Ulipristal acetate (UPA) used as emergency contraception has a mechanism distinct from levonorgestrel. UPA's primary contraceptive mechanism involves:

• A Competitive estrogen receptor antagonism in the hypothalamus blocking negative feedback
• B Direct luteolytic effect on the corpus luteum reducing progesterone and preventing implantation
• C Selective progesterone receptor modulator activity — inhibiting LH surge and delaying/suppressing ovulation even after the LH surge has commenced ✓
• D Prevention of sperm capacitation via inhibition of calcium CatSper channels in cervical mucus

Explanation

Ulipristal acetate is a selective progesterone receptor modulator (SPRM). Unlike levonorgestrel, which primarily inhibits or delays ovulation before the LH surge, UPA can postpone or inhibit follicle rupture even after the LH surge has begun (when LNG is no longer effective). UPA binds to progesterone receptors with high affinity, inhibiting endogenous progesterone's positive feedback effect on the hypothalamic-pituitary axis and directly inhibiting follicle maturation and rupture. This extends the window of emergency contraceptive efficacy to 120 hours (5 days). Anti-estrogenic effects, luteolysis, and CatSper inhibition are not its primary mechanisms.

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

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Written and medically reviewed by the StethoPrep medical team.