HGH Fragment 176-191 Research

HGH Fragment 176-191 is the C-terminal sixteen-residue fragment of human growth hormone, sold as a research chemical. No published study has given this molecule to a person. This page is short because that is the honest state of the evidence.

Research-grade HGH Fragment 176-191 is supplied for laboratory research use only.

Identity, and the molecule the research was actually done on

HGH Fragment 176-191 is PubChem CID 16131230, CAS 66004-57-7, molecular weight 1799.1, sequence Phe-Leu-Arg-Ile-Val-Gln-Cys-Arg-Ser-Val-Glu-Gly-Ser-Cys-Gly-Phe ^[1]. It is cyclized by a disulfide bridge between Cys7 and Cys14, which are Cys182 and Cys189 of the full-length hormone ^[1]. AOD-9604 is a separate record, CID 71300630, CAS 221231-10-3, molecular weight 1815.1, one oxygen atom heavier ^[1]. It is Tyr-hGH(177-191), carrying a synthetic N-terminal tyrosine in place of the native Phe176 ^[2].

Essentially all published lipolysis work used AOD-9604, or AOD-9401, a third peptide from the same research program, rather than unmodified 176-191 ^[1][2]. The World Anti-Doping Agency lists AOD-9604 and hGH 176-191 as separately named growth hormone fragments ^[3]. A 2026 review nonetheless writes the compound as "AOD9604 (hGH 176-191)", so the merge has reached the peer-reviewed literature ^[2].

Findings produced with AOD-9604 or AOD-9401 are not findings about 176-191.

What the laboratory and animal work found

Every study below used AOD-9401 or AOD-9604, and all are animal or in vitro.

The earliest primary paper in this program reported a null on the mechanism the product is named for. In rats, synthetic hGH 177-191, the peptide later designated AOD-9401, showed antilipogenic activity but no significant lipolytic effect ^[4][5]. The authors concluded growth hormone's main lipid effect is on lipogenesis, not lipolysis, and that paper came from the same laboratory as the later positive work ^[4].

In obese Zucker rats, AOD-9401 and AOD-9604 each reduced body-weight gain, with increased lipolytic activity in isolated adipose tissue ^[5]. In genetically obese ob/ob mice, thirty days of oral AOD-9401 lowered body-weight gain without any change in food consumption ^[6]. That mouse study also reported comparable effects on isolated adipose tissue from obese humans, which is tissue in a dish rather than a person ^[6]. That result is very likely the origin of the circulating claim that this fragment works in humans. The inference is this page's reading, not a conclusion of the paper.

In obese ob/ob mice, with lean controls, AOD-9604 reduced body-weight gain over fourteen days, with increased fat oxidation and raised plasma glycerol ^[7]. In beta-3 adrenergic receptor knockout mice the chronic weight effect disappeared, while acute energy-expenditure effects persisted ^[8]. Beta-3 adrenoceptor-mediated lipolysis is strongest in rodent adipocytes, while human fat cells respond poorly, partly because they carry less receptor messenger RNA ^[9]. That species difference is one general reason why rodent lipolysis results translate poorly to people. The compound's most recent primary animal study concerns cartilage in a rabbit model of osteoarthritis, and not fat at all ^[10].

In cells transfected with the human growth hormone receptor, AOD-9604 neither competed for that receptor nor induced proliferation ^[7]. For unmodified 176-191, no receptor or molecular target has been reported. That is an absence in the record rather than a proven absence in biology, and it leaves no mechanism by which these rodent findings could extend to people.

Human evidence

ClinicalTrials.gov lists no interventional trials of HGH Fragment 176-191, and none of AOD-9604, queried 27 August 2026 ^[11]. The Australian and European registers were not searched, and the 2002 development predates mandatory trial registration ^[11].

Human development did happen in this program, but it happened for AOD-9604 rather than for this fragment. A 2004 drug-pipeline profile records that phase IIa trials of AOD-9604 in obesity were underway by February 2002 ^[12]. No efficacy or safety result from that program is retrievable from the indexed peer-reviewed literature ^[11][12]. Whether those trials succeeded or failed cannot be stated here.

Both AOD-9604 and hGH 176-191 are prohibited at all times under Section S2 of the 2026 WADA Prohibited List, and AOD-9604 has been identified in seized preparations ^[3][13]. That is a sport-regulation record and an enforcement history, not a medicines-agency finding about safety.

A US regulatory record also exists, and again it is for AOD-9604 rather than for this fragment. AOD-9604 was nominated as a bulk drug substance for use in pharmacy compounding, and that nomination was later withdrawn ^[14]. FDA states it has identified serious adverse events that may be associated with AOD-9604, though causality is not clear ^[14].

Why an approved drug in the same catalog group is not evidence here

Tesamorelin is the only compound discussed in this catalog group that holds a marketing authorization anywhere. FDA approved it on 10 November 2010 under application 022505, for reduction of excess abdominal fat in adults with HIV-associated lipodystrophy ^[15]. The approval remains in force, with supplements approved as recently as 25 March 2025 ^[15].

Tesamorelin never obtained a European marketing authorization, because the applicant, Ferrer Internacional, withdrew the application while it was under CHMP review in 2012 ^[16]. It was not refused, and no refusal decision was ever issued ^[16]. At the time of the withdrawal the CHMP held the provisional opinion that the benefits did not outweigh the risks ^[16].

The approval belongs to the molecule tesamorelin and to one indication. It is not a family credential and must never be written as one. There is also no mechanistic bridge here. Tesamorelin acts at the GHRH receptor to raise endogenous growth hormone and, downstream of it, IGF-1 ^[15]. For this fragment itself, no GH-releasing action and no molecular target of any kind have been reported.

A second approval claim circulates within this group of compounds. GHRP-2, under the name pralmorelin, is reported to hold a Japanese approval as a diagnostic agent for pituitary function testing ^[17]. The 2004 development profile behind that report records only that the agent was awaiting Japanese approval ^[17]. Routine Japanese use of the GHRP-2 diagnostic test is documented in the clinical literature through at least 2023 ^[17]. The approval itself remains unverified against any primary regulatory database, and a diagnostic provocative-test approval is not comparable to tesamorelin's ^[17].

The honest contrast is not that tesamorelin works and the others might too. It is that tesamorelin is the only one of these compounds that has been through the process that would let anyone know.

What has not been studied

The IGF-1 and cancer epidemiology that accompanies this compound family is deliberately not carried onto this page. That literature rests on endogenous IGF-1 concentrations measured over many years in large prospective cohort studies. This fragment has never been shown to raise IGF-1 in a person.

There is no human pharmacokinetic data for this fragment, so any half-life, duration or active window quoted for it is extrapolated or invented. No chronic safety study of 176-191 itself exists in any species, and no controlled human result exists, published or registered.

HGH Fragment 176-191 is supplied for laboratory research use only. It is not for human consumption.

Frequently Asked Questions

Has HGH Fragment 176-191 been given to humans in a study?

No published study administers this molecule to a person, and ClinicalTrials.gov lists no interventional trials of it ^[11]. The Australian and European registers were not searched, and the 2002 development predates mandatory trial registration ^[11]. Human development did occur for AOD-9604, a different molecule, which reached phase IIa with no published result ^[11][12].

Is HGH Fragment 176-191 the same thing as AOD-9604?

No. AOD-9604 is Tyr-hGH(177-191), carrying a synthetic N-terminal tyrosine in place of the native Phe176 ^[2]. They are separate PubChem compound records whose molecular formulas differ by exactly one oxygen atom ^[1].

What does the animal evidence actually show?

It shows effects of AOD-9401 and AOD-9604 in obese rodents and in isolated human adipose tissue, which is a dish not a person ^[5][6][7]. The earliest paper in this program, on the peptide later designated AOD-9401, found no significant lipolytic effect ^[4][5].

References

1. 1

   PubChem CID 16131230 (CAS 66004-57-7, "Somatotropin (176-191)", C78H123N23O22S2) and PubChem CID 71300630 (CAS 221231-10-3, "AOD-9604", C78H123N23O23S2). NIH/NLM compound records, queried 27 August 2026. Sequence and Cys182-Cys189 disulfide verified against UniProt P01241.
2. 2

   Cox HD, Smeal SJ, Hughes CM, Cox JE, Eichner D. Detection and in vitro metabolism of AOD9604. Drug Testing and Analysis. 2015. PMID 25208511. DOI: 10.1002/dta.1715. Corroborating review for the persistence of the naming conflation: Dominikowski A, et al. Frontiers in Endocrinology. 2026. PMID 42395176. DOI: 10.3389/fendo.2026.1822475.
3. 3

   World Anti-Doping Agency. The 2026 Prohibited List, Section S2, Peptide Hormones, Growth Factors, Related Substances, and Mimetics. In force 1 January 2026.
4. 4

   Wu Z, Ng FM. Antilipogenic action of synthetic C-terminal sequence 177-191 of human growth hormone. Biochemical and Molecular Biology International. 1993. PMID 8358331. No DOI assigned. Compound studied: hGH 177-191, later designated AOD-9401.
5. 5

   Ng FM, et al. Journal of Molecular Endocrinology. 2000. PMID 11116208. DOI: 10.1677/jme.0.0250287. Compound studied: AOD9401, defined in that paper as the hGH lipolytic domain containing residues 177-191. Companion paper, on AOD9604 rather than AOD9401: Hormone Research. 2000. PMID 11146367. DOI: 10.1159/000053183.
6. 6

   Heffernan MA, et al. American Journal of Physiology, Endocrinology and Metabolism. 2000. PMID 10950816. DOI: 10.1152/ajpendo.2000.279.3.E501. Compound studied: AOD-9401.
7. 7

   Heffernan MA, et al. International Journal of Obesity and Related Metabolic Disorders. 2001. PMID 11673763. DOI: 10.1038/sj.ijo.0801740. Compound studied: AOD9604.
8. 8

   Heffernan M, et al. Endocrinology. 2001. PMID 11713213. DOI: 10.1210/endo.142.12.8522. Compound studied: AOD9604.
9. 9

   Langin D, Tavernier G, Lafontan M. Regulation of beta 3-adrenoceptor expression in white fat cells. Fundamental and Clinical Pharmacology. 1995. PMID 7628838. DOI: 10.1111/j.1472-8206.1995.tb00268.x. Review, resolved on PubMed 27 August 2026; states that rodent adipocytes respond most strongly to beta-3 agonists while human fat cells are poorly responsive.
10. 10

    Kwon DR, Park GY. Annals of Clinical and Laboratory Science. 2015. PMID 26275694. No DOI assigned.
11. 11

    ClinicalTrials.gov API v2 and PubMed E-utilities queries, run 27 August 2026. Zero studies returned for "AOD9604", "AOD-9604" and "hGH fragment 176-191" under both intervention and general-term searches. PubMed returns 23 records for AOD-9604, none a clinical trial reporting human outcomes. ANZCTR, EudraCT and the WHO ICTRP were not searched, and trial registration became a condition of publication only from 2005.
12. 12

    Wilding J. AOD-9604 Metabolic Pharmaceuticals. Current Opinion in Investigational Drugs. 2004. PMID 15134286. No DOI in the PubMed record.
13. 13

    Thomas A, et al. Journal of Separation Science. 2016. PMID 26578461. DOI: 10.1002/jssc.201501060. Seizure case report: PMID 24976118. DOI: 10.1002/dta.1687.
14. 14

    US Food and Drug Administration, Human Drug Compounding programme. "Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks", nominated-but-withdrawn table, entry AOD-9604. Page content current 22 April 2026. The entry names AOD-9604 only, and not hGH fragment 176-191.
15. 15

    US Food and Drug Administration. Application 022505, approval letter 10 November 2010; supplement S-020 approved 25 March 2025; Structured Product Labeling effective 29 July 2026, sections 1 and 12.1.
16. 16

    European Medicines Agency. Egrifta (tesamorelin), EMEA/H/C/002427, application withdrawn. Ferrer Internacional, S.A. notified the CHMP on 21 June 2012 and EMA announced the withdrawal on 26 June 2012 (EMA/431454/2012; EMA/CHMP/475021/2012). The CHMP position recorded at withdrawal was provisional.
17. 17

    Adis development profile, pralmorelin. Drugs in R&D. 2004. PMID 15230633. DOI: 10.2165/00126839-200405040-00011. Validation study: Chihara K, et al. European Journal of Endocrinology. 2007. PMID 17609397. DOI: 10.1530/EJE-07-0066. Contemporary use of the GHRP-2 test: Teramoto S, et al. Growth Hormone and IGF Research. 2023. PMID 37295337. DOI: 10.1016/j.ghir.2023.101545.