kp1 (56-87)

Klotho-derived Peptide 1 (56-87) (human) TFA, a peptide derived from the human Klotho protein, disrupts TGF-β signaling through binding interactions with TGF-β receptor type 1 (TGFBR1) and TGF-β receptor type 2 (TGFBR2), with Kd values of 1.41 and 14.6 µM, respectively. Preincubation with Klotho-derived Peptide 1 (56-87) (human) TFA at 10 µg/mL inhibits TGF-β-induced increases in fibronectin and α-smooth muscle actin (α-SMA) expression in NRK-49F rat fibroblasts. In vivo investigations demonstrate that Klotho-derived Peptide 1 (56-87) (human) TFA, administered at 1 mg/kg per day, preferentially accumulates in damaged kidneys and significantly reduces serum creatinine and blood urea nitrogen levels while decreasing renal fibrosis in mouse models of unilateral ureteral obstruction (UUO) and unilateral ischemia-reperfusion injury-induced renal fibrosis. Klotho-derived Peptide 1 (56-87) (human) TFA is therefore valuable for investigations involving renal fibrosis, TGF-β signaling modulation, and kidney injury-associated molecular pathways.