Maturing pipeline of next-generation therapeutic innovations including antibodies, bispecific antibodies, small molecules, vaccines and cell therapeutics
QIMR Berghofer is developing therapeutic interventions for a number of disease areas, including oncology, infectious disease and autoimmune disorders. These exciting new technologies use cutting-edge modalities such as bi-specific antibodies and cellular therapies.
Breast cancer is the leading cause of female cancer deaths worldwide and with an estimated 1.7 million new cases every year. The histone methyltransferase enzyme G9a is over expressed in many malignancies, including breast cancer, and effects regulation of genes involved in tumour progression. G9a is also an epigenetic regulator of the known oncogene MYC; long viewed as a potential target for novel therapeutics. QIMR Berghofer researchers, in partnership with drug discovery CRO Domainex, have developed a small molecule inhibitor of G9a which shows promising in vitro and in vivo efficacy against breast cancer. We have demonstrated that tumours derived from tamoxifen resistant cell lines are resensitized to tamoxifen when combined with a G9a inhibitor, with the combination inducing tumour regression.
Colorectal cancer (CRC) is a leading cause of cancer incidence and mortality worldwide, accounting for an estimated 862,000 deaths in 2017. While patients with early stage, non-metastatic CRC respond well to surgical resection and adjuvant chemotherapy, patients with late stage and/or metastatic CRC have a 5-year relative survival rate of about 12%. Recently, the FDA approved immune checkpoint inhibitor (e.g., anti-PD1 and anti-CTLA-4) targeted therapies for certain metastatic CRC patients. RANKL blockade has been clinically proven to increase T cell infiltration of tumours, and has shown promising preclinical and clinical efficacy in combination with anti-PD1 mAbs. QIMR Berghofer researchers have developed a bi-specific anti-RANKL/PD1 antibody that displays promising results in mouse models of CRC. This bivalent tool compound exhibits at least equivalent activity compared to the combination of anti-RANKL plus anti-PD1, and in some cases is superior to the combination therapy.