If you have been reading about REV-ERB agonist and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Updated 2026-08-01. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic small-molecule REV-ERB agonist | Not a hormone or natural product |
| Primary targets | REV-ERBα and REV-ERBβ | Nuclear receptors involved in circadian and metabolic regulation |
| Appearance | White to off-white solid | Typical for purified research samples |
| Solubility | Soluble in DMSO and ethanol; low water solubility | Laboratory solubility depends on solvent and purity |
| Common synonyms | SR9009; Stenabolic | Stenabolic is a colloquial name, not a formal chemical name |
At the molecular level, SR9009 binds REV-ERBα and REV-ERBβ and alters their repressive activity on target genes. These nuclear receptors help regulate the circadian clock, lipid synthesis, glucose metabolism, and inflammatory pathways. By changing transcription, the compound can shift the timing or magnitude of downstream metabolic processes in model systems. It does not act through androgen receptors or adenosine receptors, which distinguishes it from several substances sold for athletic performance. Whether the same transcriptional changes occur in humans at tolerable exposures remains an open question because controlled human studies are lacking.
Preclinical reports describe effects on exercise endurance, mitochondrial content, and lipid profiles in rodents, but these findings come from specific experimental conditions. Many studies use high doses or delivery methods that may not translate directly to human use. SR9009 has been reported to have low oral bioavailability and a short half-life, which complicates interpretation of oral dosing studies. It is not established as safe or effective for any indication. Literature discussions often separate its pharmacological mechanism from unverified claims made in fitness and supplement markets.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not an approved medicine and has no established human therapeutic use. The compound appears in scientific literature as a tool for probing circadian and metabolic regulation. Online sellers often label it as a research chemical, sometimes using the nickname Stenabolic. Its chemical identity is distinct from selective androgen receptor modulators, stimulants, and peroxisome proliferator-activated receptor delta agonists. Researchers use it mainly in cell and animal experiments.
Most published work on SR9009 consists of preclinical studies. It is widely sold as a research chemical, a category that does not imply safety, efficacy, or pharmaceutical-grade quality. Sports anti-doping organizations have listed SR9009 as a prohibited substance, and its presence in an athlete sample can lead to sanctions. Legal status differs by country; in several jurisdictions it is not approved for human consumption and may be treated as an unapproved new drug.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not a steroid, peptide, or natural hormone. In scientific literature, it appears under the code SR9009 and in non-scientific contexts as Stenabolic. The compound was identified through chemical screening efforts aimed at targeting circadian clock components. Its status remains investigational, and no regulatory agency has approved it as a human medicine.
SR9009 binds REV-ERB receptors and alters their repressive activity on target genes. This action can change transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. In rodent studies, treated animals have shown changes in muscle oxidative capacity and exercise performance, though effects vary by dose, duration, and model. The precise molecular steps connecting receptor binding to whole-body outcomes are still an active area of investigation. Findings in animals do not automatically translate to humans.
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.
=== Effect on the immune microenvironment === CAFs can produce cytokine TGF-β which has inhibitory effect on T cells, macrophages and neutrophils thus they are not able to promote immune response against the tumor. Immune system is greatly affected by CAFs. CAFs promote the recruitment of monocytes and induce their differentiation into pro-tumorigenic macrophage subset M2. In breast cancer secretion of monocyte chemotactic protein-1, stromal-derived factor 1 and chitinase 3-like 1 is a signal for monocyte migration and differentiation into M2 subset. Similar effect was observed in prostate carcinoma. In pancreatic cancer, other cytokines have central role in monocyte differentiation into M2 subset such as M-CSF1, IL-6 and CCL2. Other cytokines such as IL-8, IL-10, TGF-β also participate. Such M2 macrophages then further activate progression of CAFs. CAFs have inhibitory effects on NK cells by releasing prostaglandin E2 (PGE2). In hepatocellular carcinoma besides PGE2, indoleamine 2,3-dioxygenase (IDO) is suppressing NK cells. In the restriction of anti-tumor immunity are crucial regulatory T cells (Treg; Foxp3+). CAFs stimulate migration, induction and maintenance of Treg cells which depends on the chemokines CCL5 and CXCL12. Critical for anti-tumor immunity are cytotoxic CD8+ T cells. CAFs decrease their infiltration into tumor by releasing chemokine CXCL12 and cytokines IL-6 and TGF-β. However, for T cell movement restriction in tumors is also responsible hypoxia, which leads to decrease of expression of adhesion molecules on endothelial cells.
== Trade == South Korea spent around $129 million in 2017 to purchase 275,000 metric tons of foreign kimchi, more than 11 times the amount it exported, according to data released by the Korea Customs Service in 2017. South Korea consumes 1.85 million metric tons of kimchi annually, or 36.1 kg per person. It imports a significant fraction of that, mostly from China, and runs a $47.3 million kimchi trade deficit.
=== Some documentary film awards === Grierson Awards Academy Award for Best Documentary Feature Joris Ivens Award, International Documentary Film Festival Amsterdam (IDFA), (named after Joris Ivens) Cinéma du Réel prizes, including the Grand Prix and Prix du premier film Loridan-Ivens / First Film Loridan-Ivens Award (formerly Joris Ivens Award), among others Filmmaker Award, Margaret Mead Film Festival Grand Prize, Visions du Réel
== Employee relations and opportunities == In February 2019, employees of three Ohio locations resigned en masse due to management changes, as well as what they alleged was a 50% reduction of the employee hourly pay rate, a claim denied by Sonic. In 2020, Sonic added a tipping feature via the online ordering app. In 2021, Sonic added an option to tip at the stalls.
In November 1953, Florey was informed that works would proceed as planned. On 27 March 1958, Florey ceremoniously opened the John Curtin School of Medical Research and received an honorary Doctor of Science degree along with Sir Norman Gregg. Menzies, Coombes, Ennor and Curtin's family were in attendance. This was not the end of Florey's association with the ANU. In 1964, he accepted the role of chancellor, a position he held from 1965 until his death in 1968.
Sources: en.wikipedia.org
The angiotensin II receptors, (ATR1) and (ATR2), are a class of G protein-coupled receptors with angiotensin II as their ligands. They are important in the renin–angiotensin system: they are responsible for the signal transduction of the vasoconstricting stimulus of the main effector hormone, angiotensin II. The AT1 and AT2 receptors share a sequence identity of ~30%, but have a similar affinity for angiotensin II, which is their main ligand. The AT1 receptor is the best elucidated angiotensin receptor. The AT1 subtype is found in the heart, blood vessels, kidney, adrenal cortex, lung and circumventricular organs of brain, basal ganglia, brainstem and mediates the vasoconstrictor effects. The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to Gq/11 and Gi/o and thus activates phospholipase C and increases the cytosolic Ca2+ concentrations, which in turn triggers cellular responses such as stimulation of protein kinase C. Activated receptor also inhibits adenylate cyclase and activates various tyrosine kinases.
Microanalysis is the chemical identification and quantitative analysis of very small amounts of chemical substances (generally less than 10 mg or 1 ml) or very small surfaces of material (generally less than 1 cm2). One of the pioneers in the microanalysis of chemical elements was the Slovenian-Austrian Nobel Prize winner Fritz Pregl. The most known methods used in microanalysis include: Most of the spectroscopy methods: ultraviolet–visible spectroscopy, infrared spectroscopy, nuclear magnetic resonance, X-ray fluorescence, Energy-dispersive X-ray spectroscopy, Wavelength-dispersive X-ray spectroscopy, and mass spectrometry Most of the chromatography methods : high-performance liquid chromatography, Gel permeation chromatography; Some thermal analysis methods: differential scanning calorimetry, thermogravimetric analysis; Electrophoresis; Field flow fractionation; X-ray diffraction; Combustion analysis. Compared to normal analyses methods, microanalysis:
In reactor fuel, the fission product xenon, since it is almost insoluble in the lattice, tends to migrate to form bubbles in the fuel. As caesium 133, 135, and 137 are formed by the beta particle decay of the corresponding xenon isotopes, this causes the caesium to become physically separated from the bulk of the uranium oxide fuel. Because 135Xe is a potent nuclear poison with the largest cross section for thermal neutron absorption, the buildup of 135Xe in the fuel inside a power reactor can lower the reactivity greatly. If a power reactor is shut down or left running at a low power level, then large amounts of 135Xe can build up through decay of 135I. When the reactor is restarted or the low power level is increased significantly, 135Xe will be quickly consumed through neutron capture reactions and the reactivity of the core will increase. Under some circumstances, control systems may not be able to respond quickly enough to manage an abrupt reactivity increase as the built-up 135Xe burns off. It is thought that xenon poisoning was one of the factors which led to the power surge which damaged the Chernobyl reactor core.
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Sources: en.wikipedia.org
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.
It binds REV-ERBα and REV-ERBβ and changes transcription of metabolic genes. This can affect circadian rhythm, lipid use, and mitochondrial function. The full downstream effects are still under study.
No. Some rodent studies show increased endurance, but controlled human trials are lacking. Claims about human performance are not established by published evidence.
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.