Hexarelin, sometimes called examorelin, is a potent growth hormone secretagogue (GHS) hexapeptide. As a member of the synthetic class of secretagogues known as growth-hormone secretagogue peptides (GHRPs), hexarelin primarily exerts its action at the pituitary level by acting as a ghrelin mimetic. According to published literature hexarelin powerfully inhibits somatostatin, recruits or activates somatotrophs (GH-producing pituitary cells), and increases appetite in mammals. Compared to growth-hormone releasing hormone (GHRH) analogs such as Modified GRF (1-29), ghrelin mimetics are more robust and less susceptible to environmental and physiological factors that degrade the peptide or inhibit the release of growth hormone.
Although GHRPs and GHRH analogs combined are synergistic, relatively speaking GHRPs have been demonstrated in a controlled environment to release a greater amount of growth hormone. Hexarelin, along with GHRP-2, GHRP-6, and ipamorelin, is among the most-studied secretagogue peptides. Of that group of four GHRPs, ipamorelin has the least GH-releasing efficacy and the least release of cortisol and prolactin, while hexarelin induces the most potent GH release along with higher levels of cortisol and prolactin.
Like other GHRPs, hexarelin also has unique properties that are not directly tied to the release of growth hormone from the pituitary. Hexarelin "reduces injury of cerebral cortex and hippocampus after brain hypoxia-ischemia in neonatal rats" according to Liu et al (2006), an effect that may overlap with full-chain ghrelin. A possible shared effect of multiple GHRPs is an antioxidant benefit on the testis through a receptor called GHS-R type 1a, present in Sertoli and Leydig cells; reduction of lipid peroxidation and increasing the activity of the body's three main antioxidant systems may additionally protect spermatozoa from free radicals. 
Finding of Pang et al suggested hexarelin holds promise of possible clinical development and use in treating atherosclerosis (2009):
Hexarelin suppressed the formation of atherosclerotic plaques and neointima, partially reversed serum HDL-c/LDL-c ratio and increased the levels of serum NO and aortic mRNAs of eNOS, GHSR and CD36 in As rats. Hexarelin also decreased [(3)H]-TdR incorporation in cultured vascular smooth muscle cell (VSMC) and calcium sedimentation in aortic wall. Furthermore, foam cell formation induced by ox-LDL was decreased by hexarelin. In conclusion, hexarelin suppresses high lipid diet and vitamin D3-induced atherosclerosis in rats, possibly through up regulating HDL-c/LDL-c ratio, vascular NO production and downregulating the VSMC proliferation, aortic calcium sedimentation and foam cell formation. These novel anti-atherosclerotic actions of hexarelin suggest that the peptide might have a clinical potential in treating atherosclerosis. 
According to Bresciani et al (2008) "hexarelin is endowed with long-lasting orexigenic activity and might represent a potential therapeutic approach for pathological conditions characterized by a decline in food intake." 
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