MetabolicTyr-hGH 177-191AOD9604

AOD-9604

Modified GH lipolytic fragment · metabolic / fat loss

AOD-9604 is a small 16-amino-acid peptide built from the tail end of human growth hormone (the C-terminal 'lipolytic' fragment, residues 177-191) with an extra tyrosine added. The idea behind it is appealing: isolate just the fat-burning piece of growth hormone, without the parts that raise IGF-1, blood sugar, or drive general growth. In obese rodents that idea worked — oral AOD-9604 reduced fat gain and increased fat breakdown without harming insulin sensitivity. What makes this compound unusual, and worth telling honestly, is that its central promise was actually put to the test in people. Metabolic Pharmaceuticals ran six randomized, double-blind, placebo-controlled human trials, and the peptide came out genuinely safe and well tolerated — no rise in IGF-1, no impairment of glucose handling, no immune reaction. But the trial that mattered, a 24-week Phase II obesity study in over 500 adults, failed to produce more weight loss than placebo, and the company discontinued obesity development in 2007. So the honest picture is the reverse of the marketing: AOD-9604's safety is well-documented, while its fat-loss benefit in humans is documented to have failed. It is not approved as a drug anywhere, was flagged by the FDA as a compounding safety concern, is unregistered for human use in Australia, and is banned in sport by WADA.

The short version

AOD-9604 is a short peptide — 16 amino acids — copied from the very end of the growth-hormone molecule. Scientists had noticed that this tail region is the part of growth hormone most responsible for breaking down fat, so the plan was to make a drug out of just that piece and leave behind the parts of growth hormone that raise blood sugar and IGF-1.

In fat rats and mice, the plan worked: given by mouth, AOD-9604 lowered fat gain and stepped up fat breakdown, and it did so without the blood-sugar problems that full growth hormone causes.

The unusual and important part is that, unlike most research peptides, AOD-9604 actually got tested properly in humans — six placebo-controlled clinical trials. The good news from those trials is real: it was safe and well tolerated, it did not raise IGF-1, and it did not mess with blood sugar.

The catch is the headline result. The big trial designed to prove it causes weight loss — about 500 adults over 24 weeks — did not beat a placebo, and the company stopped developing it for obesity in 2007. So when you see AOD-9604 marketed as a proven fat-loss peptide, the honest reading is the opposite: its safety held up, but its fat-loss benefit in people did not.

Molecular identity

Specs

Molecular formula: C78H123N23O23S2
Molecular weight: 1,815.1 g/mol
Monoisotopic mass: 1,813.86 Da
CAS / UNII: 221231-10-3 · 7UP768IP4M

Compound class: Peptide — modified hGH C-terminal lipolytic fragmentPubChem CID 71300630
Amino-acid sequence: Tyr-Leu-Arg-Ile-Val-Gln-Cys-Arg-Ser-Val-Glu-Gly-Ser-Cys-Gly-Phe (16 aa; Cys7–Cys14 disulfide)PubChem CID 71300630
Parent fragment: Human GH 177-191 (lipolytic C-terminal domain) + N-terminal TyrStier et al. 2013, J Endocrinol Metab
Molecular target: No direct receptor; lipolytic action not β3-AR-mediated (modulates β3 expression)PMID 11713213
Half-life: ~3 min (pig IV plasma); no published human half-life despite six human trialsMoré & Kenley 2014, J Endocrinol MetabHalf-life curve →
Regulatory status: Not approved any country; obesity development discontinued 2007Research / developer record
US compounding status: FDA 503A Category 2 (significant safety concerns) 2023; removed 2024 on nominator withdrawalFDA interim 503A bulk-substances list
Anti-doping status: Prohibited at all times (WADA: S0 in the 2013 statement; now explicitly named under S2, GH fragments)WADA Prohibited List / WADA 2013 statement

Plain English

Mechanism

Growth hormone has long been known to break down fat, and research traced much of that fat-burning activity to its C-terminal tail. AOD-9604 is an engineered version of that tail — the fragment spanning residues 177-191 of human growth hormone, with a tyrosine added at the front. The design goal was to keep the lipolytic (fat-breakdown) and anti-lipogenic (fat-storage-blocking) actions of growth hormone while discarding the parts that drive IGF-1 release, raise blood glucose, and promote general tissue growth.

The animal evidence supports that separation. In obese Zucker rats, oral AOD-9604 reduced body-weight gain by more than half over 19 days and increased fat-tissue lipolytic activity (the rate at which fat is broken down) — and, importantly, a euglycemic clamp (a lab test that holds blood sugar steady to measure how well insulin works) showed no adverse effect on insulin sensitivity, in contrast to full growth hormone. This is the core mechanistic claim: fat mobilization without growth hormone's metabolic downside, demonstrated in rodents.

A common shorthand says AOD-9604 works through the β3-adrenergic receptor (a fat-cell switch that, when activated, tells the cell to burn fat), but the primary data are more careful than that. In obese mice, both growth hormone and AOD-9604 raised β3-adrenergic-receptor expression (the number of those switches the cells make) — yet in β3-receptor knockout mice (animals genetically engineered to lack that receptor) the chronic fat-loss effect was lost while an acute (short-term) rise in energy expenditure (calories burned at rest) persisted. The researchers concluded that the lipolytic action is not mediated directly through the β3 receptor, even though the compound increases β3-receptor expression. So the accurate statement is that AOD-9604 modulates β3-receptor expression, not that it acts on the receptor as its target.

In humans, the part of the mechanism that did hold up is the 'clean' profile: across the clinical program AOD-9604 produced no rise in serum IGF-1 and no impairment of glucose handling, consistent with the design intent. What did not hold up was the downstream payoff — that this fat-mobilizing mechanism would translate into meaningful weight loss in people.

Sources:PMID 11146367 PMID 11713213 DOI 10.4021/jem157w

Why people reach for it

Potential benefits

AOD-9604 is unusual: its central fat-loss promise was actually tested in humans — and didn't pan out. So the honest appeal is the inverse of the marketing, led by what the trials genuinely showed.

A genuinely clean safety record — Its real, well-documented strength: across six randomized, placebo-controlled human trials it was well tolerated and indistinguishable from placebo — no immune reaction, no serious adverse events.
No IGF-1 rise — the design held — Unlike full growth hormone, it produced no increase in IGF-1 across the human program, confirming the intent to keep the fat-related signaling without GH's growth-promoting baggage.
No blood-sugar penalty — It showed no impairment of glucose handling in the human trials — the metabolic downside people worry about with growth hormone stayed clean.
A targeted lipolytic concept — It isolates the C-terminal lipolytic fragment of growth hormone, and in obese rodents that fragment reduced fat gain and raised fat breakdown — the idea people pursue it for, demonstrated in animals.
Pairs into GH-axis routines — Because it carries no IGF-1 or glucose effect, people slot it alongside GH secretagogues like CJC-1295 + Ipamorelin or Tesamorelin — though any added fat-loss benefit is reasoned, not shown.

Sources:DOI 10.4021/jem157w PMID 11146367 PMID 11713213

What people reach for AOD-9604 for, based on what the research reports and how it's used — not proven human outcomes or medical claims. Be clear-eyed: its safety is well-documented, but its fat-loss benefit in people is documented to have failed its pivotal trial.

Implied timing

Best time to dose

Implied best time

Morning, fasted (or pre-cardio)

Most people take AOD-9604 first thing in the morning on an empty stomach, sometimes right before fasted cardio.

The convention is fasted because insulin blunts fat-mobilizing (lipolytic) signaling — an empty-stomach dose is meant to ride the body's natural overnight fat-burning window rather than fight a post-meal insulin spike.
A morning, pre-cardio dose lines the lipolytic concept up with a fasted training session, when free fatty acids are most available to burn — the same logic used across GH-fragment protocols.
There's no published human pharmacokinetics to pin a clock to, so the timing is mechanism-and-habit reasoning, not a measured optimum — and the honest caveat is that the human trial failed even with structured dosing, so timing is unlikely to be the deciding factor.
Practically, people wait roughly 15–30 minutes after the injection before eating, to keep insulin low around the dose.

No study establishes an ideal time of day for AOD-9604 — this is reasoned from its lipolytic mechanism and how it's used, not a measured schedule. Most peptide dosing defaults to the midday-to-evening window, but for a fasted fat-loss fragment the lean is the morning, on an empty stomach.

Sources:DOI 10.4021/jem157w

How to run it

Dosing & protocol

AOD-9604 is dosed here as a subcutaneous injection — the research-peptide form the calculator is built for. Before the numbers: its pivotal human obesity trial (≈502 adults, 24 weeks) did not beat placebo for fat loss, and obesity development was discontinued in 2007. That means there is no proven effective human dose. The figures below are community-and-practitioner convention, built from the calculator pre-fill and informal practice — not from a trial that showed they work.

Community convention on a failed-efficacy compound: AOD-9604 is not approved anywhere, its Phase IIb fat-loss trial did not beat placebo, and it is prohibited in sport at all times (WADA S2). Every number here is a usage pattern, not evidence of effect.

Tiered dose ranges

Community convention organizes AOD-9604 SubQ doses into two informal tiers.

Standard:: 300 mcg once daily SubQ — the most common convention, taken on an empty stomach. This is the calculator default; it sits far below the multi-milligram oral doses used in the human safety trials, where efficacy was not demonstrated.
Higher range:: Up to 500–600 mcg once daily SubQ — sometimes used by those who have run the standard dose without effect; convention only, no trial supports the increase in outcome.

Subcutaneous administration

AOD-9604 is injected into subcutaneous fat; site, timing, and the food window are the actionable choices.

Injection site:: Abdomen (a couple of inches clear of the navel), love-handle area, or outer thigh. Rotate sites between doses to prevent local irritation and lipohypertrophy (fatty lumps from repeated injection in one spot).
Measuring the dose:: Drawn on a U-100 insulin syringe from the reconstituted vial. At the standard mix (5 mg vial + 2 mL bacteriostatic water = 2,500 mcg/mL): 300 mcg = 12 IU. The on-page calculator handles any vial size.
Time of day:: Fasted, first thing in the morning is the most common convention — rationale being that insulin blunts lipolytic signaling, so an empty-stomach injection maximizes any fat-mobilizing window the compound might have. The caveat: the human trial failed even with structured dosing, so the timing is convention, not demonstrated to matter.
Food window:: Wait 15–30 minutes after injection before eating; the community reasoning is minimizing an insulin spike around the dose. No human PK data support a specific interval.

Cycle & washout

AOD-9604 is typically run as a defined block rather than indefinitely — the animal work used 14–19-day continuous dosing; community cycles extrapolate from there.

Standard cycle:: 8–12 weeks of daily dosing. The human obesity trial ran 24 weeks and found no benefit over placebo, so longer is not substantiated by outcome data.
Washout:: 4 weeks off between cycles. Because the compound's GH-fragment class is prohibited in sport at all times (WADA S2), athletes should not run it at all.
The honest expectation:: The trial that ran long enough to detect fat loss in humans found none. Any cycle is therefore run on hope of individual response, not on evidence of fat-loss efficacy in the population studied.

Reconstitution at a glance

Mixing math only — the on-page calculator does this live. Quick reference for the standard 5 mg vial:

Mixing:: 5 mg vial + 2 mL bacteriostatic water = 2,500 mcg per mL. On a 100-unit (1 mL) insulin syringe: 300 mcg = 12 IU · 500 mcg = 20 IU · 600 mcg = 24 IU.
Why 2 mL into a 5 mg vial:: Keeps the concentration moderate so you're drawing a practical syringe volume — not a near-invisible 2–3 IU that's hard to measure accurately.

Sources:PMID 11146367 DOI 10.4021/jem157w

Substrate the signal needs

Nutritional cofactor precision

AOD-9604 is marketed for fat loss — but its pivotal Phase IIb human trial did not beat placebo, and obesity development was discontinued in 2007. That failure reframes the cofactor question entirely: the things that actually drive fat loss in a controlled human setting are the 'cofactors' here — calorie deficit, protein, resistance training. They do the work the compound didn't. These cards name what to do and how much; no nutrient rescues efficacy the trial didn't show.

Fat-loss physiology, not an AOD-9604 nutrition study. Every item below is evidence-based for fat loss as a process — none is evidence that AOD-9604 works. This is the honest read on a failed-efficacy compound: the inputs matter, the compound's own RCT did not.

The honest baseline — calorie deficit (what actually drives fat loss)

The trial that ran long enough to detect fat loss in 502 humans found none over placebo. A sustained calorie deficit is the variable the trial held equal and the one that actually moves body weight.

Target:: A deficit of roughly 300–500 kcal/day is the range that produces consistent fat loss while being sustainable; larger cuts accelerate muscle loss and increase dropout.
Why this card exists:: Because AOD-9604 didn't beat placebo, the single highest-yield 'cofactor' is the dietary change the peptide was supposed to make unnecessary. Run the deficit first; the compound does not substitute for it.

Protein + resistance training (lean-mass preservation)

When calories drop, some loss comes from muscle. Protein and resistance exercise are the well-established levers that keep the weight loss fat, not lean mass.

Protein target:: 1.6–2.0 g per kilogram of body weight per day (about 0.7–0.9 g/lb) — the range consistently shown to preserve lean mass during a calorie deficit. Prioritize this before any other supplement.
Resistance training:: At least 3 sessions per week of compound lifts or resistance-band work. This is not a 'cofactor to AOD-9604' — it is the independent driver the compound trial failed to replicate through peptide action alone.
Protein + fiber for satiety:: Protein and dietary fiber blunt hunger and make the deficit sustainable — the mechanism behind GLP-1-class drug success. Eat them at every meal.

Electrolytes + micronutrient support (calorie-cut basics)

On a calorie cut, water and mineral shifts are real and predictable; these are the inputs that prevent the diet from feeling worse than it needs to.

Electrolytes:: Sodium 1,500–2,300 mg, potassium 2,000–3,500 mg, magnesium 300–400 mg — offset the shifts that come with eating and carbohydrating less. Most people on a cut feel better within 48 hours of addressing these.
Sleep:: 7–9 hours. Appetite-regulating hormones (ghrelin, leptin) are directly impaired by sleep restriction — adherence to the deficit breaks down in practice before the body composition math does.
Honest frame:: No electrolyte or micronutrient rescues a failed efficacy endpoint. Everything in this card supports the calorie-deficit process — the thing the trial showed matters.

Combinations + timing

Stacking notes + timing windows

Any stack built around AOD-9604 inherits its core problem: the compound's fat-loss efficacy failed in a proper Phase IIb human trial. Naming a stack partner doesn't fix that. The cards below are community pairings reasoned from mechanism — they are named because users combine them, not because any trial showed the combination works.

User combinations on a failed-efficacy compound — doubly unproven. AOD-9604 did not beat placebo for fat loss; none of its stack partners rescues that finding. Community convention only.

AOD-9604 + Tesamorelin

The GH-axis pairing — AOD-9604 for the C-terminal lipolytic fragment, Tesamorelin for direct GHRH-receptor stimulation of GH pulse.

Why it works (the reasoning):: Tesamorelin has actual Phase III RCT evidence for visceral fat reduction in HIV-associated lipodystrophy — one of the few peptides with a real human efficacy result in a fat-related endpoint. Pairing it with AOD-9604 (which lacks that result) adds the fragment on the hope of additive fat-mobilizing action from two different GH-axis angles. The reasoning is mechanistically plausible; the combination is not studied.
The protocol:: Tesamorelin 2 mg SubQ once daily at bedtime (its established dosing from the clinical program); AOD-9604 300 mcg SubQ in the morning fasted. Two separate injections, different times of day, different sites.
Outcome:: Reached for by users targeting visceral or abdominal fat. Honest caveat: Tesamorelin carries its evidence on its own; AOD-9604 adds a mechanistically plausible fragment whose own trial was negative. The pairing is not additive in any demonstrated way.

AOD-9604 + CJC-1295 (no DAC) / Ipamorelin

The GH secretagogue combination — CJC-1295 + Ipamorelin stimulate endogenous GH release; AOD-9604 adds the isolated C-terminal lipolytic fragment.

Why it works (the reasoning):: CJC-1295 (GHRH analog) + Ipamorelin (GHRP) together produce a synergistic GH pulse; the combination is the most common GH-secretagogue stack in the community. AOD-9604 is added on the logic that the C-terminal fragment might contribute independent lipolytic signaling on top of the full-GH pulse. Whether the fragment adds anything to an already-elevated GH state is unknown.
The protocol:: CJC-1295 no-DAC 100 mcg + Ipamorelin 100 mcg, co-injected SubQ at bedtime; AOD-9604 300 mcg SubQ in the morning fasted. Keep them on separate schedules — the secretagogue pair is timed to the overnight GH pulse window, the fragment to a fasted morning window.
Outcome:: Community fat-loss and body-recomposition stack. Honest caveat: the secretagogue pair drives whatever GH-mediated fat mobilization occurs; AOD-9604's independent contribution is undemonstrated since its own trial was negative.

AOD-9604 + Fragment 176-191

The fragment family pair — Fragment 176-191 is the bare C-terminal core that AOD-9604 was built from; its fat-loss reputation is largely borrowed from AOD-9604's animal work.

Why this card needs a honesty note first:: Fragment 176-191 (hGH residues 176-191, without AOD-9604's N-terminal tyrosine) is a different molecule. Its fat-loss marketing draws on the same rodent lipolysis story as AOD-9604 — but Fragment 176-191 never ran the Phase IIb human trial that AOD-9604 ran and failed. The pairing stacks two molecules from the same unproven family; neither has human fat-loss efficacy.
The protocol:: If combining: AOD-9604 300 mcg + Fragment 176-191 200–300 mcg, both SubQ in the morning fasted, drawn separately or as nearby-site injections. Community doses only — no human efficacy trial for either.
Outcome:: Reached for by users exploring the GH C-terminal fragment space. Read it as convention built on a family resemblance, not as two confirmed fat-loss compounds stacked together.

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

On safety, AOD-9604 has a genuinely reassuring and well-documented record — which is the honest positive of the page. Across six randomized, double-blind, placebo-controlled human trials (the gold-standard study design, in which neither the participants nor the researchers know who got the real compound versus a dummy), its safety and tolerability were indistinguishable from placebo: no rise in IGF-1, no negative effect on glucose tolerance (blood-sugar handling), no anti-drug antibodies (immune proteins the body makes against a foreign substance) detected, and no treatment-related serious adverse events or withdrawals.

The critical framing is that this is a tolerability finding, not an efficacy (whether it actually works) finding. 'Safe and well tolerated' is true and meaningful, but it is not the same as 'works.' The pivotal obesity trial showed the compound was safe while failing to deliver the weight loss it was designed to produce.

It is not approved as a medicine in any country and all human development for obesity was discontinued in 2007. In the United States the FDA placed AOD-9604 in Category 2 of its interim 503A bulk-compounding list in 2023 — 503A is the rule that governs which raw substances pharmacies may compound (mix to order) into medicines, and Category 2 is the bucket for substances raising significant safety concerns (citing issues such as immunogenicity risk — the chance the body mounts an immune reaction against it — and limited human safety data); it was removed from that list in 2024 because the nominator withdrew the nomination, not because it was cleared. In Australia it is not registered for human use. This page presents the research literature only and makes no therapeutic claims.

Sources:DOI 10.4021/jem157w FDA 503A bulk-substances list

As reported in literature

Research dosing ranges

These are the doses actually used in the published studies — the evidence the practical figures above lean on, shown separately so research data is never mistaken for a proven human dose. There is no approved therapeutic dose for AOD-9604: it is not approved as a drug in any country, and obesity development was discontinued in 2007, so this page makes no dosing or how-to recommendation. What follows is the published evidence base — the animal models and the human clinical program in which the compound was actually studied, including the routes and dose ranges tested and what they showed. The single most important entry is the last one — the human efficacy trial that did not beat placebo.

Dose	Route	Model	Outcome	Sources:
500 µg/kg, oral, 19 days	Oral	Obese Zucker rats	Reduced body-weight gain by >50% and increased adipose lipolytic activity; a euglycemic clamp showed no adverse effect on insulin sensitivity (unlike full growth hormone)	PMID 11146367
Chronic, 14 days	Injection	Obese mice + β3-receptor knockout mice	Both growth hormone and AOD-9604 reduced body weight/fat and raised β3-receptor expression; the chronic effect was LOST in β3-knockout mice, while an acute rise in energy expenditure persisted — lipolysis is not mediated directly via the β3 receptor	PMID 11713213
25–400 µg/kg, single dose	Intravenous	Humans (placebo-controlled)	Well tolerated; no rise in serum IGF-1; no impairment of glucose tolerance	DOI 10.4021/jem157w
0.25–54 mg/day, multiple-dose	Oral	Humans (placebo-controlled)	Safety and tolerability indistinguishable from placebo; no anti-drug antibodies; no treatment-related serious adverse events	DOI 10.4021/jem157w
Oral, ~24 weeks	Oral	Phase IIb obesity trial (~502 randomized adults)	FAILED its primary endpoint — produced no greater weight loss than placebo; obesity development was discontinued in 2007. (This pivotal 24-week failure was never published as a peer-reviewed, PubMed-indexed trial; only the earlier, positive 12-week study appeared, as a 2005 conference abstract.)

Labs before / during / after

Cofactor blood markers to track

The most useful and well-documented marker finding for AOD-9604 is a negative one, and it is genuinely to the compound's credit: across the human clinical program it produced no rise in serum IGF-1 (insulin-like growth factor 1 — the blood hormone through which growth hormone drives most tissue growth). That confirms the design intent — it does not act through the IGF-1 pathway the way full growth hormone does, which is the basis for the claim that it carries less of growth hormone's growth-promoting and metabolic baggage.

It likewise showed no impairment of glucose tolerance or carbohydrate metabolism (how well the body handles blood sugar) in the human trials — again a favorable, honest finding. In short, the markers you would worry about with growth hormone (IGF-1, blood sugar) stayed clean with AOD-9604. The important caveat is that a clean marker profile is a safety/mechanism observation, not evidence of fat-loss benefit — which is precisely where the human efficacy trial fell short.

Sources:DOI 10.4021/jem157w

Quick answers

Frequently asked

Does AOD-9604 cause weight loss in people?

Not in the trial built to prove it. AOD-9604 lowered fat in obese rodents, and that is real — but its pivotal human obesity trial (about 500 adults over 24 weeks) failed to produce more weight loss than placebo, and the developer discontinued obesity development in 2007. It is one of the few peptides whose fat-loss marketing claim was actually tested in a proper human trial and did not pan out.

Is AOD-9604 safe?

Its safety record is actually its strongest point. Across six placebo-controlled human trials it was well tolerated and indistinguishable from placebo, with no rise in IGF-1, no impairment of blood sugar, and no immune reaction. The honest distinction is that 'safe' is well-documented while 'effective for fat loss' is documented to have failed. It is still not an approved drug, and the FDA has flagged the peptide class for safety concerns in compounding.

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

AOD-9604 is a modified version of that fragment. It is the growth-hormone C-terminal lipolytic region (residues 177-191) with an extra tyrosine added at the front (Tyr-hGH 177-191). The added tyrosine is a synthetic modification, not part of natural growth hormone at that position. AOD-9604 is the molecule that actually carried a clinical development program; the plain fragment did not.

Does AOD-9604 work through the β3 fat-burning receptor?

Not directly, despite the common claim. In knockout-mouse experiments the lipolytic effect did not require the β3-adrenergic receptor, even though AOD-9604 (like growth hormone) raises the receptor's expression. The accurate statement is that it modulates β3-receptor expression, not that the β3 receptor is its target.

Is AOD-9604 approved or legal to use?

It is not approved as a medicine in any country — human development was discontinued in 2007. In the US the FDA placed it in a 'significant safety concerns' category for compounding in 2023 (removed in 2024 only because the nomination was withdrawn). In Australia it is not registered for human use. It is also prohibited in sport at all times under the WADA Prohibited List: WADA's 2013 statement classified it under S0 (non-approved substances) because it was not yet explicitly listed, and it is now explicitly named as a growth-hormone fragment under S2 (peptide hormones).

Primary sources

References

PubChem CID 71300630PubChem CID 71300630 (AOD-9604; C78H123N23O23S2, ~1815.1 g/mol; CAS 221231-10-3)
PMID 11146367Ng et al., Horm Res 2000 (synthetic lipolytic domain AOD9604: weight gain ↓>50% in obese Zucker rats; no insulin-sensitivity penalty)
PMID 11713213Heffernan et al., Endocrinology 2001 (hGH & AOD9604 in obese mice + β3-AR knockouts; lipolysis NOT directly β3-mediated)
DOI 10.4021/jem157wStier, Vos & Kenley, J Endocrinol Metab 2013 (human safety across six placebo-controlled trials: well tolerated, no IGF-1 rise, no glucose impairment, no immunogenicity)
FDA 503A bulk-substances listFDA — Interim policy on 503A bulk drug substances (AOD-9604 placed in Category 2, significant safety concerns, 2023; removed 2024 on nominator withdrawal)
WADA Prohibited List, S2 / 2013 statementWADA Prohibited List — prohibited at all times (S0 non-approved substances per the 2013 WADA statement; now explicitly named as a GH fragment under S2, peptide hormones)

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