Repositioning Candidate Details
| Candidate ID: | R0334 |
| Source ID: | DB00924 |
| Source Type: | approved |
| Compound Type: | small molecule |
| Compound Name: | Cyclobenzaprine |
| Synonyms: | (3-Dibenzo[a,d]cyclohepten-5-ylidene-propyl)-dimethyl-amine; Cyclobenzaprine; N,N-dimethyl-5H-dibenzo(a,d)cycloheptene-Δ5,γ-propylamine |
| Molecular Formula: | C20H21N |
| SMILES: | CN(C)CCC=C1C2=CC=CC=C2C=CC2=CC=CC=C12 |
| Structure: |
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| DrugBank Description: | Cyclobenzaprine, a centrally-acting muscle relaxant, was first synthesized in 1961 and has been available for human use since 1977. It was initially studied for use as antidepressant given its structural similarity to tricyclic antidepressants - it differs from by only a single double bond. Since its approval, it has remained relatively popular as an adjunctive, short-term treatment for acute skeletal muscle spasms secondary to musculoskeletal injury. |
| CAS Number: | 303-53-7 |
| Molecular Weight: | 275.3874 |
| DrugBank Indication: | 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. |
| DrugBank Pharmacology: | 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. |
| DrugBank MoA: | 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. |
| Targets: | 5-hydroxytryptamine receptor 2A antagonist; 5-hydroxytryptamine receptor 2B antagonist; 5-hydroxytryptamine receptor 2C antagonist; 5-hydroxytryptamine receptor 6 antagonist; Sodium-dependent serotonin transporter inhibitor; Sodium-dependent noradrenaline transporter inhibitor; 5-hydroxytryptamine receptor 7 antagonist; Toll-like receptor 4 inhibitor; Aldehyde oxidase inhibitor |
| Inclusion Criteria: | Target associated |
