Mifepristone (RU-486) acts as an anti-progestogen for medical abortion. Its mechanism of action at the cellular level is:
- A Inhibition of 17α-hydroxylase, reducing progesterone synthesis in the corpus luteum
- B Stimulation of prostaglandin F2α receptor on decidual cells, causing luteolysis
- C Inhibition of placental 11β-HSD, increasing fetal cortisol and inducing labour
- D Competitive antagonism at progesterone receptor (PR), blocking progesterone-induced gene transcription and sensitising myometrium to prostaglandins ✓
Explanation
Mifepristone is a potent competitive antagonist at the progesterone receptor (PR-A and PR-B). It binds the receptor with 3–5× higher affinity than progesterone without activating transcription, causing progesterone withdrawal. This leads to decidual degeneration, cervical softening (ripening), sensitisation of myometrium to prostaglandins, and (at high doses) anti-glucocorticoid effects. The combination with misoprostol exploits this prostaglandin sensitisation to achieve uterine evacuation. It does not act on 17α-hydroxylase (which would block synthesis), prostaglandin receptors directly, or 11β-HSD.
Reference: Shaw's Textbook of Gynaecology, 17th ed.
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Written and medically reviewed by the StethoPrep medical team.