Ulipristal acetate (UPA) is a selective progesterone receptor modulator (SPRM) used as emergency contraception up to 120 hours post-coitus. Its efficacy beyond 72 hours compared to levonorgestrel is explained by:

• A UPA is a partial agonist/antagonist at PR, capable of inhibiting or delaying ovulation even after the LH surge has started (up to the point of follicular rupture), whereas levonorgestrel loses efficacy after the LH surge begins ✓
• B UPA undergoes conversion to a long-acting sulphate conjugate that persists in follicular fluid for 5 days
• C UPA inhibits 17-hydroxyprogesterone synthesis, preventing luteal progesterone production essential for implantation
• D UPA blocks the LH receptor competitively, preventing LH-induced follicular rupture regardless of pre-ovulatory LH levels

Explanation

Levonorgestrel (a progestin) prevents ovulation primarily by inhibiting the LH surge when given before the surge begins; once the LH surge is underway, its efficacy drops sharply. Ulipristal acetate, as a selective progesterone receptor modulator with mixed antagonist/partial agonist properties at PR, can inhibit or delay follicular rupture even after the LH surge has started — because it acts at the level of the follicle (blocking progesterone-induced changes needed for rupture). This explains its superior efficacy in the 72–120-hour window. UPA does not block LH receptors directly, does not form sulphate conjugates with special pharmacokinetics, and does not inhibit 17-hydroxyprogesterone synthesis.

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

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Written and medically reviewed by the StethoPrep medical team.