Deferiprone

Cell lines

Ventricular myocytes isolated from 1 ~ 3 d old Sprague Dawley rats

Reaction Conditions

50, 100 and 500 μM deferiprone

Applications

Deferiprone (100 and 500 μM) rapidly entered myocytes and displaced iron from its complex with doxorubicin. Deferiprone (3 mM) also greatly reduced hydroxyl radical production by the iron(III)-doxorubicin complex in the xanthine oxidase/xanthine superoxide generating system. Therefore, deferiprone could protect against doxorubicin-induced damage to myocytes by displacing iron bound to doxorubicin, or chelating free or loosely bound iron, thus preventing site-specific iron-based oxygen radical damage.

Animal models

A rabbit model of subarachnoid hemorrhage (SAH)

Dosage form

100 mg/kg

Administered orally 8 hours after SAH, with the last dose administered 8 hours before the animals were killed, for a total of five doses

Applications

Deferiprone reduced the average luminal cross-sectional area of the basilar artery by 24% in SAH rabbits, significantly attenuating the vasospastic response after SAH. Because of its stability, lipophilicity, and ability to penetrate the blood-brain barrier, deferiprone could serve as an attractive candidate for the treatment of cerebral vasospasm.

Note

The technical data provided above is for reference only.

References:

1. Barnabé N, Zastre JA, Venkataram S, et al. Deferiprone protects against doxorubicin-induced myocyte cytotoxicity. Free Radical Biology and Medicine, 2002, 33(2): 266-275.

2. Arthur AS, Fergus AH, Lanzino G, et al. Systemic administration of the iron chelator deferiprone attenuates subarachnoid hemorrhage-induced cerebral vasospasm in the rabbit. Neurosurgery, 1997, 41(6): 1385-1391.