Oral contraceptives containing levonorgestrel suppress gonadotropins, thereby inhibiting ovulation. Specifically, levonorgestrel binds to progesterone and androgen receptors and slows the release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. This process results in suppression of the normal physiological rise in luteinizing hormone (LH) that precedes ovulation. It inhibits the rupture of follicles and the release of viable eggs from the ovaries. Levonorgestrel has been shown to be more effective when administered prior to ovulation.
Orally administered levonorgestrel is absorbed in the gastrointestinal tract, whereas levonorgestrel administered via a hormonal IUD is absorbed in the endometrium. Protein binding of levonorgestrel ranges from 97.5-99%. The liver enzymes CYP3A4 and CYP3A5 are mainly involved in metabolism. Approximately 45% of the oral dose and its metabolites are excreted in the urine. Approximately 32% of the oral dose is excreted in the feces.
When taken concomitantly with drugs that induce the liver enzyme CYP3A4, levonorgestrel may be metabolized more rapidly and may be less effective. These include, but are not limited to, barbiturates, bosentan, carbamazepine, felbamate, griseofulvin, oxcarbazepine, phenytoin, rifampin, St. John's wort, and topiramate.