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1. Hydrocortisone 17-butyrate 21-propionate
2. Hydrocortisone Buteprate
3. Pandel
1. Hydrocortisone Buteprate
2. 72590-77-3
3. Pandel
4. Hydrocortisone Butyrate Propionate
5. Hydrocortisone 17-butyrate 21-propionate
6. Ts 408
7. Hydrocortisone Probutate [usan]
8. Hydrocortisone Probutat
9. 11beta,17,21-trihydroxypregn-4-ene-3,20-dione 17-butyrate 21-propionate
10. [(8s,9s,10r,11s,13s,14s,17r)-11-hydroxy-10,13-dimethyl-3-oxo-17-(2-propanoyloxyacetyl)-2,6,7,8,9,11,12,14,15,16-decahydro-1h-cyclopenta[a]phenanthren-17-yl] Butanoate
11. Chebi:31675
12. O6550d6k3a
13. Ts-408
14. Hydrocortisone Butyrate Propionate [jan]
15. Hydrocortisone Probutate (usan)
16. 11beta,17alpha,21-trihydroxypregn-4-ene-3,20-dione 17-butyrate, 21-propionate
17. Hydrocortisone Butyrate Propionate (jan)
18. Unii-o6550d6k3a
19. Ncgc00183276-01
20. Einecs 276-726-9
21. Pandel (tn)
22. Schembl4778
23. Dsstox_cid_28529
24. Dsstox_rid_82801
25. Dsstox_gsid_48603
26. Chembl1200953
27. Dtxsid3048603
28. Zinc4213519
29. Tox21_112938
30. 17-butyryloxy-11-beta-hydroxy-21-propionyloxy-4-pregnene-3,20-dione
31. Lmst02030128
32. Db14543
33. Hydrocortisone Buteprate [mart.]
34. Hydrocortisone Buteprate [vandf]
35. Hydrocortisone Probutat [who-dd]
36. Hydrocortisone Probutate [vandf]
37. Pregn-4-ene-3,20-dione, 11-hydroxy-17-(1-oxobutoxy)-21-(1-oxopropoxy)-, (11-beta)-
38. Pregn-4-ene-3,30-dione, 11-beta,17,21-trihydroxy-, 17-butyrate, 21-propionate
39. Cas-72590-77-3
40. Hy-106673
41. Cs-0026321
42. Cortisol, 17-butyrate, 21-propionate
43. Hydrocortisone Probutate [orange Book]
44. D01886
45. 11beta-hydroxy-17-(1-oxobutoxy)-21-(1-oxopropoxy)pregn-4-ene-3,20-dione
46. 11.beta.,17,21-trihydroxypregn-4-ene-3,20-dione 17-butyrate 21-propionate
47. 11.beta.-hydroxy-17-(1-oxobutoxy)-21-(1-oxopropoxy)pregn-4-ene-3,20-dione
48. Pregn-4-ene-3,20-dione, 11-hydroxy-17-(1-oxobutoxy)-21-(1-oxopropyl)-, (11beta)-
49. Pregn-4-ene-3,20-dione,11-hydroxy-17-(1-oxobutoxy)-21-(1-oxopropoxy)-, (11b)-
| Molecular Weight | 488.6 g/mol |
|---|---|
| Molecular Formula | C28H40O7 |
| XLogP3 | 4.2 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 7 |
| Rotatable Bond Count | 9 |
| Exact Mass | 488.27740361 g/mol |
| Monoisotopic Mass | 488.27740361 g/mol |
| Topological Polar Surface Area | 107 Ų |
| Heavy Atom Count | 35 |
| Formal Charge | 0 |
| Complexity | 938 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 7 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease.
Hydrocortisone is the most important human glucocorticoid. It is essential for life and regulates or supports a variety of important cardiovascular, metabolic, immunologic and homeostatic functions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger a variety of important cardiovascular, metabolic, immunologic and homeostatic effects. Glucocorticoids are distinguished from mineralocorticoids and sex steroids by having different receptors, target cells, and effects. Technically, the term corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid. Glucocorticoids suppress cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most important of which is the IL-2. Reduced cytokine production limits T cell proliferation. Glucocorticoids also suppress humoral immunity, causing B cells to express lower amounts of IL-2 and IL-2 receptors. This diminishes both B cell clonal expansion and antibody synthesis. The diminished amounts of IL-2 also leads to fewer T lymphocyte cells being activated.
Anti-Inflammatory Agents
Substances that reduce or suppress INFLAMMATION. (See all compounds classified as Anti-Inflammatory Agents.)
D - Dermatologicals
D07 - Corticosteroids, dermatological preparations
D07A - Corticosteroids, plain
D07AB - Corticosteroids, moderately potent (group ii)
D07AB11 - Hydrocortisone buteprate
Absorption
Topical corticosteroids can be absorbed from normal intact skin. Inflammation and/or other disease processes in the skin increase percutaneous absorption.
Route of Elimination
Corticosteroids are metabolized primarily in the liver and are then excreted by the kidneys. Some of the topical corticosteroids and their metabolites are also excreted into the bile.
Primarily hepatic via CYP3A4
6-8 hours
Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.
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