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Systemic iron-binding proteins, primarily transferrin and ferritin, are essential for the safe transport and storage of iron throughout the body (UniProt P02787; UniProt P02794). Transferrin facilitates the movement of iron through the bloodstream to tissues, while ferritin acts as a buffer against iron deficiency and toxicity by sequestering iron in a non-reactive form (NIH, 2023). In conditions of chronic iron overload, such as thalassemia or hereditary hemochromatosis, these proteins become saturated, leading to the accumulation of non-transferrin-bound iron (NTBI) which generates reactive oxygen species and damages vital organs (StatPearls, 2023). Therapeutic agents known as iron chelators, such as deferoxamine and deferasirox, interact with the iron bound to these proteins or within the labile iron pool to form stable complexes (PubChem). These complexes are then excreted via the urine or feces, effectively reducing the systemic iron burden and preventing long-term complications like cirrhosis and heart failure (PubMed, 2021).
Iron chelators bind to ferric iron (Fe3+) associated with systemic proteins or the labile iron pool, forming stable, non-toxic complexes that are subsequently excreted from the body (StatPearls, 2023).
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