ARA 290 10mg*10vials

Figure 1 ARA290 treatment suppressed inflammatory response in pristane‐induced SLE mice. (A) The levels of IL‐6, IL‐10, MCP‐1, IFN‐γ, TNF‐α, IL‐12p70 and TGF‐β in the serum following treatment described in Figure 1 were detected (n = 6). (B) The inflammatory macrophage F4/80 infiltration was significantly suppressed by ARA 290 intervention compared to PBS control. (C) The spleen and lymph node weights were measured following ARA290 treating in SLE mice (n = 6). Scale bars represent 30 μm.

Source:PubMed^[6]

Reduction of Inflammatory Cytokine Levels: ARA-290 decreases serum concentrations of inflammatory cytokines IL-6, MCP-1, and TNF-α in SLE mice, reducing inflammation and alleviating disease symptoms ^[6].

Decreased Apoptosis: ARA-290 reduces the number of apoptotic cells in kidneys, protects renal cells, and inhibits inflammatory activation of macrophages while promoting their phagocytosis of apoptotic cells in vitro, regulating the immune system and holding potential for SLE treatment ^[6].

Mitigation of Chemotherapeutic Drug Toxicity

Reduction of DNA Damage: In doxorubicin (DOX)-induced cytotoxicity models, ARA-290 significantly reduces DOX-induced DNA damage, such as decreasing tail DNA percentage in comet assays and micronucleus frequency, protecting cellular genetic material and reducing chemotherapeutic damage to normal cells ^[7].

Alleviation of Oxidative Stress and Inflammation: ARA-290 mitigates DOX-induced impairment of antioxidant enzyme activity, reduces inflammation and apoptosis, and protects against DOX-induced oxidative stress and cell damage, potentially including cardiac cells, to alleviate adverse effects in chemotherapy patients ^[7].

Prevention and Treatment of Alzheimer’s Disease

Slowed Pathological Progression and Improved Cognition: Early administration of ARA-290 in young APP/PS1 mice (early Alzheimer’s model) slows β-amyloid (Aβ) pathological progression and improves cognitive function, highlighting its significance for early intervention^[8].

Regulation of Monocyte Function: ARA-290 specifically stimulates the generation of Ly6C⁻ patrolling monocyte subsets, increases their circulating levels, promotes Aβ clearance from cerebral blood vessels, reduces brain Aβ burden, and delays disease progression. However, it is less effective in late-stage models (aged APP/PS1 mice), underscoring the importance of early intervention ^[8].

Promotion of Diabetic Wound Healing

Accelerated Wound Closure: In streptozotocin-induced diabetic incisional wound rat models, local ARA-290 application significantly accelerates wound closure, shortens reepithelialization time, and improves wound healing efficiency^[9] .

Regulation of Tissue Repair Markers: ARA-290 increases collagen and protein content in repair tissues, regulates serum insulin, blood glucose, lipid levels, antioxidant status, and pro-inflammatory cytokine levels, creating a microenvironment conducive to wound healing and providing new strategies for treating diabetic foot ulcers ^[9].

Pain Relief

Inhibition of TRPV1 Channel Activity: ARA-290 relieves capsaicin-induced mechanical allodynia by inhibiting transient receptor potential vanilloid subtype 1 (TRPV1) channel activity, directly targeting peripheral nociceptors and providing new therapeutic targets and approaches for pain treatment ^[4].

Conclusion  

ARA-290 is an EPO-derived polypeptide with anti-inflammatory, anti-apoptotic, and anti-oxidative effects. It can treat pain in diabetes and sarcoidosis, promote nerve fiber regeneration, combat nephrotoxicity, SLE, depression, and alleviate pain by antagonizing TRPV1. With potential in early Alzheimer’s intervention and other fields, it holds broad clinical application prospects.

Scientific Journal Author

Al-Onaizi, Mohammed is a scholar with deep expertise in the field of biomedicine. He has close ties with several renowned academic and research institutions, including Dasman Diabetes Institute (DDI), Kuwait University, Laval University, Western University (University of Western Ontario), and Hebrew University of Jerusalem. His research interests are broad, covering Neurosciences & Neurology, Biochemistry & Molecular Biology, Immunology, Psychiatry, and other topics in Life Sciences & Biomedicine. These disciplines are crucial for gaining a deeper understanding of human physiological mechanisms, disease processes, and the development of new treatments. Al-Onaizi, Mohammed’s research has achieved significant results in basic sciences and has provided vital theoretical support and practical guidance for clinical medicine and biomedical research.. Al-Onaizi, Mohammed is listed in the reference of citation [8].

▎Relevant Citations

[1]  Dahan A, Brines M, Niesters M, et al. Targeting the innate repair receptor to treat neuropathy[J]. Pain Reports, 2016,1(1):e566.DOI:10.1097/PR9.0000000000000566.

[2]   Ghassemi-Barghi N, Ehsanfar Z, Mohammadrezakhani O, et al. Mechanistic Approach for Protective Effect of ARA290, a Specific Ligand for the  Erythropoietin/CD131 Heteroreceptor, against Cisplatin-Induced Nephrotoxicity,  the Involvement of Apoptosis and Inflammation Pathways[J]. Inflammation, 2023,46(1):342-358.DOI:10.1007/s10753-022-01737-7.

[3]   Wang R, Yang Z, Huang Y, et al. Erythropoietin‐derived peptide ARA290 mediates brain tissue protection through the $\beta$‐common receptor in mice with cerebral ischemic stroke[J]. CNS Neuroscience \& Therapeutics, 2024,30. https://api.semanticscholar.org/CorpusID:268414491.

[4]   Zhang W, Yu G, Zhang M. ARA 290 relieves pathophysiological pain by targeting TRPV1 channel: Integration  between immune system and nociception[J]. Peptides, 2016,76:73-79.DOI:10.1016/j.peptides.2016.01.003.

[5]   Xu G, Zou T, Deng L, et al. Nonerythropoietic Erythropoietin Mimetic Peptide ARA290 Ameliorates Chronic  Stress-Induced Depression-Like Behavior and Inflammation in Mice[J]. Frontiers in Pharmacology, 2022,13:896601.

DOI:10.3389/fphar.2022.896601.

[6]   Huang B, Jiang J, Luo B, et al. Non-erythropoietic erythropoietin-derived peptide protects mice from systemic  lupus erythematosus[J]. Journal of Cellular and Molecular Medicine, 2018,22(7):3330-3339.DOI:10.1111/jcmm.13608.

[7]   Shokrzadeh M, Etebari M, Ghassemi-Barghi N. An engineered non-erythropoietic erythropoietin-derived peptide, ARA290,  attenuates doxorubicin induced genotoxicity and oxidative stress[J]. Toxicology in Vitro, 2020,66:104864.

DOI:10.1016/j.tiv.2020.104864.

[8]   Al-Onaizi M A, Thériault P, Lecordier S, et al. Early monocyte modulation by the non-erythropoietic peptide ARA 290 decelerates  AD-like pathology progression[J]. Brain Behavior and Immunity, 2022,99:363-382.

DOI:10.1016/j.bbi.2021.07.016.

[9]   Mashreghi M, Bayrami Z, Sichani N, et al. An in vivo investigation on the wound-healing activity of Specific ligand for the innate repair receptor, ARA290, using a diabetic animal model[M]. 2023.DOI:10.21203/rs.3.rs-2520194/v1.

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