It is unlikely that ulipristal acetate could effectively be used as an abortifacient, since it is used in much lower doses (30 mg) than the roughly equipotent mifepristone (600 mg), and since mifepristone has to be combined with a prostaglandin for the induction of abortion. However, data on embryotoxicity in humans are very limited, and it is not clear what the risk for an abortion or for teratogenicity (birth defects) is. Of the 29 women studied who became pregnant despite taking ulipristal acetate, 16 had induced abortions, six had spontaneous abortions, six continued the pregnancies, and one was lost to follow-up. Lactation
It is not recommended to breast feed within seven days of taking the drug since ulipristal acetate is excreted into the breast milk, and possible effects on the infant have not been studied. Side effects
The most common side effects include headache, nausea (feeling sick), abdominal pain (stomach ache), and dysmenorrhea (period pains). Interactions
Ulipristal acetate is metabolized by CYP3A4 in vitro. Ulipristal acetate is likely to interact with substrates of CYP3A4, like rifampicin, phenytoin, St Johns wort, carbamazepine or ritonavir, therefore concomitant use with these agents is not recommended. It might also interact with hormonal contraceptives and progestogens such as levonorgestrel and other substrates of the progesterone receptor, as well as with glucocorticoids. Pharmacology
Pharmacodynamics
As an SPRM, ulipristal acetate has partial agonistic as well as antagonistic effects on the progesterone receptor. Ulipristal acetate exhibits similar potency to antagonize progesterone receptor as mifepristone in vitro.
It also binds to the androgen receptor and the glucocorticoid receptor, but is only a weak antiandrogen and antiglucocorticoid relative to flutamide and mifepristone, respectively. Ulipristal acetate has no relevant affinity to the estrogen and mineralocorticoid receptors. Phase II clinical trials suggest that the mechanism might consist of blocking or delaying ovulation and of delaying the maturation of the endometrium. Pharmacokinetics
In animal studies, the drug was quickly and nearly completely absorbed from the gut. Intake of food delays absorption, but it is not known whether this is clinically relevant.Ulipristal acetate is metabolized in the liver, most likely by CYP3A4, and to a small extent by CYP1A2 and CYP2D6. The two main metabolites have been shown to be pharmacologically active, but less than the original drug. The main excretion route is via the feces. History
Ulipristal acetate was granted marketing authorization by the European Medicines Agency (EMA) in May 2009. In 2014, the EMA recommended ulipristal be made available without a prescription in the European Union.The U.S. Food and Drug Administration (FDA) approved the drug for use in the United States on 13 August 2010, following the FDA advisory committees recommendation. Watson Pharmaceuticals announced the availability of ulipristal acetate in the United States on 1 December 2010, in retail pharmacies, clinics, and one on-line pharmacy, KwikMed. Society and culture
Brand names
Ulipristal acetate is marketed in the United States under the brand name Ella and in Canada under the brand name Fibristal.