Micromolar concentrations of the parent compound can be found in the blood plasma within the first hour after oral administration. Trials have shown that the pharmacokinetics of mifepristone follows two distinct patterns depending on whether a high or low dose is administered. At low doses (50mg), the pharmacokinetics follows an open, two-compartment model with a long half-life of over 27hrs. With higher doses (100-800mg) there is an initial redistribution phase of 6-10hrs, followed by zero-order kinetics of up to 24hrs or more.

It is believed that the serum binding protein for mifepristone in man, AAG (&-1-acid glycoprotein), has a binding capacity lower than the therapeutic dose. It is thought that at high doses the serum binding sites become saturated and hence the remaining mifepristone starts to be extravasated into the tissues. This would explain the flattened serum peak concentrations of mifepristone at higher doses. The return of the drug form the tissues back to the circulation thereafter explains the zero-order kinetics. The higher the dose exceeding the AAG binding capacity, the greater is the extravasation, and the longer is the zero-order pharmacokinetics substantiated by the return of mifepristone from the tissues into the circulation. When AAG becomes saturated, mifepristone and it's metabolites bind to another serum binding protein, albumin. It is believed that the 50mg dose of mifepristone dose not saturate the AAG binding sites and hence first-order kinetics are observed.