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Sermorelin Acetate

Sermorelin — GHRH(1-29) analog

Sermorelin Acetate (Sermorelin — GHRH(1-29) analog) research vial
$99.00

At a Glance

Molecular Properties

Molecular FormulaC149H246N44O42S (free peptide; supplied as the acetate salt)
Molecular Weight3357.9 Da (free peptide)
SequenceGHRH(1-29): the first 29 residues of human growth-hormone-releasing hormone (Tyr-Ala-Asp-Ala-Ile-Phe-Thr-Asn-Ser-Tyr-Arg-Lys-Val-Leu-Gly-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Met-Ser-Arg)

Overview

Compound Description

Sermorelin is a synthetic 29-amino-acid peptide corresponding to GHRH(1-29)-NH2, the N-terminal fragment of human growth-hormone-releasing hormone that retains the full intrinsic activity of the parent 44-residue hormone. As a growth-hormone-releasing hormone (GHRH) analog, it is studied in research contexts for its interactions with the somatotropic axis, particularly the release of endogenous growth hormone from the anterior pituitary. This profile is provided strictly for research and educational purposes and does not describe any therapeutic use or human application.

Mechanism of Action

Research-Identified Pathways

Sermorelin corresponds to GHRH(1-29) and, in published research, binds the growth-hormone-releasing hormone receptor (GHRH-R), a class B G-protein-coupled receptor expressed on anterior-pituitary somatotrophs. Receptor engagement research indicates coupling primarily through Gs, activation of adenylyl cyclase and elevation of intracellular cAMP, with additional MAPK signaling described in the literature; these pathways are associated in research models with both the synthesis and the pulsatile secretion of growth hormone (GH).

Research indicates that GHRH-analog signaling is embedded within a regulated feedback network: hypothalamic somatostatin exerts an opposing inhibitory tone at the somatotroph, and downstream GH and hepatic insulin-like growth factor 1 (IGF-1) provide negative feedback that dampens further GH release. Because of this interplay, the GH response to a GHRH analog observed in research is state-dependent, varying with prevailing somatostatin tone and IGF-1 levels rather than producing an unregulated release. No therapeutic or medical-benefit claims are made or implied.

Key Research Findings

Published Study Highlights

  • Research established that the N-terminal GHRH(1-29) fragment retains essentially the full growth-hormone-releasing activity of the intact 44-residue GHRH molecule, defining the minimal bioactive core studied as sermorelin.
  • In investigational endocrine studies, intravenous administration of the GHRH(1-29) analog elicited a relatively rapid and specific rise in circulating growth hormone, and it has been examined as a provocative probe of pituitary somatotroph capacity.
  • Controlled research in normal male subjects demonstrated that exogenous growth hormone inhibits GHRH-induced GH secretion, illustrating negative feedback within the somatotropic axis relevant to GHRH-analog signaling.
  • Preclinical and mechanistic literature characterizes GHRH-R as a Gs-coupled receptor whose activation raises cAMP and engages MAPK cascades linked to GH synthesis and pulsatile release.
  • Longitudinal investigational studies of once-daily subcutaneous GHRH(1-29) reported changes in growth-hormone dynamics over multi-month observation windows, informing research on the durability of somatotroph responsiveness to GHRH-analog stimulation.

Areas of Research Interest

Why Researchers Are Investigating This Compound

This compound has attracted significant research attention in the following areas. These represent active fields of scientific inquiry, not validated therapeutic claims. No medical benefits are stated or implied.

  • Somatotropic-axis signaling: study of GHRH-receptor engagement, cAMP/MAPK transduction, and the coupling between receptor activation and endogenous GH release in cellular and animal models.
  • GH-secretion and diagnostic research: use of a GHRH(1-29) analog as a mechanistic probe of pituitary somatotroph reserve and of GH pulsatility, feedback, and provocative-response paradigms.
  • Aging endocrinology models: investigation of age-related shifts in GHRH responsiveness and the GH/IGF-1 axis, using GHRH analogs to interrogate somatotroph function across the lifespan in research settings.
  • Feedback-regulation research: characterization of how somatostatin tone and GH/IGF-1 negative feedback modulate the magnitude and timing of GHRH-analog-driven GH secretion — a research question, not a validated benefit.

Published Research

Peer-Reviewed References

  1. Prakash A, Goa KL "Sermorelin: a review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency." BioDrugs (1999). doi:10.2165/00063030-199912020-00007
  2. Ishida J, Saitoh M, Ebner N, Springer J, Anker SD, von Haehling S "Growth hormone secretagogues: history, mechanism of action, and clinical development." JCSM Rapid Communications (2020). doi:10.1002/rco2.9
  3. Rosenthal SM, Hulse JA, Kaplan SL, Grumbach MM "Exogenous growth hormone inhibits growth hormone-releasing factor-induced growth hormone secretion in normal men." Journal of Clinical Investigation (1986). doi:10.1172/jci112273
  4. Thorner M, Rochiccioli P, Colle M, Lanes R, Grunt J, Galazka A, Landy H, Eengrand P, Shah S "Once daily subcutaneous growth hormone-releasing hormone therapy accelerates growth in growth hormone-deficient children during the first year of therapy (Geref International Study Group)." The Journal of Clinical Endocrinology & Metabolism (1996). doi:10.1210/jcem.81.3.8772599
  5. Lanes R, Carrillo E (Venezuelan Collaborative Study Group) "Long term therapy with a single daily subcutaneous dose of growth hormone releasing hormone (1-29) in prepubertal growth hormone deficient children." Journal of Pediatric Endocrinology and Metabolism (1994). doi:10.1515/jpem.1994.7.4.303

Research Use Only

The information presented on this page is compiled from peer-reviewed scientific literature and is provided solely for educational and research purposes. This compound is intended exclusively for laboratory and scientific research use. It is not a drug, pharmaceutical, or dietary supplement. It is not intended to diagnose, treat, cure, or prevent any disease or medical condition. No claims of therapeutic efficacy are made or implied.

Researchers are advised to consult the original published studies referenced above for complete methodological details, study limitations, and the authors' own conclusions. Atlas Peptide Research does not endorse any specific research application and provides this information as a reference resource only.

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For research use only. Not for human consumption. Products are intended solely for laboratory and scientific research purposes.