Research Studies: Inflammation Studies and ARA-290 Peptide
ARA-290 is a polypeptide composed of a sequence of 11 amino acids. It is obtained from the tertiary conformation of erythropoietin, a naturally occurring peptide. The primary role of erythropoietin is to initiate erythropoiesis, generating red blood cells within the bone marrow while exerting additional physiological effects. [i]
Studies suggest that due to its nonhematopoietic nature, ARA-290, an erythropoietin analog, may not induce erythropoiesis, the red blood cell generation process. Instead, research suggests it may modulate various other mechanisms, such as neuroprotection, blood pressure modulation, and promoting cellular growth.
What is the mechanism of action of ARA-290?
In order to comprehend the mechanism of action of ARA-290, it is important to consider that due to its derivation from erythropoietin, its mechanism of action is expected to exhibit significant similarities.
The primary focus of scientific research in ARA-290 pertains to its potential capacity for reducing the severity of neuropathic pain. This mechanism is achieved through the modulation of the innate repair receptor (IRR) and the subsequent suppression of inflammatory pathways, leading to a reduction in inflammation.
Researchers speculate that ARA-290 may potentially suppress the functionality of the TRPV1 channel, a key mediator of heat perception and the sensation of burning pain. This channel is predominantly associated with neuropathic conditions, wherein test subjects may commonly experience discomfort. [ii]
In alternative instances of small fiber neuropathy, there is potential for severing small peripheral nerve fibers in the skin, resulting in pain, burning, and tingling sensations. Scientists hypothesize ARA-290 may alleviate this pain by augmenting the number of small nerve fibers. [iii]
Studies suggest one significant action of ARA-290 may be intricately associated with its alleged anti-inflammatory characteristic. The compound may exhibit macrophage activation inhibition properties and exhibits a likely affinity towards protective tissue receptors (TPR) located on cellular surfaces. As a result, pro-inflammatory cytokines such as IL-2, IL-6, and tumor necrosis factor may be downregulated.
Research suggests any cellular entity that exhibits TPR expression may undergo direct modulation due to the influence of ARA-290. The aforementioned cellular components, namely macrophages, dendritic cells, mast cells, and lymphocytes, collectively constitute integral constituents of the innate immune response.
Reducing the cellular population within the immune system may subsequently impede other detrimental processes typically associated with an inflammatory response, while concurrently facilitating skin and tissue regeneration.
ARA-290 Peptide: Potential Properties
Studies suggest that ARA-290 may exhibit the potential to mitigate neuropathic pain through the inhibition of TRPV1 receptors. It is suggested that this peptide may hold significant potential as a mitigating agent for pain stemming from peripheral neuropathy linked to type 2 diabetes, multiple sclerosis, and sarcoidosis. [iv]
A study suggested that the presentation of ARA-290 to test models with neuropathic pain induced by sarcoidosis have resulted, according to study literature, in a noteworthy 50% enhancement in pain relief. This provides support for the speculation that ARA-290 may exhibit a substantial enhancement in the overall health of test models. [v]
Researchers speculate that in instances of diabetic retinopathy, ARA-290 suggests a capacity to exert neuroprotective properties, safeguarding the retina against neuroglial and vascular degeneration. Scientists hypothesize it may enhance the density of nerve fibers in the cornea, potentially mitigating the risk of vision impairment in subjects diagnosed with diabetes mellitus. [vi]
Studies suggest that due to its potentially anti-inflammatory properties, this peptide may exhibit significant potential in mitigating pain experienced by subjects with autoimmune disorders. An illustrative instance is rheumatoid arthritis, wherein the predominant cause of joint pain can be attributed to the presence of immune cells.
In addition to acquired and autoimmune diseases, research suggests ARA-290 may modulate chronic pain that may arise due to medical interventions like chemotherapy and amputation. [vii]
The transplanted islet cells typically exhibit limited viability due to post-operative inflammatory responses. In this scenario, the presentation of ARA-290 may have suppressed inflammatory cytokine secretion from macrophages, consequently promoting the prolonged survival of the transplanted cells. [viii]
ARA-209 has suggested its efficacy in mitigating burn injuries through its wound-healing potential, possibly mitigating the need for skin grafting procedures. [ix]
Several studies have also suggested that ARA-290 may reduce ischemic myocardial injury in rats with various cardiac conditions. [x]
ARA-290 vs. Thymosin Alpha 1
ARA-290 is derived from erythropoietin, a hormone the kidneys produce that is considered to regulate red blood cell production. Thymosin Alpha 1, on the other hand, is derived from the thymus gland, an organ involved in immune system function. Consequently, both of these peptides are endogenously present. Studies suggest both substances may significantly reduce inflammation, although their supposed mechanisms vary.
Research suggests ARA-290 may exhibit affinity towards tissue receptors on cellular surfaces, inhibiting pro-inflammatory cytokines. Conversely, Thymosin Alpha 1 may engage with toll-like receptors, facilitating immune system modulation.
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References
[i] Brines, M., Patel, N. S., Villa, P., Brines, C., Mennini, T., De Paola, M., Erbayraktar, Z., Erbayraktar, S., Sepodes, B., Thiemermann, C., Ghezzi, P., Yamin, M., Hand, C. C., Xie, Q. W., Coleman, T., & Cerami, A. (2008). Nonerythropoietic, tissue-protective peptides derived from the tertiary structure of erythropoietin. Proceedings of the National Academy of Sciences of the United States of America, 105(31), 10925–10930.
[ii] Brandt, M. R., Beyer, C. E., & Stahl, S. M. (2012). TRPV1 Antagonists and Chronic Pain: Beyond Thermal Perception. Pharmaceuticals (Basel, Switzerland), 5(2), 114–132.
[iii] Hoitsma, E., De Vries, J., & Drent, M. (2011). The small fiber neuropathy screening list: Construction and cross-validation in sarcoidosis. Respiratory medicine, 105(1), 95–100.
[iv] van Velzen, M., Heij, L., Niesters, M., Cerami, A., Dunne, A., Dahan, A., & Brines, M. (2014). ARA 290 for treatment of small fiber neuropathy in sarcoidosis. Expert opinion on investigational drugs, 23(4), 541–550.
[v] Niesters, M., Swartjes, M., Heij, L. R., Brines, M., Cerami, A., Dunne, A., Hoitsma, E., & Dahan, A. (2013). The erythropoietin analog ARA 290 for treatment of sarcoidosis-induced chronic neuropathic pain. Expert Opinion on Orphan Drugs, 1(1), 77–87.
[vi] McVicar, C. M., Hamilton, R., Colhoun, L. M., Gardiner, T. A., Brines, M., Cerami, A., & Stitt, A. W. (2011). Intervention with an erythropoietin-derived peptide protects against neuroglial and vascular degeneration during diabetic retinopathy. Diabetes, 60(11), 2995–3005.
[vii] Joshi, D., Abraham, D., Shiwen, X., Baker, D., & Tsui, J. (2014). Potential role of erythropoietin receptors and ligands in attenuating apoptosis and inflammation in critical limb ischemia. Journal of vascular surgery, 60(1), 191–201.e2012.
[viii] Watanabe, M., Lundgren, T., Saito, Y., Cerami, A., Brines, M., Östenson, C. G., & Kumagai-Braesch, M. (2016). A Nonhematopoietic Erythropoietin Analogue, ARA 290, Inhibits Macrophage Activation and Prevents Damage to Transplanted Islets. Transplantation, 100(3), 554–562.
[ix] Bohr, S., Patel, S. J., Shen, K., Vitalo, A. G., Brines, M., Cerami, A., Berthiaume, F., & Yarmush, M. L. (2013). Alternative erythropoietin-mediated signaling prevents secondary microvascular thrombosis and inflammation within cutaneous burns. Proceedings of the National Academy of Sciences of the United States of America, 110(9), 3513–3518. https://doi.org/10.1073/pnas.1214099110
[x] Ahmet, I., Tae, H. J., Brines, M., Cerami, A., Lakatta, E. G., & Talan, M. I. (2013). Chronic administration of small nonerythropoietic peptide sequence of erythropoietin effectively ameliorates the progression of postmyocardial infarction-dilated cardiomyopathy. The Journal of pharmacology and experimental therapeutics, 345(3), 446–456. https://doi.org/10.1124/jpet.113.202945.
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