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Significance AlthoughMET is an established oncogene that drives tumorigenesis, metastasis, and resistance to therapy, antibody therapeutics targeting Met have thus far eluded successful clinical development. Met is a particularly challenging target because bivalent antibodies typically agonize Met, whereas monovalent antibodies lack potency and the capacity to downregulate it. We report the design and preclinical development of a purely antagonistic anti-Met antibody that potently blocks both ligand-dependent and ligand-independent signaling by exploiting the concept of avidity. MM-131 is a bispecific antibody that is monovalent for Met, but exhibits high avidity by concurrently binding to the tumor-specific antigen epithelial cell adhesion molecule. Preclinically, MM-131 inhibits proliferation in Met-driven cancer cells, inhibits hepatocyte growth factor (HGF)-mediated cell migration, and inhibits tumor growth in HGF-dependent and -independent mouse xenograft models.

MM-131, a bispecific anti-Met/EpCAM mAb, inhibits HGF-dependent and HGF-independent Met signaling through concurrent binding to EpCAM