Repositioning Candidate Details
Candidate ID: | R0150 |
Source ID: | DB00443 |
Source Type: | approved; vet_approved |
Compound Type: | small molecule |
Compound Name: | Betamethasone |
Synonyms: | 16β-Methyl-1,4-pregnadiene-9α-fluoro-11β,17α,21-triol-3,20-dione; 9-Fluoro-16β-methylprednisolone; 9α-Fluoro-16β-methylprednisolone; beta-Methasone alcohol; Betadexamethasone; Betamethasone |
Molecular Formula: | C22H29FO5 |
SMILES: | [H][C@@]12C[C@H](C)[C@](O)(C(=O)CO)[C@@]1(C)C[C@H](O)[C@@]1(F)[C@@]2([H])CCC2=CC(=O)C=C[C@]12C |
Structure: |
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DrugBank Description: | Betamethasone is a long-acting corticosteroid with immunosuppressive and antiinflammatory properties. It can be used topically to manage inflammatory skin conditions such as eczema, and parenterally to manage several disease states including autoimmune disorders. Betamethasone has potent glucocorticoid activity and negligible mineralocorticoid activity. |
CAS Number: | 378-44-9 |
Molecular Weight: | 392.4611 |
DrugBank Indication: | As a member of the corticosteroid family, betamethasone is indicated for the treatment of several inflammatory conditions. As topical monotherapy, betamethasone is indicated to relieve pruritic and inflammatory symptoms of corticosteroid-responsive-dermatoses. Betamethasone can be used topically in combination with a vitamin D analog such as calcipotriene to treat plaque psoriasis. The corticosteroid is also available as an injectable suspension and can be used to manage a range of inflammatory conditions including endocrine disorders, gastrointestinal disorders, and rheumatic disorders among other conditions. |
DrugBank Pharmacology: | Corticosteroids bind to the glucocorticoid receptor inhibiting pro-inflammatory signals, while promoting anti-inflammatory signals. Corticosteroids have a wide therapeutic window as patients may require doses that are multiples of what the body naturally produces. Patients who require long-term treatment with a corticosteroid should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections. |
DrugBank MoA: | Glucocorticoids inhibit neutrophil apoptosis and demargination, and inhibit NF-Kappa B and other inflammatory transcription factors. They also inhibit phospholipase A2, leading to decreased formation of arachidonic acid derivatives. In addition, glucocorticoids promote anti-inflammatory genes like interleukin-10. Corticosteroids like betamethasone can act through nongenomic and genomic pathways. The genomic pathway is slower and occurs when glucocorticoids activate glucocorticoid receptors and initiate downstream effects that promote transcription of anti-inflammatory genes including phosphoenolpyruvate carboxykinase (PEPCK), IL-1-receptor antagonist, and tyrosine amino transferase (TAT). On the other hand, the nongenomic pathway is able to elicit a quicker response by modulating T-cell, platelet and monocyte activity through the use of existing membrane-bound receptors and second messengers. |
Targets: | Glucocorticoid receptor agonist |
Inclusion Criteria: | Therapeutic strategy associated |

Strategy ID | Strategy | Synonyms | Related Targets | Related Drugs | |
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S13 | Anti-apoptosis | hepatocyte apoptosis; hepatic autophagy; apoptosis | Pan-caspase inhibitor | Emricasan | Details |
S05 | Anti-inflammatory | inflammatory | Bile acid; TNF-a inhibitor; Dual PPAR-α and -δ agonists; Toll-Like Receptor; (TLR)-4 antagonist; Caspase inhibitor; ASK-1 inhibitor | Ursodeoxycholic Acid; Pentoxifylline; Elafibranor; JKB-121; Emricasan; Selonsertib; | Details |
Target ID | Target Name | GENE | Action | Class | UniProtKB ID | Entry Name |
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Diseases ID | DO ID | Disease Name | Definition | Class |
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