If you have been reading about REV-ERB agonist and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Last reviewed on 2025-08-11. Where a claim depends on a specific study, the study is described rather than over-claimed.
At the molecular level, SR9009 binds REV-ERBα and REV-ERBβ and alters their repressive activity on target genes. These nuclear receptors help regulate the circadian clock, lipid synthesis, glucose metabolism, and inflammatory pathways. By changing transcription, the compound can shift the timing or magnitude of downstream metabolic processes in model systems. It does not act through androgen receptors or adenosine receptors, which distinguishes it from several substances sold for athletic performance. Whether the same transcriptional changes occur in humans at tolerable exposures remains an open question because controlled human studies are lacking.
Preclinical reports describe effects on exercise endurance, mitochondrial content, and lipid profiles in rodents, but these findings come from specific experimental conditions. Many studies use high doses or delivery methods that may not translate directly to human use. SR9009 has been reported to have low oral bioavailability and a short half-life, which complicates interpretation of oral dosing studies. It is not established as safe or effective for any indication. Literature discussions often separate its pharmacological mechanism from unverified claims made in fitness and supplement markets.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C20H24ClN3O4S | Derived from published structure. |
| Molecular weight | 437.94 g/mol | Calculated value. |
| Appearance | White to off-white solid | Typical for purified research samples. |
| Solubility | DMSO, ethanol; low in water | Class: poorly water-soluble. |
| Typical storage | -20 °C, desiccated, protected from light | Limits degradation. |
SR9009 is not approved as a medicine by major regulatory agencies. It is commonly sold as a research chemical, a category that may fall outside customary drug approval and quality rules. In sports, the World Anti-Doping Agency lists SR9009 as a prohibited substance. Athletes who use it can face sanctions if it is detected in a sample. Legal status varies by country, and importation may be restricted. Enforcement practices differ across borders.
Detection of SR9009 in biological samples usually employs liquid chromatography coupled with tandem mass spectrometry. This method can identify the parent compound and sometimes metabolites in urine or blood. Because exposure can be low and clearance may be rapid, sample timing and limits of detection matter. Laboratories validate assays for sensitivity and specificity. Results are interpreted alongside chain-of-custody and quality-control records. Urine is the common matrix for anti-doping analysis, while blood may be used in research settings.
Handling recommendations for SR9009 in a laboratory setting include storing the solid at low temperature, protected from light and moisture. The compound is often dissolved in dimethyl sulfoxide or ethanol for experiments. Solutions should be prepared with appropriate personal protective equipment and disposed of according to local rules. Stability data for long-term storage are limited, so stock solutions are typically kept cold and used within defined periods. Records of preparation date and concentration support reproducibility.
Laboratory samples of SR9009 are typically handled as research chemicals rather than pharmaceuticals. Suppliers usually state that the material is for research use only and not for human or veterinary administration. Storage recommendations generally call for a freezer at approximately −20 °C, protection from light, and a desiccated environment. The solid is often described as a white to off-white powder. Solubility is commonly reported in organic solvents such as dimethyl sulfoxide and ethanol, with low solubility in water.
Analytical identification and purity assessment often use high-performance liquid chromatography with ultraviolet detection or mass spectrometry. Liquid chromatography–tandem mass spectrometry is used to detect and quantify SR9009 in biological matrices, including urine and blood, for anti-doping or pharmacokinetic studies. Nuclear magnetic resonance spectroscopy can confirm molecular structure. Stability depends on form and storage: the solid is generally more stable than solutions, and repeated freeze–thaw cycles may degrade samples. Purity is typically reported as a percentage from a certificate of analysis.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ, also called NR1D1 and NR1D2. These receptors help regulate circadian rhythms and metabolic gene programs. The compound was developed for laboratory research, not as an approved therapeutic. Its identity is distinct from steroid hormones and selective androgen receptor modulators. Scientific interest centers on how REV-ERB activation changes gene expression in cells and animal models.
At the molecular level, SR9009 binds the ligand-binding domain of REV-ERB and strengthens recruitment of corepressor proteins such as NCoR and HDAC3. This increases repression of target genes, including Bmal1 and other clock-controlled and metabolic genes. In rodent studies, such changes have been linked to altered lipid handling, glucose metabolism, and energy expenditure. The precise chain of events between receptor binding and whole-body effects remains an active area of research. Findings in animals do not automatically translate to humans.
==== Military music ==== The very first stage of Western adaptation in the Meiji period is associated with the military field. A little before the reopening of Japan, the first military academy based on Dutch model was founded in Nagasaki where, alongside the military training, military music was taught, since it was acknowledged to be an important component of the martial arts. The first military band, called kotekitai, consisted of woodwind instruments and drums, was organized there. Gradually, Western music became an integral part of the Japanese culture where the importance of Western music was undertaken as a part of a social project. The military bands played prominent role in the society. That included public concerts of Western music, which were held in a famous Rokumeikan Hall and Hibiya Open-Air stage in Tokyo, performing marches, patriotic music and European composers’ works (Richard Wagner, Charles Gounod, Peter Tchaikovsky). With the contribution of foreign and Japanese authors, the first military music score collections were completed and published. In the military field, the Japanese conducting school was formed, the founders of which were English, French and German cultural figures such as John William Fenton, Charles Leroux, and Franz Eckert. Under their leadership, the first Japanese military conductors were raised: Suketsune Nakamura and Yoshitoyo Yotsumoto.
b: black – The black mutation was discovered in 1910 by Thomas Hunt Morgan. The black mutation results in a darker colored body, wings, veins, and segments of the fruit fly's leg. This occurs due to the fly's inability to create beta-alanine, a beta amino acid. The phenotypic expression of this mutation varies based on the genotype of the individual; for example, whether the specimen is homozygotic or heterozygotic results in a darker or less dark appearance. This genetic mutation is x-linked recessive. bw: brown – The brown eye mutation results from inability to produce or synthesize pteridine (red) pigments, due to a point mutation on chromosome II. m: miniature – One of the first records of the miniature mutation of wings was also made by Thomas Hunt Morgan in 1911. He described the wings as having a similar shape as the wild-type phenotype. However, their miniature designation refers to the lengths of their wings, which do not stretch beyond their body and, thus, are notably shorter than the wild-type length. He also noted its inheritance is connected to the sex of the fly and could be paired with the inheritance of other sex-determined traits such as white eyes. The wings may also demonstrate other characteristics deviant from the wild-type wing, such as a duller and cloudier color. Miniature wings are 1.5 times shorter than wild-type but are believed to have the same number of cells. This is due to the lack of complete flattening by these cells, making the overall structure of the wing seem shorter in comparison.
=== Origin === Timing: Bokov and Steinberg (2009) "unwrapped" the 23S rRNA structure into several layers of contact. In their model, the PTC is the original element of 23S rRNA, to which structural features were later added. An opposing view from Caetano-Anollés and Sun (2014) is that the tRNA's acceptor arm and the aaRS's catalytic domain came earlier than the genetic code and the PTC. Ancestor:
Sources: en.wikipedia.org
== Selected publications == Kiessling, Laura L.; Pohl, Nicola L. (1996-02-01). "Strength in numbers: non-natural polyvalent carbohydrate derivatives". Chemistry & Biology. 3 (2): 71–77. doi:10.1016/S1074-5521(96)90280-X. ISSN 1074-5521. PMID 8807830. Ko, Kwang-Seuk; Jaipuri, Firoz A.; Pohl, Nicola L. (2005-09-28). "Fluorous-Based Carbohydrate Microarrays". Journal of the American Chemical Society. 127 (38): 13162–13163. Bibcode:2005JAChS.12713162K. doi:10.1021/ja054811k. ISSN 0002-7863. PMID 16173741. Wacker, Michael; Feldman, Mario F.; Callewaert, Nico; Kowarik, Michael; Clarke, Bradley R.; Pohl, Nicola L.; Hernandez, Marcela; Vines, Enrique D.; Valvano, Miguel A.; Whitfield, Chris; Aebi, Markus (2006-05-02). "Substrate specificity of bacterial oligosaccharyltransferase suggests a common transfer mechanism for the bacterial and eukaryotic systems". Proceedings of the National Academy of Sciences. 103 (18): 7088–7093. Bibcode:2006PNAS..103.7088W. doi:10.1073/pnas.0509207103. ISSN 0027-8424. PMC 1459022. PMID 16641107.
=== Daniel Van Deventer === Daniel Van Deventer (Alex Akpobome), nicknamed “DVD,” is a Pierpoint trader transferred from New York to London during plans to consolidate the two offices. A former protégé of Eric Tao, DVD’s rapid rise places him in direct competition with Eric, ultimately contributing to Eric’s demotion after the loss of Felim Bichan as a client. DVD assumes Eric’s responsibilities as CPS MD and begins a sexual relationship with Harper, encouraging her to consider relocating to New York as the London office faces closure. He later suspends Harper after secretly listening in on a call in which she helps Jesse Bloom unload positions at Pierpoint’s expense. DVD grows disillusioned with Pierpoint after being instructed by Adler to ignore Nicole Craig’s sexual assault of Venetia Berens, and sympathizes with Harper upon learning she was also assaulted by Nicole. He agrees to leave the firm with Harper, Eric, and Rishi, but is ultimately betrayed when Harper and Eric strike a deal with Adler to preserve a reduced London operation by branding DVD and Rishi as disloyal. DVD is fired along with much of the London office, discovering his dismissal only when his security badge stops working.
Some vented bottles, as well as bottles which use a collapsible liner collapses as the formula is drained, have been assessed favorably. They were reported to be comparable to a breastfeeding group in terms of milk intake, sucking patterns, and oxygenation. A 2012 study comparing two types of vented bottles with anti-vacuum features found no differences in infant growth between randomized groups. "Bottle A", a partial anti-vacuum design, was rated by parents as easier to assemble and clean. Infants fed using "Bottle A" were reported to engage in less "fussing", but no difference were found in "crying" or "colic" or in rates of ear infection. Health recommendations for the storage and handling of human milk typically focus on preventing the growth of dangerous bacteria, but some research is also being done on nutrition. Experimental studies have shown a degradation of retinol (Vitamin A) and α-Tocopherol (Vitamin E) content dependent upon the formation of bubbles in expressed breast milk and in formula. Seven models of bottles were studied, from six companies. Less degradation occurred when using a bottle feeding system designed to minimize the mixing of air with the bottle's contents.
Sources: en.wikipedia.org
SR9009 is a synthetic REV-ERB agonist used in laboratory research. It is not an approved drug, and its effects in humans are not well characterized. It is often sold as a research chemical under the name Stenabolic.
No. SR9009 targets the nuclear receptors REV-ERBα and REV-ERBβ, not the androgen receptor. This mechanism differs from selective androgen receptor modulators and from exercise mimetics that act on PPARδ.
Published evidence is mainly preclinical, using cell cultures and animal models. Controlled human trials are not well documented in the public literature. Claims about human performance or health effects therefore remain unsupported by robust clinical data.
It is a synthetic compound that acts as an agonist at REV-ERBα and REV-ERBβ. It is used mainly as a research chemical to study circadian and metabolic pathways. It is not approved for human therapeutic use.