Emergency Contraception - Mechanism of Action

Mechanism of Action

The primary mechanism of action of combined estrogen-progestogen emergency contraceptive pills is to prevent fertilization by inhibition of ovulation.

The primary mechanism of action of progestogen-only emergency contraceptive pills is to prevent fertilization by inhibition of ovulation. The best available evidence is that they do not have any post-fertilization effects such as the prevention of implantation. The European EMA-approved labels and the U.S. FDA-approved labels for levonorgestrel emergency contraceptive pills (based on labels for regular oral contraceptive pills) both say they may cause endometrial changes that discourage implantation. Daily use of regular oral contraceptive pills can alter the endometrium (although this has not been proven to interfere with implantation), but the isolated use of a levonorgestrel emergency contraceptive pill does not have time to alter the endometrium. In March 2011, the International Federation of Gynecology and Obstetrics (FIGO) issued a statement that: "review of the evidence suggests that LNG ECPs cannot prevent implantation of a fertilized egg. Language on implantation should not be included in LNG ECP product labeling." In June 2012, a New York Times editorial called on the FDA to remove from the label the unsupported suggestion that levonorgestrel emergency contraceptive pills inhibit implantation.

The primary mechanism of action of progesterone receptor modulator emergency contraceptive pills like low-dose (10 mg) and mid-dose (25 mg) mifepristone and ulipristal acetate (micronized 30 mg) is to prevent fertilization by inhibition or delay of ovulation. One clinical study found that post-ovulatory administration of ulipristal acetate altered the endometrium, but whether the changes would inhibit implantation is unknown. The European EMA-approved labels for ulipristal acetate emergency contraceptive pills do not mention an effect on implantation, but the U.S. FDA-approved label says: "alterations to the endometrium that may affect implantation may also contribute to efficacy."

The primary mechanism of action of copper-releasing intrauterine devices (IUDs) as emergency contraceptives is to prevent fertilization because of copper toxicity to sperm and ova. The very high effectiveness of copper-releasing IUDs as emergency contraceptives means they must also prevent some pregnancies by post-fertilization effects such as prevention of implantation.