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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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When GH levels are optimized through CJC-1295, two critical metabolic processes are enhanced: Stimulating Muscle Protein Synthesis GH signals the liver to produce IGF-1 (Insulin-like Growth Factor 1)

To this end, we utilized a functional immune co-culture bioassay comprising Raji antigen-presenting cells and Jurkat T cells stably expressing a luciferase reporter gene under the control of an NFAT-response element