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Chemical Compound Review

Exjade     4-[(3Z,5E)-3,5-bis(6-oxo-1- cyclohexa-2,4...

Synonyms: Deferasirox, Deferasiroxum, PubChem20503, ICL-670, SureCN62042, ...
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Disease relevance of Exjade


High impact information on Exjade


Chemical compound and disease context of Exjade

  • The rapid accessibility of the oral chelators deferasirox and deferiprone to intracellular labile iron compartments renders them potentially efficacious for protection from and possibly reversal of cardiac damage induced by iron overload [7].
  • Two molecules of deferasirox can form a complex with ferric iron (Fe-[ICL670]2) that can be excreted, reducing body iron overload [8].
  • Recent clinical studies indicate that oral ICL670 treatment is well tolerated and is as effective as parenteral DFO used at the standard dose of 40 mg/kg of body weight/day [9].

Biological context of Exjade

  • In the context of the pharmacokinetic properties of deferasirox and Fe-[ICL670]2, the data indicate the importance of plasma protein binding for their disposition and support a comparison of the pharmacokinetics of deferasirox and its iron complex across species [8].
  • Investigations with isolated proteins pointed to serum albumin as the principal binding protein for deferasirox and its iron complex in human plasma [8].
  • These results suggested that ICL670A has the most efficient antitumoral effect, blocks cell proliferation by a pathway different of O-trensox and may constitute a potential drug for anticancer therapy [10].
  • O-trensox and ICL670A induced a cell cycle blockade in G0-G1 and S phases respectively [10].
  • Competition binding experiments indicated that deferasirox at high concentrations displaced markers from the two main drug binding sites of human albumin, whereas Fe-[ICL670]2 displaced only warfarin [8].

Anatomical context of Exjade

  • This occurred in spite of the fact that ICL670A quickly and efficiently removed iron(III) from its complex with doxorubicin, and rapidly entered myocytes and displaced iron from a fluorescence-quenched trapped intracellular iron-calcein complex [5].
  • The new orally active iron chelator ICL670A exhibits a higher antiproliferative effect in human hepatocyte cultures than O-trensox [10].
  • Deferiprone is licensed in Europe and India, and deferasirox (ICL670) holds out important promise because it has not been shown to affect blood cell counts [11].

Associations of Exjade with other chemical compounds

  • Abnormal laboratory studies with deferasirox were occasionally associated with mild non-progressive increases in serum creatinine and reversible elevations in liver function tests [6].
  • RESULTS: Following 48 weeks of treatment in the phase III study, patients' liver iron concentrations (a key endpoint variable) had decreased an average of 2.4 mg of iron (Fe)/g dry weight (dw) and 2.9 mg Fe/g dw in the deferasirox and deferoxamine groups, respectively, despite continued blood transfusions in both cohorts [12].

Gene context of Exjade

  • In particular, comparison of the iron-clearing properties of DFO, L1, CP94 and HBED in marmosets and humans demonstrated the predictive value of the model and justify our expectation that if iron chelators such as CGP65015, ICL670A and CGP75254A are active in marmosets, they will be active in humans as well [13].

Analytical, diagnostic and therapeutic context of Exjade


  1. A phase 3 study of deferasirox (ICL670), a once-daily oral iron chelator, in patients with beta-thalassemia. Cappellini, M.D., Cohen, A., Piga, A., Bejaoui, M., Perrotta, S., Agaoglu, L., Aydinok, Y., Kattamis, A., Kilinc, Y., Porter, J., Capra, M., Galanello, R., Fattoum, S., Drelichman, G., Magnano, C., Verissimo, M., Athanassiou-Metaxa, M., Giardina, P., Kourakli-Symeonidis, A., Janka-Schaub, G., Coates, T., Vermylen, C., Olivieri, N., Thuret, I., Opitz, H., Ressayre-Djaffer, C., Marks, P., Alberti, D. Blood (2006) [Pubmed]
  2. Oral chelators deferasirox and deferiprone for transfusional iron overload in thalassemia major: new data, new questions. Neufeld, E.J. Blood (2006) [Pubmed]
  3. Deferasirox, an iron-chelating agent, as salvage therapy for rhinocerebral mucormycosis. Reed, C., Ibrahim, A., Edwards, J.E., Walot, I., Spellberg, B. Antimicrob. Agents Chemother. (2006) [Pubmed]
  4. The iron chelator deferasirox protects mice from mucormycosis through iron starvation. Ibrahim, A.S., Gebermariam, T., Fu, Y., Lin, L., Husseiny, M.I., French, S.W., Schwartz, J., Skory, C.D., Edwards, J.E., Spellberg, B.J. J. Clin. Invest. (2007) [Pubmed]
  5. The oral iron chelator ICL670A (deferasirox) does not protect myocytes against doxorubicin. Hasinoff, B.B., Patel, D., Wu, X. Free Radic. Biol. Med. (2003) [Pubmed]
  6. A randomised comparison of deferasirox versus deferoxamine for the treatment of transfusional iron overload in sickle cell disease. Vichinsky, E., Onyekwere, O., Porter, J., Swerdlow, P., Eckman, J., Lane, P., Files, B., Hassell, K., Kelly, P., Wilson, F., Bernaudin, F., Forni, G.L., Okpala, I., Ressayre-Djaffer, C., Alberti, D., Holland, J., Marks, P., Fung, E., Fischer, R., Mueller, B.U., Coates, T. Br. J. Haematol. (2007) [Pubmed]
  7. Action of chelators in iron-loaded cardiac cells: accessibility to intracellular labile iron and functional consequences. Glickstein, H., El, R.B., Link, G., Breuer, W., Konijn, A.M., Hershko, C., Nick, H., Cabantchik, Z.I. Blood (2006) [Pubmed]
  8. In vitro blood distribution and plasma protein binding of the iron chelator deferasirox (ICL670) and its iron complex Fe-[ICL670]2 for rat, marmoset, rabbit, mouse, dog, and human. Weiss, H.M., Fresneau, M., Camenisch, G.P., Kretz, O., Gross, G. Drug Metab. Dispos. (2006) [Pubmed]
  9. Objectives and mechanism of iron chelation therapy. Hershko, C., Link, G., Konijn, A.M., Cabantchik, Z.I. Ann. N. Y. Acad. Sci. (2005) [Pubmed]
  10. The new orally active iron chelator ICL670A exhibits a higher antiproliferative effect in human hepatocyte cultures than O-trensox. Chantrel-Groussard, K., Gaboriau, F., Pasdeloup, N., Havouis, R., Nick, H., Pierre, J.L., Brissot, P., Lescoat, G. Eur. J. Pharmacol. (2006) [Pubmed]
  11. New therapies for sickle cell disease. Okpala, I.E. Hematol. Oncol. Clin. North Am. (2005) [Pubmed]
  12. Deferasirox for the treatment of chronic iron overload in transfusional hemosiderosis. Shashaty, G., Frankewich, R., Chakraborti, T., Choudary, J., Al-Fayoumi, S., Kacuba, A., Castillo, S., Robie-Suh, K., Rieves, D., Weiss, K., Pazdur, R. Oncology (Williston Park, N.Y.) (2006) [Pubmed]
  13. Chelator-induced iron excretion in iron-overloaded marmosets. Sergejew, T., Forgiarini, P., Schnebli, H.P. Br. J. Haematol. (2000) [Pubmed]
  14. ICL670A: a new synthetic oral chelator: evaluation in hypertransfused rats with selective radioiron probes of hepatocellular and reticuloendothelial iron stores and in iron-loaded rat heart cells in culture. Hershko, C., Konijn, A.M., Nick, H.P., Breuer, W., Cabantchik, Z.I., Link, G. Blood (2001) [Pubmed]
  15. Iron chelator research: past, present, and future. Tam, T.F., Leung-Toung, R., Li, W., Wang, Y., Karimian, K., Spino, M. Current medicinal chemistry. (2003) [Pubmed]
  16. Safety, tolerability, and pharmacokinetics of ICL670, a new orally active iron-chelating agent in patients with transfusion-dependent iron overload due to beta-thalassemia. Galanello, R., Piga, A., Alberti, D., Rouan, M.C., Bigler, H., Séchaud, R. Journal of clinical pharmacology. (2003) [Pubmed]
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