REV-ERB agonist raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
This page was last updated on 2025-11-15 and is reviewed periodically as new material appears.
SR9009 is a synthetic small molecule studied as an agonist of REV-ERB nuclear receptors. REV-ERB alpha and REV-ERB beta help regulate circadian rhythms and metabolic gene expression. In laboratory research, SR9009 has been used to probe how these receptors affect skeletal muscle, liver, and adipose tissue. The compound was identified in academic drug-discovery work and is often described in scientific literature by its chemical name and research code. It is not an approved medicine, and human clinical data remain limited or absent.
SR9009 binds REV-ERB receptors and alters their repressive activity on target genes. This action can change transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. In rodent studies, treated animals have shown changes in muscle oxidative capacity and exercise performance, though effects vary by dose, duration, and model. The precise molecular steps connecting receptor binding to whole-body outcomes are still an active area of investigation. Findings in animals do not automatically translate to humans.
Because REV-ERB receptors are core clock components, SR9009 has been examined for effects on daily rhythms as well as metabolism. Research has explored whether the compound can shift or reinforce circadian gene expression in tissues such as liver and muscle. Some studies report improved metabolic markers in obese or diabetic mice, while others show context-dependent responses. Questions remain about which effects are direct, which are secondary to timing, and how they might differ across species.
At the molecular level, SR9009 binds REV-ERBα and REV-ERBβ and alters their repressive activity on target genes. These nuclear receptors help regulate the circadian clock, lipid synthesis, glucose metabolism, and inflammatory pathways. By changing transcription, the compound can shift the timing or magnitude of downstream metabolic processes in model systems. It does not act through androgen receptors or adenosine receptors, which distinguishes it from several substances sold for athletic performance. Whether the same transcriptional changes occur in humans at tolerable exposures remains an open question because controlled human studies are lacking.
Preclinical reports describe effects on exercise endurance, mitochondrial content, and lipid profiles in rodents, but these findings come from specific experimental conditions. Many studies use high doses or delivery methods that may not translate directly to human use. SR9009 has been reported to have low oral bioavailability and a short half-life, which complicates interpretation of oral dosing studies. It is not established as safe or effective for any indication. Literature discussions often separate its pharmacological mechanism from unverified claims made in fitness and supplement markets.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small-molecule nuclear receptor ligand |
| Appearance | Off-white to pale yellow solid | Typical for research-grade powder |
| Solubility class | Soluble in DMSO; low water solubility | Common stock solutions use organic solvent |
| Typical stock solvent | Dimethyl sulfoxide | Used for laboratory assays |
| Common analytical method | HPLC with UV or mass detection | Used for identity and purity checks |
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.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. These receptors help regulate circadian rhythms and metabolic gene expression. In laboratory experiments, SR9009 binds these receptors and alters transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. It is not a naturally occurring compound and has no approved therapeutic use. Research interest stems from its ability to modify energy metabolism in cells and animal models.
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.
SR9009 is frequently discussed in fitness and research-chemical contexts, yet it has no approved medical indication. Regulatory agencies have not authorized it for human use, and it is not a standard prescription drug. Some sports organizations list it as a prohibited substance because of its potential performance-enhancing properties. Published human data are sparse, so claims about its effects in people often rely on animal models or anecdotal reports. Quality and identity of online materials can vary widely.
SR9009 is a synthetic small molecule studied as a REV-ERB agonist. REV-ERBα and REV-ERBβ are nuclear receptors that help regulate circadian rhythms and metabolic gene expression. The compound was identified in academic screening efforts to find synthetic ligands for these receptors. In cell and animal studies, SR9009 alters transcription of genes involved in lipid and glucose metabolism, and it can shift circadian behavior. It is not an approved therapeutic agent.
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.
SR9009 is a synthetic small molecule developed as an agonist of the nuclear receptors REV-ERBα (NR1D1) and REV-ERBβ (NR1D2). These receptors help regulate circadian rhythms and metabolic gene expression. In cell and animal studies, SR9009 alters transcription of genes involved in lipid metabolism, inflammation, and mitochondrial function. It is not an approved medicine, and its pharmacological profile in humans remains largely uncharacterized. The compound is frequently discussed in the context of circadian biology and metabolic research rather than clinical use.
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.
Stone Nation, the Tupamaros, the 19th of April Movement and the Sandinista National Liberation Front in Nicaragua, the ANC in South Africa, the Provisional Irish Republican Army, ETA, Action Directe, the Red Brigades, and the Red Army Faction in Europe, and the Armenian Secret Army, the Japanese Red Army, the Free Aceh Movement, and the Moro National Liberation Front in the Philippines. Gaddafi was indiscriminate in the causes he funded, sometimes switching sides in a conflict, as in the Eritrean War of Independence. Throughout the 1970s these groups received financial support from Libya, which became a leader in the Third World's struggle against colonialism and neocolonialism. Though many of these groups were labelled "terrorists" by critics, Gaddafi rejected this characterization, instead considering them revolutionaries engaged in liberation struggles.
=== Ra === Efraim Racker (1913–1991). Austrian-American biochemist at Cornell University, notable for work on ATP synthase. Member Natl. Acad. Sci. USA. George Radda FRS (1936–2024). Hungarian biochemist at Oxford University, known for applying nuclear magnetic resonance to complex biological material, and many other contributions. Ronald T. Raines (b. 1958). American biochemist at the University of Wisconsin–Madison and MIT, known for work on enzymes and other proteins. Venkatraman Ramakrishnan FRS (President) (b. 1952). Indian-British-American structural biologist at the MRC Laboratory of Molecular Biology, Cambridge, known for work on the ribosome. Nobel Prize in Chemistry in 2009. Philip Randle (1926–2006). British biochemist at the University of Bristol known for work on diabetes. Samuel Mitja Rapoport (1912–2004). Austrian and German biochemist at the Humboldt University, Berlin noted for studies of mitochondria, and for discovering a method for preserving blood for transfusions. Leader of biochemistry in the German Democratic Republic. Member of the German Academy of Sciences at Berlin. Tom Rapoport (b. 1947). German-American cell biologist at Harvard Medical School who studies protein transport in cells.
While other plants have δ15N values that range from 2 to 6‰, legumes have lower 14N/15N ratios (close to 0‰, i.e. atmospheric N2) because they can fix molecular nitrogen, rather than having to rely on soil nitrates and nitrites. Therefore, one potential explanation for lower δ15N values in human remains is an increased consumption of legumes or animals that eat them. 15N values increase with meat consumption, and decrease with legume consumption. The 14N/15N ratio could be used to gauge the contribution of meat and legumes to the diet.
Merck Foundation - founded in 1957, the foundation has donated over $1 billion to charitable causes to promote health equity. In 2012, the foundation ended its donations to the Boy Scouts of America citing its discrimination against gay people. Patient assistance programs to offer access to pharmaceuticals to those unable to afford its medications. Provides funding to Hilleman Laboratories, an India-based non-profit research organization dedicated to the development of low-cost vaccines for use in developing countries. Merck for Mothers prevents maternal mortality. Merck produces Mectizan (ivermectin), an anti-parasitic medicine traditionally used to treat onchocerciasis, solely for donation to people in Africa, Latin America, and Yemen. The donation program has significantly reduced the incidence of the disease.
Sources: en.wikipedia.org
=== Lysine price fixing === In 1986, the Ajinomoto Group produced lysine at its Iowa factory of Heartland Lysine Co. U.S.A., followed by production in its Pathum Thani factory in Ajinomoto, Thailand, in 1986, and Bio Italia, BioPro in Italy in 1992, gradually upgrading its worldwide production bases. In the United States, competitors increased their own lysine production, which resulted in lower prices due to an overabundance of lysine on the market. To raise prices again, several companies, including Ajinomoto, price fixed lysine in the 1990s. Along with Kyowa Hakko Kogyo and Sewon America, Inc., Ajinomoto admitted to price fixing and settled with the United States Department of Justice Antitrust Division in September 1996. Each firm and an executive from each pleaded guilty as part of a plea bargain to aid in further investigation. Their cooperation led to Archer Daniels Midland settling charges with the US government in October 1996 for $100 million, a record antitrust fine at the time. Cartels were able to raise lysine prices 70% within the first six months of cooperating.
Established uitlanders, including the mining magnates, wanted political, social, and economic control over their lives. These rights included a stable constitution, a fair franchise law, an independent judiciary and a better educational system. The Boers recognised that the more concessions they made to the uitlanders the greater the likelihood—with approximately 30,000 white male Boer voters and potentially 60,000 white male uitlanders—that their independent control of the Transvaal would be lost, and the territory absorbed into the British Empire. The uitlanders resented the taxes levied by the Transvaal government, particularly when this was not spent on Johannesburg or uitlander interests but diverted to projects elsewhere in the Transvaal. For example, as the gold-bearing ore sloped away from the outcrop underground to the south, more and more blasting was necessary to extract it, and mines consumed vast quantities of explosives. A box of dynamite costing five pounds included five shillings tax. Not only was this tax perceived as exorbitant, but British interests were offended when President Paul Kruger gave monopoly rights for the manufacture of the explosive to a non-British branch of the Nobel company, which infuriated Britain. The so-called "dynamite monopoly" became a casus belli. British imperial interests were alarmed when in 1894–95 Kruger proposed building a railway through Portuguese East Africa to Delagoa Bay, bypassing British-controlled ports in Natal and Cape Town and avoiding British tariffs.
=== Disorder in the bound state (fuzzy complexes) === Intrinsically disordered proteins can retain their conformational freedom even when they bind specifically to other proteins. The structural disorder in bound state can be static or dynamic. In fuzzy complexes structural multiplicity is required for function and the manipulation of the bound disordered region changes activity. The conformational ensemble of the complex is modulated via post-translational modifications or protein interactions. Specificity of DNA binding proteins often depends on the length of fuzzy regions, which is varied by alternative splicing. Some fuzzy complexes may exhibit high binding affinity, although other studies showed different affinity values for the same system in a different concentration regime.
NIP7: Knockdown reduced mTORC2 activity that is indicated by decreased phosphorylation of mTORC2 substrates. RICTOR: Overexpression leads to metastasis and knockdown inhibits growth factor-induced PKC-phosphorylation. Constitutive deletion of Rictor in mice leads to embryonic lethality, while tissue specific deletion leads to a variety of phenotypes; a common phenotype of Rictor deletion in liver, white adipose tissue, and pancreatic beta cells is systemic glucose intolerance and insulin resistance in one or more tissues. Decreased Rictor expression in mice decreases male, but not female, lifespan. mTOR: Inhibition of mTORC1 and mTORC2 by PP242 [2-(4-Amino-1-isopropyl-1H-pyrazolo[3,4-d]pyrimidin-3-yl)-1H-indol-5-ol] leads to autophagy or apoptosis; inhibition of mTORC2 alone by PP242 prevents phosphorylation of Ser-473 site on AKT and arrests the cells in G1 phase of the cell cycle. Genetic reduction of mTOR expression in mice significantly increases lifespan. PDK1: Knockout is lethal; hypomorphic allele results in smaller organ volume and organism size but normal AKT activation. AKT: Knockout mice experience spontaneous apoptosis (AKT1), severe diabetes (AKT2), small brains (AKT3), and growth deficiency (AKT1/AKT2). Mice heterozygous for AKT1 have increased lifespan. TOR1, the S. cerevisiae orthologue of mTORC1, is a regulator of both carbon and nitrogen metabolism; TOR1 KO strains regulate response to nitrogen as well as carbon availability, indicating that it is a key nutritional transducer in yeast.
=== Enlargement to Central Europe === Following the Revolutions of 1989, the OECD began assisting countries in Central Europe (especially the Visegrád Group) to prepare market economy reforms. In 1990, the Centre for Co-operation with European Economies in Transition (now succeeded by the Centre for Cooperation with Non-Members) was established, and in 1991, the programme "Partners in Transition" was launched to offer a partnership to Czechoslovakia, Hungary and Poland, including a membership option for these countries. As a result of this, Poland, Hungary, the Czech Republic and Slovakia, as well as South Korea and Mexico, became members of the OECD between 1996 and 2000.
Sources: en.wikipedia.org
SR9009 is a synthetic research compound that acts on REV-ERB nuclear receptors. It is not approved for human use and is sold only as a research chemical. Its effects have been studied mainly in cells and rodents.
It binds REV-ERB alpha and REV-ERB beta and changes the expression of genes tied to metabolism and circadian rhythm. These changes can affect mitochondria and energy use in animal models. The exact chain from receptor binding to physiological outcome is still being mapped.
No reliable human trials show that SR9009 improves athletic performance. Some rodent studies report endurance changes, but these results are not proof of human benefit. Its use in sport is prohibited, and quality and safety data are lacking.
SR9009 is a synthetic REV-ERB agonist used in laboratory research. It is not an approved drug, and its effects in humans are not well characterized. It is often sold as a research chemical under the name Stenabolic.