The short version of REV-ERB agonist fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2026-04-02 and is reviewed periodically as new material appears.
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.
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.
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.
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.
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.
Scientific discussion of SR9009 often separates animal evidence from human anecdote. Rodent studies provide controlled data on endurance, metabolism, and gene expression, but they use specific strains, doses, and treatment durations. Human reports are mostly uncontrolled and cannot establish cause and effect. Open questions include oral bioavailability, tissue distribution, metabolic stability, and long-term effects. Review articles generally call for more rigorous pharmacokinetic and safety research before any clinical use could be considered.
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.
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.
Overall, automated synthesis has improved the efficiency for the parallel synthesis and combinatorial methods of polymers. These techniques aim to design new materials, in addition to studying the relationships of their structure and properties. However, while screening for polymers enables this investigation, it becomes increasingly demanding for researchers to create the libraries for these synthetic compositions. In addition, preparation requires a large number of repetitive reactions to be completed, leading to an immense burden of planning and labor. Using automated synthesis, this process can be refined, increasing the efficiency of the reaction and removing the impact of human error.
The engine had a physics system permitting new features, such as monsters hurling corpses at the player or dying characters realistically crumbling into pieces, instead of requiring pre-built animations. Although Troika had ignored first-person engines due to technical limitations, such as a low polygon count and limited texture memory, as the technology improved, it thought it could create a real-time action game without sacrificing the immersion and story of a role-playing game. Describing the choice of developing a game based on the existing White Wolf property over creating their own, Boyarsky said that although an original property lacked the constraints of an existing one, the downside was that it had not been tested and could be rejected by its potential audience; an existing property was proven. Troika tried to stay as close as possible to the White Wolf rules while reducing the number of abilities and disciplines to those relevant to Bloodlines gameplay.
In September 2015, the FDA issued a warning related to canagliflozin (Invokana) and canagliflozin/metformin (Invokamet) due to decreased bone mineral density and therefore increased risk of bone fractures. Using gliflozins in combination therapy with metformin can lower the risk of hypoglycemia compared to other type 2 diabetes treatments such as sulfonylureas and insulin. Increased risk of lower limb amputation is associated with canagliflozin, but further data is needed to confirm this risk associated with different gliflozins. A European Medicines Agency review concluded that there is a potential increased risk of lower limb amputation (mostly affecting the toes) in people taking canagliflozin, dapagliflozin and empagliflozin. In August 2018, the FDA issued a warning of an increased risk of Fournier gangrene in patients using SGLT2 inhibitors. The absolute risk is considered very low. In the FDA Adverse Event Reporting System an increase was reported in events of acute kidney injury associated with SGLT2 inhibitors, though data from clinical trials actually showed a reduction in such events with SGLT-2 treatment.
Sources: en.wikipedia.org
Liquid carbon dioxide forms only at pressures above 0.51795(10) MPa (5.11177(99) atm); the triple point of carbon dioxide is 216.592(3) K (−56.558(3) °C) at 0.51795(10) MPa (5.11177(99) atm) (see phase diagram). The critical point is 304.128(15) K (30.978(15) °C) at 7.3773(30) MPa (72.808(30) atm). Another form of solid carbon dioxide observed at high pressure is an amorphous glass-like solid. This form of glass, called carbonia, is produced by supercooling heated CO2 at extreme pressures (40–48 GPa, or about 400,000 atmospheres) in a diamond anvil. This discovery confirmed the theory that carbon dioxide could exist in a glass state similar to other members of its elemental family, like silicon dioxide (silica glass) and germanium dioxide. Unlike silica and germania glasses, however, carbonia glass is not stable at normal pressures and reverts to gas when pressure is released. At temperatures and pressures above the critical point, carbon dioxide behaves as a supercritical fluid known as supercritical carbon dioxide.
This craze died down amid warnings of kojic acid, reports of contamination in home-made cultures, and insufficient capabilities for industrial production. In addition, Chen Jin-Shu of National Chung Hsing University noted that kombucha was briefly home-made in Taiwan under the name hóngchá gū (Chinese: 紅茶菇; from Japanese kōcha kinoko) in the 1960s.
The reason is simple: no recognition, no normalisation. Just boycott, divestment and sanctions, until the apartheid state is defeated. I never debate with Israelis nor speak to their media. If they want to speak about Palestine – the address is the PLO. Galloway later said on his Twitter feed that he had been "misled", writing that "Christ Church never informed us that the debate would be with an Israeli. Simple." The organiser, Mahmood Naji, denied Galloway's allegations in an open letter, explaining: "At no point during my email exchange with Mr Galloway's secretary was Eylon's nationality ever brought up or mentioned ... nor do I expect to have to tell the speaker what his opponent's nationality is." Galloway's behaviour was criticised by Julian Huppert, the Liberal Democrat MP for Cambridge, and The Times. The Palestinian Boycott, Divestment and Sanctions (BDS) National Committee subsequently released a statement indicating that, while it does support a "boycott of Israel", the campaign rejects boycotting an individual "because she or he happens to be Israeli or because they express certain views." In a debate at The Oxford Union the following October, Galloway compared the support of debating Israeli Zionists with that of supporting South African apartheid. Referring indirectly to his encounter with Aslan-Levy, Galloway said that he had worked with Jewish anti-apartheid activists in South Africa, adding "So Jews don't have to be on the side of apartheid".
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.