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What drug is Soma based on? The pharmacological connection to meprobamate

3 min read

First approved in 1959, the muscle relaxant Soma has a pharmacological history tied to a well-known tranquilizer. This article explains what drug is Soma based on and the significant role its main metabolite plays in its effects and potential for dependence.

Quick Summary

Soma (carisoprodol) is based on the sedative-hypnotic meprobamate, its main active metabolite. This connection explains Soma's muscle relaxant and sedative effects, its abuse potential, and its classification as a controlled substance.

Key Points

  • Pharmacological Basis: Soma is based on the tranquilizer meprobamate, which is its primary active metabolite.

  • Metabolic Conversion: The body's liver enzyme CYP2C19 metabolizes carisoprodol (Soma) into meprobamate.

  • Mechanisms of Action: While carisoprodol works centrally to alter pain perception, meprobamate acts on GABA-A receptors, contributing sedative and anxiety-reducing effects.

  • Dependence Potential: Meprobamate's history of abuse and addiction explains why Soma also has a high potential for dependence, especially with prolonged use.

  • Controlled Substance Status: In 2012, the DEA classified carisoprodol as a Schedule IV controlled substance due to its abuse potential, reflecting the legacy of its meprobamate metabolite.

  • Duration and Effects: Carisoprodol has a rapid onset, but the longer half-life of its meprobamate metabolite means its effects can linger and accumulate over time.

In This Article

Carisoprodol and its link to meprobamate

Soma is the brand name for the prescription drug carisoprodol, a centrally-acting skeletal muscle relaxant used for the short-term relief of discomfort from acute, painful musculoskeletal conditions. While the parent drug carisoprodol has its own muscle-relaxing effects, it is fundamentally and pharmacologically linked to meprobamate, a former popular tranquilizer. The connection arises because carisoprodol is metabolized in the liver to form meprobamate as its main active metabolite.

The history of meprobamate

Before the rise of benzodiazepines, meprobamate was widely prescribed for anxiety and tension in the 1950s and 60s. Marketed under brand names like Miltown, it was considered a groundbreaking "minor tranquilizer" at the time. However, it soon became clear that meprobamate had significant potential for abuse, addiction, and dependence. Its sedative-hypnotic properties could lead to dangerous withdrawal symptoms upon abrupt discontinuation, similar to barbiturates. These risks eventually led to meprobamate being classified as a Schedule IV controlled substance.

The metabolic pathway

When a person takes Soma, the carisoprodol is metabolized primarily in the liver by the cytochrome P450 enzyme CYP2C19. This process converts carisoprodol into meprobamate. Due to individual genetic differences, some people, known as poor metabolizers, have lower levels of the CYP2C19 enzyme. This can lead to higher levels of carisoprodol and lower levels of meprobamate, potentially causing greater side effects.

How carisoprodol and meprobamate affect the body

The pharmacology of carisoprodol's muscle-relaxing effects is not fully understood, but it is believed to act on the central nervous system (CNS) to alter pain perception. The formation of meprobamate, however, is a key component of Soma's overall effect. Meprobamate is known to act on GABA-A receptors, the brain's primary inhibitory neurotransmitter system. This action produces a sedating and anxiolytic effect, contributing to the drowsiness and relaxed feeling that can result from taking Soma. It is the combined effect of carisoprodol's central action and its conversion into meprobamate that drives its therapeutic and recreational potential.

Comparison of carisoprodol and meprobamate

While closely related, carisoprodol and meprobamate have distinct characteristics. A clear comparison helps illustrate their relationship and why Soma carries significant risks.

Feature Carisoprodol (Soma) Meprobamate (Metabolite)
Drug Class Skeletal muscle relaxant Sedative-hypnotic, tranquilizer
Status (USA) Schedule IV controlled substance (since 2012) Schedule IV controlled substance
Onset of Action Rapid, within 30 minutes Slower onset, but longer duration
Half-Life Approximately 8 hours Nearly eight-fold longer than carisoprodol
Primary Effect Muscle relaxation (via CNS) Sedation, tranquilizing, anxiolytic
Metabolism Metabolized to meprobamate by CYP2C19 enzyme Active metabolite of carisoprodol

The dangers of carisoprodol

The fact that Soma is based on meprobamate is the root cause of its significant abuse and dependence potential. Despite initial marketing claims of low addiction risk, evidence has accumulated over decades demonstrating its habit-forming nature.

  • High abuse potential: Carisoprodol is often abused for its sedative and euphoric effects. It is sometimes combined with other CNS depressants, like opioids or benzodiazepines, to enhance their effects in a dangerous cocktail known as "The Holy Trinity".
  • Dependence and withdrawal: Prolonged use can lead to physical and psychological dependence. Abrupt discontinuation after long-term use can trigger severe withdrawal symptoms, including insomnia, anxiety, and potentially life-threatening seizures.
  • Safety concerns: Due to these risks, carisoprodol's market authorization was suspended in the European Union in 2008. In the United States, the DEA classified it as a Schedule IV controlled substance in 2012 to address the rising problem of abuse.

Conclusion: The hidden legacy in Soma

The answer to "What drug is Soma based on?" reveals a critical aspect of its pharmacology. It is not just carisoprodol but also its main active metabolite, meprobamate, that dictates its effects and risks. The drug was essentially designed as a pro-drug for meprobamate, a known substance of abuse. The sedative-hypnotic properties inherited through this metabolic link are what make Soma effective as a muscle relaxant but also what gives it a high potential for dependence and misuse. This pharmacological relationship is why Soma is limited to short-term use and carefully regulated by authorities. For those with acute musculoskeletal pain, it is crucial to understand this legacy and follow a physician's guidance closely to minimize health risks. More information on carisoprodol and its side effects can be found on authoritative health websites like Drugs.com.

Frequently Asked Questions

Soma is the brand name for the drug carisoprodol, a prescription muscle relaxant used for the short-term treatment of acute musculoskeletal pain and spasms.

Yes, Soma (carisoprodol) is metabolized in the liver to produce meprobamate as its primary active metabolite. This metabolic link means that the effects of Soma are largely based on the pharmacology of meprobamate.

Soma was classified as a Schedule IV controlled substance in 2012 because of its potential for abuse and dependence. This risk is directly tied to its conversion into the sedative meprobamate.

Yes, while carisoprodol is a direct muscle relaxant, its metabolite meprobamate is a more potent sedative and anxiolytic. Carisoprodol also has a more rapid, but shorter, duration of action compared to meprobamate.

Prolonged use of Soma can lead to physical and psychological dependence due to the accumulation of meprobamate. Abruptly stopping the medication can cause severe withdrawal symptoms, including seizures.

Due to its abuse potential stemming from its relationship with meprobamate, Soma is often considered a less safe option than many newer muscle relaxants, such as cyclobenzaprine or methocarbamol. Many European countries have even removed carisoprodol from the market.

No, combining Soma with other central nervous system depressants, such as opioids, benzodiazepines, or alcohol, is extremely dangerous. This combination can cause profound respiratory depression, coma, or death.

References

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Medical Disclaimer

This content is for informational purposes only and should not replace professional medical advice.