A practical reference on HPLC-MS: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2026-02-27 and is reviewed periodically as new material appears.
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.
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.
| 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 |
Laboratory identification of SR9009 typically relies on chromatographic separation coupled to mass spectrometry, often with ultraviolet detection as a secondary check. Nuclear magnetic resonance spectroscopy can confirm molecular structure when a reference standard is available. Because many suppliers sell the compound as a research chemical, independent identity testing is important for experimental reproducibility. A single retention time is not sufficient proof of identity, especially when related compounds may be present. Purity assessments usually report a percentage based on area normalization.
SR9009 is generally described as poorly soluble in water and more soluble in organic solvents such as dimethyl sulfoxide and ethanol. Stock solutions are commonly prepared in an organic solvent before dilution into an aqueous buffer or vehicle. Precipitation can occur if the organic fraction is reduced too quickly or if the final concentration exceeds the compound's solubility limit. Sonication or gentle warming may aid dissolution in some protocols, but excessive heat can promote degradation. Container material and pH can also influence observed solubility.
SR9009 is not approved as a medicine by major regulatory agencies. It is commonly sold as a research chemical, a category that may fall outside customary drug approval and quality rules. In sports, the World Anti-Doping Agency lists SR9009 as a prohibited substance. Athletes who use it can face sanctions if it is detected in a sample. Legal status varies by country, and importation may be restricted. Enforcement practices differ across borders.
Detection of SR9009 in biological samples usually employs liquid chromatography coupled with tandem mass spectrometry. This method can identify the parent compound and sometimes metabolites in urine or blood. Because exposure can be low and clearance may be rapid, sample timing and limits of detection matter. Laboratories validate assays for sensitivity and specificity. Results are interpreted alongside chain-of-custody and quality-control records. Urine is the common matrix for anti-doping analysis, while blood may be used in research settings.
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.
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.
A CAMP test is used to differentiate between Streptococcus agalactiae and other species of beta-hemolytic Streptococcus. This biochemical test uses the fact that Streptococcus agalactiae excretes a CAMP substance, making it slightly more hemolytic, which can be observed on blood agar media.
It was in this context that the UGT and the PSOE broke up for the first time in their history. The rift began when the government stopped applying the electoral program that in economic and social matters the PSOE had agreed with UGT and instead implemented a harsh economic policy of adjustments, "flexibilized" the labor market and began the "industrial reconversion", in addition to delaying the introduction of the forty-hour workweek. The first public confrontation occurred in 1985, on the occasion of the Pension Bill, not agreed by the government with the UGT, that increased from 10 to 15 the years of contribution necessary to be entitled to receive a pension and extended from two to eight years the contribution period for the calculation of the pension. The secretary general of UGT Nicolás Redondo, a socialist deputy in Congress, voted against the law and Felipe González stopped attending the May 1 demonstration. The definitive rupture was staged before the television cameras on February 19, 1987, during the bitter debate between Nicolás Redondo and the then Minister of Economy and Finance Carlos Solchaga. A few months later Redondo left his seat in the Congress of Deputies, together with the also leader of UGT Antón Saracíbar. The rupture resulted in confrontation when the government presented its Youth Employment Plan which UGT and Comisiones Obreras rejected and which motivated the call for a general strike on December 14, 1988, under the slogan "Por el giro social" ("For the social turn"). The strike was a total success and the country was completely paralyzed.
Pancreatic elastase;Feces-Pancreatic elastase;Clinical Biochemistry Laboratory; Adenovirus DNA PCR;Adenovirus DNA PCR - Feces; Clinical Microbiology Laboratory; "Hemoglobin;F";Feces-Blood; Clinical biochemistry laboratory; "Calprotectin;F";"Fecal Calprotectin;massfr."; Clinical biochemistry laboratory; Worms, eggs and cysts (microscopy of formalin-ether concentrate);Worms, eggs and cysts (microscopy of formalin-ether concentrate); Clinical Microbiology Laboratory; Larviculture (Strongyloides, hookworms);Larviculture (Strongyloides, hookworms); Clinical Microbiology Laboratory; Clostridioides difficile;Clostridioides difficile DNA/RNA (PCR quicktest); Clinical Microbiology Laboratory; Tarmpato e parasites;PCR (Tarmprotozoer); Clinical Microbiology Laboratory; Diarrhea investigation;Diarrhea investigation; Clinical Microbiology Laboratory; Alternative list Gastrointestinal stool and parasite tests The following analyses (Normal Order Name; Designation in the laboratory; Laboratory) can be performed on fecal samples.
Sources: en.wikipedia.org
== Physical properties == The compound appears as a dense, very refractive, colorless liquid with a pungent odor, insoluble in cold water, and prone to hydrolysis. Its tendency to smoke in air is low when the compound is pure, while the smoke increases with the presence of chlorosulfuric acid impurities, which are more prone to hydrolysis.
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=== Pharmacodynamics === The mechanism of action of traneurocin is either unknown or undisclosed. However, it has been described as acting as a positive allosteric modulator of the AMPA receptor and has been found to increase brain-derived neurotrophic factor (BDNF) levels. It has also been found to act as a positive allosteric modulator of the GABAA receptor. The drug is described as having neuroprotective, neurogenesis-stimulating, and pro-cognitive or nootropic effects. It has also been reported to have antihypoxic and anxiolytic properties.
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 a synthetic compound that acts as an agonist at REV-ERBα and REV-ERBβ. It is used mainly as a research chemical to study circadian and metabolic pathways. It is not approved for human therapeutic use.