| Indication | For the treatment of chronic iron overload due to blood transfusions (transfusional hemosiderosis) in patients 2 years of age and older. |
| Pharmacodynamics | Deferasirox is an orally active chelator that is selective for iron (as Fe3+). It is a tridentate ligand that binds iron with high affinity in a 2:1 ratio. Although deferasirox has very low affinity for zinc and copper there are variable decreases in the serum concentration of these trace metals after the administration of deferasirox. The clinical significance of these decreases is uncertain. |
| Mechanism of action | Two molecules of deferasirox are capable of binding to 1 atom of iron. Deferasirox works in treating iron toxicity by binding trivalent (ferric) iron (for which it has a strong affinity), forming a stable complex which is eliminated via the kidneys. |
| Absorption | The absolute bioavailability (AUC) of deferasirox tablets for oral suspension is 70% compared to an intravenous dose. |
| Volume of distribution | |
| Protein binding | Deferasirox is highly (~99%) protein bound almost exclusively to serum albumin. |
| Metabolism | Hepatic. CYP450-catalyzed (oxidative) metabolism of deferasirox appears to be minor in humans (about 8%). Glucuronidation is the main metabolic pathway for deferasirox, with subsequent biliary excretion. |
| Route of elimination | Deferasirox and metabolites are primarily (84% of the dose) excreted in the feces. Renal excretion of deferasirox and metabolites is minimal (8% of the administered dose). |
| Half life | The mean elimination half-life ranged from 8 to 16 hours following oral administration. |
| Clearance | Not Available |
| Toxicity | Not Available |
Deferasirox (marketed as Exjade, Desirox, Defrijet, Desifer...) is an iron chelator. Its main use is to reduce chronic iron overload in patients who are receiving long-term blood transfusions for conditions such as beta-thalassemia and other chronic anemias. Deferasirox
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