Carisoprodol: Wikis


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Systematic (IUPAC) name
2-{[(aminocarbonyl)oxy]methyl}-2-methylpentyl isopropylcarbamate
CAS number 78-44-4
ATC code M03BA02
PubChem 2576
DrugBank APRD00417
ChemSpider 2478
Chemical data
Formula C12H24N2O4 
Mol. mass 260.33 g/mol
SMILES eMolecules & PubChem
Pharmacokinetic data
Protein binding 60%
Metabolism Hepatic (CYP2C19-mediated)
Half life 2 hours
Excretion Renal
Therapeutic considerations
Pregnancy cat. C
Legal status -only (US) , CIV in some states.
Routes Oral
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Carisoprodol is a centrally-acting skeletal muscle relaxant. Carisoprodol is a colorless, crystalline powder, having a mild characteristic odor and a bitter taste. It is slightly soluble in water and freely soluble in alcohol, chloroform and acetone. Its solubility is practically independent of pH. It is marketed in the United States under the brand name Soma, and in the United Kingdom and other countries under the brand names Sanoma and Carisoma. Carisoprodol is available by itself or mixed with aspirin and in one preparation (Soma Compound With Codeine) along with codeine and caffeine as well.



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.[1] It had been developed by Dr. Frank M. Berger at Wallace Laboratories and had been named carisoprodol (trade name Soma).

Carisoprodol was developed on the basis of meprobamate, in the hope that it would have better muscle relaxing properties, less potential for abuse, and less risk of overdose than meprobamate.[2] 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.

The brand name Soma is shared with the Soma/Haoma of ancient India, a drug mentioned in ancient Sanskrit writings.[note 1] Soma is also the name of the fictional drug featured in Aldous Huxley's Brave New World.[3]

Usage and legal status

Although reports from Norway have shown that carisoprodol has abuse potential[4] as a product of meprobamate and/or potentiator of hydrocodone, dihydrocodeine, codeine and similar drugs, it continues to be prescribed in North America, alongside orphenadrine and cyclobenzaprine. In Europe, doctors favor cyclobenzaprine. In the United Kingdom, benzodiazepines are preferred instead. All of the above plus chlorzoxazone are used in Canada.

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 has considered other drugs used with the same indications as carisoprodol to have the same or better effects without the risks of the drug.[5] In May 2008 it was taken of the market in Norway as well. [6]

In the EU, the European Medicines Agency has issued a release recommending that member states suspend marketing authorization for this product in the treatment of acute (not chronic) back pain.[7]

As of February 2010 carisoprodol is considered to be a schedule CIV by the states of Alabama, Arizona, Arkansas, Florida, Georgia, Hawaii, Indiana, Kentucky, Louisiana, Massachusetts, Minnesota, Mississippi, New Mexico, Nevada, Oklahoma, Oregon and Texas (scheduled using the states new controlled substance program which requires physicians to obtain, and include, a state "DPS" number as well as a DEA number on all Scheduled drugs) and Washington State. It is a schedule CIII in West Virginia.[8] The rest of the United States, excluding the above named states, falls under the DEA scheduling for the drug, which considers carisoprodol a non-scheduled chemical, meaning that carisoprodol is considered a general prescription medication by the federal government of the United States, with oversight provided solely by the U.S. Food and Drug Administration (FDA).[9]


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


Side effects

The usual dose of 350 mg is unlikely to engender prominent side effects other than somnolence. The medication is well tolerated and without adverse effects in the majority of patients for which 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, motorcycle, 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 opioids, essentially all opioids and other centrally-acting analgesics, but especially those of the codeine-derived subgroup of the semi-synthetic class (codeine, ethylmorphine, dihydrocodeine, morphine, meperidine, buprenorphine, hydrocodone, oxycodone, nicocodeine, benzylmorphine, the various acetylated codeine derivatives including thebacon and 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 injury and/or muscle 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.

Meprobamate and other muscle relaxing drugs often were subjects of misuse and abuse in the 1950s and 1960s.[10][11] Overdose cases were reported as early as 1957 and have been reported on several occasions since then.[12][13][14][15][16][17][18]

Carisoprodol, meprobamate, and related drugs such as tybamate have the potential to produce physical dependence with prolonged use. Withdrawal of the drug after extensive use may require hospitalization in medically-compromised patients.

Because of potential for more severe side effects, this drug is on the list to avoid in the elderly. (See NCQA’s HEDIS Measure: Use of High Risk Medications in the Elderly,


Carisoprodol has a rapid, 30 minute onset of action, with the aforementioned effects lasting for approximately 2–6 hours. It is metabolized in the liver via the cytochrome P450 oxidase isozyme CYP2C19, excreted by the kidneys and has an approximate 8 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.


  1. ^ Various classical and modern researchers have theorised that Soma/Haoma could be anything from ephedra to mushrooms of the genus Amanita with hallucinogenic and psychedelic properties related to the muscarinic drugs contained therein to various anticholinergic plants to opium -- or a still unknown hallucinogen, stimulant and/or narcotic of unknown chemical class and origin or even coca or other drugs ported from the Western Hemisphere by an as yet unknown pre-Viking, pre-Columbian contact.


  1. ^ Miller JG, ed. The pharmacology and clinical usefulness of carisoprodol. Detroit:Wayne State University; 1959.
  2. ^ Berger F, Kletzkin M, Ludwig B, Margolin S. The history, chemistry, and pharmacology of carisoprodol. Annals of the New York Academy of Sciences. 1959;86:90-107
  3. ^ "Brave New Soma - TIME".,9171,892617,00.html. Retrieved 2007-08-20. 
  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. doi:10.1111/j.1365-2125.2007.02847.x. 
  5. ^ "Marknadsföringen av Somadril och Somadril comp rekommenderas upphöra tillfälligt". 16 NOV 2007. Retrieved 9 MAY 2009. 
  6. ^ "Somadril trekkes fra markedet". 20 April 2008. Retrieved 12 March 2010. 
  7. ^ "Carisprodol press release" (PDF). EMEA. Retrieved 2008-05-12. 
  8. ^ Respective state Boards of Pharmacy and controlled substance authorities.
  9. ^ "Florida Senate House Bill 351" (PDF). 
  10. ^ Kamin I, Shaskan D. (1959). "Death due to massive overdose of meprobamate". Am J Psychiatry 115 (12): 1123–1124. 
  11. ^ Hollister LE (1983). "The pre-benzodiazepine era". J Psychoactive Drugs 15 (1-2): 9–13. 
  12. ^ 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. doi:10.1016/S0379-0738(97)02128-2. 
  13. ^ Allen MD, Greenblatt DJ, Noel BJ (1977). "Meprobamate overdosage: a continuing problem". Clin Toxicol 11 (5): 501–515. 
  14. ^ Kintz P, Tracqui A, Mangin P, Lugnier AA (1988). "Fatal meprobamate self-poisoning". Am J Forensic Med Pathol 9 (2): 139–140. doi:10.1097/00000433-198806000-00009. 
  15. ^ 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. doi:10.1007/BF00262904. 
  16. ^ Lhoste F, Lemaire F, Rapin M (1977). "Treatment of hypotension in meprobamate poisoning". N Engl J Med 296 (17): 1004. 
  17. ^ Bedson H (1959). "Coma due to meprobamate intoxication. Report of a case confirmed by chemical analysis". Lancet 273 (1): 288–290. doi:10.1016/S0140-6736(59)90209-0. 
  18. ^ Blumberg A, Rosett H, Dobrow A (1959). "Severe hypotension reactions following meprobamate overdosage". Ann Intern Med 51: 607–612. 

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