Carisoprodol
Discover related
4 sources
Collated from PsychonautWiki, TripSit, Pharmacology, DailyMed. Where sources differ (e.g. dosing), Compare shows them side by side.
Also known as Carisoprodol, SomaPW
Fatal overdose may occur when GABAergic substances are combined with other depressants such as opiates, benzodiazepines, barbiturates, gabapentinoids, thienodiazepines or alcohol.[1] It is strongly discouraged to combine these substances, particularly in common to heavy doses.PW
Oral
Route dataPsychonautWiki
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| 50 mg | 100–325 mg | 325–500 mg | 500–750 mg | 750 mg+ |
| Onset | 15–60 minutes |
|---|---|
| Peak | 2–5 hours |
| After-effects | 1–12 hours |
Dangerous interactionsPW
Caution / uncertainPW
Mechanism of actionPHDM
The mechanism of action of carisoprodol in relieving discomfort associated with acute painful musculoskeletal conditions has not been confirmed. In studies using animal models, the muscle relaxation that is induced by carisoprodol is associated with a change in the interneuronal activity of the spinal cord and of the descending reticular formation, located in the brain. The abuse potential of this drug is attributed to its ability to alter GABAA function. This drug has been shown to modulate a variety of GABAA receptor subunits. GABAA receptor modulation can lead to anxiolysis due to inhibitory effects on neurotransmission.
Carisoprodol is a CNS depressant which has sedative and skeletal muscle relaxant effects. The precise mechanism of action of the drug is not known. The skeletal muscle relaxant effects of orally administered carisoprodol are minimal and are probably related to its sedative effect. The drug does not directly relax skeletal muscle and, unlike neuromuscular blocking agents, does not depress neuronal conduction, neuromuscular transmission, or muscle excitability. In animals, carisoprodol appears to modify central perception of pain without abolishing peripheral pain reflexes and to have slight antipyretic activity, but these effects have not been demonstrated in clinical studies.
Carisoprodol is an increasingly abused, centrally-acting muscle relaxant. Despite the prevalence of carisoprodol abuse, its mechanism of action remains unclear. Its sedative effects, which contribute to its therapeutic and recreational use, are generally attributed to the actions of its primary metabolite, meprobamate, at GABA(A) receptors (GABA(A)R). Meprobamate is a controlled substance at the federal level; ironically, carisoprodol is not currently classified as such. Using behavioral and molecular pharmacological approaches, we recently demonstrated carisoprodol, itself, is capable of modulating GABA(A)R function in a manner similar to central nervous system depressants. Its functional similarities with this highly addictive class of drugs may contribute to the abuse potential of carisoprodol. The site of action of carisoprodol has not been identified; based on our studies, interaction with benzodiazepine or barbiturate sites is unlikely. ...
PharmacodynamicsPHDM
Carisoprodol is a centrally acting skeletal muscle relaxant that does not act directly on skeletal muscle but acts directly on the central nervous system (CNS). This drug relieves the painful effects of muscle spasm. A metabolite of carisoprodol, _meprobamate_, possesses both anxiolytic and sedative properties. Clinical studies have shown that this drug causes impairment of psychomotor performance in neuropsychological tests.
Pharmacokinetics
Half-lifePH
The terminal half-life is approximately 2 hours.
Carisoprodol is eliminated by both renal and non-renal routes with a terminal elimination half-life of approximately 2 hours. The half-life of meprobamate is approximately 10 hours.
The plasma half-life of carisoprodol is approximately 8 hours.
AbsorptionPHDM
The absolute bioavailability of carisoprodol has not yet been established. The mean time to peak plasma concentrations (Tmax) of this drug was about 1.5-2 hours in clinical studies. Co-administration of a fatty meal with carisoprodol (350 mg tablet) had no impact on carisoprodol pharmacokinetics.
Carisoprodol is eliminated by the kidneys as well as other routes. The half-life of meprobamate is approximately 10 hours.
0.93 to 1.3 L/kg, according to 4 different clinical studies.
Following an oral dose of carisoprodol, the oral clearance (Cl/F) was 39.52 ± 16.83 L/hour.
Carisoprodol crosses the placenta. The drug distributes into milk in concentrations 2-4 times higher than concurrent maternal plasma concentrations.
Plasma concentrations of carisoprodol required for sedative, skeletal muscle relaxant, or toxic effects are not known. One manufacturer reports that plasma concentrations of 4-7 ug/mL were attained in 4 hours following oral administration of 350 mg of carisoprodol to healthy adults. Following usual therapeutic dosages, the onset of action is usually within 30 minutes and the duration of action is 4-6 hours.
MetabolismPH
The main pathway of carisoprodol is liver metabolism is by the cytochrome enzyme CYP2C19 to form meprobamate. This enzyme exhibits genetic polymorphism, which may affect the metabolism of this drug.
The major pathway of carisoprodol metabolism is via the liver by cytochrome enzyme CYP2C19 to form meprobamate. This enzyme exhibits genetic polymorphism.
Carisoprodol is metabolized in the liver; animal studies indicate the drug may induce liver microsomal enzymes. Animal studies also indicate that the drug is excreted in urine, principally as hydroxycarisoprodol and hydroxymeprobamate, and to a lesser extent as meprobamate; trace amounts of carisoprodol are excreted unchanged in urine. The drug may be removed by hemodialysis or peritoneal dialysis.
Carisoprodol is a muscle relaxant analgesic, which has an active metabolite i.e. meprobamate. We conducted an open three-panel single-dose administration study with 15 healthy volunteers: five poor metabolizers of mephenytoin, five poor metabolizers of debrisoquine and five extensive metabolizers of both substrates. The aim was to investigate if the elimination of carisoprodol and meprobamate is dependent on the two metabolic polymorphisms of mephenytoin and debrisoquine. The subjects were given single oral doses of 700 mg carisoprodol and 400 mg meprobamate on separate occasions. The disposition of carisoprodol was clearly correlated to the mephenytoin hydroxylation phenotype. The mean serum clearance of carisoprodol was four times lower in poor metabolizers of mephenytoin than in extensive metabolizers, which confirms the hypothesis from our previous study that N-dealkylation of carisoprodol cosegregates with the mephenytoin hydroxylation polymorphism. However, mean serum clearance of meprobamate did not differ between the two groups. Also, polymorphic debrisoquine hydroxylation did not influence the elimination of carisoprodol or meprobamate. Poor metabolizers of mephenytoin thus have a lower capacity to metabolize carisoprodol and may therefore have an increased risk of developing concentration dependent side-effects such as drowsiness and hypotension, if treated with ordinary doses of carisoprodol.
Hepatic. Metabolized in the liver via the cytochrome P450 oxidase isozyme CYP2C19.
Route of Elimination: Carisoprodol is eliminated by both renal and non-renal routes.
Half Life: 8 hours
Protein bindingPH
Approximately 60%.
Plan a dose of Carisoprodol
Loading the fact-sheet…
Logging a dose needs somewhere to keep it. Start a free session — no signup; it and everything in it expire in 7 days.
External links
Fact-sheets from PsychonautWiki. Harm-reduction reference only — not medical advice.