Misplaced Pages

:WikiProject Chemicals/Chembox validation/VerifiedDataSandbox and Carisoprodol: Difference between pages - Misplaced Pages

Article snapshot taken from Wikipedia with creative commons attribution-sharealike license. Give it a read and then ask your questions in the chat. We can research this topic together.
(Difference between pages)
Page 1
Page 2
Content deleted Content addedVisualWikitext
Revision as of 11:12, 16 February 2012 editBeetstra (talk | contribs)Edit filter managers, Administrators172,031 edits Saving copy of the {{drugbox}} taken from revid 477026068 of page Carisoprodol for the Chem/Drugbox validation project (updated: 'DrugBank').  Latest revision as of 02:59, 12 January 2025 edit Arthurfragoso (talk | contribs)Extended confirmed users3,659 edits dark mode fix 
Line 1: Line 1:
{{Short description|Muscle relaxant medication}}
{{ambox | text = This page contains a copy of the infobox ({{tl|drugbox}}) taken from revid of page ] with values updated to verified values.}}
{{Use American English|date=August 2017}}
{{Drugbox
{{Use dmy dates|date=December 2019}}
| Verifiedfields = changed
{{cs1 config |name-list-style=vanc |display-authors=6}}
| verifiedrevid = 457451240
{{Infobox drug
| IUPAC_name = 2-{methyl}-2-methylpentyl isopropylcarbamate
| Watchedfields = changed
| image = Carisoprodol-2D-skeletal.png
| verifiedrevid = 477165578
| image2 = Carisoprodol3d.png
| image = Carisoprodol.svg
| image_class = skin-invert-image
| width =
| alt =
| caption =


<!--Clinical data--> <!-- Clinical data -->
| pronounce = {{IPAc-en|k|ə|r|ˌ|aɪ|s|ʌ|ˈ|p|r|oʊ|d|ɒ|l}}<br />{{respell|kahr|EYE|suh|PROH|dol}}
| tradename = Soma
| tradename = Soma, others<ref name="drugs.com">{{cite web |title = Carisoprodol |url = https://www.drugs.com/international/carisoprodol.html |website = drugs.com |access-date = 16 April 2017 }}</ref>
| Drugs.com = {{drugs.com|monograph|carisoprodol}} | Drugs.com = {{drugs.com|monograph|carisoprodol}}
| MedlinePlus = a682578 | MedlinePlus = a682578
| DailyMedID = Carisoprodol
| pregnancy_category = C
| pregnancy_AU = <!-- A / B1 / B2 / B3 / C / D / X -->
| pregnancy_AU_comment =
| pregnancy_category =
| addiction_liability = Low<ref>{{cite web | title=Drug Scheduling | website=U.S. ] (DEA) | url=https://www.dea.gov/drug-information/drug-scheduling | access-date=24 March 2024}}</ref>{{failed verification|date=May 2024}}
| routes_of_administration = ]<ref name="Soma FDA label" />
| class = ]<ref name="Soma FDA label" />
| ATC_prefix = M03
| ATC_suffix = BA02
| ATC_supplemental =

<!-- Legal status -->
| legal_AU = S4
| legal_AU_comment =
| legal_BR = <!-- OTC, A1, A2, A3, B1, B2, C1, C2, C3, C4, C5, D1, D2, E, F -->
| legal_BR_comment =
| legal_CA = <!-- OTC, Rx-only, Schedule I, II, III, IV, V, VI, VII, VIII -->
| legal_CA_comment = Canceled<ref>{{cite web | title=Soma Product information | website=] | date=14 March 2003 | url=https://health-products.canada.ca/dpd-bdpp/info?lang=eng&code=205 | access-date=20 May 2024}}</ref>
| legal_DE = <!-- Anlage I, II, III or Unscheduled -->
| legal_DE_comment =
| legal_NZ = <!-- Class A, B, C -->
| legal_NZ_comment =
| legal_UK = <!-- GSL, P, POM, CD, CD Lic, CD POM, CD No Reg POM, CD (Benz) POM, CD (Anab) POM or CD Inv POM / Class A, B, C -->
| legal_UK_comment =
| legal_US = Schedule IV | legal_US = Schedule IV
| legal_US_comment = <ref name="Soma FDA label">{{cite web | title=Soma- carisoprodol tablet | website=DailyMed | date=15 May 2023 | url=https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=6297cf20-830a-11dc-94c8-0002a5d5c51b | access-date=20 May 2024}}</ref>
| routes_of_administration = Oral
| legal_EU =
| legal_EU_comment =
| legal_UN = <!-- N I, II, III, IV / P I, II, III, IV -->
| legal_UN_comment =
| legal_status = <!-- For countries not listed above -->


<!--Pharmacokinetic data--> <!-- Pharmacokinetic data -->
| bioavailability =
| protein_bound = 60% | protein_bound = 60%
| metabolism = ] (]-mediated) | metabolism = ] (]-mediated)
| metabolites = ]
| elimination_half-life = 2 hours
| onset = Rapid (30 minutes<ref name="PLM">{{cite book | vauthors = Carrasco A |chapter-url=https://www.medicamentosplm.com/Home/Medicamentos_Sustancia/carisoprodol/222 |language=es |access-date=13 June 2021 |page=222 |date=13 September 2019 |volume=I |edition=65th |isbn=978-607-625-072-3 |location=] |title=Diccionario de Especialidades Farmaceúticas PLM |chapter=Letra C (Carisoprodol) |publisher=PLM Latinoamérica | veditors = Carrasco Ruiz MA, Chavez Pulido X, Morales E }}</ref>{{failed verification|date=June 2021}})
| excretion = ]
| elimination_half-life = 2.5 hours ], its main active metabolite, which in turn has a half-life of 10 hours.<ref name="PLM" />}}]
| duration_of_action =
| excretion = ]


<!--Identifiers--> <!-- Identifiers -->
| CASNo_Ref = {{cascite|correct|CAS}}
| CAS_number_Ref = {{cascite|correct|??}} | CAS_number_Ref = {{cascite|correct|??}}
| CAS_number = 78-44-4 | CAS_number = 78-44-4
| ATC_prefix = M03 | CAS_supplemental =
| ATC_suffix = BA02
| PubChem = 2576 | PubChem = 2576
| IUPHAR_ligand = 7610
| DrugBank_Ref = {{drugbankcite|changed|drugbank}}
| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
| DrugBank = DB00395 | DrugBank = DB00395
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}} | ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
Line 40: Line 77:
| ChEMBL_Ref = {{ebicite|correct|EBI}} | ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 1233 | ChEMBL = 1233
| NIAID_ChemDB =
| PDB_ligand =
| synonyms =


<!--Chemical data--> <!-- Chemical and physical data -->
| IUPAC_name = (''RS'')-2-{methyl}-2-methylpentyl isopropylcarbamate
| C=12 | H=24 | N=2 | O=4
| C = 12
| molecular_weight = 260.33 g/mol
| H = 24
| smiles = O=C(OCC(COC(=O)NC(C)C)(C)CCC)N
| N = 2
| InChI = 1/C12H24N2O4/c1-5-6-12(4,7-17-10(13)15)8-18-11(16)14-9(2)3/h9H,5-8H2,1-4H3,(H2,13,15)(H,14,16)
| O = 4
| InChIKey = OFZCIYFFPZCNJE-UHFFFAOYAJ
| SMILES = O=C(N)OCC(C)(CCC)COC(=O)NC(C)C
| StdInChI_Ref = {{stdinchicite|correct|chemspider}} | StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C12H24N2O4/c1-5-6-12(4,7-17-10(13)15)8-18-11(16)14-9(2)3/h9H,5-8H2,1-4H3,(H2,13,15)(H,14,16) | StdInChI = 1S/C12H24N2O4/c1-5-6-12(4,7-17-10(13)15)8-18-11(16)14-9(2)3/h9H,5-8H2,1-4H3,(H2,13,15)(H,14,16)
| StdInChI_comment =
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}} | StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = OFZCIYFFPZCNJE-UHFFFAOYSA-N | StdInChIKey = OFZCIYFFPZCNJE-UHFFFAOYSA-N
| density =
| density_notes =
| melting_point =
| melting_high =
| melting_notes =
| boiling_point =
| boiling_notes =
| solubility =
| sol_units =
| specific_rotation =
}} }}

<!-- Definition and medical uses -->

'''Carisoprodol''', sold under the brand name '''Soma''' among others, is a medication used for ] pain.<ref name=AHFS2019/> Effects generally begin within half an hour and last for up to six hours.<ref name=AHFS2019/> It is taken orally (]).<ref name=AHFS2019>{{cite web |title=Carisoprodol Monograph for Professionals |url=https://www.drugs.com/monograph/carisoprodol.html |website=Drugs.com |publisher=American Society of Health-System Pharmacists |access-date=8 April 2019 }}</ref>

<!-- Side effects and mechanism -->
Common side effects include headache, dizziness, and sleepiness.<ref name=AHFS2019/> Serious side effect may include ], ]s, and ]s.<ref name=AHFS2019/> In people with a ] certain formulations may result in problems.<ref name=AHFS2019/> Safety during ] and ] is not clear.<ref name=AHFS2019/><ref>{{cite web |title=DailyMed - carisoprodol tablet |url=https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ab22f1be-16c8-45b6-adaf-09e08bf7a545 |website=dailymed.nlm.nih.gov |access-date=8 April 2019}}</ref> How it works is not clear.<ref name=AHFS2019/> Some of its effects are believed to occur following metabolic conversion into ], carisoprodol's main active metabolite.<ref name=AHFS2019/>

<!-- History and culture -->
Carisoprodol was approved for medical use in the United States in 1959.<ref name=AHFS2019/> Its approval in the European Union was withdrawn in 2008.<ref>{{cite web |title=Carisoprodol |url=https://www.ema.europa.eu/en/medicines/human/referrals/carisoprodol |website=European Medicines Agency |access-date=8 April 2019 |date=15 November 2007}}</ref> It is available as a ].<ref name=AHFS2019/> In 2019, it was the 343rd most commonly prescribed medication in the United States, with more than 800{{nbsp}}thousand prescriptions.<ref>{{cite web | title = Carisoprodol - Drug Usage Statistics | website = ClinCalc | url = https://clincalc.com/DrugStats/Drugs/Carisoprodol | access-date = 7 October 2022}}</ref> In the United States, it is a ] controlled substance.<ref name=AHFS2019/>

== Medical uses ==

] (acetaminophen), and ]]]
Carisoprodol is meant to be used along with rest, ] and other measures to relax muscles after ], ] and muscle injuries.<ref name="medpluscariso">{{cite web |title=Carisoprodol |url=https://medlineplus.gov/druginfo/meds/a682578.html |website=MedlinePlus |publisher=National Library of Medicine |access-date=6 May 2019}}</ref> It comes in tablet format and is taken by the mouth three times a day and before bed.<ref name="medpluscariso" />

== Side effects ==

The usual dose of 350&nbsp;mg is unlikely to engender prominent side effects other than ], and mild to significant ] or ], 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,{{Citation needed|reason=This entire paragraph is full of bold claims and not a single relevant source|date=August 2022}} 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 containing ], 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: ], ], ], fast ], ], ] and ].<ref name="medpluscariso" />

There are 368 drugs known to interact with carisoprodol including 28 major drug interactions.<ref>{{cite web |title=Carisoprodol Drug Interactions |url=https://www.drugs.com/drug-interactions/carisoprodol-index.html |website=Drugs.com |publisher=] |access-date=4 June 2024}}</ref> 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|date=July 2019}}

Meprobamate and other muscle-relaxing drugs often were subjects of misuse in the 1950s and 60s.<ref>{{cite journal | vauthors = Kamin I, Shaskan DA | title = Death due to massive overdose of meprobamate | journal = The American Journal of Psychiatry | volume = 115 | issue = 12 | pages = 1123–1124 | date = June 1959 | pmid = 13649976 | doi = 10.1176/ajp.115.12.1123-a }}</ref><ref>{{cite journal | vauthors = Hollister LE | title = The pre-benzodiazepine era | journal = Journal of Psychoactive Drugs | volume = 15 | issue = 1–2 | pages = 9–13 | year = 1983 | pmid = 6350551 | doi = 10.1080/02791072.1983.10472117 }}</ref> Overdose cases were reported as early as 1957, and have been reported on several occasions since then.<ref>{{cite journal | vauthors = Gaillard Y, Billault F, Pépin G | title = Meprobamate overdosage: a continuing problem. Sensitive GC-MS quantitation after solid phase extraction in 19 fatal cases | journal = Forensic Science International | volume = 86 | issue = 3 | pages = 173–180 | date = May 1997 | pmid = 9180026 | doi = 10.1016/S0379-0738(97)02128-2 }}</ref><ref>{{cite journal | vauthors = Allen MD, Greenblatt DJ, Noel BJ | title = Meprobamate overdosage: a continuing problem | journal = Clinical Toxicology | volume = 11 | issue = 5 | pages = 501–515 | date = December 1977 | pmid = 608316 | doi = 10.3109/15563657708988216 }}</ref><ref>{{cite journal | vauthors = Kintz P, Tracqui A, Mangin P, Lugnier AA | title = Fatal meprobamate self-poisoning | journal = The American Journal of Forensic Medicine and Pathology | volume = 9 | issue = 2 | pages = 139–140 | date = June 1988 | pmid = 3381792 | doi = 10.1097/00000433-198806000-00009 }}</ref><ref>{{cite journal | vauthors = Eeckhout E, Huyghens L, Loef B, Maes V, Sennesael J | title = Meprobamate poisoning, hypotension and the Swan-Ganz catheter | journal = Intensive Care Medicine | volume = 14 | issue = 4 | pages = 437–438 | year = 1988 | pmid = 3403779 | doi = 10.1007/BF00262904 | s2cid = 2784867 }}</ref><ref>{{cite journal | vauthors = Lhoste F, Lemaire F, Rapin M | title = Treatment of hypotension in meprobamate poisoning | journal = The New England Journal of Medicine | volume = 296 | issue = 17 | pages = 1004 | date = April 1977 | pmid = 846530 | doi = 10.1056/NEJM197704282961717 }}</ref><ref>{{cite journal | vauthors = Bedson HS | title = Coma due to meprobamate intoxication; report of a case confirmed by chemical analysis | journal = Lancet | volume = 1 | issue = 7067 | pages = 288–290 | date = February 1959 | pmid = 13632000 | doi = 10.1016/S0140-6736(59)90209-0 }}</ref><ref>{{cite journal | vauthors = Blumberg AG, Rosett HL, Dobrow A | title = Severe hypotensive reactions following meprobamate overdosage | journal = Annals of Internal Medicine | volume = 51 | issue = 3 | pages = 607–612 | date = September 1959 | pmid = 13801701 | doi = 10.7326/0003-4819-51-3-607 }}</ref>

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 or ].<ref name="toxnetcariso">{{cite web |title=CARISOPRODOL |url=http://toxnet.nlm.nih.gov/cgi-bin/sis/search2/r?dbs+hsdb:@term+@DOCNO+3021 |website=TOXNET |publisher=National Library of Medicine |access-date=6 May 2019}}</ref> Because of potential for more severe side effects, this drug is on the list to avoid for elderly people.<ref> {{webarchive |url=https://web.archive.org/web/20100201113909/http://www.ncqa.org/Portals/0/Newsroom/SOHC/Drugs_Avoided_Elderly.pdf |date=1 February 2010 }}</ref>

=== Withdrawal ===

Carisoprodol, meprobamate, and related drugs such as ], 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 ] including the potentially lethal ].

Psychological dependence has also been linked to carisoprodol use<ref>{{cite web |date=2021-03-19|title=What is Carisoprodol used for?|url=https://painosoma.com/blog/what-is-carisoprodol-used-for/|access-date=2021-04-29|website=Pain o Soma medicines }}</ref> 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 (particularly ]s or alcohol). It may reach clinical significance before physiological tolerance and dependence have occurred and (as with ]s) 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, ], hair-trigger agitation/aggression, chronic ], new or aggravated (often illogical) ], reduced IQ, short term and long-term memory loss, and dozens of other sequelae.<ref>{{cite journal | vauthors = Barker MJ, Greenwood KM, Jackson M, Crowe SF | title = Persistence of cognitive effects after withdrawal from long-term benzodiazepine use: a meta-analysis | journal = Archives of Clinical Neuropsychology | volume = 19 | issue = 3 | pages = 437–454 | date = April 2004 | pmid = 15033227 | doi = 10.1016/S0887-6177(03)00096-9 | doi-access = free }}</ref> 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 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 as ] or ] 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). ] and ] 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.{{Citation needed|date=October 2021}}

Carisoprodol withdrawal can be life-threatening (especially in high dose users and those who attempt to quit "]"). Medical supervision is recommended, with gradual reduction of dose of carisoprodol or a substituted medication, typical of other depressant drugs.

===Non-medical use===
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".<ref name="horsfallpharma">{{cite journal | vauthors = Horsfall JT, Sprague JE | title = The Pharmacology and Toxicology of the 'Holy Trinity' | journal = Basic & Clinical Pharmacology & Toxicology | volume = 120 | issue = 2 | pages = 115–119 | date = February 2017 | pmid = 27550152 | doi = 10.1111/bcpt.12655 | s2cid = 25909460 | doi-access = free }}</ref>

Recreational users of carisoprodol usually seek its potentially heavy sedating, relaxant, and ] effects.<ref>{{cite web |access-date = 29 April 2011 |url = http://www.deadiversion.usdoj.gov/drugs_concern/carisoprodol.htm |title = DEA Drugs & Chemicals of Concern "Carisoprodol" |url-status = dead |archive-url = https://web.archive.org/web/20110417095759/http://www.deadiversion.usdoj.gov/drugs_concern/carisoprodol.htm |archive-date = 17 April 2011 }}</ref> Also, because of its potentiating effects on ]s, it is often used in conjunction with many ] drugs. Also it is not detected on standard ]ing screens. On 26 March 2010 the DEA issued a ] on proposed rule making in respect to the placement of carisoprodol in schedule IV of the ].<ref>{{cite web |url = http://www.pharmcast.com/FederalRegistrar/Yr2010/Mar2010/032210/Carisoprodol032610.htm |title =Schedules of Controlled Substances: Placement of Carisoprodol Into Schedule IV; Announcement of Hearing |access-date = 19 April 2010 |url-status = dead |archive-url = https://web.archive.org/web/20110715074835/http://www.pharmcast.com/FederalRegistrar/Yr2010/Mar2010/032210/Carisoprodol032610.htm |archive-date = 15 July 2011 }}</ref> The DEA ended up classifying it under schedule IV.<ref name="DEA">{{cite web | url= https://deadiversion.usdoj.gov/drug_chem_info/carisoprodol/carisoprodol.pdf | work = Drug Enforcement Administration, Diversion Control Division, Drug & Chemical Evaluation Section | publisher = U.S. Department of Justice |title = Carisoprodol |date = December 2019}}</ref> Carisoprodol is sometimes mixed with ]s.<ref>{{cite journal | vauthors = Madea B, Musshoff F | title = Knock-out drugs: their prevalence, modes of action, and means of detection | journal = Deutsches Ärzteblatt International | volume = 106 | issue = 20 | pages = 341–347 | date = May 2009 | pmid = 19547737 | pmc = 2689633 | doi = 10.3238/arztebl.2009.0341 }}</ref>

== Overdose ==

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.<ref>{{Cite web |title=Carisoprodol - an overview {{!}} ScienceDirect Topics |url=https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/carisoprodol#:~:text=Carisoprodol%20overdosage%20should%20be%20regarded,have%20been%20observed%20(4). |access-date=2023-10-22 |website=www.sciencedirect.com}}</ref> Overdose symptoms are similar to those of other GABAergics including excessive sedation and unresponsiveness to stimuli, severe ], ], ], ], ] and inappropriate (potentially violent) behavior. Severe overdoses may present with ] (and subsequent ]), ], and ].<ref>{{Cite web |title=What Does a Soma Overdose Look Like? |url=https://projectknow.com/overdose/soma/ |access-date=2023-10-22 |website=Project Know }}</ref>

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 or ], which are generally unresponsive to light. Carisoprodol (as with its metabolite meprobamate) is particularly dangerous in combination with alcohol. ] (the benzodiazepine antidote) is not effective in the management of carisoprodol overdose as carisoprodol acts at the barbiturate binding site. Treatment mirrors that of ]s and is generally supportive, including the administration of ] and ] as indicated and, in rare cases, ]. Total amnesia of the experience is not uncommon following recovery.{{citation needed|date=January 2018}}

In 2014 actress ] died of an overdose due to the combined effects of carisoprodol, ] and ].<ref>{{cite web |url=https://www.cnn.com/2014/07/20/showbiz/obit-skyemccolebartusiak/index.html |title='Patriot' actress Skye McCole Bartusiak dead at 21 | vauthors = Duke A |date=July 22, 2014 |website=CNN Entertainment |access-date=February 24, 2019 }}</ref>

In 1999 actress ] died after taking carisoprodol (Soma) along with a few doses of a ] painkiller (Lortab), in an overdose that was ruled a suicide.<ref>{{cite news |date=May 21, 1999 |title=Death of 'Diff'rent Strokes' Actress Ruled A Suicide |newspaper=] |url=https://www.chicagotribune.com/news/ct-xpm-1999-05-21-9905220016-story.html |access-date=June 3, 2024 |archive-url=https://web.archive.org/web/20190324025542/https://www.chicagotribune.com/news/ct-xpm-1999-05-21-9905220016-story.html |archive-date=2019-03-24}}</ref>

== Pharmacology ==

===Pharmacodynamics===
Carisoprodol, has a chemical structure similar to ], a neurotransmitter, and dimethylglycine.

Carisoprodol's structural similarity to ] indicates GABAergic activity, including GABA<sub>A</sub> agonism, similar to the mechanism of benzodiazepines.<ref name="PLM2">{{cite book | vauthors = Conermann T, Christian D | chapter = Carisoprodol |date=2022 | chapter-url= http://www.ncbi.nlm.nih.gov/books/NBK553077/ |title = StatPearls|place=Treasure Island (FL)|publisher=StatPearls Publishing|pmid=31971718|access-date=2022-02-23 }}</ref>
This will allow for further muscle relaxation and anxiety reduction. Therefore, carisoprodol, at low to moderate dosages, may be clinically indicated for absent seizures, yet exacerbate ]s.{{medcn|date=December 2023}}

===Pharmacokinetics===
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 ] ] ], 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).<ref>{{cite journal | vauthors = Dean L | title = Carisoprodol Therapy and CYP2C19 Genotype | journal = Medical Genetics Summaries | date = 4 April 2017 | pmid = 28520382 | url = https://www.ncbi.nlm.nih.gov/books/NBK425390 | veditors = Pratt VM, Scott SA, Pirmohamed M, Esquivel B, Kattman BL, Malheiro AJ, Dean L }}</ref> A considerable proportion of carisoprodol is metabolized to ], 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 slightly ] in ] and freely soluble in ], ] and ]. The drug's solubility is practically independent of ].

== History ==
In June 1959, several American pharmacologists convened at ] in ] to discuss a newly discovered ] of ]. The substitution of one ] atom with an ] group on one of the ] ]s was intended to yield a drug with new pharmacological properties. It had been developed by ] at ] and was named carisoprodol.<ref>Miller JG, ed. The pharmacology and clinical usefulness of carisoprodol. Detroit:Wayne State University; 1959.</ref>

Building on ]'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 and ] effects.<ref>{{cite journal | vauthors = Berger FM, Kletzkin M, Ludwig BJ, Margolin S | title = The history, chemistry, and pharmacology of carisoprodol | journal = Annals of the New York Academy of Sciences | volume = 86 | issue = 1 | pages = 90–107 | date = March 1960 | pmid = 13799302 | doi = 10.1111/j.1749-6632.1960.tb42792.x | s2cid = 11909344 | bibcode = 1960NYASA..86...90B }}</ref>

== Usage and legal status ==

=== Norway ===
Reports from Norway have shown carisoprodol has addictive potential<ref>{{cite journal | vauthors = Bramness JG, Furu K, Engeland A, Skurtveit S | title = Carisoprodol use and abuse in Norway: a pharmacoepidemiological study | journal = British Journal of Clinical Pharmacology | volume = 64 | issue = 2 | pages = 210–218 | date = August 2007 | pmid = 17298482 | pmc = 2000626 | doi = 10.1111/j.1365-2125.2007.02847.x }}</ref> as a prodrug of ] and/or ] of ], ], ], and similar drugs. In May 2008 it was taken off the market in Norway.<ref>{{cite web |access-date = 12 March 2010 |url = http://www.legemiddelverket.no/templates/InterPage____71544.aspx |title = Somadril trekkes fra markedet | trans-title = Somadril is withdrawn from the market | language = no | work = Norwegian Medicines Agency |date = 20 April 2008 |url-status = dead |archive-url = https://web.archive.org/web/20110716163724/http://www.legemiddelverket.no/templates/InterPage____71544.aspx |archive-date = 16 July 2011 }}</ref>

=== 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.<ref>{{cite web |url = http://www.emea.europa.eu/pdfs/human/press/pr/Pressrelease_Carisoprodol_52046307en.pdf |title = Carisprodol press release |publisher = EMEA |access-date = 12 May 2008 |url-status = dead |archive-url = http://arquivo.pt/wayback/20090718092048/http://www.emea.europa.eu/pdfs/human/press/pr/Pressrelease_Carisoprodol_52046307en.pdf |archive-date = 18 July 2009 }}</ref>

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.<ref>{{cite web |access-date = 9 May 2009 |url = http://www.lakemedelsverket.se/Tpl/NewsPage____6712.aspx |title = Marknadsföringen av Somadril och Somadril comp rekommenderas upphöra tillfälligt |date = 16 November 2007 |url-status = dead |archive-url = https://archive.today/20140723055206/http://www.lakemedelsverket.se/Alla-nyheter/NYHETER-2007/Marknadsforingen-av-Somadril-och-Somadril-comp-rekommenderas-upphora-tillfalligt/ |archive-date = 23 July 2014 |language = sv |trans-title = Marketing of Somadril and Somadril is recommended to cease temporarily }}</ref>

=== United States ===
In December 2011, the ] (DEA) issued the final ruling placing carisoprodol on Schedule IV of the ] (CSA). The placement of carisoprodol on Schedule IV was effective in January 2012.<ref>{{cite journal |author = US Department of Justice |year = 2011 |title = Schedules of Controlled Substances: Placement of Carisoprodol into Schedule IV |journal = Federal Register |volume = 76 |issue = 238 |pages = 77330–77360 |url = http://www.gpo.gov/fdsys/pkg/FR-2011-12-12/pdf/2011-31542.pdf |access-date = 1 February 2012 }}</ref>

=== Canada ===
Federally, carisoprodol is a prescription drug (Schedule I, sub-schedule F1).<ref>{{cite web |url = http://napra.ca/pages/Schedules/Search.aspx |format = ASP |title = NAPRA – Search National Drug Schedule |publisher = National Association of Pharmacy Regulatory Authorities |year = 2009 |access-date = 7 January 2014 |archive-url = https://web.archive.org/web/20140201220518/http://napra.ca/pages/Schedules/Search.aspx |archive-date = 1 February 2014 |url-status = dead |df = dmy-all }}</ref> Provincial regulations vary.<ref>For British Columbia, see {{Webarchive|url=https://web.archive.org/web/20131217080015/http://library.bcpharmacists.org/D-Legislation_Standards/D-4_Drug_Distribution/5012-Drug_Schedules_Regulation.pdf |date=17 December 2013 }}</ref> It is no longer readily available.{{medical citation needed|date=April 2013}}

=== Indonesia ===
* In September 2013, carisoprodol was taken off the market due to problems with diversion, dependence and side effects.
* In September 2017, one child died and 50 had seizures when PCC, which stands for "Paracetamol Caffeine Carisoprodol" was mixed (probably illicit) into children's drinks in elementary and junior high schools in ].<ref>{{cite web | vauthors = | url=http://jakartaglobe.id/news/one-schoolchild-dies-50-suffer-seizures-consuming-pills-southeast-sulawesi/ | title=One Schoolchild Dies, More Than 50 Suffer Seizures After Consuming Pills in Southeast Sulawesi | work = Jakarta Globe | date=14 September 2017}}</ref>

==Notes==
{{reflist|group=nb}}

== References ==
{{Reflist}}

== Further reading ==
{{refbegin}}
* {{cite book | vauthors=Dean L | title=Medical Genetics Summaries | chapter=Carisoprodol Therapy and CYP2C19 Genotype | chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK425390/ | veditors=Pratt VM, McLeod HL, Rubinstein WS, Scott SA, Dean LC, Kattman BL, Malheiro AJ | display-editors=3 | publisher=] (NCBI) | year=2017 | pmid=28520377 | id=Bookshelf ID: NBK425390 | url=https://www.ncbi.nlm.nih.gov/books/NBK61999/ }}
{{refend}}

{{Muscle relaxants}}
{{GABAA receptor positive modulators}}
{{Ionotropic glutamate receptor modulators}}
{{Portal bar | Medicine}}
{{Authority control}}

]
]
]
]
]
]
]
]
]
]