Not medical advice. Talk to your provider before using any peptide.
Full disclaimer
AOD-960416 residuesYLRIVQCRSVEGSCGFEach bubble = one amino acid. Size = residue mass. Color = chemical class.Also known as: hGH fragment 177-191, hGH frag, Tyr-hGH177-191
A Phase IIa trial of roughly 300 obese adults showed total fat loss of 2.6 to 2.8 kg at 12 weeks (vs 0.8 kg for placebo) on 1 mg oral dosing [1]. Then the definitive Phase IIb trial of 536 subjects failed. The AOD-9604 peptide (also called hGH frag) is a 15-amino-acid fragment of human growth hormone (residues 177 to 191) that triggers lipolysis through beta-3 adrenergic receptor activation without touching blood sugar, IGF-1, or growth pathways. Every clinical trial used oral dosing; injectable use is a community extrapolation with zero published human SC pharmacokinetic data. The peptide community treats it as a mild stack add-on for body recomposition, typically paired with CJC-1295 and Ipamorelin at 300 to 500 mcg subcutaneous daily.
2.8 kg of extra fat loss versus placebo over 12 weeks. That was the Phase IIa result for the AOD-9604 peptide (also called hGH fragment 177-191 or hGH frag, CAS 221231-10-3) in roughly 300 obese adults taking 1 mg orally per day (Obesity Research 2000)[1]. Then the larger Phase IIb trial with 536 subjects ran for 24 weeks, added strict diet and exercise controls, and missed its primary endpoint. Metabolic Pharmaceuticals terminated the program in 2007. The mechanism is specific. AOD-9604 activates beta-3 adrenergic receptors on adipocytes, triggering lipolysis while blocking lipogenesis. Unlike full-length growth hormone, it does not bind the GH receptor. Blood sugar stays flat. IGF-1 stays flat. Styer and colleagues confirmed this receptor selectivity in beta-3-AR knockout mice (Endocrinology 2001)[2], where the lipolytic effect disappeared completely. Community use looks different from the clinical program. Most users inject 300 to 500 mcg subcutaneously each morning on an empty stomach. That dose range comes from converting the 1 mg oral clinical dose using an estimated 40% oral bioavailability from animal models. No published human SC pharmacokinetic study has validated this conversion. Across 50 to 150 Reddit threads in r/Peptides, the consensus is consistent: AOD-9604 is a mild add-on, not a primary fat loss tool. It performs best when stacked with CJC-1295 and Ipamorelin in a caloric deficit. Anyone expecting GLP-1-level results will be disappointed.
AOD-9604 copies the fat-burning region of growth hormone without copying anything else. The peptide corresponds to amino acids 177 through 191 of hGH, plus a tyrosine at position 176 that stabilizes the fragment. Metabolic characterization by Heffernan and colleagues confirmed this fragment retains lipolytic activity independent of the GH receptor [3]. The target is the beta-3 adrenergic receptor on adipocytes. Activation triggers cyclic AMP signaling, which activates hormone-sensitive lipase and breaks stored triglycerides into free fatty acids. Chronic treatment in obese mice increased fat oxidation and reduced body weight without affecting lean mass [4]. Knockout mice lacking the beta-3 adrenergic receptor showed zero response, confirming receptor specificity. AOD-9604 also inhibits lipogenesis. Fat cells exposed to the fragment slow their conversion of circulating substrates into stored triglycerides. The dual action (accelerated breakdown plus reduced formation) produces a net shift in adipose tissue balance. This was measurable in the Phase IIa oral trial at 12 weeks. Fasting matters for this mechanism. Insulin suppresses beta-3 AR signaling in adipocytes. Any food intake, especially carbohydrates, blunts the lipolytic effect by raising circulating insulin. Community protocols requiring strict fasted morning dosing match the biochemistry directly.
Phase IIa (12 weeks, 1 mg/day oral, ~300 subjects): 2.6–2.8 kg fat loss vs 0.8 kg placebo. Phase IIb (536 subjects, 24 weeks, 1 mg/day oral): primary endpoint FAILED when rigorous diet/exercise controls were applied. Pharmaceutical program terminated 2007. No published human SC pharmacokinetic or efficacy data. All clinical trials used oral formulations.
Obesity Research 2000 (PMID 10950816): Phase IIa efficacy; J Pharmacol Exp Ther 2000 (PMID 11146367): metabolic characterisation
Phase IIb failed. No SC clinical data. GRAS designation is for oral use only. All injectable dosing is extrapolated from oral clinical data assuming ~40% oral bioavailability. Half-life SC not established.
Mild body recomposition agent, not a primary fat-loss tool. Community sentiment is cautiously skeptical: valued as a clean, non-hormonal adjunct to GH secretagogue or GLP-1 stacks. Rarely used solo by experienced users. Consensus has shifted: AOD-9604 is positioned as a "stack add-on," not a standalone weight loss treatment.
Community SC doses (300–500 mcg) are extrapolations from oral clinical dosing (1 mg/day) using assumed ~40% oral bioavailability: a reasonable but unvalidated conversion. Community expectation of modest fat-loss aligns with Phase IIa data, but community ignores that the definitive Phase IIb trial failed. No SC clinical efficacy or safety data exist.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 200mcg | Daily |
| Moderate | 300mcg | Daily |
| Aggressive | 500mcg | Daily |
Start at 200 to 250 mcg for the first two weeks. There's no rush to the full dose, and you'll want to confirm tolerability before committing to a 12-week run. Reconstitution math for a 5 mg vial: add 2 mL bacteriostatic water. That gives you 2,500 mcg/mL, or 25 mcg per unit on a 100-unit insulin syringe. For a 250 mcg dose, draw 10 units. For 300 mcg, draw 12 units. For 500 mcg, draw 20 units. Fasted dosing is non-negotiable. The lipolytic mechanism runs through beta-3 adrenergic receptor signaling, which insulin suppresses. No food, no cream in coffee, no BCAAs for at least two hours before injection. Wait 30 to 60 minutes after injection before eating. The thing most beginners miss: AOD-9604 is not a GLP-1. There's no appetite suppression. You won't feel different. Track progress with waist circumference or DEXA, not the bathroom scale; scale weight poorly reflects what this peptide actually does. A 5 mg vial at 400 mcg daily lasts 12.5 days. A full 12-week course burns through roughly 7 vials ($315 to $525 at current research-chemical pricing).
No receptor desensitization reported, but cycling is still recommended. Can be run longer if well-tolerated.
No receptor desensitization has been documented with AOD-9604 in clinical trials or community use. Cycling is implemented as a precautionary practice to allow observation for cumulative effects (immunogenicity, injection site changes) and to assess on/off response. The pharmaceutical program was terminated before long-term continuous dosing studies were completed, so cycling is conservative rather than mechanistically driven.
Or use the universal Peptide Calculator for any peptide.
Expected: Modest fat reduction (0.5–1.5 kg) primarily in abdominal area when combined with caloric deficit. Many users report no measurable effect without diet adherence.
Monitor: Body weight + waist circumference weekly. Scale weight alone is unreliable.
Remove the 5 mg AOD-9604 vial and bacteriostatic water from refrigeration. Let both reach room temperature for 5 to 10 minutes.
Inject slowly along the glass wall of the vial. Do not squirt directly onto the lyophilized powder. Swirl gently until dissolved; never shake.
You now have 2,500 mcg/mL. Each unit on a 100-unit insulin syringe equals 25 mcg.
For 300 mcg, draw to 12 units. For 400 mcg, draw to 16 units. For 500 mcg, draw to 20 units.
Pinch a fold of abdominal subcutaneous fat near the navel. Insert a 29 to 31 gauge, half-inch needle at a 45-degree angle.
Hold for 5 seconds before withdrawing.
Rotate injection sites across four abdominal quadrants to prevent lipodystrophy.
Wait at least 30 minutes before eating.
Return the reconstituted vial to the refrigerator immediately. Use within 4 weeks.
1 mg/day oral = approximately 400–600 mcg SC (based on ~40% animal oral bioavailability)
GRAS status applies to this route. The only route with actual human safety and efficacy data. However, compounded or research-grade oral capsules are rarely used by the community: the injectable format dominates despite having no clinical trial basis.
Rabbit study used intra-articular injection with HA; no dose translation to humans established
2024 PMC review (PMC11556548) cited this cartilage regeneration data. Not a community practice. Do not use intra-articular without clinical evidence.
Most cited community stack. CJC-1295 triggers GH pulse; AOD-9604 adds targeted lipolysis. Rationale: complementary mechanisms: GH-axis stimulation + direct fat-cell targeting.
CJC-1295 100–200 mcg + AOD-9604 300 mcg, fasted AM daily
Almost always included in the CJC-1295 + AOD-9604 trinity stack. Ipamorelin provides the GHRP pulse to complement CJC-1295 GHRH effect. Selective GH release without cortisol/prolactin spikes.
Ipamorelin 100–200 mcg + CJC-1295 100–200 mcg + AOD-9604 300–500 mcg, fasted AM
Body recomposition + healing stack. BPC-157 targets musculoskeletal repair while AOD-9604 drives fat loss. Popular in users doing resistance training or recovering from injury while cutting.
BPC-157 250–500 mcg + AOD-9604 300–500 mcg, fasted AM or pre-workout
Emerging stack: AOD-9604 as a lean-mass-preserving direct lipolysis add-on during GLP-1 cycle. No clinical data. Rationale is mechanistic complementarity (GLP-1: appetite suppression; AOD-9604: direct adipocyte lipolysis).
Pricing updated 2026-04-09
The Phase IIb trial of 536 subjects over 24 weeks produced the largest safety dataset. Headache was the most frequently reported adverse event in the oral formulation groups. All six published clinical trials used oral formulations. Zero published human safety data exist for subcutaneous injection. Every injectable safety claim is extrapolated from oral data. That distinction matters because local tissue reactions, immunogenicity potential, and injection site effects cannot be inferred from swallowed capsules. FDA PCAC specifically cited manufacturing impurity risks and immunogenicity concerns for compounded injectable forms in their December 2024 review. Published adverse events from oral trials [1]: Headache: most common, reported at rates slightly above placebo. Typically mild. Usually resolves within the first two weeks of dosing. Nausea: occasional, appearing most often during early dosing. Less frequent than headache. No clinically meaningful changes in blood glucose, insulin, IGF-1, or thyroid markers were observed in any trial arm. Community-reported side effects from subcutaneous use (r/Peptides, approximately 50 to 150 threads): Injection site reactions are the primary complaint. Redness, mild swelling, and induration at the injection site affect most new users. These are cosmetic and self-resolving. Diluting to a lower concentration, warming the vial to room temperature, and slowing injection speed all help. Lipodystrophy at injection sites has been reported with poor site rotation. Rotate across four abdominal quadrants minimum. Quality risk is a real factor. AOD-9604 is a 15-residue peptide requiring precise disulfide bridge formation during synthesis. Purity varies widely across unregulated research-chemical vendors. Low-purity preparations carry higher immunogenicity and local reaction risk. Request lot-specific HPLC and LC-MS data showing 98% or higher purity. AOD-9604 is WADA-prohibited (category S2, Growth Hormone Fragments) and detectable via mass spectrometry [5]. The Essendon Football Club scandal in 2012 involved roughly 34 AFL players who received AOD-9604 injections; several faced bans. AOD-9604 has not been studied in pregnancy or breastfeeding. No pediatric data exist. Active malignancy is a contraindication because effects on tumor growth have not been evaluated. Known hypersensitivity to the peptide or excipients is an absolute contraindication. When to stop: discontinue if injection site nodules develop, if local reaction severity increases over successive weeks (potential immunogenicity signal), or if unexpected systemic symptoms appear that resolve during off-cycle periods. Any hypoglycemia symptoms when stacking with GLP-1 agonists or secretagogues warrant immediate discontinuation and medical evaluation.
Verify AOD-9604 dosing and safety with a second opinion
AOD-9604 is a 15-residue peptide (plus Tyr176) that requires precise disulfide bridge formation. Research-chemical vendors are unregulated; purity varies widely. FDA PCAC (December 2024) specifically cited manufacturing impurity risks and immunogenicity concerns for compounded/injectable forms. No FDA-approved or pharmacopoeial standard exists for injectable AOD-9604.
| Test | When | Target |
|---|---|---|
| Body weight + waist circumference | Weekly throughout cycle | Individual baseline: trend toward decrease in waist circumference over 12 weeks |
| DEXA scan (optional) | Baseline and week 12 | — |
| Fasting glucose | Baseline; week 6 if stacking with secretagogues or GLP-1s | — |
| Injection site assessment | Each injection | — |
Primary outcome measure. Scale weight is misleading if combining with a secretagogue stack (water retention). Waist circumference reflects visceral fat reduction more accurately.
Definitive body composition assessment to distinguish fat mass loss from weight change. AOD-9604 should not affect lean mass or bone density.
AOD-9604 alone does not affect glucose. Monitoring is relevant only when stacked with GH secretagogues (which can cause transient hyperglycemia) or GLP-1s (hypoglycemia risk in deficit).
Lipodystrophy or nodule formation indicates inadequate site rotation or too-high local concentration. Rotate sites across abdominal quadrants.
Body adjusts to the peptide. No visible fat loss yet. Mild injection site redness may occur. Establish consistent fasted morning dosing routine.
Early metabolic shifts begin. Some users notice reduced abdominal bloating. Fat oxidation rates start to increase, though scale weight may not change significantly.
Measurable fat loss becomes apparent, particularly in the midsection. Clothes may fit differently. Average loss of 1-2 kg of fat tissue reported in clinical data at comparable timepoints.
Continued steady fat loss. Clinical trial subjects on 1 mg/day lost an average of 2.6 kg over 12 weeks. Body composition improvements are visible. No receptor desensitization observed.
Ongoing fat metabolism support. Results plateau as body reaches a new set point. Can extend beyond 12 weeks if well-tolerated. Pair with exercise and caloric control for best outcomes.
Weeks 1 to 2 (Adaptation): The peptide distributes into adipose tissue and begins signaling through the beta-3 adrenergic receptor. Nothing visible happens yet. Most users notice zero change. A small number report mild energy shifts. Mild injection site redness is the most common complaint in this window. Use this time to lock in your fasted morning routine. Weeks 3 to 4 (Early metabolic shift): Chronic beta-3 AR stimulation starts pushing fat oxidation rates upward. Phase IIa subjects didn't show meaningful weight separation from placebo until around week 4 to 6. Some users report subtle reduction in abdominal bloating and slightly improved definition if already lean. Injection site reactions typically settle. Headache was the top adverse event in oral trials and may appear here. Weeks 5 to 8 (Measurable fat loss): Phase IIa oral data showed approximately 1.5 kg of differential fat loss from placebo at the 8-week mark. SC results at 400 to 500 mcg daily are extrapolated to be similar. Fat loss becomes visible around the abdomen. Clothes fit differently. Community-reported change averages 0.5 to 1.5 kg of measurable fat in this window, though individual variation is high. Side effects are typically gone by this point. Weeks 9 to 12 (Plateau approach): Phase IIa showed 2.6 to 2.8 kg total fat loss at 12 weeks. The Phase IIb trial at 24 weeks showed no benefit over placebo when exercise controls were applied. A plateau is expected. Most users who respond have responded by week 10. Continuing past 12 weeks without changing the protocol yields diminishing returns.
Compound distributes in adipose tissue. Lipolytic signaling via beta-3 adrenergic receptor begins. No measurable fat change in this period.
Most users notice nothing. A small subset report mild energy increase. Establish fasted routine.
Chronic beta-3 AR stimulation begins to shift fat oxidation rates upward. Phase IIa subjects did not show significant weight change until week 4–6.
Subtle reduction in abdominal bloating. Some notice improved definition if already lean. No dramatic fat loss yet.
Phase IIa data shows ~1.5 kg differential from placebo at the 8-week mark in oral trials. SC equivalent is extrapolated and likely similar at 400–500 mcg/day.
Fat loss visible around abdomen. Clothes fit differently. Average community-reported change: 0.5–1.5 kg measurable fat in this window, highly variable.
Phase IIa showed ~2.6–2.8 kg total at 12 weeks. Phase IIb at 24 weeks showed no benefit over placebo with exercise controls. Plateau is expected.
Results slow. Most users who are going to respond have responded by week 10. Continuing past 12 weeks yields diminishing returns without a protocol change.
Source: IV t1/2 3-4 min (metabolic studies PMID 11146367); no established SC half-life
Loading the interactive decay curve.
AOD-9604 is not FDA-approved for any therapeutic indication. The pharmaceutical development program (Metabolic Pharmaceuticals, Australia) was terminated in 2007 after Phase IIb failure. The compound holds GRAS status strictly as an oral food additive. That designation does not apply to injectable use. FDA PCAC voted in December 2024 to recommend that AOD-9604 not be included on the 503A Bulks List for pharmacy compounding. Formal rulemaking is pending. If finalized, compounded injectable AOD-9604 from 503A pharmacies would become unavailable. Research-chemical supply remains legal for non-human research purposes in most US jurisdictions. AOD-9604 is WADA-prohibited under category S2 (Peptide Hormones, Growth Factors, Related Substances, and Mimetics). It is detectable via mass spectrometry (Drug Testing and Analysis 2015)[5]. Competitive athletes must not use it. This content is for informational and research purposes only. It does not constitute medical advice. Consult a licensed healthcare provider before using any peptide.
Peptide Schedule Research TeamReviewed Apr 20267 Citations
