HIF prolyl hydroxylase inhibition results in endogenous erythropoietin induction, erythrocytosis, and modest fetal hemoglobin expression in rhesus macaques
Open accessAbstract
The hypoxia-inducible factor (HIF) pathway is crucial in mitigating the deleterious effects of oxygen deprivation. HIF-alpha is an essential component of the oxygen-sensing mechanisms and under normoxic conditions is targeted for degradation via hydroxylation by HIF-prolyl hydroxylases. Several HIF-prolyl hydroxylase inhibitors (PHIs) induced erythropoietin (epo) expression in vitro and in mice, with peak epo expression ranging from 5.6- to 207-fold above control animals. Furthermore, several PHIs induced fetal hemoglobin (HbF) expression in primary human erythroid cells in vitro, as determined by flow cytometry. One PHI, FG-2216, was further tested in a nonhuman primate model without and with chronic phlebotomy. FG-2216 was orally bioavailable and induced significant and reversible Epo induction in vivo (82- to 309-fold at 60 mg/kg). Chronic oral dosing in male rhesus macaques was well tolerated, significantly increased erythropoiesis, and prevented anemia induced by weekly phlebotomy. Furthermore, modest increases in HbF-containing red cells and reticulocytes were demonstrated by flow cytometry, though significant increases in HbF were not demonstrated by high-pressure liquid chromatography (HPLC). HIF PHIs represent a novel class of molecules with broad potential clinical application for congenital and acquired anemias.
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Pharmacological inactivation of PHD enzymes with 2OG analogs increases serum EPO levels in animal models and in humans.
“Pharmacological inactivation of PHD enzymes with 2OG analogs increases serum EPO levels in animal models and in humans”
From Regulation of erythropoiesis by hypoxia-inducible factors (2013) · cites this paper as [236]
Pharmacological inactivation of PHD enzymes with 2OG analogs has the potential to benefit patients with anemia that results from inadequate EPO production.
“and has the potential to benefit patients with anemia that results from inadequate EPO production.”
From Regulation of erythropoiesis by hypoxia-inducible factors (2013) · cites this paper as [236]
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- Authors
- Hsieh, M. M., Linde, N. S., Wynter, A., Metzger, M., Wong, C., Langsetmo, I., Lin, A., Smith, R., Rodgers, G. P., Donahue, R. E., Klaus, S. J., & Tisdale, J. F.
- Affiliations
- National Institutes of Health (US)
- FibroGen (United States) (US)
- ORCID
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2007-09-15
- Volume
- 110
- Issue
- 6
- Pages
- 2140-2147
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC1976368
- OpenAlex
- W1965209932
- Cited by
- 171
- References
- 54
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 3 · 2023: 2 · 2022: 5 · 2021: 6 · 2020: 2 · 2019: 1 · 2018: 1 · 2017: 7 · 2016: 10 · 2015: 10 · 2014: 8 · 2013: 13 · 2012: 11
- FWCI
- 13.84
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases
- Topics
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Health Sciences › Medicine › Genetics › Hemoglobinopathies and Related Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hemoglobin structure and function
- Keywords
- HIF prolyl hydroxylase inhibitors, hypoxia-inducible factor, erythrocytosis, fetal hemoglobin, rhesus monkeys, anemia, erythropoiesis, oral bioavailability
- MeSH terms
- Administration, Oral, Animals, Hypoxia, Chronic Disease, Enzyme Inhibitors, Erythrocytes, Erythropoietin, Fetal Hemoglobin, Flow Cytometry, Carcinoma, Hepatocellular, Humans, Liver Neoplasms, Macaca mulatta, Male, Oxygen, Polycythemia, Procollagen-Proline Dioxygenase, Reticulocytes, Erythroid Precursor Cells, Phlebotomy, Erythroid Cells, Mice
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