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Iron Balance Study of DFO and GT56-252 in Patients With Transfusional Iron Overload Secondary to Beta-Thalassemia

2014-07-23 21:52:15 | BioPortfolio

Summary

A clinical trial designed to compare the safety and iron excretion properties of desferoxamine (DFO) and deferitrin (GT56-252), an experimental oral iron chelator.

Study Design

Allocation: Non-Randomized, Control: Active Control, Endpoint Classification: Safety/Efficacy Study, Intervention Model: Crossover Assignment, Masking: Open Label, Primary Purpose: Treatment

Conditions

Beta-Thalassemia

Intervention

Deferitrin (GT56-252), desferoxamine (DFO)

Location

The New York Presbyterian Hospital-Weill Medical College of Cornell University
New York
New York
United States
10021

Status

Completed

Source

Genzyme

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-07-23T21:52:15-0400

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Medical and Biotech [MESH] Definitions

A disorder characterized by reduced synthesis of the beta chains of hemoglobin. There is retardation of hemoglobin A synthesis in the heterozygous form (thalassemia minor), which is asymptomatic, while in the homozygous form (thalassemia major, Cooley's anemia, Mediterranean anemia, erythroblastic anemia), which can result in severe complications and even death, hemoglobin A synthesis is absent.

A hereditary disorder characterized by reduced or absent DELTA-GLOBIN thus effecting the level of HEMOGLOBIN A2, a minor component of adult hemoglobin monitored in the diagnosis of BETA-THALASSEMIA.

An abnormal hemoglobin composed of four beta chains. It is caused by the reduced synthesis of the alpha chain. This abnormality results in ALPHA-THALASSEMIA.

An adult hemoglobin component normally present in hemolysates from human erythrocytes in concentrations of about 3%. The hemoglobin is composed of two alpha chains and two delta chains. The percentage of HbA2 varies in some hematologic disorders, but is about double in beta-thalassemia.

A group of enzymes that catalyzes the hydrolysis of terminal, non-reducing beta-D-galactose residues in beta-galactosides. Deficiency of beta-Galactosidase A1 may cause GANGLIOSIDOSIS, GM1.

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