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Sustained over-activation of glutamate receptors subsequently induces synergistic injury mechanisms, including oxidative stress, mitochondrial metabolic dysfunction, endoplasmic reticulum (ER) stress, and nicotinamide adenine dinucleotide (NAD + ) homeostasis disruption

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In Gaugler J

This observation, coupled with the added stability contributed by C-terminal amidation and the desire to increase the hydrophobicity of the peptide, led to the generation of a series of compounds with the structure N -acyl-Tyr-Ile-(6) amino-hexanoic amide

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