This review gives an overview of the mechanisms of action of oral emergency contraception pills (ECPs), focusing on the levonorgestrel (LNG) and ulipristal acetate (UPA) containing ECPs. In vivo and in vitro studies have addressed the effect of EC on various possible targets. Based on these studies as well as on clinical trials it is clear that the efficacy of ECPs to prevent an unintended pregnancy depends on their mechanism of action as well as on their use in relation to the fertile window. While the main effect of both available ECPs is to prevent or delay ovulation the window of action for UPA is wider than that of LNG. This provides the biological explanation for the difference observed in clinical trials and the higher efficacy of UPA. Neither LNG nor UPA impairs endometrial receptivity or embryo implantation. Correct knowledge on the mechanism of action of ECPs is important to avoid overestimating their effectiveness and to advise women on correct use.