. . . . . . . . "Fried, J.; U.S. Patent 2,852,51 September 16,1958; assigned to Olin Mathieson Chemical Corporation. \u2028Lincoln, F.H. Jr., Schneider, W.P. and Spero, G.B.; US. Patent 2,867,637; January 6, 1959; assigned to The Upjohn Company\u2028. Lincoln, F.H. Jr., Schneider, W.P. and Spero, G.B.; U.S. Patent 2,867,638; January 6, 1959; assigned to The Upjohn Company. \u2028Magerlein, B.J., Kagan, F. and Schlagel, C.A.; U.S. Patent 3,038,914; June 12, 1962; assigned to The Upjohn Company."@en . . . . "NSC 33001"@en . "Fluor-OP"@en . "Side effects may include acute anterior uveitis and perforation of the globe. Keratitis, conjunctivitis, corneal ulcers, mydriasis, conjunctival hyperemia, loss of accommodation and ptosis have occasionally been reported following local use of corticosteroids. LD₅₀ = 234 mg/kg (rats)"@en . . . . . . . . "Fluorometholonum"@en . . . . . . . . . "Fluorometholon"@en . . "For the ophthalmic treatment of corticosteroid-responsive inflammation of the palpebral and bulbar conjunctiva, cornea and anterior segment of the globe."@en . . " "@en . "Fluorometolona"@en . . . . "approved"@en . . . . . . . . . . . . . . . "Oxylone"@en . . "Fluorometholone"@en . . . . . . "Humans and other mammals"@en . . . . . . . . . "(1R,2S,8S,10S,11S,14R,15S,17S)-14-acetyl-1-fluoro-14,17-dihydroxy-2,8,15-trimethyltetracyclo[8.7.0.02,7.011,15]heptadeca-3,6-dien-5-one"@en . . . . . . . "Fluorometholone"@en . "9-Fluoro-11beta,17-dihydroxy-6alpha-methylpregna-1,4-diene-3,20-dione"@en . "A glucocorticoid employed, usually as eye drops, in the treatment of allergic and inflammatory conditions of the eye. It has also been used topically in the treatment of various skin disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p732)"@en . . . . . . "There is no generally accepted explanation for the mechanism of action of ocular corticosteroids. 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. Their primary target is 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."@en . . . . "Fluorom\u00E9tholone"@en . . . . . . . . . . . . . . . . " "@en . . "426-13-1"@en . . . . . . .