Focal Adhesion Kinase (FAK) is a non-receptor tyrosine kinase that mediates signaling downstream of integrins & growth factor receptors. Expression of focal adhesion kinase (FAK) is greater in many tumor types as compared to normal tissue, particularly in cancers that have high invasive and metastatic capability. FAK has many kinase-dependent functions, including control of cell movement, invasion, survival and gene expression.

FAK Inhibition

FAK is critical for multiple aspects of tumor progression

Research at Verastem Oncology has further advanced the understanding of of FAK kinase inhibition ability to overcome three key drug resistance mechanisms in the tumor microenvironment:

Plays key roles in metastasis and drug resistance

Cancer stem cells can evade both current therapies and the immune system to mediate recurrence and metastasis. FAK is essential for both the survival and tumor-initiating capability of CSCs.1

Reduces stromal density, facilitates entry of cytotoxic T cells into tumor

A tumor’s growth may prevent effective immune cell infiltration as well as potentially limiting penetration of cancer therapies. FAK inhibition decreases components of tumor-protective stroma.2,3

Reduces immune suppressive cell populations in the tumor microenvironment

FAK inhibition can improve the immune balance in the tumor microenvironment resulting in an improvement in the efficacy of immune checkpoint inhibitors.3,4