@article {Edsb{\"a}cker403, author = {S Edsb{\"a}cker and P Andersson and C Lindberg and J Paulson and A Ryrfeldt and A Thal{\'e}n}, title = {Liver metabolism of budesonide in rat, mouse, and man. Comparative aspects.}, volume = {15}, number = {3}, pages = {403--411}, year = {1987}, publisher = {American Society for Pharmacology and Experimental Therapeutics}, abstract = {The metabolism of budesonide, (22RS)-16 alpha, 17 alpha-butylidenedioxy-11 beta,21-dihydroxypregna-1,4-diene- 3,20-dione, was studied in the 9000g supernatant fraction of livers from rat, mouse, and man. The two budesonide C-22 epimers produced different metabolites. This was explained by substrate-selective oxidation of the nonsymmetric 16 alpha, 17 alpha-acetal substituent. Epimer 22R gave 16 alpha-hydroxyprednisolone, while epimer 22S produced a metabolite tentatively identified as 23-hydroxybudesonide. Otherwise, budesonide followed the general metabolic pathways reported for synthetic glucocorticoids. Thus, oxidative metabolism predominated, 6 beta-hydroxybudesonide and delta 6-budesonide being identified in all investigated species. Reductive metabolism, giving 4,5 beta-dihydrobudesonide and 3,4,5 beta-tetrahydrobudesonide, was most pronounced in the rat. Rates and routes of budesonide metabolism were most similar in mouse and human livers. This implies that the mouse is a more relevant species than the rat in studies of the pharmacology and toxicology of budesonide.}, issn = {0090-9556}, URL = {https://dmd.aspetjournals.org/content/15/3/403}, eprint = {https://dmd.aspetjournals.org/content/15/3/403.full.pdf}, journal = {Drug Metabolism and Disposition} }