Modified human-growth-hormone C-terminal fragment supplied as a lyophilized laboratory reference material for analytical and metabolism research. Research use only. Not for human or veterinary use.
Reference characteristics for laboratory research materials.
CAS Number
221231-10-3
Purity
≥98%
Molecular Formula
C78H123N23O23S2
Molecular Weight
1815.08
Appearance
White lyophilized powder
Storage
-20°C
Research Classification
Research Use Only (RUO). Not for human or veterinary use.
SCIENTIFIC OVERVIEW
Scientific background and research classification for this laboratory reference material.
AOD-9604 is a synthetic modified analog of the C-terminal lipolytic domain of human growth hormone: an N-terminal tyrosine appended to the hGH(177-191) sequence, giving the 16-residue peptide Tyr-Leu-Arg-Ile-Val-Gln-Cys-Arg-Ser-Val-Glu-Gly-Ser-Cys-Gly-Phe (YLRIVQCRSVEGSCGF) with an intramolecular disulfide bridge between Cys7 and Cys14. CAS 221231-10-3; molecular formula C78H123N23O23S2. It is supplied as a lyophilized peptide reference material for laboratory research use only. 'AOD-9604' and 'hGH Fragment 176-191' are established compound-identity names and do not describe a demonstrated effect of this research material.
As the modified fragment, AOD-9604 is a distinct molecular entity from native/unmodified hGH 176-191 and from full-length growth hormone; it retains the disulfide-bridged loop of the parent domain but is not a growth-hormone-axis agonist.
Molecular interaction profile describing how this research material engages receptor systems and influences downstream biological signaling pathways.
No cloned or definitively characterized direct molecular receptor for AOD-9604 has been established. In animal and in-vitro models the peptide has been reported to stimulate lipolysis and fat oxidation and to reduce lipogenesis (Ng et al., 2000; Heffernan et al., 2001), and this reported activity is described as not mediated by the growth-hormone receptor, with later work reporting effects independent of the beta3-adrenergic receptor. Accordingly no direct molecular target or biological pathway is asserted for this material within the governed vocabulary; the reported lipolytic and fat-oxidation findings are model-specific observations at the stated evidence level, not a demonstrated human mechanism.
Primary Organ Systems
Metabolic System
Research Documentation
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In Laboratory Testing
Laboratory Documentation In Progress
Identity
Purity
Endotoxin
Fentanyl
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Research Library
Curated peer-reviewed literature selected to provide scientific context for this research material.
Mechanistic Study•Hormone Research•2000
Metabolic studies of a synthetic lipolytic domain (AOD9604) of human growth hormone
Foundational report characterizing a synthetic lipolytic domain (AOD9604) derived from the C-terminal region of human growth hormone and its metabolic activity in laboratory models — the origin of AOD-9604 as a defined research peptide.
Velora Research Insight
Discovery/characterization of AOD9604 as a synthetic lipolytic-domain fragment. Ng / Monash (Metabolic Pharmaceuticals) originating lineage. Findings are laboratory/animal-model, foundational — not human-efficacy evidence.
The effects of human GH and its lipolytic fragment (AOD9604) on lipid metabolism following chronic treatment in obese mice and beta(3)-AR knock-out mice
Preclinical study of chronic AOD9604 treatment on lipid metabolism in obese mice and beta3-adrenergic-receptor knock-out mice, reporting lipolytic/metabolic effects and probing beta3-AR dependence.
Velora Research Insight
Preclinical mechanism/lipid-metabolism evidence; the beta3-AR knock-out arm is the basis for representing AOD-9604's activity as not straightforwardly beta3-AR-mediated. SAME Ng/Monash originating lineage (Ng FM co-author) — investigator concentration disclosed.
Preclinical Study•International Journal of Obesity and Related Metabolic Disorders•2001
Increase of fat oxidation and weight loss in obese mice caused by chronic treatment with human growth hormone and a modified C-terminal fragment
Preclinical study in obese mice reporting increased fat oxidation with chronic treatment by human growth hormone and a modified C-terminal fragment, examining the growth-hormone-receptor dependence of the effect.
Velora Research Insight
Preclinical fat-oxidation mechanism; supports the representation that the fragment's reported activity is distinguishable from full-length GH receptor signaling. SAME Ng/Monash originating lineage — not an additional independent lineage. Reported in an animal model only; not human-efficacy evidence.
Independent analytical study developing detection methods for AOD9604 and characterizing its in-vitro metabolism, relevant to identity/analytical science rather than efficacy.
Velora Research Insight
Independent later analytical/metabolism work (anti-doping laboratory; no originating-group overlap) — the only fully independent publication in this set. Anchors identity/analytical science and preserves the distinction between analytical characterization and any efficacy interpretation.