Buy Soma Drug Test
Carisoprodol (trade name Soma) is a centrally-acting skeletal muscle relaxant. Carisoprodol is slightly soluble in water and freely soluble in alcohol, chloroform and acetone. The drug's solubility is practically independent of pH. Carisoprodol is manufactured and marketed in the United States by Meda Pharmaceuticals Inc. 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 (Soma Compound With Codeine) along with codeine and caffeine as well.
History
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. It had been developed by Dr. Frank M. Berger at Wallace Laboratories and was named carisoprodol.
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. 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. Various classical and modern researchers have theorized that Soma/Haoma could be anything from ephedra or opium to mushrooms of the genus Amanita with hallucinogenic effects, or other anti-cholinergic-drug containing plantor 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.
Soma is also the name of the fictional drug featured in Aldous Huxley's Brave New World.
Usage and legal status
Although reports from Norway have shown that carisoprodol has abuse potential as a prodrug 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. In May 2008 it was taken off the market in Norway as well.
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.
In the United States, while carisoprodol is not a controlled substance under federal regulations, as of February 2010, carisoprodol is considered to be a schedule IV controlled substance 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 state's new controlled substance program which requires physicians to obtain, and include, a state "DPS" number as well as a DEA number on all controlled substances prescriptions), Utah, and Washington. It is a Schedule III controlled substance in West Virginia. The rest of the United States, excluding the above named states, falls under the DEA scheduling for the medication, 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).
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.
Abusers of carisoprodol usually seek its potential dissociative, euphoric, and heavy sedating, relaxant, and anxiolytic effects. Also, because of its potentiating effects on narcotics, it is often abused in conjunction with many opioid drugs.
As with most psychoactive substances, tolerance can form very rapidly. This causes the abuser to continually increase dosage to obtain desired effects. As with any drug, this can be dangerous for a multitude of reasons. For this reason, those with a background of addiction should not be prescribed carisoprodol.
Effects
- Analgesia
- Anxiolysis
- Muscle relaxation (and relief from hypertonia)
- Sedation
- Somnolence
Side effects
The usual dose of 350mg is unlikely to engender prominent side effects other than somnolence, and possibly mild euphoria or dysphoria. 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, 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 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 in the 1950s and 1960s. Overdose cases were reported as early as 1957 and have been reported on several occasions since then.
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.
Pharmacokinetics
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.
Chemistry
Carisoprodol is a carbamic acid ester. It is a racemic mixture of two stereoisomers.
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.
- F.M. Berger, B.J. Ludwig, U.S. Patent 2,937,119 (1960).