The short version of REV-ERB fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2026-04-05. Anything still debated is marked as such rather than presented as settled.
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.
Handling recommendations for SR9009 in a laboratory setting include storing the solid at low temperature, protected from light and moisture. The compound is often dissolved in dimethyl sulfoxide or ethanol for experiments. Solutions should be prepared with appropriate personal protective equipment and disposed of according to local rules. Stability data for long-term storage are limited, so stock solutions are typically kept cold and used within defined periods. Records of preparation date and concentration support reproducibility.
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.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not an approved medicine and has no established human therapeutic use. The compound appears in scientific literature as a tool for probing circadian and metabolic regulation. Online sellers often label it as a research chemical, sometimes using the nickname Stenabolic. Its chemical identity is distinct from selective androgen receptor modulators, stimulants, and peroxisome proliferator-activated receptor delta agonists. Researchers use it mainly in cell and animal experiments.
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.
| Property | Value | Notes |
|---|---|---|
| Regulatory status | Not approved as a medicine in major jurisdictions | Sold as a research chemical; legal status varies |
| Anti-doping status | Prohibited by the World Anti-Doping Agency | Listed under non-approved substances or related category |
| Typical analytical method | LC-MS/MS | Used for detection and confirmation in biological samples |
| Storage temperature | −20 °C or lower for solid | Desiccated and protected from light |
| Common solution solvents | DMSO; ethanol | Aqueous solubility is limited |
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.
For long-term storage, SR9009 is typically kept as a solid at low temperature, protected from moisture and light. Desiccated conditions limit hydrolysis, while opaque containers reduce photochemical breakdown. Solutions are less stable than solids and are often stored frozen in aliquots to avoid repeated freeze-thaw cycles. Stability data are not standardized across all suppliers, so users should rely on certificate-of-analysis information when available. Degradation may appear as color change, precipitate, or decreased chromatographic purity.
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.
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.
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.
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.
==== Personality profiles ==== Cooper, Noakes, Dunne, Lambert, and Rochford identified that AAS-using individuals are more likely to score higher on borderline (4.7 times), antisocial (3.8 times), paranoid (3.4 times), schizotypal (3.1 times), histrionic (2.9 times), passive-aggressive (2.4 times), and narcissistic (1.6 times) personality profiles than non-users. Other studies have suggested that antisocial personality disorder is slightly more likely among AAS users than among non-users (Pope & Katz, 1994). Bipolar dysfunction, substance dependency, and conduct disorder have also been associated with AAS use.
For his seminal contributions to organic and to medicinal chemistry including the synthesis in solution of an enzyme (ribonuclease), his stimulation of peptide research in the Pharmaceutical Industry and for his leadership role in fostering interdisciplinary research in academia and in industry, which led to the discovery of several widely prescribed medications for human and animal health. Hirschmann received the Arthur C. Cope Award for achievement in the field of organic chemistry research from the American Chemical Society in 1999 and the American Institute of Chemists Gold Medal in 2003. The Ralph F. Hirschmann Award in Peptide Chemistry is given out "to recognize and encourage outstanding achievements in the chemistry, biochemistry, and biophysics of peptides." The award was established in 1988 by Merck Research Laboratories.
== Cause == Opioid use disorder can develop for many reasons, including systemic failures such as pervasive marketing strategies, over-prescribing, and self-medication. Scoring systems have been derived to assess the likelihood of opiate addiction in chronic pain patients. Healthcare practitioners have long been aware that despite the effective use of opioids for managing pain, empirical evidence supporting long-term opioid use is minimal. Many studies of patients with chronic pain have failed to show any sustained improvement in their pain or ability to function with long-term opioid use. A 2024 literature review suggests that adverse childhood experiences (ACEs) are significantly associated with opioid use disorder later in life. ACEs include witnessing violence, experiencing abuse and neglect, and growing up with a family member with a mental health or substance abuse problem.
Sources: en.wikipedia.org
== Pathophysiology == Episcleritis is caused by inflammation due to the activation of immune cells, including lymphocytes and macrophages. In most cases, the cause of episcleritis is never determined (idiopathic). An identifiable cause is discovered in about one third of cases. Several diseases are associated with episcleritis, including systemic vasculitis (polyarteritis nodosa, granulomatosis with polyangiitis, Behçet's disease), connective tissue diseases (rheumatoid arthritis, relapsing polychondritis, systemic lupus erythematosus), psoriatic arthritis, ankylosing spondylitis, Cogan syndrome, rosacea, gout, atopy, Crohn's disease, and ulcerative colitis. 59 percent of patients with relapsing polychondritis have either episcleritis or scleritis. Rarely, episcleritis may be caused by scleritis. Very rarely, episcleritis is associated with infections, including Lyme disease, tuberculosis, syphilis, and herpes zoster. The redness in the eye associated with episcleritis is due to engorgement of the large episcleral blood vessels, which run in a radial direction from the limbus. Typically, there is no uveitis, or thickening of the sclera.
==== Functional struts ==== The porous-framework material [Cu3(btc)2(H2O)3], also known as HKUST-1, contains large cavities having windows of diameter ~6 Å. The coordinated water molecules are easily removed, leaving open Cu(II) sites. Kaskel and co-workers showed that these Lewis acid sites could catalyze the cyanosilylation of benzaldehyde or acetone. The anhydrous version of HKUST-1 is an acid catalyst. Compared to Brønsted vs. Lewis acid-catalyzed pathways, the product selectivity are distinctive for three reactions: isomerization of α-pinene oxide, cyclization of citronellal, and rearrangement of α-bromoacetals, indicating that indeed [Cu3(btc)2] functions primarily as a Lewis acid catalyst. The product selectivity and yield of catalytic reactions (e.g. cyclopropanation) have also been shown to be impacted by defective sites, such as Cu(I) or incompletely deprotonated carboxylic acid moities of the linkers. MIL-101, a large-cavity MOF having the formula [Cr3F(H2O)2O(BDC)3], is a cyanosilylation catalyst. The coordinated water molecules in MIL-101 are easily removed to expose Cr(III) sites. As one might expect, given the greater Lewis acidity of Cr(III) vs. Cu(II), MIL-101 is much more active than HKUST-1 as a catalyst for the cyanosilylation of aldehydes. Additionally, the Kaskel group observed that the catalytic sites of MIL-101, in contrast to those of HKUST-1, are immune to unwanted reduction by benzaldehyde.
==== GABA precursor ==== Glutamate also serves as the precursor for the synthesis of the inhibitory gamma-aminobutyric acid (GABA) in GABA-ergic neurons. This reaction is catalyzed by glutamate decarboxylase (GAD). GABA-ergic neurons are identified (for research purposes) by revealing its activity (with the autoradiography and immunohistochemistry methods) which is most abundant in the cerebellum and pancreas. Stiff person syndrome is a neurologic disorder caused by anti-GAD antibodies, leading to a decrease in GABA synthesis and, therefore, impaired motor function such as muscle stiffness and spasm. Since the pancreas has abundant GAD, a direct immunological destruction occurs in the pancreas and the patients will have diabetes mellitus.
Sources: en.wikipedia.org
Its legal status depends on the country and intended use. It is not an approved medicine in major jurisdictions. In sport, it is prohibited by anti-doping rules.
Laboratories typically use LC-MS/MS to detect SR9009 and related compounds in urine or blood. The method is sensitive but depends on sample collection timing. Confirmatory analysis follows quality-control procedures.
Solid material is generally kept cold, dry, and protected from light. Solutions are often stored in sealed containers at low temperature. Stability beyond recommended periods is not well documented.
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.