250 (PB030) - Targeting acidosis to improve immunotherapy in a pancreatic ductal adenocarcinoma model

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Background: Solid tumors are acidic due to the combination of high rates of glycolysis with poor perfusion. The consequent establishment of the acidosis state leads to an immunosuppressive mechanism in the tumor microenvironment, inhibiting T-cell activation and leading to tumor growth. We previously showed that neutralization of tumor acidity using sodium bicarbonate could be additive or synergistic with checkpoint blockade (anti-PD1 and anti-CTLA4) in pre-clinical models. However, the buffer therapy phase I/IIa clinical trials failed due to poor patient compliance.