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Met pathway inhibitor

Enhanced Met signaling in tumors can occur from increased levels of HGF provided by the tumor cells and/or supporting cells, activating mutations within Met, and/or receptor overexpression with or without gene amplification.^6,7 Activation of Met via its ligand, HGF, is the predominant mechanism by which Met becomes activated. Inhibition of ligand binding by targeting the extracellular region of Met can block Met-induced tumor cell growth and survival, as well as metastasis of ligand-dependent tumor cells.^4,5,9,10

MetMAb is a monovalent anti-Met monoclonal antibody consisting of a single Fab region. Its monovalent design enables MetMAb to bind Met and effectively inhibit HGF binding and receptor activation without inducing Met dimerization.^3,9,10 In preclinical studies, MetMAb demonstrated antiproliferative, anti-angiogenic, and pro-apoptotic effects.^9,10

1. MetMAb was specifically designed as a monovalent antibody to avoid agonistic activity that can occur when divalent antibodies bind and crosslink Met receptors.^9,10

   

2. MetMAb binds to the Sema domain of Met, a region which is essential for binding HGF.^3,6,9

   

3. MetMAb prevents HGF from binding to Met, thereby blocking HGF-induced dimerization and receptor activation.^9,10

   

4. Blockade of Met activation and inhibition of its downstream pathways may prevent cancer cell growth, survival, and metastasis.^6,9,10

   

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