Differential binding in vitro to glucocorticoid receptors of deflazacort and prednisolone

Abstract

Deflazacort, a new steroidal anti-inflammatory agent, has remarkable glucocorticoid activity in both animals and humans. Its biologically active form, 21-desacetyl deflazacort, displaces [3H]dexamethasone from its cytosol receptor sites in rat kidney, thymus and liver in vitro. Although less active than prednisolone in its binding to glucocorticoid receptors, deflazacort 'stabilizes' the resulting steroid-receptor complex more effectively than the former in the kidney and thymus but not in the liver. This property might explain the greater activity of deflazacort than of prednisolone in the rat.