The short version of REV-ERB fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2025-10-11. Anything still debated is marked as such rather than presented as settled.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Appearance | White to off-white powder | Common supplier description |
| Solubility | Soluble in DMSO and ethanol | Low solubility in water |
| Typical storage | −20 °C, desiccated, dark | For research samples |
| Analytical method | LC-MS/MS | Used for detection and quantification |
| Regulatory status | Prohibited in sport | WADA metabolic modulator class |
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.
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 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.
== Diagnosis == Diagnosis of amyloidosis generally requires tissue biopsy. The biopsy is assessed for evidence of characteristic amyloid deposits. The tissue is treated with various stains. The most useful stain in the diagnosis of amyloid is Congo red, which, combined with polarized light, makes the amyloid proteins appear apple-green on microscopy. Also, thioflavin T stain may be used. A number of imaging techniques such as a Nuclear Medicine PYP scan, DPD scan or SAP scan are also in use. A sample of tissue can be biopsied or obtained directly from the affected internal organ, but the first-line site of biopsy is subcutaneous abdominal fat, known as a "fat pad biopsy", due to its ease of acquisition. An abdominal fat biopsy is not completely sensitive and may result in false negatives, which means a negative result does not exclude the diagnosis of amyloidosis. However, direct biopsy of the affected organ may still be unnecessary as other less invasive methods of biopsy can also be used, including rectal mucosa, salivary gland, lip, or bone marrow biopsy which can achieve a diagnosis in up to 85% of people. In the amyloid deposition of the joints, there will be a decreased signal in both T1 and T2 weighted MRI images. In amyloidoma, there will be low T1 signal with gadolinium injection and low T2 signal.
== Mechanism == The mechanism for MMP-3 is a variation on a larger theme seen in all matrix metalloproteinases. In the active site, a water molecule is coordinated to a glutamate residue (Glu202) and one of the zinc ions present in the catalytic domain. First, the coordinated water molecule performs a nucleophilic attack on the peptide substrate's scissile carbon while the glutamate simultaneously abstracts a proton from the water molecule. The abstracted proton is then removed from the glutamate by the nitrogen of the scissile amide. This forms a tetrahedral gem-diolate intermediate that is coordinated to the zinc atom. In order for the amide product to be released from the active site, the scissile amide must abstract a second proton from the coordinated water molecule. Alternatively, it has been shown for thermolysin (another metalloproteinase) that the amide product can be released in its neutral (R-NH2) form. The carboxylate product is released after a water molecule attacks the zinc ion and displaces the carboxylate product. The release of the carboxylate product is thought to be the rate-limiting step in the reaction. In addition to the water molecule directly involved in the mechanism, a second water molecule is suggested to be a part of the MMP-3 active site. This auxiliary water molecule is thought to stabilize the gem-diolate intermediate as well as the transition states by lowering the activation energy for their formation. This is demonstrated in the mechanism and reaction coordinate diagram below.
=== Early modern era === The Portuguese planted fruit trees and vegetables on Saint Helena, a stopping point for homebound voyages from Asia, and left their sick who had scurvy and other ailments to be taken home by the next ship if they recovered. These travel accounts did not prevent further maritime tragedies caused by scurvy, partly because of the lack of communication between travelers and those responsible for their health, and because fruits and vegetables could not be kept for long on ships. In the 1519-1521 circumnavigation, Magellan's crew suffered from scurvy: "above all other calamities this was the worst: in some men the gums grew over the teeth, both lowers and uppers, so that they could not eat in any way and thus they died of this sickness. Nineteen men died." In 1536, the French explorer Jacques Cartier, while exploring the St. Lawrence River, used the local St. Lawrence Iroquoians' knowledge to save his men dying of scurvy. He boiled the needles of the aneda tree (generally believed to have been eastern white cedar) to make a tea that was later shown to contain 50 mg of vitamin C per 100 grams. Such treatments were not available aboard ship, where the disease was most common. Later, possibly inspired by this incident, several European countries experimented with preparations of various conifers, such as spruce beer, as cures for scurvy. In 1579, the Spanish friar and physician Agustin Farfán published a book in which he recommended oranges and lemons for treating scurvy, a remedy that was already known in the Spanish navy.
Sources: en.wikipedia.org
As the tepid reaction to the German Anschluss with Austria had shown, the governments of France, the United Kingdom and Czechoslovakia were set on avoiding war at any cost. The French government did not wish to face Germany alone and took its lead from the British government, led by Prime Minister Neville Chamberlain. He contended that Sudeten German grievances were justified and believed that Hitler's intentions were limited. That made Britain and France advise Czechoslovakia to concede to the German demands. Beneš resisted, and on 20 May 1938, a partial mobilisation was under way in response to the possible German invasion. It is suggested that the mobilisation could have been launched on basis of Soviet misinformation about Germany being on verge of invasion, which aimed to trigger war in Western Europe. On 30 May, Hitler signed a secret directive for war against Czechoslovakia to begin no later than 1 October. In the meantime, the British government demanded for Beneš to request a mediator. Not wishing to sever his government's ties with Western Europe, Beneš reluctantly accepted. The British appointed Lord Runciman and instructed him to persuade Beneš to agree to a plan acceptable to the Sudeten Germans. On 2 September, Beneš submitted the Fourth Plan, which granted nearly all of the demands of the Karlsbader Programm. Intent on obstructing conciliation, however, the SdP held demonstrations that provoked the police in Ostrava on 7 September. The Sudeten Germans broke off negotiations on 13 September, and violence and disruption ensued.
DavePhos, the first reported dialkylbiaryl phosphine ligand, was initially used in Pd-catalyzed Suzuki-Miyaura cross-coupling reactions as well as Buchwald-Hartwig aminations. Complexes of this ligand also catalyze a wide array of reactions, including the arylation of ketones and esters, borylation of aryl chlorides, and the arylation of indoles. Many modified versions of DavePhos have been synthesized. t-BuDavePhos has been shown to be an even more reactive variant of DavePhos in the room temperature Suzuki-Miyaura coupling of aryl bromides and chlorides. The biphenyl equivalent (PhDavePhos) is also available.
Bauman Moscow State Technical University, founded in 1830, is located in the city center; the university educates 18,000 undergraduate and 1,000 postgraduate students in science and engineering, offering technical degrees.
== Function == GPX1 is ubiquitously expressed in many tissues, where it protects cells from oxidative stress. Within cells, it localizes to the cytoplasm and mitochondria. As a glutathione peroxidase, GPx1 functions in the detoxification of hydrogen peroxide, specifically by catalyzing the reduction of hydrogen peroxide to water. The glutathione peroxidase also catalyzes the reduction of other organic hydroperoxides, such as lipid peroxides, to the corresponding alcohols. GPx1 typically uses glutathione (GSH) as the reductant, but when glutathione synthetase (GSS) is, as in brain mitochondria, γ-glutamylcysteine can serve as the reductant instead. The protein encoded by this gene protects from CD95-induced apoptosis in cultured breast cancer cells and inhibits 5-lipoxygenase in blood cells, and its overexpression delays endothelial cell death and increases resistance to toxic challenges, especially oxidative stress. This protein is one of only a few proteins known in higher vertebrates to contain selenocysteine, which occurs at the active site of glutathione peroxidase and is coded by the nonsense (stop) codon TGA.
Sources: en.wikipedia.org
Severe aortic stenosis with or without symptoms Aortic regurgitation with NYHA functional class III-IV symptoms Mitral stenosis with NYHA functional class II-IV symptoms Mitral regurgitation with NYHA functional class III-IV symptoms Aortic and/or mitral valve disease resulting in severe pulmonary hypertension (pulmonary pressure greater than 75% of systemic pressures) Aortic and/or mitral valve disease with severe LV dysfunction (EF less than 0.40) Mechanical prosthetic valve requiring anticoagulation Marfan syndrome with or without aortic regurgitation
TCEP (tris(2-carboxyethyl)phosphine) is a reducing agent frequently used in biochemistry and molecular biology applications. It is often prepared and used as a hydrochloride salt (TCEP-HCl) with a molecular weight of 286.65 gram/mol. It is soluble in water and available as a stabilized solution at neutral pH and immobilized onto an agarose support to facilitate removal of the reducing agent.
Further, it is not clear how low-carbohydrate dieting affects cardiovascular health, although two reviews showed that carbohydrate restriction may improve lipid markers of cardiovascular disease risk. Carbohydrate-restricted diets are no more effective than a conventional healthy diet in preventing the onset of type 2 diabetes, but for people with type 2 diabetes, they are a viable option for losing weight or helping with glycemic control. There is limited evidence to support routine use of low-carbohydrate dieting in managing type 1 diabetes. The American Diabetes Association recommends that people with diabetes should adopt a generally healthy diet, rather than a diet focused on carbohydrate or other macronutrients. An extreme form of low-carbohydrate diet – the ketogenic diet – is established as a medical diet for treating epilepsy. Through celebrity endorsement during the early 21st century, it became a fad diet as a means of weight loss, but with risks of undesirable side effects, such as low energy levels and increased hunger, insomnia, nausea, and gastrointestinal discomfort. The British Dietetic Association named it one of the "top 5 worst celeb diets to avoid in 2018".
The standard enthalpy change can be determined by calorimetry or by using the Van 't Hoff equation, though the calorimetric method is preferable. When both the standard enthalpy change and stability constant have been determined, the standard entropy change is easily calculated from the equation above. The fact that stepwise formation constants of complexes of the type MLn decrease in magnitude as n increases may be partly explained in terms of the entropy factor. Take the case of the formation of octahedral complexes.
Binding of CNP to NPR-B catalyzes the synthesis of cGMP, which is responsible for mediating the anti-fibrotic effects of CNP. Fibrotic heart tissue is associated with an increase risk of ventricular dysfunction which can ultimately lead to heart failure. Thus, anti-fibrotic strategies are a promising approach in the prevention and treatment of heart failure.
Sources: en.wikipedia.org
Legality depends on the country and the intended use. In many places it is sold as a research chemical, but sports and medicine regulations restrict it.
Detection commonly uses liquid chromatography–tandem mass spectrometry. This method can identify the compound in urine or blood at low concentrations.
Typical guidance is −20 °C, dry, and protected from light. Solutions should be aliquoted and limited freeze–thaw cycles should be used.
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.