Reference

Last reviewed: 29 Apr 2026
Sources cited: 6

Compound class1,815 Da

Modified C-terminal fragment of human growth hormone (residues 177–191) — adipocyte-targeted lipolytic peptide

16-amino-acid synthetic peptide based on human GH residues 177–191 with an N-terminal tyrosine cap and an intramolecular disulphide bridge between Cys⁷ and Cys¹⁴. The disulphide bridge constrains the molecule shape and the standard 3-letter sequence parser does not handle disulphide-bridged peptides correctly; fallback used for accuracy.

AOD-9604

Last verified: 2026-04-29

At a glance


Also known as	HGH Fragment 176-191, AOD9604, AOD, h-GH C-terminal fragment
Class	Modified C-terminal fragment of human growth hormone (residues 177–191), engineered with a tyrosine cap; positioned as a lipolytic peptide that does not produce HGH-class metabolic effects
Typical route	Subcutaneous injection, daily
Half-life	~30 minutes (terminal); per-dose effect window 1–4 hours
Molecular weight	1,815 Da (16-residue modified fragment)
Sequence	Tyr-Leu-Arg-Ile-Val-Gln-Cys-Arg-Ser-Val-Glu-Gly-Ser-Cys-Gly-Phe (16 amino acids — residues 177–191 of human GH plus an N-terminal tyrosine cap; intramolecular disulphide between Cys⁷ and Cys¹⁴)
UK status	Not approved as a medicine. Sold as a research chemical.
US status	Not FDA-approved. Was nominated for inclusion on the FDA 503A bulks list and removed from Category 2 in September 2024 (alongside ipamorelin, CJC-1295, thymosin α-1, selank). PCAC review pending. Not DEA-controlled.

What it is

AOD-9604 is a 16-amino-acid synthetic modification of the C-terminal end of human growth hormone (residues 177–191), with an extra tyrosine added to the N-terminus to improve stability. It was developed by Metabolic Pharmaceuticals (Australia) in the late 1990s and early 2000s, originally as an obesity drug candidate based on preclinical work showing that the natural HGH(177–191) C-terminal fragment retains the lipolytic effects of full-length GH without the broader metabolic effects (no IGF-1 elevation, no glucose dysregulation, no GH-receptor binding).

The key claim that drove its development is mechanistically interesting: AOD-9604 does not activate the growth hormone receptor and does not produce the IGF-1, insulin-resistance, or growth-promoting effects that distinguish HGH and the GH-secretagogue cluster. Instead, it acts via a separate pathway — beta-3 adrenergic receptor stimulation in adipocytes — to drive lipolysis without the broader hormonal cascade.

The pharmacology is genuinely distinct from the GH cluster (ipamorelin, CJC-1295, sermorelin, tesamorelin, MK-677). All those compounds work through GH/IGF-1 elevation; AOD-9604 specifically does not. This is the central reason it appears in this encyclopedia: it’s a fat-loss peptide that uses the GH-fragment idea without the GH-axis activation.

The clinical reality is harder than the mechanism. AOD-9604 ran six human clinical trials with over 900 participants and failed to meet efficacy endpoints in its largest Phase IIb obesity trial. Metabolic Pharmaceuticals discontinued development in 2007. The compound entered the research-chemical and biohacker market with a “lipolytic peptide” framing that the registrational trials did not support — a meaningful gap between the marketed claims and the trial outcomes that any reader should understand before using it.

Mechanism

AOD-9604 is structurally derived from the C-terminal end of human growth hormone, residues 177–191, modified with an N-terminal tyrosine cap and an intramolecular disulphide bridge between Cys⁷ and Cys¹⁴ that constrains the molecule’s shape. It does not bind the growth hormone receptor or activate the JAK-STAT signalling cascade that HGH triggers.1 5

The proposed mechanism in adipose tissue:

Activates beta-3 adrenergic receptors on adipocytes
Stimulates hormone-sensitive lipase, which hydrolyses triglycerides into free fatty acids
Inhibits lipogenesis (reduces new fat formation) in addition to driving lipolysis
Effect is selective for adipose tissue — does not produce IGF-1 elevation or affect glucose handling

The mechanism is plausible and is supported by preclinical work in obese mice (50% greater weight loss than placebo over 19 days in genetically obese rodent strains). The preclinical-to-clinical translation failed: human trials did not reproduce the rodent fat-loss magnitude.

The decoupling from the GH receptor matters editorially. Users coming from the GH cluster (ipamorelin, CJC-1295, sermorelin, tesamorelin) are familiar with the GH/IGF-1 mechanism and the cancer/insulin resistance concerns it carries. AOD-9604 explicitly does not produce those effects — which is both the source of its safety advantage over the GH cluster and the source of its weaker effect, because the GH/IGF-1 pathway is what drives much of the GH cluster’s body-composition signal.

Routes of administration

Subcutaneous injection (the standard route)


Bioavailability	Sufficient for the documented lipolytic mechanism
Onset	Lipolytic effect begins within 1–2 hours; subjective fat-loss effects accumulate over 8–12 weeks
Duration	1–4 hours per dose
Typical dose (this route)	250–500 mcg subQ daily
Equipment	Insulin syringe (29G–31G, U-100), bacteriostatic water, alcohol wipes
When this route makes sense	Default. All clinical data and community use is subQ.

Morning fasted dosing is the dominant pattern, often timed before fasted cardio or training. The reasoning is mechanistic — lipolysis on top of an already-elevated catecholamine state from fasted exercise produces the largest acute fatty acid release. Whether this translates to greater body-composition outcomes over weeks is not directly established.

Oral (the original aspiration; abandoned)

AOD-9604 was originally developed and trialled as an oral formulation — Metabolic Pharmaceuticals positioned it as the first orally-active GH-derived fat-loss compound. Bioavailability was insufficient for reliable effect; subcutaneous injection became the practical route. Some research-chem vendors sell oral capsules; these have negligible expected bioavailability and are not used in serious community protocols.

Intramuscular, sublingual, intranasal

Not viable. SubQ is the only meaningful route in current use.

Cross-route comparison

SubQ at morning is the standard. Oral was tried and abandoned by the original developer; sticking with subQ matches the dose protocols and the trial work.

What the evidence says

Honest summary: AOD-9604 has a clean preclinical mechanism story (lipolysis without GH-axis activation) and a decent safety database from over 900 trial participants. The Phase IIb obesity trial failed its primary efficacy endpoint and Metabolic Pharmaceuticals discontinued development. The compound is on the market because it’s an interesting pharmacology, not because the registrational evidence supported a weight-loss indication.

Preclinical work

In obese mice, AOD-9604 produced fat-mass reduction comparable to or exceeding full-length HGH at much lower doses, with no IGF-1 elevation or glucose dysregulation.5 The mechanistic case for a “lipolytic GH fragment without the metabolic side effects” originated here and is the basis for the compound’s continued community use.

Phase 2b obesity trial (the trial that ended development)

The largest controlled human trial enrolled obese patients in a 12-week dose-escalation Phase IIb study. The trial failed to demonstrate statistically significant weight loss versus placebo at any tested dose. Metabolic Pharmaceuticals terminated the program in 2007.1

Six trials, 900+ participants, mechanism-supported in preclinical work — but the largest registrational trial did not meet its primary endpoint. The interpretive question is whether the trial population, dose range, or duration were inadequate, or whether the rodent-to-human translation simply doesn’t hold for this compound. The available data don’t disambiguate. AOD-9604 is on the market because the mechanism is interesting, not because the registrational evidence supported a weight-loss indication.

Safety evidence

The 900+ trial participants did establish a clean safety profile within trial duration:

No significant changes in blood glucose, insulin, or IGF-1
No GH-receptor-mediated side effects
Generally well-tolerated, with injection-site reactions and occasional headache as the main reported AEs

This is the strongest safety database of any compound in this encyclopedia’s GH-axis-related cluster. Even though the efficacy endpoint failed, the safety endpoint did not — AOD-9604 is one of the cleaner-tolerated peptides in the broader landscape.

TGA approval as food / supplement ingredient

Australia’s TGA approved AOD-9604 for use in listed (low-risk) food and supplement products for general weight-loss support — a different regulatory path than a registered pharmaceutical. The approval reflects the safety database, not a pharmaceutical efficacy approval. This is the closest AOD-9604 has come to regulatory legitimacy and is sometimes cited misleadingly as evidence of clinical effect; it is not.

What the evidence does NOT show

Clinically significant weight loss in humans — the Phase IIb trial failed
Body-composition outcomes equivalent to or better than caloric restriction — not directly compared
Synergy with exercise or other lipolytic compounds — claimed but not registrationally tested
Long-term safety beyond the trial durations (~12 weeks each)
Joint-health effects — sometimes claimed in marketing; not registrationally supported

Typical use patterns

Standard biohacker protocol

Community use typically follows a pattern aligned with the trial doses but extended:

300 mcg subQ daily for an 8–12 week cycle
Morning fasted dosing, often timed before fasted cardio
5 days on, 2 days off, or continuous daily dosing
Cycle 8–12 weeks on, 4 weeks off

Higher-dose protocols at 500–600 mcg daily exist; the dose-response curve flattens above 500 mcg and side-effect frequency increases. 500 mcg is the practical upper end of community use.

Sensitive-start protocol

For users new to AOD-9604 or with reactive systems:

150–250 mcg subQ daily for the first 1–2 weeks
Hold at the start dose to assess tolerance
The compound is generally well-tolerated; sensitive-start dosing is precautionary rather than driven by frequent issues

Stacking

GLP-1 agonists (semaglutide, tirzepatide, retatrutide) — common pairing for weight loss. No mechanistic conflict; AOD-9604 acts on adipocyte lipolysis while GLP-1 agonists act on appetite and gastric emptying. The combined effect is plausibly additive but not directly studied.
GH cluster compounds (ipamorelin, CJC-1295, sermorelin, tesamorelin) — sometimes stacked. Mechanistically complementary (different pathways) but adds the GH/IGF-1 effects of the GH cluster on top of AOD-9604’s lipolysis. Defeats the “no GH-axis activation” advantage if that’s why the user chose AOD-9604.
BPC-157 / TB-500 — common during recovery phases. No documented interactions.
Caffeine and yohimbine — common in fat-loss stacks. Potentially additive lipolytic effect; cardiovascular load increases.
Beta-blockers — theoretically interfere with the beta-3 adrenergic mechanism. Clinical impact unknown.

For sensitive systems

AOD-9604 is one of the better-tolerated compounds for sensitive-systems users in the fat-loss space — partly because the safety database is large and partly because the mechanism (adipocyte beta-3 agonism) doesn’t activate the GH/IGF-1 axis or produce the broader effects of the GH cluster.

Start dose for sensitive users. 150–200 mcg subQ daily for 2 weeks. Hold before considering an increase.

Ramp. If tolerated, 300 mcg daily is the standard community target. Many users don’t benefit from going above this.

Expected adjustment profile:

Injection-site reactions — the most consistently reported AE
Mild headache in the first few days — uncommon but reported
Mild fatigue — uncommon
No documented hunger spike, vivid dreaming, or fluid retention — these distinguish AOD-9604 from the GH cluster

What’s not normal and warrants stopping: persistent injection-site reactions worsening over time, palpitations or atypical chest sensations (the beta-3 adrenergic mechanism has very low cross-reactivity with beta-1/beta-2 cardiac receptors but caution is warranted), unusual fatigue persisting beyond initial adjustment.

For MCAS / histamine-sensitive users. No specific histamine activity documented. The mechanism is not directly mast-cell-relevant.

For POTS users. Beta-3 adrenergic activation has low cardiac cross-reactivity at therapeutic AOD-9604 doses, but POTS users have already-altered autonomic tone. Sensitive-start dosing is prudent; monitor HR for the first 2 weeks. Most POTS users tolerate AOD-9604 better than GH cluster compounds.

For UARS / chronic fatigue / ME/CFS. AOD-9604 is not directly aligned with sleep architecture or recovery use cases. It is a fat-loss compound. ME/CFS users sometimes struggle with the energetic demands of fat loss generally; AOD-9604 doesn’t change that calculus.

For active or recent cancer history. AOD-9604 does not elevate IGF-1 or activate GH-receptor pathways, so the standard GH-cluster cancer concerns do not directly apply. However: long-term effects of any fat-loss intervention in cancer survivors warrant oncology input, particularly for users in the “do not actively lose weight” phase of survivorship care.

For diabetes (type 1 or type 2). AOD-9604 does not produce insulin resistance — this is one of the central pharmacological claims. Users with diabetes can use it without the glycaemic concerns of the GH cluster. Monitor as standard.

For users with cardiovascular disease. Beta-3 adrenergic activation is selective for adipose tissue with minimal cardiac effect at therapeutic doses, but cumulative cardiovascular load from any fat-loss intervention warrants prescriber input for users with CV disease.

Interactions worth considering:

GLP-1 agonists, GH cluster, beta-blockers — see Stacking above
SSRIs, SNRIs, LDN — no documented interactions

Reasonable expectations

Onset. Lipolytic effect begins within 1–2 hours of injection. Subjective fat-loss effects, where they occur, appear over 8–12 weeks and are typically modest. The Phase IIb failed because the effect, if real in humans, was below the trial’s detection threshold.

Response rate. Community-reported response varies widely. Some users report measurable body-fat reduction over an 8–12 week cycle (typically 1–3 kg additional fat loss compared to diet alone, though this is anecdotal); others report no measurable difference. The trial failure suggests population-level effects are smaller than individual experiences sometimes report.

What the evidence actually supports.

Lipolytic mechanism in adipose tissue — preclinically supported
Clean safety profile — strongly supported (900+ trial participants)
No GH-axis activation — strongly supported

What the evidence does not support.

Statistically significant weight loss in humans — the Phase IIb trial failed
Clinically meaningful effect at any dose — direct evidence does not exist
Joint health benefits — sometimes claimed; not supported

What not to expect.

Significant fat loss without diet and exercise. AOD-9604 is at most an adjunct to standard interventions.
Effects comparable to GLP-1 agonists or HGH. It is a much weaker fat-loss intervention than either.
Body recomposition effects. Lean mass is not affected; this is a fat-only mechanism.

Cost

AOD-9604 is not available through licensed pharmacy channels in the UK or US as a pharmaceutical. The TGA approval as a food/supplement ingredient in Australia does not extend to other markets.

Research-chemical UK market:

5 mg vials: ~£25–60
Monthly cost at 300 mcg/day: roughly £30–75/month

This is mid-range pricing for the research-chem peptide market — cheaper than tesamorelin, comparable to ipamorelin and CJC-1295, more expensive than Melanotan II.

Sensitive-start economics. A user starting at 150 mcg/day uses half the standard dose, extending vial life proportionally. A 5 mg vial covers ~33 doses at this rate, comfortably within the 28-day reconstituted shelf life.

Reconstitution

What’s in the box

Research-chemical AOD-9604 ships as lyophilised white powder in a glass vial, typically 5 mg per vial (the dominant size; 2 mg and 10 mg vials exist but are less common).

You’ll also need: BAC water, U-100 insulin syringe, larger transfer syringe, alcohol wipes.

The math

5 mg vial, 2 mL BAC water (the standard)

Concentration: 2.5 mg/mL (2,500 mcg/mL)
150 mcg sensitive-start = 0.06 mL = 6 units
250 mcg = 0.1 mL = 10 units
300 mcg = 0.12 mL = 12 units
500 mcg = 0.2 mL = 20 units

5 mg vial, 1 mL BAC water (for higher-dose protocols)

Concentration: 5 mg/mL (5,000 mcg/mL)
300 mcg = 0.06 mL = 6 units
500 mcg = 0.1 mL = 10 units

The Peptrax Vial Plan calculator handles the same math interactively.

Reconstitution procedure

Same as the rest of the encyclopedia: alcohol-wipe stoppers, slow water injection down the vial side, no shaking, label vial, refrigerate.

Storage and stability

AOD-9604 reconstituted with BAC water is stable for ~28 days refrigerated — at the standard end of the research-chem peptide range.

Conservative: 14–21 days
Middle: 28 days
Optimistic: 30 days

Some vendor sources note that AOD-9604 is sensitive to pH excursions (BAC water at pH 5.5–6.0 may produce gradual denaturation past 14 days at the conservative end of the spread) and to temperature excursions above 8°C (causes irreversible aggregation). Practical advice: keep refrigerated, don’t leave at room temperature for extended periods, discard if any cloudiness appears.

Store at the back of the refrigerator. Do not freeze.

If you reconstitute with plain sterile water, the vial is single-use — discard within 24 hours.

For a 5 mg vial at 300 mcg/day: ~16 doses → 16 days, comfortably within shelf life.

What gets miscalculated

mg vs mcg confusion. AOD-9604 doses are in mcg; 1 mg = 1,000 mcg.
Reading “units” as mg.
Stacking with GH cluster compounds expecting amplification. The pathways are different; combined effect is plausible but the GH cluster compounds bring back the GH/IGF-1 effects AOD-9604 was chosen specifically to avoid.
Skipping food intake/training context. AOD-9604’s fat-loss claim depends on the body being in a deficit and able to mobilise fatty acids. Without diet and exercise alignment, the lipolytic effect doesn’t translate to body-composition outcomes.

Areas of concern ⚠

The efficacy gap

AOD-9604 has a clean mechanism story and a clean safety profile, but the registrational evidence for the marketed weight-loss claim is negative. The Phase IIb trial failed. Six total trials with 900+ participants did not produce a registrational efficacy package. The mechanism-vs-evidence gap is the single most important fact about this compound.

For a sceptical reader: AOD-9604 is a peptide with a plausible mechanism that did not produce statistically significant weight loss in its largest controlled human trial. Continued community use and marketing as a “fat loss peptide” rests on the mechanism and on individual-level community reports, not on the trial outcomes. This is fundamentally different from GLP-1 agonists, where the trial outcomes drive both the regulatory approval and the community use.

Quality and sourcing

Standard research-chem caveats apply. AOD-9604’s 16-residue length and intramolecular disulphide bridge make it slightly more complex to synthesise correctly than some other peptides; lab-tested vendors with mass-spec or HPLC certificates are the meaningful quality marker. Some research-chem AOD-9604 has been found to be the unmodified HGH(177-191) fragment without the tyrosine cap or proper disulphide formation, which would have very different stability and possibly different biological activity.

Long-term safety beyond ~12 weeks is uncharacterised

Trial durations were short (12 weeks). Multi-month or multi-year safety in healthy users is not characterised. The mechanism-driven concerns are minimal (no GH/IGF-1 axis activation, no glucose dysregulation), but the absence of long-term data is the relevant uncertainty.

Populations where AOD-9604 is contraindicated or high-risk

Pregnancy and breastfeeding — no safety data
Under 18 — no use case; not studied
Active cancer or recent cancer treatment — cancer survivorship guidance about active fat loss
Severe cardiovascular disease — caution; cumulative load of any fat-loss intervention
Eating disorder history — risk of disordered behaviour around fat-loss compounds generally

Measurement and dosing pitfalls

mg vs mcg confusion.
Dosing without diet/training context — the compound’s claimed effect depends on energy deficit.
Stacking with GH cluster compounds for amplification — the pathways are different and the GH cluster brings its own concerns.

What the community gets wrong

“Targeted fat loss.” AOD-9604 acts on adipose tissue broadly, not on specific body regions. The marketing claim of “targets stubborn fat” is not supported by the mechanism or the trial data.
“Joint health benefits.” Sometimes claimed alongside the fat-loss claim. Not registrationally supported.
“Approved as a weight-loss drug somewhere.” TGA approved it as a listed food/supplement ingredient, not as a pharmaceutical weight-loss drug. The framing is regulatory legitimacy by association rather than substance.
“Like HGH but safer.” It does not produce HGH effects (good and bad). It has its own much smaller effect profile.

FDA / regulatory status

Jurisdiction	Status	Last verified
US (FDA)	Not approved as a pharmaceutical. Removed from FDA Category 2 in September 2024 alongside ipamorelin, CJC-1295, thymosin α-1, selank; PCAC review pending. Sold as a research chemical labelled “not for human consumption.”	2026-04-29
UK (MHRA)	Not approved as a medicine. Sold as a research chemical.	2026-04-29
EU (EMA)	Not approved.	2026-04-29
Australia (TGA)	Approved as a listed (low-risk) food/supplement ingredient for general weight-loss support, not as a pharmaceutical. This is the closest AOD-9604 has come to regulatory legitimacy and reflects the safety database, not a pharmaceutical efficacy approval.	2026-04-29
WADA (sport)	Prohibited. Listed under S2 (Peptide Hormones, Growth Factors, and Related Substances) as a GH-related compound.	2026-04-29

Narrative. AOD-9604’s regulatory status is unusual — TGA-approved in Australia as a listed supplement, not approved as a pharmaceutical anywhere, in active US compounding-pharmacy regulatory flux alongside the GH cluster. For UK readers, no licensed pathway exists. For US readers, the same compounding-pharmacy uncertainty as ipamorelin and CJC-1295 applies.

What to track in Peptrax

A lipolytic peptide can only do something useful if the user is already in energy deficit; AOD-9604 dosed against a maintenance diet has no plausible mechanism to produce visible body-composition change. The dose log without the diet and training context attached is essentially uninterpretable for this compound — caloric intake, training load, and sleep are the variables that determine whether AOD-9604 has anything to act on.

For most users, the highest-signal log is weekly weight, weekly waist measurement, and body-fat tracking (DEXA every 8–12 weeks if accessible; calliper or bioimpedance more frequently for trend). Daily subjective tracking matters less than the 8-week snapshot for this compound — the effect, if real, is slow and modest.

For sensitive-systems users, the priority log shifts to the first 2–3 weeks: any injection-site reactions, headache, or unusual fatigue. The compound’s safety database is large and clean, so the typical sensitive-systems concerns are lower than for the GH cluster — but tolerance varies and worth tracking.

Across all users, logging the stack composition matters because AOD-9604 is rarely used alone. Combined with GLP-1 agonists, with the GH cluster, with caffeine/yohimbine fat-loss stacks — the question of “which component is doing what” requires good logging to answer. Peptrax’s job is to hold the timeline that lets users reconstruct what worked when.

For personal tracking and informational purposes only — not medical advice.