REV-ERB agonist is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Updated 2026-04-22. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
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.
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.
| 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 |
SR9009 is a synthetic small molecule developed as a REV-ERB agonist. It binds to REV-ERBα and REV-ERBβ, nuclear receptors that help regulate circadian rhythms and metabolic gene expression. In cell and animal studies, the compound alters lipid and glucose handling and influences skeletal muscle oxidative capacity. Its exact effects in humans remain largely uncharacterized because controlled clinical trials have not been reported. The molecule is frequently described in preclinical literature as a metabolic modulator.
Research interest in SR9009 grew from studies showing improved running endurance in mice after short treatment periods. Those experiments linked the compound to increased mitochondrial content and fatty acid oxidation in muscle, but the findings come from animal models and specific dosing schedules. Independent replication has been limited, and the pathways connecting REV-ERB activation to exercise performance are still being mapped. Whether similar responses occur in humans is an open question.
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.
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.
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.
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.
Methyl blue is a chemical compound with the molecular formula C37H27N3Na2O9S3. It is used as a stain in histology, and stains collagen blue in tissue sections. It can be used in some differential staining techniques such as Mallory's trichrome stain and Gömöri trichrome stain, and can be used to mediate electron transfer in microbial fuel cells. Fungal cell walls are also stained by methyl blue. Methyl blue is also available in mixture with water blue, under name Aniline Blue WS, Aniline blue, China blue, or Soluble blue; and in a solution of phenol, glycerol, and lactic acid under the name Lactophenol cotton blue (LPCB), which is used for microscopic visualization of fungi.
=== Mechanism of action === While it is unclear how fluoxetine exerts its effect on mood, it has been suggested that fluoxetine elicits an antidepressant effect by inhibiting serotonin reuptake in the synapse by binding to the reuptake pump on the neuronal membrane to increase serotonin availability and enhance neurotransmission. Over time, this leads to a downregulation of pre-synaptic 5-HT1A receptors, which is associated with an improvement in passive stress tolerance, and delayed downstream increase in expression of brain-derived neurotrophic factor, which may contribute to a reduction in negative affective biases. Norfluoxetine and desmethylfluoxetine are metabolites of fluoxetine and also act as serotonin reuptake inhibitors, increasing the duration of action of the drug. Prolonged exposure to fluoxetine changes the expression of genes involved in myelination, a process that shapes brain connectivity and contributes to symptoms of psychiatric disorders. The regulation of genes involved with myelination is partially responsible for the long-term therapeutic benefits of chronic SSRI exposure.
=== Strabismus === Ophthalmologists specializing in eye muscle disorders (strabismus) had developed the method of EMG-guided injection (using the electromyogram, the electrical signal from an activated muscle, to guide injection) of local anesthetics as a diagnostic technique for evaluating an individual muscle's contribution to an eye movement. Because strabismus surgery frequently needed repeating, a search was undertaken for non-surgical, injection treatments using various anesthetics, alcohols, enzymes, enzyme blockers, and snake neurotoxins. Finally, inspired by Daniel B. Drachman's work with chicks at Johns Hopkins, Alan B. Scott and colleagues injected botulinum toxin into monkey extraocular muscles. The result was remarkable; a few picograms induced paralysis that was confined to the target muscle, long in duration, and without side effects. After working out techniques for freeze-drying, buffering with albumin, and assuring sterility, potency, and safety, Scott applied to the FDA for investigational drug use, and began manufacturing botulinum type A neurotoxin in his San Francisco lab. He injected the first strabismus patients in 1977, reported its clinical utility in 1980, and had soon trained hundreds of ophthalmologists in EMG-guided injection of the drug he named Oculinum ("eye aligner"). In 1986, Oculinum Inc, Scott's micromanufacturer and distributor of botulinum toxin, was unable to obtain product liability insurance, and could no longer supply the drug. As supplies became exhausted, people who had come to rely on periodic injections became desperate.
In order for the acyl-CoA to enter the mitochondrion the carnitine shuttle is used: Acyl-CoA is transferred to the hydroxyl group of carnitine by carnitine palmitoyltransferase I, located on the cytosolic faces of the outer and inner mitochondrial membranes. Acyl-carnitine is shuttled inside by a carnitine-acylcarnitine translocase, as a carnitine is shuttled outside. Acyl-carnitine is converted back to acyl-CoA by carnitine palmitoyltransferase II, located on the interior face of the inner mitochondrial membrane. The liberated carnitine is shuttled back to the cytosol, as an acyl-CoA is shuttled into the mitochondrial matrix. Beta oxidation, in the mitochondrial matrix, then cuts the long carbon chains of the fatty acids (in the form of acyl-CoA molecules) into a series of two-carbon (acetate) units, which, combined with co-enzyme A, form molecules of acetyl CoA, which condense with oxaloacetate to form citrate at the "beginning" of the citric acid cycle. It is convenient to think of this reaction as marking the "starting point" of the cycle, as this is when fuel - acetyl-CoA - is added to the cycle, which will be dissipated as CO2 and H2O with the release of a substantial quantity of energy captured in the form of ATP, during the course of each turn of the cycle and subsequent oxidative phosphorylation.
Sources: en.wikipedia.org
UDP-N-acetyl-D-glucosamine + [protein]-L-serine → UDP + [protein]-3-O-(N-acetyl-D-glucosaminyl)-L-serine UDP-N-acetyl-D-glucosamine + [protein]-L-threonine → UDP + [protein]-3-O-(N-acetyl-D-glucosaminyl)-L-threonine First, the hydroxyl group of serine is deprotonated by histidine 498, a catalytic base in this proposed reaction. Lysine 842 is also present to stabilize the UDP moiety. The oxygen ion then attacks the sugar-phosphate bond between the glucosamine and UDP. This results in the splitting of UDP-N-acetylglucosamine into N-acetylglucosamine – peptide and UDP. Proton transfers take place at the phosphate and histidine 498. This mechanism is spurred by OGT gene containing O-linked N-acetylglucosamine transferase. Aside from proton transfers the reaction proceeds in one step, as shown in Figure 2. Figure 2 uses a lone serine residue as a representative of the peptide with a reactive hydroxyl group. Threonine could have also been used in the mechanism.
Best was elected a foreign member of the Royal Netherlands Academy of Arts and Sciences in 1946. He was elected a foreign honorary member of the American Academy of Arts and Sciences in 1948. He was elected to both the American Philosophical Society and the United States National Academy of Sciences in 1950. In 1967 he was made a Companion of the Order of Canada in recognition for "his contribution to medicine, particularly as co-discoverer of insulin." He was a commander of the Civil Division of the Order of the British Empire and was made a member of Order of the Companions of Honour in 1971 "for services to Medical Research". He was a fellow of the Royal Society of London, the Royal Society of Canada, and was the first Canadian to be elected into the Pontifical Academy of Sciences. As a recipient of the Order of Canada, he was awarded the Canadian version of the Queen Elizabeth II Silver Jubilee Medal in 1977. In 1994 he was inducted into the Canadian Medical Hall of Fame. In 2004, he was inducted into the National Inventors Hall of Fame. Dr. Charles Best Secondary School in Coquitlam, British Columbia, Dr. Charles Best Public School in Burlington, Ontario, and Charles H. Best Middle School in Toronto, Ontario, are named in his honour. His birthplace in Maine is listed on the United States National Register of Historic Places.
Additionally, the relative (and quantitative) success of the shock therapies, despite the considerable risks they posed to patients, also helped to inspire doctors in the field to pioneer ever more drastic forms of medical interventions, including lobotomies. The clinician-historian Joel Braslow argues that from malarial therapy onward to lobotomy, physical psychiatric therapies "spiral closer and closer to the interior of the brain", with this organ increasingly taking "center stage as a source of disease and site of cure". For medical historian Roy Porter, the often violent and invasive psychiatric interventions developed during the 1930s and 1940s are indicative of both the well-intentioned desire of psychiatrists to find some medical means of alleviating the suffering of the vast number of patients then in psychiatric hospitals and also the relative lack of social power of those same patients to resist the increasingly radical and even reckless interventions of asylum doctors. Many doctors, patients, and family members of the period believed that, despite potentially catastrophic consequences, the results of lobotomy were seemingly positive in many instances or were at least deemed as such when measured next to the apparent alternative of long-term institutionalisation. Lobotomy has always been controversial, but for a period of the medical mainstream, it was regarded as a legitimate last-resort remedy for categories of patients who were otherwise regarded as hopeless.
Sources: en.wikipedia.org
TIMPs inhibit all MMPs except TIMP-1 which does not inhibit MT-1-MMP. There are some differences in the inhibitory preferences of TIMPs. TIMP-1 for example favors to inhibit MMP-9. Other examples are TIMP-2 and TIMP-4 which are more potent MMP-2 inhibitors than MMP-9 inhibitors. TIMPs could potentially be useful against illnesses like cardiovascular disease and cancer. The application of TIMPs as therapeutic instrument through gene therapy or direct protein application is still in early stages of development. It is preferable to inhibit specific MPPs that play a role in pathological conditions. Since TIMPs inhibit multiple MMPs it is desirable to develop engineered TIMPs with altered specificity.
"Bad and Boujee" is a song by American hip-hop group Migos featuring American rapper Lil Uzi Vert. Written alongside producer Metro Boomin and co-producer G Koop, it was originally released to the Quality Control Music YouTube channel on August 27, 2016 before being officially released on October 28 by Quality Control Music, 300 Entertainment, and Atlantic Records as the lead single from the group's second studio album Culture (2017). In late December 2016, "Bad and Boujee" became an Internet phenomenon, spawning many memes with the lyrics "rain drop, drop top". This viral trend, combined with Donald Glover's shoutout at the 2017 Golden Globes, would help its commercial performance and cause the song to spike into the top ten and later peak at number one on the US Billboard Hot 100 for the week of January 21, 2017, making it the first number one single for both Migos and Lil Uzi Vert. There were also many memes about member Takeoff's omission from the song. The single received a nomination for Best Rap Performance at the 60th Annual Grammy Awards. The track has acquired over 1 billion Spotify plays as of August 2025.
Encapsulin shells compromise icosahedral complexes (12 vertices, 20 faces, 30 edges) formed as a result of self-assembly of protomers. These encapsulin shells have diameters between 24 and 42 nm and are defined by the HK97-fold of their shell protein. The HK97-fold protomer has a roughly triangular shape and consists of three conserved domains: the axial domain, the peripheral domain, and the extended loop. The size and symmetry of the capsid are defined by a triangulation number (T), which determines the number of subunits in the assembly. For example: T = 1 encapsulins (Thermotoga martima) consist of 60 protomers. T = 3 encapsulins (Pyrococcus furiosus) consist of 180 protomers. T = 4 encapsulins (Quasibacillus thermotolerans) consist of 240 protomers.
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 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.