| Candidate ID: | R0261 |
| Source ID: | DB00741 |
| Source Type: | approved; vet_approved |
| Compound Type: |
small molecule
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| Compound Name: |
Hydrocortisone
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| Synonyms: |
(11β)-11,17,21-trihydroxypregn-4-ene-3,20-dione; 11beta-hydrocortisone; 11beta,17alpha,21-Trihydroxy-4-pregnene-3,20-dione; 11β-hydrocortisone; 17-Hydroxycorticosterone; 4-pregnen-11β,17α,21-triol-3,20-dione; Cortisol; Hydrocortisone; Kendall's compound F; Reichstein's substance M
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| Molecular Formula: |
C21H30O5
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| 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)CC[C@]12C
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| Structure: |
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| DrugBank Description: |
Hydrocortisone, or cortisol, is a glucocorticoid secreted by the adrenal cortex. Hydrocortisone is used to treat immune, inflammatory, and neoplastic conditions. It was discovered in the 1930s by Edward Kendall and named Compound F, or 17-hydroxycorticosterone.
Hydrocortisone was granted FDA approval on 5 August 1952.
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| CAS Number: |
50-23-7
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| Molecular Weight: |
362.4599
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| DrugBank Indication: |
Otic solutions are indicated for infections of the external auditory canal caused by susceptible organisms and with inflammation. Hydrocortisone tablets are indicated for certain endocrine, rheumatic, collagen, allergic, ophthalmic, respiratory, hematologic, neoplastic, edematous, gastrointestinal, and other conditions. A hydrocortisone enema is indicated for ulcerative colitis, a topical ointment with antibiotics is indicated for corticosteroid responsive dermatoses with infections, and a topical cream with is indicated to treat cold sores. Oral granules of hydrocortisone are used as a replacement therapy for Adrenocortical Insufficiency (AI) in children under 17 years of age.
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| DrugBank Pharmacology: |
Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes. Hydrocortisone has a wide therapeutic index and a moderate duration of action. Patients should stop taking the medication if irritation or sensitization occurs.
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| 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.
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| Targets: |
Glucocorticoid receptor agonist; Annexin A1 agonist
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| Inclusion Criteria: |
Therapeutic strategy associated
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