Antiprogesterone preparations such as gestrinone, anordin, and ORF 3971 were ineffective and dangerous in preventing the implantation of fertilized egg to prevent pregnancy. Trilostane and epostane, inhibitors of 3-beta-hydroxysteroid dehydrogenase, have not been approved in clinical practice. RU-486 is a synthetic 19-norsteroid 1st reported in 1982 with antiprogesterone and antiglucocorticoid activity. Its use in 7-8 weeks pre gnancy caused detachment of the placenta by competitive inhibition of progesterone receptors in the decidua. The resultant increased prostaglandin levels induced uterine contractions expulsing the conceptus. Administration during 22-25 days of menstruation caused the inhibition of the luteal body. RU-486 decreased the gonadotropin level in 3 healthy women on the 22nd day of menstruation irrespective of dosage. The reduction of luteinizing hormone (LH) secretion can be prevented by treatment with RU-486. The administration of 10 ngm/kg of RU-486 to monkeys resulted in significant elevation of ACTH (adrenocorticotropic hormone) and cortisol blood levels for 4 hours. The human dosage is 200 mg/day. 100 mg/day in women treated did not induce elevated ACTH, cortisol, or aldosterone blood levels. An 1982 experiment indicated a dose of 200 mg/day for 4 days for terminating a pregnancy of 6-10 weeks or a single dose of 400-600 mg. In 2nd trimester pregnancy RU-486 can be used for termination of fetal abnormality. It could also aid in term delivery by its ability to dilate the cervix. Early treatment in tubal (ectopic) pregnancy allowed removal of the conceptus without endangering a later pregnancy. As a post-coital agent administration of 5 mg/kg of RU-486 was effective in destroying the ovulated follicle. In breast cancer treatment RU-486 administration induced a positive response in 20% of patients.