SR9009 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 2025-09-08. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Stability depends on physical form, temperature, light exposure, and solvent. Solid SR9009 is generally stored cold and dry, with protection from light to limit degradation. Dimethyl sulfoxide stocks are common for laboratory work, but repeated freeze-thaw cycles can reduce compound integrity. Aqueous solutions may be less stable than organic stocks, and the ethyl ester in the structure can be susceptible to hydrolysis under certain conditions. Researchers typically validate storage conditions and recheck purity before quantitative experiments, especially when using archived material.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Common synonyms | SR9009; Stenabolic | Nickname is not a chemical name. |
| Typical analytical method | LC-MS/MS | Often with isotope-labeled internal standard. |
| Storage temperature | -20 °C | Desiccated and protected from light. |
| Solution stability | DMSO stock; avoid freeze-thaw | Store at -20 to -80 °C. |
| Regulatory status | Not approved; varies by country | May be restricted as research chemical. |
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.
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.
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.
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.
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.
Physicochemical behavior influences handling. SR9009 is described as a solid with limited aqueous solubility, so organic solvents such as dimethyl sulfoxide or ethanol are common in research stock solutions. Aqueous dilution can produce precipitates if the organic content is too low. Light, heat, and repeated freeze-thaw cycles may affect stability. Storage recommendations usually specify a desiccated freezer environment protected from light, but exact stability data depend on the formulation and matrix.
Detection in biological samples can be complicated by rapid metabolism and low circulating concentrations. Some studies report phase I and phase II metabolites, and analytical methods may need to target those species in addition to the parent compound. Immunoassays are not broadly available, so mass spectrometry remains the main confirmatory approach. For anti-doping testing, laboratories look for SR9009 and its metabolites using validated LC-MS methods. Open questions include how long metabolites remain detectable and how different routes of administration alter detection windows.
In laboratory settings, SR9009 is typically characterized by liquid chromatography–mass spectrometry (LC-MS) or high-performance liquid chromatography with ultraviolet detection (HPLC-UV). These methods can confirm identity and estimate purity, but they require reference standards for accurate quantification. Because SR9009 is not a licensed pharmaceutical, no harmonized pharmacopeial monograph exists. Laboratories often validate in-house methods for matrices such as plasma, urine, or cell culture media. Sample preparation may involve protein precipitation or liquid-liquid extraction before analysis.
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Clerodane acid A high-throughput library screen identified Clerodane acid, a natural product from Dodonaea viscosa, to be a selective activator of ERAP1 for small substrates and an inhibitor of peptide trimming. This compound was found active in blocking ERAP1-dependent antigen presentation (EC50 = 1μΜ) and to bind to the regulatory site of ERAP1 that normally accommodates C-termini of peptide substates. Clerodane acid was also found to induce strong immunopeptidome shifts in cancer cells.
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The American Medical Association (AMA) declared war on Christian Scientists; in 1895 its journal called Christian Science and similar ideas "molochs to infants, and pestilential perils to communities in spreading contagious diseases." Juries were nevertheless reluctant to convict when defendants believed they were helping the patient. There was also opposition to the AMA's effort to strengthen medical licensing laws. Historian Shawn Peters writes that, in the courts and public debate, Christian Scientists and Jehovah's Witnesses linked their healing claims to early Christianity to gain support from other Christians. Vaccination was another battleground. A Christian Scientist in Wisconsin won a case in 1897 that allowed his son to attend public school despite not being vaccinated against smallpox. Others were arrested in 1899 for avoiding vaccination during a smallpox epidemic in Georgia. In 1900 Eddy advised adherents to obey the law, "and then appeal to the gospel to save ...[themselves] from any bad results." In October 1902, after seven-year-old Esther Quimby, the daughter of Christian Scientists, died of diphtheria in White Plains, New York (she had received no medical care and had not been quarantined), the authorities pursued manslaughter charges. The controversy prompted Eddy to declare that "until public thought becomes better acquainted with Christian Science, the Christian Scientists shall decline to doctor infectious or contagious diseases", and from that time the church required Christian Scientists to report contagious diseases to health boards.
Sources: en.wikipedia.org
==== Other drugs ==== Acamprosate (Alcomed; Aotal; calcium acetylhomotaurinate; Campral; Campral EC; NS-11; Regtect; Sobriol; Zulex) – various actions – alcoholism Baclofen (Baclocur) – GABAB receptor agonist – alcoholism Calcium carbimide (Temposil) – aldehyde dehydrogenase 2 (ALDH2) inhibitor – alcoholism Cyanamide – aldehyde dehydrogenase 2 (ALDH2) inhibitor – alcoholism Disulfiram (Antabuse, Antabus) – aldehyde dehydrogenase 2 (ALDH2) inhibitor – alcoholism Flumazenil (flumazepil; Anexate) – GABAA receptor negative allosteric modulator/benzodiazepine antidote – benzodiazepine overdose Lofexidine (BA-168; BritLofex; Lucemyra; MDL-14042; MDL-14042A; RMI-14042A) – α2-adrenergic receptor agonist – opioid-related disorders Sodium oxybate (Alcover; SMO immediate release formulation) – GABAB and GHB receptor agonist – alcoholism
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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.
Solid material is usually kept at -20 °C, desiccated, and protected from light. Dimethyl sulfoxide stocks should be stored cold and subjected to minimal freeze-thaw cycles. Aqueous solutions are generally less stable and should be prepared fresh when possible.
Legality depends on the country and the intended use. It is not an approved medicine, and some places restrict or ban sales for human consumption. Buyers should verify local rules and product documentation before procurement.
No. It is an investigational compound without approved therapeutic indications. It is sold for research purposes only in many jurisdictions.