Iron chelation — the trapping of harmful, unbound iron — is a possible therapy for FA. A 2008 study in research mice that didn’t produce frataxin in their hearts showed that iron chelation significantly decreased iron levels in the heart and limited the harmful increase in the size of the cardiac muscle normally seen in frataxin-deficient mice. An ongoing study to evaluate the effects of an iron chelator called deferiprone in people with FA in Europe may increase understanding of whether iron chelation should be part of an FA therapy regimen.
There is some evidence that combining an antioxidant with an iron chelator may be beneficial. A 20-person study for which results were announced in 2010 found that a combination of idebenone and deferiprone had a “stabilizing effect” on neurological function and reduced abnormal heart-muscle enlargement in people with FA who received the two-drug combination for 11 months.