Deferiprone (Deferidone) is an Iron Chelator. The mechanism of action of deferiprone is as an Iron Chelating Activity.

At a concentration of 1 mM, Deferiprone causes a significant decrease in complex I-III activity in iron-overloaded cardiomyocytes. It exhibits cytotoxic effects on human tumor cell lines HSC-2, HSC-3, and HL-60, with IC50 values of 13.5 μg/mL, 9.9 μg/mL, and 10.6 μg/mL, respectively. The cytotoxicity of HK1 against HL-60 and HSC-2 cells is reduced in the presence of FeCl3. At 100 μg/mL, Deferiprone induces inter-nucleosomal DNA fragmentation in HL-60 cells, a process inhibited by the addition of FeCl3. Protection of myocytes from doxorubicin-induced lactate dehydrogenase release is observed with 100 μM Deferiprone. It effectively inhibits the transfer of radiolabeled iron from iron-loaded cardiomyocytes and protects or restores mitochondrial respiratory enzyme activity in a xanthine oxidase/hypoxanthine superoxide generating system at a concentration of 0.3 mM. Furthermore, 0.5 mM Deferiprone enhances the clearance of free iron from RBC membranes in a time- and dose-dependent manner. A 3 mM concentration significantly reduces hydroxyl radical production from the iron(III)-adriamycin complex in the xanthine oxidase/hypoxanthine superoxide generating system.

Administration of 100 mg/kg Deferiprone resulted in a 24% reduction in the average cross-sectional area of the basilar artery in rabbits. When combined with subarachnoid hemorrhage (SAH), Deferiprone also demonstrated variability in the waviness of the internal elastic lamina in rabbits.