If you have been reading about REV-ERB 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 2026-03-26. Numbers and descriptions here follow the published literature rather than marketing material.
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.
Handling recommendations for SR9009 in a laboratory setting include storing the solid at low temperature, protected from light and moisture. The compound is often dissolved in dimethyl sulfoxide or ethanol for experiments. Solutions should be prepared with appropriate personal protective equipment and disposed of according to local rules. Stability data for long-term storage are limited, so stock solutions are typically kept cold and used within defined periods. Records of preparation date and concentration support reproducibility.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Regulatory status | Not approved as a medicine in major jurisdictions | Sold as a research chemical; legal status varies |
| Anti-doping status | Prohibited by the World Anti-Doping Agency | Listed under non-approved substances or related category |
| Typical analytical method | LC-MS/MS | Used for detection and confirmation in biological samples |
| Storage temperature | −20 °C or lower for solid | Desiccated and protected from light |
| Common solution solvents | DMSO; ethanol | Aqueous solubility is limited |
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.
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.
Regulatory treatment of SR9009 reflects its investigational status. The compound has no approved human therapeutic indication, and sports authorities prohibit its use. It appears on anti-doping lists as a non-approved substance or metabolic modulator, depending on the list version. Products sold online as research chemicals are not quality-controlled medicines, so their identity and purity can differ from the label. Such products may also contain unlisted compounds, which complicates both testing and safety assessment.
Scientific discussion of SR9009 often separates animal evidence from human anecdote. Rodent studies provide controlled data on endurance, metabolism, and gene expression, but they use specific strains, doses, and treatment durations. Human reports are mostly uncontrolled and cannot establish cause and effect. Open questions include oral bioavailability, tissue distribution, metabolic stability, and long-term effects. Review articles generally call for more rigorous pharmacokinetic and safety research before any clinical use could be considered.
For long-term storage, SR9009 is typically kept as a solid at low temperature, protected from moisture and light. Desiccated conditions limit hydrolysis, while opaque containers reduce photochemical breakdown. Solutions are less stable than solids and are often stored frozen in aliquots to avoid repeated freeze-thaw cycles. Stability data are not standardized across all suppliers, so users should rely on certificate-of-analysis information when available. Degradation may appear as color change, precipitate, or decreased chromatographic purity.
Laboratory identification of SR9009 typically relies on chromatographic separation coupled to mass spectrometry, often with ultraviolet detection as a secondary check. Nuclear magnetic resonance spectroscopy can confirm molecular structure when a reference standard is available. Because many suppliers sell the compound as a research chemical, independent identity testing is important for experimental reproducibility. A single retention time is not sufficient proof of identity, especially when related compounds may be present. Purity assessments usually report a percentage based on area normalization.
SR9009 is generally described as poorly soluble in water and more soluble in organic solvents such as dimethyl sulfoxide and ethanol. Stock solutions are commonly prepared in an organic solvent before dilution into an aqueous buffer or vehicle. Precipitation can occur if the organic fraction is reduced too quickly or if the final concentration exceeds the compound's solubility limit. Sonication or gentle warming may aid dissolution in some protocols, but excessive heat can promote degradation. Container material and pH can also influence observed solubility.
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.
=== Depletion of adenine nucleotides === Having eliminated loss of respiration, Albrich et al. proposes that the cause of death may be due to metabolic dysfunction caused by depletion of adenine nucleotides. Barrette et al. studied the loss of adenine nucleotides by studying the energy charge of HClO-exposed cells and found that cells exposed to HClO were unable to step up their energy charge after addition of nutrients. The conclusion was that exposed cells have lost the ability to regulate their adenylate pool, based on the fact that metabolite uptake was only 45% deficient after exposure to HClO and the observation that HClO causes intracellular ATP hydrolysis. It was also confirmed that, at bacteriocidal levels of HClO, cytosolic components are unaffected. So it was proposed that modification of some membrane-bound protein results in extensive ATP hydrolysis, and this, coupled with the cells inability to remove AMP from the cytosol, depresses metabolic function. One protein involved in loss of ability to regenerate ATP has been found to be ATP synthetase. Much of this research on respiration reconfirms the observation that relevant bacteriocidal reactions take place at the cell membrane.
Bryant Park contains a carousel called Le Carrousel Magique, located in the southern section of the park. The carousel was designed by Marvin Sylvor, created by the Fabricon Carousel Company, and installed in 2002. The company was selected after a carousel installation in Bryant Park was approved in 1997. The carousel has a diameter of 22 feet (6.7 m), weighs 12,000 pounds (5,400 kg), and contains 14 animal casts, of which 12 are capable of moving vertically. In keeping with the French theme of the park, it plays French music. It underwent a restoration in 2009. The carousel also has a ticket booth, measuring 7 feet (2.1 m) tall and 4 feet (1.2 m) wide, which was constructed in 1928 and was relocated from Paragon Park in Hull, Massachusetts.
After hypothyroidism was found to cause a lower basal metabolic rate, this was used as a marker to guide adjustments in therapy in the early 20th century (around 1915). However, a low basal metabolic rate was known to be non-specific, also present in malnutrition. The first laboratory test to help assess thyroid status was the serum protein-bound iodine, which came into use around the 1950s. In 1971, the thyroid stimulating hormone (TSH) radioimmunoassay was developed, which was the most specific marker for assessing thyroid status in patients. Many people who were being treated based on basal metabolic rate, minimizing hypothyroid symptoms, or based on serum protein-bound iodine, were found to have excessive thyroid hormone. The following year, in 1972, a T3 radioimmunoassay was developed, and in 1974, a T4 radioimmunoassay was developed.
Sources: en.wikipedia.org
== Hospitals == People's Hospital of Ningxia Hospital of Traditional Chinese Medicine of Ningxia Ningxia Medical College Affiliated Hospital Yinchuan Hospital of Traditional Chinese Medicine Yinchuan People's Hospital Yinchuan Stomatological Hospital Yinchuan Women and Children's Healthcare Center Women and Children's Healthcare Center of Ningixa Yinchuan No.1 People's Hospital Yinchuan No.2 People's Hospital Yinchuan No.3 People's Hospital Shizuishan No.2 People's Hospital Guyuan Hospital of Ningxia
For these reasons, quantum dots are sometimes referred to as artificial atoms, emphasizing their bound and discrete electronic states, like naturally occurring atoms or molecules. It was shown that the electronic wave functions in quantum dots resemble the ones in real atoms. Quantum dots have properties intermediate between bulk semiconductors and discrete atoms or molecules. Their optoelectronic properties change as a function of both size and shape. Larger QDs of 5–6 nm diameter emit longer wavelengths, with colors such as orange, or red. Smaller QDs (2–3 nm) emit shorter wavelengths, yielding colors like blue and green. The specific emission energy of a QD depends on its dimensions, band gap energy, effective excited electron mass, and effective excited hole mass. Potential applications of quantum dots include single-electron transistors, solar cells, LEDs, lasers, single-photon sources, second-harmonic generation, quantum computing, cell biology research, microscopy, and medical imaging. Their small size allows for some QDs to be suspended in solution, which may lead to their use in inkjet printing, and spin coating. They have been used in Langmuir–Blodgett thin films. These processing techniques result in less expensive and less time-consuming methods of semiconductor fabrication.
=== Alzheimer's disease === The "amyloid hypothesis" — that Aβ, either already in plaques, or as oligomers that may act outside of plaques, is responsible for the pathology of Alzheimer's disease — has been the dominant hypothesis for around thirty years as of 2025, but is not conclusively established, especially because over time it has become clear that there are many causes of Alzheimer's (outside of people who develop early-onset Alzheimer's disease which is clearly driven by Aβ), and because many people who have plaques never develop Alzheimer's. Scientists in the field have wondered if plaques may be a response to the disease process, rather than the cause of it. Research suggests that soluble oligomeric forms of the amyloid beta may be causative agents in the development of Alzheimer's disease. It is generally believed that Aβ oligomers are the most toxic. Several genetic, cell biology, biochemical and animal studies using experimental models support the concept that Aβ plays a central role in the development of Alzheimer's disease pathology. Brain Aβ is elevated in people with sporadic Alzheimer's disease. Aβ is the main constituent of brain parenchymal and vascular amyloid; it contributes to cerebrovascular lesions and is neurotoxic. It is unresolved how Aβ accumulates in the central nervous system and subsequently initiates the disease of cells.
Sources: en.wikipedia.org
Its legal status depends on the country and intended use. It is not an approved medicine in major jurisdictions. In sport, it is prohibited by anti-doping rules.
Laboratories typically use LC-MS/MS to detect SR9009 and related compounds in urine or blood. The method is sensitive but depends on sample collection timing. Confirmatory analysis follows quality-control procedures.
Solid material is generally kept cold, dry, and protected from light. Solutions are often stored in sealed containers at low temperature. Stability beyond recommended periods is not well documented.
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.