Deferiprone is a lipophilic iron chelator that binds to iron at a molar ratio of 3:1 (ligand: iron). Its active form is available orally, making it the only oral iron chelator. Deferiprone is a member of the 4-pyridone family and is a pyridine 4-4 (1H) -one, with a methyl substitution at positions 1 and 2 and a hydroxyl substitution at position 3. By binding to iron, Deferiprone can remove excess iron from the body and prevent serum iron overload in patients with transfusion-dependent thalassemia. It has chelation and protective effects and is primarily used to treat thalassaemia.
3-Hydroxy-1,2-dimethyl-4(1H)-pyridone (OH-pyridone) may be used in the bacterial killing assays. It has been employed as hydroxyketone chelating agent and its cytotoxic action against oral human normal and tumor cell lines has been evaluated.
A chelator that could replace disferrioxamine. It is orally and parenterally effective in the removal of iron in vivo from rabbits and mice and also from transferrin and ferritin in vitro
ChEBI: Deferiprone is a member of the class of 4-pyridones that is pyridin-4(1H)-one substituted at positions 1 and 2 by methyl groups and at position 3 by a hydroxy group. A lipid-soluble iron-chelator used for treatment of thalassaemia. It has a role as an iron chelator and a protective agent.
3-Hydroxy-1,2-dimethyl-4(1H)-pyridone (Hdpp, Deferiprone) is a hydroxy ketone derivative. It reacts with uranyl salts [UO2(NO3)2] in aqueous acidic solution to afford mono nuclear complexes ([UO2(dpp)(Hdpp)2(H2O)]ClO4). X-ray studies have been conducted to examine the structure and geometry of these complexes.
Orally administered chelator:
Treatment of transfusional iron overload
Deferiprone is hepatically metabolised to an inactive
glucuronide metabolite and is excreted mainly in the urine
as the metabolite and the iron-deferiprone complex, with
a small amount of unchanged drug.
1) Hider and Hoffbrand (2018),?The Role of Deferiprone in Iron Chelation; N. Engl. J. Med.,?379?2140
2) Sripetchwandee?et al.?(2016),?A combination of an iron chelator with an antioxidant effectively diminishes the dendritic loss, tau-hyperphosphorylation, amyloid-β accumulation and brain mitochondrial dynamic disruption in rats with chronic iron-overload., Neuroscience?332?191
3) Liu?et al.?(2018),?Iron and Alzheimer’s Disease: From Pathogenesis to Therapeutic Implications;?Front. Neurosci,?12?632
