Abstract
Meeting abstracts Although durable responses to single agent immune checkpoint inhibitors have been reported, additional approaches are needed to extend this therapeutic benefit to a greater proportion of cancer patients. Accordingly, substantial efforts are ongoing to identify agents that can
Highlights
Durable responses to single agent immune checkpoint inhibitors have been reported, additional approaches are needed to extend this therapeutic benefit to a greater proportion of cancer patients
In addition to the potency of the small molecule Focal Adhesion Kinase (FAK)/PYK2 inhibitors defactinib (VS-6063) and VS-4718 to target cancer stem cells, we have reported that these agents inhibited monocyte-derived macrophages, decreased IL-6 production from macrophages in vitro, and reduced tumor-associated macrophages in xenograft models
We report that defactinib and VS-4718 stimulate proliferation of CD8+ cytotoxic T cells
Summary
Durable responses to single agent immune checkpoint inhibitors have been reported, additional approaches are needed to extend this therapeutic benefit to a greater proportion of cancer patients. FAK/PYK2 inhibitors defactinib and VS-4718 enhance immune checkpoint inhibitor efficacy Substantial efforts are ongoing to identify agents that can augment T cell-mediated killing of tumor cells and potentiate the effects of checkpoint inhibitors.
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