Everything below concerns certificate of analysis. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2025-10-22. Where a claim depends on a specific study, the study is described rather than over-claimed.
In rodent studies, SR9009 has been reported to increase mitochondrial content in skeletal muscle and improve exercise endurance under some conditions. These findings led to popular descriptions such as an exercise mimetic, although that term oversimplifies the biology. Effects vary by dose, timing, tissue, and model. The compound's influence on circadian pathways means that time of administration can matter in experiments. Whether similar metabolic changes occur in humans remains largely unexplored in controlled published trials.
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.
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 not approved as a medicine by major regulatory agencies. It is commonly sold as a research chemical, a category that may fall outside customary drug approval and quality rules. In sports, the World Anti-Doping Agency lists SR9009 as a prohibited substance. Athletes who use it can face sanctions if it is detected in a sample. Legal status varies by country, and importation may be restricted. Enforcement practices differ across borders.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic small-molecule REV-ERB agonist | Not a hormone or natural product |
| Primary targets | REV-ERBα and REV-ERBβ | Nuclear receptors involved in circadian and metabolic regulation |
| Appearance | White to off-white solid | Typical for purified research samples |
| Solubility | Soluble in DMSO and ethanol; low water solubility | Laboratory solubility depends on solvent and purity |
| Common synonyms | SR9009; Stenabolic | Stenabolic is a colloquial name, not a formal chemical name |
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.
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.
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.
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.
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.
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.
In Europe the field followed its own pathway; for example in Germany the parallel interventional society began to break free of the DR society in 2008. In the UK, interventional radiology was approved as a sub-specialty of clinical radiology in 2010. While many countries have an interventional radiology society, there is also the European-wide Cardiovascular and Interventional Radiological Society of Europe, whose aim is to support teaching, science, research and clinical practice in the field by hosting meetings, educational workshops and promoting patient safety initiatives. Furthermore, the Society provides an examination, the European Board of Interventional Radiology (EBIR), which is a highly valuable qualification in interventional radiology based on the European Curriculum and Syllabus for IR.
Required a retrievable record of all purchases, identifying the name and address of each party, to be kept for two years Required verification of proof of identity of all purchasers Required protection and disclosure methods in the collection of personal information Required reports to the Attorney General of any suspicious payments or disappearances of the regulated products Required training of employees with regard to the requirements of the CMEA. Retailers must self-certify as to training and compliance. The non-liquid dose form of regulated products may only be sold in unit dose blister packs Regulated products must be stored behind the counter or in a locked cabinet in such a way as to restrict public access Sales limits (per customer): Daily sales limit—must not exceed 3.6 grams of pseudoephedrine base without regard to the number of transactions 30-day (not monthly) sales limit—must not exceed 7.5 grams of pseudoephedrine base if sold by mail order or "mobile retail vendor" 30-day purchase limit—must not exceed 9 grams of pseudoephedrine base. (A misdemeanor possession offense under 21 U.S.C. § 844a for the person who buys it.) The requirements were revised in the Methamphetamine Production Prevention Act of 2008 to require that a regulated seller of scheduled listed chemical products may not sell such a product unless the purchaser:
The cause of the 2006 death of Alexander Litvinenko, a former Russian FSB agent who had defected to the United Kingdom in 2001, was identified to be poisoning with a lethal dose of 210Po; it was subsequently determined that the 210Po had probably been deliberately administered to him by two Russian ex-security agents, Andrey Lugovoy and Dmitry Kovtun. As such, Litvinenko's death was the first (and, to date, only) confirmed instance in which polonium's extreme toxicity has been used with malicious intent. In 2011, an allegation surfaced that the death of Palestinian leader Yasser Arafat, who died on 11 November 2004 of uncertain causes, also resulted from deliberate polonium poisoning, and in July 2012, concentrations of 210Po many times more than normal were detected in Arafat's clothes and personal belongings by the Institut de Radiophysique in Lausanne, Switzerland. Even though Arafat's symptoms were acute gastroenteritis with diarrhoea and vomiting, the institute's spokesman said that despite the tests the symptoms described in Arafat's medical reports were not consistent with 210Po poisoning, and conclusions could not be drawn. In 2013 the team found levels of polonium in Arafat's ribs and pelvis 18 to 36 times the average, even though by this point in time the amount had diminished by a factor of 2 million. Forensic scientist Dave Barclay stated, "In my opinion, it is absolutely certain that the cause of his illness was polonium poisoning. ...
Furthermore, it was shown that the codons do not overlap with each other in the DNA sequence encoding a protein, and that each sequence is read from a fixed starting point. To actually decipher the code, it took an extensive series of experiments in biochemistry and bacterial genetics, between 1961 and 1966—most importantly the work of Nirenberg and Khorana. During 1962–1964, numerous conditional lethal mutants of a bacterial virus were isolated. These mutants were used in several different labs to advance fundamental understanding of the functions and interactions of the proteins employed in the machinery of DNA replication, DNA repair, DNA recombination, and in the assembly of molecular structures.
== Sulfur content of food == Generally, a low sulfur diet involves reduction of meats, dairy products, eggs, onions, peas and cruciferous vegetables (cauliflower, cabbage, kale, watercress, broccoli and other leafy vegetables), .
Sources: en.wikipedia.org
Cetshwayo was captured a month after his defeat, and then exiled to Cape Town. The British passed rule of the Zulu kingdom onto 13 "kinglets", each with his own subkingdom. Conflict soon erupted between these subkingdoms, and in 1882, Cetshwayo was allowed to visit England. He had audiences with Queen Victoria and other famous personages before being allowed to return to Zululand to be reinstated as king. In 1883, Cetshwayo was put in place as king over a buffer reserve territory, much reduced from his original kingdom. Later that year, however, Cetshwayo was attacked at Ulundi by Zibhebhu, one of the 13 kinglets. Cetshwayo was wounded and fled. Cetshwayo died in February 1884, possibly poisoned. His son, Dinuzulu, then 15, inherited the throne. The academic Roberto Breschi notes that Zululand had a flag from 1884 to 1897 but this is pure conjecture as A.P. Burgers notes in his book. It consisted of three horizontal bands in equal width of gold, green and red.
Type I: Properdin levels are unable to be detected Type II: Properdin levels are from 1-10% in comparison to normal levels; function is intact Type III: Properdin levels are normal but the function is absent Evaluations for properdin deficiency may take place in patients with frequenct Neisserial infections with a functioning classical complement pathway (CH50). The AH50 assay is based on the lysis of unsensitized rabbit erythrocytes, however, normal results have been reported in patients with Type I properdin deficiency. Family history of X-linked inheritance should be considered. Further testing includes: Factor D Function by Hemolytic Assay, Properdin Level by ELISA, and gene sequencing to detect mutations for confirmation. Patients with Factor D deficiency or properdin deficiency are advised to receive meningococcal vaccinations and frequent evaluations for meningococcal antibodies. For those with recurring infections, prophylactic antibiotics are administered.
=== Myocardial excitability === Calcium (calcium chloride or calcium gluconate) reduces the cardiac toxicity of hyperkalemia by restoring normal conduction velocity. The traditional explanation held that calcium raises the threshold potential, restoring the gradient between threshold potential and resting membrane potential, which is elevated in hyperkalemia. However, a 2024 experimental study found that calcium restored cardiac conduction velocity and normalized the QRS complex without restoring resting membrane potential, suggesting the mechanism involves L-type calcium channel-dependent propagation rather than membrane potential stabilization. These findings provide a mechanistic basis for the clinical observation that calcium is most effective when ECG changes reflect conduction abnormalities (QRS widening) rather than repolarization changes alone (peaked T waves). A standard ampule of 10% calcium chloride is 10 mL and contains 6.8 mmol of calcium. A standard ampule of 10% calcium gluconate is also 10 mL but has only 2.26 mmol of calcium. Clinical practice guidelines recommend giving 6.8 mmol for typical ECG findings of hyperkalemia. This is 10 mL of 10% calcium chloride or 30 mL of 10% calcium gluconate. Though calcium chloride is more concentrated, it is caustic to veins and should generally be administered through a central line; calcium gluconate is preferred for peripheral venous access in stable patients.
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Sources: en.wikipedia.org
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.
It binds REV-ERBα and REV-ERBβ and changes transcription of metabolic genes. This can affect circadian rhythm, lipid use, and mitochondrial function. The full downstream effects are still under study.
No. Some rodent studies show increased endurance, but controlled human trials are lacking. Claims about human performance are not established by published evidence.
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.