Everything below concerns REV-ERB agonist. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-07-17. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Laboratory studies often administer SR9009 by injection because oral absorption appears poor in rodents. Reported pharmacokinetic properties include rapid metabolism and low systemic exposure after oral dosing. Human pharmacokinetic data are sparse, so absorption, distribution, metabolism, and excretion in people are not well defined. Some research explores related REV-ERB compounds with improved drug-like properties. Regulatory approval for any REV-ERB agonist as a human medicine has not been granted to date.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic small molecule | Studied as a REV-ERB agonist |
| Molecular formula | C20H24ClN3O4S | Reported for the neutral compound |
| Appearance | Off-white to pale yellow solid | Typical research-grade material |
| Solubility | Sparingly soluble in water | Soluble in solvents such as DMSO |
| Common synonyms | SR9009; Stenabolic | Stenabolic is an informal alias |
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.
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.
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.
Smoking earlier in life and smoking cigarettes with higher tar content increases the risk of these diseases. Additionally, other forms of environmental tobacco smoke exposure, known as passive smoke and third-hand smoke, have manifested harmful health effects in people of all ages. Tobacco use is also a significant risk factor in miscarriages among pregnant women who smoke. It contributes to several other health problems for the fetus, such as premature birth and low birth weight, and increases the chance of sudden infant death syndrome (SIDS) by 1.4 to 3 times. The incidence of erectile dysfunction is approximately 85 percent higher in men who smoke compared to men who do not smoke. Many countries have taken measures to control tobacco consumption by restricting its usage and sales. They have printed warning messages on packaging. Moreover, smoking bans in public places like workplaces, theaters, bars, and restaurants have been enacted to reduce exposure to passive smoke. Tobacco taxation inflating the price of tobacco products, have also been imposed. In the late 1700s and the 1800s, the idea that tobacco use caused certain diseases, including mouth cancers, was initially accepted by the medical community. In the 1880s, automation dramatically reduced the cost of cigarettes, cigarette companies greatly increased their marketing, and use expanded. From the 1890s onwards, associations of tobacco use with cancers and vascular disease were regularly reported.
=== Significant dates === According to legend, the coffee plant was discovered in Ethiopia by a goat herder named Kaldi around 850 AD, who observed increased physical activity in his goats after they consumed coffee beans. First cultivation in India (Chikmagalur) – 1600 First cultivation in Europe – 1616 First cultivation in Java – 1699 First cultivation in Caribbean (Cuba, Hispaniola, Jamaica, Puerto Rico) – 1715–1730 First cultivation in Dutch East Indies – 1720 First cultivation in South America – 1730 Roasted beans first sold on retail market (Pittsburgh) – 1865 Various coffee extracts, and powdered instant coffee, developed in the late 19th century
On the first day of June, which would be known as "Black Friday", 521 B-29s escorted by 148 P-51s were dispatched in a daylight raid against Osaka. While en route to the city, the Mustangs flew through thick clouds, and 27 of the fighters were destroyed in collisions. Nevertheless, 458 heavy bombers and 27 P-51s reached the city, and the bombardment killed 3,960 Japanese and destroyed 3.15 square miles (8.2 km2) of buildings. On 5 June 473 B-29s struck Kobe by day and destroyed 4.35 square miles (11.3 km2) of buildings for the loss of 11 bombers. A force of 409 B-29s attacked Osaka again on 7 June; during this attack, 2.21 square miles (5.7 km2) of buildings were burnt out and the Americans did not suffer any losses. Osaka was bombed for the fourth time that month, on 15 June, when 444 B-29s destroyed 1.9 square miles (4.9 km2) of the city and another 0.59 square miles (1.5 km2) of nearby Amagasaki; 300,000 houses were destroyed in Osaka. This attack marked the end of the first phase of XXI Bomber Command's attack on Japan's cities. During May and June, the bombers had destroyed much of the country's six largest cities, killing between 112,000 and 126,762 people and rendering millions homeless. The widespread destruction and high number of casualties from these raids caused many Japanese to realize that their country's military was no longer able to defend the home islands. American losses were low compared to Japanese casualties; 136 B-29s were downed during the campaign. In Tokyo, Osaka, Nagoya, Yokohama, Kobe, and Kawasaki, "over 126,762 people were killed ...
Sources: en.wikipedia.org
=== Mechanism of toxicity in humans === After FIAU is converted to FIAU-TP, it is not only available to viral polymerase, in humans it can also be taken up into mitochondria and used by mitochondrial DNA polymerase γ (POLG). When FIAU is incorporated into mitochondrial DNA (mtDNA), it disrupts mtDNA replication, which leads to mtDNA depletion. With less mtDNA, cells can make fewer proteins for the electron transport chain, so oxidative phosphorylation fails. The consequences are lactic acidosis (shift to anaerobic metabolism) and microvascular steatosis (impaired fatty-acid oxidation), especially in the liver
=== Naming === In Mendeleev's nomenclature for unnamed and undiscovered elements, meitnerium would be called eka-iridium. In 1979, during the Transfermium Wars (but before the synthesis of meitnerium), IUPAC published recommendations per which the element was to be called unnilennium (symbol Une), a systematic element name as a placeholder, until the element is discovered (and the discovery then confirmed) and a permanent name is decided on. Though widely used in the chemical community on all levels, from chemistry classrooms to advanced textbooks, the recommendations were mostly ignored among scientists in the field, who either called it "element 109", with the symbol E109, (109) or even simply 109, or used the proposed name "meitnerium". The naming of meitnerium was discussed in the Transfermium Wars regarding the names of elements 104–109, but meitnerium was the only proposal and thus was never disputed. The name meitnerium (Mt) was suggested by the GSI team in September 1992 in honor of Austrian physicist Lise Meitner, a co-discoverer of protactinium (with Otto Hahn), and one of the discoverers of nuclear fission. In 1994 the name was recommended by IUPAC, and was officially adopted in 1997. It is thus the only element named solely after a non-mythical woman (curium is named for both Pierre and Marie Curie).
Lithium-ion batteries can be a safety hazard since they contain a flammable electrolyte and may become pressurized if they become damaged. A battery cell charged too quickly could cause a short circuit, leading to overheating, explosions, and fires. A Li-ion battery fire can be started due to
Sources: en.wikipedia.org
SR9009 is a synthetic research compound that activates the REV-ERBα and REV-ERBβ nuclear receptors. It is not an approved drug and has no established human therapeutic use. Most published biological data come from cell and rodent studies.
No. SR9009 is frequently mislabeled as a SARM in online discussions, but it does not target androgen receptors. Its known mechanism involves REV-ERB nuclear receptors and circadian-metabolic gene regulation.
Human clinical data are very limited. There is no approved human use, and safety and efficacy in people are not established. Most evidence comes from preclinical models, so effects observed in animals may not apply to humans.
It is usually detected by LC-MS or HPLC-UV against a reference standard. In biological matrices, metabolite targeting can improve detection. No universal immunoassay is widely available.