Repositioning Candidate Details
| Candidate ID: | R0311 |
| Source ID: | DB00860 |
| Source Type: | approved; vet_approved |
| Compound Type: | small molecule |
| Compound Name: | Prednisolone |
| Synonyms: | (11β)-11,17,21-trihydroxypregna-1,4-diene-3,20-dione; 1,4-pregnadiene-11β,17α,21-triol-3,20-dione; 1,4-pregnadiene-3,20-dione-11β,17α,21-triol; 3,20-dioxo-11β,17α,21-trihydroxy-1,4-pregnadiene; delta-dehydrocortisol; delta-dehydrohydrocortisone; delta-hydrocortisone; delta(1)-Dehydrocortisol; delta(1)-Dehydrohydrocortisone; delta(1)-Hydrocortisone; Hydroretrocortine; Metacortandralone; PRDL; Prednisolone |
| Molecular Formula: | C21H28O5 |
| SMILES: | [H][C@@]12CC[C@](O)(C(=O)CO)[C@@]1(C)C[C@H](O)[C@@]1([H])[C@@]2([H])CCC2=CC(=O)C=C[C@]12C |
| Structure: |
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| DrugBank Description: | Prednisolone is a glucocorticoid similar to used for its anti-inflammatory, immunosuppressive, anti-neoplastic, and vasoconstrictive effects. Prednisolone was granted FDA approval on 21 June 1955. |
| CAS Number: | 50-24-8 |
| Molecular Weight: | 360.444 |
| DrugBank Indication: | Prednisolone is indicated to treat endocrine, rheumatic, and hematologic disorders; collagen, dermatologic, ophthalmic, respiratory, and gastrointestinal diseases; allergic and edematous states; and other conditions like tuberculous meningitis. |
| DrugBank Pharmacology: | Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Prednisolone has a short duration of action as the half life is 2.1-3.5 hours. Corticosteroids have a wide therapeutic window as patients make 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 |
| 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 |
| Target ID | Target Name | GENE | Action | Class | UniProtKB ID | Entry Name |
|---|