In our previous research, all the data showed that FGF-2 was very possible to be a new target for inhibiting lung fibrosis. Therefore, we plan to find the specific and small peptides to block FGF-2 signaling, hoping to develop a new scheme to treat pulmonary fibrosis better than FGF.

Receptor extracellular domain. As a result, we biopanned several peptides through phage display technology, and finally got G8 which is the strongest peptide binding to FGF-2. Studies have found that G8 is almost non-toxic to L929 mouse lung fibroblast cells. In mouse bleomycin-induced pulmonary fibrosis model, the lung coefficient of the rats decreased significantly after 30 days of G8 treatment, the ground glass shadow decreases in CT scan, also the collagen deposition was alleviated dramatically (Masson staining), which suggests that the pulmonary fibrosis has been inhibited dramatically. And all above results are better than Pirfenidone (PFD) treatment group. The studies suggests obviously that G8 antagonizes the promoting effect of FGF-2 in the lung fibrotic process, which has a predictable applicating prospect.