The short version of SR9009 fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2026-01-16. Anything still debated is marked as such rather than presented as settled.
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.
Detection of SR9009 in biological samples usually relies on liquid chromatography coupled to tandem mass spectrometry. This approach separates the compound from matrix components and identifies it by mass transitions. Because SR9009 can undergo metabolism, laboratories often look for both parent drug and specific metabolites. Sample preparation may involve protein precipitation or solid-phase extraction. Method validation examines sensitivity, carryover, and interference from related substances, and reference standards are required for accurate calibration.
Storage recommendations for SR9009 reference material typically specify a freezer at -20 °C or lower, with protection from moisture and light. Repeated freeze-thaw cycles can degrade small molecules and introduce variability. Stock solutions in dimethyl sulfoxide are often aliquoted to avoid repeated handling. Stability studies may examine degradation under heat, humidity, and light exposure. The compound's thiophene and nitro groups can participate in reactions that alter analytical signals over time, so such changes affect quantitative results.
| 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 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.
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.
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.
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.
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.
== Interactions == Products containing multivalent cations, such as aluminium- or magnesium-containing antacids, and products containing calcium, iron, or zinc invariably result in marked reduction of oral absorption of fluoroquinolones. Other drugs that interact with fluoroquinolones include sucralfate, probenecid, cimetidine, theophylline, warfarin, antiviral agents, phenytoin, cyclosporine, rifampin, pyrazinamide, and cycloserine. Administration of quinolone antibiotics to a benzodiazepine-dependent individual can precipitate acute benzodiazepine withdrawal symptoms due to quinolones displacing benzodiazepines from their binding sites. Fluoroquinolones have varying specificity for cytochrome P450, so may have interactions with drugs cleared by those enzymes; the order from most P450-inhibitory to least, is enoxacin > ciprofloxacin > norfloxacin > ofloxacin, levofloxacin, trovafloxacin, gatifloxacin, moxifloxacin.
=== Biofilm formation === The first step in the formation of biofilms is adhesion. The initial bacterial adhesion to surfaces involves the adhesin–receptor interactions. Certain polysaccharides, lipids and proteins in the matrix function as the adhesive agents. EPS also promotes cell–cell cohesion (including interspecies recognition) to facilitate microbial aggregation and biofilm formation. In general, the EPS-based matrix mediates biofilm assembly as follows. First, the EPS formation takes place at the site of adhesion, it will be either produced on bacterial surfaces or secreted on the surface of attachment, and form an initial polymeric matrix promoting microbial colonization and cell clustering. Next, continuous production of EPS further expands the matrix in 3 dimensions while forming a core of bacterial cells. The bacterial core provides a supporting framework, and facilitates the development of 3D clusters and aggregation of microcolonies. Studies on P. aeruginosa, B. subtilis, V. cholerae, and S. mutans suggested that the transition from initial cell clustering to microcolony appears to be conserved among different biofilm-forming model organisms. As an example, S. mutans produces an exoenzyme, called glucosyltransferase (Gtf), which synthesizes glucans in situ using host diet sugars as substrates. Gtfs even bind to the bacteria that do not synthesize Gtfs, and therefore, facilitate interspecies and interkingdom coadhesion.
A biological half-life or elimination half-life is the time it takes for a substance (drug, radioactive nuclide, or other) to lose one-half of its pharmacologic, physiologic, or radiological activity. In a medical context, the half-life may also describe the time that it takes for the concentration of a substance in blood plasma to reach one-half of its steady-state value (the "plasma half-life"). The relationship between the biological and plasma half-lives of a substance can be complex, due to factors including accumulation in tissues, active metabolites, and receptor interactions. While a radioactive isotope decays almost perfectly according to first order kinetics, where the rate constant is a fixed number, the elimination of a substance from a living organism usually follows more complex chemical kinetics. For example, the biological half-life of water in a human being is about 9 to 10 days, though this can be altered by behavior and other conditions. The biological half-life of caesium in human beings is between one and four months. The concept of a half-life has also been utilized for pesticides in plants, and certain authors maintain that pesticide risk and impact assessment models rely on and are sensitive to information describing dissipation from plants. In epidemiology, the concept of half-life can refer to the length of time for the number of incident cases in a disease outbreak to drop by half, particularly if the dynamics of the outbreak can be modeled exponentially.
Sources: en.wikipedia.org
== Reaction == In the catalytic cycle, the immediate one-electron oxidized product is monodehydroascorbate (MDHA). MDHA is either enzymatically reduced back to ascorbate by monodehydroascorbate reductase (MDAR) or two MDHA molecules disproportionate to ascorbate and dehydroascorbate (DHA).
It stated that "China does not challenge or seek to replace the United States and welcomes its prosperity and development", but also that any attempts to contain China would end in failure. It also added that rather than seeing the relationship as a zero-sum game, the US should cooperate with China to solve global problems. In Taiwan, international experts analyzed the Trump–Xi meeting and concluded that Trump maintained an ambiguous stance on Taiwan policy. However, the content of Trump's remarks revealed that while the US government uses Taiwan policy as part of its negotiating strategy, its existing "One China policy" remains unchanged.
. Salts of these species have been isolated in the cases of dibenzocyclooctatetraene, various tertiary amines, and some polymethylated derivatives of azulene. Radical cations, like radical anions, have one unpaired electron, i.e. they are paramagnetic.
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.
Liquid chromatography-tandem mass spectrometry is a common approach. It can detect the parent compound and its metabolites in biological matrices.