Fig. 5: Analyses of the synergism between F9H4 and a panel of anti-EGFR antibodies. | Nature Communications

Fig. 5: Analyses of the synergism between F9H4 and a panel of anti-EGFR antibodies.

From: A monoclonal antibody that inhibits the shedding of CD16a and CD16b and promotes antibody-dependent cellular cytotoxicity against tumors

Fig. 5: Analyses of the synergism between F9H4 and a panel of anti-EGFR antibodies.

A Male adult hFcR mice were inoculated subcutaneously with 1.5 × 106 LLC1-hEGFR cells and tumors were measured by digital caliper. Treatments with F9H4-hIgG1-DANA, EGFR antibodies, and isotype controls (0.1 mg/antibody/per mouse) were done on days 5, 6, and once per week. Only the combinations of F9H4 with cetuximab and necitumumab inhibited tumor growth to greater extents compared to F9H4 without EGFR antibodies, as highlighted by data in the right graph (Day 27). Isotypes (DANA + hIgG1) n = 10, F9H4-DANA + hIgG1 isotype n = 10, F9H4-DANA + zalutumumab n = 9, F9H4-DANA + nimotuzumab n = 10, F9H4-DANA + necitumumab n = 10, F9H4-DANA + cetuximab n = 10. F9H4 synergizes with an Fc-enhanced version of cetuximab (cetuximab-GAALIE) to promote NK cell degranulation (B) and interferon-γ production (C) against a panel of human lung cancer cell lines. Primary NK cells were co-cultured with the indicated cell lines and in the presence of the indicated antibodies, followed by analyses of CD107a and intracellular interferon-γ by flow cytometry. Data represent three (B, C) or are pooled of two (A) independent experiments, are mean ± standard error of triplicates (B, C), and were analyzed by two-way ANOVA with Bonferroni’s test (A) or Dunnett’s test (B, C). *p < 0.05, **p < 0.01, ***p < 0.001.

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