<unk>  has a number of potential drug interactions with other medications.<unk>  is a substrate of the cytochrome P450 (CYP450) enzyme CYP3A, and inhibitors and inducers of CYP3A4 may alter the metabolism of<unk>  and increase or decrease its circulating levels. The strong CYP3A4 inhibitor ketoconazole has been found to increase peak levels of and total exposure to a single 150 mg dose of<unk>  by about 2-fold. Paradoxically, rifampin, a strong inducer of CYP3A4 and other CYP450 enzymes, increased peak levels of and total exposure to a single 150 mg dose of<unk>  as well. A single dose of rifampin increased peak levels of<unk>  by 4.4-fold and total exposure by 5.6-fold, whereas continuous rifampin therapy increased peak levels of<unk>  by 2-fold and total exposure by 1.7-fold. The use of<unk>  at 200 mg twice per day concomitantly with rifampin is not recommended, whereas the concomitant use of<unk>  at 150 mg once per day with rifampin should be limited to 6 months. No significant changes in exposure to<unk>  were observed with concomitant administration of rosuvastatin (a substrate of OATP1B1, OATP1B3, and BCRP), sertraline (a moderate inhibitor of CYP2D6 and CYP2B6), or fluconazole (a strong inhibitor of CYP2C19 and a moderate inhibitor of CYP2C9 and CYP3A4).<unk>  is a substrate of the hepatic OATP1B1 transporter. Levels of<unk>  have been found to be increased by 78% in people with a genotype characterized by reduced OATP1B1 transporter function. The concomitant use of<unk>  with medications that inhibit OATP1B1 may increase<unk>  levels, and the use of<unk>  with strong OATP1B1 inhibitors like ciclosporin and gemfibrozil, which may markedly increase<unk>  exposure, is contraindicated.<unk>  is a weak to moderate inducer of CYP3A, and may decrease levels of medications that are substrates of CYP3A4. In addition,<unk>  is an inhibitor of P-glycoprotein, and may increase levels of medications that are substrates of P-glycoprotein, such as digoxin.<unk>  has been found to increase exposure to digoxin and ethinylestradiol, whereas it has been found to decrease exposure to rosuvastatin, midazolam, norethisterone, norelgestromin, and norgestrel. Because combined birth control pills and other forms of combined birth control contain an estrogen, and because<unk>  treats endometriosis by decreasing estrogen levels in the endometrium, these form of hormonal birth control are likely and expected to decrease the effectiveness of<unk>  in the treatment of this condition. The effect of progestogen-only birth control on the effectiveness of<unk>  in endometriosis is unknown. However, progestogens are antiestrogenic in the uterus, and high-dose progestin therapy is known to be effective in the treatment of endometriosis similarly to GnRH antagonists. On the basis of limited clinical research, combined birth control pills have also been found to be effective in the treatment of endometriosis, but are likely not as effective as GnRH modulator monotherapy. It is advised that women use non-hormonal methods of birth control during<unk>  therapy and for one week following discontinuation of<unk> .
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