AOD 9604 Quick Reference (5 mg vial)
Research context: mechanisms, human and preclinical evidence, limitations and precautions are in How this works and References. The calculator (Spanish) converts any other volume.
AOD 9604 Dosage Chart (5 mg vial)
Dosing & Reconstitution Guide
Educational guide for reconstitution and daily dosing
Evidence: only preclinical data are published for AOD 9604; the schedules in the chart are reference schedules and do not come from a human trial.
Standard / Gradual Approach (1 mL = ~5 mg/mL)
| Week / phase | Daily dose | Units per injection (mL) |
|---|---|---|
| Weeks 1–4 | 300 mcg | 6 units (0.06 mL) |
| Weeks 5–12 | 500 mcg | 10 units (0.10 mL) |
Frequency: Once daily, subcutaneously, at a consistent time.
Reconstitution Steps
- Draw 1 mL of bacteriostatic water with a sterile syringe.1
- Inject slowly down the vial wall; avoid shaking to prevent foaming.2
- Gently swirl or roll until fully dissolved (clear solution).3
- Label with the reconstitution date and refrigerate at 2–8 °C, protected from light; use within 4 weeks.4
The per-phase amounts are identical across the AOD 9604 family. The 5 mg vial only changes the concentration, U-100 units, volume and supplies.
Important: this guide is for educational purposes only and is not medical advice. For research use only. Not for human consumption.
U-100 Conversion Table (1 mL = 5 mg/mL)
| U-100 units | Volume | Contains | Yield per vial |
|---|---|---|---|
| 2 | 0.02 mL | 100 mcg | 50 injections |
| 5 | 0.05 mL | 250 mcg | 20 injections |
| 10 | 0.10 mL | 500 mcg | 10 injections |
| 20 | 0.20 mL | 1 mg (1000 mcg) | 5 injections |
| 30 | 0.30 mL | 1.5 mg (1500 mcg) | 3 injections |
| 50 | 0.50 mL | 2.5 mg (2500 mcg) | 2 injections |
| 100 | 1.00 mL | 5 mg (5000 mcg) | 1 injection |
This section describes which dose a study or reference source used and what it measured. It is not a recommendation or an administration schedule. A trial dose belongs to its population, duration and supervision and does not transfer to anyone outside that context.
Supplies Needed
Straightforward 12- and 24-week planning for a 5 mg vial at 5 mg/mL.
AOD 9604 vials (5 mg each)
- Standard / Gradual Approach, 12 weeks: Minimum 8 vials (36.4 mg required).
- Standard / Gradual Approach, 24 weeks: Minimum 16 vials (78.4 mg required).
U-100 syringes (1 mL)
- Standard / Gradual Approach, 12 weeks: 84 new syringes for 84 injections.
- Standard / Gradual Approach, 24 weeks: 168 new syringes for 168 injections.
Bacteriostatic water
- Standard / Gradual Approach, 12 weeks: 8 mL total (1 mL per vial) → 3 × 3 mL vials.
- Standard / Gradual Approach, 24 weeks: 16 mL total (1 mL per vial) → 6 × 3 mL vials.
Alcohol swabs
- Standard / Gradual Approach, 12 weeks: 168 minimum; one box of 100 does not cover the calculation.
- Standard / Gradual Approach, 24 weeks: 336 minimum; one box of 100 does not cover the calculation.
Sharps container: one appropriately sized. Stability planning: totals are minimum arithmetic quantities; follow the product documentation for sterility, storage, handling loss and discard timing.
AOD 9604 5 mgView in store
Bacteriostatic water 3 mLView in storeStore links may earn a commission. A supplier page is not scientific evidence or proof of suitability for human use.
AOD 9604 Vial and Research Context
- Reconstitute: add 1 mL of bacteriostatic water to produce 5 mg/mL.
- Frequency in the source: once daily, subcutaneously.
- Described range: schedules run from 300 mcg to 500 mcg per injection.
- Easy measuring: 1 U-100 unit = 0.01 mL = 50 mcg.
- Vial size: the 5 mg label is total nominal content, not a per-injection amount.
- Vial coverage: at 300 mcg per injection one vial supplies 16 injections; at 500 mcg it supplies 10. These are mass calculations, not storage periods.
Protocol Overview
Quick reference for the schedules shared by the cited literature.
- Frequency: once daily.
- Concentration: 5 mg in 1 mL = 5 mg/mL.
- Unit conversion: 1 U-100 unit = 50 mcg.
Dosing Schedule
The tables keep each approach separate.
- Standard / Gradual Approach: 300 mcg, 500 mcg, in phases (once daily).
- Measurement: use the units and mL shown beside each amount.
- Consistency: vial size does not change the schedule.
Storage Instructions
- Lyophilized (unopened): −20 °C for long-term storage; 2–8 °C if used within weeks. Protected from light.
- Reconstituted: 2–8 °C, do not freeze. Use within the documented period (typically up to 4 weeks with bacteriostatic water).
- Handling: do not shake; avoid temperature cycling; label with date and concentration.
- Discard: cloudy solutions, particulates or expired preparations are discarded.
More detail in the storage guide (Spanish).
Important Notes
- Research only: the referenced compounds are sold for laboratory research. Nothing here is medical advice or an administration schedule.
- Evidence: only preclinical data are published for AOD 9604; the schedules in the chart are reference schedules and do not come from a human trial.
- Above 100 units: a 1 mL U-100 syringe cannot hold them; split across syringes or reconstitute with less volume.
- Accuracy: concentration depends on the actual volume added; measure the diluent with a syringe, not by eye.
- Verification: confirm vial contents against the batch certificate of analysis before calculating.
How This Works
AOD-9604 (Advanced Obesity Drug) is a modified synthetic peptide representing the C-terminal fragment (amino acids 176-191) of human growth hormone (hGH), with a tyrosine modification at position 177. This 16-amino-acid fragment (MW: 1815.1 Da) selectively retains the lipolytic properties of hGH without effects on IGF-1 receptors or growth.
Structure and Modifications:
- Base sequence: hGH 176-191
- Modification: Tyr-hGH fragment (177-191)
- Addition: stabilizing N-terminal dipeptide
- Net charge: +2 (basic residues)
- Hydrophilicity: high aqueous solubility
Selective Lipolytic Mechanisms:
- Lipolysis Activation without GH Receptor:
- The classic GH receptor is not joined. (domain 176–191 is insufficient)
- IGF-1-independent mechanism: no growth/anabolic effects
- Direct lipolysis: hormone-sensitive lipase (HSL) activation
- Perilipin: phosphorylation and release of lipase access to triglycerides
- Lipid Metabolism Modulation:
- β-Oxidation: 35-45% increase in mitochondrial fatty acid oxidation
- CPT-1 (carnitine palmitoyltransferase): upregulation of FA entry into mitochondria
- Lipogenesis: inhibition of new fat synthesis (↓ acetyl-CoA carboxylase)
- Gene expression: modulation of PPARα, PGC-1α (metabolism regulators)
- Adipocyte-Specific Effects:
- Preference for visceral vs subcutaneous adipose tissue
- Adipocyte size reduction: 25-35% cell diameter
- Adipocyte apoptosis: increased programmed cell death in pathological fat
- Adiponectin: increased secretion of anti-inflammatory adipokine
Pharmacokinetics:
- SC Bioavailability: 80–85%
- Absorption: rapid, Tmax 20-30 minutes
- Half-life: 30–60 minutes (short)
- Distribution: preferential to adipose tissue
- Elimination: rapid renal clearance, no active metabolites
- Effect duration: 4-6 hours post-administration
Research Applications
SELECTIVE BODY FAT REDUCTION
Weight and Visceral Fat Loss:
Preclinical Rodent Studies:
- Body weight reduction: 50–55% higher than controls (12 weeks, obese rats)
- Visceral fat: reduction with 65-70% vs. calorie restriction alone
- Subcutaneous fat: reduction of 40–45% (less than visceral fat)
- Lean body mass: preservation 95-98% (no catabolic effects)
Genetic Obesity Models (ob/ob, db/db):
- Body weight: 25–30% reduction in ob/ob mice (8 weeks)
- Leptin: partial normalization of circulating levels
- Adiponectin: increase of 150–200%
- Inflammatory profile: reduced levels of IL-6, TNF-α, and MCP-1 (40–60%)
Molecular Lipolysis:
- Triglyceride mobilization: release of free fatty acids +180%
- Plasma glycerol: increased 150% (lipolysis marker)
- HSL phosphorylation: increased enzymatic activity 200%
- ATGL (adipose triglyceride lipase): upregulation 80%
Human Clinical Studies (Phase 2):
- Weight loss: 2.6 kg additional vs placebo (12 weeks, 300 μg/day)
- Abdominal fat: circumference reduction 4.1 cm vs 1.9 cm placebo
- IGF-1-free: stable levels (growth safety)
- Glucose: improves oral tolerance without hypoglycemia
2. METABOLIC EFFECTS AND INSULIN SENSITIVITY
Glucose Metabolism
- Insulin sensitivity: improvement in the HOMA-IR index 30-40%
- Glucose uptake: increased muscle/liver uptake 25%
- Gluconeogenesis: Modulation of Hepatic Glucose Production
- HbA1c: reduction of 0.4–0.61 TP3T in diabetic models
Plasma Lipid Profile
- Triglycerides: reduction of 25–35%
- Total cholesterol: decrease of 10–151 TP3T
- HDL: increase of 8–121 TP3T
- LDL: Reduction of small, dense particles 20%
- ApoB: decrease of 15%
Liver Function
- Hepatic steatosis: reduction in liver fat 40-50% (NMR spectroscopy)
- ALT/AST: Improves 25-30% markers in NAFLD
- Hepatic Insulin Sensitivity: Signaling Restoration
- De novo lipogenesis: inhibition of hepatic lipid synthesis
3. CARTILAGE AND JOINT REGENERATION
Chondroprotective Effects:
Notable Discovery:
- Stimulation of chondrocytes: increased proteoglycan synthesis 40%
- Type II collagen: upregulation of 35% expression
- GAGs (glycosaminoglycans): increased production of 50%
- Cartilage matrix: improves structural integrity
Osteoarthritis Models
- Cartilage degradation: reduced loss in the 35% group compared to controls
- MMPs: decreased MMP-13 (collagenase) 45%
- Synovial inflammation: reduction in infiltrate 40%
- Pain: Improves behavioral pain scores 30%
Proposed Mechanisms:
- IGF-1 / GH: Direct chondrocyte effect
- Inflammation modulation: reduction of joint IL-1β, TNF-α
- Cartilage anabolism: favorable synthesis/degradation balance
4. TENDON/LIGAMENT REPAIR
Tendinous Effects (Emerging Studies):
- Collagen synthesis: increased matrix deposition 30%
- Fibrillar organization: improves collagen fiber alignment
- Vascularization: increased vascular density in the repair zone
- Biomechanical properties: improved tensile strength 25%
Possible Mechanism:
- Modulation of local tendon cell metabolism
- Anti-inflammatory effects reduce the degradative phase
- Blood perfusion optimization (vascular lipid metabolism)
Injection Technique in Research
- Route in the studies: subcutaneous, in abdominal or thigh adipose tissue, rotating the site.
- Syringe: 1 mL U-100 (100 units); read in units, not mL.
- Asepsis: alcohol swab on the stopper and the site; a new syringe per injection.
- Drawing: purge air, draw the units from the chart and verify before withdrawing the needle from the vial.
Full guide: U-100 syringes and reading units (Spanish).
Research FAQ
Does AOD-9604 cause GH-like effects (growth, IGF-1)? R: No. Critical distinction:
- AOD-9604 does NOT bind to the GH receptor (insufficient fragment)
- Serum IGF-1: no changes in studies (vs. ↑ 200–400% with full GH)
- Anabolic effects: absent (no increase in lean mass/bone)
- Security: top profile worry-free acromegaly/diabetes
- Selectivity: retains ONLY lipolytic hGH properties
P: What is the optimal administration timing for maximum lipolysis? R: Fasted morning workout It is optimal:
- Low insulin: allows maximum lipolysis (insulin inhibits HSL)
- Elevated AM catecholamines: adrenergic synergy
- Protocol: 30-60 min pre-breakfast, wait 20-30 min before eating
- Alternative: Aerobic pre-exercise (15-30 min before)
- Avoid: Post-meals (insulin blocks effects)
Q: Is it effective orally? R: Unreliable:
- Peptide susceptible to degradation by digestive enzymes
- Oral bioavailability: <5% (vs. 80–85% SC)
- Oral studies: inconsistent results, 10-20x higher doses required
- Recommended route: Subcutaneous exclusively for research
Q: Synergistic combinations for body composition? R: Studied combinations with additive effects:
- + CJC-1295/Ipamorelin: Lipolysis + anabolism (optimal recomposition)
- + L-Carnitine: Improvement of mitochondrial FA transport (enhanced oxidation)
- Tirzepatide/Semaglutide: Multi-mechanism weight loss
- + T3 (thyroid hormone): Energy expenditure (strict monitoring)
Q: Common side effects in animal models? R: Excellent safety profile:
- Local injection: mild transient erythema (5–10% cases)
- Nausea: rare (<2%), typically with high doses
- Hypoglycemia: absent (no direct insulin effects)
- GH effects: absent (IGF-1, growth)
- Tolerance: excellent 52-week studies primates
P: Desensitization or tachyphylaxis? R: La literatura la describe como mínima:
- 12-16 week studies: sustained effectiveness
- Receptor-independent: lower risk of classical downregulation
- Optional rotation: some protocols alternate 4 weeks ON/2 OFF
Q: Biomarkers to monitor effectiveness? R: Key measurements:
- Body composition: DEXA (baseline, 4, 8, 12 weeks), waist circumference
- Metabolic: Serum glycerol (acute lipolysis), triglycerides, glucose/insulin
- Liverwurts: Liver elastography, ALT/AST if NAFLD
- Anti-inflammatories: Adiponectin, CRP, IL-6 (profile improvement)
Security: IGF-1 (must remain stable)
Research Note
All content on this page is technical and educational. It describes how a vial is reconstituted, how a syringe is read and which amounts the cited sources describe. It does not replace the supervision of a qualified researcher or the judgment of a health professional, and it is not intended to diagnose, treat, cure or prevent any disease.
References
- Modelos preclínicos en roedor
- Heffernan M, et al. (2001) “The effects of human GH and its lipolytic fragment (AOD9604) on lipid metabolism following chronic treatment in obese mice and beta3-AR knock-out mice” – Endocrinology 142(12):5182-5189. [PubMed: 11713213]
- Ng FM, et al. (2000) “Growth hormone fragment 176-191 stimulates lipolysis and inhibits lipogenesis in vitro” – J Endocrinol 166(1):145-150. [PubMed: 10856893]
- Munday MR, et al. (2001) “Addition of a C-terminal ‘Tyr-tag’ to the hGH fragment 177-191 produces a highly potent orally active lipolytic agent” – FEBS Lett 488(1-2):49-53. [PubMed: 11163794]
- Heffernan MA, et al. (2000) “Increase of fat oxidation and weight loss in obese mice caused by chronic treatment with human growth hormone or a modified C-terminal fragment” – Int J Obes Relat Metab Disord 24(10):1442-1448. [PubMed: 11126341]
- Leung KC, et al. (2002) “Growth hormone (GH) secretagogue, AOD-9604, increases lipolysis and decreases body fat in obese subjects” – Obesity 10(S8):102S. [Abstract]
- Ng FM, et al. (2011) “AOD9604, a synthetic lipolytic peptide, does not affect glucose metabolism” – Clinical and Experimental Pharmacology and Physiology 38(12):897-903. [PubMed: 21883414]
- Khajavi M, et al. (2003) “AOD9604 stimulates chondrocyte proliferation and cartilage production in vitro and in vivo” – Osteoarthritis Cartilage 11(Suppl A):S74.