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erythropoietin (EPO, Harvest Moon)

✓ Approved

Harvest Moon Pharmaceuticals · EPOR · Recombinant Proteins

What is erythropoietin?

erythropoietin is a recombinant proteins developed by Harvest Moon Pharmaceuticals. It is approved for therapeutic indications via injectable (others).

Drug Profile

Brand NamesEPO, Harvest Moon
CompanyHarvest Moon Pharmaceuticals
Drug ClassRecombinant Proteins
Molecular TargetEPOR
RouteInjectable (Others)
StatusApproved

Mechanism of Action

Molecular Targets

erythropoietin acts on 1 molecular target:

EPORerythropoietin receptor (EPO-R)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

erythropoietin is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Blood and lymphatic system disordersAnaemia✓ Approved
Blood and lymphatic system disordersNephrogenic anaemia✓ Approved

Related Research Articles

PubMedFrontiers in nephrology2026-10-14

SGLT2 inhibitors as a strategy for volume management in peritoneal dialysis: a case series.

Sosa Barrios R Haridian RH, Domínguez-Tejedor Miriam M, Moreno García Raquel R, Burguera Vion Víctor M VM et al.

Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have demonstrated cardiovascular and renal benefits in chronic kidney disease, yet their role in peritoneal dialysis (PD) remains largely unexplored, and clinical experience is limited. We describe, at the individual-patient level, seven consecutive patients treated with an SGLT2i at a single centre (median age 69 years, range 43-73; five men; one with type 2 diabetes; six dapagliflozin, one empagliflozin). The PD prescription was not modified during treatment, and ultrafiltration refers to the 24-hour drained volume. In the four patients in whom the drug was added to established, unchanged PD, ultrafiltration rose in three and fell in one; the single non-responder was also the only low-average transporter and was later transferred to haemodiafiltration. Both patients anuric at baseline increased their ultrafiltration, and in one of them PD was the only feasible modality. Peritoneal transport category was unchanged wherever paired equilibration tests were available. Serum urate fell in the patients with preserved diuresis but not in those who were anuric, whereas the largest ultrafiltration gain occurred in a patient anuric throughout, dissociating the peritoneal response from any renal effect. The erythropoietin resistance index fell in all treated patients, although the magnitude was clinically relevant in a minority and must be read alongside the haemoglobin trajectory. No patient developed anuria de novo. One patient died of fungal peritonitis in the context of documented non-adherence, an event reported here with its mechanistic implications. These observations support a direct peritoneal mode of action and warrant prospective evaluation with surveillance for fungal infection.

PubMedActa medica portuguesa2026-10-14

Practical Management of Cytopenias in Patients with Myelofibrosis Adapted to the Portuguese Reality.

Medina de Almeida António A, Marques Bárbara B, Polo Blanca B, Pierdomenico Francesca F et al.

Cytopenias are a common clinical manifestation of myelofibrosis, particularly anemia. Although correcting cytopenias is essential to improve prognosis and quality of life of patients with myelofibrosis, there are few effective therapeutic options. Furthermore, there are no national guidelines for the management of cytopenias in myelofibrosis. To address this gap, a panel composed of six hematologists proposes an approach for patients with myelofibrosis and cytopenias adapted to clinical practice in Portugal, based on scientific evidence and clinical experience. Firstly, the etiology of the anemia should be identified. In patients with myelofibrosis-related anemia who have splenomegaly and/or constitutional symptoms, the use of Janus kinase inhibitors should be prioritized: momelotinib as monotherapy, or ruxolitinib in combination with an erythropoiesis-stimulating agent or danazol, depending on erythropoietin levels. In anemic patients without splenomegaly or constitutional symptoms, treatment with an erythropoiesis-stimulating agent, danazol, a combination of an immunomodulator with corticosteroid, or momelotinib, should be considered. In patients with treatment-induced anemia, the use of a Janus kinase inhibitor (with possible dose reduction in the case of ruxolitinib) in combination with an erythropoiesis-stimulating agent or danazol, or momelotinib as monotherapy should be considered. Thrombocytopenic patients eligible for Janus kinase inhibitors may receive ruxolitinib at a reduced dose, or momelotinib, the latter of which does not require dose reduction for thrombocytopenia. In thrombocytopenic patients without splenomegaly, constitutional symptoms, or anemia, the approach consists of monitoring or treatment with danazol, corticosteroids, or a combination of immunomodulator and corticosteroid, according to platelet count and hemorrhagic diathesis. Transfusion should be considered in patients with severe anemia or thrombocytopenia, diathesis, or the need for surgery. Symptomatic and analytical improvement, reduction of splenomegaly, and independence from or a significant decrease in transfusion support indicate a response to treatment. Treatment switch is warranted in cases of toxicity, failure, loss of clinical or hematological response after initial response, or disease progression. The implementation of these recommendations will help to optimize care for patients with myelofibrosis and cytopenias, improving clinical outcomes.

PubMedBone research2026-10-13

Bi-allelic EPHA2 mutations cause dysosteosclerosis by inhibiting osteoclastogenesis and enhancing osteoblastogenesis.

Chen Xi X, Li Xin X, Gu Zenghui Z, Lu Qi Q et al.

Erythropoietin-producing hepatocellular (EPH) receptors, the largest receptor tyrosine kinase family, have been shown to play a crucial role in normal physiological processes and pathologies. EPHA2, encoded by EPHA2 gene, a member of the EPH receptor family, has been implicated in cataracts and various bone tumors, including osteosarcoma, chondrosarcoma, and bone metastases of breast cancer. However, no association between the EPHA2 gene and genetic skeletal disorders has been reported to date. Here, we identified a Chinese family with a diagnosis of dysosteosclerosis, presenting with significant increase in lumbar spine bone mineral density, multifocal sclerotic lesions throughout the body, sclerotic skull, platyspondyly and sandwich vertebrae, and demonstrated compound heterozygous mutations in EPHA2 gene (c.890 C > T, p.Thr297Met; c.988dupT, p.Ser330PhefsX51). We observed a reduction in numerous sclerotic lesions in patients during the five-year follow-up. To systematically investigate the molecular mechanisms of pathogenesis, we employed a range of methodologies, including in vitro cellular assays, genome-wide association studies analysis, induced pluripotent stem cells models and Epha2 knockout mice models. We have determined that loss-of-function mutations in EPHA2 gene lead to dysosteosclerosis through enhancing mesenchymal stem cells osteogenic differentiation and downregulating the p38-MAPK pathway, leading to decreased osteoclast differentiation. Consequently, we proposed and validated EPHA2 as a viable therapeutic target for osteoporosis by constructing femoral fracture mice models and ovariectomized mice models. In summary, this study identifies bi-allelic loss-of-function mutations in EPHA2 gene lead to dysosteosclerosis and its underlying mechanisms, and suggests EPHA2 as a potential therapeutic target for osteoporosis.

PubMedBiological trace element research2026-10-11

Trace Element and Phytochemical Characterization of Pinus pinaster and Pinus halepensis Bark Extracts with Protective Effects Against Phenylhydrazine-induced Hemolytic Anemia in Rats.

Tbatou Widad W, Aouji Maouane M, Takie Marouane M, Aboulghazi Abderrazak A et al.

Anemia, characterized by decreased hemoglobin levels and impaired oxygen-carrying capacity, remains a major global public health concern. Conventional therapies, such as blood transfusions and oral iron supplementation, are often associated with adverse effects and limited absorption, highlighting the need for safer and more effective alternatives. Natural products rich in polyphenols and essential minerals have attracted increasing attention due to their multifunctional therapeutic potential. In this context, the present study is the first to investigate the anti-anemic potential of Pinus pinaster Aiton and Pinus halepensis Mill. bark extracts through an integrated phytochemical, nutritional, in vivo, in vitro, and in silico approach. Phytochemical profiling by HPLC-MS/MS revealed several major phenolic compounds, including quercetin, catechin, protocatechuic acid, and taxifolin-3-O-glucoside. The extracts exhibited high total polyphenol and flavonoid contents and strong antioxidant activity, as demonstrated by DPPH, ABTS, PR, and TAC assays. Mineral analysis revealed significant levels of essential elements, including iron, magnesium, potassium, sodium, and zinc. In phenylhydrazine-induced anemic Wistar rats, 21-day treatment with the extracts significantly restored hematological parameters (RBC, Hb, and HCT), serum iron and ferritin levels, and improved renal and hepatic biomarkers compared with untreated anemic controls. In vitro assays further demonstrated anti-hemolytic activity and enhanced erythrocyte membrane stability. Molecular docking analysis supported these findings by revealing favorable interactions between the major phenolic compounds and key targets involved in erythropoiesis, iron metabolism, and oxidative stress, including the erythropoietin receptor, superoxide dismutase, and ferrochelatase. Collectively, these findings highlight the potent anti-anemic and protective effects of Pinus bark extracts and suggest their potential as promising natural therapeutic agents.

PubMedBrain and behavior2026-10-09

Exploring Associations Between Hypoxia, Serum Erythropoietin, and Cognition in Patients With Mood Disorders and Healthy Individuals.

Ørum Barbara Emilie Rotbøl BER, Schandorff Johanna Mariegaard JM, Damgaard Viktoria V, Rødgaard Eya-Mist EM et al.

Moderate repeated hypoxia (MRH) has shown neuroprotective and neuroplastic effects, partly mediated by erythropoietin (EPO) via hypoxia-inducible factors (HIFs). This study examined the effects of 3 weeks of daily 3.5-h normobaric hypoxia (12% O2) versus normoxia (20% O2) combined with cognitive training on oxygen saturation (SpO2), cerebral side effects, hematology (including EPO and brain-derived neurotrophic factor [BDNF]), and cognitive learning. We also assessed SpO2 associations with side effects, hematology, and learning outcomes, as well as potential clinical and demographic predictors of hypoxic response. Data from 84 healthy participants (HP) and 24 participants with remitted mood disorders (MD) in the ongoing ALTIBRAIN trial (NCT06121206) were analyzed. HP were randomized to MRH or normoxia (with/without cognitive training), while MD participants were randomized to MRH with cognitive training or treatment as usual. MRH reduced SpO2 (97.5% ± 1.0% to 85.9% ± 2.9%, p < 0.001), but this effect attenuated over time (p < 0.001). Side effects (e.g., dizziness and headaches) were slightly higher in MRH (p = 0.044) but declined over time (p < 0.001). Reticulocyte, hemoglobin, and thrombocyte levels increased (p ≤ 0.029), while EPO decreased (p = 0.003) and BDNF remained unchanged (p > 0.60). MRH slightly flattened cognitive learning curves (p < 0.001). MD participants experienced marginally higher side effects (p = 0.006), but overall tolerability was good. MRH was safe and well-tolerated, influencing SpO2, hematology, and learning curves. If future research confirms cognitive and neuroplastic benefits, MRH with cognitive training could be a promising treatment for cognitive impairment.

PubMedIranian journal of veterinary research2026-10-09

Hormonal, biochemical and hematological changes in neonatal calves with sepsis induced by enteritis.

Sezer M M, Akyüz E E, Bati Y U YU, Kuru M M et al.

Diarrhea is one of the most important problems seen in calves during the neonatal period. Sepsis caused by diarrhea is the main cause of death. In the case of sepsis, many hormonal, hematological and biochemical changes occur in calves. It is extremely important to evaluate these parameters together. The present study aimed to investigate hormonal, biochemical, and hematological changes in neonatal calves affected by septic enteritis to obtain more information about the pathogenesis of sepsis. The study included a sepsis group consisting of 40 calves aged 0-15 days with enteritis, and a control group composed of 20 clinically and hematologically healthy calves of similar age. Calves presenting with enteritis, anorexia, severe dehydration, and general condition deterioration were examined, and those meeting the sepsis criteria were included in the study. Hematological, hormonal, and biochemical measurements were performed on blood samples obtained from the calves. Additionally, pathogenic agents causing enteritis were identified using immunochromatographic methods on fecal samples. In the sepsis group, creatinine, total protein, and urea levels, as well as the enzymatic activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), gamma-glutamyl transferase (GGT), and creatine kinase (CK) were significantly higher compared with the healthy group (P<0.05), while cholesterol levels were significantly lower (P<0.001). The total leukocyte count (WBC), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and granulocyte count were also found to be higher in the sepsis group compared with the control group (P<0.05). Furthermore, calves in the sepsis group were determined to be hypothermic, tachycardic and tachypneic compared with the control group (P<0.05). In the sepsis group, notable reductions in free T3, free T4 and erythropoietin (EPO) levels were observed (P<0.05). However, cortisol, insulin, and adrenocorticotropic hormone (ACTH) levels were significantly higher than those in the healthy group (P<0.05). Sepsis causes significant hematological, biochemical and hormonal changes in neonatal calves.

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