Drug class
Hepcidin Mimetics
Hepcidin mimetics are a class of synthetic peptide or small-molecule therapeutics that functionalize or replicate the activity of endogenous hepcidin, the primary systemic regulator of iron homeostasis. Read more about Hepcidin Mimetics
1 drugs in this class 1 manufacturers
Drugs in Hepcidin Mimetics
Hepcidin mimetics are a class of synthetic peptide or small-molecule therapeutics that functionalize or replicate the activity of endogenous hepcidin, the primary systemic regulator of iron homeostasis.
These agents exert their principal therapeutic effect by binding to ferroportin—the sole cellular iron exporter—inducing its internalization and degradation to sequester iron within reticuloendothelial storage sites and reduce dietary iron absorption.
By restricting systemic iron availability, hepcidin mimetics curtail excess erythropoiesis and attenuate iron overload.
Clinically, this class is primarily utilized and investigated for the management of myeloproliferative disorders like polycythemia vera—where it limits red blood cell overproduction and reduces phlebotomy dependence—as well as primary and secondary iron overload conditions such as hereditary hemochromatosis and non-transfusion-dependent beta-thalassemia.
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fda.gov
Hepcidin mimetics are a class of synthetic peptide or small-molecule therapeutics that functionalize or replicate the activity of endogenous hepcidin, the primary systemic regulator of iron homeostasis By restricting systemic iron availability, hepcidin mimetics curtail excess erythropoiesis and attenuate iron overload Clinically, this class is primarily utilized and investigated for the management of myeloproliferative disorders like polycythemia vera—where it limits red blood cell overproducti...
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nih.gov
Hepcidin mimetics are a class of synthetic peptide or small-molecule therapeutics that functionalize or replicate the activity of endogenous hepcidin, the primary systemic regulator of iron homeostasis These agents exert their principal therapeutic effect by binding to ferroportin—the sole cellular iron exporter—inducing its internalization and degradation to sequester iron within reticuloendothelial storage sites and reduce dietary iron absorption By restricting systemic iron availability, hepc...
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cetaf.org
These agents exert their principal therapeutic effect by binding to ferroportin—the sole cellular iron exporter—inducing its internalization and degradation to sequester iron within reticuloendothelial storage sites and reduce dietary iron absorption
-
nih.gov
Clinically, this class is primarily utilized and investigated for the management of myeloproliferative disorders like polycythemia vera—where it limits red blood cell overproduction and reduces phlebotomy dependence—as well as primary and secondary iron overload conditions such as hereditary hemochromatosis and non-transfusion-dependent beta-thalassemia
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nih.gov
Clinically, this class is primarily utilized and investigated for the management of myeloproliferative disorders like polycythemia vera—where it limits red blood cell overproduction and reduces phlebotomy dependence—as well as primary and secondary iron overload conditions such as hereditary hemochromatosis and non-transfusion-dependent beta-thalassemia
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