This page is provided for research and educational purposes only and does not provide medical advice, diagnosis, treatment recommendations, dosing instructions, or instructions for human use. Research findings should be interpreted within the population, model, formulation, route, outcomes, and study design reported by each cited source.
Ara-290 (16 mg Vial)
Ara-290 (cibinetide) is an 11–amino acid non-erythropoietic peptide derived from erythropoietin’s helix-B domain[1]. It selectively activates the innate repair receptor (IRR), an EPOR/CD131 heterodimer, to promote anti-inflammatory and tissue-protective effects without stimulating red blood cell production[2]. Clinical trials have demonstrated benefits for diabetic neuropathy and sarcoidosis-related small-fiber neuropathy[3][4].
Quick Reference
What is Ara-290?
Research overview based on the cited scientific literature.
• Goal: Support tissue protection, anti-inflammatory signaling, and neuropathic symptom management via IRR activation[2].
• Storage: Lyophilized refrigerated or frozen; reconstituted refrigerated up to 28 days.
Storage Instructions
Proper storage preserves peptide integrity and potency.
• Lyophilized: Refrigerate at 2–8 °C (35.6–46.4 °F) for up to 2 years; freeze at −20 °C (−4 °F) for extended storage up to 3 years[6].
• Reconstituted: Refrigerate at 2–8 °C (35.6–46.4 °F); use within 28 days and do not freeze the liquid solution[7].
• Allow vials to reach room temperature before opening to minimize condensation; protect from light.
• Discard if discoloration, cloudiness, or particulate matter is observed.
How is Ara-290 studied?
Ara-290 (cibinetide) binds to the innate repair receptor (IRR), a heterodimer of EPOR and CD131 (βc subunit), which is distinct from the classical erythropoietin receptor[1][2]. This selective binding triggers anti-apoptotic and anti-inflammatory signaling cascades that protect tissues and promote repair without stimulating erythropoiesis[9]. Preclinical research demonstrates that Ara-290 can reprogram a pro-inflammatory, tissue-damaging environment into one favoring healing and regeneration[10]. Additionally, analgesic effects have been observed through immunomodulation and direct inhibition of TRPV1 ion channels activated by capsaicin[11].
What does the research report about Ara-290?
Observations from preclinical and clinical literature.
• Neuroprotection: Clinical trials in diabetic neuropathy showed improvements in HbA1c, lipid profiles, and neuropathic pain scores with 4 mg daily dosing[3].
• Nerve regeneration: In sarcoidosis-associated small-fiber neuropathy, treatment led to significant increases in corneal nerve fiber density (objective nerve regrowth) and improved symptoms compared to placebo[4].
• Tissue protection: Anti-inflammatory and anti-apoptotic effects observed across multiple organ systems in preclinical models[9].
• No erythropoietic effects: Unlike full EPO, Ara-290 does not stimulate red blood cell production, avoiding related side effects[2].
• Tolerability: Well tolerated in clinical studies; occasional mild injection-site reactions (redness, transient discomfort) may occur with subcutaneous administration.
Important Note
This content is provided for scientific research and educational purposes only. It does not provide medical advice, diagnosis, treatment, dosing, or administration instructions. The compounds discussed may be investigational and are not presented as approved for human use.
What are the limitations of the research on Ara-290?
Evidence should be interpreted within the population, experimental model, formulation, route, outcome measures, and study design used in each cited source. Preclinical or early-stage findings do not establish clinical efficacy, safety, or approved human use. Where human evidence is available, results should not be generalized beyond the populations and conditions actually studied.
