The short version of hGH fragment fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2026-05-18. Anything still debated is marked as such rather than presented as settled.
Research interest in AOD-9604 often focuses on whether it can influence lipid metabolism without the growth-promoting or glucose-related effects of full-length hGH. This question remains unresolved, and findings depend on model, dose, and measurement method. Some reviews treat the peptide as a historical obesity candidate rather than an active therapeutic. Others cite it in discussions of peptide fragments, metabolic signaling, and performance-enhancing substances. Clear conclusions are limited by the small number of rigorous, independent human studies.
AOD-9604 has been investigated primarily as a potential treatment for obesity and related metabolic conditions. Early laboratory work examined its effects on fat cells, and later studies moved into animal models and human clinical trials. Some trials reportedly reached Phase II, but the program did not lead to an approved medicine. Published summaries often note that weight-loss results were modest or inconsistent. The full trial data are not all publicly available in detail.
Clinical development of AOD-9604 included trials in people with obesity. Reports from early-phase and mid-phase studies described modest or inconsistent changes in body weight. A phase IIb program did not meet its primary endpoint, and the compound was not approved for medical use. Differences in formulation, delivery route, and participant characteristics may explain some of the variation. Later investigations explored whether the peptide might have effects in other tissues, including cartilage.
Regulatory treatment of AOD-9604 is shaped by its classification as a peptide hormone. The World Anti-Doping Agency lists it as a prohibited substance, and many national anti-doping organizations adopt that list. It does not hold approval as a prescription medicine in the United States, the European Union, or other major markets. Products sold online are frequently labeled for research use only and may not undergo independent quality testing. Import and possession rules differ by country, so legal status depends on local law.
Proposed mechanisms for AOD-9604 focus on fat cells. Laboratory studies suggest the peptide can increase lipolysis, the breakdown of stored fat, and reduce lipogenesis, the formation of new fat. Unlike full human growth hormone, it does not appear to stimulate substantial IGF-1 production in the studies reported so far. Some evidence points to beta-adrenergic signaling, but the precise receptor targets and downstream pathways remain unresolved. The fragment is not thought to act through the classical growth hormone receptor.
| Property | Value | Notes |
|---|---|---|
| Primary research area | Obesity and metabolic regulation | Studied in cell, animal, and human models |
| Highest reported trial phase | Phase II | Public summaries describe mixed results |
| Common route in trials | Subcutaneous injection | Typical for peptide therapeutics |
| Regulatory example | 2013 Australian anti-doping review | Classification was debated at the time |
| Approval status | Not approved as a human medicine | Status can change by jurisdiction |
Interest in AOD-9604 arose from attempts to separate metabolic effects from growth effects attributed to hGH. Early work explored whether the fragment could influence lipolysis or fat oxidation without promoting growth. Those questions remain partly unresolved because human data are limited and results have varied across studies. The peptide is not a hormone replacement for hGH and is not equivalent to hGH in clinical use. Its research history includes both laboratory studies and commercial marketing claims that are not the same as regulatory approval.
AOD-9604 is a synthetic peptide whose structure corresponds to a C-terminal segment of human growth hormone. It is often described as hGH fragment 176-191, a 16-amino-acid sequence. The peptide was designed to isolate a region of hGH associated with fat metabolism while avoiding the full hormone's growth-promoting actions. Laboratory and commercial materials typically present it as a lyophilized powder for research use. Its identity is defined by amino acid sequence, not by a single brand.
Identity and purity are usually assessed with reversed-phase high-performance liquid chromatography and mass spectrometry. Reversed-phase HPLC separates the peptide from related impurities and can estimate purity by ultraviolet absorbance, while mass spectrometry confirms the molecular mass and detects modifications. Peptide mapping, amino acid analysis, and disulfide mapping may be used when the sequence or disulfide arrangement must be verified. Because AOD9604 contains cysteine residues, oxidation and disulfide isomers are possible quality concerns in synthetic batches.
Quality varies among research-grade suppliers, so certificates of analysis and independent testing are important for verification. A typical certificate reports purity by HPLC, identity by mass spectrometry, appearance, and sometimes residual solvents or water content. AOD9604 is often sold as a research chemical not intended for human consumption, and labels can be inaccurate. Common misconceptions include treating the peptide as a form of growth hormone, assuming supplement status, or expecting approved-drug quality from unregulated products.
In December 1990, Iraq made a proposal to withdraw from Kuwait provided foreign troops left the region and that an agreement was reached regarding the Palestinian problem and the dismantlement of Israel's and Iraq's weapons of mass destruction. The White House rejected the proposal. The PLO's Yasser Arafat expressed that neither he nor Saddam insisted that solving the Israel–Palestine issues should be a precondition to solving the issues in Kuwait, though he did acknowledge a "strong link" between these problems. The US and UK stuck to their position there would be no negotiations until Iraq withdrew, and should not grant Iraq concessions, lest they give the impression Iraq benefited from its military campaign. When US secretary of state James Baker met with Tariq Aziz in Geneva, for last minute peace talks in early 1991, Aziz reportedly made no concrete proposals and did not outline any hypothetical Iraqi moves. On 14 January 1991, France proposed that the UN Security Council call for "a rapid and massive withdrawal" from Kuwait along with a statement to Iraq that Council members would bring their "active contribution" to a settlement of the region's other problems, "in particular, of the Arab–Israeli conflict and in particular to the Palestinian problem by convening, at an appropriate moment, an international conference" to assure "the security, stability and development of this region of the world." The proposal was supported by Belgium, Germany, Spain, Italy, Algeria, Morocco, Tunisia, and several non-aligned states.
== Principle == As an analytical biochemistry assay and a "wet lab" technique, ELISA involves detection of an analyte (i.e., the specific substance whose presence is being quantitatively or qualitatively analyzed) in a liquid sample by a method that continues to use liquid reagents during the analysis (i.e., controlled sequence of biochemical reactions that will generate a signal which can be easily quantified and interpreted as a measure of the amount of analyte in the sample) that stays liquid and remains inside a reaction chamber or well needed to keep the reactants contained. This is in contrast to "dry lab" techniques that use dry strips. Even if the sample is liquid (e.g., a measured small drop), the final detection step in "dry" analysis involves reading of a dried strip by methods such as reflectometry and does not need a reaction containment chamber to prevent spillover or mixing between samples. As a heterogenous assay, ELISA separates some components of the analytical reaction mixture by adsorbing certain components onto a solid phase which is physically immobilized. In ELISA, a liquid sample is added onto a stationary solid phase with special binding properties and is followed by multiple liquid reagents that are sequentially added, incubated, and washed, followed by some optical change (e.g., color development by the product of an enzymatic reaction) in the final liquid in the well from which the quantity of the analyte is measured.
=== Rediscovery of glucagon === The hormone glucagon was discovered by C.P. Kimball and John R. Murlin in 1923 as a hyperglycaemic (blood-sugar elevating) substance among the pancreatic extracts. The biological importance of glucagon was not known and the name itself was essentially forgotten. It was a still a mystery at the time de Duve joined Bouckaert at Leuven University to work on insulin. Since 1921, insulin was the first commercial hormonal drug originally produced by the Eli Lilly and Company, but their extraction methods introduced an impurity that caused mild hyperglycaemia, the very opposite of what was expected or desired. In May 1944 de Duve realised that crystallisation could remove the impurity. He demonstrated that Lilly's insulin process was contaminated, showing that, when injected into rats, the Lilly insulin caused initial hyperglycaemia and the Danish Novo insulin did not. Following his research published in 1947, Lilly upgraded its methods to eliminate the impurity. By then de Duve had joined Carl Cori and Gerty Cori at Washington University in St. Louis, where he worked with a fellow researcher Earl Wilbur Sutherland, Jr., who later won the Nobel Prize in Physiology or Medicine in 1971. Sutherland had been working on the puzzle of the insulin-impurity substance, which he had named hyperglycemic-glycogenolytic (HG) factor. He and de Duve soon discovered that the HG factor was synthesised not only by the pancreas but also by the gastric mucosa and certain other parts of the digestive tract.
=== EC 1.3.99 With unknown physiological acceptors === EC 1.3.99.1: The activity is included in EC 1.3.5.1, succinate dehydrogenase (quinone) EC 1.3.99.2: Now EC 1.3.8.1, butyryl-CoA dehydrogenase. EC 1.3.99.3: now EC 1.3.8.7, medium-chain acyl-CoA dehydrogenase, EC 1.3.8.8, long-chain acyl-CoA dehydrogenase and EC 1.3.8.9, very-long-chain acyl-CoA dehydrogenase EC 1.3.99.4: 3-oxosteroid 1-dehydrogenase EC 1.3.99.5: 3-oxo-5α-steroid 4-dehydrogenase (acceptor) EC 1.3.99.6: 3-oxo-5β-steroid 4-dehydrogenase EC 1.3.99.7: Now EC 1.3.8.6, glutaryl-CoA dehydrogenase EC 1.3.99.8: 2-furoyl-CoA dehydrogenase EC 1.3.99.9: Now EC 1.21.99.1, β-cyclopiazonate dehydrogenase EC 1.3.99.10: Now EC 1.3.8.4, isovaleryl-CoA dehydrogenase EC 1.3.99.11: transferred to EC 1.3.5.2, dihydroorotate dehydrogenase EC 1.3.99.12: Now classified as EC 1.3.8.5, 2-methyl-branched-chain-enoyl-CoA reductase EC 1.3.99.13: Now EC 1.3.8.8, long-chain-acyl-CoA dehydrogenase EC 1.3.99.14: cyclohexanone dehydrogenase EC 1.3.99.15: Now EC 1.3.7.8 EC 1.3.99.16: isoquinoline 1-oxidoreductase EC 1.3.99.17: quinoline 2-oxidoreductase EC 1.3.99.18: quinaldate 4-oxidoreductase EC 1.3.99.19: quinoline-4-carboxylate 2-oxidoreductase EC 1.3.99.20: Now EC 1.3.7.9, 4-hydroxybenzoyl-CoA reductase EC 1.3.99.21: Now EC 1.3.8.3, (R)-benzylsuccinyl-CoA dehydrogenase EC 1.3.99.22: Now EC 1.3.98.3, coproporphyrinogen dehydrogenase EC 1.3.99.23: all-trans-retinol 13,14-reductase EC 1.3.99.24: Now EC 1.3.8.16, 2-amino-4-deoxychorismate dehydrogenase EC 1.3.99.25: carvone reductase EC 1.3.99.26: all-trans-ζ-carotene desaturase EC 1.3.99.27: 1-hydroxycarotenoid 3,4-desaturase EC 1.3.99.28: phytoene desaturase (neurosporene-forming) EC 1.3.99.29: phytoene desaturase (zeta-carotene-forming) EC 1.3.99.30: phytoene desaturase (3,4-didehydrolycopene-forming) EC 1.3.99.31: phytoene desaturase (lycopene-forming) EC 1.3.99.32: glutaryl-CoA dehydrogenase (non-decarboxylating) EC 1.3.99.33: urocanate reductase EC 1.3.99.34: Now classified as EC 1.3.7.11, 2,3-bis-O-geranylgeranyl-sn-glycero-phospholipid reductase EC 1.3.99.35: Now EC 1.3.7.15, chlorophyllide a reductase * EC 1.3.99.36: cypemycin cysteine dehydrogenase (decarboxylating) EC 1.3.99.37: 1-hydroxy-2-isopentenylcarotenoid 3,4-desaturase EC 1.3.99.38: menaquinone-9 β-reductase EC 1.3.99.39: carotenoid φ-ring synthase EC 1.3.99.40: carotenoid χ-ring synthase
Sources: en.wikipedia.org
In 2022 Novo Nordisk would give up their rights to Macrilen, returning them and all associated licensing to Aeterna Zentaris. The US Food and Drug Administration (FDA) considers it to be a first-in-class medication.
in vivo (of a scientific experiment or biological process) Occurring or made to occur inside the cells or tissues of a living organism; or, in the broadest sense, in any natural, unmanipulated setting. Contrast ex vivo and in vitro.
Knowing Nixon's fears, Kissinger told him that if he did nothing, "it shows that you're weak, Mr. President. The fact that some idiot can publish all the diplomatic secrets of this country on his own is damaging to your image as far as the Soviets are concerned and it could destroy our ability to conduct foreign policy". Daniel Ellsberg, the man who leaked the Pentagon Papers to the New York Times, had been consulted by Kissinger for ideas about Vietnam in late 1968–early 1969, but when he leaked the papers, Kissinger told Nixon that he was a left-wing "fanatic" and a "drug abuser". Kissinger depicted Ellsberg to Nixon as a drug-crazed, sexually perverted degenerate of questionable mental stability out to ruin his administration. Reflecting his increasing frustration with the war, Nixon often talked to Kissinger in a bloodthirsty manner about a "fantasy holocaust" in which he would have U.S. forces kill every living thing in North Vietnam and then pull out, leading the latter appalled by his own account. By early 1972, Nixon boasted that he had pulled out 400,000 U.S. soldiers from Vietnam since July 1969, and battle deaths had fallen from an average of 200 per week in 1969 down to an average of 10 per week in 1972. The policy of Vietnamization had, as Laird predicted, tamed the antiwar movement as most Americans objected not to the war in Vietnam per se, only to Americans dying in it.
The CBC measures the amounts of platelets and red and white blood cells, along with the hemoglobin and hematocrit values. Red blood cell indices—MCV, MCH and MCHC—which describe the size of red blood cells and their hemoglobin content, are reported along with the red blood cell distribution width (RDW), which measures the amount of variation in the sizes of red blood cells. A white blood cell differential, which enumerates the different types of white blood cells, may be performed, and a count of immature red blood cells (reticulocytes) is sometimes included.
== Reactions == Esters are less reactive than acid halides and anhydrides. As with more reactive acyl derivatives, they can react with ammonia and primary and secondary amines to give amides, although this type of reaction is not often used, since acid halides give better yields.
Sources: en.wikipedia.org
No major medicines regulator appears to have approved AOD-9604 for human therapeutic use. It has been studied in clinical trials, but those programs did not result in a marketed drug.
It became prominent during a 2013 Australian sports investigation that examined whether it was a prohibited growth-hormone-related substance. Subsequent interpretations and list updates have varied, so current rules should be checked directly.
Published summaries generally report limited or inconsistent weight-loss effects, and complete trial data are not widely available. The studies were not sufficient to establish it as an effective obesity treatment.
No. Major drug regulators have not approved AOD-9604 for weight loss or any other therapeutic indication. It remains an investigational compound studied in research settings.