The short version of SR9009 fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2026-05-24. Anything still debated is marked as such rather than presented as settled.
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.
REV-ERB proteins typically suppress gene expression by recruiting corepressor complexes to DNA response elements. SR9009 binds these receptors and strengthens that repressive action in cell-based assays. Studies in rodents have reported changes in lipid handling, mitochondrial function, and exercise capacity after treatment. Such findings are often cited as evidence for metabolic effects, but species differences and limited pharmacokinetic data make direct translation to humans uncertain. Researchers continue to examine which effects are robust and which depend on specific experimental conditions.
SR9009 is frequently discussed alongside other REV-ERB ligands, including synthetic agonists and natural heme-related molecules. Its selectivity for REV-ERB over related nuclear receptors has been measured in binding and reporter assays, though off-target activity at higher concentrations is possible. The compound is prohibited in sport by the World Anti-Doping Agency, and it is not approved for any medical use in major jurisdictions. Products sold online may be labeled as research chemicals, and their identity and purity are not guaranteed by regulatory review.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Small-molecule ligand; not a hormone or peptide |
| Molecular formula | C20H24ClN3O4S | Reported for the free base |
| CAS Registry Number | 1379686-30-2 | Unique chemical identifier |
| Common synonyms | SR9009; stenabolic | Stenabolic is informal and not an official name |
| Reported targets | REV-ERBα and REV-ERBβ | Nuclear receptors linked to circadian and metabolic regulation |
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.
Analytical chemists detect SR9009 with liquid chromatography-tandem mass spectrometry, commonly abbreviated LC-MS/MS. Sample preparation may involve protein precipitation, liquid-liquid extraction, or solid-phase extraction before analysis. Laboratories can target the parent compound or its metabolites, depending on the matrix and the purpose of testing. Anti-doping methods require sensitive and specific assays because concentrations in biological samples can be low. Reference standards and validated methods are essential for reliable identification and quantification.
Regulatory agencies have not approved SR9009 for human therapeutic use. It is typically sold as a research chemical with labels stating that it is not for human consumption. The World Anti-Doping Agency prohibits the substance in sport, generally under the category of non-approved substances. Customs and national laws may restrict importation, sale, or possession. Product quality and legal status can vary by country and vendor, and therapeutic claims are not permitted in regulated advertising because the compound lacks approval.
Several misconceptions surround SR9009. It is often described as a SARM, a steroid, or an exercise pill, but its known target is the REV-ERB receptor family. Rodent studies have examined exercise capacity and metabolic markers, yet human outcomes remain unproven. Oral bioavailability appears low in animals, and human pharmacokinetics are not well characterized. Online products may contain impurities or different compounds, so identity and purity testing are important for research use.
Raleigh-Durham International Airport (IATA: RDU, ICAO: KRDU, FAA LID: RDU), the region's primary airport and the second largest in North Carolina, located northwest of downtown Raleigh via Interstate-40 between Raleigh and Durham, serves the city and greater Research Triangle metropolitan region, as well as much of eastern North Carolina. The airport offers service to nearly 75 domestic and international destinations and serves approximately 15 million passengers a year. RDU is served by 16 air carriers, flying to a multitude of nonstop destinations on 350+ flights daily. The airport also offers facilities for cargo and general aviation. The airport authority tripled the size of its Terminal 2 (formerly Terminal C) in January 2011. Private general aviation airports in Raleigh include Triple W Airport (ICAO: K5W5, FAA LID: 5W5).
== Factors in hemostasis and fibrinolysis == Stimulators of coagulation: All factors in the coagulation cascade. While the endothelium does produce some factor VIII, the majority of factor VIII is produced in the liver. Inhibitors of coagulation: Inactivate an enormous variety of proteinases α2-macroglobulin α1-antitrypsin Antithrombin III Protein S Protein C Fibrinolysis: Breakdown of fibrin clots Plasminogen Inhibitors of fibrinolysis α2-antiplasmin Complement components C1-9, complement component 3 (C3)
== Further reading == Spiegelhalter, David J.; Abrams, Keith R.; Myles, Jonathan P. (2004). "Randomised Controlled Trials". Bayesian Approaches to Clinical Trials and Health-Care Evaluation. Chichester: John Wiley & Sons. pp. 181–249. ISBN 0-471-49975-7. Chin, Jane Y. (1 August 2004). "The Clinical Side: Clinical trial endpoints". Pharmaceutical Representative. Archived from the original on 5 October 2011.
=== Signal transduction === GHRH binding to GHRHR results in increased GH production mainly by the cAMP-dependent pathway, but also by the phospholipase C pathway (IP3/DAG pathway), and other minor pathways. The cAMP-dependent pathway is initiated by the binding of GHRH to its receptor, causing receptor conformation that activates Gs alpha subunit of the closely associated G-Protein complex on the intracellular side. This results in stimulation of membrane-bound adenylyl cyclase and increased intracellular cyclic adenosine monophosphate (cAMP). cAMP binds to and activates the regulatory subunits of protein kinase A (PKA), allowing the free catalytic subunits to translocate to the nucleus and phosphorylate the transcription factor cAMP response element-binding protein (CREB). Phosphorylated CREB, together with its coactivators, p300 and CREB-binding protein (CBP) enhances the transcription of GH by binding to CREs cAMP-response elements in the promoter region of the GH gene. It also increases transcription of the GHRHR gene, providing positive feedback. In the phospholipase C pathway, GHRH stimulates phospholipase C (PLC) through the βγ-complex of heterotrimeric G-proteins. PLC activation produces both diacylglycerol (DAG) and inositol triphosphate (IP3), the latter leading to release of intracellular Ca2+ from the endoplasmic reticulum, increasing cytosolic Ca2+ concentration, resulting in vesicle fusion and release of secretory vesicles containing premade growth hormone.
Sources: en.wikipedia.org
==== Alzheimer's disease ==== A case-control study in a Japanese population showed that deficiency of ALDH2 activity influences the risk for late-onset Alzheimer's disease. The ALDH2 knockout mice display age-related memory deficits in various tasks, as well as endothelial dysfunction, brain atrophy, and other Alzheimer's disease-associated pathologies, including marked increases in lipid peroxidation products, amyloid-beta, p-tau and activated caspases. These behavioral and biochemical Alzheimer's disease-like deficits were efficiently ameliorated when these mice were treated with isotope-reinforced lipids (deuterated polyunsaturated fatty acids).
Vaccine production and storage has great potential in transgenic plants. Vaccines are expensive to produce, transport, and administer, so having a system that could produce them locally would allow greater access to poorer and developing areas. As well as purifying vaccines expressed in plants it is also possible to produce edible vaccines in plants. Edible vaccines stimulate the immune system when ingested to protect against certain diseases. Being stored in plants reduces the long-term cost as they can be disseminated without the need for cold storage, don't need to be purified, and have long term stability. Also being housed within plant cells provides some protection from the gut acids upon digestion. However the cost of developing, regulating, and containing transgenic plants is high, leading to most current plant-based vaccine development being applied to veterinary medicine, where the controls are not as strict. Genetically modified crops have been proposed as one of the ways to reduce farming-related CO2 emissions due to higher yield, reduced use of pesticides, reduced use of tractor fuel and no tillage. According to a 2021 study, in EU alone widespread adoption of GE crops would reduce greenhouse gas emissions by 33 million tons of CO2 equivalent or 7.5% of total farming-related emissions.
Although most species of psilocybin-containing mushrooms bruise blue when handled or damaged due to the oxidization of phenolic compounds, this reaction is not a definitive method of identification or determining a mushroom's potency.
Sources: en.wikipedia.org
== Distribution == Rotheca myricoides is native to mountains from Eritrea to South Africa. It is native to Angola, Botswana, Burundi, Caprivi Strip, Democratic Republic of the Congo, Djibouti, Eswatini, Eritrea, Ethiopia, Kenya, KwaZulu-Natal, Malawi, Mozambique, Namibia, Northern Provinces, Rwanda, Somalia, Sudan, Tanzania, Uganda, Zambia, and Zimbabwe. It was introduced to Trinidad-Tobago, Australia, and Brazil.
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== Clinical significance == Cavin-2/SDPR is shown to act as a metastasis suppressor by xenograft studies utilizing breast cancer cell lines. Cavin-2 may elicit its metastasis suppressor function by directly interacting with ERK and limiting its pro-survival role. Moreover, it is suggested that cavin-2 is silenced during breast cancer progression by promoter DNA methylation. Metastasis suppressor role of cavin-2 may go beyond breast cancer since tumor samples from bladder, colorectal, lung, pancreatic, and ovarian cancers as well as sarcomas also exhibited loss of cavin-2 expression.
Sources: en.wikipedia.org
SR9009 is a synthetic compound investigated as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is used in preclinical research on circadian rhythm and metabolism. It is not an approved drug.
No. It has no approved medical indication, and human safety and efficacy data are limited. It appears in research chemical markets and is banned by some sports authorities.
Natural ligands include heme and certain metabolites; SR9009 is a synthetic small molecule with higher potency and selectivity in some assays. Its effects depend on cell type and timing. It is not a naturally occurring compound.
SR9009 is a synthetic research compound that binds and modulates the nuclear receptors REV-ERBα and REV-ERBβ. It is used in laboratory studies of circadian biology and metabolism, not as an approved medicine. It is also known by the informal name Stenabolic.