The steroidal derivative RU 486 (17 beta-hydroxy-11 beta-(4-dimethyl-aminophenyl 1)-17 alpha-(prop-1-ynyl)-estra-4,9-dien-3-one) is the first potent antiprogestin in medical use. Acting reversibly at the molecular level of receptor binding, RU 486 blocks progesterone action and allows endocrine functions to return quickly to normal after its use. However, target cells dynamics that depend upon a continuity of progesterone action will be irreversibly disrupted. In normal women RU 486 acts during the luteal phase in the endometrium, provoking bleeding, and also decreases LH secretion which results in luteolysis. In pregnant women, if affects the decidual, increases myometrial contractility and ripening of the cervix, and ultimately leads to termination of pregnancy. Detachment of the trophoblast leads to a fall in chronic gonadotrophin. Clinical studies indicate that RU 486 can be a very efficient agent for the termination of early pregnancy, and as a postcoital menstrual regulator. The failures observed when RU 486 is given alone may be overcome by the additional use of oxytocics. A small amount of prostaglandin given at the end of RU 486 treatment gives satisfactory results at up to 8 weeks of amenorrhea. Treatment with RU 486 is short term, and apparently has no significant side-effects despite the compound's antiglucocorticosteroid activity.