MetabolichGH 176-191Frag 176-191

HGH Fragment 176-191

Unmodified GH C-terminal fragment · metabolic / fat loss

HGH Fragment 176-191 is the unmodified tail end of human growth hormone — the last 16 amino acids (residues 176-191) of the 191-amino-acid hormone. Decades of research traced much of growth hormone's effect on fat to this C-terminal region, and the appeal is the same as for its better-known cousin AOD-9604: capture the fat part of growth hormone without the parts that raise IGF-1 or blood sugar. The honest problem is the evidence base. The bare 176-191 fragment has never been tested in a published human trial — every placebo-controlled human study, and the well-known Phase II obesity failure, belongs to AOD-9604, which is a DIFFERENT, chemically modified molecule (the 177-191 piece with an added tyrosine). And the original laboratory work on the isolated fragment is more modest than its reputation: the founding 1993 study found it blocked fat storage (anti-lipogenic) but produced no significant fat breakdown (lipolysis) in fat tissue. So the popular image of 176-191 as a potent stand-alone fat-burner is borrowed — from AOD-9604 and from animal studies — rather than demonstrated for the fragment itself. It is not an approved drug in any country and is prohibited in sport at all times under the WADA Prohibited List, which names it explicitly.

The short version

HGH Fragment 176-191 is literally a piece of growth hormone — the last 16 building blocks of the molecule, snipped off and made on its own. Researchers had found that this tail end is the part of growth hormone most tied to its effect on body fat, so the idea was to use just that piece.

Here is the part the marketing usually skips. The fragment by itself has never been tested in a published human study. The famous human trials — and the famous human failure — were done on a related but different compound, AOD-9604, which is this fragment slightly rebuilt with an extra amino acid stuck on the front. Results from AOD-9604 are routinely sold as if they were results for 176-191. They are not the same molecule.

Even the original lab work is more modest than the reputation. The founding 1993 study on the isolated fragment found it blocked the storage of new fat but did not actually break down existing fat in the tissue tested. The picture of 176-191 as a powerful stand-alone fat-burner is borrowed from animal studies and from AOD-9604, not shown for the fragment itself.

It is not an approved medicine anywhere, there is no published human safety or dosing data for the bare fragment, and it is banned in sport at all times — the WADA list names it directly.

Molecular identity

Specs

Molecular formula: C78H123N23O22S2
Molecular weight: ~1799.1 g/mol
Monoisotopic mass: 1797.87 Da
CAS number: 66004-57-7

Compound class: Peptide — unmodified hGH C-terminal fragment (residues 176-191)PubChem CID 16131230
Amino-acid sequence: Phe-Leu-Arg-Ile-Val-Gln-Cys-Arg-Ser-Val-Glu-Gly-Ser-Cys-Gly-Phe (16 aa; Cys7–Cys14 = hGH Cys182–189 loop)UniProt P01241
Parent molecule: C-terminal 16 residues of mature human growth hormone (191 aa)UniProt P01241
Relationship to AOD-9604: AOD-9604 is a DIFFERENT molecule — the 177-191 sub-fragment plus an added N-terminal tyrosine (Tyr-hGH 177-191)FDA PCAC materials
Molecular target: No direct receptor; anti-lipogenic in fat tissue — not a β3-AR agonist (the β3 data belong to the AOD-9604 analog, where lipolysis was not β3-mediated)PMID 8358331 · PMID 11713213
Half-life: Not established (no published human pharmacokinetics for the bare fragment; any '~30 min' figure online is unsourced)Not establishedHalf-life curve →
Regulatory status: Not an approved drug in any country; no published human trial of the bare fragmentResearch / regulatory record
Anti-doping status: Prohibited at all times (WADA S2.2.3, GH analogues & fragments — names 'hGH 176-191')WADA Prohibited List

Plain English

Mechanism

Growth hormone acts on body fat, and decades of work localized much of that activity to its C-terminal tail. HGH Fragment 176-191 is exactly that tail — the final 16 residues of the 191-amino-acid hormone, made as a stand-alone peptide. The hoped-for advantage is the same as for AOD-9604: keep growth hormone's effect on fat while leaving behind the regions that bind the growth-hormone receptor and drive IGF-1, blood-sugar changes, and general growth.

The most important and most misrepresented primary finding concerns what the fragment actually does. In the founding study — performed on the closely related 177-191 sequence — the synthetic C-terminal fragment showed anti-lipogenic activity — it blocked the formation of new fat — essentially identical to that of intact growth hormone, but the authors found no significant lipolytic (fat-breakdown) effect in the fat tissue they tested. That is close to the opposite of how the peptide is marketed: the documented action is blocking fat storage, not actively burning fat.

The β3-adrenergic-receptor story that is attached to this fragment online actually comes from work on AOD-9604, the modified analog, not the bare fragment. In obese mice both growth hormone and AOD-9604 raised the expression of the β3-adrenergic receptor, but in β3-receptor knockout mice the chronic fat-loss effect was lost — the investigators concluded the action is not mediated directly through the β3 receptor. The accurate statement, and one that belongs to AOD-9604 rather than to 176-191, is that the compound modulates β3-receptor expression; it is not a β3 agonist.

One mechanistic point that runs counter to the 'metabolically harmless' framing: earlier work on growth-hormone C-terminal fragments found they carry growth hormone's diabetogenic side — in rats, fragments spanning this region raised blood glucose and insulin and reduced insulin sensitivity. So the C-terminal tail is not automatically the 'safe, blood-sugar-neutral' part of growth hormone that the fragment is often sold as.

Sources:PMID 8358331 PMID 11713213 PMID 645904

Why people reach for it

Potential benefits

HGH Fragment 176-191 has a big fat-loss reputation — but that reputation is largely borrowed. Here's the honest version of what draws people to it, with the gaps stated plainly.

A documented anti-lipogenic action — What the founding lab study actually showed: the isolated fragment blocked the formation of new fat (anti-lipogenic), roughly like intact growth hormone — note this is blocking fat storage, not actively burning fat.
The 'fat part' of growth hormone, isolated — It's the natural C-terminal tail of growth hormone made on its own, with the appeal of capturing GH's effect on fat without the regions that bind the GH receptor — the design idea people pursue it for.
A simple, low-volume daily routine — Community convention runs it at a small once-daily microgram dose, easy to measure and fit into a fasted-morning habit alongside training.
Sits inside a familiar GH-axis stack — People pair it with its better-known sibling AOD-9604 or with GH secretagogues like CJC-1295 and Ipamorelin — though any combined fat-loss effect is reasoned, not shown.

Sources:PMID 8358331 PMID 645904 PMID 11713213

What people reach for HGH Fragment 176-191 for, based on how it's used and the (mostly borrowed) research around it — not proven outcomes or medical claims. Be clear-eyed: there's no published human trial of the bare fragment, its documented action is anti-lipogenic rather than fat-burning, and animal data flag a blood-sugar (diabetogenic) signal.

Implied timing

Best time to dose

Implied best time

Morning or bedtime, fasted

Convention is to inject HGH Fragment 176-191 on an empty stomach — fasted in the morning (often before cardio) and/or fasted at bedtime.

The fasted rule is the core of the convention: insulin blunts fat-mobilizing (lipolytic) signaling, so an empty-stomach dose is meant to avoid fighting a post-meal insulin spike — the same logic carried over from AOD-9604 and GH-axis practice.
A morning, pre-cardio dose pairs the GH-fragment concept with a fasted training window; a fasted bedtime dose follows the GH-axis habit of dosing into the overnight window — people use one or both.
There is no published human pharmacokinetics for the bare fragment, so any timing is convention borrowed from AOD-9604, not a measured optimum for this molecule.
Practically, the fasted window means roughly 30–60 minutes clear of food around the dose.

No study establishes an ideal time of day for HGH Fragment 176-191 — there's no human pharmacokinetic data for the bare fragment at all, so this is convention reasoned from its GH-fragment class, not a measured schedule. Most peptide dosing defaults to the midday-to-evening window; for a fasted fat-loss fragment the lean is fasted morning or bedtime.

How to run it

Dosing & protocol

Fragment 176-191 is dosed here as a subcutaneous injection — the research-peptide form and the route the on-page calculator is built for. There is no human clinical trial of the bare fragment, so every dose and schedule below is community convention borrowed from AOD-9604 lore and animal work. Read it as a map of how people run this peptide in practice — not a validated protocol, and not proof of the fat-loss mechanism it is marketed for.

Convention on borrowed, thin evidence: there is no published human trial of the bare 176-191 fragment and no established human dose. The dose ranges below are community extrapolations from AOD-9604 and rodent data. Fragment 176-191 is not an approved drug and is prohibited in sport at all times (WADA S2.2.3).

Tiered dose ranges

Community convention scales the subcutaneous daily dose within a narrow microgram range.

Conservative start:: 250 mcg once daily — used to assess individual response before committing to a full cycle. Borrowed from AOD-9604 convention; no fragment-specific human starting dose exists.
Standard range:: 250–500 mcg once daily — the range most commonly used in user community and practitioner circles. 500 mcg/day is the upper end of what AOD-9604 trials used in an injectable form.
Split dosing:: Some users run 250 mcg twice daily (500 mcg total) when targeting more consistent coverage across the day, though there is no pharmacokinetic rationale for the bare fragment — half-life is not published.

Subcutaneous administration

Fragment 176-191 is injected into subcutaneous fat; site, timing, and the food window are the actionable decisions.

Injection site:: The abdomen (a couple of inches clear of the navel), the outer thigh, or the love-handle area. Rotate sites between doses to avoid local irritation and lipohypertrophy (fatty lumps from repeated injection into the same spot).
Measuring the dose:: Drawn on a U-100 insulin syringe from the reconstituted vial. At the standard 5 mg vial + 2 mL BAC water mix (2,500 mcg/mL): 250 mcg = 10 IU · 300 mcg = 12 IU · 500 mcg = 20 IU. The on-page calculator does this live for any vial size.
Timing:: Convention — borrowed from GH-axis logic — is to inject fasted, in the morning before the first meal (often pre-cardio) and/or fasted at bedtime, on the reasoning that food raises insulin and insulin blunts GH-related fat effects (see Best time to dose above). A second dose, if split, is typically placed at midday fasted or immediately before training.
Food window:: The fasted window (30–60 minutes before eating) is community convention, not a fragment-specific finding. It mirrors the logic used in AOD-9604 protocols and general GH secretagogue practice.

Cycle & washout

No validated cycle length exists for the bare fragment; the following is borrowed from AOD-9604 and GH-analog convention.

Standard cycle:: 8–12 weeks of daily dosing. AOD-9604's Phase II trials ran 12–24 weeks; user community typically mirrors the shorter end.
Washout:: 4 weeks off between cycles. During the break, body-composition tracking (DEXA or circumference measurements) helps assess whether any change occurred — important given the absence of human trial data confirming efficacy.
Glucose awareness during cycle:: Given the animal evidence that C-terminal hGH fragments raise blood glucose and insulin, monitoring fasting glucose periodically during a cycle is a sensible precaution that the lore usually omits.

Reconstitution at a glance

The on-page calculator does this live; the quick reference for the 5 mg vial (calculator default):

Mixing:: 5 mg vial + 2 mL bacteriostatic water = 2,500 mcg per mL. On a 100-unit (1 mL) insulin syringe: 250 mcg = 10 IU · 300 mcg = 12 IU · 400 mcg = 16 IU · 500 mcg = 20 IU.
Why 2 mL for a 5 mg vial:: Keeps the mcg-per-IU ratio in a practical syringe range — small microgram doses land on measurable unit markings rather than near-invisible fractions.

Sources:PMID 8358331 PMID 11713213 PMID 645904

Substrate the signal needs

Nutritional cofactor precision

Fragment 176-191 is marketed for fat loss. Its most honest cofactors are the things that actually drive fat loss — the nutritional and training inputs that determine whether a calorie deficit translates into lost fat rather than lost muscle. These support the fat-loss PROCESS, not this compound; the fragment's own evidence is thin (anti-lipogenic in rat tissue, no human trial), and the diabetogenic animal signal adds a glucose-awareness layer most protocols skip.

Reasoned from the fat-loss process plus the fragment's diabetogenic animal signal — not a Fragment 176-191 cofactor study. Supplement doses are general-population conventions. Every cofactor here would matter whether or not the fragment has any human effect.

SUPPLY — protein + calorie deficit (the actual fat-loss engine)

The two inputs that determine whether fat actually comes off. Nothing substitutes for them.

Protein (lean-mass anchor):: 1.6–2.0 g per kg of body weight per day (approximately 0.7–0.9 g per lb). This is the minimum needed to preserve muscle in a deficit — so the weight lost is fat rather than lean tissue, which is the entire point of a 'body-composition' peptide. Spread across 3–4 meals; leucine-rich sources (meat, eggs, dairy, whey) perform best at preserving muscle under energy restriction.
Calorie deficit:: A sustained 300–500 kcal/day deficit is the driver. No peptide with thin human evidence substitutes for this; it is what the cofactors and the compound are both meant to optimize.
Dietary fiber:: 25–35 g/day from whole plant foods. Fiber raises satiety, slows gastric emptying, and blunts post-meal glucose spikes — relevant given the fragment's diabetogenic animal signal.

AMPLIFY — resistance training (the muscle-sparing, metabolic lever)

Exercise is what converts a calorie deficit into fat loss instead of fat-and-muscle loss.

Resistance training:: 3–4 sessions per week of compound-movement strength work. Muscle tissue is metabolically expensive — building or preserving it raises resting calorie burn and is the most reliable way to shift body composition. Timing Fragment 176-191 on training days (morning dose before the session) follows GH-axis convention.
High-intensity cardio (optional):: 2–3 sessions per week of HIIT or moderate-intensity cardio for additional caloric output, if recovery allows. The borrowed GH-axis rationale for fasted morning dosing aligns with fasted morning cardio as a convention — again, this is AOD-9604-derived, not fragment-specific.

MITIGATE — glucose awareness (the honest safety cofactor)

The animal data shows C-terminal hGH fragments are diabetogenic — this is the one signal the popular protocol skips and shouldn't.

Glucose monitoring:: Fasting glucose check at baseline, at 4 weeks, and at end of cycle. Given that rat studies found C-terminal hGH fragments raised blood glucose and reduced insulin sensitivity, treating this as a zero-cost precaution is reasonable. Normal fasting glucose is below 100 mg/dL; anything trending upward mid-cycle is a reason to pause.
Magnesium (insulin sensitivity support):: 300–400 mg magnesium glycinate or malate daily, preferably with the evening meal. Magnesium supports insulin receptor sensitivity and is commonly depleted on calorie-restricted diets — two reasons it fits the cautious protocol here.
Electrolytes on aggressive cuts:: Sodium, potassium, and magnesium can run short when food intake drops sharply. Low electrolytes cause fatigue and cramps that are often attributed to the peptide — replace them first before troubleshooting the protocol.

Combinations + timing

Stacking notes + timing windows

Fragment 176-191 sits inside the GH-axis, fat-loss-fragment family, and its stacks flow from that context. The closest and most honest pairing is its Tyr-modified sibling AOD-9604 — the molecule that actually owns the human trial data the fragment's reputation borrows. GH secretagogues are the second class, pushing the broader GH axis the fragment is a piece of.

User combinations reasoned from GH-axis context — none studied head-to-head. The fat-loss premise for the bare fragment is borrowed, not demonstrated in humans. Every stack is doubly unproven. Keep the diabetogenic animal signal in view across the whole GH-axis stack.

Fragment 176-191 + AOD-9604

The sibling that owns the human data — the honest borrowed-reputation relationship, made explicit.

Why it works:: AOD-9604 is Tyr-hGH 177-191 — a slightly modified version of the same C-terminal sequence that went through six human trials. The working hypothesis for combining them is that the unmodified fragment's anti-lipogenic action (blocking fat storage) could run alongside AOD-9604's more tested profile. That said: AOD-9604 itself failed its Phase IIb obesity trial in humans in 2007. This stack is built on thin evidence layered on thinner.
The protocol:: Fragment 176-191 250 mcg + AOD-9604 250 mcg, both as separate subcutaneous injections, fasted morning. Alternatively, 300 mcg each for a combined 600 mcg/day total C-terminal fragment load. Both are dosed by the same site-rotation and food-window rules.
Outcome:: The combination users reach for when they want to 'cover both angles' on the GH C-terminal fat-loss hypothesis. The honest framing: you are stacking a molecule whose fat-loss mechanism was not shown in humans on top of one whose fat-loss effect was not replicated in its Phase IIb trial. Body-composition tracking is essential to assess any real-world signal.

Fragment 176-191 + CJC-1295 or Ipamorelin

Pairing the fragment with a GH secretagogue — the GH-axis amplification stack.

Why it works:: CJC-1295 (a GHRH analog) and Ipamorelin (a GHRP) prompt the pituitary to release more of the body's own growth hormone. Running the fragment alongside them is meant to capture both endogenous GH pulse amplification and the C-terminal fragment's direct anti-lipogenic action at the fat-cell level — two different levers on the GH-fat axis. Note: endogenous GH released by secretagogues is the full hormone; the fragment is the isolated tail. Mechanistically complementary, not the same molecule twice.
The protocol:: Fragment 176-191 250–500 mcg fasted morning + Ipamorelin 200–300 mcg subcutaneously (typically 2–3× daily, including pre-sleep for the GH pulse). CJC-1295 without DAC (MOD-GRF 1-29) is often substituted at 100 mcg per injection. The fragment dose does not change when a secretagogue is added.
Outcome:: Reached for on fat-loss and body-recomposition goals where users want full GH-axis support alongside the fat-focused fragment. The diabetogenic animal signal applies across the whole stack: GH-axis amplification can raise fasting glucose; glucose monitoring is more relevant here, not less.

Reconstitution math

Reconstitution calculator

Calculated for a 1 mL U-100 insulin syringe (100 units/mL).

Peptide per vial

BAC water added

Desired dose

Units per dose

Draw to this mark on a U-100 syringe

Volume per dose: 0.12 mL
Doses per vial: 16
Concentration: 2.5 mg/mL

One vial lasts

Daily: 16 days
Every other day: 33 days
5×/week: 23 days

Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.

From the studies

Side effects from research

There is no published human safety data for the bare HGH Fragment 176-191, because it has never been studied in a human trial. Any 'well tolerated in clinical studies' claim you see is almost certainly imported from AOD-9604, a different molecule. The honest statement is that the human safety profile of the fragment itself is simply unknown.

The one mechanistically-grounded signal comes from animal work and cuts against the marketing: growth-hormone C-terminal fragments spanning this region raised blood glucose and insulin and reduced insulin sensitivity in rats. So the popular framing of 176-191 as the 'blood-sugar-neutral' piece of growth hormone is not supported — the C-terminal tail carries growth hormone's diabetogenic activity in those studies.

It is not approved as a medicine in any country, and there is no published human pharmacokinetic data (measurements of how the body absorbs, distributes, and clears the drug) — any specific half-life (the time for blood levels to fall by half) figure circulating online should be treated as unsourced. (Note that the FDA's compounding-safety actions and Australia's non-registration status that are often quoted apply specifically to AOD-9604, the modified analog, rather than to the bare fragment by name.) This page presents the research literature only and makes no therapeutic claims.

Sources:PMID 645904

As reported in literature

Research dosing ranges

This is the research-evidence table — the actual primary studies the practical framing above leans on, shown separately so study data is never mistaken for a human dose. There is no approved therapeutic dose for HGH Fragment 176-191, and — crucially — there is no published human trial of the bare fragment at all, so there is no human dose range to report. The evidence here is animal and in-vitro (test-tube / isolated-tissue) only: the laboratory studies on the isolated C-terminal fragment, plus the β3 study that is often cited for it but was in fact done on the modified analog AOD-9604. Doses that are reported per kilogram of body weight (1 kg ≈ 2.2 lb) are noted as such. Note what these studies did and did not show.

Dose	Route	Model	Outcome	Sources:
In-vitro / ex-vivo	Tissue	Rat adipose tissue (isolated hGH 177-191 fragment)	Anti-lipogenic activity essentially identical to intact growth hormone (blocked formation of new fat) — but NO significant lipolytic (fat-breakdown) effect was found	PMID 8358331
~5 nmol/kg	Injection	Rats (hGH C-terminal fragments, residues 178-191 region)	Raised blood glucose and plasma insulin and reduced insulin sensitivity — the C-terminal region carries growth hormone's diabetogenic action, not a 'glucose-safe' profile	PMID 645904
Chronic, 14 days	Injection	Obese mice + β3-receptor knockout mice (AOD-9604, NOT the bare fragment)	AOD-9604 raised β3-receptor expression and reduced fat; the chronic effect was lost in β3-knockout mice — lipolysis not mediated directly via β3. Attributed to AOD-9604, the modified analog	PMID 11713213
Human	—	Bare 176-191 fragment in humans	NO published human trial exists for the bare fragment. The placebo-controlled human trials, the failed 24-week Phase IIb obesity study, and the 2007 discontinuation all belong to AOD-9604 — a different, chemically modified molecule — and must not be read as data on 176-191

Quick answers

Frequently asked

Does HGH Fragment 176-191 burn fat?

The evidence is much weaker than the marketing suggests. The bare fragment has never been tested in a published human study, so there is no human fat-loss data for it at all. And the founding laboratory study found it blocked the storage of new fat (anti-lipogenic) but did NOT produce significant fat breakdown (lipolysis) in the tissue tested. The image of it as a potent fat-burner is borrowed from animal work and from the related compound AOD-9604.

How is HGH Fragment 176-191 different from AOD-9604?

They are different molecules, and this is the key point. HGH Fragment 176-191 is the unmodified tail of growth hormone — the natural 16-residue sequence. AOD-9604 takes a slightly shorter piece (residues 177-191) and adds an extra tyrosine at the front (Tyr-hGH 177-191), a synthetic modification. AOD-9604 is the one that actually went through a clinical development program with six human trials; the bare fragment did not. Human results for AOD-9604 are routinely, and incorrectly, sold as results for 176-191.

Is HGH Fragment 176-191 safe? Does it affect blood sugar?

There is no published human safety data for the bare fragment. The relevant animal evidence actually argues against the 'blood-sugar-neutral' reputation: studies of growth-hormone C-terminal fragments in rats found they raised blood glucose and insulin and reduced insulin sensitivity. So the claim that this is the harmless, glucose-safe part of growth hormone is not supported by the primary literature.

Is HGH Fragment 176-191 approved or legal to use?

It is not an approved medicine in any country, and there is no published human trial of the bare fragment. It is also prohibited in sport at all times under the WADA Prohibited List, which names 'hGH 176-191' explicitly under its section on growth hormone, its analogues and fragments (S2.2.3). The FDA compounding-safety and Australian non-registration actions often quoted in this context apply specifically to the modified analog AOD-9604, not to the bare fragment by name.

Primary sources

References

PubChem CID 16131230PubChem CID 16131230 (Somatotropin 176-191; C78H123N23O22S2, ~1799.1 g/mol; CAS 66004-57-7)
UniProt P01241UniProt P01241 — Somatotropin (human growth hormone); mature sequence and disulfides (verifies residues 176-191 = FLRIVQCRSVEGSCGF, Cys182–189 loop)
PMID 8358331Wu & Ng, Biochem Mol Biol Int 1993 (synthetic hGH 177-191: anti-lipogenic like intact GH; NO significant lipolytic effect)
PMID 645904Ng & Bornstein, Am J Physiol 1978 (hGH C-terminal fragments raise blood glucose/insulin and reduce insulin sensitivity in rats — diabetogenic)
PMID 11713213Heffernan et al., Endocrinology 2001 (hGH & AOD-9604 in obese mice + β3-AR knockouts; β3 expression raised but lipolysis NOT directly β3-mediated — AOD-9604, not the bare fragment)
WADA Prohibited List, S2.2.3WADA Prohibited List — prohibited at all times; names 'hGH 176-191' under S2.2.3 (GH, its analogues and fragments)

Research use only · Not medical advice · Updated 2026-06-01