This IP seeks to treat omodysplasia by targeting the Wnt signaling pathway. Through the creation of mouse models with variants in the Frizzled2 gene—which mimic the human omodysplasia phenotype—preliminary data has shown that administering a small molecule intra-peritoneally to pregnant dams can rescue some skeletal defects in mouse embryos. By leveraging the known effects of Wnt agonists on skeletal development, the IP holds promise for addressing the skeletal defects associated with omodysplasia. As research progresses, the potential applications of this IP may extend beyond omodysplasia to other skeletal dysplasias and related conditions. The ability to target the Wnt signaling pathway opens doors to a range of therapeutic possibilities, offering hope to patients and clinicians seeking effective treatments for skeletal disorders. The IP embodies a significant advancement in the field of skeletal dysplasia research and holds promise for translating pre-clinical findings into potential therapeutic interventions. With continued development and collaboration, it has the potential to make a meaningful impact on the lives of individuals affected by omodysplasia and related conditions.