Most felids are at risk of extinction in the wild. Conservation breeding aims to preserve these species ex situ, but success is limited by subfertility, shrinking gene pools, and logistical constraints. Assisted reproduction could improve breeding performance, but further optimization is needed to address unpredictable ovarian responses to exogenous gonadotropins, low pregnancy rates, and small litter sizes. Chapter I reviewed reproductive physiology of female felids, prior investigations of ovarian response and reproductive success after gonadotropin stimulation, and relevant research in non-carnivores that could inform new felid studies. In non-carnivores, baseline serum anti-Müllerian hormone (AMH) concentrations were associated with subsequent ovarian responses to exogenous gonadotropins, and potentially with assisted reproduction outcomes such as fertilization rate, embryo quality, or pregnancy success. To determine whether AMH has similar prognostic utility in felids, Chapter II explored associations between baseline serum AMH concentrations and gonadotropin stimulation responses in cheetahs and domestic cats. Results suggested favorable outcomes in animals with greater baseline AMH concentrations, including more ovulations, greater rates of embryo cleavage, and the first reported cheetah births after in vitro fertilization and embryo transfer. AMH concentrations also reliably distinguished domestic cats based on ovulatory responses to exogenous gonadotropins, though AMH did not predict ovarian responses in naturally estrous cats after simulated coitus. Non-carnivore studies also demonstrated endometrial defects after gonadotropin stimulation that reduced uterine receptivity to embryos. Previous felid research focused on the effects of exogenous gonadotropins on gamete or embryo function, and descriptions of the intrauterine environment during gonadotropin-stimulated cycles are lacking. To address this gap, Chapter III used RNA-sequencing and histology to describe gene expression and tissue morphology in domestic cat peri-implantation endometria after gonadotropin stimulation or simulated coitus. Concentrations of soluble cytokines and total protein within uterine luminal fluid were also compared. Results demonstrated pronounced endometrial dysfunction in gonadotropin-treated cats, evidenced by dysregulated gene expression, tissue remodeling, and secretory activity. The severity of some endometrial defects related to the degree of ovarian hyperstimulation after gonadotropin treatment. Finally, Chapter IV considered how these findings can guide future research and proposed several ideas to address remaining questions.