The short version of REV-ERB agonist fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2025-09-09. Anything still debated is marked as such rather than presented as settled.
Detection of SR9009 in biological samples usually employs liquid chromatography coupled with tandem mass spectrometry. This method can identify the parent compound and sometimes metabolites in urine or blood. Because exposure can be low and clearance may be rapid, sample timing and limits of detection matter. Laboratories validate assays for sensitivity and specificity. Results are interpreted alongside chain-of-custody and quality-control records. Urine is the common matrix for anti-doping analysis, while blood may be used in research settings.
Handling recommendations for SR9009 in a laboratory setting include storing the solid at low temperature, protected from light and moisture. The compound is often dissolved in dimethyl sulfoxide or ethanol for experiments. Solutions should be prepared with appropriate personal protective equipment and disposed of according to local rules. Stability data for long-term storage are limited, so stock solutions are typically kept cold and used within defined periods. Records of preparation date and concentration support reproducibility.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Regulatory status | Not approved as a medicine in major jurisdictions | Sold as a research chemical; legal status varies |
| Anti-doping status | Prohibited by the World Anti-Doping Agency | Listed under non-approved substances or related category |
| Typical analytical method | LC-MS/MS | Used for detection and confirmation in biological samples |
| Storage temperature | −20 °C or lower for solid | Desiccated and protected from light |
| Common solution solvents | DMSO; ethanol | Aqueous solubility is limited |
At the molecular level, SR9009 binds REV-ERBα and REV-ERBβ and alters their repressive activity on target genes. These nuclear receptors help regulate the circadian clock, lipid synthesis, glucose metabolism, and inflammatory pathways. By changing transcription, the compound can shift the timing or magnitude of downstream metabolic processes in model systems. It does not act through androgen receptors or adenosine receptors, which distinguishes it from several substances sold for athletic performance. Whether the same transcriptional changes occur in humans at tolerable exposures remains an open question because controlled human studies are lacking.
Preclinical reports describe effects on exercise endurance, mitochondrial content, and lipid profiles in rodents, but these findings come from specific experimental conditions. Many studies use high doses or delivery methods that may not translate directly to human use. SR9009 has been reported to have low oral bioavailability and a short half-life, which complicates interpretation of oral dosing studies. It is not established as safe or effective for any indication. Literature discussions often separate its pharmacological mechanism from unverified claims made in fitness and supplement markets.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not an approved medicine and has no established human therapeutic use. The compound appears in scientific literature as a tool for probing circadian and metabolic regulation. Online sellers often label it as a research chemical, sometimes using the nickname Stenabolic. Its chemical identity is distinct from selective androgen receptor modulators, stimulants, and peroxisome proliferator-activated receptor delta agonists. Researchers use it mainly in cell and animal experiments.
Analytical methods for SR9009 typically rely on liquid chromatography coupled with tandem mass spectrometry. The technique can separate the parent compound from related substances and detect low concentrations in biological matrices. Urine and blood are common samples in anti-doping testing, while in vitro studies may use cell culture media. Rapid metabolism and low expected concentrations make method validation important for reliable identification. Exact metabolite patterns can vary by species and are not fully mapped.
Regulatory treatment of SR9009 reflects its investigational status. The compound has no approved human therapeutic indication, and sports authorities prohibit its use. It appears on anti-doping lists as a non-approved substance or metabolic modulator, depending on the list version. Products sold online as research chemicals are not quality-controlled medicines, so their identity and purity can differ from the label. Such products may also contain unlisted compounds, which complicates both testing and safety assessment.
Scientific discussion of SR9009 often separates animal evidence from human anecdote. Rodent studies provide controlled data on endurance, metabolism, and gene expression, but they use specific strains, doses, and treatment durations. Human reports are mostly uncontrolled and cannot establish cause and effect. Open questions include oral bioavailability, tissue distribution, metabolic stability, and long-term effects. Review articles generally call for more rigorous pharmacokinetic and safety research before any clinical use could be considered.
Each parent with the condition poses a 50% risk of passing the genetic defect on to any child due to its autosomal dominant nature. Most individuals with MFS have another affected family member. About 75% of cases are inherited. On the other hand, about 15–30% of all cases are due to de novo genetic mutations; such spontaneous mutations occur in about one in 20,000 births. Marfan syndrome is also an example of dominant negative mutation and haploinsufficiency. It is associated with variable expressivity; complete penetrance has been definitively documented.
Similarly, Sumo wrestlers are typically categorized by BMI as "severely obese" or "very severely obese", but one study of college-aged Sumo wrestlers found that 40% of them were no longer categorized as obese when body fat percentage (with a cutoff of <25%) was used instead of BMI; this was attributed to their very high lean body mass. The Edmonton Obesity Staging System (EOSS), developed in Canada, supplements BMI-based classification by incorporating medical, functional, and mental-health factors into a five-stage clinical framework.
The first woman elected president of a country was Vigdís Finnbogadóttir of Iceland, who won the 1980 presidential election as well as three subsequent elections, remaining in office for a total of 16 years, which makes her the longest-serving non-hereditary female head of state in history. Vigdís was also the first woman to win a presidential election where the second place candidate was another woman: she defeated Sigrún Þorsteinsdóttir in the 1988 presidential election. The first democratically elected female prime minister of a Muslim majority country was Benazir Bhutto of Pakistan, who led her party to victory in the 1988 general election and later in 1993, making her the first woman democratically elected leader of any Muslim nation. Bhutto was also the first of only two non-hereditary female world leaders who gave birth to a child while serving in office, the other being Jacinda Ardern of New Zealand. The longest-tenured female non-hereditary head of government is Sheikh Hasina of Bangladesh. She served as the country's prime minister from June 1996 to July 2001 and again from January 2009 until August 2024, for a combined total of over 20 years. Finland was the first republic in which women served concurrently as both the head of state and head of government, with both Anneli Jäätteenmäki and Mari Kiviniemi serving as prime ministers under president Tarja Halonen.
Sources: en.wikipedia.org
Block copolymers can "microphase separate" to form periodic nanostructures, such as styrene-butadiene-styrene block copolymer. The polymer is known as Kraton and is used for shoe soles and adhesives. Owing to the microfine structure, transmission electron microscope or TEM was used to examine the structure. The butadiene matrix was stained with osmium tetroxide to provide contrast in the image. The material was made by living polymerization so that the blocks are almost monodisperse to create a regular microstructure. The molecular weight of the polystyrene blocks in the main picture is 102,000; the inset picture has a molecular weight of 91,000, producing slightly smaller domains.
). The question raised but not answered by this study was whether the illness caused subtle immune deficiency that led to reactivation of HHV-6, or whether reactivation of HHV-6 led to the symptoms of the illness. Subsequent studies employing only serological techniques that do not distinguish active from latent infection have produced mixed results: most, but not all, have found an association between CFS and HHV-6 infection. Other studies have employed assays that can detect active infection: primary cell culture, PCR of serum or plasma, or IgM early antigen antibody assays. The majority of these studies have shown an association between CFS and active HHV-6 infection, although a few have not. In summary, active infection with HHV-6 is present in a substantial fraction of patients with CFS. Moreover, HHV-6 is known to infect cells of the nervous system and immune system, organ systems with demonstrable abnormalities in CFS. Despite this association, it remains unproven that reactivated HHV-6 infection is a cause of CFS.
Ester local anesthetics are metabolized by pseudocholinesterases which in people with myasthenia gravis taking anticholinesterase drugs may lead to excessive levels of these ester anesthetics. Amide local anesthetics are not metabolized by psuedocholineesterases. Based on these considerations, amide local anesthetics are strongly preferred over ester local anesthetics in people with myasthenia gravis. Other Drugs: Rare cases of myasthenia gravis exacerbations have been reported in people treated with: 1) penicillins, i.e., ampicillin and amoxicillin; 2) anti-cancer medications, i.e., lorlatinib, nilotinib, imatinib (these three drugs are tyrosine kinase inhibitors that may also cause myasthenia gravis), dabrafenib, and trametinib; 3) antipsychotic drugs, i.e., chlorpromazine, pimozide, thioridazine, clozapine, olanzapine, haloperidol, quetiapine, and risperidone; 4) IFN-α (may also cause myasthenia gravis); and 5) the chemical element, lithium. These agents can be used in people with myasthenia gravis because reports on their exacerbation (or induction) of myasthenia gravis are rare.
== Structure, bonding, and characterization == Phenyl compounds are derived from benzene (C6H6), at least conceptually and often in terms of their production. In terms of its electronic properties, the phenyl group is related to a vinyl group. It is generally considered an inductively withdrawing group (-I), because of the higher electronegativity of sp2 carbon atoms, and a resonance donating group (+M), due to the ability of its π system to donate electron density when conjugation is possible. The phenyl group is hydrophobic. Phenyl groups tend to resist oxidation and reduction. Phenyl groups (like all aromatic compounds) have enhanced stability in comparison to equivalent bonding in aliphatic (non-aromatic) groups. This increased stability is due to the unique properties of aromatic molecular orbitals. The bond lengths between carbon atoms in a phenyl group are approximately 1.4 Å. In 1H-NMR spectroscopy, protons of a phenyl group typically have chemical shifts around 7.27 ppm. These chemical shifts are influenced by aromatic ring current and may change depending on substituents.
Sources: en.wikipedia.org
Its legal status depends on the country and intended use. It is not an approved medicine in major jurisdictions. In sport, it is prohibited by anti-doping rules.
Laboratories typically use LC-MS/MS to detect SR9009 and related compounds in urine or blood. The method is sensitive but depends on sample collection timing. Confirmatory analysis follows quality-control procedures.
Solid material is generally kept cold, dry, and protected from light. Solutions are often stored in sealed containers at low temperature. Stability beyond recommended periods is not well documented.
It is a synthetic compound that acts as an agonist at REV-ERBα and REV-ERBβ. It is used mainly as a research chemical to study circadian and metabolic pathways. It is not approved for human therapeutic use.