Carisoprodol

[2-(carbamoyloxymethyl)-2-methylpentyl] N-propan-2-ylcarbamate

Overview

Carisoprodol belongs to Depressants.

Key safety note: Carisoprodol is a sedating CNS depressant with a barbiturate-like profile and moderate-to-high abuse liability.[3][2]
Effects
Subjective effects vary. What a substance feels like depends on dose, individual physiology, mindset, and setting. The points below describe commonly reported effects, not guaranteed, uniform, or desirable outcomes.
  • Muscle relaxation and sedation: drowsiness, dizziness and reduced muscle tension are the intended and most common effects.
  • At higher or recreational doses, barbiturate-like intoxication: euphoria, disinhibition, marked sedation and impaired coordination.
  • Tolerance and physical dependence develop with sustained use. A barbiturate-type withdrawal syndrome (including seizures) can follow abrupt cessation.
Dosing & duration
Harm-reduction note: These are commonly cited reference ranges, not a recommendation or a “safe” dose. Potency, purity, body chemistry, tolerance, and drug combinations vary widely. Start low, go slow, wait for full effects before redosing, and never assume an unknown product matches these figures. Missing data is not evidence of safety.

Oral tablets (250 mg, 350 mg, also combined with aspirin ± codeine). Prescription-only oral muscle relaxant intended for short-term use (usually up to 2–3 weeks). Efficacy beyond that is not established. Strongly sedating, not to be combined with alcohol or other CNS depressants. These are medical reference ranges, not recreational guidance.

Dose ranges

Adult (acute musculoskeletal pain)

250–350 mg three times daily and at bedtime

Lower effective dose

250 mg TID + bedtime is often as effective as 350 mg with less sedation

Maximum duration

Short-term use only (≈2–3 weeks)

Duration

onset

~30 minutes

total

Effects up to ~4–6 hours per dose

Chemical & Physical Properties
FormulaC12H24N2O4
Molar mass260.33 g/mol
StateSolid
Melting point92 °C
Boiling pointunavailable: true. reason: the only figure available is a software prediction (~423 °C at 1 atm), which is not physically meaningful: carisoprodol is a crystalline solid that thermally decomposes well before boiling, so no reliable experimental boiling point exists
DensityNot reported
Vapor pressureNot reported
pKa15.06 (Strongest acidic)
LogP2.1
Solubilityless than 1 mg/mL at 19.5 °C (NTP, 1992), slightly soluble, Soluble in most common organic solvents. Practically insoluble in vegetable oils
Refractive indexNot reported
Identifiers & Synonyms
CAS78-44-4
CAS (enantiomer)
PubChem CID2576
InChIKeyOFZCIYFFPZCNJE-UHFFFAOYSA-N
InChIInChI=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)
SMILESCCCC(C)(COC(=O)N)COC(=O)NC(C)C

Synonyms

  • Soma
  • Carisoprodol
  • N-isopropylmeprobamate
Pharmacodynamics & Biochemistry

Carisoprodol (brand name Soma) is a centrally acting skeletal muscle relaxant prescribed short-term for acute musculoskeletal pain. Despite the 'muscle relaxant' label it has no direct action on skeletal muscle: its effects are central and sedative, and both the parent drug and its metabolite act on the GABA-A receptor. Carisoprodol itself directly gates and allosterically modulates GABA-A receptors in a barbiturate-like way: its actions are blocked by barbiturate antagonists but not by the benzodiazepine antagonist flumazenil, and occur at a site distinct from the classic benzodiazepine and barbiturate sites. This GABA-A activity is independent of, and additional to, that of its metabolite. Carisoprodol is also a prodrug. It is metabolised by CYP2C19 to meprobamate, an anxiolytic that is itself a barbiturate-like GABA-A drug and a controlled substance (US Schedule IV). Meprobamate is longer-lived than the parent and accumulates, so much of carisoprodol's sedative and dependence-producing effect is mediated through it. The combined GABA-A actions of parent and metabolite produce sedation, muscle relaxation and, at higher doses, barbiturate-like intoxication, reinforcing effects and physical dependence: the basis of its abuse liability.

Biological targets

  • GABA-A
Pharmacokinetics
BioavailabilityWell absorbed orally, onset ~30 minutes, effects lasting up to ~4–6 hours
TmaxNot reported
Half-lifeCarisoprodol ≈2 h, meprobamate ≈10 h
VdNot reported
Protein bindingNot reported
MetabolismHepatic CYP2C19 → meprobamate. Poor CYP2C19 metabolisers can have ~4× higher carisoprodol and lower meprobamate levels
ExcretionNot reported
Toxicology & Safety
Harm-reduction note: Toxicity and risk depend on dose, route, purity, combinations, setting, and individual health factors. Missing harms should never be interpreted as evidence of safety.

Not reported

Carisoprodol is a sedating CNS depressant with a barbiturate-like profile and moderate-to-high abuse liability. Regular use can produce physical dependence of the barbiturate type, and abrupt discontinuation can trigger a withdrawal syndrome (anxiety, insomnia, tremor and, in severe cases, seizures). Overdose causes CNS and respiratory depression, and the danger rises sharply when carisoprodol is combined with alcohol, opioids, benzodiazepines or other depressants: combinations implicated in numerous fatal poisonings. Its abuse potential and intoxication risk led the EU to withdraw it from the market in 2008 and the US to reschedule it as a controlled substance in 2012.[3][2]

Legal Status
Legal note: Legal status can change over time and may vary by country, region, formulation, analogue status, prescription context, and enforcement practice. Always confirm with current official sources before relying on this section.
Interactions & Contraindications

Drug interactions

Alcohol, Opioids, Benzodiazepines Additive CNS and respiratory depression, potentially fatal and the basis of many carisoprodol-related deaths.[3]
CYP2C19 inhibitors (omeprazole, fluvoxamine, azoles) Omeprazole or fluvoxamine raise carisoprodol levels and reduce meprobamate formation.[2]
CYP2C19 inducers (rifampicin) Rifampicin lowers carisoprodol levels and raises meprobamate formation.[2]

Contraindications

Acute intermittent or related porphyria acute intermittent porphyria.[2]
Known hypersensitivity to the drug hypersensitivity to carisoprodol, meprobamate or other carbamates.[3]
History of stimulant or substance use disorder history of sedative or substance-use disorder (high risk of misuse and dependence).[3]
Kidney or liver impairment caution in severe hepatic or renal impairment.[3]
Usage & Context
  • Prescription skeletal muscle relaxant (as Soma and combination products with aspirin ± codeine) for short-term relief of acute musculoskeletal pain, typically limited to 2–3 weeks.
  • Widely misused for its sedative, barbiturate-like effects: often combined with opioids and benzodiazepines (the so-called 'Soma coma' / 'Holy Trinity' combinations), which markedly raises overdose risk.
  • Withdrawn from the European market since 2008. No longer marketed in Germany or most of the EU.
Sources & Evidence

Further Information