Everything below concerns anti-doping. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-04-27. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic REV-ERB agonist | Binds REV-ERBα and REV-ERBβ in preclinical models |
| Molecular formula | C20H24ClN3O4S | Reported for the parent compound |
| CAS Registry Number | 1379686-30-2 | Common identifier in chemical databases |
| Appearance | Off-white to pale yellow solid | Typical research chemical solid |
| Solubility | Soluble in DMSO and ethanol; low in water | Class: small organic molecule |
Laboratory identification of SR9009 typically relies on chromatographic separation coupled to mass spectrometry, often with ultraviolet detection as a secondary check. Nuclear magnetic resonance spectroscopy can confirm molecular structure when a reference standard is available. Because many suppliers sell the compound as a research chemical, independent identity testing is important for experimental reproducibility. A single retention time is not sufficient proof of identity, especially when related compounds may be present. Purity assessments usually report a percentage based on area normalization.
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.
Regulatory agencies have not approved SR9009 for human therapeutic use. It is typically sold as a research chemical with labels stating that it is not for human consumption. The World Anti-Doping Agency prohibits the substance in sport, generally under the category of non-approved substances. Customs and national laws may restrict importation, sale, or possession. Product quality and legal status can vary by country and vendor, and therapeutic claims are not permitted in regulated advertising because the compound lacks approval.
Several misconceptions surround SR9009. It is often described as a SARM, a steroid, or an exercise pill, but its known target is the REV-ERB receptor family. Rodent studies have examined exercise capacity and metabolic markers, yet human outcomes remain unproven. Oral bioavailability appears low in animals, and human pharmacokinetics are not well characterized. Online products may contain impurities or different compounds, so identity and purity testing are important for research use.
Analytical chemists detect SR9009 with liquid chromatography-tandem mass spectrometry, commonly abbreviated LC-MS/MS. Sample preparation may involve protein precipitation, liquid-liquid extraction, or solid-phase extraction before analysis. Laboratories can target the parent compound or its metabolites, depending on the matrix and the purpose of testing. Anti-doping methods require sensitive and specific assays because concentrations in biological samples can be low. Reference standards and validated methods are essential for reliable identification and quantification.
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.
Storage conditions for research-grade SR9009 generally involve a freezer at approximately minus twenty degrees Celsius, sometimes lower for long-term preservation. Containers should remain tightly closed and protected from light. Desiccants may be used to limit moisture uptake. Solutions are often stored in aliquots to avoid repeated warming and cooling. Stability data for the compound under various conditions are limited, so laboratories typically follow supplier recommendations and verify performance through periodic analytical checks rather than assuming indefinite stability.
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.
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.
=== Specificity === Proteolysis can be highly promiscuous such that a wide range of protein substrates are hydrolyzed. This is the case for digestive enzymes such as trypsin, which have to be able to cleave the array of proteins ingested into smaller peptide fragments. Promiscuous proteases typically bind to a single amino acid on the substrate and so only have specificity for that residue. For example, trypsin is specific for the sequences ...K\... or ...R\... ('\'=cleavage site). Conversely some proteases are highly specific and only cleave substrates with a certain sequence. Blood clotting (such as thrombin) and viral polyprotein processing (such as TEV protease) requires this level of specificity in order to achieve precise cleavage events. This is achieved by proteases having a long binding cleft or tunnel with several pockets that bind to specified residues. For example, TEV protease is specific for the sequence ...ENLYFQ\S... ('\'=cleavage site).
In much of the British Empire, slavery was subject to abolition in 1833, throughout the United States it was abolished in 1865 as a result of the Civil War, which was fought after the attempted secession of the South in order to protect its "Peculiar Institution" (i.e. slavery). In Cuba slavery was abolished in 1886. The last country in the Americas to abolish slavery was Brazil, in 1888. Chattel slavery survived longest in the Middle East. After the trans-Atlantic slave trade had been suppressed, the ancient trans-Saharan slave trade, the Indian Ocean slave trade and the Red Sea slave trade continued to traffic slaves from the African continent to the Middle East. During the 20th century, the issue of chattel slavery was addressed and investigated globally by international bodies created by the League of Nations and the United Nations (UN), such as the Temporary Slavery Commission in 1924–1926, the Committee of Experts on Slavery in 1932, and the Advisory Committee of Experts on Slavery in 1934–1939. By the time of the UN Ad Hoc Committee on Slavery in 1950–1951, legal chattel slavery still existed only in the Arabian Peninsula: in Oman, in Qatar, in Saudi Arabia, in the Trucial States and in Yemen. Legal chattel slavery was finally abolished in the Arabian Peninsula in the 1960s: Saudi Arabia and Yemen in 1962, in Dubai in 1963, and Oman as the last in 1970. The last country to abolish slavery, Mauritania, did so in 1981.
== The route == Though the route changes to accommodate various ports of call, the race typically departs Europe in October, and in recent editions has had either 9 or 10 legs, with in-port races at many of the stopover cities. The 2008–09 race started in Alicante, Spain, on October 11, 2008. The route for the 2008–2009 race was altered from previous years to include stopovers in India and Asia for the first time. The 2008–09 route covered nearly 39,000 nmi (72,000 km), took over nine months to complete, and reached a cumulative TV audience of 2 billion people worldwide. During the nine months of the 2011–12 Volvo Ocean Race, which started in Alicante, Spain, in October 2011 and concluded in Galway, Ireland, in July 2012, the teams were scheduled to sail over 39,000 nmi (72,000 km) of the world's most treacherous seas via Cape Town, Abu Dhabi, Sanya, Auckland, around Cape Horn to Itajaí, Miami, Lisbon, and Lorient. As in the previous editions, the 2014–15 Volvo Ocean Race started in Alicante, Spain, on October 11. Destination was Gothenburg, Sweden, scheduled for June 2015, with stopovers in the ports of Cape Town, Abu Dhabi, Sanya, Auckland, Itajaí, Newport, Lisbon, Lorient, and with a Pitstop at The Hague through the last leg.
=== Retrial === At a hearing on 25 September 2023, the Crown Prosecution Service confirmed that there would be a retrial on one of the six attempted‑murder counts on which the original jury had been unable to reach a verdict. The retrial was scheduled to take place after the Court of Appeal had considered whether Letby would be granted permission to appeal her existing convictions. The retrial began on 10 June 2024. On 2 July, Letby was found guilty of attempted murder, and on 5 July she received a further whole‑life order. On 24 October 2024, Letby applied for permission to appeal this conviction, arguing that prejudicial media coverage should have prevented the trial from proceeding. The Court of Appeal rejected the application.
Sources: en.wikipedia.org
=== Online resale === Buc-ee's does not operate its own online store. However, several third-party resellers offer Buc-ee's products through various platforms, including Amazon, Walmart Marketplace, eBay, Etsy, and dedicated websites such as Texas Snax, True Texas Merch, and Johnny's Goods. These resellers operate under the first-sale doctrine, which permits the resale of legitimately purchased products. Buc-ee's states on its Web site that such resellers "are not affiliated with, authorized, sponsored, or endorsed by Buc-ee's in any way." Texas Snax, founded by Chris J. Koerner in 2020, emerged as one of the largest dedicated Buc-ee's resellers after Koerner initially contacted the company about a partnership and received no response. When Buc-ee's legal team learned of his venture, they permitted it on the condition that he change the original Web site name and add a disclaimer clarifying that Texas Snax is not affiliated with Buc-ee's. Online prices for Buc-ee's products are typically marked up significantly compared to in-store prices.
=== Regulation of the 20S by the 19S === The 19S regulatory particle is responsible for stimulating the 20S to degrade proteins. A primary function of the 19S regulatory ATPases is to open the gate in the 20S that blocks the entry of substrates into the degradation chamber. The mechanism by which the proteasomal ATPase open this gate has been recently elucidated. 20S gate opening, and thus substrate degradation, requires the C-termini of the proteasomal ATPases, which contains a specific motif (i.e., HbYX motif). The ATPases C-termini bind into pockets in the top of the 20S, and tether the ATPase complex to the 20S proteolytic complex, thus joining the substrate unfolding equipment with the 20S degradation machinery. Binding of these C-termini into these 20S pockets by themselves stimulates opening of the gate in the 20S in much the same way that a "key-in-a-lock" opens a door. The precise mechanism by which this "key-in-a-lock" mechanism functions has been structurally elucidated in the context of human 26S proteasome at near-atomic resolution, suggesting that the insertion of five C-termini of ATPase subunits Rpt1/2/3/5/6 into the 20S surface pockets are required to fully open the 20S gate, confirming work previously done on yeast proteasome.
=== Frederick Banting and the discovery of insulin === At the end of 1920, Macleod was approached by Frederick Banting, a young Canadian physician who had the idea of curing diabetes using an extract from a pancreas whose functioning had been disrupted. Macleod was not enthusiastic, because (unlike Banting) he knew about unsuccessful experiments in this direction by other researchers. He thought it more likely that the nervous system had a crucial role in regulating blood glucose concentration. Even though Banting had virtually no experience of physiology, he managed to convince Macleod to lend him laboratory space during a holiday in Scotland that summer. In addition to the laboratory, Macleod provided experimental animals and his student Charles Best, who worked as a demonstrator. Macleod also advised on project planning and the use of analytical techniques, and assisted with the operation on the first dog. While Macleod was away, Banting and Best achieved a breakthrough: they isolated an internal secretion of the pancreas and succeeded in reducing the blood sugar level of another dog, whose pancreas had been surgically removed.
Sources: en.wikipedia.org
SR9009 is a synthetic small molecule studied as an agonist of the REV-ERB nuclear receptors. It is not an approved medicine, and its effects in humans are not well characterized.
No. It is a synthetic ligand that binds nuclear receptors, not a steroid or peptide hormone. Its activity depends on receptor binding rather than endocrine secretion.
Clinical evidence is limited. Most published data come from cell and animal experiments. Human safety and efficacy remain uncertain.
It is a synthetic REV-ERB agonist used mainly in preclinical research. It is not an approved medicine for human use.