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Iron-Chelating Therapy and Friedreich Ataxia

NCT00224640 · Status: COMPLETED · Phase: PHASE1/PHASE2 · Type: INTERVENTIONAL · Enrollment: 15

Last updated 2009-03-04

No results posted yet for this study

Summary

Friedreich ataxia, an autosomal recessive condition, ascribed to frataxin gene expansion, has been shown to result from an iron- induced injury to the mitochondrial respiratory chain. Buffering free radicals with short-chain quinones (Idebenone) protects the patients against cardiomyopathy but not CNS involvement. Removing CNS iron should limit the impact of the neurological symptoms of the disease.

Conditions

  • Friedreich Ataxia

Interventions

DRUG

Iron chelating intervention

Iron chelating intervention

Sponsors & Collaborators

  • Assistance Publique - Hôpitaux de Paris

    lead OTHER

Principal Investigators

  • Arnold MUNNICH, Pr,MD,PhD · Assistance Publique - Hôpitaux de Paris

Study Design

Allocation
NON_RANDOMIZED
Purpose
TREATMENT
Masking
NONE
Model
SINGLE_GROUP

Eligibility

Min Age
13 Years
Sex
ALL
Healthy Volunteers
No

Timeline & Regulatory

Start
2005-03-31
Primary Completion
2008-03-31
Completion
2008-03-31

Countries

  • France

Study Locations

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Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT00224640 on ClinicalTrials.gov