HGH Fragment 176-191

Dosing from the Literature

Published for fat loss: rodent data, and oral trial doses for its cousin AOD-9604. Not published: any human dose of the fragment itself.

No FDA-approved dose exists for HGH Fragment 176-191 or AOD-9604. No trial has given the fragment to people: the community rows are what online protocols describe, and the trial doses are AOD-9604’s, taken by mouth.

The AOD-9604 trials gave it by mouth, not by injection: in the 12-week trial, 1 mg a day came with 2.6 kg of weight loss against 0.8 kg on placebo and 10 mg a day with less, and the 24-week trial, whose top dose was 1 mg a day, found no significant weight loss (Stier et al., J Endocrinol Metab 2013; Valentino et al., Clin Pharmacol Ther 2010; PMID 20445536). Oral and injected doses are not interchangeable, so the trial doses say nothing about whether community SubQ doses of 250–500 mcg are high or low, and no controlled human trial of the parent fragment exists.

Online protocols describe taking it on an empty stomach, in the morning before food or at bedtime, and waiting 1–2 hours before eating. No study has tested timing.

What It Is

HGH Fragment 176-191 is a synthetic peptide corresponding to the carboxy-terminal region of the 22 kilodalton isoform of human growth hormone — specifically amino acid residues 176 through 191. Synthetic versions of this stretch were studied from the 1970s onward (Ng & Bornstein, Am J Physiol 1978; PMID 645904), in structure-activity work aimed at dissecting which region of the 191-amino-acid GH molecule was responsible for its lipolytic (fat-mobilizing) effect, versus the regions responsible for its growth-promoting (IGF-1-mediated) and diabetogenic (insulin-resistance-inducing) effects.

Frank Ng and colleagues at Monash University published the seminal C-terminal GH fragment research in the 1980s–1990s, demonstrating that the lipolytic activity of GH could be localized to the C-terminal domain and was structurally and functionally separable from the central helical domain responsible for GH-receptor binding. Most of that work used hGH 177-191 (one residue shorter) and the tyrosine-modified AOD-9604 rather than hGH 176-191 itself: in rodent fat tissue and obese rodents these peptides mimicked GH’s effects on fat, and chronic treatment did not cause the insulin resistance or glucose intolerance seen with full-length GH (Ng et al., J Mol Endocrinol 2000; PMID 11116208; Heffernan et al., Int J Obes 2001; PMID 11673763). The one early study of hGH 176-191 itself, in normal rats, found a short-lived rise in blood glucose and insulin (Ng & Bornstein, Am J Physiol 1978; PMID 645904).

Metabolic Pharmaceuticals (Australia) developed a commercial analog, AOD-9604 (Anti-Obesity Drug 9604), which is hGH 177-191 with an added N-terminal tyrosine (Tyr-hGH177-191): the same 16 residues as hGH 176-191 except that tyrosine replaces the native phenylalanine at position 176, a change the developer describes as stabilizing the peptide (Stier et al., J Endocrinol Metab 2013). A 2026 review notes that AOD-9604 is itself sometimes labelled “hGH 176-191” or simply “GH fragment” (Dominikowski et al., Front Endocrinol 2026; PMID 42395176). AOD-9604 entered formal clinical development for obesity in the early 2000s, progressed through Phase I and Phase II trials (six placebo-controlled trials between 2001 and 2006; Stier et al., J Endocrinol Metab 2013), and ultimately failed to meet registrational weight-loss endpoints in adequately powered Phase IIb studies. The obesity clinical development program was terminated in 2007 (Valentino et al., Clin Pharmacol Ther 2010; PMID 20445536).

The parent compound HGH Fragment 176-191 itself has never been advanced into a formal human clinical development program. Its community use and compounding-pharmacy-era protocols for fat loss were built on mechanistic inference from preclinical literature and extrapolation from AOD-9604's short-term lipolytic data — not from direct controlled human efficacy trials of the parent fragment. HGH Fragment 176-191 is not on any FDA 503A bulk-substance list.

The structural rationale for the fragment is worth unpacking. The 191-amino-acid GH molecule folds into a four-helix bundle, and residues in three separate stretches (2–19, 54–74 and 167–191) take part in binding the GH receptor (Cunningham & Wells, Science 1989; PMID 2471267), so the C-terminal stretch the lipolytic peptides come from overlaps one of the receptor-binding sites. Synthetic C-terminal peptides tested from the 1970s carried part of GH’s insulin-antagonistic activity (Ng & Bornstein, Am J Physiol 1978; PMID 645904), and the Ng laboratory later located GH’s antilipogenic activity in residues 177–191 (Wu & Ng, Biochem Mol Biol Int 1993; PMID 8358331). Made synthetically, hGH 177-191 forms a ring through a disulfide bond between its two cysteines and keeps some of the shape that stretch has in intact GH (Ogru et al., J Pept Res 2000; PMID 11152298). It does not bind the GH receptor, and its effect on fat is not mediated directly through the β3-adrenergic receptor either; no other receptor has been identified (Heffernan et al., Int J Obes 2001; PMID 11673763; Heffernan et al., Endocrinology 2001; PMID 11713213).

The practical implication: HGH Fragment 176-191 is not a growth-hormone analog in the pharmacological sense. It does not replace any function of GH for GH-deficient patients. It does not elevate IGF-1. It does not drive tissue growth, recovery, or sleep-architecture changes. Anyone expecting "GH effects without GH side effects" from the fragment is mis-framing what the fragment is — it is a selective lipolytic peptide whose utility, if any, is narrow to the fat-loss hypothesis.

Mechanism of Action

Most mechanism work used hGH 177-191 and AOD-9604 rather than the fragment itself: in rodent fat tissue they limited fat synthesis and raised markers of fat breakdown without binding the GH receptor (Ng et al., 2000; Heffernan et al., 2001).

• Lipolysis stimulation (beta-adrenergic pathway interaction) — In obese mice, 14 days of AOD-9604 injections reduced body weight and body fat and raised β3-adrenergic receptor RNA in fat; in β3-receptor knock-out mice, long-term AOD-9604 neither reduced weight nor raised lipolysis, though it still raised energy expenditure and fat oxidation acutely, and the authors conclude that its lipolytic action is not mediated directly through the β3 receptor (Heffernan et al., Endocrinology 2001; PMID 11713213).
• Lipogenesis inhibition — In isolated rat fat tissue, hGH 177-191 (AOD9401, the sequence one residue shorter than the fragment) inhibited acetyl-CoA carboxylase and stimulated hormone-sensitive lipase, as intact GH does (Ng et al., J Mol Endocrinol 2000; PMID 11116208).
• No engagement of the classical GH receptor (GHR) — The direct test was done on AOD-9604: in cells carrying the human GH receptor, it did not compete with GH for binding and, unlike GH, did not make the cells proliferate (Heffernan et al., Int J Obes 2001; PMID 11673763); in its human trials it did not change IGF-1 (Stier et al., J Endocrinol Metab 2013).
• Insulin and glucose: early and later studies differ — Full-length GH is diabetogenic — it opposes insulin action in liver and muscle, producing glucose intolerance at pharmacologic doses. Early rat studies found that the C-terminal peptides carry some of this activity: hGH 176-191 itself briefly raised blood glucose and insulin, and an insulin-antagonistic core was placed within residues 178 to 190 (Ng & Bornstein, Am J Physiol 1978; PMID 645904; Wade et al., Acta Endocrinol 1982; PMID 6751009). Later chronic studies in obese rodents found no insulin resistance or glucose intolerance with hGH 177-191 (Ng et al., J Mol Endocrinol 2000; PMID 11116208) or AOD-9604 (Ng et al., Horm Res 2000; PMID 11146367), and AOD-9604 did not raise blood glucose in obese mice (Heffernan et al., Int J Obes 2001; PMID 11673763).
• Oxidation of free fatty acids — In obese mice given AOD-9604 by mini-pump for 14 days, weight gain fell while fat oxidation and plasma glycerol, a marker of fat breakdown, rose (Heffernan et al., Int J Obes 2001; PMID 11673763).
• Cartilage regenerative effects (secondary claim) — Some preclinical work on AOD-9604 suggested chondroprotective effects in models of osteoarthritis; this is a secondary claim and has not been reproduced at scale. In 32 rabbits with collagenase-induced knee osteoarthritis, weekly injections of 0.25 mg AOD-9604 into the joint left less cartilage damage than saline, and AOD-9604 with hyaluronic acid did better than either alone (Kwon & Park, Ann Clin Lab Sci 2015; PMID 26275694).
• Appetite — In obese mice given hGH 177-191 (AOD-9401) by mouth for 30 days, food intake did not differ from saline-treated controls, though weight gain was lower from day 16 (Heffernan et al., Am J Physiol Endocrinol Metab 2000; PMID 10950816).

What the Research Shows

The evidence divides into rodent and fat-tissue work, mostly on hGH 177-191 and AOD-9604 rather than the fragment itself, and human trials of AOD-9604 taken by mouth (Stier et al., J Endocrinol Metab 2013); no human trial has tested the fragment.

• hGH 176-191 itself in rats: a rise in blood glucose (Ng & Bornstein, Am J Physiol 1978; PMID 645904) — In normal rats, synthetic hGH 176-191 and three related C-terminal peptides (172-191, 177-191 and 178-191) produced a short-lived rise in blood glucose and a more sustained rise in plasma insulin, and a single dose (5 nmol/kg) of the peptides containing residues 178-191 reduced insulin sensitivity in insulin tolerance tests. A 1982 follow-up that shortened a modified hGH 177-191 peptide placed this insulin-antagonistic activity within residues 178 to 190 (Wade et al., Acta Endocrinol 1982; PMID 6751009).
• C-terminal GH fragment: antilipogenic, not lipolytic (Wu & Ng, Biochem Mol Biol Int 1993; PMID 8358331) — The synthetic hGH 177-191 fragment matched intact human growth hormone’s antilipogenic activity in rat fat tissue and showed no significant lipolytic effect (glycerol release from rat epididymal fat pads). The authors concluded that GH acts on fat mainly by limiting fat synthesis.
• hGH 177-191 in obese mice (Natera et al., Biochem Mol Biol Int 1994; PMID 7987248) — Long-term treatment of obese (ob/ob) mice with hGH 177-191, one residue shorter than the fragment and without AOD-9604’s added tyrosine, reduced their cumulative body-weight gain and fat-tissue mass and significantly inhibited fat synthesis in their fat tissue.
• AOD-9604 preclinical characterization (Heffernan et al., Endocrinology 2001; PMID 11713213) — In obese mice, 14 days of AOD-9604 (or hGH) injections reduced body weight and body fat and raised β3-adrenergic receptor RNA in fat; in β3-receptor knock-out mice the long-term weight and lipolysis effects did not appear.
• AOD-9604 in obese rats (Ng et al., 2000) — An oral dose of 500 µg/kg daily for 19 days cut body-weight gain by more than half against controls (15.8 g against 35.6 g), raised lipolytic activity in adipose tissue and, unlike chronic intact hGH, did not impair insulin sensitivity.
• AOD-9604 12-week trial — In 300 obese adults taking it by mouth for 12 weeks, the 1 mg a day group lost an average of 2.6 kg against 0.8 kg on placebo and the 10 mg group lost less (Valentino et al., Clin Pharmacol Ther 2010; PMID 20445536); the result comes from the developer’s reports, not a journal paper (Dominikowski et al., Front Endocrinol 2026; PMID 42395176).
• AOD-9604 Phase IIb 24-week obesity trial (Metabolic Pharmaceuticals, 2006–2007) — The pivotal weight-loss study in obese adults. The 24-week study did not demonstrate a clinically meaningful separation between AOD-9604 and placebo on the primary body-weight endpoint, leading to termination of the obesity clinical-development program in 2007 (Valentino et al., Clin Pharmacol Ther 2010; PMID 20445536).
• No direct human clinical trial of the parent HGH Fragment 176-191 — The parent fragment itself (without the N-terminal tyrosine modification) has never been advanced into controlled human clinical trials. All parent-fragment claims are extrapolated from AOD-9604 data and rodent work.
• After obesity: cellulite cream and osteoarthritis (AOD-9604) — After the obesity program ended, Phosphagenics licensed AOD-9604 in 2009 for a transdermal cosmetic aimed at cellulite (Valentino et al., Clin Pharmacol Ther 2010; PMID 20445536), and the developer’s parent company, Calzada, turned to osteoarthritis; in April 2013 it said that work had been done only in preclinical studies (Calzada Ltd, ASX announcement, 26 April 2013). No human trial of AOD-9604 is registered on ClinicalTrials.gov. The osteoarthritis claim remains mechanistically interesting and clinically unproven in humans (Dominikowski et al., Front Endocrinol 2026; PMID 42395176).
• Class-level framing — lipolytic peptides without GH axis — The HGH Fragment 176-191 / AOD-9604 research program is the most serious attempt to pharmacologically separate GH's lipolytic effect from its somatogenic and diabetogenic effects. The failure to deliver a clinically meaningful weight-loss endpoint does not mean the biology is wrong — it means the effect size is smaller than weight-loss regulatory pathways require, or that the peripheral-lipolytic mechanism is insufficient without concurrent central appetite / energy-balance modulation. Modern GLP-1 class agents (semaglutide, tirzepatide) deliver weight loss through precisely the central mechanism that HGH Fragment 176-191 does not engage.

Human Data

Human data for the parent HGH Fragment 176-191 is essentially absent; human data for the AOD-9604 analog is the closest available reference.

• AOD-9604 Phase I and early Phase II — Single IV doses (25–400 µg/kg) in 15 healthy men, single IV doses in 23 obese men, and single or 7-day oral doses (9–54 mg) in obese men were well tolerated; the 54 mg oral dose brought more headache, diarrhea and flatulence. None of the trials gave it by SubQ injection (Stier et al., J Endocrinol Metab 2013).
• AOD-9604 short-term studies — The published summary of the single-dose and 7-day studies reports safety, glucose and IGF-1, not fat-breakdown markers; in the first IV study, no significant glycerol, glucose or IGF-1 trends were seen with AOD-9604 (Stier et al., J Endocrinol Metab 2013).
• AOD-9604 12-week trial — In a 12-week randomized trial in 300 obese adults, AOD-9604 was taken by mouth once a day at 1 to 30 mg (Stier et al., J Endocrinol Metab 2013); those on 1 mg lost an average of 2.6 kg against 0.8 kg on placebo, and those on 10 mg lost less (Valentino et al., Clin Pharmacol Ther 2010; PMID 20445536).
• AOD-9604 Phase IIb 24-week obesity trial — The pivotal trial failed to demonstrate clinically meaningful weight loss vs placebo; obesity development program terminated 2007 (Valentino et al., Clin Pharmacol Ther 2010; PMID 20445536). A 2026 review notes that this conclusion rests mainly on the developer’s reports of its phase 2 programme rather than on peer-reviewed trial papers (Dominikowski et al., Front Endocrinol 2026; PMID 42395176).
• AOD-9604 safety database — Clinical trial safety profile did not reveal dose-limiting toxicities; most reported adverse events were mild and transient. In a summary of the six placebo-controlled trials (about 900 adults) written by authors with ties to the developer, AOD-9604 did not change serum IGF-1 or oral glucose tolerance against placebo, and no antibodies to it were found in the patients tested (Stier et al., J Endocrinol Metab 2013).
• No published human clinical trial of the parent HGH Fragment 176-191 — All community use is extrapolation.
• Bioavailability and route — AOD-9604 was developed as an oral drug: its 12- and 24-week trials used capsules or tablets (Stier et al., J Endocrinol Metab 2013), and in pigs oral AOD-9604 was well absorbed but broken down quickly (Moré & Kenley, J Endocrinol Metab 2014; doi:10.14740/jem213w). We found no study measuring how much of hGH 176-191 itself reaches the blood by any route; SubQ remains the dominant community route.
• Competitive landscape post-2007 — After the AOD-9604 obesity program termination, the weight-loss pharmaceutical landscape was re-shaped by GLP-1 receptor agonists (exenatide approved 2005; liraglutide 2010; semaglutide 2017; tirzepatide 2022) — agents that deliver substantially greater clinical weight loss through central appetite mechanisms. The peripheral-lipolytic fragment hypothesis has been substantially displaced as a pharmaceutical weight-loss paradigm, though mechanistic interest persists in niche research and community settings.

Reconstitution & Storage

Sellers list HGH Fragment 176-191 as a lyophilized powder in 2 mg or 5 mg vials.

• Reconstitution — Reconstitution guides describe adding the water slowly down the vial wall and swirling rather than shaking.
• Injection sites — Practitioner reports describe injecting under the skin of the abdomen or thigh, rotating sites.

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Side Effects & Risks

• Headache — More frequent at the 54 mg oral dose of AOD-9604 in its early trials (Stier et al., J Endocrinol Metab 2013).
• Gastrointestinal — Diarrhea and flatulence were more frequent at the same 54 mg oral dose (Stier et al., J Endocrinol Metab 2013).
• AOD-9604 trial safety signal — In the Phase I/II AOD-9604 clinical trials, the safety profile was benign with no dose-limiting toxicities; most adverse events were mild and transient (Stier et al., J Endocrinol Metab 2013).
• Efficacy shortfall — AOD-9604’s Phase IIb weight-loss endpoint was not met (Valentino et al., Clin Pharmacol Ther 2010; PMID 20445536).
• No long-term human safety data for the parent fragment — The parent HGH Fragment 176-191 has never been administered in controlled human trials. Long-term safety is inferred from the closely-related AOD-9604, which was tested to approximately 24 weeks. In animal studies by authors from the developer and its consultant, AOD-9604 given by mouth every day for 6 months to rats and 9 months to cynomolgus monkeys was generally safe, and it showed no genotoxic activity in three standard tests (Moré & Kenley, J Endocrinol Metab 2014; doi:10.14740/jem213w).
• IGF-1 — AOD-9604 did not change serum IGF-1 against placebo in its trials (Stier et al., J Endocrinol Metab 2013); no study has measured IGF-1 with the fragment itself.

Bloodwork & Monitoring

No trial, label or guideline sets monitoring for HGH Fragment 176-191. The AOD-9604 trials measured serum IGF-1, oral glucose tolerance and antibodies to the peptide (Stier et al., J Endocrinol Metab 2013).

Commonly Stacked With

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Legal Status

Related Compounds

What HGH Frag 176-191 users compare against:

Next Steps

References

1. Heffernan M, Summers RJ, Thorburn A, Ogru E, Gianello R, Jiang WJ, Ng FM. 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. Endocrinology. 2001;142(12):5182-5189. PMID: 11713213.
2. Ng FM, Sun J, Sharma L, Libinaka R, Jiang WJ, Gianello R. Metabolic studies of a synthetic lipolytic domain (AOD9604) of human growth hormone. Horm Res. 2000;53(6):274-278. PMID: 11146367. (AOD-9604 preclinical metabolic characterization.)
3. Heffernan MA, Jiang WJ, Thorburn AW, Ng FM. Effects of oral administration of a synthetic fragment of human growth hormone on lipid metabolism. Am J Physiol Endocrinol Metab. 2000;279(3):E501-E507. PMID: 10950816. (Oral bioavailability and lipid-metabolism effects of the GH fragment.)
4. Ng FM, Bornstein J. Hyperglycemic action of synthetic C-terminal fragments of human growth hormone. Am J Physiol. 1978;234(5):E521-E526. PMID: 645904. (Early structural dissection of GH C-terminal activity.)
5. Stier H, Vos E, Kenley D. Safety and Tolerability of the Hexadecapeptide AOD9604 in Humans. J Endocrinol Metab. 2013;3(1-2):7-15. doi:10.4021/jem157w. (AOD-9604 human tolerability data; authors tied to the developer.)
6. Calzada Ltd. AOD9604 – Important Clarifications. ASX announcement, 26 April 2013. announcements.asx.com.au/asxpdf/20130426/pdf/42fh15rvm7p65t.pdf. Read October 3, 2026. (The developer’s parent company: six trials in 925 patients, no clinically meaningful weight loss, obesity program terminated February 2007; osteoarthritis work preclinical only; regulatory status.)
7. U.S. Food and Drug Administration. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A — Category 2 list. FDA.gov.
8. Stone W. The wellness world is eager for RFK Jr.’s promised move on peptides. NPR, March 31, 2026. npr.org/2026/03/31/nx-s1-5768206/peptides-rfk-fda-compounding-pharmacies. Read October 3, 2026. (The HHS secretary’s late-February podcast remarks, “about 14” peptides; reported, not a rule.)
9. Wu Z, Ng FM. Antilipogenic action of synthetic C-terminal sequence 177-191 of human growth hormone. Biochem Mol Biol Int. 1993;30(1):187-196. PMID: 8358331. (hGH 177-191, the sequence without residue 176.)
10. Ng FM, Jiang WJ, Gianello R, Pitt S, Roupas P. Molecular and cellular actions of a structural domain of human growth hormone (AOD9401) on lipid metabolism in Zucker fatty rats. J Mol Endocrinol. 2000;25(3):287-298. PMID: 11116208. (AOD9401 is hGH 177-191.)
11. Heffernan MA, Thorburn AW, Fam B, Summers R, Conway-Campbell B, Waters MJ, Ng FM. Increase of fat oxidation and weight loss in obese mice caused by chronic treatment with human growth hormone or a modified C-terminal fragment. Int J Obes Relat Metab Disord. 2001;25(10):1442-1449. PMID: 11673763. (The modified C-terminal fragment is AOD-9604.)
12. Natera SH, Jiang WJ, Ng FM. Reduction of cumulative body weight gain and adipose tissue mass in obese mice: response to chronic treatment with synthetic hGH 177-191 peptide. Biochem Mol Biol Int. 1994;33(5):1011-1021. PMID: 7987248.
13. Wade JD, Ng FM, Bornstein J, Pullin CO, Pearce JS. Effect of C-terminal chain shortening on the insulin-antagonistic activity of human growth hormone 177--191. Acta Endocrinol (Copenh). 1982;101(1):10-14. PMID: 6751009.
14. Kwon DR, Park GY. Effect of Intra-articular Injection of AOD9604 with or without Hyaluronic Acid in Rabbit Osteoarthritis Model. Ann Clin Lab Sci. 2015;45(4):426-432. PMID: 26275694.
15. Valentino MA, Lin JE, Waldman SA. Central and peripheral molecular targets for antiobesity pharmacotherapy. Clin Pharmacol Ther. 2010;87(6):652-662. PMID: 20445536. (Review: the 12-week AOD-9604 trial result and the end of the obesity program in 2007.)
16. Dominikowski A, Rękoś Z, Olejarz M, Szczepanek-Parulska E, Domin R, Ruchała M. The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration. Front Endocrinol (Lausanne). 2026;17:1822475. PMID: 42395176. (Narrative review.)
17. Moré MI, Kenley D. Safety and Metabolism of AOD9604, a Novel Nutraceutical Ingredient for Improved Metabolic Health. J Endocrinol Metab. 2014;4(3):64-77. doi:10.14740/jem213w. (Animal toxicology and pharmacokinetics; authors from the developer and its consultant.)
18. Cunningham BC, Wells JA. High-resolution epitope mapping of hGH-receptor interactions by alanine-scanning mutagenesis. Science. 1989;244(4908):1081-1085. PMID: 2471267.
19. Ogru E, Wilson JC, Heffernan M, Jiang WJ, Chalmers DK, Libinaki R, Ng F. The conformational and biological analysis of a cyclic anti-obesity peptide from the C-terminal domain of human growth hormone. J Pept Res. 2000;56(6):388-397. PMID: 11152298. (The peptide is hGH 177-191.)
20. World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S2.2.3, Growth hormone (GH), its analogues and fragments. wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf. Read October 3, 2026.

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