The short version of REV-ERB agonist fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2026-03-05. Anything still debated is marked as such rather than presented as settled.
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.
Laboratory samples of SR9009 are typically handled as research chemicals rather than pharmaceuticals. Suppliers usually state that the material is for research use only and not for human or veterinary administration. Storage recommendations generally call for a freezer at approximately −20 °C, protection from light, and a desiccated environment. The solid is often described as a white to off-white powder. Solubility is commonly reported in organic solvents such as dimethyl sulfoxide and ethanol, with low solubility in water.
Analytical identification and purity assessment often use high-performance liquid chromatography with ultraviolet detection or mass spectrometry. Liquid chromatography–tandem mass spectrometry is used to detect and quantify SR9009 in biological matrices, including urine and blood, for anti-doping or pharmacokinetic studies. Nuclear magnetic resonance spectroscopy can confirm molecular structure. Stability depends on form and storage: the solid is generally more stable than solutions, and repeated freeze–thaw cycles may degrade samples. Purity is typically reported as a percentage from a certificate of analysis.
Regulatory treatment of SR9009 varies by country and context. It is not approved as a therapeutic drug by agencies such as the United States Food and Drug Administration or the European Medicines Agency. Sports authorities list it as a prohibited substance; the World Anti-Doping Agency classifies it among hormone and metabolic modulators. Legal status for personal possession or sale differs across jurisdictions, and some countries may restrict it under analog or research chemical laws. Buyers who seek verified material often rely on independent laboratory testing because online product labels may not match contents.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small molecule; not a steroid or peptide. |
| Primary targets | NR1D1 and NR1D2 | Also known as REV-ERBα and REV-ERBβ. |
| Studied routes | Intraperitoneal in rodents | Oral bioavailability in humans is not established. |
| Human approval | No approved therapeutic indication | No recognized clinical use. |
| Key uncertainty | Human physiological effects | Preclinical findings may not translate. |
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.
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.
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.
=== Sources === Cleveland Clinic. "LADA Diabetes." Cleveland Clinic, https://my.clevelandclinic.org/health/diseases/lada-diabetes. Accessed 9 Apr. 2026. Diabetes UK. "Latent Autoimmune Diabetes (LADA)." Diabetes UK, https://www.diabetes.org.uk/about-diabetes/other-types-of-diabetes/latent-autoimmune-diabetes. Accessed 9 Apr. 2026. Eisenbarth, George S., ed. (2010). Immunoendocrinology: Scientific and Clinical Aspects. Contemporary Endocrinology. Humana Press. ISBN 978-1-603-27477-7. Flynn, John A.; Michael J. Choi; L. Dwight Wooster, eds. (2013). Oxford American Handbook of Clinical Medicine. Oxford American Handbooks in Medicine. Oxford University Press. ISBN 978-0-195-18849-3. HealthNormal. "Latent Autoimmune Diabetes in Adults." HealthNormal, https://www.healthnormal.com/latent-autoimmune-diabetes-in-adults/. Accessed 9 Apr. 2026. "Latent Autoimmune Diabetes in Adults: Current Status and New Horizons." SN Comprehensive Clinical Medicine, 2025, https://link.springer.com/article/10.1007/s42399-025-02003-1. Accessed 9 Apr. 2026. "Management of Latent Autoimmune Diabetes in Adults." Diabetes, vol. 69, no. 10, 2020, https://diabetesjournals.org/diabetes/article/69/10/2037/16062. Accessed 9 Apr. 2026. Munden, Julie, ed. (2006). Diabetes Mellitus: A Guide to Patient Care. Lippincott Williams & Wilkins. ISBN 978-1-58255-732-8. Haskins, Jacqueline. Kickass Healthy LADA: How to Thrive with Latent Autoimmune Diabetes in Adults. Hachette Go (2023). ISBN 9780306830730.
=== Josh Thomas and Lachlan Keeffe === Lachlan Keeffe (drafted to Collingwood in 2008) and Josh Thomas (drafted to Collingwood in 2009) are the most recent players to breach the anti-doping code. They both tested positive for clenbuterol which led to a 2-year ban as well as a $50,000 fine. The banned substance was detected in their systems after taking illicit drugs during a night out. Both players were banned from playing AFL for 2 years and were delisted by the Collingwood Football Club, before being redrafted by Collingwood in the 2016 Rookie Draft.
However, even after the initial recruitment phase, when head-shaving is no longer required, many soldiers maintain a completely or partially shaven hairstyle (such as a "high and tight", "flattop" or "buzz cut") for personal convenience or neatness. Head-shaving is not required and is often not permitted for women in military service, although they must have their hair cut or tied to regulation length. For example, the shortest hair a female soldier can have in the U.S. Army is 1/4 inch from the scalp.
Sources: en.wikipedia.org
low: hs-CRP level under 1.0 mg/L average: between 1.0 and 3.0 mg/L high: above 3.0 mg/L Normal levels increase with aging. Higher levels are found in late pregnant women, mild inflammation and viral infections (10–40 mg/L), active inflammation, bacterial infection (40–200 mg/L), severe bacterial infections and burns (>200 mg/L). CRP cut-off levels indicating bacterial from non-bacterial illness can vary due to co-morbidities such as malaria, HIV and malnutrition and the stage of disease presentation. In patients presenting to the emergency department with suspected sepsis, a CRP/albumin ratio of less than 32 has a negative predictive value of 89% for ruling out sepsis. CRP is a more sensitive and accurate reflection of the acute phase response than the ESR (erythrocyte sedimentation rate). ESR may be normal while CRP is elevated. CRP returns to normal more quickly than ESR in response to therapy.
==== Ketoacid ==== Currently, the best available evidence suggests that the ketoacid is originally attached to the chromophore core (as L-glutamate) when it is synthesized from D-tyrosine, L-2,4-diaminobutyric acid, and L-glutamate. It is unclear how this is later altered to the other congenerate (i.e., a-ketoglutarate, succinate/succinamide, etc.) forms.
==== Comparison with other antidepressants ==== In general, sertraline efficacy is similar to that of other antidepressants. For example, a meta-analysis of 12 new-generation antidepressants showed that sertraline and escitalopram are the best in terms of efficacy and acceptability in the acute-phase treatment of adults with depression. Comparative clinical trials demonstrated that sertraline is similar in efficacy against depression to moclobemide, nefazodone, escitalopram, bupropion, citalopram, fluvoxamine, paroxetine, venlafaxine, and mirtazapine. Sertraline may be more efficacious for the treatment of depression in the acute phase (first four weeks) than fluoxetine. There are differences between sertraline and some other antidepressants in their efficacy in the treatment of different subtypes of depression and in their adverse effects. For severe depression, sertraline is as good as clomipramine but is better tolerated. Sertraline appears to work better in melancholic depression than fluoxetine, paroxetine, and mianserin and is similar to the tricyclic antidepressants such as amitriptyline and clomipramine. In the treatment of depression accompanied by OCD, sertraline performs significantly better than desipramine on the measures of both OCD and depression. Sertraline is equivalent to imipramine for the treatment of depression with co-morbid panic disorder, but it is better tolerated. Compared with amitriptyline, sertraline offered a greater overall improvement in quality of life of depressed patients.
Sources: en.wikipedia.org
== Pathogenesis == The exact cause for the varied collection of symptoms found in the different ALD phenotypes is not clear. The white matter of the brain, the Leydig cells of the testes and the adrenal cortex are the most severely affected systems. The excess VLCFA can be detected in almost all tissues of the body, despite the localization of symptoms. The lack of Coenzyme A does not permit the disintegration of the VLCFA, accumulating the same in the white matter, adrenal glands, and the testes more specifically in the Leydig cells not allowing the proper function of these organs. Successful treatment of the demyelination process that affects the brain with either stem cell transplant or gene therapy does not immediately normalize the VLCFA levels in body tissues. The levels of VLCFA can be normalized by treatment with Lorenzo's oil, but this does not alter the progression of the disease. It is unclear whether the accumulation of VLCFA is associated with the pathogenesis of the disease in a specific way, or if it is a biochemical phenotype, useful for identification. Several studies link inflammation from viral infection or head trauma to development or worsening of symptoms.
== Health economics == Economic analyses suggest that TOPS may be cost-effective compared with fusion. These findings are based on improvements in quality of life, faster recovery, and reduced need for reoperation over time.
Because many proteases are nonspecific, they are highly regulated in the cell. Without regulation, proteases will destroy many proteins which are essential to physiological processes. One way the body regulates proteases is through protease inhibitors. Protease inhibitors can be other proteins, small peptides, or molecules. There are two types of protease inhibitors: reversible and irreversible. Reversible protease inhibitors form non-covalent interactions with the protease limiting its functionality. They can be competitive inhibitors, uncompetitive inhibitors, and noncompetitive inhibitors. Competitive inhibitors compete with the peptide to bind to the protease active site. Uncompetitive inhibitors bind to the protease while the peptide is bound but do not let the protease cleave the peptide bond. Noncompetitive inhibitors can do both. Irreversible protease inhibitors covalently modify the active site of the protease so it cannot cleave peptides.
Sources: en.wikipedia.org
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.
REV-ERB receptors generally repress transcription when bound by natural heme. SR9009 is described as an agonist that enhances this repressive activity. The result is altered expression of clock and metabolic genes.
Published controlled human trials are lacking. Some sources cite limited or unofficial reports, but these do not establish safety or efficacy. Claims about human performance effects remain unverified.
Legality depends on the country and the intended use. In many places it is sold as a research chemical, but sports and medicine regulations restrict it.