REV-ERB agonist 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.
Last reviewed on 2026-07-18. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Pharmacokinetic data for SR9009 are limited in published literature. Some reports indicate low oral bioavailability and rapid clearance in animals, which complicates interpretation of exposure and effect. Researchers often use injected routes in preclinical work to achieve measurable systemic levels. Analytical studies rely on mass spectrometry to detect the parent compound and its metabolites. Questions about tissue distribution, active metabolites, and long-term consequences remain open. Species differences in metabolism can affect observed half-life and target engagement.
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 and metabolic gene expression. In laboratory experiments, SR9009 binds these receptors and alters transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. It is not a naturally occurring compound and has no approved therapeutic use. Research interest stems from its ability to modify energy metabolism in cells and animal models.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C20H24ClN3O4S | Reported for the free base |
| Molecular weight | 437.9 g/mol | Calculated from the formula |
| Primary target | REV-ERBα and REV-ERBβ | Nuclear receptors involved in circadian regulation |
| Solubility | Soluble in DMSO and ethanol | Poorly soluble in water |
| Typical storage | -20 °C, desiccated | Protect from light and moisture |
REV-ERB proteins help regulate daily cycles in gene expression, including genes tied to lipid and glucose metabolism. SR9009 binds these receptors and alters their activity in cell and animal experiments. Consequences observed in rodents include changes in skeletal muscle oxidative capacity, blood lipid levels, and exercise performance. The precise chain from receptor occupancy to whole-body effects is still an active area of study. Human responses cannot be assumed from rodent data.
Most published work on SR9009 consists of preclinical studies. It is widely sold as a research chemical, a category that does not imply safety, efficacy, or pharmaceutical-grade quality. Sports anti-doping organizations have listed SR9009 as a prohibited substance, and its presence in an athlete sample can lead to sanctions. Legal status differs by country; in several jurisdictions it is not approved for human consumption and may be treated as an unapproved new drug.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not a steroid, peptide, or natural hormone. In scientific literature, it appears under the code SR9009 and in non-scientific contexts as Stenabolic. The compound was identified through chemical screening efforts aimed at targeting circadian clock components. Its status remains investigational, and no regulatory agency has approved it as a human medicine.
Identity and purity testing for SR9009 commonly uses liquid chromatography coupled with tandem mass spectrometry. This method separates the compound from matrix components and detects it by mass-to-charge transitions, providing sensitive and specific confirmation. Nuclear magnetic resonance spectroscopy can support structural identification, while high-performance liquid chromatography with ultraviolet detection may estimate purity. Because online products labeled as SR9009 may contain other substances or no active compound at all, independent verification is important in research settings. Certificates of analysis are useful but not a substitute for in-house testing.
Laboratory samples of SR9009 are typically supplied as a white to off-white powder. The compound dissolves readily in organic solvents such as dimethyl sulfoxide and ethanol, while its solubility in water is low. Because of this solubility profile, researchers often prepare concentrated stock solutions in an organic solvent before diluting them into aqueous assay buffers. Light exposure, moisture, and repeated freeze-thaw cycles can degrade many small molecules, so handling procedures usually aim to minimize these factors. Purity is commonly checked before use.
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.
Quality control for research materials includes identity confirmation by nuclear magnetic resonance and purity assessment by high-performance liquid chromatography. Mass spectrometry provides molecular weight confirmation and can detect related impurities. Purchasers should request a certificate of analysis that lists lot-specific data. Online products advertised for human use often lack such documentation. Distinguishing legitimate research material from mislabeled or contaminated samples is a recurring challenge in independent testing, and independent laboratories may use orthogonal methods to verify identity.
Detection of SR9009 in biological samples usually relies on liquid chromatography coupled to tandem mass spectrometry. This approach separates the compound from matrix components and identifies it by mass transitions. Because SR9009 can undergo metabolism, laboratories often look for both parent drug and specific metabolites. Sample preparation may involve protein precipitation or solid-phase extraction. Method validation examines sensitivity, carryover, and interference from related substances, and reference standards are required for accurate calibration.
Storage recommendations for SR9009 reference material typically specify a freezer at -20 °C or lower, with protection from moisture and light. Repeated freeze-thaw cycles can degrade small molecules and introduce variability. Stock solutions in dimethyl sulfoxide are often aliquoted to avoid repeated handling. Stability studies may examine degradation under heat, humidity, and light exposure. The compound's thiophene and nitro groups can participate in reactions that alter analytical signals over time, so such changes affect quantitative results.
== Structure == Larazotide is a synthetic octapeptide derived from research on an enterotoxin secreted by Vibrio cholerae, the causative agent of cholera. It has the amino acid sequence GGVLVQPG, IUPAC condensed descriptor of H-Gly-Gly-Val-Leu-Val-Gln-Pro-Gly-OH, and the systematic name glycylglycyl-L-valyl-L-leucyl-L-valyl-L-glutaminyl-L-prolyl-glycine.
Isobutyryl-coenzyme A is a necessary cofactor required for Polyketide synthase (PKS) enzyme(s), to catalyze the a,b-dehydrogenation of acyl-CoA esters to make many natural products via Polyketide synthase (PKS) assembly lines, as well as PKS-NRPS hybrid assembly lines. The resulting products comprise antibiotics and other bioactive molecules. Notably, isobutyryl-coenzyme A is also an intermediate in the metabolism of the amino acid valine, and it is structurally similar to intermediates in the catabolism of other small amino acids. Defective Isobutyryl-coenzyme A, produced by the body, often results in a metabolic disease.
==== 1400–1499 ==== Valuation Timetable (Scotland) Amendment (No.2) Order 1993 (S.I. 1993/1400) Nene Valley Light Railway (Transfer) Order 1993 (S.I. 1993/1402) Home-Grown Cereals Authority (Rate of Levy) Order 1993 (S.I. 1993/1405) Offshore Installations (Safety Zones) Order 1993 (S.I. 1993/1406) High Court and County Courts Jurisdiction (Amendment) Order 1993 (S.I. 1993/1407) Foreign Fields (Specification) Order 1993 (S.I. 1993/1408) Aeroplane Noise (Limitation on Operation of Aeroplanes) Regulations 1993 (S.I. 1993/1409) Fire Safety and Safety of Places of Sport Act 1987 (Commencement No. 7) Order 1993 (S.I. 1993/1411) Sports Grounds and Sporting Events (Designation) (Scotland) Amendment Order 1993 (S.I. 1993/1412) Food Protection (Emergency Prohibitions) (Paralytic Shellfish Poisoning) (No. 2) Order 1993 (S.I. 1993/1413) Removal, Storage and Disposal of Vehicles (Prescribed Sums and Charges etc.) (Amendment) (No. 2) Regulations 1993 (S.I. 1993/1415) Goods Vehicles (Operators' Licences) (Temporary Use in Great Britain) (Amendment) Regulations 1993 (S.I. 1993/1416) Hackney, Haringey and Islington (London Borough Boundaries) Order 1993 (S.I. 1993/1417) Non-Domestic Rating Act 1993 (Commencement No. 1) Order 1993 (S.I. 1993/1418) Suckler Cow Premium Regulations 1993 (S.I. 1993/1441) Feeding Stuffs (Amendment) Regulations 1993 (S.I. 1993/1442) East London Boroughs (London Borough Boundaries) Order 1993 (S.I. 1993/1443) East London Boroughs (London Borough Boundaries) (No. 2) Order 1993 (S.I. 1993/1444) City and London Borough Boundaries Order 1993 (S.I.
Biological activities of metal ion-binding compounds can be changed in response to the increment of the metal concentration, and based on the latter compounds can be classified as "metal ionophores", "metal chelators" or "metal shuttles". If the biological effect is augmented by increasing the metal concentration, it is classified as a "metal ionophore". If the biological effect is decreased or reversed by increasing the metal concentration, it is classified as a "metal chelator". If the biological effect is not affected by increasing the metal concentration, and the compound-metal complex enters the cell, it is classified as a "metal shuttle". The term ionophore (from Greek ion carrier or ion bearer) was proposed by Berton Pressman in 1967 when he and his colleagues were investigating the antibiotic mechanisms of valinomycin and nigericin. Many ionophores are produced naturally by a variety of microbes, fungi and plants, and act as a defense against competing or pathogenic species. Multiple synthetic membrane-spanning ionophores have also been synthesized. The two broad classifications of ionophores synthesized by microorganisms are:
Autosomal-dominant mutations in APP cause hereditary early-onset Alzheimer's disease (familial AD, fAD). This form of AD accounts for no more than 10% of all cases, and the vast majority of AD is not accompanied by such mutations. However, familial Alzheimer's disease is likely to result from altered proteolytic processing. This is evidenced by the fact that many mutations that lead to fAD occur near γ-secretase cleavage sites on APP. One of the most common mutations causing fAD, London Mutation, occurs at codon 717 of the APP gene, and results in a valine to isoleucine amino acid substitution. Histochemical analysis of the APP V717I mutation has revealed extensive Aβ pathology throughout neuroaxis as well as widespread cerebral amyloid angiopathy (CAA). The gene for the amyloid precursor protein is located on chromosome 21, and accordingly people with Down syndrome have a very high incidence of Alzheimer's disease.
Sources: en.wikipedia.org
IDF soldiers have three types of insignia, other than rank insignia, which identify their corps, specific unit, and position. A pin attached to the beret identifies a soldier's corps. Soldiers serving in staffs above corps level are often identified by the General Corps pin, despite not officially belonging to it, or the pin of a related corps. New recruits undergoing tironut (basic training) do not have a pin. Beret colors are also often indicative of the soldier's corps. Most non-combat corps do not have their own beret, and sometimes wear the color of the corps to which the post they're stationed in belongs. Individual units are identified by a shoulder tag attached to the left shoulder strap. Most units in the IDF have their own tags, although those that do not, generally use tags identical to their command's tag (corps, directorate, or regional command). While one cannot always identify the position/job of a soldier, two optional factors help make this identification: an aiguillette attached to the left shoulder strap and shirt pocket, and a pin indicating the soldier's work type, usually given by a professional course. Other pins may indicate the corps or additional courses taken. An optional battle pin indicates a war that a soldier has fought in.
Symptoms depend on the type and severity of thalassemia. Carriers of thalassemia genes may have no symptoms or very mild symptoms with occasional crisis; those with three or more (out of four) affected genes will have severe and life threatening symptoms. Full alpha thalassemia with all four genes failing to synthesise alpha-globin, is generally fatal to the unborn child. The absence of alpha globin means that zero functional hemoglobin is produced during gestation. Unmatched gamma globin chains cluster to form hemoglobin Bart's, which is ineffective at transporting oxygen. In this situation, a fetus will develop hydrops fetalis, a form of edema, which can be detected on prenatal ultrasound. The child will normally die before or shortly after birth, unless intrauterine blood transfusion is performed. Less severe alpha thalassemia may affect growth and development. If thalassemia is untreated or undetected in the infant, this can lead to developmental issues such as slowed growth, delayed puberty, bone abnormalities, and intellectual impairment. More generally, impaired production of hemoglobin causes anemia, resulting in tiredness and a general lack of energy, shortness of breath, rapid or irregular heartbeat, dizziness, pale skin, yellowing of the skin and eyes (jaundice). In thalassemia, ineffective erythropoiesis causes the bone marrow to expand. This expansion is a compensatory response to the damage caused to red blood cells by the imbalanced production of globin chains. Bone marrow expansion can lead to abnormal bone structure, particularly in the skull and face.
=== Gene therapy === Researchers are working on a gene editing method to correct a mutation that leads to Duchenne muscular dystrophy (DMD). Researchers used a technique called CRISPR/Cas9-mediated genome editing, which can precisely remove a mutation in the dystrophin gene in DNA, allowing the body's DNA repair mechanisms to replace it with a normal copy of the gene. Genome editing through the CRISPR/Cas9 system is not currently feasible in humans. However, it may be possible, through advancements in technology, to use this technique to develop therapies for DMD in the future. In 2007, researchers did the world's first clinical (viral-mediated) gene therapy trial for Duchenne MD. Biostrophin is a delivery vector for gene therapy in the treatment of Duchenne muscular dystrophy and Becker muscular dystrophy.
The Court of Justice held that the Directive could be relied on by her because equality was also a general principle of EU law. Fourth, if the defendant is an emanation of the state, even if not central government, it can still be bound by Directives. In Foster v British Gas plc the Court of Justice held that Mrs Foster was entitled to bring a sex discrimination claim against her employer, British Gas plc, which made women retire at age 60 and men at 65, if (1) pursuant to a state measure, (2) it provided a public service, and (3) had special powers. This could also be true if the enterprise is privatised, as it was held with a water company that was responsible for basic water provision. Fifth, national courts have a duty to interpret domestic law "as far as possible in the light of the wording and purpose of the directive". Textbooks (though not the Court itself) often called this "indirect effect". In Marleasing SA v La Comercial SA the Court of Justice held that a Spanish Court had to interpret its general Civil Code provisions, on contracts lacking cause or defrauding creditors, to conform with the First Company Law Directive article 11, that required incorporations would only be nullified for a fixed list of reasons. The Court of Justice quickly acknowledged that the duty of interpretation cannot contradict plain words in a national statute. But, if a member state has failed to implement a Directive, a citizen may not be able to bring claims against other non-state parties. It must instead sue the member state itself for failure to implement the law.
Sources: en.wikipedia.org
It is a synthetic REV-ERB agonist used mainly in preclinical research. It is not an approved medicine for human use.
It binds to REV-ERBα and REV-ERBβ, nuclear receptors involved in circadian and metabolic gene regulation. This can alter transcription of genes related to lipid and glucose metabolism in experimental models.
No controlled human trials have established that effect. Endurance findings come primarily from rodent studies, and human responses remain unknown.
It is a synthetic research compound that activates REV-ERB nuclear receptors. It is not an approved drug or dietary supplement. Most information comes from cell and animal studies.