The corticosteroids, such as prednisolone and methylprednisolone, provide diverse antiinflammatory and immunosuppressive effects which typically show responses with slow onset and prolonged duration. This report summarizes modeling efforts which are successful in describing such steroid effects. Clinical effects with such a pattern, including adrenal suppression and altered trafficking of basophils and helper T-cells, can be related to plasma drug concentrations by models containing an inhibition function and differential equations for controlling input and disposition of the response variable. Some responses have circadian-controlled inputs which add time-dependent complexities to the models. Kinetic/dynamic data for several corticosteroid effects yield IC50 values which agree well with receptor KD values. A relationship of linear AUC of effect versus log AUC of steroid in plasma is found with these models over a large range of doses. Gene-mediated effects of corticosteroids are initiated by receptor-binding which causes a cascade effect altering DNA transcription, RNA, mRNA and proteins or enzymes accounting for drug effects. Models for such behavior have been developed in animals for hepatic tyrosine aminotransferase (TAT) enzyme activity. Studies with methylprednisolone formulated in liposomes show tissue sequestration of steroid, prolonged receptor-binding and extended inhibition of splenocyte proliferation. The data and models usually show good correspondence of the AUC of receptor occupancy with the AUC of pharmacologic response.