Deferiprone is the only orally active iron-chelating drug to be used therapeutically in conditions of transfusional iron overload.
Target：
Deferiprone is an orphan drug designed and developed primarily by academic initiatives for the treatment of iron overload in thalassaemia. Deferiprone has been used in several other iron or other metal imbalance conditions and has prospects of wider clinical applications. Deferiprone has high affinity for iron and interacts with almost all the iron pools at the molecular, cellular, tissue and organ levels. Doses of 50-120 mg/kg/day appear to be effective in bringing patients to negative iron balance. Deferiprone increases urinary iron excretion, which mainly depends on the iron load of patients and the dose of the drug.
Deferiprone is a potent iron chelating agent that is orally active, capable of penetrating the brain, cells, and skin. It is effective in inhibiting tumor cell proliferation and migration, while also promoting apoptosis. Additionally, deferiprone possesses anti-anemic, neuroprotective, anti-inflammatory, antioxidant, and antidotal properties, making it useful in studies related to cancer, cardiovascular disease, infection, inflammation, and neurological diseases[1].[2].[3].[4].[5].[6].[7].[8].
体内研究
Deferiprone (100 mg/kg daily for 4 weeks, ingested) demonstrates a neuroprotective effect in a mouse model of tauopathy, the rTg(tauP301L)4510[6].
Deferiprine (50-200 mg/kg daily, orally for 5-10 days) alleviates nephrotoxicity in a rat model of acute renal failure induced by Cisplatin[7].
Deferiprone (13.82 and 27.64 mg/kg per day, ingested for 4 weeks) exhibits anti-apoptotic and neuroprotective activities in a rat model of Alzheimer’s disease[8].
体外研究
Deferiprone (ranging from 66 to 660 μM, over 48 to 96 hours) significantly inhibits cell proliferation in TRAMP-C2, Myc-CaP, and 22rv1 cells[1].
At a concentration of 100 μM and up to 192 hours, deferiprone hampers cell migration in the same cell lines[1].
Deferiprone (100 μM, 24 hours) reduces both the expression and activity of mitochondrial aconitase (m-Acon) in TRAMP-C2, Myc-CaP, and 22rv1 cells[1].
Deferiprone (up to 1 μM, between 0.5 and 24 hours) lowers free iron levels in thalassemic red blood cells[2].
Deferiprone (10 minutes) inhibits human platelet aggregation stimulated by arachidonic acid (AA), adenosine diphosphate (ADP), epinephrine, and collagen, with IC50 values of 0.24, 0.25, 3.36, and 3.73 mM, respectively[3].
Deferiprone (0.1-3.2 μM, 5 minutes) inhibits COX-1 activity with an IC50 of 0.33 μM[3].
Deferiprone (4 mM, 5 minutes) prevents ADP-induced formation of cAMP[3].
Deferiprone (156.25 μg/mL, 24 hours) enhances the survival rate and reduces LDH levels, maintaining normal cell morphology in aged fibroblasts[4].
Deferiprone (25 μM, 6 hours) increases the antibacterial efficacy of conventional antibiotics against S. epidermidis[5].
搜索
