16AA Preclinical / In Vitro
Fragment 176-191
The native hGH lipolytic tail—12.5× more potent at fat oxidation than full-length GH, with zero IGF-1 or insulin disruption in preclinical models.
In Plain English:
Fragment 176-191 is the 16-amino acid C-terminal tail of human growth hormone (residues 176–191), isolated because this region carries hGH's fat-burning signal. Unlike full HGH, it does not bind the GH receptor, does not raise IGF-1, and does not cause insulin resistance or hyperglycemia. Animal studies show it stimulates lipolysis (fat breakdown) and inhibits lipogenesis (new fat formation) with substantially greater potency than the intact hormone. It also lowers blood glucose in obese rodents. A 2022 in-vitro study found it enhanced doxorubicin toxicity against MCF-7 breast cancer cells via molecular docking with Ki-67, estrogen receptor, and Mind Bomb protein targets. No independent human clinical trials have been published; most safety data is extrapolated from its close structural analog AOD-9604 (which adds an N-terminal tyrosine). Community researchers typically dose 250–500 mcg/day SC in two fasted injections.
Research Maturity
Preclinical / In Vitro (23 PubMed-indexed results (hGH fragment 176-191 / AOD-9604); preclinical/in vitro; no independent human RCTs+ Studies)
Focus
Body Composition
Metabolic Health
Origin
Native C-terminal fragment of human growth hormone (hGH residues 176–191); cyclic disulfide between Cys7 and Cys14 of the fragment. First characterized by Ng et al. at the University of Hong Kong in the early 1990s.
Mechanism
Stimulates lipolysis and inhibits lipogenesis in adipose tissue via beta-3 adrenergic receptor upregulation and elevated intracellular cAMP; phosphorylates hormone-sensitive lipase (HSL). Does not bind the GH receptor, does not elevate IGF-1, and does not impair glucose tolerance or insulin sensitivity. A distinct pathway from full hGH: AOD-9604 (the N-Tyr-extended analog) confirmed these effects persist in beta-3-AR knockout mice, indicating additional non-beta-3-AR mechanisms.
Outcome
Lipolysis/fat oxidation (preclinical); inhibition of lipogenesis in rat and human adipose tissue; body weight reduction in obese rodent models; blood glucose lowering in obese mice; MCF-7 breast cancer cell toxicity enhancement in vitro (2022). No human fat-loss endpoint has been tested independently.
