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In vivo studies with long-acting glucagon analogue suggest that hypoaminoacidaemia could be an important contributing mechanism to the observed increase in energy expenditure with glucagon agonism, but it also leads to enhanced lean mass loss [63]

and (3) glutathione S-transferases (GST) to conjugate GSH with endogenous substances (e.g., estrogens), exogenous electrophiles (e.g., arene oxides, unsaturated carbonyls, organic halides), and diverse xenobiotics

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Failure to meet these thresholds typically results in treatment discontinuation, as cost-effectiveness is not demonstrated with lesser responses