
AOD-9604
AOD-9604 is a modified HGH fragment 176-191 with disulfide bridge modification, studied for lipolytic activity without IGF-1 or insulin resistance effects — with FDA GRAS designation and Phase IIb human trial data.
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HGH Fragment 176-191 is a 16-amino-acid GH C-terminal peptide studied in preclinical adipose models for lipolysis promotion without IGF-1 stimulation, anabolic effects, or insulin resistance.
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Lyophilized and lot-tracked
Sterile-filtered, freeze-dried, sealed under inert gas. Each vial carries its own lot ID — full chain of custody from fill to delivery.
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How it works
HGH Fragment 176-191 activates lipolytic pathways in adipocytes through proposed β3-adrenoreceptor interaction, stimulating fat breakdown and inhibiting lipogenesis independently of GH receptor activation. In rodent models, it produces body fat reduction without the anabolic, growth-promoting, or diabetogenic effects of full-length GH — mechanistically dissecting GH's lipolytic dimension from its other biological activities.
Compound profile
Product definition
HGH Fragment 176-191 is a 16-amino-acid GH C-terminal peptide studied in preclinical adipose models for lipolysis promotion without IGF-1 stimulation, anabolic effects, or insulin resistance.
HGH Fragment 176-191 is a peptide fragment of the C-terminal helical region of human growth hormone, developed by researchers at Monash University (Melbourne) to isolate the lipolytic activity of GH from its growth-promoting and diabetogenic effects. The fragment spans residues 176 to 191 of the 191-amino-acid GH sequence. The critical mechanistic discovery was that this C-terminal region — a helical structure — activates lipolysis in fat cells through a receptor pathway distinct from the GH receptor. The proposed mechanism involves β3-adrenoreceptor-like interaction, producing adenylyl cyclase activation and downstream lipolysis (triglyceride hydrolysis) and inhibition of lipogenesis (triglyceride synthesis from glucose). In the Monash research series and subsequent published studies, fragment 176-191 produced statistically significant body fat reduction in obese rodent models versus vehicle controls, with the fat loss concentrated in visceral adipose depots. Critically, these effects were achieved without IGF-1 elevation (confirming lack of GH receptor engagement), without insulin resistance (confirming no GH-like diabetogenic effect), and without growth plate stimulation (confirming no growth-promoting activity).
Research audience
HGH Fragment 176-191 is used by researchers in adipose tissue biology, GH pharmacology, lipolysis mechanisms, fat cell metabolism, and metabolic disease. It is specifically valuable for investigators who need to study GH-associated lipolytic mechanisms without the confounding effects of GH's anabolic and diabetogenic receptor activities.
Research context
The Monash University research program on HGH Fragment 176-191 was motivated by the observation that full-length GH's clinical utility in treating obesity was limited by insulin resistance induction — essentially trading metabolic benefit (fat loss) for metabolic harm (glucose dysregulation). The hypothesis was that the lipolytic and anabolic/diabetogenic activities of GH were separable at the molecular level. The fragment 176-191 work confirmed this hypothesis: the C-terminal helical region activates fat cell metabolism through a distinct pathway from the growth hormone receptor that mediates anabolic and diabetogenic effects. The Monash group published body composition studies in genetically obese (ob/ob) mice and diet-induced obesity models showing visceral fat reduction without metabolic liabilities. The compound was also investigated briefly in early human research (Phase I/II metabolic studies in Australia) before development was discontinued for commercial reasons. The published preclinical and early clinical data remain in the literature as the mechanistic foundation for fragment 176-191 research. AOD-9604 is a related compound — a modified version of fragment 176-191 with a disulfide bridge — that was developed in parallel from the same Monash research program and achieved FDA GRAS designation.
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