. . . . . . "clobetasol 17-propionate"@en . . . . . . . . . . . . . "For short-term topical treatment of the inflammatory and pruritic manifestations of moderate to severe corticosteroid-responsive dermatoses of the scalp."@en . . . . . . . . . . . . . . . . . . . . . "Corticosteroids are metabolized primarily in the liver and are then excreted by the kidneys. Some of the topical corticosteroids, including clobetasol propionate and its metabolites, are also excreted into the bile."@en . " "@en . . . . . . . . . . . . . . . . . . . . . . . . "Elks, J., Phillipps, G.H. and May, P.J.; US. Patent 3,721,687; March 20, 1973; assigned to Glaxo Laboratories Limited, England."@en . "approved"@en . . . . . "25122-46-7"@en . . . . . "Clobetasol propionate"@en . . . . . . . "21-chloro-9-fluoro-11\u03B2,17-dihydroxy-16\u03B2-methylpregna-1,4-diene-3,20-dione 17-propionate"@en . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . "Humans and other mammals"@en . . . . . . "Oral LD₅₀ in rat and mouse is >3000 mg/kg. Topically applied clobetasol can be absorbed in sufficient amounts to produce systemic effects. Symptoms of overdose include thinning of skin and suppression of adrenal cortex (decreased ability to respond to stress)."@en . . . . "clobetasol 17-propanoate"@en . . . . . . . . . . "Topical corticosteroids can be absorbed from intact healthy skin. The extent of percutaneous absorption of topical corticosteroids is determined by many factors, including the vehicle and the integrity of the epidermal barrier. Occlusion, inflammation and/or other disease processes in the skin may also increase percutaneous absorption."@en . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . "A derivative of prednisolone with high glucocorticoid activity and low mineralocorticoid activity. Absorbed through the skin faster than fluocinonide, it is used topically in treatment of psoriasis but may cause marked adrenocortical suppression. [PubChem]"@en . . . . . . . . . . . . "The precise mechanism of the antiinflammatory activity of topical steroids in the treatment of steroid-responsive dermatoses, in general, is uncertain. However, corticosteroids are thought to act by the induction of phospholipase A₂ inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A₂. Initially, however, clobetasol, like other corticosteroids, bind to the glucocorticoid receptor, which complexes, enteres the cell nucleus and modifies genetic transcription (transrepression/transactivation)."@en . .