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It is therefore clear that currently available GLP-1RAs, mimicking on the peripheral action of GLP-1 (7-36) NH2 , not only ignore the yet unknown physiology of GLP-1 (9-36) NH2 or its metabolites, but they also fail to address the tissue specific physiology of GLP-1 (7-36) NH2 , while pushing to supra-physiological limits the endocrine GLP-1 receptor axis, likely explaining the reported side-effects and only partial success in the treatment of T2D

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To address this, we have used a HEK293 cell-based system where GNE is either knocked down or the cells over-express mutant GNE recombinant protein

Well, science reality has a name: GHK-Cu peptide