Introduction:Basic information about CAS 77326-96-6|FLUNISOLIDE, including its chemical name, molecular formula, synonyms, physicochemical properties, and safety information, etc.
| Common Name | FLUNISOLIDE |
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| CAS Number | 77326-96-6 | Molecular Weight | 887.01100 |
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| Density | 1.33 g/cm3 | Boiling Point | 581.8ºC at 760 mmHg |
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| Molecular Formula | C48H64F2O13 | Melting Point | / |
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| MSDS | / | Flash Point | 305.7ºC |
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Names
| Name | Flunisolide [anhydrous] |
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FLUNISOLIDE BiologicalActivity
| Description | Flunisolide hemihydrate is a corticosteroid, which is an orally active glucocorticoid receptor activator with anti-inflammatory activity. Flunisolide hemihydrate can induce eosinophil apoptosis, and is used for the research of asthma or rhinitis, and inflammation[1][2]. |
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| Related Catalog | Signaling Pathways >>Apoptosis >>ApoptosisResearch Areas >>EndocrinologyResearch Areas >>Inflammation/ImmunologySignaling Pathways >>GPCR/G Protein >>Glucocorticoid Receptor |
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| In Vitro | Flunisolide hemihydrate (0.1-10 μM, 1 h) inhibits lung fibroblast (Isolated from lung) activation[1]. Flunisolide hemihydrate (10 μM, 24 h) reduces MMP-9, TIMP-1, TGF-β and fibronectin release by sputum cells (isolated frommild to moderate asthmatics), and induces sputum eosinophil apoptosis[2]. Flunisolide hemihydrate (0.1-10 µM μM, 24 h) effectively inhibits ICAM-1 expression and GM-CSF and IL-5 release induced by TNF-alpha in BEAS-2B cells[3]. Flunisolide hemihydrate (115 µM, 0-3 h) can be transported in a polarized way in the apical (ap) to basolateral (bl) direction in Calu-3 cells and is demonstrated to be ATP-dependent[4]. Apoptosis Analysis[2] Cell Line: Eosinophil Concentration: 10 μM Incubation Time: 24 h Result: Induced sputum eosinophil apoptosis. |
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| In Vivo | Flunisolide hemihydrate (Intranasal administration, 0.3-10 µg/mouse, daily, from days 21–27) inhibits lung inflammation, fibrosis, and airway hyper-reactivity, also improves clearance of silica particles from the lungs in silicotic mice[1]. Flunisolide hemihydrate (Intranasal administration, 0.3-10 µg/mouse, daily, from days 21–27) inhibits silica-induced macrophage and myofibroblast accumulation in the lung tissue[1]. Animal Model: Male Swiss Webster mice (instilled, intranasally, with crystalline silica, 10 mg/50 µL, particle size 0.5-10 µm)[1] Dosage: 0.3-10 µg/mouse, daily, from days 21–27 Administration: Intranasal administration Result: Reduced both granulomatous response, collagen deposition, concerning granuloma formation caused by silica particles. Reduced the number of F4/80 and α-SMA positive cells. |
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| References | [1]. Tatiana Paula Teixeira Ferreira, et al. Intranasal Flunisolide Suppresses Pathological Alterations Caused by Silica Particles in the Lungs of Mice. Front Endocrinol (Lausanne). 2020 Jun 17;11:388. [2]. M Profita, et al. In vitro effects of flunisolide on MMP-9, TIMP-1, fibronectin, TGF-beta1 release and apoptosis in sputum cells freshly isolated from mild to moderate asthmatics. Allergy. 2004 Sep;59(9):927-32. [3]. S Boero, et al. Modulation by flunisolide of tumor necrosis factor-alpha-induced stimulation of airway epithelial cell activities related to eosinophil inflammation. J Asthma. 2010 May;47(4):381-7. [4]. B I Florea, et al. Evidence of P-glycoprotein mediated apical to basolateral transport of flunisolide in human broncho-tracheal epithelial cells (Calu-3). Br J Pharmacol. 2001 Dec;134(7):1555-63. |
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Chemical & Physical Properties
| Density | 1.33 g/cm3 |
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| Boiling Point | 581.8ºC at 760 mmHg |
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| Molecular Formula | C48H64F2O13 |
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| Molecular Weight | 887.01100 |
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| Flash Point | 305.7ºC |
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| Exact Mass | 886.43100 |
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| PSA | 195.35000 |
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| LogP | 4.48510 |
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| InChIKey | MIXMJCQRHVAJIO-TZHJZOAOSA-N |
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| SMILES | CC1(C)OC2CC3C4CC(F)C5=CC(=O)C=CC5(C)C4C(O)CC3(C)C2(C(=O)CO)O1.CC1(C)OC2CC3C4CC(F)C5=CC(=O)C=CC5(C)C4C(O)CC3(C)C2(C(=O)CO)O1.O |
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| Storage condition | -20°C |
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Safety Information
| RIDADR | NONH for all modes of transport |
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