REV-ERB agonist is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Updated 2026-06-15. 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, 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.
Laboratory studies often administer SR9009 by injection because oral absorption appears poor in rodents. Reported pharmacokinetic properties include rapid metabolism and low systemic exposure after oral dosing. Human pharmacokinetic data are sparse, so absorption, distribution, metabolism, and excretion in people are not well defined. Some research explores related REV-ERB compounds with improved drug-like properties. Regulatory approval for any REV-ERB agonist as a human medicine has not been granted to date.
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.
| 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 |
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.
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.
=== Laboratory uses === Urea in concentrations up to 10 M is a protein denaturant as it disrupts the noncovalent bonds in the proteins. This property can be exploited to increase the solubility of some proteins. A mixture of urea and choline chloride is used as a deep eutectic solvent (DES), a substance similar to ionic liquid. When used in a deep eutectic solvent, urea gradually denatures the proteins that are solubilized. Urea in concentrations up to 8 M can be used to make fixed brain tissue transparent to visible light while still preserving fluorescent signals from labeled cells. This allows for much deeper imaging of neuronal processes than previously obtainable using conventional one photon or two photon confocal microscopes.
In December 2017 the company announced that in the summer of 2018 Geoffrey Babidge, who had been nearing retirement age, would step down and Jayne Hrdlicka would take over as CEO; at that time she was CEO of a subsidiary of Qantas. She took over in July 2018. At that time the company was experiencing strong growth via sales in China and had ramped up spending to further increase Chinese sales and to expand the US market. Hrdlicka resigned as CEO in December 2019, after her husband was found to have a kidney tumour. On her departure Geoffrey Babidge returned, as interim CEO. In August 2020 David Bortolussi was appointed CEO and managing director.
=== Architecture === Cole, John Y. and Henry Hope Reed. The Library of Congress: The Art and Architecture of the Thomas Jefferson Building (1998) excerpt and text search Small, Herbert, and Henry Hope Reed. The Library of Congress: Its Architecture and Decoration (1983)
Sources: en.wikipedia.org
The Germans also made use of CH for their own passive radar system, known as Klein Heidelberg. This used CH's transmissions as their source, and a series of antennas along the Channel coast as the receiver. By comparing the time of arrival of the signals from a selected aircraft, its range and direction could be determined with some accuracy. Since the system sent out no signals of its own, the allies were not aware of it until they overran the stations in 1944. Most of the stations had only just been built when they were overrun.
=== Dentin graft === Dentin bone, made from extracted teeth, comprises more than 85% of tooth structure, the enamel consists of HA mineral and comprises 10% of tooth structure. Dentin is similar to bone in its chemical composition, by volume 70–75% is HA mineral and 20% organic matrix, mostly fibrous type I collagen. Dentin, like bone, may release growth and differentiating factors while being resorbed by osteoclasts. In order to make the dentin graft usable and bacteria-free, some companies have developed clinical procedures which include grinding, sorting and cleaning of the teeth for immediate or future use. In Korea, the Korea Tooth Bank performed bio-recycling of 38 000 patients' own teeth from January 2009 until October 2012.
In chemistry, the molar mass (M) (sometimes called molecular weight or formula weight, but see related quantities for usage) of a chemical substance (element or compound) is defined as the ratio between the mass (m) and the amount of substance (n, measured in moles) of any sample of the substance: M = m/n. The molar mass is a bulk, not molecular, property of a substance. The molar mass is a weighted average of many instances of the element or compound, which often vary in mass due to the presence of isotopes. Most commonly, the molar mass is computed from the standard atomic weights and is thus a terrestrial average and a function of the relative abundance of the isotopes of the constituent atoms on Earth. The molecular mass (for molecular compounds) and formula mass (for non-molecular compounds, such as ionic salts) are commonly used as synonyms of molar mass, as the numerical values are identical (for all practical purposes), differing only in units (dalton vs. g/mol or kg/kmol). However, the most authoritative sources define it differently. The difference is that molecular mass is the mass of one specific particle or molecule (a microscopic quantity), while the molar mass is an average over many particles or molecules (a macroscopic quantity). The molar mass is an intensive property of the substance, that does not depend on the size of the sample. In the International System of Units (SI), the coherent unit of molar mass is kg/mol. However, for historical reasons, molar masses are almost always expressed with the unit g/mol (or equivalently in kg/kmol).
Sources: en.wikipedia.org
Aprataxin is 342 amino acids long and consists of FHA domain and HIT-ZnF catalyc core. It works by binding to adenylated DNA and removing AMP by catalytic side. Aprataxin is localised in the nucleus and mitochondria, which means aprataxin participates in mitochondrial DNA repair. This protein participates in base excision repair (BER) by returning abortive DNA ligation into scheduled repair by DNA polymerase beta, which would remove 5'-deoxyribosephosphate residue (dRP) and fill the gap; consequently, DNA ligase III-XRCC1 complex would seal the gap; consequently this mechanism is hampered in AOA1. Also, it might participate in microhomology-mediated end joining (MMEJ) by associating with XRCC1 and DNA ligase III and safeguarding DNA from abortive ligations by DNA ligase I, which might, again, be hampered in AOA1. iPSC with AOA1-associated mutation showed hindered differentiation into neurons which could be responsinble for early onset. Additionally, these neurons showed increased levels of cleaved PARP1 and decreased levels of APEX1. Due to the unique structure of chromatin in Purkinje cells, DNA damage (caused by aprataxin dysfunction) would hamper RNA polymerase II function, which would lead to improper splicing of some genes (such as: ITPR1, GRID2, CA8) and consequeent formation of R-loops; R-loops can exacerbate DNA damage. Because of dysregulation of genes, this would lead to ataxia. Decreased levels of albumin and elevated alpha-fetoprotein in AOA1 might be caused by transcriptional dysregulation in the liver.
However its participation in the legislative process still remains limited because no member can actually or pass legislation without the Commission and Council, meaning power ("kratia") is not in the hands of directly elected representatives of the people ("demos"): in the EU it is not yet true that "the administration is in the hands of the many and not of the few".
Harry Raymond Eastlack, Jr. (17 November 1933 – 11 November 1973) was an American man who became the subject of the most recognized cases of fibrodysplasia ossificans progressiva (FOP), a disease characterized by the ossification of fibrous connective tissue. His case is also particularly acknowledged, by scientists and researchers, for his contribution to medical advancement. After living with a rare, debilitating, and currently incurable genetic disease, Eastlack decided to have his skeleton and medical history donated to the Mütter Museum of the College of Physicians of Philadelphia in support of FOP research. His skeleton is one of the few FOP-presenting, fully articulated ones in existence, and it has proved valuable to the study of the disease. As is characteristic of FOP patients, Eastlack did not demonstrate any possible sign of a disease at birth except for a malformation of the big toes. At the time it was not recognized as the first clinical sign of FOP. It was not until 1937 when the first heterotopic ossification symptom surfaced. By the time of his death, Eastlack's skeleton bore sheets of bone along the vertebrae that fused to and locked his skull, and branches of bone along his limbs, which immobilized his shoulders, elbows, hips, and knees. He died in Philadelphia of bronchial pneumonia, aged 39.
Increased body temperature >38 °C (>100.4 °F) Confused or altered consciousness Excessive sweating Severely rigid muscles Autonomic imbalance The first symptoms of neuroleptic malignant syndrome are usually muscle cramps and tremors, fever, symptoms of autonomic nervous system instability such as unstable blood pressure, and sudden changes in mental status (agitation, delirium, or coma). Other possible symptoms include sweating, trouble swallowing, incontinence, and mutism. Once symptoms appear, they may progress rapidly and reach peak intensity in as little as three days. These symptoms can last anywhere from eight hours to forty days, with the median duration of symptoms, with treatment, being nine days. The median onset of symptoms is four days after initiating the offending medication, but in some cases symptoms may begin up to 30 days later. Symptoms are sometimes misinterpreted by doctors as symptoms of mental illness which can result in delayed treatment. Symptoms may also be mistaken for similarly presenting conditions such as malignant hyperthermia, serotonin syndrome, and substance intoxication from illicit drugs such as cocaine, methamphetamine, or MDMA. Neuroleptic malignant syndrome (NMS) usually presents with a "lead pipe rigidity" in which the muscles are stiffened and resistance is observed throughout the range of motion on testing. Severe cases may present as catatonia in which the person is not responsive to stimuli. The deep tendon reflexes in NMS are usually preserved whereas serotonin syndrome presents with myoclonus or hyperactive muscle reflexes.
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.
SR9009 is a synthetic research compound that acts on REV-ERB nuclear receptors. It is not approved for human use and is sold only as a research chemical. Its effects have been studied mainly in cells and rodents.