Muscle relaxant medication
Carisoprodol, sold under the brand name Soma among others, is an oral medication used for musculoskeletal pain. Effects generally begin within half an hour and last for up to six hours.
Common side effects include headache, dizziness, and sleepiness. Serious side effect may include addiction, allergic reactions, and seizures. In people with a sulfa allergy certain formulations may result in problems. Safety during pregnancy and breastfeeding is not clear. How it works is not clear. Some of its effects are believed to occur following metabolic conversion into meprobamate, carisoprodol's main active metabolite.
Carisoprodol was approved for medical use in the United States in 1959. Its approval in the European Union was withdrawn in 2008. It is available as a generic medication. In 2019, it was the 343rd most commonly prescribed medication in the United States, with more than 800,000 prescriptions. In the United States, it is a Schedule IV controlled substance.
Safety at a Glance
High Risk- It is strongly recommended that one use harm reduction practices when using this drug.
- Tolerance will develop to the sedative-hypnotic effects of carisoprodol after prolonged use. It is unknown exactly ho...
- Toxicity: Carisoprodol likely has moderate toxicity relative to dose. However, carisoprodol is potentially lethal when mixed wi...
- Dangerous with: Atropa belladonna, Cake, Datura, Deschloroetizolam (+23 more)
- Overdose risk: Depressant overdose from Carisoprodol is a life-threatening medical emergency. The primary mechan...
If someone is in crisis, call 911 or Poison Control: 1-800-222-1222
Dosage
oral
Duration
oral
Total: 3.5 hrs – 18.6 hrsHow It Feels
Carisoprodol arrives like a warm tide rolling in across the body. Within twenty to forty minutes, the first wave brings a pronounced loosening of muscular tension -- not just the surface tension of stress but a deeper, structural relaxation, as though the connective tissue itself were sighing with relief. The shoulders drop, the lower back unclenches, and there is a spreading warmth through the torso and limbs that carries with it a distinct sense of physical pleasure. This is not a subtle medication; it announces itself boldly.
The come-up ushers in a euphoria that sets carisoprodol apart from most muscle relaxants. There is a giddy, almost intoxicating lightness to the mood -- a feeling of well-being that goes beyond mere pain relief into genuine recreational territory. Conversations become easier, inhibitions lower, and there is a sociability that resembles the best moments of mild alcohol intoxication but with a cleaner, more focused quality. The body feels simultaneously heavy and weightless: heavy in the sense that the limbs are deeply relaxed and disinclined to move, weightless in the sense that physical discomfort has been lifted like a veil.
At peak effects, the experience walks a line between euphoria and sedation. The mental state is warm and hazy, thoughts drifting pleasantly without direction or urgency. There is a notable impairment of coordination; walking becomes a loose-jointed, slightly swaying affair, and fine motor tasks require concentrated effort. The visual world seems to shimmer slightly at the edges, and there is a mild perceptual slowing, as though reality were being projected at a slightly reduced frame rate. Physical touch feels amplified and rewarding, and there is a characteristic heaviness to the eyelids that makes keeping them open an act of will. The euphoria has a dreamy, narcotic quality that some compare to the edges of an opioid experience -- warm, enveloping, and deeply content.
The descent is a slow slide into profound drowsiness. The euphoria fades first, leaving behind the deep muscular relaxation and a growing desire for sleep. Consciousness becomes thin and translucent, and the boundary between waking and dreaming blurs. Sleep, when it arrives, is thick and restorative. The following morning may bring a lingering heaviness in the limbs and a slight cognitive fog that lifts gradually, like mist burning off under a rising sun.
Subjective Effects
The effects listed below are based on the Subjective Effect Index (SEI), an open research literature based on anecdotal reports and personal analyses. They should be viewed with a healthy degree of skepticism. These effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects.
Physical Effects
Physical(11)
- Decreased libido— Decreased libido is a diminished interest in and desire for sexual activity, commonly caused by subs...
- Dehydration— A state of insufficient bodily hydration manifesting as persistent thirst, dry mouth, and physical d...
- Dizziness— A sensation of spinning, swaying, or lightheadedness that impairs balance and spatial orientation, o...
- Motor control loss— A distinct decrease in the ability to control one's physical body with precision, balance, and coord...
- Muscle relaxation— The experience of muscles throughout the body losing their rigidity and tension, becoming noticeably...
- Nausea— An uncomfortable sensation of queasiness and stomach discomfort that may or may not lead to vomiting...
- Pain relief— A suppression of negative physical sensations such as aches and pains, ranging from dulled awareness...
- Physical euphoria— An intensely pleasurable bodily sensation that can manifest as waves of warmth, tingling electricity...
- Respiratory depression— A dangerous slowing and shallowing of breathing that can progress from barely noticeable reductions ...
- Sedation— A state of deep physical and mental calming that manifests as a progressive desire to remain still, ...
- Seizure— Uncontrolled brain electrical activity causing convulsions and loss of consciousness -- a life-threa...
Cognitive & Perceptual Effects
Visual(1)
- Drifting— The visual experience of perceiving stationary objects, textures, and surfaces as appearing to flow,...
Cognitive(12)
- Amnesia— A complete or partial inability to form new memories or recall existing ones during and after substa...
- Analysis suppression— Analysis suppression is a cognitive impairment in which the capacity for logical reasoning, critical...
- Anxiety— Intense feelings of apprehension, worry, and dread that can range from a subtle background unease to...
- Anxiety suppression— A partial to complete suppression of anxiety and general unease, producing a calm, relaxed mental st...
- Cognitive euphoria— A cognitive and emotional state of intense well-being, elation, happiness, and joy that manifests as...
- Compulsive redosing— An overwhelming, difficult-to-resist urge to continuously take more of a substance in order to maint...
- Delusion— A delusion is a fixed, false belief that is held with unshakeable certainty and is impervious to con...
- Depression— A persistent state of low mood, emotional numbness, hopelessness, and diminished interest or pleasur...
- Disinhibition— A marked reduction in social inhibitions, self-consciousness, and behavioral restraint that manifest...
- Language suppression— A diminished ability to formulate, comprehend, or articulate language, ranging from difficulty findi...
- Psychosis— Psychosis is a serious psychiatric state involving a fundamental break from consensus reality — char...
- Thought deceleration— The experience of thoughts occurring at a markedly reduced pace, as if the mind has been placed into...
Pharmacology
Carisoprodol is a prodrug that is metabolized to meprobamate, besides having its own effects. The precise mechanism of meprobamate is not completely understood. However it is believed that meprobamate acts similarly to benzodiazepines and barbiturates, acting as a positive allosteric modulator of a GABAA receptor. Unlike barbiturates and benzodiazepines, in animal studies meprobamate has been shown to retain most of its effects without having gamma-aminobutyric acid present.
Carisoprodol is metabolized by the cytochrome P450 2C19 enzyme in the liver and has a biological half-life of about two hours. Carisoprodol and its metabolites are excreted by the kidneys in urine.
moderate toxicity relative to dose. However, carisoprodol is lethal when mixed with depressants like alcohol or opioids]]. Carisoprodol has been taken off the market is several countries such as Sweden and Indonesia due to side effects and abuse.
It is strongly recommended that one use harm reduction practices when using this drug. -extremely physically and psychologically addictive. Carbamate withdrawal, like barbiturate withdrawal, is medically serious and can potentially cause a life-threatening withdrawal syndrome that can cause seizures, psychosis, and death. Drugs which lower the seizure threshold such as tramadol and amphetamine should be avoided during withdrawal.
Tolerance will develop to the sedative-hypnotic effects of carisoprodol after prolonged use. It is unknown exactly how long it takes for tolerance to reach baseline.
In most jurisdictions, carisoprodol is considered a prescription-only and/or controlled drug.
Germany:** Carisoprodol is a prescription medicine, according to Anlage 1 AMVV.
United States: In the United States, carisoprodol is a Schedule IV Controlled Substance. Therefore, it is prescription-only and anyone caught in possession of the substance with or without intent to distribute is punishable by law.
Carisoprodol (Wikipedia)
Carisoprodol (Erowid Vault)
Carisoprodol (Isomer Design)
Detection Methods
Standard Drug Panel Inclusion
Carisoprodol is NOT included on standard 5-panel or 10-panel drug screens. However, some extended panels, particularly those used in pain management clinics and substance abuse treatment programs, may include carisoprodol and its active metabolite meprobamate. Meprobamate is a Schedule IV controlled substance and was historically included on some expanded barbiturate/sedative panels. Standard immunoassay methods for meprobamate exist but are not universally deployed.
Urine Detection
Carisoprodol is detectable in urine for approximately 2 to 4 days. It is metabolized by CYP2C19 to its primary active metabolite meprobamate, which has a longer half-life (6 to 17 hours versus 2 to 3 hours for the parent compound) and serves as the primary urinary biomarker. Meprobamate may remain detectable for 3 to 7 days in chronic users. Some drug testing panels specifically target meprobamate rather than carisoprodol, as the metabolite persists longer and is itself pharmacologically active.
Blood and Serum Detection
Blood detection windows are 1 to 3 days for the parent compound. Therapeutic blood concentrations of carisoprodol range from 1 to 10 mcg/mL. Meprobamate concentrations in blood are typically 2 to 5 times higher than carisoprodol due to the longer half-life. Blood concentrations of meprobamate above 50 mcg/mL are associated with severe toxicity.
Hair Follicle Detection
Hair analysis for carisoprodol and meprobamate is feasible with LC-MS/MS methods but is rarely performed. Detection windows extend to approximately 90 days.
Confirmatory Methods
GC-MS and LC-MS/MS provide definitive confirmation of both carisoprodol and meprobamate. Laboratories testing for carisoprodol should always include meprobamate in the panel, as the metabolite is pharmacologically active and may be the only detectable analyte in specimens collected more than 24 hours after the last dose.
Reagent Testing
No established reagent testing protocols exist for carisoprodol. Standard harm reduction reagents do not produce reliable diagnostic reactions. Pharmaceutical-grade products obtained from pharmacies do not require additional testing.
Interactions
| Substance | Status | Note |
|---|---|---|
| Atropa belladonna | Dangerous | Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure |
| Cake | Dangerous | Combined CNS depression; risk of respiratory failure |
| Datura | Dangerous | Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure |
| Deschloroetizolam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Desomorphine | Dangerous | Severe respiratory depression risk; leading cause of polydrug overdose |
| Diclazepam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Diphenhydramine | Dangerous | Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure |
| Dissociatives | Dangerous | — |
| Eszopiclone | Dangerous | Combined CNS depression; risk of respiratory failure |
| Etizolam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Flubromazepam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Flubromazolam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Flunitrazepam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Flunitrazolam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Gaboxadol | Dangerous | Combined CNS depression; risk of respiratory failure |
| Harmala alkaloid | Dangerous | Unpredictable potentiation of CNS depression; risk of respiratory failure |
| Lorazepam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Mephenaqualone | Dangerous | Combined CNS depression; risk of respiratory failure |
| Metizolam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Midazolam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Naloxone | Dangerous | Severe respiratory depression risk; leading cause of polydrug overdose |
| Nicotine | Dangerous | Combined CNS depression; risk of respiratory failure |
| Nifoxipam | Dangerous | Combined CNS depression; risk of respiratory failure |
| Peganum harmala | Dangerous | Unpredictable potentiation of CNS depression; risk of respiratory failure |
| Pentobarbital | Dangerous | Combined CNS depression; risk of respiratory failure |
| Phenobarbital | Dangerous | Combined CNS depression; risk of respiratory failure |
| SAMe | Dangerous | Combined CNS depression; risk of respiratory failure |
| 3-Cl-PCP | Caution | Both cause CNS depression; increased risk of vomiting, unconsciousness, and respiratory depression |
| 3-FMA | Caution | Masks the effects of each drug; risk of overdosing when one wears off before the other |
| 3-HO-PCE | Caution | Both cause CNS depression; increased risk of vomiting, unconsciousness, and respiratory depression |
| 3-HO-PCP | Caution | Both cause CNS depression; increased risk of vomiting, unconsciousness, and respiratory depression |
| 3-MeO-PCE | Caution | Both cause CNS depression; increased risk of vomiting, unconsciousness, and respiratory depression |
| 1,3-Butanediol | Low Risk & Decrease | Depressants dull psychedelic effects; benzodiazepines are commonly used as trip-killers |
| 25E-NBOH | Low Risk & Decrease | Depressants dull psychedelic effects; benzodiazepines are commonly used as trip-killers |
| 2C-T | Low Risk & Decrease | Depressants dull psychedelic effects; benzodiazepines are commonly used as trip-killers |
| 2C-T-2 | Low Risk & Decrease | Depressants dull psychedelic effects; benzodiazepines are commonly used as trip-killers |
| 2C-T-21 | Low Risk & Decrease | Depressants dull psychedelic effects; benzodiazepines are commonly used as trip-killers |
History
Carisoprodol belongs to the depressant class of psychoactive substances, which encompasses a diverse range of compounds that reduce central nervous system activity.
The history of CNS depressants in medicine stretches back millennia, from the ancient use of alcohol and opium to the development of barbiturates in the early 1900s and benzodiazepines in the 1960s. Each generation of depressant drugs was initially heralded as safer than its predecessors, only for patterns of dependence and misuse to emerge with wider use.
The development of benzodiazepines represented a significant improvement in the therapeutic index over barbiturates, though concerns about dependence and long-term cognitive effects have moderated initial enthusiasm. Newer GABAergic compounds, including the Z-drugs and various research chemicals, continue this pattern of iterative development.
Carisoprodol is situated within this evolving pharmacological landscape, with its own specific history of development, clinical application, and patterns of use.
Harm Reduction
It is strongly recommended that one use harm reduction practices when using this drug. -extremely physically and psychologically addictive. Carbamate withdrawal, like barbiturate withdrawal, is medically serious and can potentially cause a life-threatening withdrawal syndrome that can cause seizures, psychosis, and death. Drugs which lower the seizure threshold such as tramadol and amphetamine should be avoided during withdrawal.
Tolerance will develop to the sedative-hypnotic effects of carisoprodol after prolonged use. It is unknown exactly how long it takes for tolerance to reach baseline.
In most jurisdictions, carisoprodol is considered a prescription-only and/or controlled drug.
Germany:** Carisoprodol is a prescription medicine, according to Anlage 1 AMVV.
United States: In the United States, carisoprodol is a Schedule IV Controlled Substance. Therefore, it is prescription-only and anyone caught in possession of the substance with or without intent to distribute is punishable by law.
Carisoprodol (Wikipedia)
Carisoprodol (Erowid Vault)
Carisoprodol (Isomer Design)
Toxicity & Safety
Carisoprodol likely has moderate toxicity relative to dose. However, carisoprodol is potentially lethal when mixed with depressants like alcohol or opioids. Carisoprodol has been taken off the market is several countries such as Sweden and Indonesia due to side effects and abuse.
It is strongly recommended that one use harm reduction practices when using this drug.
Tolerance and addiction potential
Carisoprodol is extremely physically and psychologically addictive. Carbamate withdrawal, like barbiturate withdrawal, is medically serious and can potentially cause a life-threatening withdrawal syndrome that can cause seizures, psychosis, and death. Drugs which lower the seizure threshold such as tramadol and amphetamine should be avoided during withdrawal.
Tolerance will develop to the sedative-hypnotic effects of carisoprodol after prolonged use. It is unknown exactly how long it takes for tolerance to reach baseline.
Dangerous interactions
Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).
Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.
Depressants (1,4-Butanediol, 2M2B, alcohol, benzodiazepines, barbiturates, GHB/GBL, methaqualone, opioids) - This combination potentiates the muscle relaxation, amnesia, sedation, and respiratory depression caused by one another. At higher doses, it can lead to a sudden, unexpected loss of consciousness along with a dangerous amount of depressed respiration. There is also an increased risk of suffocating on one's vomit while unconscious. If nausea or vomiting occurs before a loss of consciousness, users should attempt to fall asleep in the recovery position or have a friend move them into it.
Dissociatives - This combination can unpredictably potentiate the amnesia, sedation, motor control loss and delusions that can be caused by each other. It may also result in a sudden loss of consciousness accompanied by a dangerous degree of respiratory depression. If nausea or vomiting occurs before consciousness is lost, users should attempt to fall asleep in the recovery position or have a friend move them into it.
Stimulants - Stimulants mask the sedative effect of depressants, which is the main factor most people use to gauge their level of intoxication. Once the stimulant effects wear off, the effects of the depressant will significantly increase, leading to intensified disinhibition, motor control loss, and dangerous black-out states. This combination can also potentially result in severe dehydration if one's fluid intake is not closely monitored. If choosing to combine these substances, one should strictly limit themselves to a pre-set schedule of dosing only a certain amount per hour until a maximum threshold has been reached.
Addiction Potential
extremely physically and psychologically addictive
Overdose Information
Depressant overdose from Carisoprodol is a life-threatening medical emergency. The primary mechanism of death is respiratory depression leading to respiratory arrest.
Signs of overdose: Extremely slow or stopped breathing, blue lips or fingertips (cyanosis), pinpoint pupils, unresponsiveness, cold/clammy skin, gurgling or snoring sounds (may indicate airway obstruction), very slow heart rate.
Emergency response:
- Call emergency services immediately
- If the person is not breathing, begin rescue breathing or CPR
- Place unconscious but breathing person in the recovery position
- Administer naloxone if opioid involvement is suspected
- Stay with the person until help arrives
- Be honest with emergency responders about all substances consumed
Critical combination risk: The combination of Carisoprodol with other depressants (alcohol, benzodiazepines, opioids) is the most common scenario for fatal depressant overdose. The respiratory depression from multiple depressants is synergistic (greater than the sum of individual effects).
Dangerous Interactions
The combinations listed below may be life-threatening. Independent research should always be conducted to ensure safety when combining substances.
Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure
Combined CNS depression; risk of respiratory failure
Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure
Combined CNS depression; risk of respiratory failure
Severe respiratory depression risk; leading cause of polydrug overdose
Combined CNS depression; risk of respiratory failure
Compounding CNS depression with anticholinergic effects; risk of cardiac events and respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Unpredictable potentiation of CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Severe respiratory depression risk; leading cause of polydrug overdose
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Unpredictable potentiation of CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Combined CNS depression; risk of respiratory failure
Tolerance
| Full | Develops within 1 - 2 weeks of daily use |
| Half | 3 - 7 days |
| Zero | 1 - 2 weeks |
Cross-tolerances
Legal Status
In most jurisdictions, carisoprodol is considered a prescription-only and/or controlled drug.
Germany:** Carisoprodol is a prescription medicine, according to Anlage 1 AMVV.
United States: In the United States, carisoprodol is a Schedule IV Controlled Substance. Therefore, it is prescription-only and anyone caught in possession of the substance with or without intent to distribute is punishable by law.
Carisoprodol (Wikipedia)
Carisoprodol (Erowid Vault)
Carisoprodol (Isomer Design)
Experience Reports (1)
Tips (3)
Inform a trusted person when using Carisoprodol, especially if alone. Depressant overdoses can cause you to lose consciousness before you can call for help. Someone should be able to check on you.
If you are considering quitting Carisoprodol after regular use, consult a medical professional. Depressant withdrawal can be medically dangerous and a supervised taper is the safest approach. Do not try to white-knuckle it.
Physical dependence on Carisoprodol can develop faster than expected with regular use. Depressant withdrawal can cause seizures, delirium, and death. Never abruptly stop after prolonged daily use; taper gradually under medical guidance.
See Also
References (3)
- PubChem: Carisoprodol
PubChem compound page for Carisoprodol (CID: 2576)
pubchem - Carisoprodol - TripSit Factsheet
TripSit factsheet for Carisoprodol
tripsit - Carisoprodol - Wikipedia
Wikipedia article on Carisoprodol
wikipedia