KZIA News & Events

Kazia Therapeutics appointed Sudha Rao as Chief Scientific Officer, or CSO. Dr. Rao has more than 20 years of experience spanning pharmaceutical R&D, biotechnology, and early clinical development. She currently holds a professorial appointment and leads the Gene Regulation and Translational Medicine Laboratory at QIMR Berghofer Medical Research Institute and previously held senior scientific roles at Sanofi/Rhone-Poulenc in the UK. She is the founder and former Chief Scientific Officer of EpiAxis Therapeutics. At Kazia, Dr. Rao will lead all research and development activities.

Kazia Therapeutics announced the in-licensing of a SETDB1-targeted epigenetic drug development platform from QIMR Berghofer. The platform includes use of an AI-integrated epigenetic drug discovery engine candidate generation. The lead drug candidate, MSETC, was discovered and optimized using this AI-integrated epigenetic drug discovery engine. MSETC is a bicyclic peptide designed to target a disease-associated nuclear SETDB1 complex. By targeting SETDB1, the program is intended to restore immune signaling in tumors that have become resistant to immunotherapy, including checkpoint inhibitors. "SETDB1 represents a compelling emerging target in oncology," said John Friend, CEO of Kazia Therapeutics. "With this acquisition, we are extending our strategy to target how cancer controls its own behavior by addressing immune resistance at the chromatin level, one of the earliest layers of tumor immune regulation, alongside transcriptional reprogramming with paxalisib and targeted protein degradation with our PD-L1 platform. Together, these programs position Kazia's pipeline to address cancer therapy across multiple layers of tumor biology."

Kazia Therapeutics announced "compelling" preclinical and translational data supporting the development of NDL2, a potentially first-in-class protein degrader that is designed to selectively eliminate nuclear PD-L1, a previously unrecognized intracellular driver of immunotherapy resistance and metastatic progression that is not addressed by currently approved PD-1/PD-L1 antibodies. Across multiple preclinical models and patient-derived samples, NDL2 demonstrated reversal of immune exhaustion, suppression of metastatic biology, and enhanced anti-tumor activity, including in combination with anti-PD-1 therapy. The data collectively support nuclear PD-L1 as a mechanistically distinct and therapeutically actionable driver of immune evasion, disease progression, and metastasis. Unlike PD-1/PD-L1 antibodies that block extracellular signalling, NDL2 is designed to target nuclear PD-L1 proteins that are linked to aggressive and therapeutically resistant mesenchymal and stem-like cancer phenotypes. In murine triple-negative breast cancer preclinical models, NDL2 reduced primary tumor volume by 49% as monotherapy and 73% in combination with anti-PD-1, with 50% reduction in lung metastases in the combination setting, with no observed toxicity, no hemolysis, preserved immune checkpoint function at the cell surface, and favorable plasma stability. Nuclear PD-L1 was shown to be enriched in immunotherapy-resistant tumor cells, metastatic lesions, and circulating tumor cells, and to regulate gene programs associated with invasion, survival, and immune suppression. These findings support a precision-guided development strategy, integrating therapy and diagnostics from the outset.