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What is Carisoprodol

Systematic (IUPAC) name:
(RS)-2-[(aminocarbonyl)oxy]methyl-2-methylpentyl isopropylcarbamate;
Clinical data:
Trade names Soma;
Legal status:
AU: Prescription Only (S4);
US: Schedule IV; Schedule II(In Louisiana);
Routes of administration:
Pharmacokinetic data;
Protein binding 60%;
Metabolism Hepatic (CYP2C19-mediated);
Half-life 2 hours;
Excretion Renal;
CAS Registry Number;
78-44-4 Yes;
ATC code;
PubChem CID 2576;
DrugBank DB00395 Yes;
ChemSpider 2478 Yes;
UNII 21925K482H Yes;
KEGG D00768 Yes;
ChEBI CHEBI:3419 Yes;
Chemical data;
Formula C12H24N2O4;
Molecular mass;
260.33 g/mol;



Carisoprodol can be 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 actually independent of pH. Carisoprodol is manufactured and marketed inside United States by Meda Pharmaceuticals[1] beneath the brand name Soma, as well as in the United Kingdom along with other countries underneath the brand names Sanoma and Carisoma. The drug is available themselves or when combined aspirin, plus one preparation with codeine and caffeine, also. Although carisoprodol has significant pharmacological activity, its benefit in treatments are likely due mostly for the meprobamate metabolite as meprobamate remains inside the system significantly longer and reaches a larger peak plasma concentration compared to parent drug some hours following administration. This is further evidenced by carisoprodol's chance to maintain relevant benefits when administered 3-4 times daily despite its short half-life of only 2 hours.
On June 1, 1959 several American pharmacologists convened at Wayne State University in Detroit, Michigan to go over a new drug. The drug, originally consideration to have antiseptic properties, was discovered to have central muscle-relaxing properties.[2] It had been put together by Frank M. Berger at Wallace Laboratories and was named carisoprodol.
Carisoprodol would have been a modification of meprobamate, intended to get better muscle relaxing properties, less possibility of abuse, and fewer risk of overdose.[3] The substitution of 1 hydrogen atom through an isopropyl group on a single of the carbamyl nitrogens was that will yield a molecule with new pharmacological properties.
Usage and legal status Abuse Potential first Noted in Norway Study Reports from Norway show carisoprodol has abuse potential[4] to be a prodrug of meprobamate and/or potentiator of hydrocodone, oxycodone, codeine and other drugs. In May 2008 it had been taken off industry in Norway.[5] It has become prescribed in North America alongside methocarbamol, cyclobenzaprine, metaxalone, tizanidine, orphenadrine, and chlorzoxazone. In the United States, carisopridol, while being recently scheduled to be a controlled substance, is as known as cyclobenzaprine, tizanidine is practically as fashionable as methocarbamol, while chlorzoxazone much cheaper than frequently prescribed at approximately the same frequency as orphenadrine. In Europe, doctors favor the safer cyclobenzaprine. In the United Kingdom, benzodiazepines are preferred, instead.


As of November 2007, carisoprodol (Somadril, Somadril comp.) has been removed the market in Sweden caused by problems with dependence and uncomfortable side effects. The agency overseeing pharmaceuticals considered other drugs in combination with the same indications as carisoprodol to get the same or better effects devoid of the risks with the drug.[6]
European Union
In the EU, the European Medicines Agency issued a release recommending member states suspend marketing authorization just for this product inside the treatment of acute (not chronic) lumbar pain.
United States
Until December 12, 2011, if your Administrator with the Drug Enforcement Administration (DEA) issued the last ruling placing the substance carisoprodol into Schedule IV on the Controlled Substances Act (CSA), carisoprodol has not been a controlled substance. The keeping of carisoprodol into Schedule IV was effective January 11, 2012.
Carisoprodol is available to be a generic in 350 mg and, now, as 250 mg tablets. There is additionally a brand formulation in 250 mg tablets.Compounded tablets with acetaminophen are also offered.
Federally, carisoprodol is really a Prescription Drug (Schedule I, sub-schedule F1). Provincial regulations can vary greatly, e.g. for BC see It is no longer readily accessible.[11] Now unscheduled, easily obtainable in powder base to be a Research Chemical
In September 2013, carisoprodol has been flourished the market in Indonesia caused by problems with diversion, dependence and uncomfortable side effects.
Because of possibility of more severe uncomfortable side effects, this drug is listed to avoid inside elderly.
Carisoprodol, meprobamate, and related drugs for instance tybamate, have the possible ways to produce physical dependence on the barbiturate type following periods of prolonged use. Withdrawal in the drug after extensive use may necessitate hospitalization in medically compromised patients. In severe cases the withdrawal can mimic the the signs of alcohol withdrawal such as potentially lethal status epilepticus.
Psychological dependence been specifically linked to carisoprodol use although this far less severe compared to meprobamate itself (presumably due towards the slower start of effects). Psychological dependence is a lot more common in those that abuse carisoprodol and individuals who have a good reputation for drug abuse (particularly sedatives and/or alcohol). It may reach clinical significance before physiological tolerance and dependence have occurred and (just like benzodiazepines) is demonstrated to persist to varying examples of severity for time after discontinuation. Withdrawal treatment
Discontinuation of carisoprodol, much like all GABA-ergics, can lead to 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, quick and extended memory loss, and a large number of other sequela.[22] The effects, severity, and duration seem slightly dose-dependent but you are mainly dependant on the patients pattern people (taken as prescribed, consumed in bulk doses, when combined other drugs, a combination on the above, etc.), genetic predisposition to drug use, and a reputation of substance abuse all improve the patients chance of persistent discontinuation syndrome symptoms.
Treatment for physical withdrawal generally involves switching the person to a long-acting benzodiazepine for example diazepam or clonazepam then slowly titrating them off of the replacement drug completely at a rate that's both reasonably comfortable for the person but rapid enough to the managing physician to contemplate the rate of progress acceptable (overly rapid dose reduction greatly increases the chance patient non-compliance like the abuse of illicitly obtained alternative sedatives and/or alcohol). Psychotherapy and cognitive behavior therapy have demonstrated moderate success in lessening the rebound anxiety which ends up upon carisoprodol discontinuation but only when along with regular and active attendance to a alcohol abuse support group.
Anecdotal reports indicate that routine work out speeds the recovery from dependence, having a long jog/swim/bike ride (etc.) effectively acting like a "rescue medication" for sudden/severe cravings and panic disorder. Claims for just a wide range of several medicine sorts of reducing persistent psychological dependence have already been made (meditation, yoga, acupuncture, chiropractic, fighting methods, supplemental I.V. nutrition, etc.,), however such claims are promoted from the practitioners of those alternative medicines and seem mostly ineffective in accordance with anecdotal reports (no formally conducted studies for the use of these alternative practices inside treatment of persistent post-withdrawal cravings).
As carisoprodol withdrawal may be life-threatening (particularly high dose users and people that attempt to quit "cold turkey"). A patient ought to contact their doctor before attempting to discontinue carisoprodol use so your physician and the individual can concur with a de-titration plan which can be safe, affordable, comfortable, and effective for the individual in order to protect the person and maximize program compliance.
Recreational use and abuse
Recreational users of carisoprodol usually seek its potentially heavy sedating, relaxant, and anxiolytic effects.[23] Also, due to its potentiating effects on narcotics, it's often abused in conjunction with a lot of opioid drugs. Also it truly 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 towards the placement of carisoprodol in schedule IV from the Controlled Substances Act.[24] Carisoprodol is sometimes when combined date rape drugs.[25]
As along with other gabaminergic drugs, combination for some other gabaminergic drugs, including alcohol, also as with sedatives generally, use a significant risk to your user from the form of overdose. Overdose symptoms act like 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 just not detected on all toxicology tests that might delay diagnosing overdose. Overdose symptoms in conjunction with opiates offer a similar experience but distinguished by miosis. Carisoprodol (similar to its metabolite meprobamate) is very dangerous in in conjunction with alcohol. Flumazenil enable you to counteract the outcomes of carisoprodol nevertheless its use is restricted by the prospect of severe uncomfortable side effects and is contraindicated in mixed overdoses for example when it is co-ingested with opiates.
Carisoprodol features a rapid, 30-minute start of action, while using aforementioned effects lasting about two to six hours. It is metabolized inside the liver through cytochrome P450 oxidase isozyme CYP2C19, excreted because of the kidneys and possesses about an eight-hour half-life. A considerable proportion of carisoprodol is metabolized to meprobamate, which can be a known drug of abuse and dependence; this will account to the abuse potential of carisoprodol (meprobamate levels reach higher peak plasma levels than carisoprodol itself following administration).


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