199331-40-3

199331-40-3 structure

Name: etiprednol dicloacetate
Chemical Name: etiprednol dicloacetate
CAS Number: 199331-40-3
Molecular Formula: C₂₄H₃₀Cl₂O₆
Molecular Weight: 485.39700
Catalog: Research Areas Inflammation/Immunology
Create Date: 2018-01-26 20:25:51
Modify Date: 2024-01-30 10:01:11
Etiprednol dicloacetate (BNP 166) is an anti-inflammatory agent. Etiprednol dicloacetate inhibits eosinophil accumulation. Etiprednol dicloacetate can be used in the research of inflammatory airway diseases, such as asthma[1][2].

Name	etiprednol dicloacetate
Synonyms	etiprednol dichloroacetate EDA BNP-166 (8S,9S,10R,11S,13S,14S,17R)-17-(2,2-Dichloro-acetoxy)-11-hydroxy-10,13-dimethyl-3-oxo-6,7,8,9,10,11,12,13,14,15,16,17-dodecahydro-3H-cyclopenta[a]phenanthrene-17-carboxylic acid ethyl ester etiprednol dichloacetate ethyl 17α-dichloroacetoxy-11β-hydroxyandrosta-1,4-dien-3-one-17β-carboxylate

Description	Etiprednol dicloacetate (BNP 166) is an anti-inflammatory agent. Etiprednol dicloacetate inhibits eosinophil accumulation. Etiprednol dicloacetate can be used in the research of inflammatory airway diseases, such as asthma[1][2].
Related Catalog	Signaling Pathways >> Others >> Others Research Areas >> Inflammation/Immunology
In Vitro	Etiprednol dicloacetate (1 nM-1 μM) inhibits LPS-induced TNF-α production by human blood[1].
In Vivo	Etiprednol dicloacetate (0-100 μg/kg, intranasal inhalation) attenuates peribronchial eosinophilia in the lung of the allergen sensitized and challenged rats[1]. Etiprednol dicloacetate (0.1 μg/kg, intranasal inhalation) inhibits eosinophil accumulation in rats (antigen-induced airway eosinophil infiltration)[3]. Etiprednol dicloacetate (0-20 mg/kg, p.o., 28 days) is well tolerated in rats and dogs[2]. Animal Model: Allergen sensitized and challenged Brown Norway rats[1] Dosage: 0.1, 1, 10, and 100 μg/kg Administration: Intranasal inhalation Result: Decreased the number of eosinophils at the perivascular area of the lung tissue. Decreased the number of mucus secreting cells and antigen-induced formation of perivascular edema.