Luspatercept: Fewer Transfusions in Beta Thalassaemia and the Iron Question

Table of Contents

1. Why Beta Thalassaemia Needs Transfusions
2. How Transfusions Bring Iron Overload
3. What Luspatercept Is and How It Works
4. FDA Approvals and What the Label Covers
5. The BELIEVE Trial in Transfusion-Dependent Thalassaemia
6. BEYOND: Thalassaemia Without Regular Transfusions
7. What Happened to Iron: Ferritin, Liver and Heart
8. Myelodysplastic Syndromes: MEDALIST and COMMANDS
9. Side Effects and Label Warnings
10. What Is Not Known
11. Key Research Papers
12. Connections
13. Featured Videos

Why Beta Thalassaemia Needs Transfusions

Haemoglobin, the protein that carries oxygen inside red blood cells, is built from two kinds of chains: alpha chains and beta chains. In beta thalassaemia a faulty gene means too few beta chains are made, or none. The alpha chains are then left without partners. A 2014 study in mice with beta thalassaemia describes what follows: the unpaired alpha chains clump together inside developing red cells, the cells die before they finish maturing, and the later stages of red-cell development are held back. The result is anaemia, a bone marrow that works hard but produces too few good cells, and disturbed iron handling.

Doctors call this ineffective erythropoiesis (erythropoiesis means making red blood cells). A 2022 review in the journal Blood describes it as a large expansion of early red-cell precursors, driven by the kidney hormone erythropoietin, together with the death of many late-stage precursors before they reach the bloodstream. The review names beta thalassaemia as one of the main inherited causes, and some types of myelodysplastic syndrome as an acquired cause.

In the severe form of the disease the anaemia is so deep that regular red-cell transfusions are the standard treatment. The BELIEVE trial, described below, enrolled adults who needed 6 to 20 units of red cells every 24 weeks, according to the United States label. People with milder disease, called non-transfusion-dependent thalassaemia, need transfusions only now and then, or not at all, but still live with anaemia and its effects.

How Transfusions Bring Iron Overload

Every unit of transfused blood carries iron, and the human body has no active way to get rid of extra iron. In the BELIEVE biomarker analysis the researchers counted 1.4 grams of iron as roughly 7 units of blood. Over years of transfusions the iron builds up in the liver, the heart and the hormone glands. This is why people with transfusion-dependent thalassaemia also take iron chelators, medicines that bind iron so it can leave the body. The chelators and their own risks are described on the Thalassaemia page and the Iron Overload and Iron Toxicity page.

Thalassaemia also loads iron without transfusions. The 2022 Blood review explains that the overgrown red-cell marrow releases signals that suppress hepcidin, the liver hormone that normally limits how much iron the gut absorbs. With hepcidin low, the gut takes in more iron than the body needs. The review calls these conditions "iron-loading anaemias" for that reason. A 2023 review of non-transfusion-dependent thalassaemia describes anaemia and iron overload as the two linked problems at the heart of that milder form.

So in thalassaemia two things feed iron overload: the transfusions themselves, and the gut's increased absorption. Luspatercept aims at the first by reducing the number of transfusions. Its effect on the second is more complicated, as the iron section below shows.

What Luspatercept Is and How It Works

Luspatercept (known in early research as ACE-536, and in the United States label as luspatercept-aamt) is a man-made fusion protein. A 2022 review describes it as part of a receptor called activin receptor type IIB, changed slightly, joined to a piece of a human antibody (the Fc part of immunoglobulin G1) that keeps it in the blood longer. Because it is a protein it cannot be swallowed; it is injected under the skin.

The drug is called a ligand trap. Instead of blocking a receptor on a cell, it floats in the blood and catches certain signalling proteins (ligands) before they reach their receptors on red-cell precursors. These signalling proteins belong to the transforming growth factor beta family. When they reach the cells, they switch on an internal pathway known as SMAD2/3, which holds back the final stages of red-cell maturation. Catching them lets more precursors finish maturing.

• The 2014 discovery work. In the founding study, the mouse version of the drug produced rapid rises in red-cell numbers in several animal species and reduced or prevented anaemia in mouse models. Unlike erythropoietin, which mainly drives early precursors to multiply, it promoted the maturation of late-stage precursors in mice. The protein bound a signalling molecule called growth differentiation factor 11 and blocked its SMAD2/3 signal; growth differentiation factor 11 itself held back red-cell maturation in mice.
• In mice with beta thalassaemia. A second 2014 study found that, in mice, the drug reduced alpha-chain clumps in red cells, lowered harmful reactive oxygen molecules, relieved anaemia, and lessened iron overload, spleen enlargement and bone damage.
• The label's summary. The United States label states that the drug binds several transforming growth factor beta family ligands and lowers SMAD2/3 signalling; that in mouse models of beta thalassaemia and myelodysplastic syndromes it increased late-stage precursors in the marrow; and that in humans it increased red-cell precursors. The label calls it an "erythroid maturation agent".

This is a different approach from erythropoietin-type drugs (erythropoiesis-stimulating agents), which push the early stages. The 2014 study found that combining the two gave a stronger red-cell response in animals than either alone.

FDA Approvals and What the Label Covers

The Drugs@FDA record for the medicine (biologics licence application 761136) lists these approvals:

• 8 November 2019: original approval, as a new molecular entity under priority review, with orphan designation. This approval covered anaemia in adults with beta thalassaemia who need regular red-cell transfusions. The label gives "Initial U.S. Approval: 2019".
• 3 April 2020: an efficacy approval. The label's use in lower-risk myelodysplastic syndromes with ring sideroblasts after an erythropoiesis-stimulating agent has failed matches the MEDALIST trial population.
• 28 August 2023: an efficacy supplement under priority review. The current label covers anaemia in adults with very-low- to intermediate-risk myelodysplastic syndromes who have not had an erythropoiesis-stimulating agent before and who may need regular transfusions, which is the COMMANDS trial population. This made it a first treatment option rather than a second one in that group.

According to the current label (revised February 2026), luspatercept is not a substitute for transfusions in people who need their anaemia corrected immediately. The label states that it is not indicated for people with non-transfusion-dependent beta thalassaemia, even though the BEYOND trial studied that group. On children, the label states that safety and effectiveness have not been established, and that, based on findings in young animals, the drug is not recommended for children. The BELIEVE trial excluded people with haemoglobin S (the sickle-cell gene) and people with alpha-thalassaemia disease, and sickle cell disease is not among the label's uses.

Doses as the label states them: for beta thalassaemia, a starting dose of 1 mg per kilogram of body weight once every 3 weeks under the skin, which may be raised to a maximum of 1.25 mg/kg if transfusion needs do not fall. For myelodysplastic syndromes, the same starting dose with a maximum of 1.75 mg/kg. The label states that haemoglobin results are reviewed before each dose and that the injection is prepared and given by a healthcare professional.

The BELIEVE Trial in Transfusion-Dependent Thalassaemia

BELIEVE was the phase 3 trial behind the 2019 approval. It enrolled 336 adults with transfusion-dependent beta thalassaemia and randomly assigned them, two to one, to luspatercept (224 people) or placebo (112 people), both on top of usual care including transfusions and iron chelation. Neither patients nor doctors knew who received which. Treatment lasted a median of about 64 weeks in both groups.

The main goal was strict: a cut of at least one third in the number of units transfused during weeks 13 to 24, and at least 2 fewer units over those 12 weeks. The published results in the New England Journal of Medicine (2020) were:

• Main goal reached: 21.4% on luspatercept vs 4.5% on placebo. The current label, using the later data, gives 21.0% (47 of 224) vs 4.5%.
• At least a one-third cut over any 12-week stretch: 70.5% vs 29.5%.
• At least a one-half cut over any 12-week stretch: 40.2% vs 6.3%.
• Blood ferritin (a marker of stored iron) at week 48: 348 micrograms per litre lower on luspatercept than on placebo.
• Transient bone pain, joint pain, dizziness, high blood pressure and raised uric acid were more common on luspatercept. Few side effects led people to stop treatment.

Put plainly, most people on the drug still needed transfusions. What changed for many of them was how many. Only about one in five met the trial's main goal in the fixed weeks 13 to 24, while about seven in ten had at least a one-third reduction at some point.

The final results, about three years on

The final BELIEVE report (2025) followed patients for a median of 163 weeks; people on placebo could switch to the drug after the trial was unblinded. Because the two groups were then treated for very different lengths of time, the researchers made no comparisons between them after week 96. In the luspatercept group:

• Transfusion needs stayed lower through week 192, with mean decreases of 6.2 units during weeks 97 to 144 and 6.4 units during weeks 145 to 192.
• 173 people (77%) had a cut of at least one third over some 12-week stretch, and 116 (52%) over some 24-week stretch. The median total time spent in such a response was 586 days.
• Among all 315 people who received the drug, including 92 who crossed over, the most common severe side effects were anaemia (3%), increased liver iron (2%) and bone pain (2%). Serious side effects of any kind occurred in 23%. No deaths were judged to be caused by treatment.

The first study, open-label

Before BELIEVE, a phase 2 study that began in 2013 gave the drug to 64 adults with either form of beta thalassaemia, with an extension of up to five years and no placebo group. Among 32 transfusion-dependent patients on the higher doses, 19 (59.4%) had at least a one-half cut in transfusions over some 12-week stretch. The median total time in response was 909 days for transfusion-dependent patients and 1,126 days for the others. Bone pain, headache and muscle pain were the most common treatment-related side effects.

BEYOND: Thalassaemia Without Regular Transfusions

BEYOND was a phase 2 trial in adults with non-transfusion-dependent beta thalassaemia whose haemoglobin was 10 g/dL or lower. It enrolled 145 people in six countries, randomly assigned two to one to luspatercept (96) or placebo (49) for 48 weeks, with neither side knowing who received which.

• The main goal was a rise of at least 1.0 g/dL in average haemoglobin over 12 weeks in weeks 13 to 24, without transfusions. It was reached by 74 of 96 people (77%) on luspatercept and none on placebo.
• Serious side effects were less common on luspatercept (12% vs 25%).
• The most common side effects on luspatercept were bone pain (37%), headache (30%) and joint pain (29%). No blood clots or deaths were reported in that first phase.

The final BEYOND report (2025) added about 2.2 years of follow-up, with median treatment of 202.8 weeks on luspatercept. Over the whole study, 94.8% on luspatercept and 22.4% on placebo had a haemoglobin rise of at least 1.0 g/dL over some 12-week stretch. Patient-reported tiredness and weakness stayed improved. Headache (45.8% vs 20.4%), bone pain (43.8% vs 6.1%), back pain (39.6% vs 12.2%) and joint pain (38.5% vs 16.3%) were the most common side effects. Masses of blood-forming tissue outside the marrow were reported in 12 people (9.0%) on luspatercept and 2 (4.1%) on placebo, although the authors note that the very different treatment times prevent a fair comparison. Four people on luspatercept had blood clots, and each had more than one risk factor.

Despite these results, the United States label states that the drug is not indicated for non-transfusion-dependent beta thalassaemia. A 2023 review by thalassaemia specialists discusses it as one of the newer agents for anaemia-related complications in this group.

What Happened to Iron: Ferritin, Liver and Heart

The hope was simple: fewer transfusions, less iron. The detailed BELIEVE biomarker analysis, published in 2024, shows the story is less simple.

• Iron coming in fell. The rate of iron loading from transfusions dropped by 20%, about 1.4 grams of iron, roughly 7 units of blood.
• Blood ferritin fell. Serum ferritin dropped 19.2%, by an average of 269.3 micrograms per litre. The authors read this as less iron stored in the scavenger cells (macrophages) that break down old red cells.
• Liver iron did not fall. Liver iron content rose from 5.3 to 6.7 mg per gram of dry liver, a change that was not statistically significant. The rise was seen in patients who still had their spleen.
• Hepcidin fell by half. Erythropoietin rose 93%, the marrow signal growth differentiation factor 15 rose 59%, soluble transferrin receptor rose 66%, reticulocytes (young red cells) rose 112%, the hormone erythroferrone rose 51%, and hepcidin fell 53%.

The authors' reading is that luspatercept makes the marrow more active, the active marrow suppresses hepcidin, and the body's iron is moved out of macrophages and into liver cells. They conclude that this means chelation still has to continue alongside the drug for iron to be managed. In the long-term BELIEVE report, "increased liver iron concentration" was one of the three most common severe side effects, in 2% of patients.

So ferritin, the blood test most people with thalassaemia know, can fall while liver iron stays the same or rises. That gap is one reason liver iron is measured separately rather than read from ferritin alone.

The heart. Heart iron is the most dangerous kind, as the Iron Overload: Heart Problems page explains. The BELIEVE papers read for this page report ferritin and liver iron, but their summaries give no figures for heart iron. Whether luspatercept changes iron in the heart is not shown in the trial reports summarised here.

Myelodysplastic Syndromes: MEDALIST and COMMANDS

Myelodysplastic syndromes (MDS) are a group of bone-marrow disorders, mostly in older adults, in which the marrow makes blood cells that do not mature properly. Many people with the lower-risk forms become anaemic and dependent on transfusions, and they too build up iron. The Myelodysplastic Syndrome page covers the condition.

MEDALIST (2020)

MEDALIST was a phase 3, placebo-controlled trial in 229 people with lower-risk myelodysplastic syndromes with ring sideroblasts (red-cell precursors with a ring of iron around the nucleus) who needed regular transfusions and for whom erythropoiesis-stimulating agents had not worked, were unlikely to work, or had to be stopped. Freedom from transfusions for at least 8 weeks during weeks 1 to 24 was reached by 38% on luspatercept vs 13% on placebo. Freedom for at least 12 weeks was reached by 28% vs 8% in weeks 1 to 24, and 33% vs 12% in weeks 1 to 48. Fatigue, diarrhoea, weakness, nausea and dizziness were the most common side effects, and side effects became less frequent over time.

COMMANDS (2023 and 2024)

COMMANDS compared luspatercept head to head with epoetin alfa, the usual first erythropoiesis-stimulating agent, in people with lower-risk myelodysplastic syndromes who had never had such an agent and who needed 2 to 6 units of blood every 8 weeks. It was an open-label trial (people knew which drug they were getting) at 142 sites in 26 countries; the median age was 74.

• The main goal was freedom from transfusions for at least 12 weeks together with a haemoglobin rise of at least 1.5 g/dL in weeks 1 to 24.
• At the interim analysis (2023), it was reached by 86 of 147 people (59%) on luspatercept vs 48 of 154 (31%) on epoetin alfa.
• At the primary analysis (2024), with all 363 people, it was reached by 110 (60%) vs 63 (35%).
• In a 2025 long-term analysis, a single transfusion-free stretch of at least one year was reached by 44.5% vs 27.6%, and of at least 1.5 years by 30.2% vs 13.8%. Progression to higher-risk disease or acute myeloid leukaemia was below 5% in both groups.
• The most common severe side effects on luspatercept in the primary analysis were high blood pressure (10%), anaemia (10%), pneumonia (5%), fainting (5%) and low white-cell and platelet counts. In the interim report one death, after a diagnosis of acute myeloid leukaemia 44 days into treatment, was considered related to luspatercept.

The interim report's authors wrote that longer follow-up is needed to confirm the results and to define them in subgroups, including people without the SF3B1 gene change or without ring sideroblasts.

Side Effects and Label Warnings

The United States label lists four warnings and precautions:

• Blood clots (thrombosis and thromboembolism). In adults with beta thalassaemia, clots were reported in 8 of 223 people (3.6%) on the drug, including deep-vein clots in the legs, clots in the lungs, a clot in the main vein to the liver (portal vein thrombosis) and strokes caused by a blocked artery. The label states that people with known risk factors, such as removal of the spleen (splenectomy) or hormone replacement therapy, may be at further increased risk, and it raises preventive clot treatment for those at higher risk. In BELIEVE, about 58% of patients in each group had had their spleen removed. A 2025 review notes that thalassaemia itself, especially after splenectomy, carries a raised clotting tendency, and that luspatercept's part in that risk still needs to be worked out.
• High blood pressure. It was reported in 63 of 554 people (11.4%) on the drug across studies; severe high blood pressure ranged from 2% to 9.6%. The label states that blood pressure is checked before each dose.
• Extramedullary haematopoietic masses. These are lumps of blood-forming tissue that grow outside the bone marrow, for example in the chest or next to the spine, as the body tries to make more red cells. In adults with transfusion-dependent thalassaemia, the label reports them in 3.2% of people on the drug, with symptoms of spinal cord compression in 1.9%. In non-transfusion-dependent thalassaemia they were seen in 6.3% on the drug vs 2% on placebo. The label lists possible risk factors as a history of such masses, splenectomy, an enlarged spleen or liver, and a low starting haemoglobin (below 8.5 g/dL). It states that treatment is stopped if the masses cause serious complications, and advises against use in people who need treatment to control growing masses. A 2024 case report describes one higher-risk patient with a past chest mass and a removed spleen who was treated without notable problems; a single case cannot show how safe the drug is in that group.
• Harm to an unborn baby (embryo-fetal toxicity). In pregnant rats and rabbits the drug caused more embryo and fetal deaths, growth changes and structural abnormalities at exposures above the highest human dose. There are no data in pregnant women. The label calls for a pregnancy test before starting and effective contraception during treatment and for at least 3 months after the last dose, and states that breastfeeding is not recommended during treatment and for 3 months after.

Common side effects in BELIEVE, per the label: headache (26%), bone pain (20%), joint pain (19%), fatigue (14%), cough (14%), abdominal pain (14%), diarrhoea (12%) and dizziness (11%). Bone pain was reported by 20% on the drug vs 8% on placebo, and was severe in 1%.

Signs that hospitals treat as urgent in anyone at risk of clots or of these masses include sudden chest pain or breathlessness, coughing up blood, a swollen and painful leg, sudden weakness or numbness of the face, arm or leg on one side, trouble speaking or seeing, and new back pain with weakness or numbness in the legs or loss of bladder or bowel control.

What Is Not Known

• Survival and long-term outcomes. The trials measured transfusion units and haemoglobin, not how long people live or whether they have fewer heart, liver or hormone complications. The 2022 Blood review states that the long-term effectiveness and safety of luspatercept still need to be evaluated in both beta thalassaemia and myelodysplastic syndromes.
• The heart. The trial reports summarised here give no figures for iron in the heart.
• Liver iron. The BELIEVE biomarker work found liver iron did not fall and rose in people with a spleen. How much this matters over many years is not known.
• Children. The label states that safety and effectiveness have not been established in children. BELIEVE, BEYOND, MEDALIST and COMMANDS enrolled adults only.
• Clotting risk. A 2025 review states that luspatercept's role in the thrombotic risk of thalassaemia patients still needs to be clarified.
• People with extramedullary masses. The evidence on this higher-risk group is limited to warnings, small numbers in trials and case reports.
• Non-transfusion-dependent thalassaemia. BEYOND was a phase 2 trial of 145 people. The United States label does not cover this group.
• Which patients respond. In BELIEVE about one in five met the main goal, and many never reached a one-half cut in transfusions. Ways to predict who will respond are not established in the papers summarised here.

Decisions about this medicine belong with a haematologist, the specialist who treats blood disorders.

Key Research Papers

1. Suragani RN, Cadena SM, Cawley SM, Sako D, Mitchell D, Li R, et al. Transforming growth factor-β superfamily ligand trap ACE-536 corrects anemia by promoting late-stage erythropoiesis. Nat Med. 2014;20(4):408-14. PubMed PMID: 24658078
2. Suragani RN, Cawley SM, Li R, Wallner S, Alexander MJ, Mulivor AW, et al. Modified activin receptor IIB ligand trap mitigates ineffective erythropoiesis and disease complications in murine β-thalassemia. Blood. 2014;123(25):3864-72. PubMed PMID: 24795345
3. Cazzola M. Ineffective erythropoiesis and its treatment. Blood. 2022;139(16):2460-2470. PubMed PMID: 34932791
4. Cappellini MD, Viprakasit V, Taher AT, Georgiev P, Kuo KHM, Coates T, et al. A Phase 3 Trial of Luspatercept in Patients with Transfusion-Dependent β-Thalassemia. N Engl J Med. 2020;382(13):1219-1231. PubMed PMID: 32212518
5. Cappellini MD, Viprakasit V, Georgiev P, Coates TD, Origa R, Khelif A, et al. Long-term efficacy and safety of luspatercept for the treatment of anaemia in patients with transfusion-dependent β-thalassaemia (BELIEVE): final results from a phase 3 randomised trial. Lancet Haematol. 2025;12(3):e180-e189. PubMed PMID: 39947215
6. Garbowski MW, Ugidos M, Risueño A, Shetty JK, Schwickart M, Hermine O, et al. Luspatercept stimulates erythropoiesis, increases iron utilization, and redistributes body iron in transfusion-dependent thalassemia. Am J Hematol. 2024;99(2):182-192. PubMed PMID: 37782758
7. Piga A, Longo F, Gamberini MR, Voskaridou E, Ricchi P, Caruso V, et al. Long-term safety and erythroid response with luspatercept treatment in patients with β-thalassemia. Ther Adv Hematol. 2022;13:20406207221134404. PubMed PMID: 36505885
8. Taher AT, Cappellini MD, Kattamis A, Voskaridou E, Perrotta S, Piga AG, et al. Luspatercept for the treatment of anaemia in non-transfusion-dependent β-thalassaemia (BEYOND): a phase 2, randomised, double-blind, multicentre, placebo-controlled trial. Lancet Haematol. 2022;9(10):e733-e744. PubMed PMID: 36007538
9. Taher AT, Viprakasit V, Kattamis A, Perrotta S, Ricchi P, Porter JB, et al. Efficacy and safety of luspatercept in non-transfusion-dependent β-thalassemia: long-term results from the BEYOND study. Blood Adv. 2025;9(23):6108-6119. PubMed PMID: 40875596
10. Saliba AN, Musallam KM, Taher AT. How I treat non-transfusion-dependent β-thalassemia. Blood. 2023;142(11):949-960. PubMed PMID: 37478396
11. Fenaux P, Platzbecker U, Mufti GJ, Garcia-Manero G, Buckstein R, Santini V, et al. Luspatercept in Patients with Lower-Risk Myelodysplastic Syndromes. N Engl J Med. 2020;382(2):140-151. PubMed PMID: 31914241
12. Platzbecker U, Della Porta MG, Santini V, Zeidan AM, Komrokji RS, Shortt J, et al. Efficacy and safety of luspatercept versus epoetin alfa in erythropoiesis-stimulating agent-naive, transfusion-dependent, lower-risk myelodysplastic syndromes (COMMANDS): interim analysis of a phase 3, open-label, randomised controlled trial. Lancet. 2023;402(10399):373-385. PubMed PMID: 37311468
13. Della Porta MG, Garcia-Manero G, Santini V, Zeidan AM, Komrokji RS, Shortt J, et al. Luspatercept versus epoetin alfa in erythropoiesis-stimulating agent-naive, transfusion-dependent, lower-risk myelodysplastic syndromes (COMMANDS): primary analysis of a phase 3, open-label, randomised, controlled trial. Lancet Haematol. 2024;11(9):e646-e658. PubMed PMID: 39038479
14. Garcia-Manero G, Santini V, Zeidan AM, Komrokji RS, Pozharskaya V, Rose S, et al. Long-Term Transfusion Independence with Luspatercept Versus Epoetin Alfa in Erythropoiesis-Stimulating Agent-Naive, Lower-Risk Myelodysplastic Syndromes in the COMMANDS Trial. Adv Ther. 2025;42(7):3576-3589. PubMed PMID: 40377899
15. Cappellini MD, Taher AT, Motta I. Thalassemia and hypercoagulability. Hematology Am Soc Hematol Educ Program. 2025;2025(1):285-290. PubMed PMID: 41348010
16. Seijari MN, Alshurafa A, Yassin MA. Luspatercept's use in a patient with transfusion-dependent beta-thalassemia and intrathoracic extramedullary hematopoiesis (EMH). Clin Case Rep. 2024;12(5):e8795. PubMed PMID: 38736568
17. Hatzimichael E, Timotheatou D, Koumpis E, Benetatos L, Makis A. Luspatercept: A New Tool for the Treatment of Anemia Related to β-Thalassemia, Myelodysplastic Syndromes and Primary Myelofibrosis. Diseases. 2022;10(4):85. PubMed PMID: 36278584

Other Sources

1. United States prescribing information for luspatercept-aamt (revised February 2026), DailyMed, U.S. National Library of Medicine. DailyMed label
2. Drugs@FDA, U.S. Food and Drug Administration: biologics licence application 761136, approval history. Drugs@FDA record

PubMed Topic Searches

1. luspatercept thalassemia
2. luspatercept iron overload
3. luspatercept myelodysplastic syndromes
4. luspatercept extramedullary hematopoiesis
5. ineffective erythropoiesis thalassemia

Connections

• Drugs — every drug page on the site
• Thalassaemia — the condition, chelation, transplant and gene therapy
• Myelodysplastic Syndrome — the other condition luspatercept is approved for
• Iron Overload: Heart Problems — what excess iron does to the heart
• Iron Overload: Liver Problems — where most transfused iron is stored
• Iron Overload and Iron Toxicity — causes, tests and chelation
• Sickle Cell Disease — another inherited haemoglobin disorder treated with transfusions

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