Ulipristal acetate (UPA), used both as emergency contraception and for uterine fibroids, acts as a selective progesterone receptor modulator (SPRM). What distinguishes its receptor pharmacology from mifepristone?

• A UPA selectively blocks progesterone synthesis in the corpus luteum while mifepristone blocks uterine receptors only
• B UPA has no anti-glucocorticoid activity unlike mifepristone, due to different receptor binding domain interactions
• C UPA is a tissue-selective partial agonist/antagonist at progesterone receptors — antagonist in endometrium and cervix but partial agonist in other tissues; mifepristone is a full progesterone and glucocorticoid receptor antagonist ✓
• D UPA is a full progesterone receptor agonist that competitively displaces endogenous progesterone in high doses

Explanation

Both ulipristal acetate and mifepristone bind progesterone receptor (PR) with high affinity, but with different tissue-selective profiles. Mifepristone is a full PR antagonist (and significant glucocorticoid receptor antagonist) — it blocks progesterone action completely in all tissues and causes antiprogesterone effects including cervical ripening and uterine sensitization to prostaglandins (used for medical abortion). UPA is an SPRM that acts as an antagonist in endometrium (suppressing endometrial proliferation in fibroids) but partial agonist in cervix and possibly myometrium. Critically, UPA has minimal anti-glucocorticoid activity unlike mifepristone, which has significant anti-cortisol effects relevant at higher doses.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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