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In the animal models studied, it did so without producing significant increases in cortisol, ACTH, or prolactin, distinguishing it from earlier growth hormone-releasing peptides.[2] Preclinical research suggests that activating both the GHRH and GHS-R1a pathways may yield greater GH output than either pathway alone, providing a mechanistic rationale for the CJC-1295/Ipamorelin stack.[2] These findings come primarily from early clinical and preclinical studies

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doi: 10.1111/acel.13034, PMID: [DOI] [PMC free article] [PubMed] [Google Scholar] 29

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