Ulipristal acetate used for emergency contraception has a broader window of efficacy (up to 120 hours) compared to levonorgestrel (72 hours) because it acts as:

• A A combined progesterone and estrogen receptor antagonist causing endometrial shedding regardless of fertilization
• B A selective progesterone receptor modulator (SPRM) that delays or inhibits follicular rupture by suppressing the LH surge even after the LH surge has begun, unlike levonorgestrel which requires pre-surge administration ✓
• C An anti-progestogen with glucocorticoid activity that prevents implantation via endometrial atrophy
• D A GnRH receptor agonist causing LH/FSH desensitization throughout the 120-hour window

Explanation

Ulipristal acetate (UPA) is a selective progesterone receptor modulator (SPRM) — it acts as a partial agonist/antagonist at progesterone receptors. Its key pharmacodynamic advantage is the ability to inhibit or delay ovulation even after the LH surge has started, a phase when levonorgestrel (which primarily inhibits the LH surge) is no longer effective. This pre-ovulatory follicular stasis effect explains UPA's superior efficacy at 72–120 hours. UPA does not reliably cause endometrial changes inconsistent with implantation at the approved dose, distinguishing it from mifepristone (full progesterone antagonist used for medical abortion).

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.