Everything below concerns nuclear receptor. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-07-16. Numbers and descriptions here follow the published literature rather than marketing material.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. These receptors help regulate circadian rhythms, lipid metabolism, and inflammatory gene expression. In cell and animal experiments, SR9009 alters transcription of clock-controlled genes and metabolic pathways. The compound is not a hormone and does not resemble classical steroid structures. Its activity depends on binding to the ligand-binding domain of REV-ERB, where it can modify corepressor recruitment.
Research interest in SR9009 grew from studies of circadian biology and metabolic disease. Preclinical reports describe effects on exercise capacity, muscle metabolism, and blood lipid levels in rodents, but these findings come from controlled laboratory settings. The compound has low oral bioavailability in animals, which limits systemic exposure after swallowing. Investigators often use injected routes in experiments to achieve measurable plasma concentrations. Human clinical data are sparse, no approved therapeutic product exists, and whether animal effects translate to humans remains an open question.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Binds REV-ERBα and REV-ERBβ in preclinical models |
| Molecular formula | C20H24ClN3O4S | Reported for the parent compound |
| CAS Registry Number | 1379686-30-2 | Common identifier in chemical databases |
| Appearance | Off-white to pale yellow solid | Typical research chemical solid |
| Solubility | Soluble in DMSO and ethanol; low in water | Class: small organic molecule |
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.
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.
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.
Quality control for research materials includes identity confirmation by nuclear magnetic resonance and purity assessment by high-performance liquid chromatography. Mass spectrometry provides molecular weight confirmation and can detect related impurities. Purchasers should request a certificate of analysis that lists lot-specific data. Online products advertised for human use often lack such documentation. Distinguishing legitimate research material from mislabeled or contaminated samples is a recurring challenge in independent testing, and independent laboratories may use orthogonal methods to verify identity.
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.
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.
Mixed connective tissue disease (MCTD) is a systemic autoimmune disease that shares characteristics with at least two other systemic autoimmune diseases, including systemic sclerosis (Ssc), systemic lupus erythematosus (SLE), polymyositis/dermatomyositis (PM/DM), and rheumatoid arthritis. The idea behind the "mixed" disease is that this specific autoantibody is also present in other autoimmune diseases such as systemic lupus erythematosus, polymyositis, scleroderma, etc. MCTD was characterized as an individual disease in 1972 by Sharp et al., and the term was introduced by Leroy in 1980. Some experts consider MCTD to be the same as undifferentiated connective tissue disease, but other experts specifically reject this idea because undifferentiated connective tissue disease is not necessarily associated with serum antibodies directed against the U1-RNP. Furthermore, MCTD is associated with a more clearly defined set of signs and symptoms.
structural formula A graphical representation of the molecular structure and geometry of a particular chemical compound, showing how the atoms are arranged in real, three-dimensional space. Chemical bonding within the molecule is also shown, either implicitly or explicitly. When known with certainty, structural formulas are very useful because they allow chemists to visualize the molecules and the structural changes that occur in them during chemical reactions.
=== Relation of PIDD1 to centrosomes === Recent investigations reveal that CASP2 activation, which is dependent on PIDD1, does not lead to cell death or activate p53 in reaction to DNA damage (such as that induced by doxorubicin) or during prolonged mitotic arrest (as observed with taxol treatment). In contrast, the p53 activation linked to centrosome amplification—a process that can occur following failed cytokinesis—undoubtedly depends on the Caspase-2−PIDDosome complex. Notably, PIDD1 appears to be integral in assessing the quantity of mature mother centrioles, utilizing a mechanism that has yet to be fully clarified. Furthermore, PIDD1 is situated at the distal ends of mature centrosomes within normal cells, suggesting its potential role in regulating centrosomal functions. The assembly of the Caspase-2−PIDDosome can be triggered by the presence of multiple mature centrioles with appendages. This activation leads to CASP2-mediated cleavage of MDM2, resulting in the accumulation of p53 and subsequent cell cycle arrest mediated by p21. Notably, these processes occur without causing significant cell death. Similarly, the depletion of centrosomes undermines the effectiveness of this pathway during instances of cytokinesis failure. In contrast, overexpressing polo-like kinase 4 (PLK4), which promotes the formation of additional centrosomes, is sufficient to activate the pathway even when cytokinesis is not compromised.
VUV absorbance spectra also exhibit feature similarity within compound classes, meaning VUV detectors can rapidly compound class characterization in complex samples through compound spectral shape and retention index information. Advances in technology reduces the typical group analysis data processing time from 15 to 30 minutes to <1 minute per sample.
Sources: en.wikipedia.org
Because nickel is resistant to corrosion, it was occasionally used as a substitute for decorative silver. Nickel was also occasionally used in some countries after 1859 as a cheap coinage metal (see above), but in the later years of the 20th century, it was replaced by cheaper stainless steel (i.e., iron) alloys, except in the United States and Canada. Nickel is an excellent alloying agent for certain precious metals and is used in the fire assay as a collector of platinum group elements (PGE). As such, nickel can fully collect all six PGEs from ores, and can partially collect gold. High-throughput nickel mines may also do PGE recovery (mainly platinum and palladium); examples are Norilsk, Russia and the Sudbury Basin, Canada. Nickel foam or nickel mesh is used in gas diffusion electrodes for alkaline fuel cells. Nickel and its alloys are often used as catalysts for hydrogenation reactions. Raney nickel, a finely divided nickel-aluminium alloy, is one common form, though related catalysts are also used, including Raney-type catalysts. Nickel is naturally magnetostrictive: in the presence of a magnetic field, the material undergoes a small change in length. The magnetostriction of nickel is on the order of 50 ppm and is negative, indicating that it contracts. Nickel is used as a binder in the cemented tungsten carbide or hardmetal industry and used in proportions of 6% to 12% by weight. Nickel makes the tungsten carbide magnetic and adds corrosion-resistance to the cemented parts, though the hardness is less than those with cobalt binder.
== Nonrennet coagulation == Many soft cheeses are produced without use of rennet, by coagulating milk with acid, such as citric acid or vinegar, or the lactic acid produced by soured milk. Cream cheese, paneer, rubing, and other acid-set cheeses are traditionally made this way. The acidification can also come from bacterial fermentation such as in cultured milk. Vegan alternatives to cheese are manufactured without using animal milk but instead use soy, wheat, rice or cashew. These can be coagulated with acid using sources such as vinegar or lemon juice.
D* → D + hν For example, A could be luminol and B could be hydrogen peroxide. D would be 3-aminophthalate (3-APA). In theory, one photon of light should be given off for each molecule of reactant. In practice, the yield ("quantum efficiency") is often low owing to side reactions. Chemiluminescence differs from fluorescence or phosphorescence in that the electronic excited state is the product of a chemical reaction rather than of the absorption of a photon. It is the antithesis of a photochemical reaction, in which light is used to drive an endothermic chemical reaction. Instead, here light is generated from a chemically exothermic reaction. The chemiluminescence might be also induced by an electrochemical stimulus and in that case, it is called electrochemiluminescence.
Sources: en.wikipedia.org
SR9009 is a synthetic small molecule studied as an agonist of the REV-ERB nuclear receptors. It is not an approved medicine, and its effects in humans are not well characterized.
No. It is a synthetic ligand that binds nuclear receptors, not a steroid or peptide hormone. Its activity depends on receptor binding rather than endocrine secretion.
Clinical evidence is limited. Most published data come from cell and animal experiments. Human safety and efficacy remain uncertain.
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.