ARA-290 16mg

ARA-290 Peptide

Erythropoietin (EPO) is a kidney-derived glycoprotein made of 11 amino acids that has been studied for its potential to promote blood vessel growth, tissue repair, cell survival, neuroprotection in the case of diabetic neuropathy, and alter blood pressure. ARA-290 is a peptide derived from the beta-helix domain of EPO.^[1] ARA-290 was developed with the intention of stimulating the pain relief and neuroprotective effects of EPO, possibly without promoting blood cell formation. ARA-290 has been proposed by researchers to exhibit anti-apoptotic, anti-inflammatory, and anti-permeability potential akin to endogenous EPO. The peptide is being evaluated for its potential for neuropathic wound healing, immunomodulation, and mitigation of Systemic Lupus Erythematosus (SLE) symptoms.

ARA-290 AND BLOOD VESSEL HEALTH
Retinal ischemia is considered to be a potential result of various diseases and may ultimately lead to damage to retinal epithelial cells. The peptide has been studied for its potential to protect endothelial colony-forming cells to repair the blood vessels and rebuild damaged tissue. Results from one study in mice models have suggested the peptide’s potential to enhance the proliferation and migration of blood cells significantly.^[2]
More specifically, the study delves into the potential role of ARA-290 in possibly exploiting an inherent system of tissue protection and repair that EPO hypothetically mediates. The innate repair receptor (IRR), which is believed to be composed of EPO receptor and CD-131 subunits, may be upregulated in response to cellular stress. This receptor is presumed to be activated by EPO and ARA-290, leading to responses that might be anti-inflammatory and reparative in a variety of cell populations such as macrophages/microglia, endothelial cells, and neurons. These reactions include the potential reduction of pro-inflammatory cytokines, apparent preservation of the blood-retinal barrier (BRB), and a speculated prevention of cell apoptosis. The researchers also share that in murine models of diabetic retinopathy (DR), the influence of ARA-290 might have resulted in the inhibition of vascular leakage and edema, protection against possible retinal degeneration, and probable improvements in metabolic control.^[2]
Further, one study investigated the mechanisms that boost endothelial colony-forming cells (ECFCs) as another potential method to foster reparative angiogenesis in retinal ischemia, a condition often linked to vision-threatening diseases. This research looked into the capacity of ARA-290 to potentially mitigate the present pro-inflammatory environment in the ischemic retina and its possible impact on ECFC-facilitated vascular regeneration. Tests were performed to estimate the influence of ARA-290 on pro-survival signaling and function within ECFC cultures. According to the findings, it appears that ARA-290 might activate pro-survival signaling and enhance cell viability in ECFCs when subjected to oxidative stress brought about by H2O2. The study ventured to evaluate the potential effectiveness of ECFC transplantation in advancing retinal vascular repair in mouse models of retinal ischemia using the oxygen-induced retinopathy (OIR) model. The outcomes of ECFC transplantation with and without ARA-290 were compared. The inflammatory cytokine profile and microglia activation were assessed, which might serve as indicators of inflammation. The results suggested that preconditioning ECFCs with either EPO or ARA-290 before transplantation did not appear to enhance their vasoreparative function in the ischemic retina. However, when ARA-290 was systemically presented to OIR mice, it appeared to reduce the expression of pro-inflammatory cytokines such as IL-1β and TNF-α in the mouse retina, possibly indicating its anti-inflammatory potential. The transplantation of ECFCs into the vitreous humor appeared to result in their incorporation into the damaged retinal vasculature. It may have led to a notable decrease in the avascular area. Interestingly, it seems that the presence of ARA-290 potentially boosted the vasoreparative function of ECFCs, whereas EPO did not exhibit a similar effect. Given these observations, the study posits that ARA-290 might enhance the regulation of the pro-inflammatory environment in the ischemic retina.^[3]