Hepcidinagonisten

Hepcidinagonisten are a class of therapeutic agents designed to mimic the action of hepcidin, a hormone that plays a crucial role in regulating iron metabolism. Hepcidin acts by binding to ferroportin, the sole known cellular iron exporter, leading to its degradation and thus reducing iron absorption from the diet and iron release from storage sites. By increasing hepcidin levels or its activity, hepcidinagonisten aim to decrease circulating iron levels.

This therapeutic strategy is primarily being investigated for conditions characterized by iron overload, such as hereditary hemochromatosis and transfusional hemosiderosis, which occurs in patients requiring frequent blood transfusions for diseases like thalassemia or sickle cell anemia. In these conditions, excessive iron accumulation can lead to significant organ damage, including the liver, heart, and endocrine glands.

The development of hepcidinagonisten represents a targeted approach to managing iron overload, offering an alternative to current treatments like phlebotomy (blood removal) or iron chelation therapy, which can have their own limitations and side effects. Research in this area focuses on developing agonists that are potent, stable, and have favorable pharmacokinetic profiles for effective and safe clinical use. While still largely in the research and development phase, hepcidinagonisten hold promise as a novel treatment for iron-related disorders.