Preventing β-catenin translocation to the nucleus through disruption of the interaction between BCL9 and β-catenin allows for disruption of oncogenic WNT-signaling, resulting in tumor cell death and a pro-inflammatory tumor microenvironment – without disruption of homeostatic WNT-function.
ST316 suppresses transcription of Wnt target genes regulating proliferation, migration, invasion and the metastatic potential of tumor cells, as well as genes regulating the immunosuppression of the tumor microenvironment.
ST316 RECRUITING PATIENTS FOR PHASE 1-2 STUDY
Following IND clearance in March 2023, the Phase 1 portion of the ST316 Phase 1-2 study is currently enrolling patients with selected advanced solid tumors likely to harbor abnormalities of the Wnt/β-catenin signaling pathway.