INDICATIONS

REBLOZYL is indicated for the treatment of anemia in adult patients with beta thalassemia who require regular red blood cell (RBC) transfusions.

REBLOZYL is indicated for the treatment of anemia failing an erythropoiesis stimulating agent and requiring 2 or more red blood cell units over 8 weeks in adult patients with very low- to intermediate-risk myelodysplastic syndromes with ring sideroblasts (MDS-RS) or with myelodysplastic/myeloproliferative neoplasm with ring sideroblasts and thrombocytosis (MDS/MPN-RS-T).

REBLOZYL is not indicated for use as a substitute for RBC transfusions in patients who require immediate correction of anemia.

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THE NEED FOR REBLOZYL: MECHANISM OF ACTION

Impaired erythroid maturation graphic Impaired erythroid maturation graphic

EARLY-STAGE ERYTHROPOIESIS

Endogenous erythropoietin regulates proliferation4

LATE-STAGE ERYTHROPOIESIS

Select TGF-β superfamily ligands help regulate maturation TGF-β superfamily signaling through Smad2/3 is abnormally high in diseases characterized by ineffective erythropoiesis, which leads to impaired erythroid maturation of RBCs5-7

For illustrative purposes only.

BFU-E=burst-forming unit erythroid; CFU-E=colony-forming unit erythroid; HSC=hematopoietic stem cell; RBC=red blood cell; TGF-beta=transforming growth factor beta.

REBLOZYL restores erythropoiesis by increasing the number and improving the quality of mature RBCs as observed in preclinical studies1

REBLOZYL® enhanced erythroid maturation graphic REBLOZYL® enhanced erythroid maturation graphic

EARLY-STAGE ERYTHROPOIESIS

Endogenous erythropoietin regulates proliferation4

LATE-STAGE ERYTHROPOIESIS

REBLOZYL regulates erythroid maturation REBLOZYL binds several TGF-β superfamily ligands, thereby diminishing Smad2/3 signaling and increasing the number of mature RBCs1,6,7

For illustrative purposes only.

In preclinical models, REBLOZYL improved Hgb levels, RBC morphology, and other hematology parameters* associated with ineffective erythropoiesis1,6

*Other hematology parameters include reducing oxidative stress in erythrocytes, reducing accumulation of α-globin aggregates in erythrocyte membranes, and improving RBC life span.

Hgb=hemoglobin.

THE NEED FOR REBLOZYL: MECHANISM OF ACTION

Impaired erythroid maturation graphic Impaired erythroid maturation graphic

EARLY-STAGE ERYTHROPOIESIS

Endogenous erythropoietin regulates proliferation4

LATE-STAGE ERYTHROPOIESIS

Select TGF-β superfamily ligands help regulate maturation TGF-β superfamily signaling through Smad2/3 is abnormally high in diseases characterized by ineffective erythropoiesis, which leads to impaired erythroid maturation of RBCs5-7

For illustrative purposes only.

BFU-E=burst-forming unit erythroid; CFU-E=colony-forming unit erythroid; HSC=hematopoietic stem cell; RBC=red blood cell; TGF-beta=transforming growth factor beta.

REBLOZYL restores erythropoiesis by increasing the number and improving the quality of mature RBCs as observed in preclinical studies1

REBLOZYL® enhanced erythroid maturation graphic REBLOZYL® enhanced erythroid maturation graphic

EARLY-STAGE ERYTHROPOIESIS

Endogenous erythropoietin regulates proliferation4

LATE-STAGE ERYTHROPOIESIS

REBLOZYL regulates erythroid maturation REBLOZYL binds several TGF-β superfamily ligands, thereby diminishing Smad2/3 signaling and increasing the number of mature RBCs1,6,7

For illustrative purposes only.

In preclinical models, REBLOZYL improved Hgb levels, RBC morphology, and other hematology parameters* associated with ineffective erythropoiesis1,6

*Other hematology parameters include reducing oxidative stress in erythrocytes, reducing accumulation of α-globin aggregates in erythrocyte membranes, and improving RBC life span.

Hgb=hemoglobin.

References: 1. REBLOZYL [US Prescribing Information]. Summit, NJ: Celgene Corporation; 2022. 2. Liang R, Ghaffari S. Advances in understanding the mechanisms of erythropoiesis in homeostasis and disease. Br J Haematol. 2016;174(5):661-673. 3. Ponka P, Koury MJ, Sheftel AD. Erythropoiesis, hemoglobin synthesis, and erythroid mitochondrial iron homeostasis. In: Ferreira GC, ed. Handbook of Porphyrin Science: With Applications to Chemistry, Physics, Materials Science, Engineering, Biology and Medicine. Vol 27. Singapore: World Scientific Publishing Co.; 2014. 4. Lodish H, Flygare J, Chou S. From stem cell to erythroblast: regulation of red cell production at multiple levels by multiple hormones. IUBMB Life. 2010;62(7):492-496. 5. Fortunel NO, Hatzfeld A, Hatzfeld JA. Transforming growth factor-β: pleiotropic role in the regulation of hematopoiesis. Blood. 2000;96(6):2022-2036. 6. Suragani RN, Cadena SM, Cawley SM, et al. Transforming growth factor-β superfamily ligand trap ACE-536 corrects anemia by promoting late-stage erythropoiesis. Nat Med. 2014;20(4):408-414. 7. Attie KM, Allison MJ, McClure T, et al. A phase 1 study of ACE-536, a regulator of erythroid differentiation, in healthy volunteers. Am J Hematol. 2014;89(7):766-770.