PD-1/PD-L1 blockade is a clinically proven cancer therapeutic strategy that releases an inhibitory brake on T-cell activation. Co-stimulation by CD137, also known as 4-1BB, has been shown to synergistically increase the activity of PD-1/PD-L1 axis blockade. Clinical application of such a combination approach, however, may be limited by toxicity associated with the systemic administration of CD137 agonists. Bispecific antibody targeting strategies afford the feasibility of localizing CD137 co-stimulation to the tumor microenvironment through simultaneous engagement of a tumor-expressed antigen and CD137 expressed on tumor infiltrating lymphocytes. In this poster,
The preclinical data presented show that PD-L1 x CD137 bispecific DART and TRIDENT molecules can switch on CD137 co-stimulation strictly in a PD-L1-dependent fashion, limiting the probability of systemic activation where PD-L1 is not expressed. Although tumor adaptive resistance via PD-L1 induction promotes immune escape, PD-L1 x CD137 bispecific molecules can exploit the upregulation of the checkpoint ligand to provide a co-stimulatory signal and further amplify concomitant checkpoint blockade. Additional investigations as a potential therapeutic approach to overcome limitations of existing PD-1/PD-L1-targeting strategies are ongoing.
The poster presented at the 30th EORTC-NCI-AACR Symposium is available for download from the Events & Presentations page on
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Jim Karrels, Senior Vice President, CFO MacroGenics, Inc.1-301-251-5172, firstname.lastname@example.org Karen Sharma, Senior Vice President MacDougall Biomedical Communications1-781-235-3060, email@example.com
Source: MacroGenics, Inc.