If you have been reading about AOD-9604 and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Last reviewed on 2025-08-19. Where a claim depends on a specific study, the study is described rather than over-claimed.
Development of AOD-9604 began in the 1990s as scientists sought to isolate metabolic effects of growth hormone without its growth-promoting actions. Early laboratory work focused on fat cells and animal models. Several human trials followed, examining changes in body composition and fat mass. Results have been mixed, and the peptide has not progressed to widespread clinical approval. Interest continues in research settings, particularly regarding its mechanism and potential metabolic targets.
Regulatory status varies by country. In the United States, AOD-9604 is not approved as a prescription drug. It is sometimes sold as a research chemical or dietary supplement, though such marketing may fall outside legal frameworks. The World Anti-Doping Agency prohibits its use in sport. Researchers must obtain it through legitimate suppliers and follow institutional rules. Its legal classification continues to evolve as authorities increasingly assess peptide products more broadly.
Clinical development of AOD9604 included trials in people with obesity, but the results did not lead to approval as a prescription medicine in major markets. Interest later shifted to research settings and to unapproved products marketed for body composition. Regulatory agencies have questioned whether the peptide qualifies as a dietary ingredient, and some have issued warnings about its presence in supplements. Long-term human safety data are limited, and questions about efficacy, dosing, and target populations remain unresolved.
AOD9604 is a synthetic peptide modeled on the C-terminal region of human growth hormone. It corresponds to a short sequence near the end of the 191-amino-acid hormone, often described as residues 176–191 or a related fragment. Researchers designed it to separate metabolic effects from the growth-promoting actions of full-length growth hormone. Early work in the 1990s explored it as a candidate for weight and lipid disorders. It is not a naturally circulating hormone fragment produced in large amounts.
Laboratory studies have reported that AOD9604 can increase lipolysis and reduce lipid accumulation in fat cells. The precise molecular target remains uncertain, and the compound does not appear to activate the growth hormone receptor in the same way as full-length hGH. Proposed mechanisms include effects on beta-adrenergic signaling and enzymes involved in fatty acid synthesis, but these pathways are not firmly established. Because most evidence comes from cell and animal models, whether the same effects occur in humans is an open question.
| Property | Value | Notes |
|---|---|---|
| Molecular class | Peptide fragment | Corresponds to hGH residues 176-191 |
| Common synonyms | AOD9604, hGH 176-191 | Also written as AOD-9604 |
| Typical form | Lyophilized powder | Often supplied in sealed vials |
| Solubility | Water-soluble | Dissolves in aqueous buffers |
| Regulatory status | Not approved as drug | Banned in sport; varies by country |
In the scientific literature, AOD-9604 appears in reviews of growth hormone fragments and in discussions of peptide-based metabolic research. Some sources distinguish it from growth hormone itself, while others group it with compounds marketed for weight management. The evidence base is small compared with approved obesity medications. Questions about long-term efficacy and clinical relevance remain open, and independent replication of key findings is limited. Most published reports are early-stage and exploratory.
AOD-9604 is a synthetic peptide modeled on the C-terminal region of human growth hormone. It is often described as hGH fragment 176-191. Research interest arose because it was designed to isolate possible effects on fat metabolism from other actions of growth hormone. It is not a full growth hormone molecule. Its development history includes early laboratory and animal studies followed by human trials. The peptide has been examined in laboratory, animal, and limited human studies.
The peptide is frequently described as a growth hormone fragment, although it is chemically distinct from full-length hGH. AOD-9604 contains 16 amino acids and includes two cysteine residues that can form an intramolecular disulfide bond. In solution, this structural feature can influence folding, aggregation, and stability. Published descriptions sometimes call it hGH 176-191 or AOD9604, with spacing and capitalization varying. Such naming differences can complicate literature searches, database entries, and product verification.
Researchers have studied the fragment in cell and animal models to understand its metabolic actions. Some experiments report effects on fat breakdown and fat storage pathways, but the underlying mechanism remains incompletely defined. AOD-9604 does not appear to stimulate the same broad growth hormone receptor signaling as full-length hGH. Whether its observed activities arise from direct receptor interactions or downstream metabolic changes is an open question. Results from different assays are not always consistent.
AOD-9604 is a synthetic peptide modeled on the C-terminal region of human growth hormone. It corresponds to residues 176-191 of the 191-amino-acid hGH sequence. The fragment is not the full hormone and lacks the receptor-binding region associated with growth and metabolic effects of hGH. Researchers developed it to isolate a specific portion of hGH for study. Its exact sequence and length are often stated in peptide catalogs and patents.
Immune evasion proteins from Staphylococcus aureus have a significant conservation of protein structures and a range of activities that are all directed at the two key elements of host immunity, complement and neutrophils. These secreted virulence factors assist the bacterium in surviving immune response mechanisms. Examples of toxins produced by strains of S. aureus include enterotoxins that cause food-poisoning, exfoliative toxins that cause scalded skin syndrome, and toxic-shock syndrome toxin (TSST) that underlies toxic shock syndrome. These toxin examples are classified as superantigens. Multi-drug resistant S. aureus strains also produce alpha toxin, classified as a pore-forming toxin, which can cause abscesses.
56. J Physiol Pharmacol. 2009 Dec;60 Suppl 7:191-6. Modulatory effect of gastric pentadecapeptide BPC 157 on angiogenesis in muscle and tendon healing. Brcic L(1), Brcic I, Staresinic M, Novinscak T, Sikiric P, Seiwerth S. Author information: (1)Institute of Pathology, University of Zagreb Medical School, Zagreb, Croatia. Angiogenesis is a natural and complex process controlled by angiogenic and angiostatic molecules, with a central role in healing process. One of the most important modulating factors in angiogenesis is the vascular endothelial growth factor (VEGF). Pentadecapeptide BPC 157 promotes healing demonstrating particular angiogenic/angiomodulatory potential. We correlated the angiogenic effect of BPC 157 with VEGF expression using in vitro (cell culture) and in vivo (crushed muscle and transected muscle and tendon) models. Results revealed that there is no direct angiogenic effect of BPC 157 on cell cultures. On the other hand, immunohistochemical analysis of muscle and tendon healing using VEGF, CD34 and FVIII antibodies showed adequately modulated angiogenesis in BPC 157 treated animals, resulting in a more adequate healing. Therefore the angiogenic potential of BPC 157 seems to be closely related to the healing process in vivo with BPC 157 stimulating angiogenesis by up-regulating VEGF expression.
8. Ir Med J. 2026 Sep 28;119(8):161. Type A Insulin Resistance Syndrome Due to a Pathogenic Variant in the INSR Gene. Afzal S, Brosnan E, Sadiq MS, Rizvi SR, Wassem Z, Iqbal F. PRESENTATION: A woman in her 40s initially diagnosed with type 1 diabetes in 1994 exhibited an atypical 30-year metabolic course, characterised by fluctuating insulin sensitivity, prolonged insulin independence and later insulin resistance despite a non-obese phenotype. DIAGNOSIS: Owing to the unusual clinical trajectory and a strong family history of young-onset diabetes, genetic testing identified a heterozygous pathogenic INSR mutation (p.M1180K), confirming Type A Insulin Resistance Syndrome (TAIRS). TREATMENT: Management evolved from insulin therapy to oral hypoglycaemic agents, including metformin and gliclazide alongside lifestyle modification resulting in partial glycaemic improvement. DISCUSSION: This case underscores the diagnostic challenge of TAIRS, which is frequently misclassified as type 1 or type 2 diabetes and highlights the importance of early genetic evaluation and multidisciplinary care.
Different isoforms of actin are present in the cell nucleus. The level of actin isoforms may change in response to stimulation of cell growth or arrest of proliferation and transcriptional activity. Research on nuclear actin is focused on isoform beta. However the use of antibodies directed against different actin isoforms allows identifying not only the cytoplasmic beta in the cell nucleus, but also alpha- and gamma-actin in certain cell types. The presence of different isoforms of actin may have a significant effect on its function in nuclear processes, as the level of individual isoforms can be controlled independently. Functions of actin in the nucleus are associated with its ability to polymerize and interact with various ABPs and with structural elements of the nucleus. Nuclear actin is involved in:
AS9000 (1997) Aerospace Basic Quality System Standard As aerospace suppliers soon found that ISO 9001 (1994) did not address the specific requirements of their customers, including the DoD, NASA, FAA, and commercial aerospace companies including Boeing, Lockheed Martin, Northrop Grumman, GE Aircraft Engines and Pratt & Whitney, they developed AS9000, based on ISO 9001, to provide a specific quality management standard for the aerospace industry. Prior to the adoption of an aerospace specific quality standard, various corporations typically used ISO 9001 and their own complementary quality documentation/requirements, such as Boeing's D1-9000 or the automotive Q standard. This created a patchwork of competing requirements that were difficult to enforce and/or comply with. The major American aerospace manufacturers collaborated to develop a unified quality standard based on ISO 9001:1994, which led to the creation of AS9000. Following its release, companies like Boeing discontinued their previous quality supplements in favor of complying with AS9000.
Sources: en.wikipedia.org
Glycogenolysis and gluconeogenesis in liver. Glycogenolysis and lactate release in skeletal muscle. Contract sphincters of Gastrointestinal tract. Thickened secretions from salivary glands. Insulin and glucagon secretion from pancreas. Inhibit histamine-release from mast cells. Increase protein content of secretions from lacrimal glands. Receptor also present in cerebellum. Bronchiole dilation (targeted while treating asthma attacks) Involved in brain - immune - communication Short-acting β2 agonists (SABA) bitolterol fenoterol hexoprenaline isoprenaline (INN) or isoproterenol (USAN) levosalbutamol (INN) or levalbuterol (USAN) orciprenaline (INN) or metaproterenol (USAN) pirbuterol procaterol salbutamol (INN) or albuterol (USAN) terbutaline Long-acting β2 agonists (LABA) arformoterol (some consider it to be an ultra-LABA) bambuterol clenbuterol formoterol salmeterol Ultra-long-acting β2 agonists (ultra-LABA) carmoterol indacaterol milveterol (GSK 159797) olodaterol vilanterol (GSK 642444)
DeepMind is known to have trained the program on over 170,000 protein structures from the Protein Data Bank, a public repository of protein sequences and structures. The program uses a form of attention network, a deep learning technique that focuses on having the AI identify parts of a larger problem, then piece it together to obtain the overall solution. The overall training was conducted on processing power between 100 and 200 GPUs.
As the salt of a weak base (ammonium) and a weak acid (acetic acid), is often used to create a buffer solution. Ammonium acetate is volatile at low pressures. Because of this, it has been used to replace cell buffers that contain non-volatile salts in preparing samples for mass spectrometry. It is also popular as a buffer for mobile phases for HPLC with ELSD and CAD-based detection for this reason. Other volatile salts that have been used for this include ammonium formate. When dissolving ammonium acetate in pure water, the resulting solution typically has a pH of 7, because the equal amounts of acetate and ammonium neutralize each other. However, ammonium acetate is a dual component buffer system, which buffers around pH 4.75 ± 1 (acetate) and pH 9.25 ± 1 (ammonium), but it has no significant buffer capacity at pH 7, contrary to common misconception.
The first few amino acids were discovered in the early 1800s. In 1806, French chemists Louis-Nicolas Vauquelin and Pierre Jean Robiquet isolated a compound from asparagus that was subsequently named asparagine, the first amino acid to be discovered. Cystine was discovered in 1810, although its monomer, cysteine, remained undiscovered until 1884. Glycine and leucine were discovered in 1820. The last of the 20 common amino acids to be discovered was threonine in 1935 by William Cumming Rose, who also determined the essential amino acids and established the minimum daily requirements of all amino acids for optimal growth. The unity of the chemical category was recognized by Wurtz in 1865, but he gave no particular name to it. The first use of the term "amino acid" in the English language dates from 1898, while the German term, Aminosäure, was used earlier. Proteins were found to yield amino acids after enzymatic digestion or acid hydrolysis. In 1902, Emil Fischer and Franz Hofmeister independently proposed that proteins are formed from many amino acids, whereby bonds are formed between the amino group of one amino acid with the carboxyl group of another, resulting in a linear structure that Fischer termed "peptide".
The Rho GTPase activating protein 31 is encoded in humans by the ARHGAP31 gene. It is a Cdc42/Rac1 GTPase regulator. ARHGAP31 encodes a GTPase-activating protein (GAP). A variety of cellular processes are regulated by Rho GTPases which cycle between an inactive form bound to GDP and an active form bound to GTP. This cycling between inactive and active forms is regulated by guanine nucleotide exchange factors and GAPs. The encoded protein is a GAP shown to regulate two GTPases involved in protein trafficking and cell growth. ARHGAP31 mutations result in a loss of available active Cdc42 and consequently disrupt actin cytoskeletal structures, causing syndromic cutis aplasia and limb anomalies. Human ARHGAP31 genome location and ARHGAP31 gene details page in the UCSC Genome Browser. This article incorporates text from the United States National Library of Medicine, which is in the public domain.
Sources: en.wikipedia.org
AOD-9604 is a synthetic peptide fragment of human growth hormone, corresponding to amino acids 176-191. It is studied for potential effects on fat metabolism, but it is not approved as a drug in most countries. Its exact mechanism remains under investigation.
No, it is a small fragment of the full growth hormone protein. It does not appear to stimulate growth or increase growth hormone levels in the same way. Its actions are thought to be more limited to metabolic pathways.
Regulatory status varies. It is not approved for medical use in the United States or many other countries. It is banned in sport by WADA, and its sale as a supplement or research chemical may be subject to legal restrictions.
AOD9604 is a synthetic peptide based on a C-terminal segment of human growth hormone. It is manufactured by chemical peptide synthesis rather than extracted from human tissue. The sequence is often described as hGH fragment 176–191 or a close variant.