Description
Deferiprone is an iron chelator that exhibits neuroprotective and immunosuppressive activities. In animal models of Alzheimer’s disease, deferiprone decreases plasma iron and cholesterol levels, phosphorylation of tau protein, and levels of amyloid-β40, amyloid-β42, and β-amyloid precursor cleaving enzyme, BACE 1. In vitro, deferiprone decreases the number of proliferating CD4+ T cells, CD8+ T cells, and CD25+ cells; in vivo, deferiprone decreases disease severity of multiple sclerosis. Deferiprone is also cardioprotective, as it reverses iron-overload cardiomyopathy in clinical heart failure.
References
Prasanthi JR, Schrag M, Dasari B, et al. Deferiprone reduces amyloid-β and tau phosphorylation levels but not reactive oxygen species generation in hippocampus of rabbits fed a cholesterol-enriched diet. J Alzheimers Dis. 2012;30(1):167-82. PMID: 22406440.
Sweeney ME, Slusser JG, Lynch SG, et al. Deferiprone modulates in vitro responses by peripheral blood T cells from control and relapsing-remitting multiple sclerosis subjects. Int Immunopharmacol. 2011 Nov;11(11):1796-801. PMID: 21807124.
Kolnagou A, Michaelides Y, Kontos C, et al. Myocyte damage and loss of myofibers is the potential mechanism of iron overload toxicity in congestive cardiac failure in thalassemia. Complete reversal of the cardiomyopathy and normalization of iron load by deferiprone. Hemoglobin. 2008;32(1-2):17-28. PMID: 18274979.
Wiwanitkit V. Quantum chemical analysis of the deferiprone-iron binding reaction. Int J Nanomedicine. 2006;1(1):111-3. PMID: 17722270.
