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 2026-08-01 and is reviewed periodically as new material appears.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small molecule; not a steroid or peptide. |
| Primary targets | NR1D1 and NR1D2 | Also known as REV-ERBα and REV-ERBβ. |
| Studied routes | Intraperitoneal in rodents | Oral bioavailability in humans is not established. |
| Human approval | No approved therapeutic indication | No recognized clinical use. |
| Key uncertainty | Human physiological effects | Preclinical findings may not translate. |
Laboratory samples of SR9009 are typically supplied as a white to off-white powder. The compound dissolves readily in organic solvents such as dimethyl sulfoxide and ethanol, while its solubility in water is low. Because of this solubility profile, researchers often prepare concentrated stock solutions in an organic solvent before diluting them into aqueous assay buffers. Light exposure, moisture, and repeated freeze-thaw cycles can degrade many small molecules, so handling procedures usually aim to minimize these factors. Purity is commonly checked before use.
Storage conditions for research-grade SR9009 generally involve a freezer at approximately minus twenty degrees Celsius, sometimes lower for long-term preservation. Containers should remain tightly closed and protected from light. Desiccants may be used to limit moisture uptake. Solutions are often stored in aliquots to avoid repeated warming and cooling. Stability data for the compound under various conditions are limited, so laboratories typically follow supplier recommendations and verify performance through periodic analytical checks rather than assuming indefinite stability.
SR9009 is not approved as a medicine by major regulatory agencies. It is commonly sold as a research chemical, a category that may fall outside customary drug approval and quality rules. In sports, the World Anti-Doping Agency lists SR9009 as a prohibited substance. Athletes who use it can face sanctions if it is detected in a sample. Legal status varies by country, and importation may be restricted. Enforcement practices differ across borders.
Detection of SR9009 in biological samples usually employs liquid chromatography coupled with tandem mass spectrometry. This method can identify the parent compound and sometimes metabolites in urine or blood. Because exposure can be low and clearance may be rapid, sample timing and limits of detection matter. Laboratories validate assays for sensitivity and specificity. Results are interpreted alongside chain-of-custody and quality-control records. Urine is the common matrix for anti-doping analysis, while blood may be used in research settings.
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.
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.
The Leaning Tower of Pizza was a proposed 30-story slanted skyscraper that would have housed Domino's Pizza's operations at its Domino's Farms campus near Ann Arbor, Michigan. In the mid-1980s, Monaghan asked Taliesin Associated Architects, the inheritors of Frank Lloyd Wright's practice, to erect a structure based on an un-built tower that Wright designed in 1956 for Chicago called the Golden Beacon. Sometime during the planning of the tower, Monaghan and the Taliesin architects parted company, allegedly because both parties felt the project may have not served justice to the spirit of Wright's architecture. Monaghan then went to Gunnar Birkerts, the architect of Domino's unusual half-mile (800 m) long headquarters office building who came up with a design for a tower that would rise at a 15-degree angle with a swooping top reminiscent of the forms of Wright's late work. Birkerts' design, no doubt, had serious intent, but would immediately and forever be dubbed with the nickname "The Leaning Tower of Pizza" after Italy's Leaning Tower of Pisa. The structure was never built but a 50-foot (15 m) tall scale model stands at the proposed site on Domino Pizza headquarters in Ann Arbor Charter Township, Michigan, outside of Ann Arbor.
== Examples and ligands == The ligands for receptors are as diverse as their receptors. GPCRs (7TMs) are a particularly vast family, with at least 810 members. There are also LGICs for at least a dozen endogenous ligands, and many more receptors possible through different subunit compositions. Some common examples of ligands and receptors include:
A number of experiments have found that decay rates of other modes of artificial and naturally occurring radioisotopes are, to a high degree of precision, unaffected by external conditions such as temperature, pressure, the chemical environment, and electric, magnetic, or gravitational fields. Comparison of laboratory experiments over the last century, studies of the Oklo natural nuclear reactor (which exemplified the effects of thermal neutrons on nuclear decay), and astrophysical observations of the luminosity decays of distant supernovae (which occurred far away so the light has taken a great deal of time to reach us), for example, strongly indicate that unperturbed decay rates have been constant (at least to within the limitations of small experimental errors) as a function of time as well. Recent results suggest the possibility that decay rates might have a weak dependence on environmental factors. It has been suggested that measurements of decay rates of silicon-32, manganese-54, and radium-226 exhibit small seasonal variations (of the order of 0.1%). However, such measurements are highly susceptible to systematic errors, and a subsequent paper has found no evidence for such correlations in seven other isotopes (22Na, 44Ti, 108Ag, 121Sn, 133Ba, 241Am, 238Pu), and sets upper limits on the size of any such effects.
Sources: en.wikipedia.org
== Discovery == In 2004 Linda B. Buck and Richard Axel won the Nobel Prize in Physiology or Medicine for their work on olfactory receptors. In 2006, it was shown that another class of odorant receptors – known as trace amine-associated receptors (TAARs) – exist for detecting volatile amines. Except for TAAR1, all functional TAARs in humans are expressed in the olfactory epithelium. A third class of olfactory receptors known as vomeronasal receptors has also been identified; vomeronasal receptors putatively function as pheromone receptors. As with many other GPCRs, there is still a lack of experimental structures at atomic level for olfactory receptors and structural information is based on homology modeling methods. In 2023 the structure of OR51E2 was found, the first elucidation of the structure of any human olfactory receptor. The limited functional expression of olfactory receptors in heterologous systems, however, has greatly hampered attempts to deorphanize them (analyze the response profiles of single olfactory receptors) This was first completed by genetically engineered receptor, OR-I7 to characterize the "odor space" of a population of native aldehyde receptors.
Membrane fusion proteins (not to be confused with chimeric or fusion proteins) are proteins that cause fusion of biological membranes. Membrane fusion is critical for many biological processes, especially in eukaryotic development and viral entry. Fusion proteins can originate from genes encoded by infectious enveloped viruses, ancient retroviruses integrated into the host genome, or solely by the host genome. Post-translational modifications (PTM) made to fusion proteins by host enzymes (in particular the addition of sugars through glycosylation or the addition of acetyl groups) can drastically affect their relative ability to fuse membranes, also known as their fusogenicity.
=== Early puberty === Anastrozole is used at a dosage of 0.5 to 1 mg/day in combination with the antiandrogen bicalutamide in the treatment of peripheral precocious puberty, for instance due to familial male-limited precocious puberty (testotoxicosis) and McCune–Albright syndrome, in boys.
Sources: en.wikipedia.org
She wore an imported black satin dress heavily beaded with tiny black jet beads, black satin slippers, beaded, and had on her rarely beautiful diamonds. ... She stood before us, seemingly slight, graceful of carriage, and exquisitely beautiful even to critical eyes. Then, still standing, she faced her class as one who knew herself to be a teacher by divine right. She turned to the student at the end of the first row of seats and took direct mental cognizance of this one, plainly knocked at the door of this individual consciousness. ... This continued until each member of the class had received the same mental cognizance. No audible word voiced the purely mental contact. It was in part because of her unusual personality that Christian Science flourished, despite the numerous disputes she initiated among her followers. "She was like a patch of colour in those gray communities," McClure's wrote, "She never laid aside her regal air; never entered a room or left it like other people." Mark Twain, a prominent critic of hers, described her in 1907 as "vain, untruthful [and] jealous", but "[i]n several ways ... the most interesting woman that ever lived, and the most extraordinary".
== Bibliography == Capoccia, Anna Rita (2006). "MAGATI, Cesare". Dizionario Biografico degli Italiani (in Italian). Vol. 67: Macchi–Malaspina. Rome: Istituto dell'Enciclopedia Italiana. ISBN 978-88-12-00032-6. Capparoni, Pietro (1932). "Cesare Magati (Padre Liberato da Scandiano dei Minori Cappuccini)". Profili Bio-bibliografici di Medici e Naturalisti Celebri Italiani Dal Secolo XV al Secolo XVIII. Rome: 70–75. Cesare Magati entry (in Italian) by Agostino Palmerini in the Enciclopedia Treccani, 1934 Putti, Vittorio (1941). "Cesare Magati (1579– 1647)". Biografie di Chirurghi Dal XVI a XIX Secolo. Bologna: 9–16. Premuda, Loris (1970). "Magati, Cesare". In Charles Coulston Gillispie (ed.). Dictionary of Scientific Biography. Vol. 9. New York: Charles Scribner's Sons. pp. 4–5.
3-Phosphoglyceric acid (3PG, 3-PGA, or PGA) is the conjugate acid of 3-phosphoglycerate or glycerate 3-phosphate (GP or G3P). This glycerate is a biochemically significant metabolic intermediate in both glycolysis and the Calvin-Benson cycle. The anion is often termed as PGA when referring to the Calvin-Benson cycle. In the Calvin-Benson cycle, 3-phosphoglycerate is typically the product of the spontaneous scission of an unstable 6-carbon intermediate formed upon CO2 fixation. Thus, two equivalents of 3-phosphoglycerate are produced for each molecule of CO2 that is fixed. In glycolysis, 3-phosphoglycerate is an intermediate following the dephosphorylation (reduction) of 1,3-bisphosphoglycerate.
Sources: en.wikipedia.org
It is a synthetic compound that acts as an agonist at REV-ERBα and REV-ERBβ. It is used mainly as a research chemical to study circadian and metabolic pathways. It is not approved for human therapeutic use.
REV-ERB receptors generally repress transcription when bound by natural heme. SR9009 is described as an agonist that enhances this repressive activity. The result is altered expression of clock and metabolic genes.
Published controlled human trials are lacking. Some sources cite limited or unofficial reports, but these do not establish safety or efficacy. Claims about human performance effects remain unverified.
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.