This is a working overview of REV-ERB agonist, 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 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.
At the molecular level, SR9009 binds the ligand-binding domain of REV-ERB and strengthens recruitment of corepressor proteins such as NCoR and HDAC3. This increases repression of target genes, including Bmal1 and other clock-controlled and metabolic genes. In rodent studies, such changes have been linked to altered lipid handling, glucose metabolism, and energy expenditure. The precise chain of events between receptor binding and whole-body effects remains an active area of research. Findings in animals do not automatically translate to humans.
Laboratory studies often administer SR9009 by injection because oral absorption appears poor in rodents. Reported pharmacokinetic properties include rapid metabolism and low systemic exposure after oral dosing. Human pharmacokinetic data are sparse, so absorption, distribution, metabolism, and excretion in people are not well defined. Some research explores related REV-ERB compounds with improved drug-like properties. Regulatory approval for any REV-ERB agonist as a human medicine has not been granted to date.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small-molecule ligand; not a hormone or peptide |
| Molecular formula | C20H24ClN3O4S | Reported for the free base |
| CAS Registry Number | 1379686-30-2 | Unique chemical identifier |
| Common synonyms | SR9009; stenabolic | Stenabolic is informal and not an official name |
| Reported targets | REV-ERBα and REV-ERBβ | Nuclear receptors linked to circadian and metabolic regulation |
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.
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.
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.
Water has a high heat of vaporization and is relatively inert, which makes it a good fire extinguishing fluid. The evaporation of water carries heat away from the fire. It is dangerous to use water on fires involving oils and organic solvents because many organic materials float on water and the water tends to spread the burning liquid. Use of water in fire fighting should also take into account the hazards of a steam explosion, which may occur when water is used on very hot fires in confined spaces, and of a hydrogen explosion, when substances which react with water, such as certain metals or hot carbon such as coal, charcoal, or coke graphite, decompose the water, producing water gas. The power of such explosions was seen in the Chernobyl disaster, although the water involved in this case did not come from fire-fighting but from the reactor's own water cooling system. A steam explosion occurred when the extreme overheating of the core caused water to flash into steam. A hydrogen explosion may have occurred as a result of a reaction between steam and hot zirconium. Some metallic oxides, most notably those of alkali metals and alkaline earth metals, produce so much heat in reaction with water that a fire hazard can develop. The alkaline earth oxide quicklime, also known as calcium oxide, is a mass-produced substance that is often transported in paper bags. If these are soaked through, they may ignite as their contents react with water.
=== Autoimmune disorders === People with type 1 diabetes are at an increased risk for developing several autoimmune disorders, particularly thyroid problems – around 20% of people with type 1 diabetes have hypothyroidism or hyperthyroidism, typically caused by Hashimoto thyroiditis or Graves' disease respectively. Celiac disease affects 2–8% of people with type 1 diabetes, and is more common in those who were younger at diabetes diagnosis, and in white people. Type 1 diabetics are also at increased risk of rheumatoid arthritis, lupus, autoimmune gastritis, pernicious anemia, vitiligo, and Addison's disease. Conversely, complex autoimmune syndromes caused by mutations in the immunity-related genes AIRE (causing autoimmune polyglandular syndrome), FoxP3 (causing IPEX syndrome), or STAT3 include type 1 diabetes in their effects.
Estradiol acts primarily as an agonist of the estrogen receptor (ER), a nuclear steroid hormone receptor. There are two subtypes of the ER, ERα and ERβ, and estradiol potently binds to and activates both of these receptors. The result of ER activation is a modulation of gene transcription and expression in ER-expressing cells, which is the predominant mechanism by which estradiol mediates its biological effects in the body. Estradiol also acts as an agonist of membrane estrogen receptors (mERs), such as GPER (GPR30), a recently discovered non-nuclear receptor for estradiol, via which it can mediate a variety of rapid, non-genomic effects. Unlike the case of the ER, GPER appears to be selective for estradiol, and shows very low affinities for other endogenous estrogens, such as estrone and estriol. Additional mERs besides GPER include ER-X, ERx, and Gq-mER. ERα/ERβ are in inactive state trapped in multimolecular chaperone complexes organized around the heat shock protein 90 (HSP90), containing p23 protein, and immunophilin, and located in majority in cytoplasm and partially in nucleus. In the E2 classical pathway or estrogen classical pathway, estradiol enters the cytoplasm, where it interacts with ERs. Once bound E2, ERs dissociate from the molecular chaperone complexes and become competent to dimerize, migrate to nucleus, and to bind to specific DNA sequences (estrogen response element, ERE), allowing for gene transcription which can take place over hours and days.
Niosomes are vesicles composed of non-ionic surfactants, incorporating cholesterol as an excipient. Niosomes are utilized for drug delivery to specific sites to achieve desired therapeutic effects. Structurally, niosomes are similar to liposomes as both consist of a lipid bilayer. However, niosomes are more stable than liposomes during formation processes and storage. Niosomes trap hydrophilic and lipophilic drugs, either in an aqueous compartment (for hydrophilic drugs) or in a vesicular membrane compartment composed of lipid material (for lipophilic drugs).
Sources: en.wikipedia.org
=== Meperidine === Meperidine is a synthetic opiate, part of the arylpiperidine class. It is a strong μ-receptor agonist with 1/10th the potency of morphine. It has historically also been used to treat rigors, and has a half-life of three to four hours. It is hepatically metabolized to the active metabolites of normeperidine, normepiridinic acid, and medperidinic acid. Normeperidine may accumulate to toxic levels in patients with renal impairment with repeated doses, and can cause CNS excitation and seizures.
Remdesivir, sold under the brand name Veklury, is a broad-spectrum antiviral medication developed by the biopharmaceutical company Gilead Sciences. It is administered via injection into a vein. During the COVID‑19 pandemic, remdesivir was approved or authorized for emergency use to treat COVID‑19 in numerous countries. Remdesivir was originally developed to treat hepatitis C, and was subsequently investigated for Ebola virus disease and Marburg virus infections before being studied as a post-infection treatment for COVID‑19. Remdesivir is a prodrug that is intended to allow intracellular delivery of GS-441524 monophosphate and subsequent biotransformation into GS-441524 triphosphate, a ribonucleotide analogue inhibitor of viral RNA polymerase. The most common side effect in healthy volunteers is raised blood levels of liver enzymes. The most common side effect in people with COVID‑19 is nausea. Side effects may include liver inflammation and an infusion-related reaction with nausea, low blood pressure, and sweating. The US Food and Drug Administration (FDA) considers it to be a first-in-class medication.
==== Huntington's Disease ==== Mutant huntingtin protein disrupts AMPAR-mediated synaptic transmission by impairing receptor trafficking, leading to synaptic dysfunction and neuronal loss in Huntington's disease models.
Sources: en.wikipedia.org
=== Manuscript locations === Before his death, Tolkien negotiated the sale of the manuscripts, drafts, proofs and other materials related to his then-published works—including The Lord of the Rings, The Hobbit and Farmer Giles of Ham—to the Department of Special Collections and University Archives at Marquette University's John P. Raynor, S.J., Library in Milwaukee, Wisconsin, United States. After his death his estate donated the papers containing Tolkien's Silmarillion mythology and his academic work to the Bodleian Library at Oxford University. The Bodleian Library held an exhibition of his work in 2018, including more than 60 items which had never been seen in public before. In 2009 a partial draft of Language and Human Nature, which Tolkien had begun co-writing with Lewis but had never completed, was discovered at the Bodleian Library.
The M242 is standard equipment on the U. S. Army M2 and M3 Bradley fighting vehicles; it is also in use on the LAV-25. Before the project was cancelled, the Mk44 Bushmaster II 30 mm chain gun (a successor to the M242) was used on the Marine Corps' Expeditionary Fighting Vehicle (EFV). The M242 is also a popular choice of primary armament for armored fighting vehicles manufactured around the world, such as Singapore's Bionix AFVs and as the Rafael Overhead Weapon Station-25 mounted on upgraded M113A2 Ultra IFVs.
Vascular shunt A vascular shunt can also bypass the capillary bed and provide a route for blood supply directly to a collecting venule. This is achieved by a metarteriole that supplies around a hundred capillaries. At their junctions are precapillary sphincters that tightly regulate the flow of blood into the capillary bed. When all of the sphincters are closed blood can flow from a metarteriole into a thoroughfare channel and into a collecting venule bypassing the capillary bed.
=== Other === Chest pain may be accompanied by sweating, nausea or vomiting, and fainting, and these symptoms may also occur without any pain at all. Dizziness or lightheadedness is common and occurs due to reduction in oxygen and blood to the brain. In females, the most common symptoms of myocardial infarction include shortness of breath, weakness, and fatigue. Females are more likely to have unusual or unexplained tiredness and nausea or vomiting as symptoms. Females having heart attacks are more likely to have palpitations, back pain, labored breath, vomiting, and left arm pain than males, although the studies showing these differences had high variability. Females are less likely to report chest pain during a heart attack and more likely to report nausea, jaw pain, neck pain, cough, and fatigue, although these findings are inconsistent across studies. Females with heart attacks also had more indigestion, dizziness, loss of appetite, and loss of consciousness. Shortness of breath is a common, and sometimes the only symptom, occurring when damage to the heart limits the output of the left ventricle, with breathlessness arising either from low oxygen in the blood or pulmonary edema. Other less common symptoms include weakness, light-headedness, palpitations, and abnormalities in heart rate or blood pressure. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system, which occurs in response to pain and, where present, low blood pressure.
Sources: en.wikipedia.org
SR9009 is a synthetic compound investigated as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is used in preclinical research on circadian rhythm and metabolism. It is not an approved drug.
No. It has no approved medical indication, and human safety and efficacy data are limited. It appears in research chemical markets and is banned by some sports authorities.
Natural ligands include heme and certain metabolites; SR9009 is a synthetic small molecule with higher potency and selectivity in some assays. Its effects depend on cell type and timing. It is not a naturally occurring compound.
SR9009 is a synthetic research compound that activates the REV-ERBα and REV-ERBβ nuclear receptors. It is not an approved drug and has no established human therapeutic use. Most published biological data come from cell and rodent studies.