4.20.2018 | Noah Black

A report had appeared demonstrating the abuse potential, ultimay contributing to a rise in concern about its effects.

(2015) Assessment of subunit-dependent direct gating and allosteric modulatory effects of Carisoprodol at GABAa receptors.

Adenosine reuptake inhibition appears to exist, which may contribute to the sedative action.

Other depressants, including ethanol, opioids, and benzodiazepines.

It is rapidly absorbed from the GI tract and distributed in the CNS.

Some countries have responded by moving away from the substance. There’s been an increase in concern about its abuse potential since the 1990s.

Even at high doses, some users primarily encounter depression, sedation, and some dysphoria. Not everyone experiences positive effects.


(2009) Abuse Potential of Soma: the GABAA Receptor as a Target.

A number of near-fatal and fatal cases have been connected to its use with opioids and benzodiazepines. But it’s also much riskier. This may lead to greater euphoria, relaxation, and sedation. It’s regularly taken with other drugs, mainly depressants. Dose-response.

Carisoprodol is sold as a racemic mixture.

(2003) Simultaneous determination of carisoprodol and acetaminophen in an attempted suicide by liquid chromatography-mass spectrometry with positive electrospray ionization.

This list may not be complete. You should always check your local laws.

Limited evidence suggests NMDA antagonist and pro-serotonin activity could exist.

One hypothesis is that overdoses with effects like agitation and muscular rigidity might be carisoprodol-dominant and suggest less metabolism has occurred.

Half-life: 1.5 to 2 hours Metabolism.

Frank M. Berger of Wallace Laboratories (later Carter-Wallace) created the drug. He was also part of the team responsible for synthesizing meprobamate, which became a popular pharmaceutical in the 1950s.

(2005) Treatment of carisoprodol dependence: a case report.

Carisoprodol is a centrally-acting muscle relaxant that’s taken for acute musculoskeletal disorders. The drug is often used alongside rest, physical therapy, and NSAIDs. It seems to reduce discomfort, but it’s only recommended for a few weeks.

Different receptor complexes are affected to varying degrees, but it clearly affects a1b2y2, the most prominent configuration in the brain. The drug acts as a positive allosteric modulator (PAM) and a direct agonist at GABAa receptors.

A post in the Federal Register explained the move with these points: Schedule 4.

More regions, including US states, scheduled the drug. 2012.

(1997) Barbiturate-like actions of the propanediol dicarbamates felbamate and meprobamate.

(2004) Commonly used muscle relaxant therapies for acute low back pain: a review of carisoprodol, cyclobenzaprine hydrochloride, and metaxalone.

It’s characterized by cheerfulness, disinhibition, socialization, physical euphoria, and sometimes psychomotor excitement (with impairment). Those who take over 1400 mg (sometimes much more) more reliably report what some have described as a hypomanic state.

The agonism is higher at b1 receptors, whereas PAM is greater at b2 receptors.

(2010) Carisoprodol legal status and patterns of abuse.

Some evidence suggests there’s one site for PAM and another for direct agonism. It differs from benzodiazepines and barbiturates, and alternative binding sites seem to play a role.

(1990) Carisoprodol concentrations from different anatomical sites: three overdose cases.

Studies in animals have shown flumazenil partially inhibits the drug’s activity.

Most overdoses primarily feature CNS depression.

(1998) Carisoprodol-induced myoclonic encephalopathy.

(2009) Carisoprodol-mediated modulation of GABAA receptors: in vitro and in vivo studies.

(2002) Carisoprodol: an unrecognized drug of abuse.

Meprobamate was greater than carisoprodol in serum by 2.5 hours.

(2012) Carisoprodol tolerance and precipitated withdrawal.

As usual, the negative effects at common doses are mild, such as drowsiness and impaired coordination.

The Drug Classroom (TDC) provides straightforward drug education that is free from bias.

It usually offers more physical euphoria than benzodiazepines. Euphoria (cognitive and physical) is most prominent at strong+ doses.

Onset: 00:15 – 00:45 Erowid Positive Negative.

Group report in Norway.

PAM. Carisoprodol’s agonist activity contributes to its more concerning effects in overdose. The fatal concentration may be as low as 140 uM, which correlates with the concentration associated with significant levels of direct activation.

A lot of the relaxation, physical impairment, anxiolysis, and euphoria is comparable to ethanol to some degree.

350 – 1050 mg is most likely to primarily cause relaxation and drowsiness, though the other aforementioned positives are possible.

Cmax: It appears to be between 2 and 7 ug/mL following a 350 mg dose.

Molecular weight: 260.334 g/mol IUPAC: N-propan-2-ylcarbamate Contents.

Case reports (non-fatal) Case 1 Case 2 Case 3 Case 4 Case 5 Case 6 Case reports (fatal) Case 1 Case 2 Case 3 Case 4. It appears using over 12 grams is potentially life-threatening, though nothing near that should even be attempted acuy.

Common: 350 mg (3 – 4x per day).

Even though it wasn’t scheduled at the federal level, individual states began scheduling it.

Some investigations found it to be an analgesic in certain situations, including in human trials.

(1984) A purinergic component in the central actions of meprobamate.

Meprobamate is active with an acute half-life of ~11.3 hours. Study.

Case reports Case 1 Case 2 Case 3 Case 4 Case 5 Case 6. Seizures are possible. Anxiety, insomnia, tremor, hallucinations, and tachycardia are common symptoms.

(2000) A review of three commonly prescribed skeletal muscle relaxants.

The efficacy isn’t affected by the presence of a gamma (y) subunit. Modulation is present at a1b1y2 and a1b2y2 (among others), with the efficacy being higher at b2 receptors than b1.

Common: 350 – 700 mg Strong: 700+ mg.

During the same year, ~10.5 million prescriptions were dispensed. SAMHSA reported a doubling of nonmedical use between 2004 and 2008. The National Forensic Laboratory Information System listed it as one of the top 25 most abused drugs in the US in 2008.

There is clearly the potential for severe withdrawal with chronic use. It’s connected in part to meprobamate, which accumulates with chronic use and has a longer half-life.

Neuromuscular symptoms and evidence of myoclonus existed in 16% of overdose cases (29 of 176) in San Francisco during 1997.

It still has notable effects on a2 and a2 receptors, but it isn’t selective for them. PAM is greater at receptors with an a1 subunit. Other mechanisms.

It’s not recommended as a first-line treatment even though it’s been widely prescribed in some regions.

Pain relief. The primary negatives in medical settings are drowsiness and psychomotor impairment.

It’s very similar to meprobamate and is structurally n-isopropyl-meprobamate. Both are carbamate derivatives.

(1960) The history, chemistry, and pharmacology of Carisoprodol.

Most of the discussion about the substance suggested it had a low abuse potential and minimal risk of physical dependence.

The Drug Classroom (TDC) provides straightforward drug education that is free from bias.

(2008) Carisoprodol (Soma). (2008) Carisoprodol withdrawal syndrome misdiagnosed as a psychotic disorder.

More claims appeared of it being used to boost or change the effects of opioids and sometimes benzodiazepines, cocaine, and ethanol.

(2007) Is the frequency of carisoprodol withdrawal syndrome increasing?

(2003) Carisoprodol – Effects on Human Performance and Behavior.

Taking it with NSAIDs may boost the overall efficacy, albeit while raising the chance of adverse CNS effects.

In this respect it was likened to atropine. The drug was found to cause clear EEG changes in animals without leading to much sedation at low doses.

2015 By The Drug Classroom.

It’s intertwined with meprobamate, a drug it’s metabolized to.

A3 is affected less than the other alpha subunits. Greater direct activation is seen at a2 receptors relative to a1 receptors, which are more abundant in the CNS.

Taking a very strong dose can lead to coma, respiratory depression, amnesia, and even death. A smaller number of reports exist detailing agitation, seizures, movement disorders, and muscular rigidity.

The metabolites include meprobamate, hydroxycarisoprodol, and hydroxymeprobamate. The drug is metabolized in the liver primarily by CYP2C19.

It became a Schedule 4 drug in the US following an apparent rise in misuse and adverse events.

A few mechanisms may be playing a role, but the most important activity occurs at GABA receptors. Part of the activity comes from carisoprodol itself and part comes from metabolism to meprobamate.

(1960) The Pharmacology and Clinical Usefulness of Carisoprodol Patreon PayPal.

(2010) Carisoprodol: abuse potential and withdrawal syndrome.

Sweden) moved away from using it. They either removed it from medical practice or further restricted its use. Some countries (e.g.

An example timeline is having insomnia appear on the first night post-cessation, followed by psychosis by 36 – 48 hours. The symptoms appear to peak 3 – 5 days after cessation and have sometimes lasted up to 8 days.

Light: 100 – 350 mg.

The greatest chance of severe effects exists when abruptly stopping the drug. It’s similar to what can occur with benzodiazepines and ethanol.

(2000) Flumazenil reversal of carisoprodol (Soma) intoxication.

(2012) Carisoprodol: update on abuse potential and legal status.

It’s sold as 250 and 350 mg tablets.

(2007) Carisoprodol withdrawal induced delirium: A case study.

Papers described it as exhibiting some of the same properties as mephenesin and meprobamate. Carisoprodol is introduced following FDA approval.

A contributing factor to the rise in nonmedical use was the availability of carisoprodol from online sellers.

One test showed 9/10 human participants extensively and quickly metabolized the drug to meprobamate, which was detectable within 20 minutes of a 700 mg administration.

Carisoprodol = Soma; Listaflex; Gencari; Genesafe; Carisoma; Myolax; Isomeprobamate; Isopropyl meprobamate PubChem: 2576 Molecular formula: C12H24N2O4.

Drugs are never going to leave society, so it only makes sense to provide real drug education.

This was opposed by the FDA at the time due to a lack of available evidence, though carisoprodol ended up becoming a “drug of concern.”. The DEA recommended federal scheduling in 1996.

It’s usually not controlled as an illicit drug, but prescriptions may be far less common than in the US. Some countries have taken it off the market.

This is reportedly seen with meprobamate as well, but carisoprodol is more active and more potent. Picrotoxin can antagonize the activation, lending support to carisoprodol truly operating at GABAA receptors.

Following reports documenting physical dependence and recreational use, concerns increased about carisoprodol. Yet, a paper found that just a small percentage of physicians understood carisoprodol’s prodrug status and they believed it had a lower abuse risk than meprobamate.

(2010) Carisoprodol withdrawal after internet purchase.

It was quickly found to have some unique pharmacological properties compared to meprobamate. A number of meprobamate derivatives were being created and tested, leading to the development of carisoprodol.

One study in humans demonstrated an elevation of the pain threshold when undergoing tooth pulp stimulation. While 700 mg of carisoprodol produced an effect, 800 mg of meprobamate did not.

(2007) Carisoprodol use and abuse in Norway: a pharmacoepidemiological study.

(1993) Carisoprodol abuse: a report from India.

Total: 2 – 5 hours.

(2004) A Near‐Fatal Overdose of Carisoprodol (SOMA): Case Report.

Total: 4 – 6 hours Onset: ~ 00:30.

(2011) Ingestions of hydrocodone, carisoprodol, and alprazolam in combination reported to Texas poison centers.

Pentobarbital and meprobamate can fully substitute for the discriminative stimulus of carisoprodol in animals. Direct agonism.

There was a significant rise in ED visits involving the drug:

Drugs are never going to leave society, so it only makes sense to provide real drug education.

As a centrally acting muscle relaxant, it doesn’t directly impact transmission at the neuromuscular junction (as opposed to tubocurarine, for example). Carisoprodol is associated with altered interneuronal activity in the spinal cord and descending reticular formation.

Tmax: 1 – 2 hours.

It was investigated in humans and animals, with it primarily being compared to meprobamate and other muscle relaxants.

There’s more acetylcholine antagonism than with meprobamate, but it’s not significant.

A fairly high incidence of hallucinations (mainly visual and auditory) has been reported. This fits with a report that claimed around 20% of meprobamate withdrawal cases feature hallucinations or other psychotic symptoms.

It also seems to increase the analgesic efficacy of opioids. Early studies showed it could produce analgesia not seen with meprobamate.

It was ranked 18 out of 123 for drugs involved in emergency department (ED) visits in the US in 1998.

Carisoprodol is a muscle relaxant that is sometimes prescribed to treat musculoskeletal disorders (e.g. It’s also been used recreationally for decades, with its effects reminiscent to some extent of barbiturates, benzodiazepines, and ethanol. back pain).

(2007) Abuse potential of carisoprodol: a retrospective review of Idaho Medicaid pharmacy and medical claims data.

(2003) Muscle relaxants for non-specific low back pain.