Non-transferrin-bound plasma iron (NTBI)

Non-transferrin-bound plasma iron (NTBI) refers to all iron species in plasma that are *not* bound to transferrin, ferritin, or heme[1][2][4]. It emerges especially in states of iron overload—when transferrin, the principal physiological iron-binding protein, becomes saturated—typically at transferrin saturation over 75%[4][7]. NTBI is highly heterogeneous: it comprises low molecular weight ferric citrate complexes, partially albumin-bound forms, glycated protein–iron complexes, and, in some cases, redox-active or chelate-bound iron[1][2][4]. Unlike transferrin-bound iron, NTBI is redox-active and catalyzes the generation of reactive oxygen species, driving lipid peroxidation and cellular damage—particularly affecting the liver, heart, pancreas, and endocrine system[2][4][6]. NTBI species are central to the pathogenesis of secondary hemochromatosis and other iron overload disorders[4][7]. There is no standardized clinical NTBI assay; methods differ in terms of which iron forms are detected and are generally used for research rather than routine patient management[4]. Clinically, iron chelators (such as deferoxamine, deferasirox, and deferiprone) interact with NTBI, removing it from the circulation to mitigate toxicity[2][3].\nNote: NTBI is *not* a protein, receptor, enzyme, or canonical therapeutic target, but rather a pathological iron pool or molecular species. It is best considered a *biomarker* and a pathophysiological entity rather than a classical drug target[1][2][4][7].

Other names

Non-transferrin-bound ironNTBInon transferrin bound iron

Chelation of free/labile iron for removal from plasma and tissues