HGH Fragment 176-191.
HGH Fragment 176-191 is a synthetic peptide corresponding to the final 16 amino acids (residues 176 to 191) of the C-terminal region of human growth hormone.
HGH Fragment 176-191 is a synthetic peptide corresponding to the final 16 amino acids (residues 176 to 191) of the C-terminal region of human growth hormone. HGH Fragment 176-191 is research / preclinical, and PepCue grades its published evidence F tier (30/100). Also known as hGH frag 176-191 · GH lipolytic fragment. This is a research reference, not medical or dosing advice.
What it is
HGH Fragment 176-191 is a synthetic peptide corresponding to the final 16 amino acids (residues 176 to 191) of the C-terminal region of human growth hormone. It derives from the observation that this domain appears to carry GH's fat-metabolizing (lipolytic) activity while lacking the growth-promoting and insulin-antagonizing actions of the whole hormone. It is closely related to, but distinct from, AOD-9604, a modified analog in which a tyrosine residue is added to the N-terminus (developed under the name Anti-Obesity Drug 9604). The plain 176-191 fragment itself is a research-only compound with almost no dedicated clinical data.
How it works
The proposed mechanism is stimulation of lipolysis, the breakdown of stored triglycerides, along with reduced fat synthesis in adipose tissue, reproducing the fat-reducing effect of GH's C-terminus without activating the GH receptor to raise IGF-1 or impair glucose handling. Work on the analog AOD-9604 implicated the beta-3-adrenergic pathway in this effect. The mechanism is characterized mainly in mouse and in vitro models, and how faithfully the unmodified 176-191 fragment reproduces it in humans is not established.
Mechanism pathways
Acting directly on fat tissue to increase fat breakdown or reduce its blood supply.
This pathway groups compounds that act on adipose tissue itself rather than on appetite. Lipolysis is the enzymatic breakdown of stored triglycerides into free fatty acids and glycerol, executed by adipose triglyceride lipase and hormone-sensitive lipase inside the fat cell. It is normally triggered by catecholamines acting on beta-adrenergic receptors, which raise cyclic AMP and activate protein kinase A. Growth hormone also stimulates lipolysis, but it does so as part of a package that includes growth promotion and a rise in insulin resistance. Several compounds here derive from the observation that growth hormone's fat-mobilising activity appears to reside in the carboxy-terminal region of the molecule, separate from the domain that binds and activates the growth hormone receptor. Isolating that region was intended to produce fat breakdown without raising IGF-1 or impairing glucose handling. Mechanistic work in rodents linked the effect to beta-3 adrenergic receptor activity rather than to growth hormone receptor signalling. One member of this group is the plain fragment; another is a modified analog with an added amino-terminal residue and considerably more development history behind it. A second, entirely different approach targets the blood supply instead of the fat cell. A homing sequence binds prohibitin, a protein unusually abundant on the endothelial cells lining blood vessels within white adipose tissue, and delivers a pro-apoptotic sequence that kills those cells once internalised. The intent is to shrink fat depots by starving them of perfusion. This is a vascular-targeting strategy borrowed from oncology and is conceptually unrelated to lipolysis. A third approach targets an enzyme, nicotinamide N-methyltransferase, which is highly expressed in adipose tissue and consumes both nicotinamide and methyl groups from S-adenosylmethionine. Inhibiting it is proposed to spare nicotinamide for NAD+ regeneration and to shift adipocytes toward energy expenditure rather than storage. Clinical relevance across this group is weak. The growth hormone fragment analog was carried into human obesity trials and did not produce clinically meaningful weight loss beyond placebo, and it was not approved as a medicine. The plain fragment has essentially no human evidence of its own and borrows its reputation from that analog. The vascular-targeting compound raised kidney toxicity concerns in primate work and did not progress. The enzyme inhibitor's downstream logic is plausible but largely inferred from animal and cell studies. None of these are approved for any use.
The evidence
Almost all supportive data come from the modified analog AOD-9604 rather than from 176-191 itself. Heffernan et al., in Endocrinology (2001, PMID 11713213), showed that AOD9604 reduced body weight and increased lipolysis in obese mice and that the effect disappeared in beta-3-adrenergic-receptor knockout mice, implicating that pathway. That was a rodent study using genetically obese and knockout strains, with short treatment periods and body-weight and tissue endpoints rather than clinical outcomes. Its central finding, dependence on a receptor whose contribution to human fat metabolism is far smaller than in rodents, is itself a reason to doubt direct translation. AOD-9604 was later carried into human obesity trials but did not produce clinically meaningful weight loss beyond placebo and was not approved as a drug. The program, run by an Australian sponsor, was discontinued after the larger placebo-controlled trial failed to separate from placebo on weight, which is the endpoint that matters for an anti-obesity indication. The compound was subsequently repositioned toward non-pharmaceutical uses, and a separate strand of published work examined intra-articular AOD9604 in a rabbit osteoarthritis model rather than obesity, which says nothing about systemic fat loss. For the unmodified 176-191 fragment specifically there is essentially no controlled human evidence, and its reputation is extrapolated from AOD-9604 data. The tyrosine added to the N-terminus of AOD-9604 was a deliberate stability modification, so the two molecules are not interchangeable, and no published head-to-head comparison establishes that the plain fragment behaves like the analog in people. The contrast with full-length somatropin is instructive: recombinant GH has approved indications, product labeling, decades of registry data, and a well-mapped metabolic profile, while the fragment has none of that. There are no human pharmacokinetic data for 176-191, no bioavailability data, no dose-ranging work, no imaging-based body-composition endpoints, and no long-term study of any kind.
The evidence, in brief
The C-terminal 16-residue fragment of human growth hormone, isolated for its lipolytic activity. Nearly all supporting data come from the modified analogue AOD-9604, which reduced weight in obese mice through a beta-3-adrenergic pathway but did not produce clinically meaningful weight loss beyond placebo in human obesity trials and was never approved. For the plain 176-191 fragment there is essentially no controlled human evidence; its reputation is borrowed from a program that failed.
- Effects of GH and its lipolytic fragment AOD9604 on lipid metabolism (beta-3-AR knockout mice)Endocrinology, 2001 (PMID 11713213)
- PubMed search: growth hormone fragment 176-191 lipolysisPubMed / NCBI
Evidence maturity
An evidence-only reading: approval status, human vs preclinical data, mechanism and safety. Popularity never raises it. Research file #029
Mostly preclinical or mechanistic; little human data.
Findings come mainly from animal models, not people.
Claim receipts
Popular claims about HGH Fragment 176-191, checked against the state of the evidence. The verdict describes evidence maturity, never an invented study result.
The lipolytic role of this domain is characterized mainly in mouse and in-vitro models.
The closely related analog AOD-9604 failed to separate from placebo on weight in obesity trials.
AOD-9604 carries an added N-terminal tyrosine, and no head-to-head work shows the plain fragment behaves the same.
No study has measured IGF-1 or glucose handling during sustained human exposure to the fragment.
Safety profile
In its trials the analog AOD-9604 was generally well tolerated over short periods, with headache and mild edema among the reported effects, but the plain 176-191 fragment has no comparable human safety record of its own. Long-term safety is unknown. The theoretical selling point of the fragment, that it separates GH's lipolytic action from the growth-promoting and insulin-antagonizing actions of the whole hormone, has never been confirmed in a controlled human study, so the assumption that it avoids GH's metabolic liabilities remains an assumption rather than a finding. Full-length growth hormone reliably raises IGF-1 and can worsen glucose tolerance and cause fluid retention, carpal tunnel symptoms, and arthralgia. Whether a C-terminal fragment is genuinely free of those effects at meaningful exposure is untested, and no study has measured IGF-1 or glucose handling during sustained exposure to the fragment. Because the peptide is administered by injection, the usual injection risks apply: local reactions, infection from non-sterile technique or non-sterile product, and immune response to a foreign fragment. Nothing published characterizes immunogenicity for this sequence. Injectable material sold online as Fragment 176-191 is unregulated research-grade product of uncertain identity and purity, frequently supplied without a certificate of analysis or with one that cannot be traced to the vial in hand, and independent testing of this market has found mislabeled and contaminated product. A proper trial would require fasting glucose and insulin, IGF-1, and lipid monitoring, together with sterility and endotoxin testing of the material, none of which happens outside a regulated setting. The safety of the fragment itself remains largely uncharacterized.
Compound notes
- HGH Fragment 176-191 is the C-terminal fragment of human growth hormone from which AOD-9604 is derived.
- It is studied for fat metabolism/lipolysis while aiming to avoid GH's growth and IGF-1 effects.
- Human evidence for meaningful fat-loss benefit is weak.
- Not FDA-approved; research-only.
- Long-term human safety and real-world efficacy are not established.
Regulatory status
HGH Fragment 176-191 is not an approved drug and is sold as research-use-only. The related AOD-9604 was investigated for obesity, failed to reach approval as a pharmaceutical, and was subsequently pursued as a food and cosmetic ingredient in some markets; neither has FDA approval as a weight-loss medicine. GH fragments of this type are prohibited in sport by WADA.
Sold research-use-only; human evidence is limited or preclinical.
By the numbers
- 01The C-terminal 16-residue (176-191) fragment of human growth hormone
- 02Isolated for GH's lipolytic activity, minus growth and insulin effects
- 03Distinct from AOD-9604, a modified analog with an added N-terminal tyrosine
- 04Human data comes almost entirely from AOD-9604, not the plain fragment
- 05AOD-9604 obesity trials showed minimal weight loss vs placebo; not approved
- 06Research-use-only; unregulated online supply; WADA-prohibited
HGH Fragment 176-191: research formats
Choose the format you are researching to see route-specific notes.
Same reconstitution profile as AOD-9604: acetic acid first, then BAC water to volume.
HGH Fragment 176-191 is the C-terminal 16-residue fragment of human growth hormone and is closely related to AOD-9604, the modified analog carrying an extra N-terminal tyrosine. Like other aggregation-prone GH fragments it is typically reconstituted with 0.6% acetic acid first, then diluted with BAC water. A 5 mg vial brought to 2.0 mL gives 2,500 mcg/mL.
Almost all of the supporting data belong to the analog AOD-9604, not to the plain 176-191 fragment. AOD-9604 reached human obesity trials and did not produce clinically meaningful weight loss beyond placebo, and the unmodified fragment has essentially no controlled human evidence of its own.
The two are not interchangeable: an added N-terminal tyrosine is a real structural difference, so data from one does not transfer cleanly to the other.
Sources
Every factual claim above resolves to a real, published source.
- Effects of GH and its lipolytic fragment AOD9604 on lipid metabolism (beta-3-AR knockout mice)Endocrinology, 2001 (PMID 11713213)
- PubMed search: growth hormone fragment 176-191 lipolysisPubMed / NCBI
- Safety and Efficacy of Approved and Unapproved Peptide Therapies for Musculoskeletal Injuries and Athletic PerformanceSports Med, 2026 (PMID 41966639)
- PubMed search: AOD9604 growth hormone fragment obesityPubMed / NCBI
- ClinicalTrials.gov search: AOD9604ClinicalTrials.gov registry
Cite this page
PepCue. “HGH Fragment 176-191: the evidence.” PepCue, reviewed June 1, 2026. https://www.pepcue.app/p/hgh-fragment-176-191.
Log your doses, run the vial math, and keep a provider-ready record in PepCue.