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Each year, cutaneous fibrosis (scarring) affects approximately 100 million patients worldwide due to traumatic injury or surgery. If not properly addressed, scarring can lead to significant functional, aesthetic, and psychological challenges. To date, there are no anti-scar therapeutics approved by the US FDA. In an effort to develop better anti-scar strategies, we explored potential solutions from developmental biology, explicitly drawing insights from fetal repair mechanisms known for their scarless healing. Through comprehensive animal models, including mice, rats, and pigs, we identified fibromodulin (FMOD), an extracellular matrix proteoglycan, as being critical for scarless fetal skin wound repair. When added exogenously, FMOD significantly benefits skin wound healing by improving gross appearance, reducing scar size, and accelerating the restoration of wound tensile strength. Interestingly, FMOD can also induce myofibroblast apoptosis. We further developed a chemically synthesized FMOD-derived peptide, SLI-F06, that retains the pro-migration, pro-contraction, and anti-fibrotic properties of FMOD. We are currently in US FDA Phase 2a clinical trials for scar reduction. Given, FMOD’s ability promote cell migration and contraction, we also tested its ability to heal wounds in preclinical diabetic chronic wound models. After verifying its efficacy in diabetic rodent and swine models, we are now planning preclinical safety testing with guidance from regulatory authorities so that we may begin first-in-man trials once safety studies are complete. Overall, this talk will describe our initial path of clinical problem identification, in vivo model establishment to identify candidate therapeutic molecules, elucidation of cellular and molecular mechanisms behind the candidate therapeutic, as well as the transition from the initial path to preclinical research, therapeutic development, and clinical trials.