This is a working overview of REV-ERB agonist, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-03-18 and is reviewed periodically as new material appears.
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.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Appearance | Off-white to pale yellow solid | Visual description varies with purity and source |
| Solubility | Soluble in DMSO and ethanol; poorly soluble in water | Organic stock solutions are common in research |
| Typical storage | -20 °C, desiccated, protected from light | Avoid repeated freeze-thaw cycles |
| Typical analytical method | LC-MS or HPLC-UV | Reference standards are needed for quantification |
| Molar mass | Approximately 437.9 g/mol | Calculated from the reported free-base formula |
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.
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.
SR9009 is often grouped with compounds studied for circadian and metabolic regulation rather than with classical anabolic steroids. Its interactions with nuclear receptors differ from those of androgen receptor ligands, and its proposed mechanisms involve transcriptional control rather than direct hormone signaling. Some sources classify it as a metabolic modulator because of observed effects on energy utilization. The distinction matters for regulation and for interpreting research results across different compound classes.
SR9009 is a synthetic small molecule developed as a REV-ERB agonist. It binds to REV-ERBα and REV-ERBβ, nuclear receptors that help regulate circadian rhythms and metabolic gene expression. In cell and animal studies, the compound alters lipid and glucose handling and influences skeletal muscle oxidative capacity. Its exact effects in humans remain largely uncharacterized because controlled clinical trials have not been reported. The molecule is frequently described in preclinical literature as a metabolic modulator.
Research interest in SR9009 grew from studies showing improved running endurance in mice after short treatment periods. Those experiments linked the compound to increased mitochondrial content and fatty acid oxidation in muscle, but the findings come from animal models and specific dosing schedules. Independent replication has been limited, and the pathways connecting REV-ERB activation to exercise performance are still being mapped. Whether similar responses occur in humans is an open question.
de Lorenzo, Victor; Schmidt, Markus (April 2016). "Synthetic bugs on the loose: containment options for deeply engineered (micro)organisms". Current Opinion in Biotechnology. 38: 90–96. doi:10.1016/j.copbio.2016.01.006. PMID 26874261.
But ΔF = Eq, where q is the total charge in the volume of the tube. The volume of the tube is equal to πr2L, so the number of charged particles in this volume is equal to nπr2L, and their total charge is q = nπr2 Lq*. Since the voltage V = EL, it follows then
=== Modulation techniques === Modulation techniques make use of the fact that technical noise usually decreases with increasing frequency (which is why it is often referred to as 1/f noise) and improve the signal to noise ratio by encoding and detecting the absorption signal at a high frequency, where the noise level is low. The most common modulation techniques are wavelength modulation spectroscopy (WMS) and frequency modulation spectroscopy (FMS). In WMS the wavelength of the light is continuously scanned across the absorption profile, and the signal is detected at a harmonic of the modulation frequency. In FMS, the light is modulated at a much higher frequency but with a lower modulation index. As a result, a pair of sidebands separated from the carrier by the modulation frequency appears, giving rise to a so-called FM-triplet. The signal at the modulation frequency is a sum of the beat signals of the carrier with each of the two sidebands. Since these two sidebands are fully out of phase with each other, the two beat signals cancel in the absence of absorbers. However, an alteration of any of the sidebands, either by absorption or dispersion, or a phase shift of the carrier, will give rise to an unbalance between the two beat signals, and therefore a net-signal. Although in theory baseline-free, both modulation techniques are usually limited by residual amplitude modulation (RAM), either from the laser or from multiple reflections in the optical system (etalon effects).
== Safety and regulatory actions == In March 2025, the FDA issued Dexcom a warning letter following inspections of facilities that manufactured G6 and G7 sensors. The agency said the devices were adulterated because manufacturing methods and controls did not conform to federal quality-system requirements. The letter cited inadequate process monitoring and validation, deficiencies in design controls and risk analysis—including risks associated with automated insulin delivery—and commercial distribution of sensors after major manufacturing changes without a required new premarket notification. In 2025, Dexcom recalled certain G6, G7, ONE, and ONE+ receivers because a speaker malfunction could prevent audible alerts for dangerously high or low glucose. The FDA classified the action as the most serious type of recall and reported at least 56 injuries and no deaths. Affected users were advised to check their receiver, request a replacement, and test its speaker whenever it was charged. In May 2026, Dexcom announced that G7 sensors from two lots which had been designated as scrap were stolen during disposal and sold by third parties. The company said one lot included sensors that were not properly sterilized, increasing the risk of skin infection, while the other had an elevated internal-testing failure rate and an increased risk of producing no readings. Dexcom advised users not to use sensors from the two lots and offered replacements; at the time of the announcement, no severe adverse events had been reported.
== Structure == Monomeric actin, or G-actin, has a globular structure consisting of two lobes separated by a deep cleft. The bottom of the cleft represents the "ATPase fold", a structure conserved among ATP and GTP-binding proteins that binds to a magnesium ion and a molecule of ATP. Binding of ATP or ADP is required to stabilize each actin monomer; without one of these molecules bound, actin quickly becomes denatured. The X-ray crystallography model of actin that was produced by Kabsch from the striated muscle tissue of rabbits is the most commonly used in structural studies as it was the first to be purified. The G-actin crystallized by Kabsch is approximately 67 x 40 x 37 Å in size, has a molecular mass of 41,785 Da and an estimated isoelectric point of 4.8. Its net charge at pH = 7 is -7.
Sources: en.wikipedia.org
Reduction of 4-nitrobenzoic acid Hoffman degradation of the monoamide derived from terephthalic acid. Food sources of PABA include liver, brewer's yeast (and unfiltered beer), kidney, molasses, mushrooms, and whole grains. Other food sources of PABA include spinach and oat seeds.
Isocitrate dehydrogenase 1 (NADP+), soluble is an enzyme that in humans is encoded by the IDH1 gene on chromosome 2. Isocitrate dehydrogenases catalyze the oxidative decarboxylation of isocitrate to 2-oxoglutarate. These enzymes belong to two distinct subclasses, one of which uses NAD+ as the electron acceptor and the other NADP+. Five isocitrate dehydrogenases have been reported: three NAD+-dependent isocitrate dehydrogenases, which localize to the mitochondrial matrix, and two NADP+-dependent isocitrate dehydrogenases, one of which is mitochondrial and the other predominantly cytosolic. Each NADP+-dependent isozyme is a homodimer. The protein encoded by this gene is the NADP+-dependent isocitrate dehydrogenase found in the cytoplasm and peroxisomes. It contains the PTS-1 peroxisomal targeting signal sequence. The presence of this enzyme in peroxisomes suggests roles in the regeneration of NADPH for intraperoxisomal reductions, such as the conversion of 2,4-dienoyl-CoAs to 3-enoyl-CoAs, as well as in peroxisomal reactions that consume 2-oxoglutarate, namely the alpha-hydroxylation of phytanic acid. The cytoplasmic enzyme serves a significant role in cytoplasmic NADPH production. Alternatively spliced transcript variants encoding the same protein have been found for this gene. [provided by RefSeq, Sep 2013]
== History == Invented by Arnold O. Beckman in 1940 , the spectrophotometer was created with the aid of his colleagues at his company National Technical Laboratories founded in 1935 which would become Beckman Instrument Company and ultimately Beckman Coulter. This would come as a solution to the previously created spectrophotometers which were unable to absorb the ultraviolet correctly. He would start with the invention of Model A where a glass prism was used to absorb the UV light. It would be found that this did not give satisfactory results, therefore in Model B, there was a shift from a glass to a quartz prism which allowed for better absorbance results. From there, Model C was born with an adjustment to the wavelength resolution which ended up having three units of it produced. The last and most popular model became Model D which is better recognized now as the DU spectrophotometer which contained the instrument case, hydrogen lamp with ultraviolet continuum, and a better monochromator. It was produced from 1941 to 1976 where the price for it in 1941 was US$723 (far-UV accessories were an option at additional cost). In the words of Nobel chemistry laureate Bruce Merrifield, it was "probably the most important instrument ever developed towards the advancement of bioscience." Once it became discontinued in 1976, Hewlett-Packard created the first commercially available diode-array spectrophotometer in 1979 known as the HP 8450A.
Despite widespread use of this type of program, further studies are needed to understand the impact of these programs on overall child health and how to better address faltering growth in a child and improve practices related to feeding children in lower to middle income countries. UNICEF has supported an initiative in Madagascar assisting parents to recognise the signs of severe malnutrition among their children.
The two substrates of this enzyme are L-arabinose and oxidised nicotinamide adenine dinucleotide (NAD+). Its products are L-arabino-1,4-lactone, reduced NADH, and a proton. This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-OH group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is L-arabinose:NAD+ 1-oxidoreductase. This enzyme participates in ascorbate and aldarate metabolism.
Sources: en.wikipedia.org
== Treatment == Treatment for neurofibrosarcoma is similar to that of other cancers. Surgery is an option; the removal of the tumor along with surrounding tissue may be vital for the patient's survival. For discrete, localized tumors, surgery is often followed by radiation therapy of the excised area to reduce the chance of recurrence. For patients who have neurofibrosarcomas in an extremity, if the tumor is vascularized (has its own blood supply) and has many nerves going through it and/or around it, amputation of the extremity may be necessary. Some surgeons argue that amputation should be the procedure of choice when possible, due to the increased chance of a better quality of life. Otherwise, surgeons may opt for a limb-saving treatment, by removing less of the surrounding tissue or part of the bone, which is replaced by a metal rod or grafts. Radiation will also be used in conjunction with surgery, especially if the limb was not amputated. Radiation is rarely used as a sole treatment. In some instances, the oncologist may choose chemotherapy drugs when treating a patient with neurofibrosarcoma, usually in conjunction with surgery. Patients taking chemotherapy must be prepared for the side effects that come with any other chemotherapy treatment, such as; hair loss, lethargy, weakness, etc.
Mitoquinone mesylate (MitoQ) is a synthetic analogue of coenzyme Q10 which has antioxidant effects. It was first developed in New Zealand in the late 1990s. It has significantly improved bioavailability and improved mitochondrial penetration compared to coenzyme Q10, and has shown potential in a number of medical indications, being widely sold as a dietary supplement. A 2014 review found insufficient evidence for the use of mitoquinone mesylate in Parkinson's disease and other movement disorders. A 2025 British study found that diabetes patients who took daily mitoquinone, a widely available antioxidant, as well as their standard treatment had healthier hearts after four months than those not given the supplement. Mitoquinone was able to reverse the early signs of diabetes-related heart failure over the course of the study.
Instant tea is a powdered mix in which water is added, in order to reconstitute it into a cup of tea. The earliest form of instant tea was developed in the United Kingdom in 1885. A patent was granted for a paste made of concentrated tea extract, sugar, and evaporated milk, which became tea when hot water was added. However, no notable developments were made until spray drying technology allowed for drying the tea concentrates at a temperature which did not damage the flavors of the product.
== Signs and symptoms == Most individuals with G6PD deficiency are asymptomatic. When it induces hemolysis, the effect is usually short-lived. Most people who develop symptoms are male, due to the X-linked pattern of inheritance, but female carriers can be affected due to unfavorable lyonization or skewed X-inactivation, where random inactivation of an X chromosome in certain cells creates a population of G6PD-deficient red blood cells coexisting with unaffected red blood cells. A female with one affected X chromosome will show the deficiency in approximately half of her red blood cells. However, in some cases, including double X-deficiency, the ratio can be much more than half, making the individual almost as sensitive as males. Red blood cell breakdown (also known as hemolysis) in G6PD deficiency can manifest in many ways, including the following:
RNA World website Link collection (structures, sequences, tools, journals) Nucleic Acid Database Images of DNA, RNA, and complexes. Anna Marie Pyle's Seminar: RNA Structure, Function, and Recognition Archived 2018-06-21 at the Wayback Machine
Sources: en.wikipedia.org
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.
The compound is generally handled as light-sensitive and stored cold and dry. Stability in solution depends on solvent, concentration, and storage time. Specific degradation rates are not fully standardized.
Limited water solubility affects formulation for cell and animal studies. Organic co-solvents are often used to dissolve it. Precipitation can confound assay results if not controlled.
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.