Patients with beta (β)-thalassemia who have high levels of fetal hemoglobin (HbF) have less
severe anemia and are often transfusion-independent. Therefore, augmentation of HbF
production has been a longstanding therapeutic objective. Three classes of HbF-inducing
agents have been investigated for the treatment of β-thalassemia including
chemotherapeutics, short-chain fatty acid derivatives, and recombinant erythropoietin. These
agents have several different mechanisms of action and have been shown to increase total …