| 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 |
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