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erythropoietin

✓ Approved

Helvetic Biopharma · EPOR · 重组蛋白

什么是 erythropoietin？

erythropoietin 是一种重组蛋白，由Helvetic Biopharma研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)。

药物档案

公司Helvetic Biopharma
药物类别重组蛋白
分子靶点EPOR
给药途径Injectable (Others)
状态Approved
来源： ClinicalTrials.gov, Helvetic Biopharma

作用机制

分子靶点

erythropoietin 作用于 1 个分子靶点：

EPORerythropoietin receptor (EPO-R)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

erythropoietin 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Vascular disordersThrombosis✓ Approved

相关研究文献

PubMedExperimental physiology2026-10-26

A 45 min bout of hot-water immersion induces transient plasma volume contraction without a detectable increase in circulating erythropoietin.

Zerilli Owain O, Killick Joseph A JA, Douglas Andrew J M AJM, Nash Dan D et al.

Heat acclimation is increasingly used to induce haematological adaptations and enhance endurance performance. Although repeated hot-water immersion (HWI) has been shown to increase haemoglobin mass, the acute physiological responses that might underpin these longer-term adaptations remain poorly understood. This study investigated the 24 h time course of plasma volume (PV) and erythropoietin (EPO) responses following a single bout of HWI. Sixteen healthy adults (four females) completed a randomised crossover study comprising 45 min of HWI (40°C) and a time-matched control condition. Changes in PV were estimated from haemoglobin concentration and haematocrit, while serum EPO concentrations were determined using an ELISA. HWI induced a substantial contraction in PV immediately after immersion (-9.5%, 95% CI [-12.5, -6.5]; P < 0.001), accompanied by marked increases in tympanic temperature and thermal strain. However, PV returned to baseline within 12 h, and no subsequent PV expansion was observed. Serum EPO concentration was unaffected by time (P = 0.183), condition (P = 0.125) or the condition × time interaction (P = 0.309). Furthermore, changes in PV were unrelated to changes in circulating EPO in both the HWI (β = 0.07; [-1.3, 1.4]; P = 0.915) and control (β = 1.10; [-1.1, 3.3]; P = 0.326) conditions. These findings demonstrate that a 45 min bout of HWI induces a substantial but transient contraction in PV that is not accompanied by a measurable increase in circulating EPO within 24 h. Acute PV contractions following HWI therefore appear insufficient to stimulate a measurable erythropoietic response, suggesting that the haematological adaptations observed following chronic heat acclimation may instead depend upon sustained alterations in PV arising from repeated heat exposures.

PMID 42929056
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PubMedMolecular medicine reports2026-10-25

Erythropoietin beyond red blood cells: Systemic and oncological functions (Review).

Danková Kristína K, Solárová Zuzana Z, Harvanik Pavol P, Šemeláková Martina M et al.

Erythropoietin (Epo) is widely recognized as the primary regulator of haematopoiesis, managing red blood cell production via erythropoietin receptor (EPOR) expressed on erythroid progenitors. Beyond erythropoiesis, Epo functions as a pleiotropic cytokine, exhibiting marked tissue‑protective effects across various non‑haematopoietic systems, including neuroprotection, cardioprotection, anti‑inflammatory effects and promotion of angiogenesis. Clinically, recombinant Epo is widely used to alleviate cancer‑related anaemia and improve haemoglobin levels. However, the presence of EPOR in malignant tissues may directly influence tumour progression or angiogenesis. The aim of the present review is to summarize current knowledge on Epo signalling across multiple organ systems, to discuss the possible applications of Epo derivatives, and to refer to emerging evidence suggesting that Epo may affect tumour biology and modulate the efficacy of chemotherapy. The review provides a comprehensive overview of current and emerging therapeutic concepts involving Epo derivatives, while emphasizing that most non‑haematopoietic applications remain under preclinical or early clinical investigation.

PMID 42924578
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PubMedFrontiers in pharmacology2026-10-25

Renal anemia: from erythropoietin deficiency to erythropoietin resistance.

Chu Aojiao A, Bu Jinyang J, Zou Xinfu X, Zhang Zheng Z et al.

Renal anemia is one of the core complications of chronic kidney disease (CKD) and is closely associated with poor patient prognosis. Renal interstitial fibrosis or impaired oxygen sensing leads to insufficient erythropoietin (EPO) production, which constitutes the fundamental mechanism initiating renal anemia. On this basis, multiple pathological factors-including the inflammatory microenvironment in CKD, iron deficiency, and mineral and bone disorders-synergistically induce EPO resistance, further exacerbating anemia and diminishing the response to existing therapies. Currently, the treatment of renal anemia has moved beyond simple EPO replacement and is progressively shifting toward a dual strategy that emphasizes both correction of EPO resistance and enhancement of drug responsiveness. This article summarizes the molecular network through which insufficient EPO synthesis and EPO resistance synergistically aggravate renal anemia, systematically reviews the pharmacological basis, limitations, and safety risks of current drug therapies, and discusses future research directions and potential therapeutic targets in this field.

PMID 42923141
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PubMedCellular signalling2026-10-25

Structural integrity of the EpoR WSXWS region is required for ligand-independent JAK2-V617F signaling and tumorigenesis.

Funakoshi-Tago Megumi M, Sakata Tomoki T, Fumihito Ueda U, Tago Kenji K

The JAK2-V617F point mutation in the tyrosine kinase Janus kinase 2 (JAK2) is a well-established driver of myeloproliferative neoplasms (MPNs). This mutant protein is constitutively activated and exerts its oncogenic potential through signaling pathways mediated by the erythropoietin receptor (EpoR). While the extracellular WSXWS motif (Trp-Ser-X-Trp-Ser) of EpoR is implicated in receptor folding and trafficking, its specific contribution to JAK2-V617F-driven oncogenesis remains to be fully elucidated. Here, we evaluated a series of EpoR WSXWS mutants (W232A, S233A, W235A, S236A, and S236N) combined with wild-type JAK2 or JAK2-V617F in Ba/F3 cells. Biochemical analyses revealed that substitutions such as W232A, S233A, W235A, and S236N caused aberrant receptor processing accompanied by reduced cell-surface expression and impaired Epo binding. In contrast, the S236A mutant displayed a glycosylation and processing profile comparable to that of wild-type EpoR, was efficiently transported to the plasma membrane, and retained substantial Epo-binding activity. Immunoprecipitation assays demonstrated that wild-type JAK2 and JAK2-V617F physically interacted with all EpoR constructs. Co-expression of S236A preserved Epo-dependent STAT5 phosphorylation and cell proliferation with both wild-type JAK2 and JAK2-V617F. Crucially, however, S236A markedly attenuated ligand-independent JAK2-V617F/STAT5 activation and failed to support robust cytokine-independent growth. Furthermore, none of the WSXWS mutants supported JAK2-V617F-driven tumorigenicity or organomegaly in the Ba/F3 transplantation model, in contrast to wild-type EpoR. Collectively, our findings demonstrate that preserved receptor cell-surface localization alone is not sufficient to drive robust JAK2-V617F activation, and that integrity of the WSXWS region is functionally required for EpoR to support ligand-independent JAK2-V617F signaling and transformation in this model.

PMID 42926027
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PubMedFrontiers in sports and active living2026-10-25

Gene, microbiome, and anti-aging doping in sport: molecular mechanisms, detection strategies, and implications for sports rehabilitation medicine.

Cotella Diego D

Advances in gene transfer have created legitimate opportunities for tissue repair, but the same tools raise the prospect of illicit use to enhance athletic performance ("gene doping"). Evidence that elite athletes harbour a distinctive gut microbiota has raised a parallel concern that microbiome manipulation, including faecal microbiota transplantation (FMT) from high-performing donors, could be used as a form of biological enhancement ("microbiome doping"). A third, related frontier is anti-aging gene therapy (telomerase and Klotho gene delivery and partial cellular reprogramming) which targets the same muscle- and stem-cell-regenerative pathways relevant to injury recovery and has already reached unregulated human self-experimentation. This narrative review summarises the principal gene-doping targets relevant to performance and recovery (erythropoietin, myostatin/activin inhibitors, insulin-like growth factor 1, PPAR-δ/AMPK reprogramming), their delivery vectors, and current detection strategies. It then reviews athlete-associated gut microbiota signatures, notably the lactate-metabolising bacterium Veillonella atypica, and the feasibility and detection challenges of microbiota transplantation, before examining the rationale, targets, and governance challenges of anti-aging gene therapy. Attention is given to the overlap between all three frontiers and legitimate regenerative, microbiota-directed, or aging-biology therapies under investigation for musculoskeletal, metabolic, and gastrointestinal conditions, an overlap that places rehabilitation clinicians in a sensitive position, particularly with older or master athletes; across all three frontiers, the same biological pathways and delivery technologies are simultaneously being developed for legitimate therapeutic use, creating a recurring dual-use dilemma for clinicians and regulators alike. I review safety risks, the regulatory framework administered by the World Anti-Doping Agency (WADA) and its gaps regarding microbiome and longevity interventions, and the practical responsibilities of rehabilitation professionals. I conclude that interdisciplinary collaboration between molecular biologists, microbiome and aging researchers, anti-doping scientists, and clinicians is essential to keep detection methods and clinical governance aligned with the pace of innovation in these three areas, and we outline specific priorities, including clarification of the regulatory status of microbiota transfer and anti-aging gene constructs, strain-level metagenomic monitoring, and biological-age biomarkers, for achieving this alignment.

PMID 42921440
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PubMedJAMA2026-10-25

Sodium-Glucose Cotransporter 2 Inhibitor Use and Levels of Hemoglobin, Markers of Iron Metabolism, and Erythropoiesis: A Systematic Review and Meta-Analysis of Randomized Clinical Trials.

Yang Yaqin Y, Yang Changyuan C, Wang Yanmei Y, Rawee Pien P et al.

In randomized clinical trials, sodium-glucose cotransporter 2 (SGLT2) inhibitor use was associated with increased hemoglobin and hematocrit compared with placebo. However, the magnitude and importance of this association remain unclear. To evaluate the associations between SGLT2 inhibitor use and levels of hemoglobin, hematocrit, and markers of iron metabolism and erythropoiesis compared with placebo or active comparator. PubMed, Web of Science, and the Cochrane Central Register of Controlled Trials (CENTRAL) were searched from inception to July 22, 2026. Randomized, double-masked clinical trials comparing SGLT2 inhibitor use with placebo or active comparators in patients with 1 or more of the following conditions: cardiovascular disease, diabetes, heart failure, and chronic kidney disease. Three reviewers independently extracted data and results were pooled using random-effects meta-analysis. Primary outcomes were changes in hemoglobin and hematocrit. Secondary outcomes were changes in red blood cell concentration, erythropoietin (EPO), and iron measures (serum iron, ferritin, transferrin saturation, and hepcidin). A total of 85 randomized clinical trials were analyzed (median [IQR] duration, 24 [12-32] weeks), including 70 543 participants (mean [SD] age, 62.4 [9.4] years; 25 334 female [35.9%]). Mean (SD) baseline hemoglobin was 13.6 (1.5) g/dL; baseline hematocrit was 41.5% (4.9). Seventy-eight clinical trials (67 208 participants) compared SGLT2 inhibitors with placebo, and 7 clinical trials (3335 participants) used active comparators, most commonly sitagliptin (2 trials [1158 participants]). From baseline to follow-up, hemoglobin changed by 0.55 g/dL (95% CI, 0.49 to 0.61 g/dL; P < .001) in the SGLT2 inhibitor group, and -0.08 g/dL (95% CI, -0.13 to -0.03 g/dL; P = .003) in the control group (difference, 0.60 g/dL; 95% CI, 0.55 to 0.66 g/dL; P < .001). From baseline to follow-up, hematocrit changed by 2.17% (95% CI, 1.95% to 2.39%; P < .001) in the SGLT2 inhibitor group and -0.13% (95% CI, -0.28% to 0.01%; P = .07) in the control group (difference, 2.36%; 95% CI, 2.19% to 2.52%; P < .001). Of the 6 secondary outcomes, 4 showed significant associations with SGLT2 inhibitors, including increased EPO (2.35 mIU/mL in SGLT2 inhibitor group vs 0.04 mIU/mL in control group; difference, 2.11 mIU/mL [95% CI, 0.5-3.71 mIU/mL]; P = .01) and decreased transferrin saturation (-2.2% in SGLT2 inhibitor group vs -0.10% in control group; difference, -0.84% [95% CI, -1.21% to -0.47%]; P < .001). In a meta-analysis of randomized clinical trials, compared with control, SGLT2 inhibitor use was associated with small statistically significant increases in hemoglobin and hematocrit levels. The clinical significance of these findings is unclear.

PMID 42925557
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