Educational information only. Nothing on this site is medical advice, and no dose mentioned here is a recommendation. Speak to a prescriber who knows your history.

HGH fragment 176-191

hGH 176-191, growth hormone fragment 176-191, HGH frag, lipolytic fragment of human growth hormone

HGH fragment 176-191 is the tail end of the human growth hormone molecule, sold widely as a fat-loss injectable. It has never been tested in a registered human clinical trial for any indication. Everything claimed about it in humans is extrapolated from rodent experiments conducted mainly in the 1990s, and from an identically sequenced analogue that failed when it was finally tested properly.

Preclinical only Metabolic & incretin Reviewed 2026-09-04

Mechanism

HGH fragment 176-191 comprises the last sixteen amino acids of mature human growth hormone, containing a disulfide-linked loop between cysteines 182 and 189. The hypothesis behind it, developed by Ng, Bornstein and colleagues from the late 1970s, was that growth hormone is functionally modular: its anabolic and growth-promoting actions run through the growth hormone receptor and IGF-1, while a separate lipolytic and antilipogenic activity resides in this C-terminal domain and can be isolated from it. If correct, the fragment would mobilise fat without raising IGF-1, without inducing insulin resistance, and without the tissue overgrowth that constrains growth hormone use.

In isolated rodent adipocytes and in whole animals, synthetic C-terminal fragments increased lipolysis, suppressed lipogenesis and altered glucose handling. The proposed mechanism was upregulation of beta-3 adrenergic receptor expression in adipose tissue, leading to increased fat oxidation. That explanation has a serious problem: work from the same research programme found that the compound retained activity in beta-3 adrenergic receptor knockout mice, meaning beta-3 signalling is not required and cannot be the mechanism. No specific receptor for this fragment has ever been identified, and no receptor-binding or structural study has established how it would act in human tissue. The mechanism, as stated on essentially every website selling it, is an unvalidated hypothesis whose named pathway has already been contradicted in the primary literature.

What the research shows

The evidence base consists almost entirely of rodent and in vitro work from the 1970s to the early 2000s, produced principally by one research group. Those studies reported antilipogenic effects of the synthetic 177-191 sequence, effects on glucose transport in rat adipocytes, and, in obese mice, increased fat oxidation and weight loss with chronic treatment. Taken on their own terms these are legitimate preclinical findings. They are also twenty-five to fifty years old, were largely conducted by parties with a commercial interest in the outcome, and have not been independently replicated at scale.

The human record is empty. A search of ClinicalTrials.gov returns no registered interventional trial administering hGH fragment 176-191 to human participants for any indication. There is no published randomised controlled trial, no published pharmacokinetic study, no dose-ranging study and no controlled study of body composition in people. This is not a case of weak or conflicting human evidence; it is a case of no human evidence.

The most informative thing available is what happened to AOD-9604. That compound has the identical 16-residue sequence, since hGH residue 176 is a tyrosine and 'Tyr plus hGH(177-191)' simply reconstitutes hGH(176-191), and it came out of the same programme. It was taken into human obesity trials. A small 12-week study produced an encouraging result. The larger 24-week phase 2b trial designed to confirm it failed to show significant weight loss, and the sponsor abandoned obesity development in 2007. That is the nearest thing to a human test this chemistry has ever received, and it was negative. Any confident claim that hGH fragment 176-191 causes fat loss in people is therefore not merely unsupported; it runs against the one relevant human result that exists.

Evidence assessment

Preclinical only

No registered or published interventional human trial of hGH fragment 176-191 exists for any indication, and all five surviving citations are rodent or in vitro studies verified as such against PubMed. The closest human test, of the sequence-identical AOD-9604, was negative.

Tiers are applied consistently across the library and re-checked when new trials read out. Read the grading method.

Key studies

Hyperglycemic action of synthetic C-terminal fragments of human growth hormone Preclinical only

Ng FM, Bornstein J · American Journal of Physiology · 1978

Preclinical; synthetic C-terminal fragments in animal models

Reported that synthetic C-terminal fragments of human growth hormone possess metabolic activity distinct from the intact hormone, the foundational observation for this compound class.

Antilipogenic action of synthetic C-terminal sequence 177-191 of human growth hormone Preclinical only

Wu Z, Ng FM · Biochemical and Molecular Biology International · 1993

Preclinical; in vitro and rodent adipose tissue

The synthetic 177-191 sequence suppressed lipogenesis in adipose tissue preparations.

Effect of an antilipogenic fragment of human growth hormone on glucose transport in rat adipocytes Preclinical only

Wijaya E, Ng FM · Biochemical and Molecular Biology International · 1993

Preclinical; isolated rat adipocytes

The growth hormone fragment altered glucose transport in isolated rat adipocytes.

Increase of fat oxidation and weight loss in obese mice caused by chronic treatment with human growth hormone or a modified C-terminal fragment Preclinical only

Heffernan MA, Thorburn AW, Fam B, Summers R, Conway-Campbell B, Waters MJ, Ng FM · International Journal of Obesity and Related Metabolic Disorders · 2001

Preclinical; chronic dosing in obese mice

Chronic treatment with the modified C-terminal fragment increased fat oxidation and reduced body weight in obese mice.

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 only

Heffernan M, Summers RJ, Thorburn A, Ogru E, Gianello R, Jiang WJ, Ng FM · Endocrinology · 2001

Preclinical; obese mice and beta-3 adrenergic receptor knockout mice

Activity was retained in beta-3 adrenergic receptor knockout mice, demonstrating that beta-3 adrenergic signalling is not required for the fragment's metabolic effects.

Safety

Nothing meaningful is known about the safety of hGH fragment 176-191 in humans, because it has never been studied in humans in a registered trial. Absence of reported harm is not evidence of safety; it reflects absence of investigation. The theoretical argument that it should be safer than growth hormone, because it does not raise IGF-1 and does not act via the growth hormone receptor, is plausible but untested for this specific product. Safety data from AOD-9604 are sometimes cited in its place. Because the two are sequence-identical that substitution is more defensible than it first appears, but it remains weak: the AOD-9604 safety data come largely from short trials using oral administration, published outside the indexed peer-reviewed literature, and say nothing about injected grey-market material. The dominant practical risk is product quality. Material sold under this name is unregulated synthesis, and analytical surveys of illicit peptide products have found incorrect identity, wrong quantity, bacterial contamination and endotoxin. Injecting an unsterile, uncharacterised peptide carries infection and immunogenicity risks entirely independent of the pharmacology. Athletes face an additional certainty: the compound is explicitly named on the WADA Prohibited List, and a positive test carries a default four-year sanction.

Regulatory status

Status summary. Regulation changes-verify against the current regulator position before relying on this.
JurisdictionStatus
United KingdomNot licensed by the MHRA for any indication. Not an authorised medicine and not an authorised food ingredient. Supplying it for human use would fall outside the Human Medicines Regulations 2012. It is sold in the UK almost exclusively through unregulated online channels.
United StatesNot approved as a drug for any indication and never submitted for approval. It has no GRAS status and no legitimate route to market as a dietary supplement. FDA has warned about unapproved peptides marketed for fat loss, and material sold to consumers is an unapproved new drug. The 'for research use only' labelling used by sellers has no regulatory meaning for a product being supplied to the public for injection.
WADA (sport)Prohibited at all times. hGH 176-191 is explicitly named in section S2.2.3 of the WADA Prohibited List under growth hormone fragments, as a non-specified substance carrying a default four-year sanction.

Questions

No. A search of ClinicalTrials.gov returns no registered interventional trial administering this peptide to humans for any indication, and there is no published randomised trial, pharmacokinetic study or body composition study in people. Every human claim made for it is extrapolation from rodent experiments, most of them conducted between the late 1970s and 2001.

In sequence, yes. Both are YLRIVQCRSVEGSCGF with a Cys182-Cys189 disulfide bond. AOD-9604 is described as a tyrosine added to hGH 177-191, and because residue 176 of growth hormone is itself a tyrosine, that reconstitutes hGH(176-191) exactly. They are the same 16-residue peptide with two names. The practical point is that AOD-9604 is the version that was actually tested in humans, and it failed its pivotal obesity trial.

That is the hypothesis the compound was built on, and it has some support in rodent data. It has never been tested in a human trial under this name. The sequence-identical AOD-9604 did appear not to raise IGF-1 in humans, but it also did not produce significant weight loss when properly tested. Selective fat loss without growth hormone's drawbacks remains an untested claim for this peptide.

Because the regulatory gap allows it. Sellers label it 'for research use only' or 'not for human consumption', which lets them supply an unapproved injectable to consumers while disclaiming that it is a drug. That phrase carries no assurance about purity, identity or sterility, and no research is implied by it. Marketing leans on genuine-sounding rodent citations from the 1990s while omitting that the human test of this chemistry was negative.