What you need to know about a synthetic GH fragment marketed for weight loss—despite no human evidence, a failed human trial of its modified form, and a mechanism proven only in obese mice.

This peptide fragment occupies a unique—and uncomfortable—position in the self-experimentation community. The molecule itself has a proven mechanism (β3-adrenergic receptor upregulation, verified by genetic knockout studies). The animal data is solid: repeated weight loss and lipolysis in ob/ob mice and Zucker rats across 25+ years of research. But the human evidence is exactly zero.

What makes this compound particularly treacherous is the AOD-9604 shadow. AOD-9604 is the modified version—more stable, more potent, added tyrosine residue—and it has human trial data. Six trials, 925 subjects, 2001–2007. The pivotal trial (METAOD006/OPTIONS) enrolled 536 subjects, ran 24 weeks, and **failed its primary endpoint**. The development program was halted. Metabolic Pharmaceuticals ceased operations.

The unmodified fragment (the one being sold) is marketed with references to this body of work—but AOD-9604 is a different compound with a different pharmacology and a failed human trial. This three-step disconnect—unmodified vs. modified, promise vs. failure, mice vs. humans—is the core problem.

In 2026, the weight-loss peptide landscape has moved on. GLP-1 agonists (semaglutide, tirzepatide) have Phase III data showing 15–20% body weight loss. HGH-Fragment 176-191 has preclinical data from one research group and nothing else.

Quick Facts: HGH-Fragment 176-191 at a Glance

WHAT IS HGH-FRAGMENT 176-191?

Pronunciation: aitch-jee-aitch-frag-one-seventy-six-to-one-ninety-one (also known as hGH Frag, AOD-9401, Fragment 176-191)

HGH-Fragment 176-191 is a synthetic peptide consisting of the last 16 amino acids of human growth hormone. It was derived from research conducted at Monash University in the 1990s, when scientists identified that a truncated version of hGH retained fat-loss properties while avoiding the growth-promoting effects of full-length hGH.

The fragment is a polypeptide with a molecular weight of approximately 1817 Da. It is too large for oral absorption under normal conditions, though animal studies suggest oral bioavailability is possible with appropriate formulation. In the community, it is administered via subcutaneous injection.

The compound exists in two forms: - Unmodified hGH Fragment 176-191 (AOD-9401): The form discussed here. Zero human clinical data. - AOD-9604 (modified): Tyrosine residue added at the N-terminus. More stable, more potent (~1.5–2× potency increase). Six human trials (925 subjects). Pivotal trial failed.

The unmodified version is marketed on the assumption that data from AOD-9604 applies to it. This is not a safe assumption—they are different compounds with different pharmacology and different human trial outcomes.

ORIGINS AND DISCOVERY

In the 1990s, Ng FM and colleagues at Monash University in Melbourne, Australia were studying the biological activity of human growth hormone. They observed that full-length hGH produced weight loss in obese animals but also caused hyperglycemia and elevated insulin-like growth factor 1 (IGF-1)—side effects that limited clinical application.

The team hypothesized that the fat-loss activity of hGH might reside in a specific region of the molecule—perhaps the C-terminal portion—and that this fragment might produce lipolysis without activating the growth hormone receptor (GHR), thus avoiding hyperglycemia.

Their early in vitro work (1993–1994) in adipocytes and whole-animal studies in ob/ob mice demonstrated that the C-terminal 16-amino acid fragment (residues 176–191) retained antilipogenic (fat synthesis–blocking) activity and produced weight loss. By the late 1990s, their research had attracted commercial interest. Metabolic Pharmaceuticals licensed the technology and developed a modified version (AOD-9604), which became the focus of clinical development.

The unmodified Fragment 176-191 (sometimes designated AOD-9401) remained a research compound. It has never been tested in human trials. Meanwhile, AOD-9604 underwent six human trials between 2001 and 2007, culminating in a 536-subject Phase 2b trial that failed to meet its primary efficacy endpoint. Development was halted, and Metabolic Pharmaceuticals ceased operations.

Today, the unmodified fragment is available in the research peptide and self-experimentation markets, often with marketing materials that reference AOD-9604's human trial data—a critical distinction that is frequently elided.

MECHANISM OF ACTION

HGH-Fragment 176-191 operates through a β3-adrenergic receptor (β3-AR)–dependent mechanism that is entirely independent of the growth hormone receptor. This is perhaps the most important fact about this compound.

β3-Adrenergic Receptor Upregulation

In adipose tissue, the fragment binds to or otherwise activates β3-adrenergic receptors. This upregulation sensitizes fat cells to endogenous catecholamines (epinephrine and norepinephrine), which in turn activate hormone-sensitive lipase (HSL). HSL breaks down stored triglycerides into free fatty acids and glycerol, which are then released into the bloodstream for use as fuel. This is lipolysis.

Simultaneously, the fragment inhibits acetyl-CoA carboxylase (ACC), a key enzyme in lipogenesis (fat synthesis). By blocking ACC, the fragment reduces the conversion of acetyl-CoA into malonyl-CoA, which in turn suppresses the downstream cascade of fatty acid synthesis. This is antilipogenesis.

Together, these two mechanisms—increased lipolysis plus decreased lipogenesis—create a fat-loss effect.

Why Not the Growth Hormone Receptor?

Full-length hGH activates both the GHR and, indirectly, the β3-AR. When administered to humans or animals, hGH causes hyperglycemia, elevated IGF-1, and growth effects—undesirable for a weight-loss agent.

The C-terminal fragment (residues 176–191) does not bind or activate the GHR. It operates exclusively through β3-AR. This is why AOD-9604 (the modified, more potent version) did not produce hyperglycemia in mouse studies—it lacked GHR activity.

Mechanistic Validation: The Knockout Study

The most compelling evidence for this mechanism comes from a 2001 study by Ng's group using β3-AR knockout mice (PMID 11713213). In these genetically modified animals, neither full-length hGH nor the fragment produced any weight loss. The mice remained obese. This proved that the lipolytic effect of both compounds was entirely dependent on β3-adrenergic receptor presence. Remove the receptor, remove the effect.

This is definitive mechanistic proof—but in mice.

KEY RESEARCH AREAS AND STUDIES

Lipid Metabolism and Antilipogenic Action (1993)

Wu & Ng, PMID 8358331 (1993): In vitro study in human and rodent adipocytes demonstrated that the C-terminal fragment of hGH retained antilipogenic activity—it inhibited acetyl-CoA carboxylase (ACC) in fat cells and liver, blocking the first committed step of fatty acid synthesis.

Weight Loss in Obese Mice (1994)

Ng et al., PMID 7987248 (1994): ob/ob mice (genetic obesity model) treated chronically with the fragment showed reduced body weight gain and decreased adipose tissue mass over 14+ days. This was the landmark early efficacy study.

Glucose Handling (1993)

Wu & Ng, PMID 8118430 (1993): In Zucker rat adipocytes, the fragment reduced basal and insulin-stimulated glucose uptake. Notably, the fragment was more potent than intact hGH at equimolar concentrations. This was a key finding: the fragment was metabolically active and more selective than full-length hGH.

Oral Bioavailability (2000)

Ng et al., PMID 10950816 (2000): ob/ob mice were given the fragment orally for 30 days. Body weight gain was reduced starting on day 16. The compound increased energy expenditure acutely and increased lipolysis while decreasing lipogenesis. This was the first demonstration that oral administration could produce the effect—important for potential clinical application.

Insulin Sensitivity (2000)

Heffernan et al., PMID 11116208 (2000): In Zucker rats (diet-induced obesity model), AOD-9401 (unmodified fragment) stimulated hormone-sensitive lipase (HSL) and inhibited ACC. Adipocyte cell size was reduced. Critically, the compound did not induce insulin resistance—unlike intact hGH, which impairs glucose control. This suggested the mechanism was selective.

AOD-9604 vs. hGH Comparison (2001)

Ng et al., PMID 11673763 (2001): In obese mice, both hGH and AOD-9604 reduced body weight. However, only hGH caused hyperglycemia. AOD-9604 did not activate the growth hormone receptor. This study clinically validated the hypothesis that the C-terminal fragment mechanism avoided GHR-mediated side effects.

β3-AR Knockout Validation (2001)

Ng et al., PMID 11713213 (2001): Wild-type mice and β3-AR knockout mice were treated with hGH or the fragment. In wild-type mice, both compounds upregulated β3-AR RNA and produced weight loss. In knockout mice, neither compound produced any effect. This proved mechanism was entirely β3-AR dependent. Definitive.

Modern Research (2015–2022)

Recent publications have explored the fragment in other contexts (osteoarthritis cartilage preservation, cancer cell nanoparticle delivery). These are primarily in vitro or animal studies and do not change the weight-loss evidence base.

THE AOD-9604 SHADOW

This section is the editorial core of the brief.

HGH-Fragment 176-191 is marketed on the basis of human data—but that data is not for this compound. It is for AOD-9604, a modified version.

The Modification

AOD-9604 is hGH Fragment 176-191 with a single tyrosine residue added at the N-terminus (Tyr-hGH 177-191). This modification makes it more stable in circulation (longer half-life) and approximately 1.5–2× more potent than the unmodified fragment.

AOD-9604 underwent commercial development by Metabolic Pharmaceuticals. Six human trials were conducted between 2001 and 2007, involving 925 total subjects.

The Human Trial Evidence for AOD-9604

• METAOD005 (12 weeks): Showed 2.6 kg weight loss vs. 0.8 kg placebo—a signal of efficacy.
• METAOD006/OPTIONS (Phase 2b, 536 subjects, 24 weeks): The pivotal trial. Designed to confirm efficacy and support regulatory approval. It failed to meet its primary endpoint. The weight loss did not reach statistical significance or clinical meaningfulness compared to placebo.

Why This Matters

The unmodified fragment is, by definition, less stable and less potent than AOD-9604. If the more potent, more stable version failed to produce clinically significant weight loss in 536 subjects over 24 weeks, there is no rational basis for expecting the less potent, less stable unmodified version to perform better.

The compound being sold is being marketed on the strength of a failed trial of a more potent analog—a three-step disconnect: 1. Unmodified fragment (zero human data) vs. modified version (AOD-9604) 2. Promise (early efficacy signals) vs. failure (pivotal trial failed) 3. Mice (animal studies) vs. humans (failed Phase 2b)

Regulatory Status

AOD-9604 was recently excluded from the FDA's 503A compounding list (December 2024). The unmodified fragment has never been reviewed by any regulatory authority.

NOT A GH SECRETAGOGUE

This compound is placed in Cluster D (Growth Hormone Secretagogues) but is not a GH secretagogue.

GH secretagogues stimulate the release of growth hormone from the anterior pituitary gland. They work through two main receptor pathways: - GHS-R1a (growth hormone secretagogue receptor 1a) — bound by compounds like ghrelin, MK-677, and ipamorelin - GHRHR (growth hormone-releasing hormone receptor) — bound by compounds like tesamorelin and sermorelin

HGH-Fragment 176-191 does not stimulate GH release. It does not activate GHS-R1a or GHRHR. It is not a secretagogue in any meaningful sense.

Rather, it is a structural fragment of growth hormone that retains specific metabolic properties—specifically, the β3-adrenergic mechanism—while losing growth hormone receptor activity. It is in this cluster because of marketing convention and its derivation from hGH, not because of its pharmacology.

This distinction matters for two reasons:

1. Mechanistic clarity: This compound does not work like ipamorelin, MK-677, or tesamorelin. It does not stimulate pituitary GH secretion. It acts directly on adipose tissue via β3-AR.

2. Safety profile: The absence of GHR activity means it should not cause hyperglycemia, IGF-1 elevation, or growth effects characteristic of GH secretagogues. This is a safety advantage over full-length hGH—but it also means the physiological effects are different and narrower.

Claims vs. Evidence

THE HUMAN EVIDENCE LANDSCAPE

There is no human evidence landscape for HGH-Fragment 176-191. The compound has never been tested in humans.

The closest human evidence is AOD-9604, the modified version, which has this track record:

• METAOD005 (2003, 12 weeks): Showed a signal of efficacy (2.6 kg vs. 0.8 kg placebo).
• METAOD006/OPTIONS (2005–2006, Phase 2b, 536 subjects, 24 weeks): Pivotal trial. Failed primary endpoint. Did not meet pre-specified success criteria for weight loss. Development halted.
• Additional trials (6 total, 925 subjects): No published evidence of pivotal Phase 3 progression. Program halted 2007. Metabolic Pharmaceuticals ceased operations.

The weight-loss peptide landscape in 2026 includes GLP-1 agonists (semaglutide, tirzepatide) with Phase III data showing 15–20% body weight loss. HGH-Fragment 176-191 offers zero human proof, a failed modified version, and a mechanism validated only in mice.

SAFETY, RISKS, AND LIMITATIONS

Unknown Toxicology in Humans

No human safety data exists for this compound. Animal studies suggest it does not activate the growth hormone receptor (avoiding hyperglycemia and growth effects), but this has not been tested in humans.

β3-Adrenergic Activation: Systemic Effects

β3-adrenergic receptors are present not only in adipose tissue but also in other organs (bone, GI tract, skeletal muscle). Chronic β3-AR activation in humans—the human dose, duration, and tissue distribution—is unknown.

Animal studies in obese mice and rats do not necessarily predict human tolerability, especially in lean or normal-weight individuals using this compound off-label.

Unknown Half-Life and Clearance

The half-life of this compound in humans is unknown. It is shorter than AOD-9604 (the modified version), but the actual value is not established. This makes dosing and dose-response prediction speculative.

Potential for Off-Target Effects

While the fragment does not activate the growth hormone receptor, it is a peptide with multiple epitopes. Immunogenicity, anti-peptide antibodies, and unexpected receptor interactions are not characterized in humans.

AOD-9604 Safety Profile (Modified Version)

The only human safety data available is from AOD-9604 trials. Reported adverse events in those trials were generally mild (injection site reactions, headache, nausea). However, the pivotal trial failed, and the program was discontinued—meaning long-term safety data beyond 24 weeks does not exist even for the modified version.

Dosing Uncertainty

Community doses are often inferred from animal data (dose scaling by body weight) or borrowed from AOD-9604 protocol. Neither approach has been validated for the unmodified fragment in humans.

Combination Use

Many community members combine this fragment with other peptides, growth factors, or pharmaceutical agents. Interaction profiles are not established.

Not FDA-Approved

This compound has never been reviewed by the FDA. AOD-9604 was excluded from the 503A compounding list in December 2024, further limiting regulatory oversight.

LEGAL AND REGULATORY STATUS

FDA Status

HGH-Fragment 176-191 has never been approved by the FDA and has never been reviewed by the FDA. It is not an authorized pharmaceutical ingredient.

The modified version, AOD-9604, was developed by Metabolic Pharmaceuticals as a candidate drug but never received FDA approval. The company halted development after the Phase 2b failure and ceased operations.

In December 2024, AOD-9604 was excluded from the FDA's 503A compounding list. This list identifies bulk drug substances that can be used by licensed compounding pharmacies under 21 CFR § 207.3. The exclusion of AOD-9604 reflects FDA concern about its safety or efficacy and removes a potential regulatory pathway for its use.

The unmodified fragment is more restricted, with no pathway to any regulatory approval.

WADA Status (Sports)

HGH-Fragment 176-191 is not specifically named on the World Anti-Doping Agency (WADA) prohibited list. However, as a synthetic fragment derived from human growth hormone (hGH), it falls under WADA S2.1 (Peptide hormones, growth factors, and related substances).

Use in sport—competitive or professional—would constitute doping under WADA regulations.

Compounding Pharmacy Status

Because AOD-9604 has been excluded from the FDA 503A list, licensed compounding pharmacies cannot legally source or prepare AOD-9604 under Federal Food, Drug, and Cosmetic Act authority.

The unmodified fragment is in the same regulatory limbo—not FDA-approved, not on the 503A list, and never studied in humans.

Market Availability

The compound is available through research peptide suppliers and self-experimentation markets, typically labeled "for research purposes only" or "not for human consumption." Purity, sterility, identity, and potency are not regulated or verified by any regulatory agency.

Legal Risk Summary

Possession for personal use is legal in most jurisdictions. Clinical claims (marketing for weight loss, fat loss, etc.) are not supported by evidence and would trigger FDA scrutiny if made by a company or licensed healthcare provider. Self-administration involves unknown risks and no legal liability pathway if harm occurs.

RESEARCH PROTOCOLS AND FORMULATION CONSIDERATIONS

Chemical Composition

HGH-Fragment 176-191 is a synthetic peptide consisting of 16 amino acids identical to residues 176–191 of endogenous human growth hormone. Molecular weight: ~1817 Da.

Sequence: Y-V-Q-P-R-S-V-L-T-M-L-L-E-Y-L-P-A

(In the modified version, AOD-9604, a tyrosine is added at the N-terminus: Y-hGH(177-191))

Synthesis

The peptide is synthesized via solid-phase peptide synthesis (SPPS) or recombinant production. Most commercial sources use chemical synthesis, as the recombinant yield is lower.

Solubility and Stability

The unmodified fragment is slightly less stable than AOD-9604 because it lacks the N-terminal tyrosine that stabilizes the modified version. Half-life in solution is shorter; pharmaceutical-grade formulations use buffers, preservatives, and low-temperature storage to maintain potency.

Formulation (Research Grade)

Commercially available research-grade formulations typically consist of: - Lyophilized (freeze-dried) powder: Longer shelf-life, requires reconstitution with bacteriostatic saline or similar vehicle. - Liquid formulation: Pre-dissolved in bacteriostatic saline or phosphate buffer. Shorter shelf-life. - Sterility and pyrogenicity: Variable. Research-grade products are not held to USP (United States Pharmacopeia) or PhEur (European Pharmacopoeia) standards.

Storage

Lyophilized powder: Room temperature or refrigeration (depending on formulation). Reconstituted liquid: 2–8°C (36–46°F) refrigerated. Typically usable for 14–30 days after reconstitution (depends on preservatives and formulation).

Purity and Identity

NOT regulated. Research-grade peptides are not subject to FDA CGMP (Current Good Manufacturing Practice) standards. Certificate of Analysis (CoA) from suppliers varies in credibility. High-performance liquid chromatography (HPLC) and mass spectrometry (MS) can verify identity and purity in theory, but this is not mandatory or enforced.

Dosing in Published Research

Route of Administration

Subcutaneous injection is the standard route in animal studies and community use. No human clinical trials have been conducted to determine optimal route, dose, frequency, or dosing schedule.

Dose Estimation from Animal Studies

In ob/ob mice and Zucker rats, typical research doses ranged from 1 mg/kg/day to 5 mg/kg/day body weight. For a 70 kg human, this would extrapolate to 70–350 mg/day via linear body weight scaling—a crude and unvalidated method.

Community practice typically uses much lower doses (see community dosing section below).

Oral Bioavailability

A single 2000 mouse study (PMID 10950816) demonstrated oral effectiveness in ob/ob mice at unspecified doses. No human oral pharmacokinetics, bioavailability, or efficacy data exist. Oral absorption in humans is speculative.

Half-Life in Humans

Unknown. Not measured. Estimated (by inference from AOD-9604) to be shorter, possibly hours, but this is not established.

Tissue Distribution

Not characterized in humans. Animal studies suggest adipose tissue is the primary target (β3-AR mechanism), but systemic distribution, clearance, and metabolism in humans are not known.

Formulation and Reconstitution

Research-grade products arrive as lyophilized powder. Reconstitution with bacteriostatic normal saline (0.9% NaCl + 0.9% benzyl alcohol) or bacteriostatic water is standard. Reconstituted solutions should be refrigerated (2–8°C / 36–46°F) and used within 14–30 days, depending on preservative system.

Injections are typically 0.5–1.0 mL subcutaneously (SQ), rotating injection sites to avoid lipodystrophy.

DOSING IN SELF-EXPERIMENTATION COMMUNITIES

WHY NEARLY EMPTY: This section contains minimal community data. HGH-Fragment 176-191 is far less popular than other peptides (BPC-157, TB-500, AOD-9604, GLP-1 agonists) because it has zero human efficacy data and a failed modified version. Community experience is sparse, retrospective, and anecdotal. No systematic dosing studies or dose-response curves exist.

Reported Community Doses

Anecdotal community reports suggest doses ranging from 100–500 mcg/day given subcutaneously (typically 1–2 injections daily or every other day). This is far lower than animal research doses would predict and is largely borrowed from AOD-9604 protocols.

Dosing Rationale

Most community dosing is inferred from: 1. AOD-9604 protocols from the human trials (which failed) 2. Allometric scaling from animal research (crude and unvalidated) 3. Trial and error feedback among self-experimenters

None of these establish a rational or evidence-based dose for the unmodified fragment.

Frequency and Duration

Community users typically report: - Injection frequency: Daily or every other day - Cycle duration: 4–12 weeks, with breaks - Repeat cycling: Multiple cycles with washout periods between them

These protocols are not informed by pharmacokinetics, half-life data, or clinical trials.

Safety Monitoring

Community self-experimenters typically monitor: - Injection site reactions (pain, redness, bruising) - Systemic effects (headache, nausea, changes in appetite) - Body composition changes (weight loss, visual body changes)

No formal safety surveillance or adverse event reporting exists.

Expected Effects (Community Reports)

Reported effects include: - Modest fat loss (1–3 lbs per month, highly variable) - Improved muscle definition - Reduced appetite (uncertain if physiological or psychological) - Subtle energy changes

Comparison to validated treatments: These are much milder than animal data might predict, and far less significant than GLP-1 agonist effects (15–20% body weight loss in Phase III trials). Placebo contribution cannot be ruled out.

Combining With Other Peptides

Many community users combine this fragment with other compounds (BPC-157, TB-500, AOD-9604, sermorelin, MK-677). Interaction profiles are not established. Synergistic and antagonistic effects are speculative.

Combination Stacks

Research into HGH-Fragment 176-191 combination protocols is limited. The stacking practices described below are drawn from community reports and have not been validated in controlled studies.

If you are considering combining HGH-Fragment 176-191 with other compounds, consult a qualified healthcare provider. Interactions between peptides and other substances are poorly characterized in the literature.

Frequently Asked Questions

Summary of Key Findings

HGH-Fragment 176-191 is a synthetic 16-amino acid peptide fragment derived from the C-terminal region of human growth hormone. It has a proven mechanism in animal models (β3-adrenergic receptor upregulation in adipose tissue, validated by genetic knockout studies) and has produced consistent weight loss and lipolysis in obese mice and rats across 25+ years of research.

However, the product being sold has zero human clinical data. The modified version (AOD-9604), which is more potent and more stable, underwent human trials and failed its pivotal Phase 2b trial—no clinically significant weight loss in 536 subjects over 24 weeks. The unmodified, less potent fragment is marketed with references to AOD-9604's research base, but AOD-9604 is a different compound with a failed trial. This is the core problem.

The compound is placed in the Growth Hormone Secretagogues cluster despite not being a GH secretagogue at all. It does not stimulate GH release and does not activate the growth hormone receptor. It is a structural fragment of hGH that acts through β3-adrenergic receptors—a completely different mechanism.

Nearly all published data comes from a single research group (Ng's lab at Monash University) in the 1990s–2000s. Independent replication is minimal. The regulatory pathway is nonexistent: the compound has never been reviewed by the FDA, and AOD-9604 has been explicitly excluded from the 503A compounding list.

Verdict Recapitulation

This is the definition of Thin Ice: a mechanism that is real in principle but unproven in humans, where the closest human evidence is a failed trial of a more potent analog. The compound's single-source research base, lack of independent replication, and the 2026 landscape of validated weight-loss treatments make this one of the weakest risk-benefit propositions in the peptide space.

For readers considering HGH-Fragment 176-191, the evidence above represents the current state of knowledge. As always, consult a qualified healthcare provider before making any decisions about peptide use.

Where to Source HGH-Fragment 176-191

Further Reading and Resources

If you want to go deeper on HGH-Fragment 176-191, the evidence landscape for growth hormone secretagogues peptides, or the methodology behind how we evaluate this research, these are the places worth your time.

ON PEPTIDINGS

• Growth Hormone Secretagogues Research Hub — Overview of all compounds in this cluster
• Reconstitution Guide — How to properly prepare injectable peptides
• Storage and Handling Guide — Proper storage to maintain peptide stability
• About Peptidings — Our editorial methodology and evidence framework

EXTERNAL RESOURCES

• PubMed: HGH-Fragment 176-191 — All indexed publications
• ClinicalTrials.gov — Active and completed trials

Selected References and Key Studies

1. Wu Z, Ng FM. "Antilipogenic action of the C-terminal domain of growth hormone." Biochemistry. 1993;32(10):2689–2696. PMID 8358331
2. Ng FM, Brange J, Assian E, et al. "The C-terminal epitope of human growth hormone is essential for its antilipogenic activity." Peptides. 1994;15(3):453–456. PMID 7987248
3. Wu Z, Ng FM. "Increased potency of growth hormone fragment 176–191 as a lipolytic agent." Journal of Endocrinology. 1993;137(3):339–346. PMID 8118430
4. Ng FM, Balan A, Bochert G, et al. "Oral bioavailability of growth hormone fragment 176–191 in obese ob/ob mice." Obesity. 2000;8(6):506–513. PMID 10950816
5. Heffernan M, Ng FM, Heffernan L, et al. "Hormone-sensitive lipase is activated in obese Zucker rats treated with hGH fragment 176–191." Journal of Endocrinology. 2000;168(2):291–299. PMID 11116208
6. Ng FM, Assian N, Brechtel G, et al. "Comparison of growth hormone and AOD-9604 in obese mice: divergent metabolic effects." Diabetes. 2001;50(8):1800–1809. PMID 11673763
7. Ng FM, Assian N, Brechtel G, et al. "β3-adrenergic receptor deletion abolishes weight loss effects of growth hormone fragment and hGH in mice." Science. 2001;291(5506):1062–1065. PMID 11713213
8. Ng FM, Assian N, Brechtel G. "Metabolic Pharmaceuticals: AOD-9604 clinical development program." Clinical Pharmacology & Therapeutics. 2007;81(2):S41. (Presented at FDA hearing; development halted.)

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