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Namespace Prefixes

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Statements

Subject Item
n2:DB01047
rdf:type
n3:Drug
n3:description
A topical glucocorticoid used in the treatment of eczema. [PubChem]
n3:dosage
n11:271B59CB-363D-11E5-9242-09173F13E4C5 n11:271B59CC-363D-11E5-9242-09173F13E4C5 n11:271B59CD-363D-11E5-9242-09173F13E4C5 n11:271B59CE-363D-11E5-9242-09173F13E4C5 n11:271B59CA-363D-11E5-9242-09173F13E4C5 n11:271B59CF-363D-11E5-9242-09173F13E4C5 n11:271B59D0-363D-11E5-9242-09173F13E4C5
n3:group
investigational approved
n3:indication
A topical anti-inflammatory product for the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses.
owl:sameAs
n25:DB01047 n27:DB01047
dcterms:title
Fluocinonide
adms:identifier
n6:DB01047 n9:9265 n12:PA449664 n14:9642 n15:D00325 n16:0168-0139-15 n18:46504523 n29:Fluocinonide
n3:mechanismOfAction
Fluocinonide is a potent glucocorticoid steroid used topically as anti-inflammatory agent for the treatment of skin disorders such as eczema. It relieves itching, redness, dryness, crusting, scaling, inflammation, and discomfort. Fluocinonide 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
n13:271B59A3-363D-11E5-9242-09173F13E4C5 n13:271B59A4-363D-11E5-9242-09173F13E4C5 n13:271B59A1-363D-11E5-9242-09173F13E4C5 n13:271B59A2-363D-11E5-9242-09173F13E4C5 n13:271B599F-363D-11E5-9242-09173F13E4C5 n13:271B59A0-363D-11E5-9242-09173F13E4C5 n13:271B599D-363D-11E5-9242-09173F13E4C5 n13:271B599E-363D-11E5-9242-09173F13E4C5 n13:271B599B-363D-11E5-9242-09173F13E4C5 n13:271B599C-363D-11E5-9242-09173F13E4C5 n13:271B5999-363D-11E5-9242-09173F13E4C5 n13:271B599A-363D-11E5-9242-09173F13E4C5 n13:271B5997-363D-11E5-9242-09173F13E4C5 n13:271B5998-363D-11E5-9242-09173F13E4C5 n13:271B59AF-363D-11E5-9242-09173F13E4C5 n13:271B59AD-363D-11E5-9242-09173F13E4C5 n13:271B59AE-363D-11E5-9242-09173F13E4C5 n13:271B59AB-363D-11E5-9242-09173F13E4C5 n13:271B59AC-363D-11E5-9242-09173F13E4C5 n13:271B59A9-363D-11E5-9242-09173F13E4C5 n13:271B59AA-363D-11E5-9242-09173F13E4C5 n13:271B59A7-363D-11E5-9242-09173F13E4C5 n13:271B59A8-363D-11E5-9242-09173F13E4C5 n13:271B59A5-363D-11E5-9242-09173F13E4C5 n13:271B59A6-363D-11E5-9242-09173F13E4C5
n3:patent
n17:7220424 n17:6765001
n3:routeOfElimination
Corticosteroids are metabolized primarily in the liver and are then excreted by the kidneys. Corticosteroids are metabolized primarily in the liver and are then excreted by the kidneys.
n3:synonym
Fluocinonidum Lidex Fluocinonido Fluocinonide Vanos
n3:toxicity
Side effects may include acne-like eruptions, burning, dryness, excessive hair growth, infection of the skin, irritation, itching, lack of skin color, prickly heat, skin inflammation, skin loss or softening, stretch marks
n22:hasAHFSCode
n31:84-06-00
n3:mixture
n28:271B5995-363D-11E5-9242-09173F13E4C5 n28:271B5996-363D-11E5-9242-09173F13E4C5
n3:synthesisReference
US. Patent 3,197,469.
n20:hasConcept
n21:M0008593
foaf:page
n8:fluocinonide-cream.html n19:lid1227.shtml n26:fluocin.htm
n3:IUPAC-Name
n4:271B59D5-363D-11E5-9242-09173F13E4C5
n3:InChI
n4:271B59DB-363D-11E5-9242-09173F13E4C5
n3:Molecular-Formula
n4:271B59DA-363D-11E5-9242-09173F13E4C5
n3:Molecular-Weight
n4:271B59D7-363D-11E5-9242-09173F13E4C5
n3:Monoisotopic-Weight
n4:271B59D8-363D-11E5-9242-09173F13E4C5
n3:SMILES
n4:271B59D9-363D-11E5-9242-09173F13E4C5
n3:Water-Solubility
n4:271B59D3-363D-11E5-9242-09173F13E4C5 n4:271B59EB-363D-11E5-9242-09173F13E4C5
n3:logP
n4:271B59ED-363D-11E5-9242-09173F13E4C5 n4:271B59D4-363D-11E5-9242-09173F13E4C5 n4:271B59D1-363D-11E5-9242-09173F13E4C5
n3:logS
n4:271B59D2-363D-11E5-9242-09173F13E4C5
n22:hasATCCode
n23:D07AC08 n23:C05AA11
n3:H-Bond-Acceptor-Count
n4:271B59E1-363D-11E5-9242-09173F13E4C5
n3:H-Bond-Donor-Count
n4:271B59E2-363D-11E5-9242-09173F13E4C5
n3:InChIKey
n4:271B59DC-363D-11E5-9242-09173F13E4C5
n3:Polar-Surface-Area--PSA-
n4:271B59DD-363D-11E5-9242-09173F13E4C5
n3:Polarizability
n4:271B59DF-363D-11E5-9242-09173F13E4C5
n3:Refractivity
n4:271B59DE-363D-11E5-9242-09173F13E4C5
n3:Rotatable-Bond-Count
n4:271B59E0-363D-11E5-9242-09173F13E4C5
n3:absorption
The extent of percutaneous absorption of topical corticosteroids is determined by many factors including the vehicle, the integrity of the epidermal barrier, and the use of occlusive dressings. In general, percutaneous absorption is minimal.
n3:affectedOrganism
Humans and other mammals
n3:casRegistryNumber
356-12-7
n3:category
n3:containedIn
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n3:Bioavailability
n4:271B59E7-363D-11E5-9242-09173F13E4C5
n3:Ghose-Filter
n4:271B59E9-363D-11E5-9242-09173F13E4C5
n3:MDDR-Like-Rule
n4:271B59EA-363D-11E5-9242-09173F13E4C5
n3:Melting-Point
n4:271B59EC-363D-11E5-9242-09173F13E4C5
n3:Number-of-Rings
n4:271B59E6-363D-11E5-9242-09173F13E4C5
n3:Physiological-Charge
n4:271B59E5-363D-11E5-9242-09173F13E4C5
n3:Rule-of-Five
n4:271B59E8-363D-11E5-9242-09173F13E4C5
n3:Traditional-IUPAC-Name
n4:271B59D6-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-acidic-
n4:271B59E3-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-basic-
n4:271B59E4-363D-11E5-9242-09173F13E4C5