Rusfertide, a peptide mimetic of natural hepcidin, targets and degrades ferroportin, thereby reducing serum iron and transferrin saturation, which helps regulate red blood cell production. It ameliorates conditions such as polycythemia vera, β-thalassemia, and hereditary hemochromatosis [1] [2].

Rusfertide reduces iron toxicity within red blood cells (RBCs) at a dosage of 1 mg/kg administered subcutaneously every two days for 49 days and decreases transferrin saturation at 2.5 mg/kg under the same administration schedule for two weeks. This enhances the oxygen-carrying capacity of RBCs and ameliorates anemia and iron accumulation in β-thalassemia and hereditary hemochromatosis mouse models [1]. Animal Model: Hbb th3/+ mice model for β-thalassemia and hereditary hemochromatosis [1] Dosage: 1 and 2.5 mg/kg Administration: s.c., once every two days, for 49 days (1 mg/kg); or for 2 weeks (2.5 mg/kg) Result: Improved the survival rate of RBCs in β-thalassemia model. Reduced transferrin-saturation and iron deposition.