ARA 290-DMO is a prospective, open label, interventional, single centre, investigator led, phase II trial to examine the effect of ARA 290 on diabetic macular oedema in patients with type 1 or 2 diabetes.
The aim or primary objective of the study was to determine whether ARA 290 administered at a daily dose of 4mg subcutaneously for 12 weeks to patients with diabetes mellitus (DM) and DMO would have a beneficial effect on mean change in best corrected visual acuity (BCVA) from baseline values to week 12.

开始日期2016-04-01

申办/合作机构

Belfast Health & Social Care Trust

[+1]

NCT02039687

/ Completed临床2期

A Double Blind, Placebo Controlled Phase 2 Dose Ranging Study of the Effects of ARA 290 on Corneal Nerve Fiber Density and Neuropathic Symptoms of Subjects With Sarcoidosis

The purpose of this study is to determine whether ARA 290, a new class of compound, is effective in the treatment of the neuropathic symptoms of sarcoidosis. Brief interaction of ARA 290 with the innate repair receptor results in anti-apoptotic and anti-inflammatory activities in myriad of cells, tissues and organs throughout the body to activate repair mechanisms and accelerate healing, including the nerve damage that can be associated with sarcoidosis. In this study, subjects with sarcoidosis and symptoms of small fiber neuropathy will administered ARA 290 or placebo by subcutaneous injection daily for 28 days. In addition to monitoring the safety of the treatment, the symptoms of the subjects will be assessed with several questionnaires, function tests, and measurement of nerve fibers in their cornea and skin (via a non-invasive test and a biopsy, respectively). The total participation time for each patient will be 16 weeks.

开始日期2014-01-01

申办/合作机构

Araim Pharmaceuticals, Inc.

NCT01933529

/ Unknown status临床2期IIT

Effects of ARA 290, a Non-hematopoietic Erythropoietin Analogue, on Glucose Tolerance, Insulin Secretion, Insulin Sensitivity and Long-term Glucose Control in Individuals With Prediabetes and/or Drug-naive Type 2 Diabetes; a Phase II Study.

The purpose of this study is to determine whether a non-hematopoietic erythropoietin analogue, ARA 290, exerts beneficial effects on blood glucose levels and insulin secretion in persons with prediabetes (impaired glucose tolerance, IGT, or impaired fasting glucose, IFG), or drug-naive type 2 diabetes.
The study will also evaluate effects of ARA 290 on insulin sensitivity and serum levels of inflammatory agents, e.g. cytokines. In addition, safety will be monitored by following parameters related to hematology, kidney and liver function and lipid levels.

开始日期2013-10-01

申办/合作机构

Karolinska Institutet

[+1]

100 项与西比奈肽相关的临床结果

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100 项与西比奈肽相关的转化医学

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100 项与西比奈肽相关的专利（医药）

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项与西比奈肽相关的文献（医药）

2025-12-01·INTERNATIONAL IMMUNOPHARMACOLOGY

Pegmolesatide ameliorates indoxyl sulfate-induced cardiomyocyte hypertrophy through modulating the EPOR-CD131-dependent JAK2/STAT3 signaling pathway

Article

作者: Zhang, Xinyu ; Lin, Tingru ; Zuo, Li ; Zhu, Li ; Gan, Liangying ; Li, Sufang

BACKGROUND:

Cardiovascular events remain the leading cause of mortality in chronic kidney disease (CKD). Pegmolesatide(P), a novel long-acting EPO receptor modulator, shows cardiovascular benefits in clinical studies. This study aims to demonstrate Pegmolesatide suppressed the formation of EPOR-CD131 heterodimer and to explore its cardioprotective mechanisms against indoxyl sulfate (IS)-induced cardiomyocyte hypertrophy.

METHODS:

H9c2 cardiomyocytes were assigned to different treatment groups (vehicle, IS, IS+P, P) and RNA sequencing was performed to identify dysregulated signaling pathways. Mechanistic exploration groups supplemented with CD131 agonist ARA290, STAT3 activator Colivelin, or STAT3 inhibitor Stattic for rescue experiments. Analyses included real-time qPCR/Western blot for cardiac hypertrophy markers and EPOR-CD131/JAK2/STAT3 axis components, phalloidin staining for cell size and co-immunoprecipitation (Co-IP) for EPOR-CD131 heterodimerization.

RESULTS:

Pegmolesatide significantly attenuated IS-induced cardiomyocyte hypertrophy, as evidenced by suppressed expression of cardiac hypertrophy markers (ANP, BNP, and β-MHC), reduced cell surface area, and improved cytoskeletal organization(P < 0.05). Mechanistically, Pegmolesatide upregulated EPOR expression while suppressing CD131 expression and activation of the JAK2/STAT3 signaling. Co-IP analysis demonstrated that Pegmolesatide suppressed the formation of EPOR-CD131 heterodimer. Functional rescue experiments showed that the cardioprotective effects of Pegmolesatide were reversed by CD131 agonist ARA290 or STAT3 activator Colivelin. Notably, combined treatment with ARA290 and STAT3 inhibitor Stattic partially restored its anti-hypertrophic activity.

CONCLUSION:

Pegmolesatide exerts protective effects against IS-induced cardiomyocyte hypertrophy by inhibiting the EPOR-CD131/JAK2/STAT3 signaling axis. It may be a promising strategy for CKD-related cardiovascular complications.

2025-06-01·EUROPEAN JOURNAL OF PHARMACOLOGY

ARA290, an alternative of erythropoietin, inhibits activation of NLRP3 inflammasome in schwann cells after sciatic nerve injury

Article

作者: Li, Wei ; Liu, Xiaoli ; Song, Meiying ; Yang, Yanyan ; Wang, Xiao ; Jiang, Suli ; Zhang, Li ; Zhang, Bei ; Wang, Luoyang ; Yang, Zijie ; Liang, Jie ; Liu, Guixian

The challenge of repairing peripheral nerve injury is a critical issue that needs to be addressed urgently. Previous research has shown that erythropoietin (EPO) and its prolonged peptides exhibit beneficial effects in neurological disorders. In our study, we demonstrated that both EPO and pyroglutamic acid helix B surface peptide (pHBSP, also known as ARA290) inhibit the early inflammatory response and promote functional recovery after sciatic nerve crush injury in rat models. Our experimental results demonstrate that significant inflammatory response occurred in Schwann cells after sciatic nerve injury, and that the activation of NLRP3 inflammasome in Schwann cells is inhibited after EPO and ARA290 treatment. Our study further demonstrated that EPO and ARA290 inhibit the activation of NLRP3 inflammasome in Schwann cells by inhibiting NF-κB phosphorylation and reducing reactive oxygen species (ROS) production. In summary, EPO and ARA290 promote repair and regeneration by inhibiting the activation of NLRP3 inflammasome after sciatic nerve injury.

2024-12-31·Toxicology Research

Mechanisms of ARA290 in counteracting cadmium-triggered neurotoxicity in PC12 cells

Article

作者: Fakhri B, Maryam S ; Motafeghi, Farzaneh ; Ghassemi Barghi, Nasrin

Abstract:

Erythropoietin (EPO) is known for its role in hematopoiesis and also exhibits anti-inflammatory, anti-apoptotic, antioxidant, and cytoprotective properties. However, its clinical application is limited by hematopoietic side effects. ARA290, a non-hematopoietic derivative of EPO, selectively activates the innate repair receptor (IRR) and replicates these protective effects without the associated hematopoietic complications. Cadmium (Cd), a prevalent environmental toxin, causes neurotoxic damage through mechanisms such as oxidative stress, genotoxicity, apoptosis, and inflammation. This study explored ARA290’s neuroprotective effects against cadmium-induced toxicity in PC12 cells, an in vitro model for neuronal health. PC12 cells pretreated with ARA290 showed significantly improved cell viability in the MTT assay, indicating reduced cytotoxicity. The comet assay revealed decreased DNA damage, suggesting reduced genotoxicity. ARA290 also alleviated oxidative stress, as evidenced by reduced levels of reactive oxygen species (ROS) and malondialdehyde (MDA), alongside increased glutathione (GSH), total antioxidant capacity (TAC), and superoxide dismutase (SOD) activities. A marker of apoptosis, TUNEL-positive cells, was significantly reduced. Additionally, ARA290 decreased inflammatory markers such as TNF alpha, IL1ß and IL 6. These findings demonstrate that ARA290, via IRR activation, provides robust neuroprotection against cadmium-induced toxicity, suggesting a multi-faceted protective mechanism. This highlights ARA290’s potential therapeutic role in managing heavy metal-induced neurotoxicity and supports further research into its long-term effects and applications in other neurodegenerative diseases or conditions involving environmental toxins.

Highlights:

项与西比奈肽相关的新闻（医药）

2025-11-05

·翰森制药

圣罗莱®最新机制研究于《国际免疫药理学》发布，证实具有潜在心血管保护作用

近日，北京大学人民医院肾内科团队在《国际免疫药理学》（International Immunopharmacology，IF:4.7）杂志上发表了一篇有关翰森制药自主研发的创新药培莫沙肽（商品名：圣罗莱®）的机制研究，揭示了圣罗莱®具有心血管保护作用，其能够通过抑制促红细胞生成素受体（EPOR）-CD131异二聚体的形成，阻断JAK2/STAT3信号通路激活，从而改善硫酸吲哚酚（IS，慢性肾脏病的一种关键毒素）诱导的心肌细胞肥大。这不仅为临床研究中所观察到的圣罗莱®相对较低的心血管不良事件发生率提供了机制依据，还可能为慢性肾脏病（CKD）相关心血管并发症提供一种有前景的治疗策略[1]。已知心血管事件是CKD患者死亡的首要原因，而肾性贫血是CKD患者心血管事件的重要致病因素。因此，贫血的早期干预对于改善CKD患者的心血管结局具有重要意义。然而，传统ESA类药物在抗贫血的同时会增加不良心血管事件风险。培莫沙肽是具有全新结构的小分子肽类化学药物，既往的Ⅲ期临床研究证实了其不仅在疗效上非劣于传统短效ESA，而且心血管不良事件的发生率更低[2,3]。本次研究结果表明： ●通过H9c2心肌细胞模型实验发现，圣罗莱®显著减轻了硫酸吲哚酚诱导的心肌细胞肥大，表现为心肌肥大标志物[包括A型利钠肽（ANP）、B型利钠肽（BNP）和β-肌球蛋白重链（β-MHC）]表达的抑制、细胞表面积的减少以及细胞骨架组织的改善（P < 0.05）。 ●圣罗莱®上调了EPOR的表达，同时抑制了CD131的表达和JAK2/STAT3信号通路的激活。共免疫沉淀分析显示培莫沙肽抑制了EPOR-CD131异二聚体的形成。功能挽救实验表明，CD131激动剂ARA290或STAT3激活剂Colivelin可逆转培莫沙肽的心脏保护作用，而联合使用ARA290和STAT3抑制剂Stattic则部分恢复了其抗肥大活性。这些发现提示了培莫沙肽可通过抑制CD131和STAT3而发挥心肌保护作用。整体而言，该研究证明了圣罗莱®能够通过抑制CD131表达、阻断EPOR-CD131异二聚体的形成，进而阻断JAK2/STAT3通路的激活，从而有效缓解硫酸吲哚酚诱导的心肌细胞肥大，揭示了一种新的心脏保护机制。值得注意的是，圣罗莱®独特的机制——通过调节CD131依赖的异二聚体化而非经典的EPO信号通路，不仅有助于避免与EPO信号通路相关的心血管风险，同时还赋予了直接的心脏保护作用。这为培莫沙肽潜在的安全性优势，包括减少心血管不良事件，以及其独特的心脏保护特性，提供了有力的机制依据。随着培莫沙肽临床应用的日益广泛，还需进一步在动物实验和CKD人群中验证其心血管获益机制。参考文献： 1.Zhang X, Li S, Lin T,et al.Pegmolesatide ameliorates indoxyl sulfate-induced cardiomyocyte hypertrophy through modulating the EPOR-CD131-dependent JAK2/STAT3 signaling pathway.Int Immunopharmacol. 2025 Oct 14;167:115643. 2.Xie J, Yang A, Qiu H,et al. Randomized Trial of Pegmolesatide for the Treatment of Anemia in Patients With Nondialysis CKD.Kidney Int Rep. 2024 Dec 6;10(3):720-729. 3.Zhang P, Jiang Y, Xu C,et al.Pegmolesatide for the treatment of anemia in patients undergoing dialysis: a randomized clinical trial.EClinicalMedicine. 2023 Oct 28;65:102273. 关于翰森制药翰森制药是中国领先的创新驱动型制药企业，下属豪森药业、常州恒邦药业、翰森生物医药等子公司，以「持续创新，提高人类生命质量」为使命，重点关注抗肿瘤、抗感染、中枢神经系统、代谢及自身免疫等重大疾病治疗领域。截至目前，公司在中国产生销售收入的创新药共7款，形成了丰富的产品管线。翰森制药连续多年位居全球制药企业百强、中国医药研发产品线最佳工业企业前3强，是国家重点高新技术企业、国家技术创新示范企业。翰森制药于2019年6月在香港联交所挂牌上市（股票代码：03692.HK）。免责声明本文仅供医疗卫生专业人士参阅，非广告用途。翰森制药不推荐任何未获批药品使用和/或未获批适应症用药，亦不对任何药品和/或适应症作推荐。本文中涉及的信息仅供参考，请遵从医生或其他医疗卫生专业人士的意见或指导。医疗卫生专业人士作出的任何与治疗有关的决定应根据患者的具体情况并遵照药品说明书。如需了解公司任何产品、医疗或疾病的相关信息，请务必咨询医疗卫生专业人士。前瞻性说明本新闻稿旨在提供关于翰森制药集团有限公司及其附属公司（包括其子公司，统称为“翰森制药”）的信息。它不构成对翰森制药或任何投资建议的信息披露。本新闻稿包含的信息可能包括与翰森制药业务和产品前景、计划、信念、预期和策略相关的前瞻性声明。这些声明是基于推测性假设的预测，并不保证未来的表现。它们受到诸如科学、商业、政治、经济、财务、法律因素以及竞争环境和社会条件等风险和不确定性的影响，这些因素很多都是翰森制药无法控制且难以预测的，因此实际结果可能与此处所述有显著差异，且过去的证券价格趋势不应作为未来行情的指导。因此，投资者在使用这些信息进行投资决策时应谨慎行事。“致力于”“预期”“相信”“预测”“意图”“预计”“可能”“将”“应该”“计划”“继续”“目标”“考虑”“估计”“指导”“潜在”“追求”以及于任何未来计划、行动或事件的讨论中使用的类似词语和术语，均表示前瞻性声明。翰森制药不承诺或保证前瞻性信息的准确性、及时性或完整性，并且不承担更新或修订这些前瞻性声明的义务。无论是翰森制药还是其任何董事、员工或代理人，均不对任何证明不准确或无法实现的前瞻性声明负责，也不对因依赖本新闻稿中提供的信息而产生的任何损失或损害负责，包括但不限于直接、偶然、间接或惩罚性的损害。

临床3期免疫疗法

100 项与西比奈肽相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11218	-	-	DB13006

研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
糖尿病性黄斑水肿	临床2期	英国	Araim Pharmaceuticals, Inc.	2016-04-01
神经结节病	临床2期	美国	Araim Pharmaceuticals, Inc.	2014-01-01
神经结节病	临床2期	荷兰	Araim Pharmaceuticals, Inc.	2014-01-01
2型糖尿病	临床2期	瑞典	Araim Pharmaceuticals, Inc.	2013-10-01
葡萄糖耐受不良	临床2期	瑞典	Araim Pharmaceuticals, Inc.	2013-10-01
糖尿病前期	临床2期	瑞典	Araim Pharmaceuticals, Inc.	2013-10-01
周围神经损伤	临床前	中国	青岛大学	2025-04-09

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临床结果

适应症

分期

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT02039687 (CTgov)	临床2期	神经结节病	64	ARA 290 (1 mg Per Day ARA 290)	簾餘選淵網廠繭醖鑰願(鑰選網蓋艱襯鹽鏇簾鹽) = 構觸憲顧積餘範廠獵壓鏇範齋製蓋蓋構遞簾鏇 (顧齋糧遞鹹衊製蓋醖觸, 759.9) 更多	-	2017-01-18
				ARA 290 (4 mg Per Day ARA 290)	簾餘選淵網廠繭醖鑰願(鑰選網蓋艱襯鹽鏇簾鹽) = 餘鏇鑰齋願蓋壓願鏇願鏇範齋製蓋蓋構遞簾鏇 (顧齋糧遞鹹衊製蓋醖觸, 1110.02) 更多
phase 2b (ANA2016)	临床2期	结节病 corneal nerve fiber area (CNFA)	64	ARA 290 1mg	顧蓋簾憲膚餘鏇簾願餘(壓艱願網蓋簾顧築壓鑰) = 衊簾廠範餘觸餘襯醖壓構鹽繭壓遞鹹壓鑰積鑰 (糧製鑰構繭鑰獵簾顧淵, 355.14 ~ 824.78)	积极	2016-10-14
				ARA 290 4mg	顧蓋簾憲膚餘鏇簾願餘(壓艱願網蓋簾顧築壓鑰) = 壓鏇選顧積淵願鏇網願構鹽繭壓遞鹹壓鑰積鑰 (糧製鑰構繭鑰獵簾顧淵, 44.92 ~ 1220.43)