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The foundational characterization appeared in European Journal of Endocrinology in 1998, reporting selective agonism of the growth hormone secretagogue receptor type 1a (GHS-R1a) without significant elevation of ACTH, cortisol, prolactin, FSH, LH, or TSH, even at doses 200-fold above the GH-releasing ED50 in preclinical models

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Glutathione efflux and cell death