This is a working overview of circadian rhythm, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-05-03 and is reviewed periodically as new material appears.
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.
Research interest in SR9009 grew from studies showing improved running endurance in mice after short treatment periods. Those experiments linked the compound to increased mitochondrial content and fatty acid oxidation in muscle, but the findings come from animal models and specific dosing schedules. Independent replication has been limited, and the pathways connecting REV-ERB activation to exercise performance are still being mapped. Whether similar responses occur in humans is an open question.
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.
| 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 |
SR9009 is a synthetic small molecule developed as an agonist of the nuclear receptors REV-ERBα (NR1D1) and REV-ERBβ (NR1D2). These receptors help regulate circadian rhythms and metabolic gene expression. In cell and animal studies, SR9009 alters transcription of genes involved in lipid metabolism, inflammation, and mitochondrial function. It is not an approved medicine, and its pharmacological profile in humans remains largely uncharacterized. The compound is frequently discussed in the context of circadian biology and metabolic research rather than clinical use.
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.
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 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.
SR9009 stability depends on temperature, moisture, light, and solvent. Solid material is generally kept cool and dry, while solutions may require protection from repeated warming and cooling. Degradation can appear as color changes, precipitate, or new chromatographic peaks. Researchers should follow supplier instructions and their own stability data. Long-term storage conditions for human use have not been established because the compound lacks approved clinical formulation.
SR9009 is supplied as a solid research chemical, often in milligram quantities. Laboratories typically weigh it in a controlled environment because fine powders can disperse. Stock solutions are commonly prepared in dimethyl sulfoxide and stored in small aliquots to reduce freeze-thaw cycles. Personal protective equipment and chemical fume hoods are standard when handling unknown or potent compounds. These practices address laboratory safety rather than human use.
Identity and purity of SR9009 samples are usually checked with chromatographic and spectrometric methods. High-performance liquid chromatography can separate the compound from related impurities, while mass spectrometry provides molecular mass confirmation. Nuclear magnetic resonance spectroscopy may be used for structural verification in research settings. No single method proves biological activity, and certificates of analysis should be reviewed alongside raw data. Independent testing is often needed because online products vary widely.
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.
Metal tagged antibodies however are viable for up to two weeks without losing signal, adding more flexibility to experiments. The stained samples can also be cryopreserved, which may be particularly useful for clinical trials when samples are collected over a longer period of time. Costs of CyTOF are high, as the metal-tagged antibodies and antibody conjunction kits are expensive. A major downside of CyTOF is that acquisition flow rate is quite slow compared to flow cytometry, by almost an order of magnitude. Because heavy metals are common in laboratory reagents, avoiding contamination during sample preparation is very important.
corrects this dilution effect by multiplying the fraction of the susceptible population over the total population. It corrects the effective/transmissible interaction between an infectious person and the rest of the community when many of the interaction is immune in the middle to late stages of the disease spreading. Thus, when
11 January – A scrub fire breaks out in Kūaotunu in the Coromandel Peninsula, consuming 36 hectares (89 acres) by the following day. 12 January – Mayor of Hamilton Paula Southgate announces that she would not be running for a third term during the 2025 New Zealand local elections. 13 January: New Zealand and the United Arab Emirates sign a comprehensive economic partnership agreement, cutting tariffs on 98.5% of New Zealand exports to that country. 14 January – Deputy Police Commissioner Jevon McSkimming is suspended from duties due to a criminal investigation by the Independent Police Conduct Authority and the New Zealand Police. 16 January: Hundreds including Police Commissioner Richard Chambers attend the funeral of slain Nelson Police officer Senior Sergeant Lyn Fleming. Health New Zealand confirms a baby who died in November 2024 as the first death caused by whooping cough since a whooping cough epidemic was declared on 22 November 2024. 17 January – Minister of Māori Development Tama Potaka announces an overhaul of the Waitangi Tribunal's membership. 18 January: A pod of about 30 whales are stranded near Pākawau in Golden Bay / Mohua, prompting a response from local iwi, the Department of Conservation(DOC) and Project Jonah. A juvenile beaked whale is stranded and refloated at New Brighton, Christchurch. 19 January: Prime Minister Christopher Luxon implements a cabinet reshuffle, resulting in the replacement of Shane Reti as health minister by Simeon Brown, and the promotion of James Meager to the new position of Minister for the South Island.
=== Sabbatical leave (1913/1914) === In 1913/1914 Robertson took 12 months sabbatical leave from the University of California. He spent four months in Adelaide, during which time he delivered two lectures: "Some Factors in the Cell Growth of Tumors [sic]", to the Microscopical Society of South Australia on 22 July 1913, and "Some Economic Aspects of Scientific Research", to the Science Association of the Adelaide University on 6 August 1913. On 12 November 1913, he submitted a 17-page report, Report on the Scope and Administration of an Institute for Scientific Research in Australia (BR.13), to the South Australian branch of the British Science Guild. The Guild's Report, with Robertson's report appended to it, was immediately given to Patrick "Paddy" McMahon Glynn, the Member for Angas, and Minister for Foreign Affairs, for him to directly hand it on to the Prime Minister, Joseph Cook. According to George Currie and John Graham (GC.1, pp.8–9), there is no evidence that Robertson's (1913) report ever reached the Prime Minister (or any other Minister) at that time. Robertson then travelled widely throughout Europe. In March 1914 he met up with Ivan Pavlov in Russia, and Pavlov gave him a personal tour of his laboratories at the Institute of Experimental Medicine in Saint Petersburg.
Sources: en.wikipedia.org
People taking rituximab had improved pain, function, reduced disease activity, and reduced joint damage based on X-ray images. After 6 months, 21% more people had improvement in their symptoms using rituximab and methotrexate. Biological agents should generally be used only if methotrexate and other conventional agents are not effective after a trial of three months. They are associated with a higher rate of serious infections as compared to other DMARDs. Biological DMARD agents used to treat rheumatoid arthritis include: tumor necrosis factor alpha inhibitors (TNF inhibitors) such as infliximab; interleukin 1 blockers such as anakinra, monoclonal antibodies against B cells such as rituximab, interleukin 6 blockers such as tocilizumab, and T cell co-stimulation blockers such as abatacept. They are often used in combination with either methotrexate or leflunomide. Biologic monotherapy or tofacitinib with methotrexate may improve ACR50, RA remission rates and function. Abatacept should not be used at the same time as other biologics. In those who are well controlled (low disease activity) on TNF inhibitors, decreasing the dose does not appear to affect overall function. Discontinuation of TNF inhibitors (as opposed to gradually lowering the dose) by people with low disease activity may lead to increased disease activity and may affect remission, damage that is visible on an x-ray, and a person's function. People should be screened for latent tuberculosis before starting any TNF inhibitor therapy to avoid reactivation of tuberculosis.
First, 2-chloro-6-methoxy-3-nitropyridine and 2-aminopropane-1,3-diol undergo nucleophilic aromatic substitution (SNAr) to form a diol, which is then protected by 2,2-dimethoxypropane to form a ketal intermediate. The intermediate is reduced with hydrogen catalyzed by Pd/C to afford an amine, which then immediately goes through substitution with ethyl bromoacetate. The resulting compound is treated with NaH, and is then oxidized with MnO2 to form the pyrazinone ring. The ketal is deprotected with aqueous HCl to regenerate the diol, and is then treated with methanesulfonic anhydride and triethylamine to form the final ring of the tricyclic core. The resulting compound goes through substitution with tert-butyl piperidin-4-ylcarbamate, acidic deprotection of the amino group, and chiral preparative HPLC to give the enantio-pure penultimate amine intermediate. Finally, a reductive amination is performed, and the product is treated with HCl in diethyl ether to form gepotidacin as a hydrochloride. This route consists of 11 steps, with 8 steps aimed at the formation of the tricyclic core.
Baikiain is an organic compound with the molecular formula C6H9NO2. Chemically, it is classified as a tetrahydropyridine substituted with a carboxylic acid. Because it contains both this carboxylic acid and an adjacent amine group, it is also an alpha-amino acid. Baikiain is one of the two enantiomers of the chiral compound 4,5-didehydropipecolic acid.
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.
It is a synthetic REV-ERB agonist used mainly in preclinical research. It is not an approved medicine for human use.