Cancer is characterized with its exceptional ability to survival via its adaptive mechanisms.  Focal Adhesion Kinase (FAK) is non-receptor tyrosine kinase  plays an important role in creating survival advantage for cancers. FAK is highly expressed in both tumor cells & cancer associated fibroblasts (CAFs), and is up-regulate/activated by a variety of chemo-, targeted and radiation therapy etc. Researchers have found that inhibiting the FAK signaling pathway is synergistic with multiple therapeutic modalities and can overcome emerging resistance of either chemo- or targeted therapy. 

FAK is one of key signaling hubs of tumor defense mechanism. Ifebemtinib, a highly selective, potent, small molecule  FAK inhibitor which is able to block FAK activation. Ifebemtinib targeting both tumor cells and cancer associated fibroblasts (CAF), consequently dismantle the tumor defense. The MOA of  Ifebemtinib  is depicted in the following figure, namely, 1)  priming tumor microenvironment, 2) transforming cell death toward immunogenic, and 3) reducing/delaying metastasis. These mechanisms of action of Ifebemtinib dismantle the survial advantages and improve all relevant efficacy endpoints in cancer treatment.