LC-MS/MS raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
This page was last updated on 2026-08-01 and is reviewed periodically as new material appears.
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 studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not a steroid, peptide, or natural hormone. In scientific literature, it appears under the code SR9009 and in non-scientific contexts as Stenabolic. The compound was identified through chemical screening efforts aimed at targeting circadian clock components. Its status remains investigational, and no regulatory agency has approved it as a human medicine.
REV-ERB proteins help regulate daily cycles in gene expression, including genes tied to lipid and glucose metabolism. SR9009 binds these receptors and alters their activity in cell and animal experiments. Consequences observed in rodents include changes in skeletal muscle oxidative capacity, blood lipid levels, and exercise performance. The precise chain from receptor occupancy to whole-body effects is still an active area of study. Human responses cannot be assumed from rodent data.
Most published work on SR9009 consists of preclinical studies. It is widely sold as a research chemical, a category that does not imply safety, efficacy, or pharmaceutical-grade quality. Sports anti-doping organizations have listed SR9009 as a prohibited substance, and its presence in an athlete sample can lead to sanctions. Legal status differs by country; in several jurisdictions it is not approved for human consumption and may be treated as an unapproved new drug.
| 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 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.
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.
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.
Regulatory treatment of SR9009 varies by country and context. It is not approved as a therapeutic drug by agencies such as the United States Food and Drug Administration or the European Medicines Agency. Sports authorities list it as a prohibited substance; the World Anti-Doping Agency classifies it among hormone and metabolic modulators. Legal status for personal possession or sale differs across jurisdictions, and some countries may restrict it under analog or research chemical laws. Buyers who seek verified material often rely on independent laboratory testing because online product labels may not match contents.
== External links == Alberts, Bruce; Johnson, Alexander; Lewis, Julian, eds. (2002). "Fibroblasts and Their Transformations: The Connective-Tissue Cell Family". Molecular Biology of the Cell (4th ed.). New York: Garland Science. ISBN 978-0-8153-3218-3. Akita, Sadanori; Akino, Kozo; Imaizumi, Toshifumi; Hirano, Akiyoshi (2008). "Basic fibroblast growth factor accelerates and improves second-degree burn wound healing". Wound Repair and Regeneration. 16 (5): 635–41. doi:10.1111/j.1524-475X.2008.00414.x. PMID 19128258. S2CID 24954846. Phan, S. H. (2008). "Biology of Fibroblasts and Myofibroblasts". Proceedings of the American Thoracic Society. 5 (3): 334–7. doi:10.1513/pats.200708-146DR. PMC 2645244. PMID 18403329. Lapouge, Gaelle; Blanpain, Cédric (September 18, 2008). Silberstein, Leslie (ed.). "Medical applications of epidermal stem cells". Stembook. doi:10.3824/stembook.1.27.1. PMID 20614607.
=== Modes of action === The cytotoxic activity of docetaxel is exerted by promoting and stabilising microtubule assembly, while preventing physiological microtubule depolymerisation/disassembly in the absence of GTP. This leads to a significant decrease in free tubulin, needed for microtubule formation and results in inhibition of mitotic cell division between metaphase and anaphase, preventing further cancer cell progeny. Because microtubules do not disassemble in the presence of docetaxel, they accumulate inside the cell and cause initiation of apoptosis. Apoptosis is also encouraged by the blocking of apoptosis-blocking bcl-2 oncoprotein. Both in vitro and in vivo analysis show the anti-neoplastic activity of docetaxel to be effective against a wide range of known cancer cells, cooperate with other anti-neoplastic agents activity, and have greater cytotoxicity than paclitaxel, possibly due to its more rapid intracellular uptake. The main mode of therapeutic action of docetaxel is the suppression of microtubule dynamic assembly and disassembly, rather than microtubule bundling leading to apoptosis, or the blocking of bcl-2.
When glutamic acid is dissolved in water, the amino group (−NH2) may gain a proton (H+), and/or the carboxyl groups may lose protons, depending on the acidity of the medium. In sufficiently acidic environments, both carboxyl groups are protonated and the molecule becomes a cation with a single positive charge, HOOC−CH(NH+3)−(CH2)2−COOH. At pH values between about 2.5 and 4.1, the carboxylic acid closer to the amine generally loses a proton, and the acid becomes the neutral zwitterion −OOC−CH(NH+3)−(CH2)2−COOH. This is also the form of the compound in the crystalline solid state. The change in protonation state is gradual; the two forms are in equal concentrations at pH 2.10. At even higher pH, the other carboxylic acid group loses its proton and the acid exists almost entirely as the glutamate anion −OOC−CH(NH+3)−(CH2)2−COO−, with a single negative charge overall. The change in protonation state occurs at pH 4.07. This form with both carboxylates lacking protons is dominant in the physiological pH range (7.35–7.45). At even higher pH, the amino group loses the extra proton, and the prevalent species is the doubly-negative anion −OOC−CH(NH2)−(CH2)2−COO−. The change in protonation state occurs at pH 9.47.
Sources: en.wikipedia.org
An animal in a study that does not receive the treatment being tested. Comparing the health of control animals with the health of treated animals allows researchers to evaluate the effects of a treatment more accurately. (NCI) Control group
=== Germination === The first stage of growth is germination, a method which first becomes apparent as a seed's radicle emerges. This is the first stage of root growth and occurs within the first 48 hours under ideal growing conditions. The first photosynthetic structures, the cotyledons, develop from the hypocotyl, the first plant structure to emerge from the soil. These cotyledons act both as leaves and as a source of nutrients for the immature plant, providing the seedling nutrition for its first 7 to 10 days.
anomer Either of a pair of cyclic hemiacetal or hemiketal saccharides that are epimers of each other, differing at only one carbon stereocenter, specifically the carbon that bears the aldehyde or ketone functional group in the compound's acyclic, open-chain configuration, known as the anomeric carbon.
=== Caps-2-PIDDosome === Another important interaction is between Caspase-2 enzyme and PIDD1 to form Caps-2-PIDDosome. The formation of the Caspase–2–PIDDosome relies on the interaction with the adaptor protein RAIDD, which is characterized by the presence of a death domain (DD) and a caspase recruitment domain (CARD). RAIDD and PIDD-CC engage through their death domains (DD) to form a high molecular weight complex. Additionally, the N-terminal caspase recruitment domain (CARD) in RAIDD acts as a docking site for the zymogen of CASP2. This interaction is specifically associated with PIDD-CC, which is derived from the human PIDD1 transcript variant 1, since a small deletion in transcript variant 3 is likely sufficient to prevent RAIDD binding. The presence of PIDD-C in the nucleus is vital for the activation of NF-κB; however, PIDD-CC has also been detected in the nucleolus, an organelle that serves various functions, including ribosome biogenesis and DNA repair.
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 studied as an agonist of REV-ERB nuclear receptors. It is not an approved medicine and has mainly been examined in laboratory and animal research.