CD39 is highly expressed in the TME and is an ectonucleotidase that converts ATP to AMP. This reduces local ATP levels and promotes the degradation pathway towards adenosine. As ATP stimulates immune reactions and adenosine is an immunosuppressive metabolite, the inhibition of CD39 can improve anti-tumor immune activity. PD-1 and CD39 are both expressed on effector T cells, and blockade of both these pathways have been found to synergize in preclinical tumor models. PM1086 is a highly potent inhibitor to PD-1 and CD39 and has improved avidity to T cells that express these markers simultaneously to reinvigorate tumor-specific T cells in the TME.