dr. Rer. Nat.

External links