This is a working overview of REV-ERB, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-05-21 and is reviewed periodically as new material appears.
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.
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.
Research interest in SR9009 grew from studies of circadian biology and metabolic disease. Preclinical reports describe effects on exercise capacity, muscle metabolism, and blood lipid levels in rodents, but these findings come from controlled laboratory settings. The compound has low oral bioavailability in animals, which limits systemic exposure after swallowing. Investigators often use injected routes in experiments to achieve measurable plasma concentrations. Human clinical data are sparse, no approved therapeutic product exists, and whether animal effects translate to humans remains an open question.
Regulatory and sporting contexts treat SR9009 as a prohibited substance in many elite competitions. Its presence on banned lists reflects concerns about performance enhancement and unknown long-term safety. Analytical chemists have developed methods to detect the parent compound and its metabolites in urine and blood. Literature discussions distinguish between in vitro potency, animal pharmacology, and anecdotal human reports. The latter are difficult to verify because products sold online may lack purity or contain different compounds.
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, lipid metabolism, and inflammatory gene expression. In cell and animal experiments, SR9009 alters transcription of clock-controlled genes and metabolic pathways. The compound is not a hormone and does not resemble classical steroid structures. Its activity depends on binding to the ligand-binding domain of REV-ERB, where it can modify corepressor recruitment.
| 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 |
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.
Mechanistically, SR9009 binds the ligand-binding domain of REV-ERBα/β and enhances recruitment of corepressor complexes. This represses target genes rather than activating them. Because REV-ERB proteins normally compete with ROR proteins at shared response elements, the net effect depends on tissue and timing. Researchers use SR9009 to probe how nuclear receptor signaling links the clock to metabolism, inflammation, and muscle biology. Findings are largely preclinical, and the precise contribution of each receptor subtype remains under study.
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.
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.
Analytical identification of SR9009 typically relies on liquid chromatography coupled with tandem mass spectrometry. In biological samples, researchers first separate the compound from matrix components using protein precipitation, liquid-liquid extraction, or solid-phase extraction. High-performance liquid chromatography with ultraviolet detection and nuclear magnetic resonance spectroscopy can support structural confirmation of reference materials. Because SR9009 is a small, relatively lipophilic molecule, reverse-phase columns and acidic mobile phases are common. Laboratories often include isotope-labeled internal standards to improve quantification and to correct for ion suppression.
Stability depends on physical form, temperature, light exposure, and solvent. Solid SR9009 is generally stored cold and dry, with protection from light to limit degradation. Dimethyl sulfoxide stocks are common for laboratory work, but repeated freeze-thaw cycles can reduce compound integrity. Aqueous solutions may be less stable than organic stocks, and the ethyl ester in the structure can be susceptible to hydrolysis under certain conditions. Researchers typically validate storage conditions and recheck purity before quantitative experiments, especially when using archived material.
Regulatory treatment of SR9009 varies by country and region. It is not approved as a pharmaceutical, and several jurisdictions restrict its sale for human consumption. Some authorities classify it as a research chemical, a prescription-only substance, or a prohibited performance-enhancing agent in sport. Purchasers may encounter certificates of analysis, but these documents do not guarantee identity, purity, or legality. In research settings, institutional safety reviews and controlled procurement help ensure that materials are handled under appropriate oversight. The absence of harmonized rules means that legal status can change and requires verification.
The second Testerman administration stabilized the city's finances, initiated urban renewal projects in Mechanicsville and East Knoxville, and consolidated Knoxville City and Knox County schools. With the help of rising entrepreneur Chris Whittle, Testerman came up with an updated downtown redevelopment plan, the "1987 Downtown Plan." This new plan called for further renovations to Market Square and the beautification of Gay Street. Victor Ashe, Testerman's successor, continued redevelopment efforts, focusing mainly on parks and blighted areas of East and North Knoxville. As the city's westward expansion along Kingston Pike had been thwarted by the incorporation of Farragut as a town in 1980, Ashe, rather than focus on large-scale annexations, turned instead to "finger" annexations, which involved annexing small parcels of land at a time. Ashe would make hundreds of such annexations during his 16-year tenure, effectively expanding the city by over 25 square miles. Preservation efforts in Knoxville, which have preserved historic structures such as Blount Mansion, the Bijou Theatre, and the Tennessee Theatre, have intensified in recent years, prompting the designation of numerous historic overlay districts throughout the city. The efforts of developers such as Kristopher Kendrick and David Dewhirst, who have purchased and restored numerous dilapidated buildings, gradually helped lure residents back to the Downtown area.
=== Lifestyle and diet === Drinking enough water may help to keep skin hydrated, especially in individuals who are chronically dehydrated. A poor diet lacking vitamins can lead to skin problems, such as scurvy, pellagra, and numerous subclinical skin pathologies that have not been studied in detail. Lack of sleep has been shown to make conditions like atopic dermatitis, eczema and psoriasis worse, and these conditions have in turn been shown to reduce sleep quality.
=== Osmow's === Osmow's is a quick-service restaurant chain known for its Mediterranean and Middle Eastern inspired menu. Founded in Mississauga in 2001, the chain now has 200 locations across North America.
== See also == Air-free technique – Chemistry laboratory technique Acidic oxide – Type of oxide, a.k.a. acid anhydride Base anhydride – Oxide of a chemical element from alkali- or alkaline earth metals Hydrate – Substance containing water or its constituent elements
Sources: en.wikipedia.org
restriction fragment length polymorphism (RFLP) Variability within a population of organisms observed in the size of the restriction fragments produced when genomic DNA (or any particular DNA molecule) is digested by one or more restriction endonucleases. This variability results from a corresponding polymorphism in the locations of restriction sites within the molecule(s) due to slight differences in nucleotide sequence between individuals. RFLP is frequently exploited in the laboratory to construct physical maps of the genome, to identify the specific locus occupied by a particular gene, and to detect genetic differences between closely related individuals or determine that different samples originated from the same individual. Analysis of restriction fragments can also reveal the presence of a mutation that may itself cause disease or be closely linked to one that does.
In the run-up to the Second World War Tolkien was earmarked as a codebreaker. In January 1939 he was asked to serve in the cryptographic department of the Foreign Office in the event of national emergency. Beginning on 27 March, he took an instructional course at the London headquarters of the Government Code and Cypher School. He was informed in October that his services would not be required. In 1945 Tolkien moved to Merton College, Oxford, becoming the Merton Professor of English Language and Literature, in which post he remained until his retirement in 1959. He served as an external examiner for University College, Galway (now the University of Galway), for many years. In 1954 Tolkien received an honorary doctorate from the National University of Ireland (of which University College, Galway, was a constituent college). Tolkien completed The Lord of the Rings in 1948, close to a decade after the first sketches.
The origins of the Cossacks are disputed. According to scientific studies, the Y-chromosomal genetic makeup of Zaporozhian, Don, and Kuban Cossacks forms the southern fragment of the East Slavic population, with minimal or no Caucasian or Asian component in their paternal gene pool. However, the term "Cossack" referred to independent horse-riding communities by the Tatars (qazaq or "free men") who inhabited the Pontic–Caspian steppe, north of the Black Sea near the Dnieper River. By the end of the 15th century, the term was also applied to Slavic peasants who had fled to the devastated regions along the lower Dnieper and Don Rivers, where they established their self-governing, cavalry-based communities. Until at least the 1630s, these Cossack groups remained ethnically and religiously autonomous. There were several major Cossack hosts in the 16th century: near the Dnieper, Don, Volga, and Ural Rivers; the Greben Cossacks in Caucasia; and the Zaporozhian Cossacks, mainly west of the Dnieper. It is unclear when people other than the Brodnici and Berladnici (which had a Romanian origin with large Slavic influences) began to settle in the lower reaches of major rivers such as the Don and the Dnieper after the demise of the Khazars. Their arrival was theorized to have been around the 13th century when the Mongols broke the power of the Cumans, who had assimilated the previous population in that region. It is known that immigrant settlers inherited a lifestyle that long pre-dated their presence, including from that of the Cumans and the Circassian Kassaks.
Sources: en.wikipedia.org
Independent of strength and performance measures, muscles can be induced to grow larger by a number of factors, including hormone signaling, developmental factors, strength training, and disease. Contrary to popular belief, the number of muscle fibres cannot be increased through exercise. Instead, muscles grow larger through a combination of muscle cell growth as new protein filaments are added along with additional mass provided by undifferentiated satellite cells alongside the existing muscle cells. Biological factors such as age and hormone levels can affect muscle hypertrophy. During puberty in males, hypertrophy occurs at an accelerated rate as the levels of growth-stimulating hormones produced by the body increase. Natural hypertrophy normally stops at full growth in the late teens. As testosterone is one of the body's major growth hormones, on average, men find hypertrophy much easier to achieve than women. Taking additional testosterone or other anabolic steroids will increase muscular hypertrophy. Muscular, spinal and neural factors all affect muscle building. Sometimes a person may notice an increase in strength in a given muscle even though only its opposite has been subject to exercise, such as when a bodybuilder finds her left biceps stronger after completing a regimen focusing only on the right biceps. This phenomenon is called cross education.
Thus, most einsteinium samples are contaminated, and their intrinsic properties are often deduced by extrapolating back experimental data accumulated over time. Other experimental techniques to circumvent the contamination problem include selective optical excitation of einsteinium ions by a tunable laser, such as in studying its luminescence properties. Magnetic properties have been studied for einsteinium metal, its oxide and fluoride. All three materials showed Curie–Weiss paramagnetic behavior from liquid helium to room temperature. The effective magnetic moments were deduced as 10.4±0.3 μB for Es2O3 and 11.4±0.3 μB for the EsF3, which are the highest values among actinides, and the corresponding Curie temperatures are 53 and 37 K.
=== Relation of PIDD1 to centrosomes === Recent investigations reveal that CASP2 activation, which is dependent on PIDD1, does not lead to cell death or activate p53 in reaction to DNA damage (such as that induced by doxorubicin) or during prolonged mitotic arrest (as observed with taxol treatment). In contrast, the p53 activation linked to centrosome amplification—a process that can occur following failed cytokinesis—undoubtedly depends on the Caspase-2−PIDDosome complex. Notably, PIDD1 appears to be integral in assessing the quantity of mature mother centrioles, utilizing a mechanism that has yet to be fully clarified. Furthermore, PIDD1 is situated at the distal ends of mature centrosomes within normal cells, suggesting its potential role in regulating centrosomal functions. The assembly of the Caspase-2−PIDDosome can be triggered by the presence of multiple mature centrioles with appendages. This activation leads to CASP2-mediated cleavage of MDM2, resulting in the accumulation of p53 and subsequent cell cycle arrest mediated by p21. Notably, these processes occur without causing significant cell death. Similarly, the depletion of centrosomes undermines the effectiveness of this pathway during instances of cytokinesis failure. In contrast, overexpressing polo-like kinase 4 (PLK4), which promotes the formation of additional centrosomes, is sufficient to activate the pathway even when cytokinesis is not compromised.
https://doi.org/10.1007/978-94-007-1060-3 Zhou, T., Li, N., Jin, Y., Zeng, Q., Prabowo, W., Liu, Y., Tian, C., Bao, L., Liu, S., Yuan, Z., Fu, Q., Gao, S., Gao, D., Dunham, R., Shubin, N. H., & Liu, Z. (2018). Chemokine C-C motif ligand 33 is a key regulator of teleost fish barbel development. Proceedings of the National Academy of Sciences, 115(22), E5018–E5027. https://doi.org/10.1073/pnas.1718603115
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 small molecule studied as an agonist of the REV-ERB nuclear receptors. It is not an approved medicine, and its effects in humans are not well characterized.