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Iron overload contributes to the complications associated with hemochromatosis, β-thalassemia, and myelodysplastic disorders. Hepcidin inhibits the activity of the cellular iron exporter ferroportin, decreasing iron absorption, recycling, and storage.
In a recent review, investigators describe hepcidin agonists currently under development. The drugs include hepcidin mimetics (minihepcidins) and agents that silence transmembrane protease serine-6 (Tmprss6), a suppressor of hepcidin production.
Minihepcidins are short peptides based on the N-terminal amino acid segment of hepcidin; they induce the degradation of ferroportin. In mouse models, minihepcidins reduced iron overload in hemochromatosis and improved anemia, ineffective erythropoiesis, …