Highly functional HBV-specific T cells within our immune system are believed to be required for long-term HBV viral control. However, HBV-specific T cells become functionally defective, and reduced in number during chronic HBV infection. One approach to boost HBV-specific T cells is to block the PD-1/PD-L1 protein-protein interaction that is one of the causes of T cell immune disfunction.
Through our comprehensive research, we have identified a class of small molecule oral PD-L1 inhibitors that we believe will allow for controlled checkpoint blockade, enable oral dosing and mitigate systemic safety issues typically seen with checkpoint antibody therapies. We are in IND-enabling studies with AB-101 that could potentially be an important part of a combination therapy for the treatment of HBV. We are also exploring oncology applications for AB-101.