C80H127N23O24S2 · 1859.1 g/mol · PubChem CID 172966176 ↗
HGH Fragment 176-191
also known as AOD9604, AOD-9604, hGH 176-191
C-terminal fragment of human growth hormone spanning amino acids 176-191, with an additional N-terminal tyrosine residue in the AOD9604 variant. Retains lipolytic activity of parent GH without IGF-1 elevation or diabetogenic effects. Animal studies demonstrate 50% reduction in weight gain and enhanced beta-3 adrenergic receptor expression in obese mice. No adverse effects on insulin sensitivity observed in euglycemic clamp studies.
- Class
- GH Fragment
- Evidence level
- Strong animal evidence
- Regulatory status
- Not FDA-approved (US) — research use only
SQ · IP (animal) · Oral (tested)
Primary target — Beta-3 adrenergic receptors on adipocytes [heffernan-2001].
Pathway — Fragment → β3-AR upregulation → Enhanced lipolytic sensitivity [heffernan-2001].
Downstream effect — Increased lipolysis and beta-3 AR mRNA expression without IGF-1 axis activation.
Origin — Synthetic peptide derived from hGH residues 176-191; AOD9604 includes N-terminal tyrosine (177-191) [cox-2015].
Feedback intact — N/A — does not interact with GH/IGF-1 axis.
| Parameter | Value |
|---|---|
| Animal dose (oral) | 500 mcg/kg body weight [ng-2000]Obese Zucker rats, 19 days. |
| Animal dose (IP) | Not specified (14-day chronic administration) [heffernan-2001]Obese mice, daily IP injection. |
| Human equivalent dose | Not established — no published human RCTs |
| Frequency | Once daily (animal models) |
| Evidence basis | Animal studies only |
| Duration tested | 14–19 days [heffernan-2001][ng-2000] |
| Detection window | 50 pg/mL LOD in urine; stable metabolite extends detection [cox-2015]WADA-banned; anti-doping testing available. |
| Oral bioavailability | Demonstrated efficacy in animal oral administration [ng-2000]Potential for oral therapeutic development. |
Reconstitution
A pure mass-to-volume utility. Enter what you have in the vial; the atlas computes the volume per dose. No prescription information.
Multiple animal models (obese Zucker rats, obese mice, β3-AR knockout mice) · 14–19 days chronic administration · No human RCTs published
| Outcome | Finding |
|---|---|
| Primary fat target | Adipose tissue (general) — beta-3 AR mediated lipolysis [heffernan-2001] |
| Weight gain reduction | 50% reduction vs control (15.8 ± 0.6 g vs 35.6 ± 0.8 g) [ng-2000]Obese Zucker rats, 19 days oral administration. |
| Body fat reduction | Significant decrease in body weight and body fat in obese mice (14 days) [heffernan-2001] |
| Lipolytic activity | Increased adipose tissue lipolytic activity [ng-2000]Direct measurement in treated animals. |
| Beta-3 AR expression | Upregulated β3-AR mRNA in obese mice to lean-comparable levels [heffernan-2001] |
| Insulin sensitivity | No adverse effect — euglycemic clamp confirmed [ng-2000]Contrasts with intact hGH diabetogenic effects. |
| IGF-1 impact | No elevation — fragment does not activate GH/IGF-1 axis |
| Beta-3 AR dependency | Effect abolished in β3-AR knockout mice [heffernan-2001]Confirms β3-AR as primary mechanism. |
| Route of administration | Efficacy demonstrated via oral and IP routes [ng-2000][heffernan-2001] |
| Human evidence | None published — pre-clinical only |
- — Competitive athletes (WADA-banned) [cox-2015]
- — Absence of human safety data — experimental use only
- 01Route
Subcutaneous injection primary route in research context. Oral administration demonstrated efficacy in animal models at 500 mcg/kg.
- 02Frequency
Once daily dosing used in animal studies. Timing not specified; GH-independent mechanism suggests flexibility.
- 03Duration
Animal protocols: 14–19 days. Human duration not established — no published trials.
- 04Storage
Lyophilized peptide storage per standard peptide protocols. Metabolite stability suggests refrigerated reconstituted solution viable.
- 05Detection
Detectable in urine via SPE-LC-MS at 50 pg/mL LOD. Extended detection window via stable metabolite CRSVEGSCG. [cox-2015]
Frequently asked
How does HGH Fragment 176-191 work?
HGH Fragment 176-191 acts on Beta-3 adrenergic receptors on adipocytes, signalling via Fragment → β3-AR upregulation → Enhanced lipolytic sensitivity. [heffernan-2001][heffernan-2001]
Is HGH Fragment 176-191 FDA-approved?
HGH Fragment 176-191 is not FDA-approved in the United States and is handled as a research compound (research use only). Regulatory status may differ in other jurisdictions.
Sources
of 59 rendered claims carry a resolvable citation.
- [cox-2015]Cox 2015 — Detection and in vitro metabolism of AOD9604.
journal, 2015 - [heffernan-2001]Heffernan 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, 2001
Demonstrates AOD-9604 lipolytic activity without IGF-1 elevation. - [ng-2000]Ng 2000 — Metabolic studies of a synthetic lipolytic domain (AOD9604) of human growth hormone.
Horm Res, 2000
AOD-9604 mechanism: beta3-AR-mediated lipolysis. Synthetic lipolytic domain of hGH.