Abstract 1990 Creating a Heparin-Binding, Hyper-Stable FGF1: Effects of a Targeted Two Mutation on the N-Terminus of Super FGF1

Approximately 4% of Americans experience poor-healing foot ulcers due to diabetes, often leading to severe complications and amputations, and costing millions in healthcare resources for intensive wound care. Fibroblast Growth Factors (FGFs), cell-signaling proteins critical for cell proliferation, metabolism, differentiation, and tissue repair, are key drivers of wound-healing processes. Recently, researchers have developed a hyper-stable FGF1 (hsFGF1) mutant that retains its diverse bioactivity while increasing its stability in isolation, eliminating repulsive electrostatic forces by mutating the amino acid sequence in the protein's C-terminus.