HGH Fragment 176-191
C-terminal fragment of human growth hormone (residues 176-191) researched for lipolysis without the growth, IGF-1, or glucose effects of full GH
Half-life
~20-30 min
Typical Dose
250-500mcg daily SC (often dosed fasted or pre-cardio)
Format
Injectable
Purity
≥98%
Overview
HGH Fragment 176-191 is the 16-amino-acid C-terminal tail of human growth hormone, the region that carries the hormone's fat-mobilizing activity [1,4]. Researchers isolated this segment to study lipolysis on its own, stripped of the growth-promoting, IGF-1-raising, and insulin-antagonistic actions of the intact hormone [1,2]. It is the direct structural cousin of AOD-9604 (which we also cover): AOD-9604 is essentially the 177-191 sequence with a tyrosine added at the N-terminus for stability, so the two share the same lipolytic domain and most of the same literature. Animal work is reasonably consistent (reduced body-weight gain and increased fat oxidation in obese mice and Zucker rats [3,5]), but human fat-loss efficacy is weak and largely unproven. The stabilized analog AOD-9604 advanced into human obesity trials and failed to beat placebo on weight over 24 weeks, and Fragment 176-191 itself has essentially no controlled human data.
Mechanism
Mimics the lipolytic C-terminus of hGH. In adipose tissue it stimulates hormone-sensitive lipase and inhibits acetyl-CoA carboxylase, which both breaks down stored triglycerides and suppresses new fat synthesis [5]. It increases beta-3 adrenergic receptor expression, though the lipolytic effect is not mediated directly through the beta-3-AR pathway [2]. Critically, it does not bind the growth hormone receptor, so it produces no rise in IGF-1, no growth signaling, and none of the insulin-antagonistic, glucose-raising effects of full GH [2,4].
Researched benefits
- Targeted lipolysis (triglyceride breakdown) in adipose tissue
- No IGF-1 elevation or growth signaling
- No documented effect on blood glucose or insulin sensitivity
- No appetite suppression
- Stacks cleanly with GH secretagogue and GLP-1 protocols
- Short half-life allows flexible, timed dosing
Frequently asked
How is HGH Fragment 176-191 different from AOD-9604?
They are close relatives. Fragment 176-191 is the unmodified C-terminal segment of hGH. AOD-9604 is the 177-191 sequence with a tyrosine added at the N-terminus to improve stability, which is why it was the version taken into formal human trials. They share the same lipolytic domain and mechanism, so most of the published research (Ng, Heffernan) applies to both. In practice, the fragment is the raw peptide and AOD-9604 is the engineered, trial-tested analog.
How is it different from full HGH?
Full growth hormone binds the GH receptor and drives growth, IGF-1 production, and insulin antagonism alongside its fat-mobilizing effect. Fragment 176-191 is only the fat-mobilizing tail. Published studies show it stimulates lipolysis and reduces lipogenesis without engaging the GH receptor, without raising IGF-1, and without the hyperglycemia associated with GH [2,4]. You get the lipolytic action isolated from the anabolic and metabolic baggage.
Does it actually work for fat loss in humans?
Honestly, the human evidence is weak. The animal data (obese mice and Zucker rats) show real reductions in body-weight gain and increased fat oxidation [3,5], but that has not translated cleanly to people. The stabilized analog AOD-9604 went through a 24-week Phase 2 obesity trial and did not produce significant weight loss versus placebo, and Fragment 176-191 itself has no controlled human efficacy data. Treat any fat-loss claim as unproven in humans.
What's the typical research dose and timing?
Common research protocols use 250-500mcg subcutaneously per day, sometimes split into two doses. It is frequently administered on an empty stomach or before fasted cardio, on the rationale that low circulating insulin favors lipolysis. Dosing is empirical: there are no human dose-response trials for the fragment, so protocols are extrapolated from the AOD-9604 and rodent literature.
How is HGH Fragment 176-191 reconstituted?
Bacteriostatic water is the standard diluent. For a 5mg vial, 2mL of BAC water yields 2.5mg/mL (so 250mcg = 0.1mL and 500mcg = 0.2mL). Add the water slowly down the vial wall, swirl gently, and never shake. Refrigerate after reconstitution and protect from light.
Can it be stacked with GH secretagogues or GLP-1 peptides?
Researchers commonly investigate it alongside CJC-1295, Ipamorelin, or GLP-1 agonists. The mechanisms are complementary: GH secretagogues raise endogenous GH pulses, GLP-1 agonists cut caloric intake centrally, and Fragment 176-191 acts locally on adipocytes to mobilize fat without touching appetite or the GH receptor. Because it does not raise IGF-1 or glucose, it layers onto these protocols without adding their metabolic effects.
Scientific Literature
References
- [1]
Ng FM, Sun J, Sharma L, et al. (2000). Metabolic studies of a synthetic lipolytic domain (AOD9604) of human growth hormone.
Hormone Research · PubMed: 11146367
- [2]
Heffernan M, Summers RJ, Thorburn A, et al. (2001). 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 · PubMed: 11713213
- [3]
Heffernan MA, Thorburn AW, Fam B, et al. (2001). Increase of fat oxidation and weight loss in obese mice caused by chronic treatment with human growth hormone or a modified C-terminal fragment.
International Journal of Obesity and Related Metabolic Disorders · PubMed: 11673763
- [4]
Heffernan MA, Jiang WJ, Thorburn AW, Ng FM. (2000). Effects of oral administration of a synthetic fragment of human growth hormone on lipid metabolism.
American Journal of Physiology - Endocrinology and Metabolism · PubMed: 10950816
- [5]
Ng FM, Jiang WJ, Gianello R, Pitt S, Roupas P. (2000). Molecular and cellular actions of a structural domain of human growth hormone (AOD9401) on lipid metabolism in Zucker fatty rats.
Journal of Molecular Endocrinology · PubMed: 11116208
Citations are provided for educational purposes. Always verify primary sources before drawing research conclusions.
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