Pharmacodynamics As an SPRM,<unk>  has partial agonistic as well as antagonistic effects on the progesterone receptor.<unk>  exhibits similar potency to antagonize progesterone receptor as mifepristone in vitro. It also binds to the androgen receptor and the glucocorticoid receptor, but is only a weak antiandrogen and antiglucocorticoid relative to flutamide and mifepristone, respectively.<unk>  has no relevant affinity to the estrogen and mineralocorticoid receptors. Phase II clinical trials suggest that the mechanism might consist of blocking or delaying ovulation and of delaying the maturation of the endometrium. Pharmacokinetics In animal studies, the drug was quickly and nearly completely absorbed from the gut. Intake of food delays absorption, but it is not known whether this is clinically relevant.<unk>  is metabolized in the liver, most likely by CYP3A4, and to a small extent by CYP1A2 and CYP2D6. The two main metabolites have been shown to be pharmacologically active, but less than the original drug. The main excretion route is via the feces.
Ulipristal acetate
Macimorelin
Linagliptin
Saxagliptin
Sitagliptin
Liraglutide
Vildagliptin
Lumacaftor