- Raw materials
- Skeletal muscle relaxants
- Muscle relaxants
- Cyclobenzaprine
Filters
Custom request?
Type
Production region
Qualifications
Country of origin
Cyclobenzaprine API Manufacturers & Suppliers
5 verified results
Commercial-scale Suppliers
Employees: 200+
All certificates
Employees: 4,000
All certificates
All certificates
All certificates
All certificates
Total market transparency
Supplier trade data access
Buyer / supplier flow comparison
Cyclobenzaprine | CAS No: 303-53-7 | GMP-certified suppliers
A medication that provides short-term relief of muscle spasms in acute musculoskeletal conditions and may aid in pain and sleep disturbances associated with fibromyalgia.
Therapeutic categories
Primary indications
- Cyclobenzaprine is indicated as a short-term (2-3 weeks) adjunct therapy, along with rest and physical therapy, for relief of muscle spasm associated with acute, painful musculoskeletal conditions
- It has not been found effective in the treatment of spasticity originating from cerebral or spinal cord disease, or spasticity in children with cerebral palsy
- Cyclobenzaprine is also occasionally used off-label for reducing pain and sleep disturbances in patients with fibromyalgia
Product Snapshot
- Cyclobenzaprine is available primarily as oral tablets and capsules, including extended-release formulations, and topical creams
- It is mainly indicated for the short-term adjunctive treatment of muscle spasms associated with acute musculoskeletal conditions
- Cyclobenzaprine is approved for use in major regulatory markets including the United States and Canada
Clinical Overview
Pharmacodynamically, cyclobenzaprine acts within the brainstem to reduce skeletal muscle spasm. The precise mechanism of action in humans remains incompletely defined but is believed to involve modulation at the supraspinal level, particularly in the locus coeruleus. The drug likely reduces alpha and gamma motor neuron efferent activity by inhibiting coeruleus-spinal and reticulospinal pathways, resulting in decreased spinal interneuron excitation. Additional evidence suggests inhibition of descending serotonergic pathways in the spinal cord via 5-HT2 receptor antagonism may also contribute to its muscle relaxant effects.
Cyclobenzaprine exhibits a relatively long half-life but a short duration of clinical effect, typically 4 to 6 hours. It undergoes hepatic metabolism primarily via cytochrome P450 isoenzymes CYP1A2, CYP2D6, and CYP3A4. Given its serotonergic activity, there is a documented risk of serotonin syndrome, particularly when combined with other serotonergic agents. Manifestations may include autonomic instability, neuromuscular abnormalities, altered mental status, and gastrointestinal symptoms; immediate discontinuation is advised if such symptoms occur.
Safety considerations include a potential to reduce the seizure threshold and cause photosensitivity. It is contraindicated in certain populations and requires caution in patients with underlying cardiac conduction disorders due to its tricyclic-like structure.
Notable branded formulations have been available globally for decades as immediate-release oral tablets, primarily targeting acute musculoskeletal discomfort. Off-label use in fibromyalgia-associated pain and sleep disturbance has been reported but lacks strong clinical endorsement.
From an API sourcing standpoint, attention should be given to consistent purity, stereochemical configuration, and compliance with relevant pharmacopeial standards. Manufacturing processes must ensure control of potential impurities related to its dibenzocycloheptene scaffold and maintain stability given susceptibility to photodegradation. Reliable supply chains with traceability and validated quality assurance are critical for formulation development and regulatory submissions.
Identification & chemistry
| Generic name | Cyclobenzaprine |
|---|---|
| Molecule type | Small molecule |
| CAS | 303-53-7 |
| UNII | 69O5WQQ5TI |
| DrugBank ID | DB00924 |
Pharmacology
| Summary | Cyclobenzaprine is a skeletal muscle relaxant that acts primarily at the brainstem level, particularly targeting the locus coeruleus to reduce motor neuron activity and spinal interneuron excitability. Its pharmacological effects involve modulation of descending serotonergic pathways through 5-HT2 receptor inhibition, contributing to decreased muscle spasm. The drug’s mechanism does not involve direct action at neuromuscular junctions or skeletal muscle. |
|---|---|
| Mechanism of action | The exact mechanism of action of cyclobenzaprine has not been fully elucidated in humans, and much of the information available regarding its mechanism has been ascertained from early animal studies. There is some evidence that cyclobenzaprine exerts its effects at the supraspinal level, specifically within the locus coeruleus of the brainstem, with little-to-no action at neuromuscular junctions or directly on skeletal musculature. Action on the brainstem is thought to result in diminished activity of efferent alpha and gamma motor neurons, likely mediated by inhibition of coeruleus-spinal or reticulospinal pathways, and ultimately depressed spinal cord interneuron activity. More recently it has been suggested that inhibition of descending serotonergic pathways in the spinal cord via action on 5-HT2 receptors may contribute to cyclobenzaprine’s observed effects. |
| Pharmacodynamics | Cyclobenzaprine is a skeletal muscle relaxant that works on areas of the brainstem to reduce skeletal muscle spasm, though its exact pharmacodynamic behaviour is currently unclear. Despite its long half-life, it is relatively short-acting with a typical duration of action of 4-6 hours. Cyclobenzaprine has been reported to contribute to the development of serotonin syndrome when used in combination with other serotonergic medications. Symptoms of serotonin syndrome may include autonomic instability, changes to mental status, neuromuscular abnormalities, or gastrointestinal symptoms - treatment with cyclobenzaprine should be discontinued immediately if any of these reactions occur during therapy. |
Targets
| Target | Organism | Actions |
|---|---|---|
| 5-hydroxytryptamine receptor 2A | Humans | antagonist |
| 5-hydroxytryptamine receptor 2B | Humans | antagonist |
| 5-hydroxytryptamine receptor 2C | Humans | antagonist |
ADME / PK
| Absorption | The oral bioavailability of cyclobenzaprine has been estimated to be between 0.33 and 0.55. C<sub>max</sub> is between 5-35 ng/mL and is achieved after 4 hours (T<sub>max</sub>). AUC over an 8 hour dosing interval was reported to be approximately 177 ng.hr/mL. |
|---|---|
| Half-life | The effective half-life of cyclobenzaprine in young healthy subjects is approximately 18 hours. These values are extended in the elderly and those with hepatic insufficiency, with a mean effective half-life of 33.4 hours and 46.2 hours in these groups, respectively. |
| Protein binding | Cyclobenzaprine is approximately 93% protein bound in plasma. It has been identified as specifically having a high affinity for human serum albumin. |
| Metabolism | Cyclobenzaprine is extensively metabolized in the liver via both oxidative and conjugative pathways. Oxidative metabolism, mainly N-demethylation, is catalyzed primarily by CYP3A4 and CYP1A2 (with CYP2D6 implicated to a lesser extent) and is responsible for the major metabolite desmethylcyclobenzaprine. Cyclobenzaprine also undergoes N-glucuronidation in the liver catalyzed by UGT1A4 and UGT2B10, and has been shown to undergo enterohepatic circulation. |
| Route of elimination | After administration of a radio-labeled dose of cyclobenzaprine, 38-51% of radioactivity was excreted in the urine while 14-15% was excreted in the feces. Cyclobenzaprine is highly metabolized, with only approximately 1% of this same radio-labeled dose recovered in the urine as unchanged drug. Metabolites excreted in the urine are likely water-soluble glucuronide conjugates. |
| Volume of distribution | The volume of distribution of cyclobenzaprine is approximately 146 L. The combination of high plasma clearance despite a relatively long half-life observed with cyclobenzaprine is suggestive of extensive tissue distribution. |
| Clearance | The approximate plasma clearance of cyclobenzaprine is 0.7 L/min. |
Formulation & handling
- Cyclobenzaprine is formulated primarily for oral administration, including immediate and extended-release capsules and tablets.
- As a small molecule with low water solubility and high lipophilicity (LogP 4.61), solubilization strategies may be needed for formulation.
- Avoid co-administration with alcohol due to potentiation of central nervous system depressant effects.
Regulatory status
| Lifecycle | The active pharmaceutical ingredient (API) has patent protection in the United States expiring between November 2023 and February 2025, with marketed products available in both the US and Canada. Following patent expiry, the market is expected to enter a phase of increased generic competition and maturity. |
|---|
| Markets | Canada, US |
|---|
Supply Chain
| Supply chain summary | The manufacturing landscape for cyclobenzaprine includes numerous originator and generic manufacturers, indicating a well-established supply chain with multiple producers involved in API sourcing and packaging. Branded products such as Amrix have a presence primarily in the US and Canadian markets. Recent patent expirations in late 2023, along with a patent expiration in early 2025, suggest existing and potential generic competition in the near term. |
|---|
Safety
| Toxicity | The oral LD<sub>50</sub> of cyclobenzaprine in mice and rats is 338 mg/kg and 425 mg/kg, respectively. Signs of overdose may develop rapidly after ingestion and commonly include significant drowsiness and tachycardia, with less common manifestations including tremor, agitation, ataxia, GI upset, and other CNS effects such as confusion and hallucinations. Potentially critical manifestations, though rare, include cardiac arrest or dysrhythmias, severe hypotension, seizures, and neuroleptic malignant syndrome. As the management of cyclobenzaprine overdose is complex and ever-changing, it is recommended that a poison control center be consulted prior to treatment. Typical management involves gastrointestinal decontamination, close cardiac monitoring, and monitoring for signs of CNS or respiratory depression. As cyclobenzaprine exists in relatively low concentrations in plasma, monitoring of drug plasma levels should not guide management and dialysis is likely of no value. |
|---|
- Cyclobenzaprine exhibits oral LD50 values of 338 mg/kg in mice and 425 mg/kg in rats, indicating moderate acute toxicity
- Overdose may rapidly induce central nervous system and cardiovascular effects, including drowsiness, tachycardia, and in rare cases, severe arrhythmias or neuroleptic malignant syndrome
- Due to complex toxicity management and limited utility of plasma level monitoring or dialysis, exposure requires specialized toxicological consultation
Cyclobenzaprine is a type of Muscle relaxants
Muscle relaxants are a subcategory of pharmaceutical active pharmaceutical ingredients (APIs) commonly used to alleviate muscle spasms and promote muscle relaxation. These medications act on the central nervous system (CNS) or directly on muscle fibers to reduce muscle tone and tension.
Muscle relaxants can be classified into two main groups: spasmolytics and neuromuscular blockers. Spasmolytics primarily target the CNS to inhibit the transmission of nerve signals, thus reducing muscle spasms. They are often prescribed for conditions such as back pain, muscle strains, and spasms caused by neurological disorders.
Neuromuscular blockers, on the other hand, act at the neuromuscular junction to prevent the transmission of nerve impulses, resulting in temporary paralysis of skeletal muscles. These medications are primarily used during surgical procedures to induce muscle relaxation and facilitate intubation.
Commonly prescribed muscle relaxants include benzodiazepines, such as diazepam and lorazepam, which have sedative properties and can provide relief from muscle spasms. Another class of muscle relaxants is the centrally acting skeletal muscle relaxants, including carisoprodol and cyclobenzaprine, which work by affecting neurotransmitters in the CNS.
It is important to note that muscle relaxants can cause side effects such as drowsiness, dizziness, and impaired coordination. They should only be used under the guidance of a healthcare professional, and the dosage and duration of treatment should be strictly followed to avoid dependence or other complications.
In conclusion, muscle relaxants are pharmaceutical APIs used to alleviate muscle spasms and promote muscle relaxation. They are available in different forms and can target the CNS or directly act on muscle fibers. It is crucial to consult a healthcare professional for proper diagnosis, prescription, and monitoring when using muscle relaxants.
Cyclobenzaprine (Muscle relaxants), classified under Skeletal muscle relaxants
Skeletal muscle relaxants are a category of pharmaceutical active pharmaceutical ingredients (APIs) that are commonly used in the treatment of musculoskeletal conditions characterized by muscle spasms, stiffness, or tension. These medications work by targeting the central nervous system to reduce muscle activity and promote relaxation.
Skeletal muscle relaxants act on various receptors in the central nervous system, such as gamma-aminobutyric acid (GABA) receptors, to inhibit the transmission of nerve impulses and decrease muscle tone. This results in a reduction in muscle spasms, pain relief, and improved mobility.
There are different classes of skeletal muscle relaxants, including benzodiazepines, antispasmodics, and centrally acting muscle relaxants. Benzodiazepines, such as diazepam and lorazepam, exert their muscle relaxant effects by enhancing the activity of GABA receptors. Antispasmodics like cyclobenzaprine work by inhibiting the release of certain neurotransmitters involved in muscle contractions. Centrally acting muscle relaxants, such as baclofen and tizanidine, directly target the spinal cord to reduce muscle hyperactivity.
Skeletal muscle relaxants are commonly prescribed for conditions like muscle spasms, back pain, fibromyalgia, and multiple sclerosis. However, they are typically used for short-term treatment due to their potential side effects, including drowsiness, dizziness, and sedation.
It is important to note that skeletal muscle relaxants should only be used under the supervision and prescription of a qualified healthcare professional. Proper dosage and duration of treatment should be determined based on the patient's condition and medical history to ensure safe and effective use of these medications.
Cyclobenzaprine API manufacturers & distributors
Compare qualified Cyclobenzaprine API suppliers worldwide. We currently have 5 companies offering Cyclobenzaprine API, with manufacturing taking place in 4 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| Derivados Quimicos | Producer | Spain | Spain | CoA, USDMF | 18 products |
| Hetero Drugs | Producer | India | India | CoA, GMP, USDMF, WC | 98 products |
| LGM Pharma | Distributor | United States | World | BSE/TSE, CEP, CoA, GMP, MSDS, USDMF | 441 products |
| Medichem | Producer | Spain | Unknown | CoA, USDMF | 39 products |
| Vasudha Pharma Chem Ltd. | Producer | India | India | CoA, EDMF/ASMF, GMP, KDMF, MSDS, USDMF, WC | 37 products |
When sending a request, specify which Cyclobenzaprine API quality you need: for example EP (Ph. Eur.), USP, JP, BP, or another pharmacopoeial standard, as well as the required grade (base, salt, micronised, specific purity, etc.).
Use the list above to find high-quality Cyclobenzaprine API suppliers. For example, you can select GMP, FDA or ISO certified suppliers. Visit our help page to learn more about sourcing APIs via Pharmaoffer.
