Ebopiprant (OBE022) is an orally available, selective and potent prostaglandin F2α (PGF2α) receptor antagonist that interferes with the binding of PGF0126α to the FPR and can be used in the study of obesity.

Ebopiprant (OBE022) and OBE002 are subjected to FP binding affinity assays through competitive binding analysis with 3H-PGF2α, utilizing HEK293 cells stably transfected with the FP receptor. The binding affinities (Ki) of Ebopiprant(OBE022) for the human and rat FP receptor are 1 nM and 26 nM, respectively. For OBE002, the Kis are 6 nM for the human FP receptor and 313 nM for the rat FP receptor. The binding of both OBE022 and OBE002 is reversible and competitive. Increasing concentrations of either compound result in successive decreases in the slope of the binding curves, indicative of an increase in the equilibrium dissociation constant (KD) without a reduction in receptor density[1].

In the time-course study of the cumulative percentage of delivered mice after RU486-induced preterm parturition at GD17, oral treatment with Ebopiprant (OBE022)or nifedipine, as well as vehicle treatment, was assessed. Both Ebopiprant (OBE022) and nifedipine treatments resulted in a delay in preterm birth caused by RU486 administration, evidenced by a rightward shift in the percentage of delivery curve. Notably, both compounds showed a trend towards an increased time to the first pup delivery. This prolongation of gestation led to the delivery of viable pups.Furthermore, the combination of Ebopiprant (OBE022) and nifedipine exhibited a synergistic effect on delaying RU486-induced preterm birth, as indicated by a more pronounced rightward shift in the percentage of delivery curve compared to Ebopiprant (OBE022) or nifedipine alone. Additionally, a larger increase in the time of the first pup delivery was observed with the combination treatment[1].