According to pilot studies, our group determined that 400 μg/mL represented an optimal dose level by reducing inflammation, promoting collagen fibers alignment, while aborting the onset of HTS in rabbit ears. A lower dose (200 μg/mL) did not prevent the exuberant phenotype whereas a higher dose (800 μg/mL) delayed reepithelialization in rats and rabbits (data not shown).


Despite all these pharmacological advantages and that GHRPs exhibit a broad safety profile, their clinical development has been erratic and irregular. This has been a deterrence factor for their definitive positioning within cardiology and intensive care medicine for years. In the meantime, novel drugs and therapeutic strategies are demanded to protect organs and tissues exposed to ischemia and other lethal insults in the clinical practice.
This peptide is a modified fragment of hGH which contains the portion of the molecule that is believed to be responsible for hGH’s anti-obesity effects. The peptide has been shown to increase fat burning without the increase in blood sugar and growth rate that has been seen with hGH itself. AOD 9604 has been deemed safe for chronic use by the FDA, receiving Human GRAS status in 2014. In addition to its utility as an anti-obesity peptide, AOD 9604 has been shown to have very favorable cartilage repair and regenerative properties, especially when paired with peptide BPC 157.
In more recent years, these data were further substantiated using again the TO-2 hamster DCM biomodel in which GHRP-2 reduced the progression of LV remodeling, dysfunction, and the ensued myocardial fibrosis by an antioxidant mechanism.36 The abovementioned myocardial fibrotic process amelioration reveals an additional potential use for GHRP in an unmet medical need. Chronic treatment with hexarelin in spontaneously hypertensive rats, in addition to decreasing ventricular hypertrophy, diastolic dysfunction, and high blood pressure, significantly reduced cardiac fibrosis by decreasing interstitial and perivascular myocardial collagen deposition and myocardial hydroxyproline content. Mechanistically, hexarelin treatment increased matrix metalloproteinase (MMP)-2 and MMP-9 activities and decreased myocardial mRNA expression of tissue inhibitor of metalloproteinase (TIMP)-1.37
Abbreviations: AKT1, RAC-alpha serine/threonine-protein kinase; AMI, acute myocardial infarction; CTGF, connective tissue growth factor; DCM, dilated cardiomyopathy; dP/dt, the rate of left ventricle maximal pressure rise in early systole; DX, doxorubicin; ECM, extracellular matrix; EGF, epidermal growth factor; ERK1/2, extracellular signal-regulated kinase 1/2; GH, growth hormone; GHRH, growth hormone-releasing hormone; GHRPs, growth hormone-releasing peptides; GHS, growth hormone secretagogues; GHS-R, growth hormone secretagogue receptor; GHS-R1a, growth hormone secretagogue receptor type 1a; HIF-1α, hypoxia-inducible factor-1 alpha; I/R, ischemia and reperfusion; IGF-1, insulin-like growth factor-1; IL-1β, interleukin-1 beta; IL-6, interleukin 6; LPS, lipopolysaccharide; LV, left ventricle; LVEF, left ventricular ejection fraction; MBP, mean blood pressure; MIF, macrophage migration inhibitory factor; MCP-1, monocyte chemoattractant protein-1; MMP, matrix metalloproteinase; MOD, Multiple Organs Damage; NEP, nitrosylation end products; NIH, National Institute of Health; PDGF, platelet-derived growth factor; PGC1α, peroxisome proliferator-activated receptor gamma coactivator 1 alpha; PI-3K, phosphatidylinositol-4,5-bisphosphate 3-kinase; PPARγ, peroxisome proliferator-activated receptor gamma; RAS, rennin–angiotensin system; rhGH, recombinant human growth hormone; ROS, reactive oxygen species; TGF-β, transforming growth factor beta; TIMP, tissue inhibitor of metalloproteinase; TNF-α, tumor necrosis factor alpha.
As both CJC1295 and Ipamorelin bind to the pituitary gland and prompt the release of GH, when used together, the production of growth hormone is over 10 times more than when used individually. As it stimulates the body’s natural growth hormone production it also causes the release of IGF-1. The advantages of the CJC peptide is that it helps increases bone density and collagen, as well as boosting the immune system. It will also produce new muscle cells which will be leaner and increases weight loss. The CJC 1295 results are part of years of scientific studies. It primarily increases the production of proteins, which leads to stable bodily functions related to the glands in the body or the endocrine system.
It has been discovered that when GHRP-6 and insulin are administered simultaneously, GH response to GHRP-6 is increased (1). However, the consumption of carbohydrates and/or dietary fats, around the administration window of GH secretagogues significantly blunts the GH release. A recent study in normal mice showed significant differences in body composition, muscle growth, glucose metabolism, memory and cardiac function in the mice being administered the GHRP-6 (2). There are still many questions regarding this fairly new compound, scientists are hoping to gain a better clinical understanding of the peptide through further research over the next few years.
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