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The four amino acid substitutions in CJC-1295 No DAC (Ala2D-Ala, Asn8Ala, Ala15Ala, Met27Leu) provide resistance to enzymatic degradation while maintaining receptor binding affinity

[1] [2] The precise mechanism in humans remains incompletely understood and is based partly on extrapolation from preclinical data and from clinical observations with approved GLP-1 receptor agonists

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In addition, the intracellular glutamine can maintain redox homeostasis through many sophisticated mechanisms (Son et al., 2013

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