“These are important data for driving our ficlatuzumab program forward, as well as for demonstrating the clinical value of AVEO’s proprietary Human Response Platform,” stated William Slichenmyer, M.D., Sc.M., chief medical officer of AVEO. “Through our platform, we were able to recognize the interplay between the EGFR and HGF/c-Met pathways. These biomarker insights, combined with the clinical data, support our continued development of ficlatuzumab in combination with an EGFR inhibitor. We look forward to further clinical investigation in lung cancer. In addition, we will be initiating a clinical study in head and neck cancer later this year.”Study Overview The open-label, two-arm, randomized exploratory Phase 2 study was designed to compare the combination of ficlatuzumab and gefitinib versus gefitinib monotherapy, in clinically selected Asian subjects with previously untreated advanced NSCLC who have a high likelihood of harboring activating EGFR mutations. Ninety-four (94) patients were randomized to gefitinib and ficlatuzumab/gefitinib arms, respectively; 144 tumor tissue samples were available for biomarker analysis. Subjects who demonstrated disease control (complete response, partial response, or stable disease for 12 weeks or longer) in the gefitinib alone arm were eligible to cross-over upon progression to a combination of gefitinib and ficlatuzumab to assess whether acquired resistance to gefitinib can be overcome with the addition of ficlatuzumab. About Ficlatuzumab and the HGF/c-MET Pathway HGF is a ligand that binds to and activates a receptor called c-Met. Activation of the HGF/c-Met pathway is believed to be important in normal processes in embryonic development and wound healing, but is also believed to trigger many activities involved in cancer development and metastasis. HGF/c-Met has been shown to be one of the most potent drivers of tumor growth in AVEO’s Human Response Platform. HGF/c-Met over-expression is observed in many solid tumors including breast, colorectal, gastric, head and neck, lung and prostate, as well as hematologic malignancies 1. Additionally, c-Met and EGFR are frequently co-amplified and co-expressed in a variety of tumor types; HGF/c-Met pathway upregulation can render EGFR-targeted therapy resistance, and vice-versa 2-4. Ficlatuzumab is a humanized IgG1 antibody that binds to the HGF ligand with high affinity and specificity to inhibit the biological activities of the HGF/c-Met pathway.