KRFK TFA, a peptide derived from TSP-1, can activate TGF-β. KRFK TFA promotes TGF-β-mediated signaling and its downstream role, independent of thrombospondin (TSP) receptors such as CD47 and CD36. KRFK TFA can be used for chronic ocular surface inflammatory disorders reseach.
KRFK TFA (50 μM; 24 h) activates the secretion of TGF-β and reduces the expression of DC maturation markers in tsp-1 deficient bone marrow-derived dendritic cells (BMDCs) [1].
KRFK TFA (5 μg/5 μL/eyes; single dose) significantly prevents the development of chronic ocular surface inflammation in TSP-1-/- mice[1].
References:
[1]. Soriano-Romaní L, et al. Topical Application of TGF-β-Activating Peptide, KRFK, Prevents Inflammatory Manifestations in the TSP-1-Deficient Mouse Model of Chronic Ocular Inflammation. Int J Mol Sci. 2018 Dec 20;20(1):9.