Everything below concerns certificate of analysis. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-05-26. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Regulatory treatment of SR9009 varies by country and region. It is not approved as a pharmaceutical, and several jurisdictions restrict its sale for human consumption. Some authorities classify it as a research chemical, a prescription-only substance, or a prohibited performance-enhancing agent in sport. Purchasers may encounter certificates of analysis, but these documents do not guarantee identity, purity, or legality. In research settings, institutional safety reviews and controlled procurement help ensure that materials are handled under appropriate oversight. The absence of harmonized rules means that legal status can change and requires verification.
Analytical identification of SR9009 typically relies on liquid chromatography coupled with tandem mass spectrometry. In biological samples, researchers first separate the compound from matrix components using protein precipitation, liquid-liquid extraction, or solid-phase extraction. High-performance liquid chromatography with ultraviolet detection and nuclear magnetic resonance spectroscopy can support structural confirmation of reference materials. Because SR9009 is a small, relatively lipophilic molecule, reverse-phase columns and acidic mobile phases are common. Laboratories often include isotope-labeled internal standards to improve quantification and to correct for ion suppression.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C20H24ClN3O4S | Reported for the free base |
| Molecular weight | 437.9 g/mol | Calculated from the formula |
| Primary target | REV-ERBα and REV-ERBβ | Nuclear receptors involved in circadian regulation |
| Solubility | Soluble in DMSO and ethanol | Poorly soluble in water |
| Typical storage | -20 °C, desiccated | Protect from light and moisture |
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.
Analytical methods for SR9009 typically rely on liquid chromatography coupled with tandem mass spectrometry. The technique can separate the parent compound from related substances and detect low concentrations in biological matrices. Urine and blood are common samples in anti-doping testing, while in vitro studies may use cell culture media. Rapid metabolism and low expected concentrations make method validation important for reliable identification. Exact metabolite patterns can vary by species and are not fully mapped.
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.
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.
REV-ERB proteins help regulate daily cycles in gene expression, including genes tied to lipid and glucose metabolism. SR9009 binds these receptors and alters their activity in cell and animal experiments. Consequences observed in rodents include changes in skeletal muscle oxidative capacity, blood lipid levels, and exercise performance. The precise chain from receptor occupancy to whole-body effects is still an active area of study. Human responses cannot be assumed from rodent data.
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.
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.
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.
== See also == Adatom Cryo-adsorption Dual-polarization interferometry Fluidized bed concentrator Hydrogen-bonded organic framework Kelvin probe force microscope Micromeritics Molecular sieve Polanyi adsorption Pressure swing adsorption Random sequential adsorption Segregation (materials science)
== State and local government == Several states have proposed and passed laws that regulate AI models and AI-generated content, including impersonations, chatbot disclosures, and synthetic political content.
=== Precision Medicine === The protease modulatory web represents opportunities to identify novel biomarkers for disease and targets for drug design. Proteolytic processed N-termini have been proposed as potential biomarkers as disease specific proteolysis has been well studied in pathologies such as inflammation and cancer. Contributions to degradomics have identified numerous characterized and novel protease substrates and continue to lead to speculation of previously unknown protease targets. More recently, proteolytic signatures of cell death have been found using N-terminomic techniques on chemotherapy patient plasma samples. Advancements in SRM and MRM clinical assays also allow for analyzing proteolytic signature biomarkers in patient samples and can be complemented by PSP quantification. Deciphering these networks will aid drug design in understanding which substrates perform useful roles versus harmful ones to determine which should be targeted by drugs.
=== Regulatory status === This medication first reached market in 1973. It is approved in 21 countries worldwide, which does not include its home country of Denmark. It was taken off the approved list in India in 2014, citing a lack of required information such as mandatory clinical trial results in its 1998 approval decision. It is approved in China.
Daphne Walker, singer (born 1930). 19 July – Lee Mummery, cricketer (Central Districts) (born 1935). 20 July – Jim Tomlin, artist, musician (Chants R&B), and art educator (Otago Polytechnic) (born 1940). 23 July – Kathryn Smits, Germanist (University of Auckland) (born 1935). 25 July – Ian Leggat, school teacher and university administrator, principal of Hagley High School (1971–1976) and Christchurch Boys' High School (1976–1988), University of Canterbury chancellor (1992–1998) (born 1929). 26 July Ian Carter, sociologist (University of Auckland) (born 1943). Keith Sorrenson, historian (University of Auckland), president of the Citizens' Association for Racial Equality (1971–1973), member of the Waitangi Tribunal (1986–2011) (born 1932). John Werry, child and adolescent psychiatrist (University of Auckland) (born 1931). 29 July – Sir Michael Hill, jeweller, businessman (Michael Hill Jeweller), and philanthropist (born 1938).
Sources: en.wikipedia.org
== See also == Hydrogen sensor Localized surface plasmon Multi-parametric surface plasmon resonance Nano-optics Plasmon Quartz crystal microbalance Spinplasmonics Spreeta Surface plasmon polariton Waves in plasmas
=== Initiation === RNA polymerase binding in bacteria involves the sigma factor recognizing the core promoter region containing the −35 and −10 elements (located before the beginning of sequence to be transcribed) and also, at some promoters, the α subunit C-terminal domain recognizing promoter upstream elements. There are multiple interchangeable sigma factors, each of which recognizes a distinct set of promoters. For example, in E. coli, σ70 is expressed under normal conditions and recognizes promoters for genes required under normal conditions ("housekeeping genes"), while σ32 recognizes promoters for genes required at high temperatures ("heat-shock genes"). In archaea and eukaryotes, the functions of the bacterial general transcription factor sigma are performed by multiple general transcription factors that work together. The RNA polymerase-promoter closed complex is usually referred to as the "transcription preinitiation complex." After binding to the DNA, the RNA polymerase switches from a closed complex to an open complex. This change involves the separation of the DNA strands to form an unwound section of DNA of approximately 13 bp, referred to as the "transcription bubble". Supercoiling plays an important part in polymerase activity because of the unwinding and rewinding of DNA. Because regions of DNA in front of RNAP are unwound, there are compensatory positive supercoils. Regions behind RNAP are rewound and negative supercoils are present.
=== Biomechanical, sensory, and physiological properties of the body-wide fascia network === Chaudhry, H.; Huang, C.V.; Schleip, R.; Ji, Z.; Bukiet, B.; Findley, T. (2007). "Viscoelastic behavior of human fasciae under extension in manual therapy". Journal of Bodywork and Movement Therapies. 11 (2): 159–167. doi:10.1016/j.jbmt.2006.08.012. Schleip, R.; Duerselen, L.; Vleeming, A.; Naylor, I.L.; Lehmann-Horn, F.; Zorn, A.; Jaeger, H.; Klingler, W. (2012). "Strain hardening of fascia: Static stretching of dense fibrous connective tissues can induce a temporary stiffness increase accompanied by enhanced matrix hydration". Journal of Bodywork and Movement Therapies. 16 (1): 94–100. doi:10.1016/j.jbmt.2011.09.003. PMID 22196433. Schleip, R.; Mechsner, F.; Zorn, A.; Klingler, W. (2014). "The bodywide fascial network as a sensory organ for haptic perception". Journal of Motor Behavior. 46 (3): 191–193. doi:10.1080/00222895.2014.880306. PMID 24628059. Schleip, R.; Zorn, A.; Klingler, W. (2014). "Clinical relevance of fascial tissue and dysfunctions". Current Pain and Headache Reports. 18 (8): 439. doi:10.1007/s11916-014-0439-y. PMID 24962403.
First, the inward current becomes primarily carried by sodium channels. Second, the delayed rectifier, a potassium channel current, increases to 3.5 times its initial strength. In order for the transition from a calcium-dependent action potential to a sodium-dependent action potential to proceed new channels must be added to the membrane. If Xenopus neurons are grown in an environment with RNA synthesis or protein synthesis inhibitors that transition is prevented. Even the electrical activity of the cell itself may play a role in channel expression. If action potentials in Xenopus myocytes are blocked, the typical increase in sodium and potassium current density is prevented or delayed. This maturation of electrical properties is seen across species. Xenopus sodium and potassium currents increase drastically after a neuron goes through its final phase of mitosis. The sodium current density of rat cortical neurons increases by 600% within the first two postnatal weeks.
=== Microfractures of the fetal membranes === Throughout gestation the fetal membranes undergo remodeling to allow for the increase in size of the uterus. The remodeling of the fetal membranes occurs at both the level of the cells and the extracellular matrix (ECM). Structural abnormalities such as areas of where collagen has degraded, known as microfractures, have been observed in the amniotic membrane layer. Microfractures are characterised by:
Sources: en.wikipedia.org
It is a synthetic REV-ERB agonist used mainly in preclinical research. It is not an approved medicine for human use.
It binds to REV-ERBα and REV-ERBβ, nuclear receptors involved in circadian and metabolic gene regulation. This can alter transcription of genes related to lipid and glucose metabolism in experimental models.
No controlled human trials have established that effect. Endurance findings come primarily from rodent studies, and human responses remain unknown.
The most common approach is liquid chromatography-tandem mass spectrometry, often after extraction from blood, urine, or tissue. Ultraviolet detection and nuclear magnetic resonance spectroscopy are used mainly for reference material characterization. Isotope-labeled internal standards improve accuracy.