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Namespace Prefixes

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Statements

Subject Item
n2:DB00591
rdf:type
n3:Drug
n3:description
A glucocorticoid derivative used topically in the treatment of various skin disorders. It is usually employed as a cream, gel, lotion, or ointment. It has also been used topically in the treatment of inflammatory eye, ear, and nose disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p732). It is also being investigated by Sivida and Alimera, under the brand name Medidur, as a sustained release intraocular implant for the treatment of diabetic macular edema.
n3:dosage
n15:271B51B4-363D-11E5-9242-09173F13E4C5 n15:271B51B5-363D-11E5-9242-09173F13E4C5 n15:271B51B6-363D-11E5-9242-09173F13E4C5 n15:271B51B7-363D-11E5-9242-09173F13E4C5 n15:271B51B8-363D-11E5-9242-09173F13E4C5 n15:271B51B9-363D-11E5-9242-09173F13E4C5 n15:271B51BA-363D-11E5-9242-09173F13E4C5 n15:271B51BB-363D-11E5-9242-09173F13E4C5 n15:271B51BC-363D-11E5-9242-09173F13E4C5 n15:271B51BD-363D-11E5-9242-09173F13E4C5 n15:271B51BE-363D-11E5-9242-09173F13E4C5 n15:271B51BF-363D-11E5-9242-09173F13E4C5 n15:271B51C0-363D-11E5-9242-09173F13E4C5
n3:generalReferences
# Goldstein DA, Godfrey DG, Hall A, Callanan DG, Jaffe GJ, Pearson PA, Usner DW, Comstock TL: Intraocular pressure in patients with uveitis treated with fluocinolone acetonide implants. Arch Ophthalmol. 2007 Nov;125(11):1478-85. Epub 2007 Oct 8. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/17923537 # Brumm MV, Nguyen QD: Fluocinolone acetonide intravitreal sustained release device--a new addition to the armamentarium of uveitic management. Int J Nanomedicine. 2007;2(1):55-64. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/17722513 # Jaffe GJ, Yang CH, Guo H, Denny JP, Lima C, Ashton P: Safety and pharmacokinetics of an intraocular fluocinolone acetonide sustained delivery device. Invest Ophthalmol Vis Sci. 2000 Oct;41(11):3569-75. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/11006254
n3:group
investigational approved
n3:halfLife
1.3-1.7 hours
n3:indication
For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also for the treatment of chronic non-infectious uveitis affecting the posterior segment of the eye (Retisert).
n3:manufacturer
n7:271B519A-363D-11E5-9242-09173F13E4C5 n7:271B519B-363D-11E5-9242-09173F13E4C5 n7:271B5198-363D-11E5-9242-09173F13E4C5 n7:271B5199-363D-11E5-9242-09173F13E4C5 n7:271B5196-363D-11E5-9242-09173F13E4C5 n7:271B5197-363D-11E5-9242-09173F13E4C5 n7:271B5195-363D-11E5-9242-09173F13E4C5 n7:271B51A2-363D-11E5-9242-09173F13E4C5 n7:271B51A3-363D-11E5-9242-09173F13E4C5 n7:271B51A0-363D-11E5-9242-09173F13E4C5 n7:271B51A1-363D-11E5-9242-09173F13E4C5 n7:271B519E-363D-11E5-9242-09173F13E4C5 n7:271B519F-363D-11E5-9242-09173F13E4C5 n7:271B519C-363D-11E5-9242-09173F13E4C5 n7:271B519D-363D-11E5-9242-09173F13E4C5 n7:271B51A4-363D-11E5-9242-09173F13E4C5 n7:271B51A5-363D-11E5-9242-09173F13E4C5
owl:sameAs
n28:DB00591 n30:DB00591
dcterms:title
Fluocinolone Acetonide
adms:identifier
n6:0168-0064-15 n8:D01825 n9:5980 n12:DB00591 n13:6215 n14:46506244 n16:Fluocinolone_acetonide n17:PA164754912
n3:mechanismOfAction
Fluocinolone Acetonide is a corticosteroid that 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. Cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In another 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. Like other glucocorticoid agents Fluocinolone acetonide acts as a physiological antagonist to insulin by decreasing glycogenesis (formation of glycogen). It also promotes the breakdown of lipids (lipolysis), and proteins, leading to the mobilization of extrahepatic amino acids and ketone bodies. This leads to increased circulating glucose concentrations (in the blood). There is also decreased glycogen formation in the liver.
n3:packager
n7:271B5188-363D-11E5-9242-09173F13E4C5 n7:271B5189-363D-11E5-9242-09173F13E4C5 n7:271B5186-363D-11E5-9242-09173F13E4C5 n7:271B5187-363D-11E5-9242-09173F13E4C5 n7:271B518A-363D-11E5-9242-09173F13E4C5 n7:271B518B-363D-11E5-9242-09173F13E4C5 n7:271B5184-363D-11E5-9242-09173F13E4C5 n7:271B5185-363D-11E5-9242-09173F13E4C5 n7:271B5183-363D-11E5-9242-09173F13E4C5 n7:271B5192-363D-11E5-9242-09173F13E4C5 n7:271B5193-363D-11E5-9242-09173F13E4C5 n7:271B5191-363D-11E5-9242-09173F13E4C5 n7:271B518F-363D-11E5-9242-09173F13E4C5 n7:271B5190-363D-11E5-9242-09173F13E4C5 n7:271B518D-363D-11E5-9242-09173F13E4C5 n7:271B518E-363D-11E5-9242-09173F13E4C5 n7:271B5194-363D-11E5-9242-09173F13E4C5 n7:271B518C-363D-11E5-9242-09173F13E4C5
n3:patent
n20:6217895
n3:routeOfElimination
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.
n3:synonym
Fluzon Tefunote Jellin 6alpha,9alpha-Difluoro-16alpha-hydroxyprednisolone 16,17-acetonide Fluocinolon acetonid Localyn Fluovitif Coriphate Omniderm Synamol Dermalar Acétonide de fluocinolone Acetónida de fluocinolona Fluocinoloni acetonidum Cortiplastol Fluocinolone 16,17-acetonide Flupollon Percutina Synandone Synemol Fluocinolonacetonid Synotic Retisert Prodermin Acetonido de fluocinolona Fluocet Derma-smoothe/fs Flucinar Iluvien Synalar Synandrone Synsac Fluonid Sinalar Fluotrex Radiocin Flucort 6alpha-Fluorotriamcinolone acetonide
n10:hasAHFSCode
n19:84-06-00
n3:mixture
n18:271B517F-363D-11E5-9242-09173F13E4C5 n18:271B5182-363D-11E5-9242-09173F13E4C5 n18:271B5180-363D-11E5-9242-09173F13E4C5 n18:271B5181-363D-11E5-9242-09173F13E4C5
n3:synthesisReference
Mills, J.S. and Bowers, A.; U.S. Patent 3,014,938; December 26, 1961; assigned to Syntex SA, Mexico.
n23:hasConcept
n24:M0008592
foaf:page
n26:retisert.htm n29:fluocinolone-acetonide-implant.html
n3:IUPAC-Name
n4:271B51C5-363D-11E5-9242-09173F13E4C5
n3:InChI
n4:271B51CB-363D-11E5-9242-09173F13E4C5
n3:Molecular-Formula
n4:271B51CA-363D-11E5-9242-09173F13E4C5
n3:Molecular-Weight
n4:271B51C7-363D-11E5-9242-09173F13E4C5
n3:Monoisotopic-Weight
n4:271B51C8-363D-11E5-9242-09173F13E4C5
n3:SMILES
n4:271B51C9-363D-11E5-9242-09173F13E4C5
n3:Water-Solubility
n4:271B51C3-363D-11E5-9242-09173F13E4C5
n3:logP
n4:271B51C1-363D-11E5-9242-09173F13E4C5 n4:271B51C4-363D-11E5-9242-09173F13E4C5 n4:271B51DC-363D-11E5-9242-09173F13E4C5
n3:logS
n4:271B51C2-363D-11E5-9242-09173F13E4C5
n10:hasATCCode
n11:S01BA15 n11:C05AA10 n11:S02BA08 n11:D07AC04
n3:H-Bond-Acceptor-Count
n4:271B51D1-363D-11E5-9242-09173F13E4C5
n3:H-Bond-Donor-Count
n4:271B51D2-363D-11E5-9242-09173F13E4C5
n3:InChIKey
n4:271B51CC-363D-11E5-9242-09173F13E4C5
n3:Polar-Surface-Area--PSA-
n4:271B51CD-363D-11E5-9242-09173F13E4C5
n3:Polarizability
n4:271B51CF-363D-11E5-9242-09173F13E4C5
n3:Refractivity
n4:271B51CE-363D-11E5-9242-09173F13E4C5
n3:Rotatable-Bond-Count
n4:271B51D0-363D-11E5-9242-09173F13E4C5
n3:absorption
Rapidly absorbed (15 minutes)
n3:affectedOrganism
Humans and other mammals
n3:casRegistryNumber
67-73-2
n3:category
n3:containedIn
n21:271B51AF-363D-11E5-9242-09173F13E4C5 n21:271B51B0-363D-11E5-9242-09173F13E4C5 n21:271B51AD-363D-11E5-9242-09173F13E4C5 n21:271B51AE-363D-11E5-9242-09173F13E4C5 n21:271B51B3-363D-11E5-9242-09173F13E4C5 n21:271B51B1-363D-11E5-9242-09173F13E4C5 n21:271B51B2-363D-11E5-9242-09173F13E4C5 n21:271B51A7-363D-11E5-9242-09173F13E4C5 n21:271B51A8-363D-11E5-9242-09173F13E4C5 n21:271B51A6-363D-11E5-9242-09173F13E4C5 n21:271B51AB-363D-11E5-9242-09173F13E4C5 n21:271B51AC-363D-11E5-9242-09173F13E4C5 n21:271B51A9-363D-11E5-9242-09173F13E4C5 n21:271B51AA-363D-11E5-9242-09173F13E4C5
n3:Bioavailability
n4:271B51D7-363D-11E5-9242-09173F13E4C5
n3:Ghose-Filter
n4:271B51D9-363D-11E5-9242-09173F13E4C5
n3:MDDR-Like-Rule
n4:271B51DA-363D-11E5-9242-09173F13E4C5
n3:Melting-Point
n4:271B51DB-363D-11E5-9242-09173F13E4C5
n3:Number-of-Rings
n4:271B51D6-363D-11E5-9242-09173F13E4C5
n3:Physiological-Charge
n4:271B51D5-363D-11E5-9242-09173F13E4C5
n3:Rule-of-Five
n4:271B51D8-363D-11E5-9242-09173F13E4C5
n3:Traditional-IUPAC-Name
n4:271B51C6-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-acidic-
n4:271B51D3-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-basic-
n4:271B51D4-363D-11E5-9242-09173F13E4C5