REV-ERB agonist comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Last reviewed on 2025-09-30. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Binds REV-ERBα and REV-ERBβ in preclinical models |
| Molecular formula | C20H24ClN3O4S | Reported for the parent compound |
| CAS Registry Number | 1379686-30-2 | Common identifier in chemical databases |
| Appearance | Off-white to pale yellow solid | Typical research chemical solid |
| Solubility | Soluble in DMSO and ethanol; low in water | Class: small organic molecule |
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, also called NR1D1 and NR1D2. These receptors help regulate circadian rhythms and metabolic gene programs. The compound was developed for laboratory research, not as an approved therapeutic. Its identity is distinct from steroid hormones and selective androgen receptor modulators. Scientific interest centers on how REV-ERB activation changes gene expression in cells and animal models.
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.
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.
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 often grouped with compounds studied for circadian and metabolic regulation rather than with classical anabolic steroids. Its interactions with nuclear receptors differ from those of androgen receptor ligands, and its proposed mechanisms involve transcriptional control rather than direct hormone signaling. Some sources classify it as a metabolic modulator because of observed effects on energy utilization. The distinction matters for regulation and for interpreting research results across different compound classes.
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.
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.
== Pathophysiology == The precise mechanism of acrocyanosis is not known. The current line of thinking goes that vasospasms in the cutaneous arteries and arterioles produce cyanotic discoloration, while compensatory dilatation in the postcapillary venules causes sweating. Arteriovenous subpapillary plexus shunting also occurs. Persistent vasoconstriction at the precapillary sphincter creates a local hypoxic environment, thus releasing adenosine into the capillary bed. Vasospasms force adenosine to enter the capillary bed, where it vasodilates the postcapillary venules. Such differences in vessel tone create a countercurrent exchange system that attempts to retain heat. Profuse sweating would then be caused by an overwhelmed countercurrent exchange system. In addition to adenosine, other hormones may contribute to acrocyanosis such as increase blood levels of serotonin. This would seem to support case studies reporting acrocyanosis as an unusual side effect for pediatric patients taking tricyclic antidepressants, as these medications can inhibit the reuptake of serotonin and thus increase their blood concentrations. Acrocyanosis has been reported in association with many other medications and substances.
BioID, also known as BirA*, is a mutant E. coli biotin ligase that catalyzes the activation of biotin by ATP. The activated biotin is short-lived and thus can only diffuse to a region proximal to BioID. Labeling is achieved when the activated biotin reacts with nearby amines, such as the lysine sidechain amines found in proteins. TurboID is a biotin ligase engineered via yeast surface display directed evolution. TurboID, an enhanced variant of BioID, enables ~10 minute labeling times instead of the ~18 hour labeling times required by BioID. Split-TurboID can be used for proximity labeling in a manner dependent on an independent protein-protein interaction requiring two halves of TurboID to colocalize. APEX is an ascorbate peroxidase derivative reliant on hydrogen peroxide for catalyzing the oxidation of biotin-tyramide, also known as biotin-phenol, to a short-lived and reactive biotin-phenol free radical. Labeling is achieved when this intermediate reacts with various functional groups of nearby biomolecules. APEX can also be used for local deposition of diaminobenzidine, a precursor for an electron microscopy stain. APEX2 is a derivative of APEX engineered via yeast surface display directed evolution. APEX2 shows improved labeling efficiency and cellular expression levels. APEX and APEX2 generate highly reactive phenoxyl radical intermediates from cell-permeable biotin-phenol. These intermediates primarily interact with tyrosine and tryptophan residues on labeled proteins and guanosine on labeled RNAs. Direct DNA labeling is significantly less efficient than RNA labeling.
=== Continued employment by the Astros === As part of a personal services contract Bagwell signed with the Astros, he served as a coach in spring training of 2007. On July 11, 2010, the Astros hired Bagwell to be their hitting coach, replacing Sean Berry. At the time of the switch, the Astros had the second-worst average (.237) in the majors and the worst OBP (.295). At the end of the season, the team marginally improved, but was still last in the league in OBP (.303) and SLG (.362) and Bagwell announced he would not return as hitting coach. After a five-year gap in contact with the Astros organization, Bagwell accepted a formal invitation from manager A. J. Hinch to be a guest instructor in spring training of 2015. He is currently a special advisor to team owner Jim Crane.
=== Cluster headaches === Preventive therapy with verapamil is believed to work because it has an effect on the circadian rhythm and on CGRPs, as CGRP-release is controlled by voltage-gated calcium channels.
Sources: en.wikipedia.org
Under Nazi rule, Germans had been forbidden to accept Nobel prizes after the Nobel Peace Prize had been awarded to Carl von Ossietzky in 1936. The Nobel Committee for Chemistry's recommendation was therefore rejected by the Royal Swedish Academy of Sciences in 1944, which also decided to defer the award for one year. When the Academy reconsidered the award in September 1945, the war was over and thus the German boycott had ended. Also, the chemistry committee had now become more cautious, as it was apparent that much research had taken place in the United States in secret, and suggested deferring for another year, but the Academy was swayed by Göran Liljestrand, who argued that it was important for the Academy to assert its independence from the Allies of World War II, and award the prize to a German, as it had done after World War I when it had awarded it to Fritz Haber. Hahn therefore became the sole recipient of the 1944 Nobel Prize for Chemistry. The invitation to attend the Nobel festivities was transmitted via the British Embassy in Stockholm. On 4 December, Hahn was persuaded by two of his Alsos captors, American Lieutenant Colonel Horace K. Calvert and British Lieutenant Commander Eric Welsh, to write a letter to the Nobel committee accepting the prize but stating that he would not be able to attend the award ceremony on 10 December since his captors would not allow him to leave Farm Hall. When Hahn protested, Welsh reminded him that Germany had lost the war.
== Physiological function == Until the late 1970s, hyaluronic acid was described as a "goo" molecule, a ubiquitous carbohydrate polymer that is part of the extracellular matrix. For example, hyaluronic acid is a major component of the synovial fluid and was found to increase the viscosity of the fluid. Along with lubricin, it is one of the fluid's main lubricating components. Hyaluronic acid is an important component of articular cartilage, where it is present as a coat around each cell (chondrocyte). When aggrecan monomers bind to hyaluronan in the presence of HAPLN1 (hyaluronic acid and proteoglycan link protein 1), large, highly negatively charged aggregates form. These aggregates imbibe water and are responsible for the resilience of cartilage (its resistance to compression). The molecular weight (size) of hyaluronan in cartilage decreases with age, but the amount increases. A lubricating role of hyaluronan in muscular connective tissues to enhance the sliding between adjacent tissue layers has been suggested. A particular type of fibroblasts, embedded in dense fascial tissues, has been proposed as being cells specialized for the biosynthesis of the hyaluronan-rich matrix. Their related activity could be involved in regulating the sliding ability between adjacent muscular connective tissues. Hyaluronic acid is also a major component of skin, where it is involved in repairing tissue. When skin is exposed to excessive UVB rays, it becomes inflamed (sunburn), and the cells in the dermis stop producing as much hyaluronan and increase the rate of its degradation.
The genealogy of lifting can be traced back to the beginning of recorded history where humanity's fascination with physical abilities can be found among numerous ancient writings. In many prehistoric tribes, they would have a big rock they would try to lift, and the first one to lift it would inscribe their name into the stone. Such rocks have been found in Greek and Scottish castles. Progressive resistance training dates back at least to Ancient Greece, when legend has it that wrestler Milo of Croton trained by carrying a newborn calf on his back every day until it was fully grown. Another Greek, the physician Galen, described strength training exercises using the halteres (an early form of dumbbell) in the 2nd century. Ancient Greek sculptures also depict lifting feats. The weights were generally stones, but later gave way to dumbbells. The dumbbell was joined by the barbell in the later half of the 19th century. Early barbells had hollow globes that could be filled with sand or lead shot, but by the end of the century these were replaced by the plate-loading barbell commonly used today. Weightlifting was first introduced in the Olympics in the 1896 Athens Olympic Games as a part of track and field, and was officially recognized as its own event in 1914. The 1960s saw the gradual introduction of exercise machines into the still-rare strength training gyms of the time. Weight training became increasingly popular in the 1970s, following the release of the bodybuilding movie Pumping Iron, and the subsequent popularity of Arnold Schwarzenegger.
=== BLT (bone marrow/liver/thymus) model === The BLT model is constituted with human HSCs, bone marrow, liver, and thymus. The engraftment is carried out by implantation of liver and thymus under the kidney capsule and by transplantation of HSCs obtained from fetal liver. The BLT model has a complete and totally functional human immune system with HLA-restricted T lymphocytes. The model also comprises a mucosal system that is similar to that of humans. Moreover, among all models the BLT model has the highest level of human cell reconstitution. However, since it requires surgical implantation, this model is the most difficult and time-consuming to develop. Other drawbacks associated with the model are that it portrays weak immune responses to xenobiotics, sub-optimal class switching and may develop GvHD.
== Immunoassay == Today, these antigen-proteins can be genetically manufactured (e.g. transgene E. coli) to produce material for a simple antigen test, which detects the presence of HBV. It is present in the sera of patients with viral hepatitis B (with or without clinical symptoms). Patients who developed antibodies against HBsAg (anti-HBsAg seroconversion) are usually considered non-infectious. HBsAg detection by immunoassay is used in blood screening, to establish a diagnosis of hepatitis B infection in the clinical setting (in combination with other disease markers) and to monitor antiviral treatment. In histopathology, the presence of HBsAg is more commonly demonstrated by the use of the Shikata orcein technique, which uses a natural dye to bind to the antigen in infected liver cells. Positive HBsAg tests can be due to recent vaccination against Hepatitis B virus but this positivity is unlikely to persist beyond 14 days post-vaccination.
Sources: en.wikipedia.org
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.
No. It is a synthetic ligand that binds nuclear receptors, not a steroid or peptide hormone. Its activity depends on receptor binding rather than endocrine secretion.
Clinical evidence is limited. Most published data come from cell and animal experiments. Human safety and efficacy remain uncertain.
It is a synthetic research compound that activates REV-ERB nuclear receptors. It is not an approved drug or dietary supplement. Most information comes from cell and animal studies.