SR9009 comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Updated 2025-11-06. 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.
Regulatory and sporting contexts treat SR9009 as a prohibited substance in many elite competitions. Its presence on banned lists reflects concerns about performance enhancement and unknown long-term safety. Analytical chemists have developed methods to detect the parent compound and its metabolites in urine and blood. Literature discussions distinguish between in vitro potency, animal pharmacology, and anecdotal human reports. The latter are difficult to verify because products sold online may lack purity or contain different compounds.
Stability depends on physical form, temperature, light exposure, and solvent. Solid SR9009 is generally stored cold and dry, with protection from light to limit degradation. Dimethyl sulfoxide stocks are common for laboratory work, but repeated freeze-thaw cycles can reduce compound integrity. Aqueous solutions may be less stable than organic stocks, and the ethyl ester in the structure can be susceptible to hydrolysis under certain conditions. Researchers typically validate storage conditions and recheck purity before quantitative experiments, especially when using archived material.
Regulatory treatment of SR9009 varies by country and region. It is not approved as a pharmaceutical, and several jurisdictions restrict its sale for human consumption. Some authorities classify it as a research chemical, a prescription-only substance, or a prohibited performance-enhancing agent in sport. Purchasers may encounter certificates of analysis, but these documents do not guarantee identity, purity, or legality. In research settings, institutional safety reviews and controlled procurement help ensure that materials are handled under appropriate oversight. The absence of harmonized rules means that legal status can change and requires verification.
Analytical identification of SR9009 typically relies on liquid chromatography coupled with tandem mass spectrometry. In biological samples, researchers first separate the compound from matrix components using protein precipitation, liquid-liquid extraction, or solid-phase extraction. High-performance liquid chromatography with ultraviolet detection and nuclear magnetic resonance spectroscopy can support structural confirmation of reference materials. Because SR9009 is a small, relatively lipophilic molecule, reverse-phase columns and acidic mobile phases are common. Laboratories often include isotope-labeled internal standards to improve quantification and to correct for ion suppression.
| 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 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.
REV-ERB proteins typically suppress gene expression by recruiting corepressor complexes to DNA response elements. SR9009 binds these receptors and strengthens that repressive action in cell-based assays. Studies in rodents have reported changes in lipid handling, mitochondrial function, and exercise capacity after treatment. Such findings are often cited as evidence for metabolic effects, but species differences and limited pharmacokinetic data make direct translation to humans uncertain. Researchers continue to examine which effects are robust and which depend on specific experimental conditions.
SR9009 is frequently discussed alongside other REV-ERB ligands, including synthetic agonists and natural heme-related molecules. Its selectivity for REV-ERB over related nuclear receptors has been measured in binding and reporter assays, though off-target activity at higher concentrations is possible. The compound is prohibited in sport by the World Anti-Doping Agency, and it is not approved for any medical use in major jurisdictions. Products sold online may be labeled as research chemicals, and their identity and purity are not guaranteed by regulatory review.
SR9009 is a synthetic small molecule that acts on the nuclear receptors REV-ERBα and REV-ERBβ. These receptors are part of the circadian clock machinery and normally repress transcription of certain target genes. In laboratory research, SR9009 is used as a chemical tool to study how REV-ERB activity influences metabolism, inflammation, and daily biological rhythms. The compound is not an approved medicine, and its effects in humans remain largely uncharacterized. It is often described as an investigational agent rather than a therapeutic product.
=== Controlling pore size === The microstructural wavelength (average pore + wall thickness) can be described as a function of the solidification velocity v (λ= Av−n) where A is dependent on solids loading. There are two ways then that the pore size can be controlled. The first is to change the solidification speed that then alters the microstructural wavelength, or the solids loading can be changed. In doing so, the ratio of pore size to wall size is changed. It is often more prudent to alter the solidification velocity seeing as a minimum solid loading is usually desired. Since microstructural size (λ) is inversely related to the velocity of the freezing front, faster speeds lead to finer structures, while slower speeds produce a coarse microstructure. Controlling the solidification velocity is, therefore, crucial to being able to control the microstructure.
=== Extraction thimbles === Extraction thimbles are rod-shape filter paper often used in soxhlet extractors or atomized extractors. It is ideal for very sensitive detection, the performance depends on the thickness of inner diameter. Also, it is usually used in areas of food control and environmental monitoring.
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Alcohol (ethanol/ethyl alcohol) – GABAA receptor positive allosteric modulator Alkyl nitrites (poppers) (e.g., amyl nitrite) – nitric oxide donors, vasodilators, muscle relaxants, inhalants Cannabinoids (e.g., THC, cannabis, synthetic cannabinoids) – cannabinoid CB1 receptor agonists Dissociative hallucinogens (e.g., ketamine, methoxetamine, phencyclidine (PCP)) – ionotropic glutamate NMDA receptor antagonists Entactogens (empathogens) (e.g., MDMA (ecstasy), mephedrone, 6-APB, borax combo) – serotonin–norepinephrine–dopamine releasing agents (SNDRAs), other actions γ-Hydroxybutyric acid (GHB; oxybate) and prodrugs (e.g., GBL, 1,4-BD) – GABAB and GHB receptor agonists Phosphodiesterase PDE5 inhibitors (e.g., sildenafil, tadalafil, vardenafil, avanafil) Psychostimulants (stimulants) (e.g., amphetamine, methamphetamine, cocaine, mephedrone (4-MMC), metaphedrone (3-MMC), MDPV) – norepinephrine–dopamine releasing agents (NDRAs) and/or norepinephrine–dopamine reuptake inhibitors (NDRIs) Serotonergic psychedelics (e.g., 2C-B, 5-MeO-DiPT, 5-MeO-MiPT) – serotonin 5-HT2A receptor agonists
Sources: en.wikipedia.org
Pillared graphene is a hybrid carbon structure, consisting of an oriented array of carbon nanotubes connected at each end to a sheet of graphene. It was first described theoretically by George Froudakis and colleagues at the University of Crete in Greece in 2008. Pillared graphene has not yet been synthesized in the laboratory, but it has been suggested that it may have useful electronic properties, or as a hydrogen storage material.
== Recent research == The Development of ELISA testing for specific diagnosis of PNP was released in 2009. The research focuses on the specific determination of autoantibodies involved in the mechanism of PNP. Specifically, antibodies against envoplakin and periplakin were being investigated. Further use of ELISA testing on these antibodies confirmed the presence of anti-envoplakin and anti-periplakin autoantibodies in patients with PNP. Further research in 2013 outlined the various types of assays that could be used to determine which antibodies were involved in PNP. Demonstration of certain antibodies in the serum was named as the basis for diagnosis of PNP. This piece labeled PNP as a "multiorgan disease characterized by antibodies against plakins, desmogleins and the α2-macroglobulin-like-1 (A2ML1) protein, in association with an underlying neoplasm". A study concluded in 2009, summarized in 2010, surrounded the surgical removal of the associated tumor as a means to treat PNP. While 7/22 of the subjects perished due to resulting infection from the body's inability to heal itself after surgery, the other 15 cases survived. This study outlined the importance of early detection and prompt treatment as of utmost important in the treatment of PNP. In 2011, a case study of a woman with ulcers on the back of her leg reported as being diagnosed with PNP. The underlying tumors are almost exclusively of B-cell lineage. However, T-cells and CD56+ Natural Killer cells have also been postulated to be associated effectors of paraneoplastic pemphigus.
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Sources: en.wikipedia.org
=== Cardiac rhythm disease management === Cardiac rhythm disease management (CRDM) is the oldest and largest of Medtronic's business units. Its work in heart rhythm therapies dates back to 1957 when Bakken developed the first wearable heart pacemaker to treat abnormally slow heart rates. Since then, it has expanded its expertise in electrical stimulation to treat other cardiac rhythm diseases. It has also made an effort to address overall disease management by adding diagnostic and monitoring capabilities to many of its devices. An independently-operating Dutch pacemaker manufacturer, Vitatron, acquired by Medtronic in 1986, is now a European subsidiary of the unit. Medtronic and Vitatron pacemakers are interrogated and programmed by Medtronic Carelink Model 2090 Programmer for Medtronic and Vitatron Devices; they use separate interfaces. In 2007, Medtronic recalled its Sprint Fidelis product, the flexible wires, or leads, which connect a defibrillator to the interior of the heart. The leads were found to be failing at an unacceptable rate, resulting in unnecessary shocks or no shocks when needed; either can be lethal. The scope of the problem continues to be a matter of research. Studies since the recall, disputed by Medtronic, suggest that the failure rate of already-implanted Sprint Fidelis leads is increasing exponentially. Medtronic's liability is limited by various court decisions.
== History == The earliest fully documented case of aortic dissection is attributed to Frank Nicholls in his autopsy report of King George II of Great Britain, who had been found dead on 25 October 1760; the report describes a dissection of the aortic arch and into the pericardium. The term "aortic dissection" was introduced by the French physician J. P. Maunoir in 1802, and René Laennec labeled the condition "dissecting aneurysm". London cardiologist Thomas Bevill Peacock contributed to the understanding of the condition by publishing two series of the cases described in the literature so far: 19 cases in an 1843 review, and 80 in 1863. The characteristic symptom of tearing pain in the chest was recognized in 1855 when a case was diagnosed in life. Surgery for aortic dissection was first introduced and developed by Michael E. DeBakey, Denton Cooley, and Oscar Creech, cardiac surgeons associated with the Baylor College of Medicine, Houston, Texas, in 1954. DeBakey developed aortic dissection himself at age 97 in 2005, and underwent surgery in 2006. Endovascular treatment of aortic dissection was developed in the 1990s.
Glycine amidinotransferase, mitochondrial is an enzyme that in humans is encoded by the GATM gene. This gene encodes a mitochondrial enzyme that belongs to the Amidinotransferase family. This enzyme is involved in creatine biosynthesis, whereby it catalyzes the transfer of a guanido group from L-arginine to glycine, resulting in guanidinoacetic acid, the immediate precursor of creatine. Mutations in this gene cause arginine:glycine amidinotransferase deficiency, an inborn error of creatine synthesis characterized by mental retardation, language impairment, and behavioral disorders.
In November 2016, Celtic Biotech Ltd received approval from the French National Agency for the Safety of Medicines and Health Products to commence Part 2 of the Phase 1 dose escalation safety study Crotoxin in Patients with Advanced Cancer using an Intravenous Route of Administration. In December 2016, Spotlight Innovation announced the formation of a Scientific Advisory Board. The board includes Professor Hengli Tang of Florida State University, Dr. Elliot Androphy of Indiana University School of Medicine and Professor Kevin Hodgetts of Brigham and Women's Hospital. In June 2017, Spotlight Innovation entered into a sponsored research agreement with Brigham and Women's Hospital in support of research conducted by Professor Kevin Hodgetts, Ph.D., intended to develop drugs for the treatment of spinal muscular atrophy. In August 2017, Spotlight Innovation announced that its subsidiary Caretta Therapeutics had developed its first commercially available over-the-counter analgesic product for the treatment of chronic pain but the product was never launched. In August 2017, Spotlight Innovation entered into a sponsored research agreement with Indiana University in support of research conducted by Dr. Elliot Androphy intended to develop drugs for the treatment of spinal muscular atrophy.
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.
The most common approach is liquid chromatography-tandem mass spectrometry, often after extraction from blood, urine, or tissue. Ultraviolet detection and nuclear magnetic resonance spectroscopy are used mainly for reference material characterization. Isotope-labeled internal standards improve accuracy.