Table 5.

Metabolic and other effects of iron chelating drugs in patients.

Increase in iron excretion and route of elimination in iron loaded patients	L1: Urinary iron. DFRA: Fecal iron. DFO: Urinary and fecal iron.
Differential iron removal from various organs. Efficacy is dose related.	L1 preferential iron removal from the heart and DFRA from the liver. DFO from the liver and to lesser extent from the heart. L1 iron removal from focal iron deposits in the brain of patients with neurodegenerative diseases.
Iron removal from diferric transferrin in iron loaded patients	About 40% at L1 concentrations > 0.1 mM, but not by DFO or DFRA.
Iron redistribution	DFO and especially L1 redistribute iron from the reticuloendothelial system to the erythron in anemic rheumatoid arthritis patients. DFO in cell studies. DFRA may cause redistribution of iron from the liver to other organs in thalassemia and other iron loaded patients.
Increase excretion of metals other than iron, e.g., zinc (Zn) and aluminum (Al).	DTPA > L1 > DFO. (Order of increased Zn excretion in iron loaded patients). DFO and L1 cause increase Al excretion in renal dialysis patients. DFRA causes Al and other xenobiotic metal absorption.
Iron mobilization and excretion of chelator metabolite iron complexes	Several DFO metabolites have iron chelation potential and cause increase in iron excretion. No increase in iron excretion by the L1 glucuronide and DFRA glucuronide metabolites.
Combination chelation therapy	L1 and DFO or L1 and DFRA or other chelator combinations are likely to be more effective than monotherapy.
Chelating drug synergism with reducing agents	Ascorbic acid acts synergistically with DFO, but not with L1 or DFRA for increasing iron excretion.
Effects on iron absorption by lipophilic and hydrophilic chelators	Increase of iron absorption by maltol, 8-hydroxyquinoline and DFRA. Decrease of iron absorption by DFO, DTPA, EDTA and L1.
Chelating drugs minimizing toxicity of other drugs	L1 and ICRF187 (Dexrazoxane), but not DFRA, inhibit doxorubicin induced cardiotoxicity.
Chelator prodrugs	ICRF 187 (Dexrazoxane) is converted in vivo to an EDTA like chelator.
Chelators with enterohepatic circulation	DFRA and cholyl hydroxamic acid.