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Last reviewed on 2026-03-27. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
SR9009 binds REV-ERB receptors and alters their repressive activity on target genes. This action can change transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. In rodent studies, treated animals have shown changes in muscle oxidative capacity and exercise performance, though effects vary by dose, duration, and model. The precise molecular steps connecting receptor binding to whole-body outcomes are still an active area of investigation. Findings in animals do not automatically translate to humans.
Because REV-ERB receptors are core clock components, SR9009 has been examined for effects on daily rhythms as well as metabolism. Research has explored whether the compound can shift or reinforce circadian gene expression in tissues such as liver and muscle. Some studies report improved metabolic markers in obese or diabetic mice, while others show context-dependent responses. Questions remain about which effects are direct, which are secondary to timing, and how they might differ across species.
SR9009 is a synthetic small molecule studied as an agonist of REV-ERB nuclear receptors. REV-ERB alpha and REV-ERB beta help regulate circadian rhythms and metabolic gene expression. In laboratory research, SR9009 has been used to probe how these receptors affect skeletal muscle, liver, and adipose tissue. The compound was identified in academic drug-discovery work and is often described in scientific literature by its chemical name and research code. It is not an approved medicine, and human clinical data remain limited or absent.
| 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 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.
SR9009 is a synthetic small molecule that acts on the nuclear receptors REV-ERBα and REV-ERBβ. These receptors are part of the circadian clock machinery and normally repress transcription of certain target genes. In laboratory research, SR9009 is used as a chemical tool to study how REV-ERB activity influences metabolism, inflammation, and daily biological rhythms. The compound is not an approved medicine, and its effects in humans remain largely uncharacterized. It is often described as an investigational agent rather than a therapeutic product.
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.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. These receptors help regulate circadian rhythms, lipid metabolism, and inflammatory gene expression. In cell and animal experiments, SR9009 alters transcription of clock-controlled genes and metabolic pathways. The compound is not a hormone and does not resemble classical steroid structures. Its activity depends on binding to the ligand-binding domain of REV-ERB, where it can modify corepressor recruitment.
Research interest in SR9009 grew from studies of circadian biology and metabolic disease. Preclinical reports describe effects on exercise capacity, muscle metabolism, and blood lipid levels in rodents, but these findings come from controlled laboratory settings. The compound has low oral bioavailability in animals, which limits systemic exposure after swallowing. Investigators often use injected routes in experiments to achieve measurable plasma concentrations. Human clinical data are sparse, no approved therapeutic product exists, and whether animal effects translate to humans remains an open question.
Handling practices for SR9009 focus on minimizing degradation and contamination. The solid is generally stored desiccated at or below -20 °C, protected from light and moisture. Stock solutions are often prepared in dimethyl sulfoxide or ethanol, then aliquoted to avoid repeated freeze–thaw cycles. Aqueous solubility is low, so formulations for animal studies may require cosolvents or suspending agents. Personnel should follow institutional chemical safety procedures, because toxicological data for humans are incomplete.
Regulatory status varies by country and intended use. Major drug agencies have not granted marketing authorization for SR9009 as a medicine, and it is not listed as a controlled substance in many jurisdictions. It is often sold as a research chemical, a category that may fall outside pharmaceutical manufacturing rules. Buyers should verify local laws and supplier documentation, including certificates of analysis. The lack of standardized quality controls raises concerns about identity, purity, and actual content in products marketed online.
Federal Prime Minister Milan Panić became frustrated with Milošević's domineering behaviour during diplomatic talks in 1992 and told Milošević to "shut up" because Milošević's position was officially subordinate to his position. Milošević later forced Panić to resign. This situation changed after 1997 when Milošević's second and last legal term as Serbian President ended. He then had himself elected Federal President, thus entrenching the power that he already de facto held. After the Federal Republic was reconstituted as a State Union, the new Assembly of the State Union was created. It was unicameral and was made up of 126 deputies, of which 91 were from Serbia and 35 were from Montenegro. The Assembly convened in the building of the old Federal Assembly of Yugoslavia, which now houses the National Assembly of Serbia. A direct, nationwide election was planned for 2005, but was subsequently delayed to 2006 in Montenegro and 2007 in Serbia to coincide with local parliamentary elections. Since the State Union dissolved before either was held, direct parliamentary elections were never held and the deputies were instead elected indirectly by the parliament of their respective republic. In 2003, after the constitutional changes and creation of the State Union of Serbia and Montenegro, a new President of Serbia and Montenegro was elected. He was also president of the Council of Ministers of Serbia and Montenegro. Svetozar Marović was the first and last President of Serbia and Montenegro until its breakup in 2006.
==== Systemic lupus erythematosus ==== Systemic lupus erythematosus (SLE) is a chronic autoimmune disease. Studies have implicated a role for neutrophil death (NETosis) in SLE. Neutrophil ferroptosis is prevalent in patients with SLE and is induced by autoantibodies and interferon-alpha (IFN-α), which suppress GPX4 expression via the transcriptional repressor CREMα. Inhibition of ferroptosis was able to ameliorate SLE disease progression in the MRL/lpr mouse model of SLE.
== Further reading == Foreman, John C.; Johansen, Torben; Gibb, Alasdair J., eds. (2010). Textbook of Receptor Pharmacology. doi:10.1201/9781420052558. ISBN 978-0-429-14730-2. Brunton L (2011). Brunton LL, Chabner B, Knollmann BC (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics (12 ed.). New York: McGraw-Hill. ISBN 978-0-07-162442-8. Whalen K (2014). Lippincott Illustrated Reviews: Pharmacology.
=== Pharmacodynamics === Teicoplanin is a glycopeptide antibiotic that inhibits bacterial cell wall synthesis. It binds to the D-alanyl-D-alanine (D-Ala-D-Ala) terminus of the peptidoglycan precursor, preventing the transpeptidation reaction necessary for cell wall cross-linking. This binding also interferes with the polymerization of peptidoglycan, ultimately leading to cell death. In addition to its binding to the D-Ala-D-Ala terminus, teicoplanin may also interact with the lipid II substrate in the bacterial cell membrane through its hydrophobic tail. This interaction could facilitate the antibiotic's proximity to the nascent peptidoglycan, enhancing its inhibitory effect. However, this mechanism has not been fully confirmed.
Sources: en.wikipedia.org
This was Merck's first use of the designation and the reduction in regulatory risk was one of the reasons management was willing to put company resources into development. In 2013, the United States Adopted Name (USAN) name was changed from lambrolizumab to pembrolizumab. In that year clinical trial results in advanced melanoma were published in The New England Journal of Medicine. This was part of the large phase I NCT01295827 trial. In September 2014, the US Food and Drug Administration (FDA) approved pembrolizumab under the Fast Track Development Program. It is approved for use following treatment with ipilimumab, or after treatment with ipilimumab and a BRAF inhibitor in advanced melanoma patients who carry a BRAF mutation. As of 2015, the only PD-1/PD-L1 targeting drugs on the market are pembrolizumab and nivolumab. By April 2016, Merck applied for approval to market the drug in Japan and signed an agreement with Taiho Pharmaceutical to co-promote it there. In July 2015, pembrolizumab received marketing approval in the European Union. In October 2015, the US FDA approved pembrolizumab for the treatment of metastatic non-small cell lung cancer (NSCLC) in people whose tumors express PD-L1 and who have failed treatment with other chemotherapeutic agents. In July 2016, the US FDA accepted for priority review an application for recurrent or metastatic head and neck squamous cell carcinoma (HNSCC) after a platinum-based chemotherapy.
=== Toxicity of trivalent arsenicals === Enzymes and receptors that contain thiol or sulfhydryl functional groups are actively targeted by arsenite (III) metabolites. These sulfur-containing compounds are normally glutathione and the amino acid cysteine. Arsenite derivatives generally have higher binding affinity compared to the arsenate metabolites. These bindings restrict activity of certain metabolic pathways. For example, pyruvate dehydrogenase (PDH) is inhibited when monomethylarsonous acid (MMAIII) targets the thiol group of the lipoic acid cofactor. PDH is a precursor of acetyl-CoA, thus the inhibition of PDH eventually limits the production of ATP in electron transport chain, as well as the production of gluconeogenesis intermediates.
== Distribution and habitat == The distribution of algal species has been fairly well studied since the founding of phytogeography in the mid-19th century. Algae spread mainly by the dispersal of spores analogously to the dispersal of cryptogamic plants by spores. Spores can be found in a variety of environments: fresh and marine waters, air, soil, and in or on other organisms. Whether a spore is to grow into an adult organism depends on the species and the environmental conditions where the spore lands. The spores of freshwater algae are dispersed mainly by running water and wind, as well as by living carriers. However, not all bodies of water can carry all species of algae, as the chemical composition of certain water bodies limits the algae that can survive within them. Marine spores are often spread by ocean currents. Ocean water presents many vastly different habitats based on temperature and nutrient availability, resulting in phytogeographic zones, regions, and provinces. To some degree, the distribution of algae is subject to floristic discontinuities caused by geographical features, such as Antarctica, long distances of ocean or general land masses. It is, therefore, possible to identify species occurring by locality, such as "Pacific algae" or "North Sea algae". When they occur out of their localities, hypothesizing a transport mechanism is usually possible, such as the hulls of ships. For example, Ulva reticulata and U. fasciata travelled from the mainland to Hawaii in this manner.
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 acts on REV-ERB nuclear receptors. It is not approved for human use and is sold only as a research chemical. Its effects have been studied mainly in cells and rodents.