Figure 8. Schematic drawing summarizing the antitumor effects of D16F7 mAb.

Treatment with D16F7 exerts antitumor activity through several mechanisms of action: a) inhibition of angiogenesis after binding to endothelial cells, thus preventing chemotaxis induced by angiogenic factors and/or sVEGFR-1 released by tumor cells and/or tumor-associated macrophages; b) inhibition of myeloid hematopoietic progenitors mobilization and of tumor mass infiltration by monocytes/macrophages. The latter play an important role in tumor angiogenesis and invasiveness by secreting angiogenic factors, matrix metalloproteases and growth factors that promote tumor cell survival and metastases; c) inhibition of tumor growth and spreading of VEGFR-1 expressing tumor cells, by directly hampering chemotaxis and ability to form capillary-like tubes (i.e., vasculogenic mimicry), which allow nutrient supply and dissemination of metastatic cells.