Repositioning Candidate Details
| Candidate ID: | R0368 |
| Source ID: | DB01013 |
| Source Type: | approved |
| Compound Type: | small molecule |
| Compound Name: | Clobetasol propionate |
| Synonyms: | 21-chloro-9-fluoro-11β,17-dihydroxy-16β-methylpregna-1,4-diene-3,20-dione 17-propionate; clobetasol 17-propanoate; clobetasol 17-propionate; Clobetasol propionate; Clobetasol propionate E |
| Molecular Formula: | C25H32ClFO5 |
| SMILES: | [H][C@@]12C[C@H](C)[C@](OC(=O)CC)(C(=O)CCl)[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: | Clobetasol propionate is a prednisolone derivative with higher specificity for glucocorticoid receptors than mineralocorticoid receptors. It has demonstrated superior activity compared to and was first described in the literature in 1974. Clobetasol Propionate was granted FDA approval on 27 December 1985. |
| CAS Number: | 25122-46-7 |
| Molecular Weight: | 466.97 |
| DrugBank Indication: | Clobetasol propionate is indicated to treat moderate to severe plaque psoriasis as well as inflammatory and pruritic manifestations of corticosteroid responsive dermatoses. |
| DrugBank Pharmacology: | Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Clobetasol propionate is generally applied twice daily so the duration of action is long. Corticosteroids have a wide therapeutic window as patients may require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections. |
| DrugBank MoA: | The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days. Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10. Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive. High doses of glucocorticoids for an extended period bind to the mineralocorticoid receptor, raising sodium levels and decreasing potassium levels. |
| Targets: | Glucocorticoid receptor agonist; Annexin A1 inducer; Mineralocorticoid receptor agonist |
| Inclusion Criteria: | Therapeutic strategy associated |
| Strategy ID | Strategy | Synonyms | Related Targets | Related Drugs | |
|---|---|---|---|---|---|
| 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 |
| Diseases ID | DO ID | Disease Name | Definition | Class |
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