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].
Deferiprone/去铁酮 细胞实验
Cell Line
Concentration
Treated Time
Description
References
Primary mouse fibroblasts
1 mM
24 h
To assess PRKN-independent mitophagy, results showed mt-Keima was more sensitive than mito-QC
Autophagy. 2021 Nov;17(11):3753-3762
HeLa cells
1 mM
24 h
To assess PRKN-independent mitophagy, results showed both mt-Keima and mito-QC could detect iron-chelation induced mitophagy, but mt-Keima was more sensitive
Autophagy. 2021 Nov;17(11):3753-3762
ARPE-19 cells
50, 100, 200 μM
2 h
DFP significantly alleviated the toxicity of A2E-loaded ARPE-19 cells under blue light exposure, restored cell viability, reduced LDH release, decreased intracellular Fe2+ levels and ROS production, and upregulated the protein expression of SLC7A11 and GPX4.
Cell Mol Biol Lett. 2025 Feb 21;30(1):22
ARPE-19 cells
1 mM
18 h
DFP rescued MNU-induced cell death in ARPE-19 cells via inhibition of parthanatos, and this protective effect was independent of mitophagy.
Cell Death Dis. 2025 May 19;16(1):402
EA.hy926 cells
100 μM
24 h
DFP significantly alleviated ZnONPs-induced death of EA.hy926 cells
Autophagy. 2021 Dec;17(12):4266-4285.
HUVECs
100 μM
24 h
DFP significantly alleviated ZnONPs-induced death of HUVECs
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