Recombinant Human Antibody (C225) is capable of binding to EGFR, expressed in HEK 293 cells. Expressed as the combination of a heavy chain (HC) containing VH from anti-EGFR mAb and CH1-3 region of human IgG1 and a light chain (LC) encoding VL from anti-EGFR proteins mAb and CL of human kappa light chain. Exists as a disulfide linked dimer of the HC and LC hetero-dimer under non-reducing condition.
Figure 1 Inhibition of VEGF (A), IL-8 (A), and bFGF (B) steady-state mRNA expression by C225 mAb in vitro.
Cells were cultured in the presence of or absence of MAb C225. mRNA was extracted after 48 h of treatment and analyzed by Northern blotting. Using image densitometry, the mRNA expression of untreated cells was assumed to be 100% of potential expression for these cells. Treatment with C225 down-regulated VEGF, IL-8, and bFGF mRNA expression in a dose-dependent fashion. β-actin served as a control for loading (exposure, 30 min).
Figure 2 Immunohistochemical staining of MAb C225-treated human TCC tumors growing in the bladders of athymic nude mice.
MAb C225-treated tumors (after 3 weeks and 5 weeks of therapy) and control tumors were stained with CD31 antibodies directed against mouse endothelial cells (A–C). Note the increased vessel density in the control tumors (A) and the 3-week C225-treated tumors (B) compared with that of the 5-week C225-treated specimen (C). Immunostaining for VEGF (D–F), IL-8 (G–I), and bFGF (J–L) is higher in the control tumors (D, G, and J) than in the MAb C225-treated specimens (E, F, H, I, K, and L) at 3 weeks and 5 weeks. Note that the down-regulation of VEGF, IL-8, and bFGF precedes the inhibition of angiogenesis.
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For Research Use Only. Not For Clinical Use.