The short version of REV-ERB fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2026-06-15 and is reviewed periodically as new material appears.
SR9009 is a synthetic small molecule that acts on the nuclear receptors REV-ERBα and REV-ERBβ. These receptors are part of the circadian clock machinery and normally repress transcription of certain target genes. In laboratory research, SR9009 is used as a chemical tool to study how REV-ERB activity influences metabolism, inflammation, and daily biological rhythms. The compound is not an approved medicine, and its effects in humans remain largely uncharacterized. It is often described as an investigational agent rather than a therapeutic product.
REV-ERB proteins typically suppress gene expression by recruiting corepressor complexes to DNA response elements. SR9009 binds these receptors and strengthens that repressive action in cell-based assays. Studies in rodents have reported changes in lipid handling, mitochondrial function, and exercise capacity after treatment. Such findings are often cited as evidence for metabolic effects, but species differences and limited pharmacokinetic data make direct translation to humans uncertain. Researchers continue to examine which effects are robust and which depend on specific experimental conditions.
SR9009 is frequently discussed alongside other REV-ERB ligands, including synthetic agonists and natural heme-related molecules. Its selectivity for REV-ERB over related nuclear receptors has been measured in binding and reporter assays, though off-target activity at higher concentrations is possible. The compound is prohibited in sport by the World Anti-Doping Agency, and it is not approved for any medical use in major jurisdictions. Products sold online may be labeled as research chemicals, and their identity and purity are not guaranteed by regulatory review.
In rodent studies, SR9009 has been reported to increase mitochondrial content in skeletal muscle and improve exercise endurance under some conditions. These findings led to popular descriptions such as an exercise mimetic, although that term oversimplifies the biology. Effects vary by dose, timing, tissue, and model. The compound's influence on circadian pathways means that time of administration can matter in experiments. Whether similar metabolic changes occur in humans remains largely unexplored in controlled published trials.
Pharmacokinetic data for SR9009 are limited in published literature. Some reports indicate low oral bioavailability and rapid clearance in animals, which complicates interpretation of exposure and effect. Researchers often use injected routes in preclinical work to achieve measurable systemic levels. Analytical studies rely on mass spectrometry to detect the parent compound and its metabolites. Questions about tissue distribution, active metabolites, and long-term consequences remain open. Species differences in metabolism can affect observed half-life and target engagement.
| Property | Value | Notes |
|---|---|---|
| Common name | SR9009 | Also marketed informally as Stenabolic |
| Chemical class | Synthetic REV-ERB agonist | Binds REV-ERBα and REV-ERBβ |
| Molecular formula | C24H30ClN3O4S | Approximate molecular weight 492 g/mol |
| CAS Registry Number | 1379686-30-2 | Identifier for the parent compound |
| Regulatory status | Not approved for human use | Prohibited in sport by WADA |
Regulatory treatment of SR9009 varies by country and context. It is not approved as a therapeutic drug by agencies such as the United States Food and Drug Administration or the European Medicines Agency. Sports authorities list it as a prohibited substance; the World Anti-Doping Agency classifies it among hormone and metabolic modulators. Legal status for personal possession or sale differs across jurisdictions, and some countries may restrict it under analog or research chemical laws. Buyers who seek verified material often rely on independent laboratory testing because online product labels may not match contents.
Laboratory samples of SR9009 are typically handled as research chemicals rather than pharmaceuticals. Suppliers usually state that the material is for research use only and not for human or veterinary administration. Storage recommendations generally call for a freezer at approximately −20 °C, protection from light, and a desiccated environment. The solid is often described as a white to off-white powder. Solubility is commonly reported in organic solvents such as dimethyl sulfoxide and ethanol, with low solubility in water.
Analytical identification and purity assessment often use high-performance liquid chromatography with ultraviolet detection or mass spectrometry. Liquid chromatography–tandem mass spectrometry is used to detect and quantify SR9009 in biological matrices, including urine and blood, for anti-doping or pharmacokinetic studies. Nuclear magnetic resonance spectroscopy can confirm molecular structure. Stability depends on form and storage: the solid is generally more stable than solutions, and repeated freeze–thaw cycles may degrade samples. Purity is typically reported as a percentage from a certificate of analysis.
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.
SR9009 stability depends on temperature, moisture, light, and solvent. Solid material is generally kept cool and dry, while solutions may require protection from repeated warming and cooling. Degradation can appear as color changes, precipitate, or new chromatographic peaks. Researchers should follow supplier instructions and their own stability data. Long-term storage conditions for human use have not been established because the compound lacks approved clinical formulation.
SR9009 is supplied as a solid research chemical, often in milligram quantities. Laboratories typically weigh it in a controlled environment because fine powders can disperse. Stock solutions are commonly prepared in dimethyl sulfoxide and stored in small aliquots to reduce freeze-thaw cycles. Personal protective equipment and chemical fume hoods are standard when handling unknown or potent compounds. These practices address laboratory safety rather than human use.
Identity and purity of SR9009 samples are usually checked with chromatographic and spectrometric methods. High-performance liquid chromatography can separate the compound from related impurities, while mass spectrometry provides molecular mass confirmation. Nuclear magnetic resonance spectroscopy may be used for structural verification in research settings. No single method proves biological activity, and certificates of analysis should be reviewed alongside raw data. Independent testing is often needed because online products vary widely.
Bantu Stephen Biko OMSG (18 December 1946 – 12 September 1977) was a South African anti-apartheid activist. Ideologically an African nationalist and African socialist, he was at the forefront of a grassroots anti-apartheid campaign known as the Black Consciousness Movement during the late 1960s and 1970s. His ideas were articulated in a series of articles published under the pseudonym Frank Talk. Raised in a poor Xhosa family, Biko grew up in Ginsberg township in the Eastern Cape. In 1966, he began studying medicine at the University of Natal, where he joined the National Union of South African Students (NUSAS). Strongly opposed to the apartheid system of racial segregation and white-minority rule in South Africa, Biko was frustrated that NUSAS and other anti-apartheid groups were dominated by white liberals, rather than by the blacks who were most affected by apartheid. He believed that well-intentioned white liberals failed to comprehend the black experience and often acted in a paternalistic manner. He developed the view that to avoid white domination, black people had to organise independently, and to this end he became a leading figure in the creation of the South African Students' Organisation (SASO) in 1968. Membership was open only to "Blacks", a term that Biko used in reference not just to Bantu-speaking Africans but also to Coloureds and Indians. He was careful to keep his movement independent of white liberals, but opposed anti-white hatred and had white friends.
== Career == Chilkoti joined Duke University in 1996 as an assistant professor of biomedical engineering. He was promoted to associate professor in 2002 and professor in 2006. He was the Theo Pilkington Chair Professor of Biomedical Engineering from 2008 to 2013, and has been the Alan L. Kaganov Distinguished Professor of Biomedical Engineering at Duke University since 2013. From 2002 till 2007, Chilkoti served as associate director of the Center for Biologically Inspired Materials and Material Systems at Duke University and was the director of the center from 2007 to 2011. In 2014, he became Chair of the Department of Biomedical Engineering at Duke University and served as chair until 2022. As Chair of the Duke BME department, he launched an incubator—BRiDGE—for Biomedical Engineering faculty and student startups, and he created the Duke Engineering Entrepreneurship program (DEEP)—a post-doctoral fellowship program for recent PhD graduates of the department interested in entrepreneurship. Since 2023, he has been serving as the senior associate dean of Pratt School of Engineering at Duke University. Chilkoti founded two Gordon Research Conferences (GRCs)—one on Biointerface Science in 2006 and a second on Bioinspired Materials in 2012. Furthermore, he is the founder of five start-ups.
Elizabeth Tracy Mae "Bethe" Wettlaufer (née Parker; born June 10, 1967) is a convicted Canadian serial killer and former registered nurse who confessed to murdering eight senior citizens and attempting to murder six other people in southwestern Ontario between 2007 and 2016. With a total of 14 victims either killed or injured by her actions, she is described as one of the deadliest serial killers in Canadian history.
=== Transcriptional dysregulation === CREB-binding protein (CBP), a transcriptional coregulator, is essential for cell function because as a coactivator at a significant number of promoters, it activates the transcription of genes for survival pathways. CBP contains an acetyltransferase domain to which HTT binds through its polyglutamine-containing domain. Autopsied brains of those who had Huntington's disease also have been found to have incredibly reduced amounts of CBP. In addition, when CBP is overexpressed, polyglutamine-induced death is diminished, further demonstrating that CBP plays an important role in Huntington's disease and neurons in general.
Sources: en.wikipedia.org
== Awards and honours == 2007 Donald F. Steiner Award for Outstanding Diabetes Research, University of Chicago 2008 Prix Galien Canada for Outstanding Pharmaceutical Research 2009 Clinical Investigator Award, Endocrine Society 2012 Claude Bernard Prize, European Association for the Study of Diabetes 2012 Fellow of the Royal Society of Canada 2013 Oon International Award for Preventative Medicine, University of Cambridge 2014 Banting Medal for Scientific Achievement, American Diabetes Association 2014 Manpei Suzuki Foundation International Prize for Diabetes, Japan 2015 Fellow of the Royal Society 2015 Officer of the Order of Canada 2017 Rolf Luft Award in Endocrinology and Diabetes Research, Karolinska Institute 2017 Harrington Prize for Innovation in Medicine, American Society for Clinical Investigation and the Harrington Institute (co-recipient with Joel Habener and Jens Juul Holst) 2019 Harold Hamm International Prize for Biomedical Research in Diabetes 2019 Novo Nordisk Foundation and European Association for the Study of Diabetes Prize for Excellence in Diabetes Research (watch the mini documentary about Drucker produced by the Novo Nordisk Foundation for the occasion) 2019 Lifetime Achievement Award, Helmholtz Diabetes Centre, Germany 2020 John Baxter Award for Entrepreneurship, Endocrine Society 2020 Transatlantic Medal, Society for Endocrinology 2020 Warren Alpert Foundation Prize for Biomedical Research (co-recipient with Joel Habener and Jens Juul Holst) 2021 International Member, National Academy of Sciences 2021 Canada Gairdner International Award (co-recipient with Joel Habener and Jens Juul Holst) 2022 Inductee of the Canadian Medical Hall of Fame 2023 Wolf Prize in Medicine 2023 International Member of the National Academy of Medicine 2023 VinFuture Prize for Innovators with Outstanding Achievements in Emerging Fields (co-recipient with Joel Habener, Jens Juul Holst and Svetlana Mojsov) 2024 Princess of Asturias Award for Technical and Scientific Research (co-recipient with Jeffrey M. Friedman, Joel Habener, Jens Juul Holst and Svetlana Mojsov) 2024 Time100 Most Influential People and Time100 Health 2024 Golden Plate Award, American Academy of Achievement 2024 Fred Conrad Koch Lifetime Achievement Award, Endocrine Society 2024 TOPS Research Achievement Award, The Obesity Society 2025 Warren Triennial Prize, Massachusetts General Hospital (co-recipient with Joel Habener and Svetlana Mojsov) 2025 BBVA Foundation Frontiers of Knowledge Award in Biology and Biomedicine (co-recipient with Joel Habener, Jens Juul Holst and Svetlana Mojsov) 2025 Solomon A. Berson Award, American Physiology Society 2025 Breakthrough Prize in Life Sciences (co-recipient with Joel Habener, Jens Juul Holst, Svetlana Mojsov and Lotte Bjerre Knudsen) 2026 Governor General's Innovation Award
=== Maluku province === Alune people Ambonese people Haruku people Hitu people Saparua people Aru people Ujir people Babar people Banda people Bati people Buano people Buru people Ambelau people Kayeli people Lisela people Masarete people Rana people Wai Apu people Wai Loa people Geser people Gorom people Kei people Tanimbar Kei people Kisar people Leti people Manipa people Masela people Mausu Ane people Meher people Nuaulu people Oirata people Tanimbarese people Teon–Nila–Serua (TNS) Nila people Serua people Teon people Teor people Von people Wemale people Wetar people Yamatitam people
== Career and research == In 1997, Sereti came to the National Institute of Allergy and Infectious Diseases as a clinical associate in the laboratory of immunoregulation. She became a staff clinician in 2003. Sereti was appointed to a clinical tenure-track position in 2009 and received tenure in 2015. She is chief of the HIV pathogenesis section. Sereti researches the pathogenesis of HIV infection emphasizing mechanisms of immune reconstitution inflammatory syndrome in advanced HIV infection and of serious non-AIDS events in treated HIV-infected patients. She also investigates the pathogenesis of idiopathic CD4 lymphocytopenia (ICL) and immune-based therapeutic strategies of HIV infection and ICL.
== Inhibitors == Glycogen synthase kinase inhibitors are different chemotypes and have variable mechanisms of action; they may be cations, from natural sources, synthetic ATP and non-ATP competitive inhibitors and substrate-competitive inhibitors. GSK3 is a bi-lobar architecture with N-terminal and C-terminal, the N-terminal is responsible for ATP binding and C-terminal which is called as activation loop mediates the kinase activity, Tyrosine located at the C-terminal it essential for full GSK3 activity.
Transforming growth factor beta (TGF-β) is a multifunctional cytokine belonging to the transforming growth factor superfamily that includes three different mammalian isoforms (TGF-β 1 to 3, HGNC symbols TGFB1, TGFB2, TGFB3) and many other signaling proteins. TGFB proteins are produced by all white blood cell lineages. Activated TGF-β complexes with cell surface TGF-β receptors to form an active serine/threonine kinase complex. After binding their TGF-β protein ligand, TGF-β receptors assemble into heterotetramers composed of two each of the type 1 and type 2 receptor subunits, both of which are serine/threonine kinases. Upon assembly, the type 2 receptor kinase phosphorylates and activates the type 1 receptor kinase to initiate a signaling cascade. This leads to the activation of different downstream substrates and regulatory proteins, inducing transcription of different target genes that function in differentiation, chemotaxis, proliferation, and activation of many immune cells. TGF-β is secreted by many cell types, including macrophages, in a latent form in which it is complexed with two other polypeptides, latent TGF-beta binding protein (LTBP) and latency-associated peptide (LAP). Serum proteinases such as plasmin catalyze the release of active TGF-β from the complex. This often occurs on the surface of macrophages where the latent TGF-β complex is bound to CD36 via its ligand, thrombospondin-1 (TSP-1). Inflammatory stimuli that activate macrophages enhance the release of active TGF-β by promoting the activation of plasmin.
Sources: en.wikipedia.org
Arapaima can reach lengths of more than 2 m (6 ft 7 in), in some exceptional cases even exceeding 2.6 m (8 ft 6 in) and over 100 kg (220 lb). The maximum recorded weight for the species is 200 kg (440 lb), while the longest recorded length verified was 3.07 m (10 ft 1 in). Anecdotal reports suggest that specimens as long as 4.57 m (15 ft 0 in) exist, but verification is deemed impossible, and thus considered questionable. As a result of overfishing, arapaima more than 2 m (6 ft 7 in) are seldom found in the wild. The arapaima is torpedo-shaped, with large, blackish-green scales and red markings. It is streamlined and sleek, with its dorsal and anal fins set near its tail. Arapaima scales have a mineralised, hard, outer layer with a corrugated surface under which lie several layers of collagen fibres in a Bouligand-type arrangement. In a structure similar to plywood, the fibres in each successive layer are oriented at large angles to those in the previous layer, increasing toughness. The hard, corrugated surface of the outer layer, and the tough internal collagen layers work synergistically to contribute to their ability to flex and deform while providing strength and protection—a solution that allows the fish to remain mobile while heavily armored. The arapaima has a fundamental dependence on surface air to breathe. In addition to gills, it has a modified and enlarged swim bladder, composed of lung-like tissue, which enables it to extract oxygen from the air.
== Mechanism of action == P11-4 is an α-peptide that self-assembles into β-sheet amyloids with a hydrogel appearance at low pH. It builds a 3-D bio-matrix with binding sites for calcium ions serving as nucleation point for hydroxyapatite (tooth mineral) formation. The high affinity to tooth mineral is based on matching distances of Ca-ion binding sites on P11-4 and Ca spacing in the crystal lattice of hydroxyapatite. The matrix formation is pH controlled and thus allows control matrix activity and place of formation.
hybrid The offspring that results from combining the qualities of two organisms of different genera, species, breeds, or varieties through sexual reproduction. Hybrids may occur naturally or artificially, as during selective breeding of domesticated animals and plants. Reproductive barriers typically prevent hybridization between distantly related organisms, or at least ensure that hybrid offspring are sterile, but fertile hybrids may result in speciation.
=== November 1972 meeting with Tho === On 20 November 1972, Kissinger met Tho again in Paris. Kissinger no longer aimed at secrecy and was followed by paparazzi as he went to a house owned by the French Communist Party, where Tho was waiting for him. Kissinger announced that the Americans wanted major changes to the peace agreement made in October to accommodate Thieu, which led Tho to accuse him of negotiating in bad faith. Tho stated: "We have been deceived by the French, the Japanese and the Americans. But the deception has never been so flagrant as of now". Kissinger insisted the changes he wanted were only minor, but in effect, he wanted to renegotiate almost the entire agreement. Kissinger wanted to eliminate all of the powers assigned to the National Reconciliation Council and for the National Liberation Front's Provisional Revolutionary Government to be prevented from signing the peace accords. Tho rejected Kissinger's terms, saying he would abide by the terms agreed to on 8 October. Putting more pressure on him, Nixon told Kissinger to break off the talks if Tho would not agree to the changes he wanted. Being re-elected for a second term meant that Nixon was no longer concerned about public opinion as before, and in November 1972, he seriously considered firing Kissinger. Though Nixon decided that Thieu's 69 amendments were unrealistic, he also wanted a demonstration of force to prove that he was still willing to stand by South Vietnam.
In 1998, the European Union's Directive 98/44/ECclarified that patents on DNA sequences were allowable. In 2010 in the US, AMP sued Myriad Genetics to challenge the latter's patents regarding two genes, BRCA1, BRCA2, which are associated with breast cancer. In 2013, the U.S. Supreme Court partially agreed, ruling that a naturally occurring gene sequence could not be patented.
Sources: en.wikipedia.org
SR9009 is a synthetic research compound that binds and modulates the nuclear receptors REV-ERBα and REV-ERBβ. It is used in laboratory studies of circadian biology and metabolism, not as an approved medicine. It is also known by the informal name Stenabolic.
No. SR9009 has not been approved as a therapeutic drug in the United States, European Union, or other major markets. Human safety and efficacy data are very limited. Its presence in consumer products does not imply regulatory approval.
The World Anti-Doping Agency lists SR9009 as a prohibited substance because it can alter gene expression and metabolic pathways relevant to performance. The ban applies at all times, not only during competition. Detection relies on laboratory methods such as mass spectrometry.
It is a synthetic research compound that activates REV-ERB nuclear receptors. It is not an approved drug or dietary supplement. Most information comes from cell and animal studies.