KY19334 is an inhibitor of CXXC5-DVL. By blocking the interaction between CXXC5 and Dvl, KY19334 activates the Wnt/β-catenin signaling pathway. It also hinders the proliferation, migration, invasion, and transformation of cancer cells through CDK1 inhibition. Moreover, KY19334 accelerates wound healing and promotes regeneration. This compound is applicable in research related to cancer, inflammation, neurological, and metabolic disorders, such as skin squamous cell carcinoma and diabetes.

KY19334 at a concentration of 5 μM over 72 hours inhibits the proliferation of human cutaneous squamous cell carcinoma (cSCC) HSC-1 and HSC-5 cells, without significantly affecting the proliferation of normal keratinocytes HaCaT. In addition, KY19334 at 5 μM for 24 hours significantly reduces both migration and invasion of HSC-1 and HSC-5 cells. Furthermore, this compound at 5 μM over two weeks suppresses colony formation in these cancer cells. KY19334, at the same concentration and duration of 24 hours, downregulates CDK1 expression and inhibits the Wnt/β-catenin signaling pathway in HSC-1 and HSC-5 cells. Conversely, at a concentration of 1 mM for 7 to 16 days, KY19334 activates the Wnt/β-catenin signaling pathway in keratinocytes, endothelial cells, and fibroblasts of wound tissue in diabetic mice. Moreover, 1 mM of KY19334 administered over 7 days enhances the expression of CD31+ endothelial cell angiogenesis-related proteins in wound tissue of diabetic mice.

KY19334, when applied topically at a concentration of 2 mM 30 minutes before TPA administration, effectively inhibits the development of skin cancer in C57BL/6 mice induced by DMBA and TPA. Additionally, a 1 mM topical application of KY19334 administered once daily for 16 consecutive days accelerates wound healing in diabetic C57BL/6 mice.