The steroidal derivative RU 486 (17 beta-hydroxy-11 beta-(4-dimethyl-aminophenyl)-17 alpha-(prop-1-ynyl) ester-4, 9-dien-3-one) is the first potent antiprogestin to be used clinically. RU 486 blocks the action of progesterone by a reversible inhibition of the action of progesterone on its own receptors. This reversibility allows endocrine functions to return quickly to normal after discontinuation of treatment. However, target cells which depend upon a continuity of progesterone action will be irreversibly disrupted by receptor blockade. In normal women, RU 486 acts during the luteal phase in the endometrium, provoking bleeding, and decreasing pituitary luteinizing hormone (LH) secretion and hence luteolysis. In pregnant women, it affects the decidua, increases myometrial contractility and ripening of the cervix and ultimately leads to termination of pregnancy. Detachment of the trophoblast leads to a further fall in gonadotropin production. Clinical studies indicate that RU 486 can be a very efficient agent for the termination of early pregnancy, and as a postcoital menstrual regulator. In about 20% of cases when RU 486 is given alone, termination of pregnancy fails. This can be overcome by taking in addition a small amount of prostaglandin.