In cervix tumor xenograft models treated with NSC 119875 alone, there is notable tumor growth inhibition compared to the control group. However, combining NSC 119875 with Mifepristone results in even more significant tumor weight reduction (p<0.05), achieving approximately a 50% decrease compared to individual treatments by the study's end^[2].

Adult male Sprague-Dawley rats undergo a 4-day binge-like ethanol (EtOH) administration regimen (3 to 5 g/kg, orally, every 8 hours), aimed at achieving peak blood EtOH levels (BELs) under 300 mg/dL. Subgroups of these animals receive subcutaneous injections of Mifepristone (20 or 40 mg/kg in peanut oil). While Mifepristone does not significantly alter the behavior of EtOH-naïve animals, pretreatment with Mifepristone (40 mg/kg) significantly reduces the severity of EtOH withdrawal. There is a notable interaction between diet and drug, F(5,55)=3.92, p<0.05, showing that EtOH-treated animals receiving either the vehicle or 20 mg/kg of Mifepristone exhibit significantly more signs of EtOH withdrawal compared to EtOH-naïve animals undergoing the same treatment. Crucially, 40 mg/kg of Mife

The identification of Mifepristone as the first competitive progesterone antagonist has sparked a vigorous pursuit of more potent and selective antiprogestins^[1].

Cell growth is assessed following a 4-day exposure to Mifepristone at 10 μM, which approximates achievable human plasma concentrations. In HeLa cells, the antiproliferative effect of NSC 119875 is enhanced when combined with Mifepristone. The IC50 for NSC 119875 in combination with Mifepristone is reduced to 14.2 μM, compared to 34.2 μM for NSC 119875 alone, indicating a roughly 2.5-fold increase in potency. Additionally, HeLa cells treated with Mifepristone show a twofold higher accumulation of intracellular NSC 119875, rising from 0.79 to 1.52 μg/mg of protein, a statistically significant difference (p=0.009) compared to NSC 119875 alone^[2].