The short version of REV-ERB agonist fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2026-03-17 and is reviewed periodically as new material appears.
REV-ERB proteins help regulate daily cycles in gene expression, including genes tied to lipid and glucose metabolism. SR9009 binds these receptors and alters their activity in cell and animal experiments. Consequences observed in rodents include changes in skeletal muscle oxidative capacity, blood lipid levels, and exercise performance. The precise chain from receptor occupancy to whole-body effects is still an active area of study. Human responses cannot be assumed from rodent data.
Most published work on SR9009 consists of preclinical studies. It is widely sold as a research chemical, a category that does not imply safety, efficacy, or pharmaceutical-grade quality. Sports anti-doping organizations have listed SR9009 as a prohibited substance, and its presence in an athlete sample can lead to sanctions. Legal status differs by country; in several jurisdictions it is not approved for human consumption and may be treated as an unapproved new drug.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not a steroid, peptide, or natural hormone. In scientific literature, it appears under the code SR9009 and in non-scientific contexts as Stenabolic. The compound was identified through chemical screening efforts aimed at targeting circadian clock components. Its status remains investigational, and no regulatory agency has approved it as a human medicine.
Several misconceptions surround SR9009. It is often described as a SARM, a steroid, or an exercise pill, but its known target is the REV-ERB receptor family. Rodent studies have examined exercise capacity and metabolic markers, yet human outcomes remain unproven. Oral bioavailability appears low in animals, and human pharmacokinetics are not well characterized. Online products may contain impurities or different compounds, so identity and purity testing are important for research use.
Analytical chemists detect SR9009 with liquid chromatography-tandem mass spectrometry, commonly abbreviated LC-MS/MS. Sample preparation may involve protein precipitation, liquid-liquid extraction, or solid-phase extraction before analysis. Laboratories can target the parent compound or its metabolites, depending on the matrix and the purpose of testing. Anti-doping methods require sensitive and specific assays because concentrations in biological samples can be low. Reference standards and validated methods are essential for reliable identification and quantification.
| Property | Value | Notes |
|---|---|---|
| Common name | SR9009 | Also referred to as Stenabolic in non-scientific contexts. |
| Chemical class | Synthetic small molecule | Not a steroid or peptide hormone. |
| Receptor target | REV-ERBα and REV-ERBβ | Nuclear receptor agonist in preclinical studies. |
| Development status | Investigational | No approved human therapeutic indication. |
| Regulatory attention | Prohibited in sport | Listed by anti-doping authorities. |
Preclinical reports have linked SR9009 to improved endurance and altered energy expenditure in rodents. Such findings have prompted interest in whether REV-ERB activation can influence skeletal muscle metabolism. However, the reported effects depend on dose, route, and experimental model, and replication across laboratories is limited. Human trials have not established comparable outcomes, so claims about exercise performance remain speculative. The absence of controlled human data is a central limitation in interpreting these observations.
The mechanism of action involves binding to REV-ERB receptors and recruiting corepressor complexes, which represses target gene transcription. This contrasts with many nuclear receptor agonists that activate transcription. Downstream effects may include changes in autophagy, mitochondrial biogenesis, and lipid handling, but the precise pathways remain an active area of study. Whether these molecular events translate into meaningful physiological effects in humans is unresolved. Most evidence comes from cultured cells and rodent models rather than human participants.
Adrenomedullin (ADM) is a multifunctional peptide hormone that plays an important role in the homeostasis of the cardiovascular system and in inflammatory response. It acts as a potent vasodilator, regulating vascular tone and blood pressure through both endothelium-dependent and independent mechanisms. ADM exerts protective effects on the cardiovascular system by inhibiting apoptosis in endothelial cells, reducing oxidative stress, and regulating vascular smooth muscle cell proliferation. In the heart, it increases cardiac output and augments myocardial contractility. Beyond its cardiovascular functions, ADM demonstrates significant anti-inflammatory properties, modulating cytokine production and secretion in macrophages. It also contributes to the maintenance of vascular integrity, potentially reducing vascular permeability during inflammatory conditions. In addition, ADM has been implicated in angiogenesis, protection of organs, and tissue repair. Because of its wide-ranging effects, it has potential therapeutic applications in a variety of diseases, including inflammatory bowel disease, sepsis, and cardiovascular disorders.
In humans, FDC-SP was first found within follicular dendritic cell isolates from the tonsil, and later was found to be specifically expressed within the periodontal ligament. FDC-SP expression can be induced in human FDC-like cell lines by exposure to tumour necrosis factor (TNF). Exposure of human peripheral blood cells to LPS can also result in FDC-SP expression, but TNF exposure does not cause FDC-SP expression and similarly LPS exposure does not cause expression within FDC-like cell lines. Expression in mouse splenocytes can be induced by LPS in a similar manner to that of human peripheral blood cells. In mice, as in humans, FDC-SP is not expressed in B cells, but FDC-SP expression in FDCs can be dependent on B cells after their stimulation by CD40. After stimulation with CD40, B cells have been shown to be able to induce phenotypic changes in FDCs through the B cell's surface TNF expression. It has therefore been suggested that the expression of TNF cytokines by B cells causes FDC-SP expression within FDCs upon contact. This reaction is said to be typical during GC formation. FDC-SP is highly expressed in the junctional epithelium and well as in the tonsils, prostate, lymph nodes and trachea. The proline rich region in the C-terminal half bears some resemblance to the antimicrobial peptide Bac5. FDC-SP may therefore have a role in microbial defense in the oral cavity.
Prof. Ralser serves since 2019 as head of the Institute of Biochemistry at the Charité – Universitätsmedizin Berlin, Germany; as well as since 2022 as group leader at the University of Oxford, UK. He studied genetics and molecular biology in Salzburg, Austria. He completed his PhD in 2006 at the Max Planck Institute for Molecular Genetics in Berlin, Germany, studying neurodegenerative diseases. This was followed by a postdoctoral fellowship at the Vrije Universiteit Amsterdam, Netherlands, where he started to explore mass spectrometry. He returned to the MPI for Molecular Genetics in 2007 to become junior group leader, but in 2011 relocated his group to the University of Cambridge, UK. He relocated again, becoming group leader at the newly opened Francis Crick Institute in London in 2013 (senior group leader since 2019). His group moved to Oxford in 2022.
The localization of ADAM17 is speculated to be an important determinant of shedding activity. TNF-α processing has classically been understood to occur in the trans-Golgi network, and be closely connected to transport of soluble TNF-α to the cell surface. Shedding is also associated with clustering of ADAM17 with its substrate, membrane bound TNF, in lipid rafts. The overall process is called substrate presentation and regulated by cholesterol. Research also suggests that the majority of mature, endogenous ADAM17 may be localized to a perinuclear compartment, with only a small amount of TACE being present on the cell surface. The localization of mature ADAM17 to a perinuclear compartment, therefore, raises the possibility that ADAM17-mediated ectodomain shedding may also occur in the intracellular environment, in contrast with the conventional model. Functional ADAM17 has been documented to be ubiquitously expressed in the human colon, with increased activity in the colonic mucosa of patients with ulcerative colitis, a main form of inflammatory bowel disease. Other experiments have also suggested that expression of ADAM17 may be inhibited by ethanol.
== Nuclear fuel == Uranium-233 has been used as fuel in several reactor types and has been proposed for use in new designs. Uranium-233 can be bred in either fast reactors or thermal reactors, unlike the uranium-238-based fuel cycles which require the superior neutron economy of a fast reactor in order to breed plutonium, that is, to produce more fissile material than is consumed. In 1968, the Molten-Salt Reactor Experiment at Oak Ridge became the first reactor to operate on uranium-233. The long-term strategy of the nuclear power program of India, which has substantial thorium reserves, is to move to a nuclear program breeding uranium-233 from thorium feedstock.
Sources: en.wikipedia.org
Treatments include dietary changes emphasizing low glycemic index food, physical activity to improve insulin sensitivity, and medications that (1) increase the amount of insulin secreted by the pancreas, (2) increase the sensitivity of target organs to insulin, (3) decrease the rate at which glucose is absorbed from the gastrointestinal tract, and (4) increase the loss of glucose through urination. Several drug classes are indicated for use in type 2 diabetes and are often used in combination. Therapeutic combinations may include several insulin isoforms or varying classes of oral antihyperglycemic agents. As of 2020, 23 unique antihyperglycemic drug combinations were approved by the FDA. The first triple combination of oral anti-diabetics was approved in 2019, consisting of metformin, saxagliptin, and dapagliflozin. Another triple combination approval for metformin, linagliptin, and empagliflozin followed in 2020.
In chemistry, racemization is a conversion, by heat or by chemical reaction, of an optically active compound into a racemic (optically inactive) form. This creates a 1:1 molar ratio of enantiomers and is referred to as a racemic mixture (i.e. contain equal amount of (+) and (−) forms). Plus and minus forms are called dextrorotation and levorotation. The D and L enantiomers are present in equal quantities, the resulting sample is described as a racemic mixture or a racemate. Racemization can proceed through a number of different mechanisms, and it has particular significance in pharmacology in as much as different enantiomers may have different pharmaceutical effects.
The International Ink Library and its Digital Ink Library are an FBI forensic database of inks. It is used to identify writing instruments, makes, models, ink types, and document authenticity. It contains over 15,000 samples of pen, marker, and printer inks dating from the 1920s. As part of the FBI Questioned Documents Branch, it is used to investigate criminal and terrorist cases, fraudulent documents, forgeries, checks, money orders, and threats to persons. It uses high-performance thin-layer chromatography, electrophoresis, ultraviolet spectra, electrospray ionization and mass spectrometry. It also analyzes chemical date tags expressly inserted by ink manufacturers. The database originated in the 1960s from the collection of Antonio Cantu, former Chief Forensic Chemist at the Secret Service, which dedicated the lab in his honor. There is no cost to access, but is limited to U.S. Secret Service directorates, students through coordinated research initiatives, and law enforcement entities. It handles over 500 cases per year. It has been used in such cases as the Jasper Johns forged documents, the Martha Stewart conviction, as well as the 9/11 attacks.
Following months of rumours and investigations, on 13 August 2013, Corcoran, along with the Essendon Football Club, senior coach James Hird, senior assistant coach Mark Thompson and club doctor Bruce Reid was charged by the AFL with bringing the game into disrepute in relation to the supplements program at the club in 2011 and 2012. The club was given 14 days to consider the charges and faced an AFL Commission hearing on 26 August 2013. On 27 August 2013, Corcoran was banned for six months with two months of that time suspended for a period of two years; effectively a four-month ban. He cannot work with any AFL club in any capacity during that period.
Sources: en.wikipedia.org
It is a synthetic compound studied as an agonist of REV-ERB nuclear receptors. It is not an approved medicine and has mainly been examined in laboratory and animal research.
No. It is a small molecule that binds nuclear receptors involved in circadian regulation. Its classification differs from anabolic steroids or peptide hormones.
Published human clinical trial data are lacking. Most safety and activity information comes from preclinical models, so effects in people remain uncertain.
Legality depends on the country and the intended use. In many places it is not approved as a medicine and may be sold only as a research chemical. Importation or possession can be restricted, and sports organizations prohibit it.