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  • Title: The antiprogesterone steroid RU 486: a short pharmacological and clinical review, with emphasis on the interruption of pregnancy.
    Author: Garfield RE, Baulieu EE.
    Journal: Baillieres Clin Endocrinol Metab; 1987 Feb; 1(1):207-21. PubMed ID: 3297023.
    Abstract:
    In this review we have briefly outlined the clinical applications and mechanism of action of the progesterone antagonist RU 486. RU 486 has been successfully used in a variety of conditions to regulate the reproductive cycle and to control fertility in women. We suggest that the mechanism by which RU 486 acts during the cycle and early pregnancy is probably by affecting mainly the endometrium. During late pregnancy, the compound has significant effects on the myometrium including the induction of gap junctions between myometrium cells, which is required for muscle contractility during labour. The use of RU 486 has helped to demonstrate that progesterone is required for maintenance of the late stages of pregnancy in women. The mechanism of action and clinical uses of RU 486, the first antiprogesterone compound to be used clinically, are summarized, emphasizing those related to termination of pregnancy. RU-486 can be used to induce menses in sexually active women (still under investigation), to intercept pregnancy postcoitally in very young women occasionally and to terminate late pregnancy in case of a dead or abnormal fetus. Other possible uses include once-a-month pill, cancer treatment, ectopic pregnancy and Cushing's syndrome. RU-486 has antiglucocorticoid action, but not at doses active on the uterus. RU-486 acts by substituting for progesterone at its receptor-binding site, while preventing activation of the receptor complex. Hormonal studies indicate that its action on the uterus is directly on the endometrium, not mediated by hormones. The effectiveness of RU-486 on all species studied has contributed to our understanding of progesterone's effects. In early pregnancy, RU-486 acts by causing release of prostaglandins, but in late pregnancy, the drug acts by blocking the maintenance of uterine quiescence by progesterone. This need for progesterone was, until the advent of RU-486, a controversial issue in women. Rhythmic, coordinated uterine contractions require synthesis of gap junctions to transmit electrical impulses between myometrial cells, and these develop rapidly after administration of RU-486. Whether induction of gap junctions is the primary action of RU-486 in late pregnancy remains to be seen.
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