Fenspiride hydrochloride

Research use only, not for human use.

Fenspiride is an oxazolidinone spiro compound used as a drug in the treatment of certain respiratory diseases.

Fenspiride is an oxazolidinone spiro compound used as a drug in the treatment of certain respiratory diseases. It is approved for use in Russia for the treatment of acute and chronic inflammatory diseases of ENT organs and the respiratory tract (like rhinopharyngitis, laryngitis, tracheobronchitis, otitis and sinusitis), as well as for maintenance treatment of asthma. (In Vitro):Fenspiride (around 100 μM) inhibits histamine-induced contraction of isolated guinea pig trachea.Fenspiride (≤1000 μM) produces less than 25% inhibition of phosphodiesterase 1 and phosphodiesterase 2 activities.(In Vivo):Fenspiride (60 mg/kg; p.o. for 3 days) reduces the lipopolysaccharide-induced early rise of tumor necrosis factor concentrations in serum and in the bronchoalveolar lavage fluid (BALF) of the model of endotoxemia.Fenspiride (60 mg/kg; p.o. for 3 days) reduces the lipopolysaccharide-induced primed stimulation of alveolar macrophages.Fenspiride (60 mg/kg; p.o. for 3 days) reduces the increased serum concentrations of extracellular type II phospholipase A 2, the intensity of the neutrophilic alveolar invasion and the lethality due to the lipopolysaccharide.

Fenspiride (around 100 μM) inhibits histamine-induced contraction of isolated guinea pig trachea.Fenspiride (≤1000 μM) produces less than 25% inhibition of phosphodiesterase 1 and phosphodiesterase 2 activities.

Fenspiride (60 mg/kg; p.o. for 3 days) reduces the lipopolysaccharide-induced early rise of tumor necrosis factor concentrations in serum and in the bronchoalveolar lavage fluid (BALF) of the model of endotoxemia.Fenspiride (60 mg/kg; p.o. for 3 days) reduces the lipopolysaccharide-induced primed stimulation of alveolar macrophages.Fenspiride (60 mg/kg; p.o. for 3 days) reduces the increased serum concentrations of extracellular type II phospholipase A 2, the intensity of the neutrophilic alveolar invasion and the lethality due to the lipopolysaccharide. Animal Model:Lipopolysaccharide-treated Male Dunkin-Hartley guinea-pigs weighing 400-600 g Dosage:60 mg/kg Administration:Orally for 3 days; pretreated Result:Reduced the lipopolysaccharide-induced early rise of tumor necrosis factor concentrations in serum (4.2 vs. 2.3 ng/ml) and in the BALF (55.7 vs. 19.7 ng/ml).Reduced the lipopolysaccharide-induced primed stimulation of alveolar macrophages, (1551.5 vs 771.5 pg/μg protein, P<0.05 for thromboxane B2 and 12.6 vs. 3.6 pg/μg protein, P<0.05 for leukotriene C4). Reduced the increased serum concentrations of extracellular type II phospholipase A 2 (3.9 vs. 1.2 nmol/ml per min), the intensity of the neutrophilic alveolar invasion and the lethality due to the lipopolysaccharide.

Decaspiride

Angiogenesis

PDE

PDE3| PDE4

Inflammation/Immunology

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5053-08-7

296.79

C15H20N2O2·HCl

>98% (HPLC)

Water: 59 mg/mL (198.79 mM); DMSO: 9 mg/mL (30.32 mM)

C1CN(CCC12CNC(=O)O2)CCC3=CC=CC=C3.Cl

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(-20℃)

With Ice Pack

≥ 2 years