["Endogenous Cushing's syndrome is caused by chronically elevated levels of cortisol. Mifepristone, a glucocorticoid receptor (GR) antagonist, is approved for the treatment of Cushing's syndrome. Currently there is an unmet clinical need for a direct biochemical method for monitoring the immediate effectiveness of mifepristone in patients with Cushing's syndrome. The glucocorticoid induction of FK506-binding protein 5 (FKBP5) expression is rapid and has been shown to be attenuated by GR antagonists in a range of in vitro and in vivo models.", 'The objective of the study was to develop a quantitative PCR assay for FKBP5 mRNA expression in blood and apply it to measure the inhibition of glucocorticoid-induced FKBP5 expression by GR antagonists in healthy human subjects.', 'Briefly, blood samples were acquired from a phase I study in which healthy human subjects were administered either a single dose of the GR agonist prednisone with and without coadministration of a single oral dose of mifepristone or glucocorticoid receptor antagonist (CORT125134) or multiple daily doses of CORT125134 over 14 days with coadministration of prednisone with the final dose. FKBP5 mRNA levels were analyzed by quantitative PCR in blood samples collected at selected time points.', 'The study was conducted at Quotient Clinical (Nottingham, United Kingdom).', 'Oral administration of the glucocorticoid prednisone to healthy human subjects resulted in a time-dependent increase of FKBP5 mRNA to peak levels of approximately 12-fold compared with unstimulated levels within 4 hours of steroid administration, followed by a reduction to baseline levels within 24 hours. Furthermore, oral administration of mifepristone or the selective GR antagonist CORT125134 had the desired effect of inhibiting prednisone-mediated activation of GR as seen by a reduction of FKBP5 mRNA levels.'] Does fKBP5 mRNA Expression be a Biomarker for GR Antagonism?