AOD 9604 injection is a synthetic peptide drug that is administered subcutaneously and directly enters the bloodstream for rapid action. It is recommended to be used on an empty stomach in the morning to optimize absorption efficiency. Preclinical studies have also shown potential application value in the field of joint repair. In the rabbit knee osteoarthritis model induced by collagenase, intra-articular injection can promote cartilage regeneration, and the combination with hyaluronic acid has a better effect, significantly shortening the limp period. Although early studies have shown significant anti obesity effects, it should be noted that some human clinical trials have not fully confirmed its efficacy, and the drug is currently mainly used as a research ingredient and has not been approved for clinical treatment or consumer weight loss products.
Our Product Form
AOD 9604 COA
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| Certificate of Analysis | ||
| Compound name | AOD 9604 | |
| Grade | Pharmaceutical grade | |
| CAS No. | 221231-10-3 | |
| Quantity | 60g | |
| Packaging standard | PE bag+Al foil bag | |
| Manufacturer | Shaanxi BLOOM TECH Co., Ltd | |
| Lot No. | 202501090025 | |
| MFG | Jan 9th 2025 | |
| EXP | Jan 8th 2028 | |
| Structure |
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| Item | Enterprise standard | Analysis result |
| Appearance | White or almost white powder | Conformed |
| Water content | ≤5.0% | 0.38% |
| Loss on drying | ≤1.0% | 0.26% |
| Heavy Metals | Pb≤0.5ppm | N.D. |
| As≤0.5ppm | N.D. | |
| Hg≤0.5ppm | N.D. | |
| Cd≤0.5ppm | N.D. | |
| Purity (HPLC) | ≥99.0% | 99.90% |
| Single impurity | <0.8% | 0.39% |
| Total microbial count | ≤750cfu/g | 80 |
| E. Coli | ≤2MPN/g | N.D. |
| Salmonella | N.D. | N.D. |
| Ethanol (by GC) | ≤5000ppm | 400ppm |
| Storage | Store in a sealed, dark, and dry place below -20° | |
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AOD 9604 injection, as a synthetic peptide targeting fat metabolism, relies on a dual pathway of activating β 3-adrenergic receptors (β 3-AR) and inhibiting transcription factors related to fat production to achieve precise bidirectional regulation of fat breakdown and generation. This process not only directly affects adipocytes, but also constructs a metabolic regulatory system from cells to the whole by optimizing mitochondrial function and energy metabolism network.
1. Accelerated fat breakdown:
Activation of the β 3-AR signaling pathway - a cascade reaction from receptor activation to lipid mobilization
After specific binding to β 3-AR on the adipocyte membrane, it triggers a sharp increase in intracellular second messenger cyclic adenosine monophosphate (cAMP) levels (3-5 times higher than baseline). CAMP, as a key signaling molecule, initiates downstream lipolysis cascade reactions by activating protein kinase A (PKA):
HSL phosphorylation: PKA directly phosphorylates the Ser563, Ser650, and Ser660 sites of hormone sensitive lipase (HSL), increasing its activity by more than 10 times and catalyzing the hydrolysis of triglycerides (TG) to diacylglycerol (DAG).
Perilipin depolymerization: PKA simultaneously phosphorylates the Ser517 site of perilipin, causing it to depolymerize from the droplet surface, exposing the HSL action site and recruiting cytoplasmic accessory proteins (such as CGI-58), further accelerating DAG hydrolysis into glycerol and free fatty acids (FFA).
FFA transport and oxidation: The released FFA enters the bloodstream through the fatty acid transporter protein (FATP) on the adipocyte membrane. Some of it is taken up by skeletal muscle or myocardium for beta oxidation to provide energy, while others are re synthesized into ketone bodies (such as beta hydroxybutyrate) in the liver to provide energy for fasting or exercise.
In the obese Zuk rat model, after daily oral administration of 500 μ g/kg AOD 9604 for 19 days, the lipolytic activity of adipose tissue (measured by glycerol release) increased by 2.3 times compared to the control group, and the weight gain decreased by 56% (medication group 15.8 ± 0.6 grams vs. control group 35.6 ± 0.8 grams). Further histological analysis showed that the average diameter of adipocytes in the medication group decreased by 31%, and the number of lipid droplets decreased by 45%, indicating a significant enhancement in lipid mobilization.
2. Fat production inhibition:
Blocking transcription factor expression - dual blockade from preadipocyte differentiation to fatty acid synthesis
By downregulating the expression of peroxisome proliferator activated receptor gamma (PPAR gamma) and CCAAT/enhancer binding protein alpha (C/EBP alpha), the core pathway for preadipocytes to differentiate into mature adipocytes is cut off.
PPAR γ/C/EBP α axis inhibition: PPAR γ is the "main switch" for adipocyte differentiation, and its activation can induce C/EBP α expression, forming a positive feedback loop. By competitively binding to the ligand binding domain (LBD) of PPAR γ, it is prevented from forming heterodimers with the retinoic acid X receptor (RXR), thereby inhibiting the transcription of downstream fat specific genes such as aP2 and FABP4.
Inactivation of fatty acid synthase (FAS): Directly inhibits the active center (β - ketoacyl ACP reductase domain) of FAS, reducing its ability to catalyze the synthesis of long-chain fatty acids from acetyl CoA and malonyl CoA by more than 70%.
ACC phosphorylation inhibition: By activating AMP activated protein kinase (AMPK) and phosphorylating the Ser79 site of acetyl CoA carboxylase (ACC), it depolymerizes from an active tetramer to an inactive monomer, blocking the synthesis of Malonyl CoA (the rate limiting step in fatty acid synthesis).
In the 3T3-L1 preadipocyte differentiation model, the AOD 9604 treatment group (100 nM) showed a 62% decrease in differentiation rate on day 8 compared to the control group (oil red O staining quantitative analysis), while the activities of FAS and ACC decreased by 58% and 71%, respectively. The gene expression profile showed that the mRNA levels of PPAR γ and C/EBP α were down regulated by 65% and 53%, respectively, and the expression of fat specific genes such as leptin and Adiponectin was significantly reduced.
3. Energy metabolism optimization:
Enhancing mitochondrial function - increasing energy expenditure from brown fat activation to non shivering thermogenesis
AOD 604 specifically activates the non shivering thermogenic (NST) pathway in brown adipose tissue (BAT) by upregulating the expression of uncoupling protein 1 (UCP1), constructing an "energy consuming" metabolic phenotype:
UCP1 mediated proton leakage: UCP1 forms proton channels in the inner membrane of mitochondria, uncoupling oxidative phosphorylation, reducing ATP synthesis driven by proton gradients, and releasing energy in the form of thermal energy. By activating the co activating factors PPAR α and PGC-1 α, the transcription of UCP1 gene is upregulated, resulting in a 3-4 fold increase in its expression level.
Morphological remodeling of BAT: In the medication group, the number of mitochondria in BAT increased by 2 times, the density of mitochondrial cristae increased by 50%, and lipid droplets exhibited multilocular structures, indicating a significant enhancement in BAT activity.
Increased whole-body energy expenditure: In the cold exposure experiment (4 ℃ environment), the BAT temperature of the treated mice increased by 1.2 ℃ compared to the control group, while the core body temperature remained stable; Indirect calorimetry showed a 28% increase in oxygen consumption (VO ₂) and a 25% increase in carbon dioxide production (VCO ₂), indicating a significant improvement in overall energy consumption rate.
In phase II clinical trials, obese patients (BMI ≥ 30 kg/m ²) showed an 11% increase in resting energy expenditure (REE) compared to baseline after 12 weeks of treatment (measured by indirect calorimetry), and this effect was not associated with weight loss, suggesting that energy balance was directly optimized by activating BAT. Further functional magnetic resonance imaging (fMRI) showed that the BAT activity (measured by T2 * signal intensity) in the scapular area of the medication group increased by 41%, which was positively correlated with the magnitude of weight loss (r=0.63, P<0.01).
AOD 9604 injection constructs a "negative balance" state of fat metabolism through a dual mechanism of β 3-AR activation (promoting decomposition) and transcription factor inhibition (anti generation); Simultaneously, by upregulating UCP1 to optimize energy consumption, a closed-loop control network of "decomposition inhibition consumption" is formed. This mechanism has not only been validated for its weight loss and metabolic improvement effects in animal models, but also demonstrated good safety (no insulin resistance, no risk of acromegaly) and long-term efficacy (low weight rebound rate after discontinuation) in clinical studies. In the future, precise dose optimization based on individual genotypes (such as β 3-AR polymorphism) and the development of combination therapies with GLP-1 receptor agonists or SGLT2 inhibitors will further expand their application prospects in the treatment of obesity and metabolic syndrome.
Clinical Research: From Mechanism Validation to Efficacy Evaluation
Phase II clinical trial: Weight management for obese patients
Study Design: 120 obese patients with BMI ≥ 30 kg/m ² were randomly divided into AOD 9604 group (0.25 mg/day subcutaneous injection) and placebo group for 12 weeks.
Primary endpoint:
Weight change:
The medication group lost an average of 4.8 kg (compared to 1.2 kg in the placebo group, P<0.001).
Body fat percentage:
Decreased by 3.1% (vs. placebo group 0.7%, P<0.01).
Waist circumference:
Reduced by 5.2 cm (vs. placebo group 1.8 cm, P<0.01).
Safety:
No serious adverse events (SAEs) have been reported.
Common adverse reactions include redness and swelling at the injection site (incidence rate 8.3%) and mild headache (5.0%), both of which are transient.
2. Subgroup analysis of patients with metabolic syndrome: improvement in multiple metabolic risks
In the Phase II trial, subgroup analysis was conducted on 42 patients with concomitant hypertension, hyperglycemia, or dyslipidemia
Blood glucose control:
Fasting blood glucose decreased from 9.2 mmol/L to 7.8 mmol/L (P<0.05), and glycated hemoglobin (HbA1c) decreased by 0.6% (P<0.01).
Blood pressure regulation:
systolic/diastolic blood pressure decreased by 11/7 mmHg (P<0.01), and 14% of patients needed to adjust the dosage of antihypertensive drugs.
Blood lipid optimization:
TG decreased by 28%, HDL-C increased by 15%, and LDL-C/HDL-C ratio improved by 22%.
3. Long term follow-up study: Weight maintenance and metabolic memory effects
Conduct a 52 week extended observation on the participants who completed the Phase II trial:
Weight rebound:
After 12 weeks of discontinuation, the weight of the medication group increased by 1.2 kg, significantly lower than that of the placebo group (3.8 kg, P<0.01).
Metabolic memory:
Even after discontinuation, AOD 9604 injection the medication group showed a 21% improvement in HOMA-IR index compared to baseline, while the placebo group recovered to baseline levels.
Industrial Big Data
Quality of life score: SF-36 scale was used to evaluate, and the physical function, physical activity, and overall health perception scores of the medication group were significantly higher than those of the control group.
Frequently Asked Questions
What does AOD-9604 do?
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AOD 9604 helps your body naturally break down fat cells and use the fat that is stored in your body. Research into this peptide has shown some patients experiencing significant weight loss thanks to this peptide.
Why was AOD-9604 banned?
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It is reported to mimic the lipolytic properties of growth hormone without the diabetogenic side effects. Therefore, AOD9604 may be used as a performance enhancing drug and is banned by the World Anti-doping Agency (WADA).
How much weight can you lose on AOD-9604?
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In a 23-week randomized clinical trial in humans, individuals taking AOD-9604 at 1 mg daily had an average of 2.8 kg weight reduction compared to a 0.8 kg weight reduction in those taking a placebo.
What are the side effects of AOD-9604?
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No Serious Adverse Events: No withdrawals or serious complications related to AOD-9604. Minimal Side Effects: Occasional injection site reactions, mild fatigue, or headache.
How quickly does AOD9604 work?
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30-60 days
Q: How long does it take for AOD 9604 therapy to work? A: There are reported cases where patients are seeing results by week two, but generally results are expected to be anywhere from 30-60 days. It is very patient specific and many other factors do play a role such as lifestyle, diet and health status.
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