161115-59-9
基本信息
環(huán)索奈德雜質(zhì)B
去異丁酰環(huán)索奈德
去異丁基環(huán)索奈德
環(huán)索奈德EP雜質(zhì)B
去異丁酸酯環(huán)索奈德
去甲丙?;h(huán)索奈德
化合物 T13646
環(huán)索奈德雜質(zhì)B(EP)
環(huán)索奈德雜質(zhì)B EP標準品
161115-59-9
Ciclesonide impurity B
Norpropionyl cyclosonide
Ciclesonide EP Impurity B
Desisobutyryl Ciclesonide
Ciclesonide impurity B CRS
21-Desisobutyryl Ciclesonide
Ciclesonide active principle
Desisobutyryl-ciclesonide (CIC-AP
物理化學性質(zhì)
常見問題列表
Glucocorticoid receptor
Ciclesonide, an inhaled corticosteroid with almost no affinity for the glucocorticoid receptor, is highly effective in downregulating in vitro pro-inflammatory activities of airway parenchymal cells when converted into the active metabolite Desisobutyryl-ciclesonide. Peripheral blood mononuclear cell proliferation to C. albicans is dose-dependently inhibited by 0.3-3.0 μM Ciclesonide and Desisobutyryl-ciclesonide but inhibition by Desisobutyryl-ciclesonide is higher. A significant proliferation to PhlP5 is observed only in cultures from atopic subjects: an effective downregulation is already detected at 0.03 μM Ciclesonide and 0.003 μM Desisobutyryl-ciclesonide (complete inhibition at 3 μM Ciclesonide and 0.03 μM Desisobutyryl-ciclesonide). 3 μM Ciclesonide and Desisobutyryl-ciclesonide reduce the PhlP5 -specific T-cell blast proliferation and interleukin 4-producing cell proportion. In PBMCs cultures from atopic patients, both Ciclesonide (CIC) and Desisobutyryl-ciclesonide (des-CIC) induce a dose-dependent downregulation of PhlP5 -induced proliferation. The effect is already significantat 0.03 μM Ciclesonide and at 0.003 μM Desisobutyryl-ciclesonide (p<0.001, each comparison),with an early complete inhibition observed at 3μM Ciclesonide and at 0.03 μM Desisobutyryl-ciclesonide. The inhibitory activity toward PhlP5 -induced PBMC proliferation is higher for Desisobutyryl-ciclesonide than for Ciclesonide at 0.003 μM (p<0.05), 0.03 μM (p<0.001) and 0.3 μM (p<0.05).