Ulobetasol (as ulobetasol propionate) is 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. It is used for the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses.
Halobetasol propionate is 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. The initial interaction, however, is due to the drug binding 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 extent of percutaneous absorption of topical corticosteroids is determined by many factors including the vehicle and the integrity of the epidermal barrier. Inflammation and/or other disease processes in the skin may increase percutaneous absorption.
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Humans and other mammals
Daniella Gutman, Shimon Chernyak, "Process for preparing a crystalline form of halobetasol propionate." U.S. Patent US20070167420, issued July 19, 2007.
Receptor for glucocorticoids (GC). Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE), both for nuclear and mitochondrial DNA, and as a modulator of other transcription factors. Affects inflammatory responses, cellular proliferation and differentiation in target tissues. Could act as a coactivator for STAT5-dependent transcription upon grow...
Mohandas S, Rai R, Srinivas CR: Halobetasol versus clobetasol: a study of potency. Indian J Dermatol Venereol Leprol. 2009 Mar-Apr;75(2):186-7. [PubMed:19293512 ]
Hofmann TG, Hehner SP, Bacher S, Droge W, Schmitz ML: Various glucocorticoids differ in their ability to induce gene expression, apoptosis and to repress NF-kappaB-dependent transcription. FEBS Lett. 1998 Dec 28;441(3):441-6. [PubMed:9891987 ]