Desisobutyryl-ciclesonide has an affinity for glucocorticoid receptors. Desisobutyryl-ciclesonide is the active metabolite of Ciclesonide.

Ciclesonide is an inhaled glucocorticoid with little affinity for glucocorticoid receptors. When converted into an active metabolite Desisobutyryl-ciclesonide, it is very effective in down-regulating the proinflammatory activity of airway parenchymal cells in vitro. 0.3-3.0μMCiclesonide and Desisobutyryl-Ciclesonide dose-dependently inhibited the proliferation of peripheral blood mononuclear cells to Candida albicans, but Desisobutyryl-Ciclesonide had a higher inhibitory effect. Significant proliferation of PhlP5 was observed only in cultures of ectopic subjects: effective downregulation has been detected at 0.03 μM Ciclesonide and 0.003 μM Desisobutyryl-Ciclesonide (at 3 μM Ciclesonide and 0.03 μM Desisobutyryl-ciclesonide Completely suppressed). 3μM Ciclesonide and Desisobutyryl-ciclesonide reduced the proportion of PhlP5-specific T cell embryonic cell proliferation and interleukin 4 producing cells. In PBMC cultures of atopic patients, both Csonide (CIC) and desisobutyryl-Crossonide (des-CIC) induced dose-dependent down-regulation of PhlP5-induced proliferation. At 0.03 μM Ciclesonide and 0.003 μM Desisobutyryl-Ciclesonide (p <0.001, each comparison), the effect is already significant (an earlier complete inhibition was observed at 3 μMCiclesonide and 0.03 μMDesisobutyryl-Ciclesonide. At 0.003 μM ( p<0.05), 0.03μM (p<0.001) and 0.3μM (p<0.05), the inhibitory activity of desisobutyryl-ciclesonide on PhlP5-induced PBMC proliferation was higher than that of Ciclesonide.