ArticleThe Journal of clinical investigation2019
Oral ferroportin inhibitor ameliorates ineffective erythropoiesis in a model of β-thalassemia.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 89 citations in OpenAlex.
- Safety and pharmacodynamics of the ferroportin inhibitor vamifeport in patients with non-transfusion-dependent β-thalassemia: results from a randomized phase 2a study.Orphanet journal of rare diseases · 2025Trial
- A TMPRSS6-inhibiting mAb improves disease in a β-thalassemia mouse model and reduces iron in healthy humans.JCI insight · 2025Trial
- Rescuing anxiety by targeting the neuronal-astrocytic iron signaling axis in male mice.Signal transduction and targeted therapy · 2026Article
- Extracellular Hemoglobin, Hypoxia, and Macrophage-Mediated Pulmonary Vascular Remodeling in Hemolytic Disease.International journal of molecular sciences · 2026Review
- Contemporary Management of Thalassemia: A Perspective on Current Standards and the Emergence of FDA-Approved Oral Therapy.Health science reports · 2026Article
- Hepcidin as a Molecular Hub of Iron Homeostasis: From BMP-SMAD Signaling to Therapeutic Modulation.Biomolecules · 2026Review
- Identification and characterization of novel hepcidin mimetics that modulate ferroportin function.Blood red cells & iron · 2026Article
- Vamifeport, a clinical stage oral ferroportin inhibitor, alleviates murine lupus nephritis: A pilot study.Clinical immunology (Orlando, Fla.) · 2026Article
- Ferroportin inhibition attenuates pulmonary hypertension in hypoxic sickle cell disease mice.Blood advances · 2026Article
- Multidimensional repair of jujube pectic oligosaccharides on bone marrow hematopoietic failure.Frontiers in nutrition · 2026Article
- Iron metabolism and ferroptosis: druggable targets to delay the progression of lupus nephritis.American journal of physiology. Renal physiology · 2026Review
- Genetic biomarkers and crucial cell subsets of iron metabolism in Beta-Thalassemia: insights from bioinformatics and experimental validation.Annals of hematology · 2025Article
- Molecular Mechanisms of Iron Metabolism and Overload.Biomedicines · 2025Review
- Antioxidant Molecules in the Human Vitreous Body During Prenatal Eye Development.Antioxidants (Basel, Switzerland) · 2025Review
- Pharmacologic Inhibition of Erythrocyte Ferroportin Expression ExacerbatesMicroorganisms · 2025Article
- Essential role of hepcidin in host resistance to disseminated candidiasis.Cell reports · 2025Article
- Current Landscape of Hepcidin Therapeutics.Advances in experimental medicine and biology · 2025Review
- Targeting ferroptosis for neuroprotection: potential therapeutic avenues in neurodegenerative and neuropsychiatric diseases.Frontiers in physiology · 2025Review
- Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects.Signal transduction and targeted therapy · 2024Review
- Vamifeport: Monography of the First Oral Ferroportin Inhibitor.Journal of clinical medicine · 2024Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
β-Thalassemia is a genetic anemia caused by partial or complete loss of β-globin synthesis, leading to ineffective erythropoiesis and RBCs with a short life span. Currently, there is no efficacious oral medication modifying anemia for patients with β-thalassemia. The inappropriately low levels of the iron regulatory hormone hepcidin enable excessive iron absorption by ferroportin, the unique cellular iron exporter in mammals, leading to organ iron overload and associated morbidities. Correction of unbalanced iron absorption and recycling by induction of hepcidin synthesis or treatment with hepcidin mimetics ameliorates β-thalassemia. However, hepcidin modulation or replacement strategies currently in clinical development all require parenteral drug administration. We identified oral ferroportin inhibitors by screening a library of small molecular weight compounds for modulators of ferroportin internalization. Restricting iron availability by VIT-2763, the first clinical stage oral ferroportin inhibitor, ameliorated anemia and the dysregulated iron homeostasis in the Hbbth3/+ mouse model of β-thalassemia intermedia. VIT-2763 not only improved erythropoiesis but also corrected the proportions of myeloid precursors in spleens of Hbbth3/+ mice. VIT-2763 is currently being developed as an oral drug targeting ferroportin for the treatment of β-thalassemia.
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