Is Soma a Benzo? Understanding the Drug Class of Carisoprodol

October 7, 2025 •

4 min read

Soma, the brand name for carisoprodol, is a prescription muscle relaxant used for short-term treatment of acute, painful musculoskeletal conditions. The question, "Is Soma a benzo?", frequently arises because of its sedative properties and potential for dependence, though it belongs to a different pharmacological class.

Quick Summary

Soma (carisoprodol) is a centrally-acting skeletal muscle relaxant, not a benzodiazepine. Its primary metabolite, meprobamate, produces sedative effects similar to benzos, contributing to Soma's potential for abuse and dependence. The medication is a Schedule IV controlled substance.

Key Points

Not a Benzo: Soma (carisoprodol) is a centrally-acting skeletal muscle relaxant, not a benzodiazepine, though it shares similar sedative effects.
Meprobamate Metabolite: The reason for the confusion is that Soma is metabolized into meprobamate, a compound with pharmacological effects similar to benzodiazepines, affecting GABA$_{A}$ receptors.
Schedule IV Controlled Substance: Due to its potential for abuse and dependence, the DEA has classified Soma as a Schedule IV controlled substance, along with many benzodiazepines.
High Abuse Potential: Soma's sedative and euphoric effects, amplified by its meprobamate metabolite, give it a significant potential for abuse, especially at higher doses.
Dangerous Drug Interactions: Combining Soma with other CNS depressants like alcohol, opioids, or benzodiazepines can cause excessive sedation, respiratory depression, overdose, and even death.
Withdrawal Syndrome: Abruptly discontinuing Soma after prolonged use can trigger a withdrawal syndrome with symptoms similar to meprobamate withdrawal, including insomnia, tremors, and anxiety.

Soma's Pharmacological Classification: A Deeper Look

Soma, known generically as carisoprodol, is not technically a benzodiazepine. Instead, it is classified as a centrally-acting skeletal muscle relaxant. Its complex pharmacology and metabolism are the sources of confusion and similarity to benzodiazepines.

While the exact mechanism of carisoprodol is not fully understood, it is believed to act by inhibiting interneuronal activity in the spinal cord and descending reticular formation of the brain. This central nervous system (CNS) depression produces muscle relaxation and also accounts for its sedative effects.

The key to understanding its benzodiazepine-like properties lies in its primary metabolite. When the body metabolizes carisoprodol, it produces meprobamate. Meprobamate is a carbamate derivative that has anti-anxiety and sedative effects by acting on GABA$_{A}$ receptors, much like benzodiazepines. This is why Soma produces similar feelings of calm and relaxation, especially at higher doses, and contributes significantly to its potential for abuse and addiction.

The Controlled Substance Status of Soma

Because of its abuse potential, the Drug Enforcement Administration (DEA) classified carisoprodol as a Schedule IV controlled substance in 2012. This designation indicates that while it has accepted medical uses, it carries a risk of misuse, dependency, and abuse. Many states, and some European countries, have also placed restrictions on its use. Other Schedule IV drugs include well-known benzodiazepines like Xanax (alprazolam) and Valium (diazepam).

Potential for Dependence and Withdrawal

Both Soma and benzodiazepines can lead to physical dependence, particularly with long-term use. For this reason, Soma is typically prescribed for short-term use only, generally no longer than two to three weeks. Abruptly stopping the medication after prolonged use can trigger a withdrawal syndrome.

Symptoms of Soma withdrawal can be serious and may include:

Insomnia
Vomiting
Tremors
Muscle twitching
Anxiety
Hallucinations
Ataxia (loss of coordination)
Delusions

It is critical to taper off Soma under a doctor's supervision to minimize the risk of severe withdrawal symptoms.

Risks of Combining Soma and Other CNS Depressants

The sedative effects of Soma are significantly magnified when combined with other CNS depressants, including alcohol, opioids, and benzodiazepines. This is one of the most dangerous risks associated with Soma use and abuse. Combining these substances increases the risk of:

Excessive drowsiness
Impaired coordination
Slowed breathing (respiratory depression)
Overdose
Death

Individuals who use a combination of Soma, opioids (like hydrocodone), and benzodiazepines (like Xanax) recreationally are at an extremely high risk. This dangerous combination is sometimes referred to as the "Houston Cocktail" or "Holy Trinity".

Comparing Soma and Benzodiazepines


Feature	Soma (Carisoprodol)	Benzodiazepines (e.g., Diazepam)
Drug Class	Skeletal muscle relaxant	Central nervous system depressants, anxiolytics
Mechanism of Action	Centrally-acting. Produces meprobamate metabolite which acts on GABA$_{A}$ receptors.	Act directly on GABA$_{A}$ receptors to enhance inhibitory effects.
Primary Use	Short-term relief of acute musculoskeletal pain.	Treatment of anxiety, seizures, and muscle spasms.
Speed of Effect	Onset typically within 30 minutes.	Onset varies, often rapid.
Duration of Effect	4 to 6 hours.	Varies, e.g., Diazepam's half-life is ~70 hours.
Abuse Potential	High potential due to meprobamate metabolite.	High potential for abuse and dependence.
Controlled Status	Schedule IV in the U.S..	Schedule IV in the U.S..
Addiction Risk	Significant, often linked to sedative/euphoric effects.	Significant, can lead to psychological and physical dependence.
Withdrawal	Symptoms can include insomnia, tremors, and hallucinations.	Symptoms can be severe and life-threatening.

Why the Distinction is Crucial

The distinction between Soma and a direct benzodiazepine is not just a matter of technicality. It is critical for healthcare providers to understand these differences to properly assess a patient's risk profile, especially for those with a history of substance abuse. While Soma and benzos share similar sedative and CNS depressant effects, their chemical structures and metabolic pathways are different. This means their interactions with other drugs, specific side effects, and long-term risks, while overlapping, are not identical.

For patients, understanding this difference can help them make informed decisions and recognize the serious risks involved, especially when tempted to misuse the medication or combine it with other substances. The presence of meprobamate, a substance with its own potential for dependence, reinforces the need for strict medical supervision during the short-term use of Soma.

Conclusion

In summary, while Soma (carisoprodol) functions as a powerful CNS depressant and produces sedative effects similar to those of benzodiazepines, it is not a benzodiazepine itself. The similarity stems from its metabolism into meprobamate, which has pharmacological properties akin to benzos. As a Schedule IV controlled substance with a significant potential for abuse, dependence, and serious interactions with other CNS depressants, Soma requires careful use under medical guidance. Understanding its distinct pharmacological profile and its metabolite's role is essential for both patients and clinicians to ensure safety and minimize risks associated with this potent medication.

For a deeper dive into carisoprodol's pharmacology, see the StatPearls article on the NCBI Bookshelf.

Frequently Asked Questions

The primary difference lies in their chemical structure and classification. Soma is a skeletal muscle relaxant that is metabolized into a compound with benzodiazepine-like effects, while a benzodiazepine is a drug class that directly acts on GABA receptors in the brain.

Soma is a controlled substance because of its potential for abuse and dependence. This potential is largely due to its main metabolite, meprobamate, which has sedative and euphoric properties that can be habit-forming.

Combining Soma with a benzodiazepine is extremely dangerous and can be fatal. Both are CNS depressants, and taking them together greatly increases the risk of excessive sedation, respiratory depression, and overdose.

Meprobamate, the primary metabolite of Soma, is believed to work by enhancing the activity of the GABA neurotransmitter in the brain. This produces sedative and anti-anxiety effects, similar to how benzodiazepines function.

Common side effects of Soma include drowsiness, dizziness, and headache. In higher doses or with prolonged use, more serious side effects like loss of coordination, fainting, and hallucinations can occur.

Soma is only prescribed for short-term use (typically 2-3 weeks) because of a lack of evidence for its long-term effectiveness and a significant risk of dependence and abuse.

Stopping Soma abruptly, especially after long-term use, can lead to withdrawal symptoms similar to those experienced with benzodiazepines or alcohol, including insomnia, tremors, and anxiety.