This chemical modification reduces the binding affinity of LMWHs for antithrombin and blocks angiogenic factors involved in the initial angiogenesis (VEGF and FGF2) and the primitive stabilization of the endothelial vascular network (platelet-derived growth factor subunit B) to inhibit multiple stages of angiogenesis, which directly leads to decreased blood perfusion throughout the tumor and inhibition of tumor growth. The gene discussed is FGF2; the disease is neoplasm.