HGH Fragment 176-191 is a synthetic 16-residue disulfide-cyclized peptide corresponding to the C-terminal region (residues 176–191) of human growth hormone. It is classified as a lipolytic/GH-fragment peptide, not a full growth hormone. The compound is prohibited at all times under WADA Section S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics). Not FDA-approved for any indication; clinical development of the related analogue AOD9604 was discontinued in 2007 after a pivotal Phase IIb obesity trial failed its primary efficacy endpoint.
Mechanism of Action
Proposed to represent a "lipolytic domain" of full-length hGH: in animal studies the related AOD9604 analogue stimulated adipose lipolysis and fat oxidation and reduced lipogenesis without the diabetogenic or growth-promoting effects of intact hGH. Effects reported as GH-receptor-independent or only weakly GH-receptor-dependent. Chronic dosing upregulated adipose β3-adrenergic receptor RNA toward lean-animal levels, but chronic lipolytic/weight effects were abolished in β3-AR knockout mice while acute energy-expenditure increases persisted—the receptor mechanism remains unresolved and only partially β3-AR-linked. No human receptor-binding or definitive molecular target has been established in the sourced literature.
Research Summary
No human data were found for the native peptide (CAS 66004-57-7, Phe176) itself. All identified human clinical work was conducted on AOD9604, a distinct N-terminal Tyr-substituted analogue: six sponsor-run, randomized, double-blind, placebo-controlled trials (Phase I–IIb, 2001–2006, ~900 total subjects, including a ~502-subject 24-week Phase IIb obesity trial) assessed safety and later weight-loss efficacy. Reported: good tolerability, no serious adverse events, no IGF-1 elevation—but the pivotal Phase IIb trial did not meet its primary weight-loss endpoint versus placebo and Metabolic Pharmaceuticals discontinued development in 2007. In obese Zucker rats, oral AOD9604 (500 µg/kg/day × 19 days) reduced body-weight gain by >50% and increased adipose lipolytic activity without impairing insulin sensitivity. In obese and lean mice, both hGH and AOD9604 reduced weight gain and increased fat oxidation and plasma glycerol; unlike hGH, AOD9604 caused no hyperglycemia and did not compete for the hGH receptor. In β3-AR knockout mice, chronic lipolytic/weight effects were lost while acute energy-expenditure increases persisted. Intra-articular AOD9604 combined with hyaluronic acid outperformed either agent alone in a rabbit collagenase-induced knee osteoarthritis model.
Verified testing for HGH Fragment 176-191
Aggregated from 1 lab-verified Certificate of Analysis uploaded directly by labs. Purity averages exclude values outside [50%, 100%] to filter unit-misreads.
1 prescriber in our directory work with HGH Fragment 176-191, each confirmed from their own website. Peptides like HGH Fragment 176-191 require a prescription from a licensed provider.
Metabolic studies of a synthetic lipolytic domain (AOD9604) of human growth hormone. 2000. PMID 11146367.
Increase of fat oxidation and weight loss in obese mice caused by chronic treatment with human growth hormone or a modified C-terminal fragment. 2001. PMID 11673763.
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. 2001. PMID 11713213.
Safety and Tolerability of the Hexadecapeptide AOD9604 in Humans. 2013.
Frequently asked questions
Has HGH Fragment 176-191 been independently lab-tested?
Disclosed Labs has collected 1 Certificate of Analysis (COA) for HGH Fragment 176-191 from 1 independent testing lab. 1 vendor has submitted material for testing. Products average 99.2% tested purity across the corpus. Full testing data is available at https://www.disclosedlabs.com/peptides/hgh-fragment-176-191/testing.
Which prescribers offer HGH Fragment 176-191 with a prescription?
1 prescriber in the Disclosed Labs directory work with HGH Fragment 176-191, each confirmed from their own website. HGH Fragment 176-191 requires a prescription from a licensed provider. Browse them at https://www.disclosedlabs.com/prescribers?peptide=HGH%20Fragment%20176-191.
How does HGH Fragment 176-191 work?
Proposed to represent a "lipolytic domain" of full-length hGH: in animal studies the related AOD9604 analogue stimulated adipose lipolysis and fat oxidation and reduced lipogenesis without the diabetogenic or growth-promoting effects of intact hGH. Effects reported as GH-receptor-independent or only weakly GH-receptor-dependent. Chronic dosing upregulated adipose β3-adrenergic receptor RNA toward lean-animal levels, but chronic lipolytic/weight effects were abolished in β3-AR knockout mice while acute energy-expenditure increases persisted—the receptor mechanism remains unresolved and only partially β3-AR-linked. No human receptor-binding or definitive molecular target has been established in the sourced literature.
What does the research say about HGH Fragment 176-191?
No human data were found for the native peptide (CAS 66004-57-7, Phe176) itself. All identified human clinical work was conducted on AOD9604, a distinct N-terminal Tyr-substituted analogue: six sponsor-run, randomized, double-blind, placebo-controlled trials (Phase I–IIb, 2001–2006, ~900 total subjects, including a ~502-subject 24-week Phase IIb obesity trial) assessed safety and later weight-loss efficacy. Reported: good tolerability, no serious adverse events, no IGF-1 elevation—but the pivotal Phase IIb trial did not meet its primary weight-loss endpoint versus placebo and Metabolic Pharmaceuticals discontinued development in 2007. In obese Zucker rats, oral AOD9604 (500 µg/kg/day × 19 days) reduced body-weight gain by >50% and increased adipose lipolytic activity without impairing insulin sensitivity. In obese and lean mice, both hGH and AOD9604 reduced weight gain and increased fat oxidation and plasma glycerol; unlike hGH, AOD9604 caused no hyperglycemia and did not compete for the hGH receptor. In β3-AR knockout mice, chronic lipolytic/weight effects were lost while acute energy-expenditure increases persisted. Intra-articular AOD9604 combined with hyaluronic acid outperformed either agent alone in a rabbit collagenase-induced knee osteoarthritis model.
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