Basic Fibroblast Growth Factor (FGF) Inhibitory Peptides

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CAT# Product Name M.W Molecular Formula Inquiry
B06001 bFGF (119-126), Basic Fibroblast Growth Factor, human, bovine 993.2 Inquiry
B06002 bFGF Inhibitory Peptide 815.9 Inquiry
B06003 bFGF Inhibitory Peptide II 2178.5 Inquiry
B06004 FGF basic (120-125) (human, bovine, ovine, rabbit) 993.18 Inquiry
B06005 H-Ala-Pro-Ser-Gly-His-Tyr-Lys-Gly-OH 815.88 Inquiry
B06006 H-Met-Trp-Tyr-Arg-Pro-Asp-Leu-Asp-Glu-Arg-Lys-Gln-Gln-Lys-Arg-Glu-OH 2178.48 Inquiry


Basic fibroblast growth factor (FGF) is a polypeptide having an activity of promoting cell mitosis and inducing cardiovascular production. FGF is closely related to tumor differentiation, growth, and invasion, metastasis and tumor angiogenesis. bFGF inhibitory peptides are kinds of receptor tyrosine kinases (PTKs) that activate signaling pathways by activating phosphorylation of specific protein substrates, controlling cell growth, differentiation and death. Novel molecularly highly sulfonated oligosaccharides PI-88 inhibits heparanase activity and competes with heparan sulfate growth factors (such as FGF and anti-vascular endothelial growth factor (VEGF)) to inhibit tumor proliferation, differentiation, and angiogenesis.

Mechanism of action

Non-specific small molecule tyrosine kinase inhibitors of the FGFRs intracellular tyrosine kinase domain targeting ATP-binding sites include E3810, Ponatinib, ENMD-2076, TSU68, Regorafenib, Nintedanib, and the like. They have an interaction with the anti-vascular endothelial growth factor receptor (VEGFR) and/or the anti-platelet-derived growth factor receptor (PDGFR). Ren et al found a high expression of FGFR mRNA in about 50% of 3059 non-small cell lung cancer specimens, and ponatinib significantly inhibited FGFR1 non-small cell lung cancer cell lines. The results indicate that ponatinib inhibits FGFR1 tyrosine kinase activity and is effective in treating patients with overexpressed FGFR1 lung cancer.

Application of Basic Fibroblast Growth Factor (FGF) Inhibitory Peptides

It has been shown that approximately 50% of proto-oncogenes have protein tyrosine kinase activity. Its abnormal expression will lead to disorder of cell proliferation, and apoptosis regulation, leading to tumor proliferation, differentiation and apoptosis of normal cells and tumor cells. Therefore, anti-tumor drugs PTKs, which selectively target FGFR, have become a hotspot in the world of anti-tumor research.


  1. Plotnikov, A. frsdN., Schlessinger, J., Hubbard, S. R., & Mohammadi, M. (1999). Structural basis for FGF receptor dimerization and activation. Cell, 98(5), 641-650.
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