Merrimack develops bispecific against c-MET oncogene

Merrimack has overcome hurdles to antibody targeting of c-MET with a bispecific that increases avidity by anchoring to a tumor surface protein.

Marketed small molecules inhibiting c-MET, which drives tumor formation, metastasis and resistance to therapy, have additional targets and lack specificity against the oncogene. Biologics antagonizing c-MET have been difficult to develop because monovalent antibodies are not potent enough and bivalent antibodies activate instead of block c-MET when its ligand, HGF/SF, is not present...