Mifepristone (RU-486) mechanism for medical abortion involves which receptor-level pharmacology?
- A Competitive partial agonist/antagonist at progesterone receptors (PR-A/PR-B) — blocks progesterone-mediated decidual support, increases myometrial prostaglandin sensitivity, and opens cervical collagen cross-links (cervical softening), requiring subsequent prostaglandin for complete uterine evacuation ✓
- B Direct inhibition of human chorionic gonadotrophin (hCG) receptor in the corpus luteum, stopping progesterone production
- C Inhibition of steroidogenic enzyme 17-hydroxylase in placental trophoblasts, reducing progesterone synthesis
- D Agonism of PGE2 receptors (EP2/EP4) in the myometrium, directly causing uterine contractions without progesterone blockade
Explanation
Mifepristone binds progesterone receptors PR-A and PR-B with high affinity (3-5 times higher than progesterone itself) but acts as a partial agonist/competitive antagonist, blocking progesterone's supportive effects on the decidua (causing endometrial breakdown) and on myometrial quiescence. Critically, mifepristone also upregulates uterine prostaglandin receptors and induces prostaglandin synthesis in decidual cells, synergising with exogenous misoprostol (a PGE1 analogue) administered 24-48 hours later. The combined effect causes cervical ripening, myometrial contractions, and complete evacuation. Mifepristone also has anti-glucocorticoid activity (blocks GR), which can elevate ACTH/cortisol.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.