CJC-1295 cas 863288-34-0 with best price and highquality 2mg/5mg/vial*10vial/kit

Product Name: CJC1295

Synonyms: CJC1295;Y(d -A)DAIFTQSYRKVLAQLSARKLLQDILSR-NH2;L-Tyrosyl-D-alanyl-L-alpha-aspartyl-L-alanyl-L-isoleucyl-L-phenylalanyl-L-threonyl-L-glutaminyl-L-seryl-L-tyrosyl-L-arginyl-L-lysyl-L-valyl-L-leucyl-L-alanyl-L-glutaminyl-L-seryl-L-alanyl-L-arginyl-L-lysyl-L-leucyl-L-leucyl-L-glutaminyl-L-alpha-aspartyl-L-isoleucyl-L-leucyl-L-seryl-L-arginyl-N6-[3-(2,5-dihydro-2,5-dioxo-1H-pyrrol-1-yl)-1-oxopropyl]-L-lysinamide;CJC-1295 CJC-1295;CJC-1295 Acetate;CJC1295 with out DAC;-L-arginyl-L-lysyl-L-leucyl-L-leucyl-L-glutaminyl;CJC-1295(2MG)

CAS: 863288-34-0

CJC-1295 Research

CJC-1295 (Mod GRF 1-29), or tetra-substituted GRF (1-29), is a synthetically developed peptide equivalent to the naturally occurring GHRH hormone. It includes the smallest possible chain of amino acids that might connect to the GHRH receptors, and comprises the initial 29 amino acids of GHRH. The primary structural differences between CJC-1295 and its naturally occurring GHRH equivalent lies in 4 substituted amino acids of GHRH’s original 29 amino acids, to possibly enhance the peptide’s resistance to breakdown by the enzyme dipeptidyl peptidase-4. More specifically, the amino acids that have been altered and substituted are the 2nd, 8th, 15th, and 27th amino acids.[1] Further, the researchers commented, “CJC-1295 caused an increase in total pituitary RNA and GH mRNA, suggesting that proliferation of somatotroph cells had occurred, as confirmed by immunohistochemistry images.” CJC-1295 appears to bind to and interact with the receptor of GHRH in the anterior pituitary gland.[2] It may potentially maintain the pulsatile production of growth hormone (GH), improving overall physiological levels.

CJC-1295 & GHRP-6 peptides have also been associated with nervous tissue protection and repair. One study explored the impact of GHRP-6 on the brain’s IGF-1 system in murine models. The actions of GH are generally considered to be mediated through IGF-I, so the study centered primarily on the modulation of the brain’s IGF system. Researchers reported that the introduction of GHRP-6 for one week appears to have led to an increase in IGF-I mRNA levels in the hypothalamus, cerebellum, and hippocampus, but not in the cerebral cortex. This may suggest that GH and GHRP-6 may enhance the expression of IGF-I in specific brain areas. The study also explored the expression of the IGF receptor and IGF-binding protein IGFBP-2, but its findings reported no considerable fluctuation in activity following peptide introduction. However, the phosphorylation of Akt and Bad appeared stimulated in areas where IGF-I was increased. The researchers noted that this finding implied that GH and GHRP-6 may activate phosphatidylinositol kinase intracellular pathways involved in cell survival in response to growth factors. Bad is a pro-apoptotic member of the Bcl-2 protein family, which is considered to play a central role in cell death. Akt is a serine/threonine-specific protein kinase that plays a key role in multiple cellular processes such as glucose metabolism, apoptosis, cell proliferation, transcription, and cell migration. No reported changes were observed in MAPK, a protein kinase-specific to the amino acids serine, threonine, and tyrosine, nor were changes reported in glycogen synthase kinase-3beta. Moreover, the antiapoptotic protein Bcl-2 was increased in the areas where IGF-I appeared increased, with no change in the proapoptotic protein Bax. This could potentially indicate a shift towards cell survival and away from apoptosis. IGFBP-5, also reported to be involved in neuron survival processes, was reported to be increased mainly in the hypothalamus, which might suggest a potential neuroendocrine role.

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