hGH 176-191 · Tyr-hGH 177-191 · GH lipolytic fragment
The last 16 amino acids of human growth hormone (positions 176–191), specifically the region responsible for GH's fat-mobilising properties. Closely related to AOD-9604 — which is the stabilised, more studied version of this fragment. Unlike AOD-9604, HGH Fragment 176-191 has no completed human clinical trials. All evidence is from animal models or extrapolated from AOD-9604 research.
01 — Research Summary
HGH Fragment 176-191 has no completed human clinical trials. This is the central fact that separates it from AOD-9604, which at least completed Phase 2 trials (even though the pivotal trial failed). All human-relevant evidence for Fragment 176-191 is either extrapolated from AOD-9604 research or drawn from animal models.
Fat reduction without lean mass loss in animal models. Studies in obese murine models consistently show body weight and fat mass reduction with Fragment 176-191 administration, linked to beta-3 adrenergic lipolytic activation. No organ growth, no IGF-1 elevation.
AOD-9604 is the stabilised, more bioavailable form of this fragment. The clinical Phase 2 data for AOD-9604 is the closest available proxy for Fragment 176-191's human effects — same sequence, different stability. AOD-9604's Phase IIb trial failure is the most relevant caution for fragment users as well.
No completed human clinical trials exist for HGH Fragment 176-191 specifically. All efficacy claims for this compound in humans are extrapolated from animal data and from the AOD-9604 clinical program. The fragment is less stable in biological systems than AOD-9604, which means bioavailability may be lower than the animal data would suggest.
02 — Mechanism of Action
HGH Fragment 176-191 and AOD-9604 share the same core mechanism — they are the same C-terminal GH sequence. The structural difference is that AOD-9604 has a tyrosine added at the N-terminus for stability. The lipolytic mechanism is identical.
Fragment 176-191 activates beta-3 adrenergic receptors on adipocytes, increasing intracellular cAMP and activating protein kinase A. This cascade activates hormone-sensitive lipase — the key enzyme in triglyceride breakdown — releasing free fatty acids for oxidation.
Concurrent downregulation of acetyl-CoA carboxylase reduces de novo fat synthesis, creating a dual effect: more fat breakdown, less fat storage. This selectivity for adipose tissue is what distinguishes the fragment from full HGH.
The fragment does not activate the classical GH receptor pathway, meaning no IGF-1 elevation, no promotion of cell proliferation, and no insulin resistance — the primary side effect concerns with full HGH therapy.
03 — Dosing Context
No validated human dosing protocol exists. Community protocols are extrapolated from AOD-9604 trial data and from rodent study doses scaled to human body weight.
| Protocol | Dose | Frequency | Timing |
|---|---|---|---|
| Common community | 200–500 mcg | Daily | Fasted — AM preferred |
| Conservative | 200 mcg | Daily | Fasted AM |
Fasted administration is essential — insulin inhibits the lipolytic pathway this fragment acts on. The glycogen disruption noted in some research (possible hyperglycaemia risk) warrants monitoring blood glucose, particularly for people with insulin resistance or pre-diabetes.
04 — Community
Community discussion of Fragment 176-191 frequently conflates it with AOD-9604 — the two are often treated as interchangeable and many suppliers label them as the same compound. They are mechanistically identical but differ in stability and bioavailability. Users who report positive outcomes typically describe modest fat loss effects similar to those attributed to AOD-9604, making it impossible to separate compound-specific from class-level effects in anecdotal reports.