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Sr9009 Identity And Mechanism — Evidence Review

By Editorial Desk · published 2025-08-11 · last reviewed 2025-09-18 · News

circadian clock 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 2025-09-18. Where a claim depends on a specific study, the study is described rather than over-claimed.

SR9009 Identity and Mechanism

SR9009 is frequently discussed alongside other REV-ERB ligands, including synthetic agonists and natural heme-related molecules. Its selectivity for REV-ERB over related nuclear receptors has been measured in binding and reporter assays, though off-target activity at higher concentrations is possible. The compound is prohibited in sport by the World Anti-Doping Agency, and it is not approved for any medical use in major jurisdictions. Products sold online may be labeled as research chemicals, and their identity and purity are not guaranteed by regulatory review.

SR9009 is a synthetic small molecule that acts on the nuclear receptors REV-ERBα and REV-ERBβ. These receptors are part of the circadian clock machinery and normally repress transcription of certain target genes. In laboratory research, SR9009 is used as a chemical tool to study how REV-ERB activity influences metabolism, inflammation, and daily biological rhythms. The compound is not an approved medicine, and its effects in humans remain largely uncharacterized. It is often described as an investigational agent rather than a therapeutic product.

Analytical Detection and Regulatory Status

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.

Sr9009 at a glance

PropertyValueNotes
Common nameSR9009Also marketed informally as Stenabolic
Chemical classSynthetic REV-ERB agonistBinds REV-ERBα and REV-ERBβ
Molecular formulaC24H30ClN3O4SApproximate molecular weight 492 g/mol
CAS Registry Number1379686-30-2Identifier for the parent compound
Regulatory statusNot approved for human useProhibited in sport by WADA

SR9009 Background and Mechanism

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.

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.

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Analytical Detection and Stability

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.

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.

Handling, Analysis, and Regulation

Laboratory samples of SR9009 are typically handled as research chemicals rather than pharmaceuticals. Suppliers usually state that the material is for research use only and not for human or veterinary administration. Storage recommendations generally call for a freezer at approximately −20 °C, protection from light, and a desiccated environment. The solid is often described as a white to off-white powder. Solubility is commonly reported in organic solvents such as dimethyl sulfoxide and ethanol, with low solubility in water.

Analytical identification and purity assessment often use high-performance liquid chromatography with ultraviolet detection or mass spectrometry. Liquid chromatography–tandem mass spectrometry is used to detect and quantify SR9009 in biological matrices, including urine and blood, for anti-doping or pharmacokinetic studies. Nuclear magnetic resonance spectroscopy can confirm molecular structure. Stability depends on form and storage: the solid is generally more stable than solutions, and repeated freeze–thaw cycles may degrade samples. Purity is typically reported as a percentage from a certificate of analysis.

Background and Pharmacological Mechanism

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.

Further detail

== Career == Somogyi was born on March 7, 1883, in the village of Zsámánd in Hungary (today Reinersdorf, part of Heiligenbrunn, Austria). He graduated in chemical engineering from the University of Budapest in 1905. After an additional year as an assistant in biochemistry, Somogyi went to the United States, where he eventually found a position as an assistant in biochemistry at Cornell University (1906–1908). He returned to Budapest where he worked at the Municipal Laboratory for the next decade. In 1914, he received his Ph.D. from the University of Budapest, submitting a dissertation on catalytic hydrogenation. During World War I he was in charge of providing food to the destitute. Somogyi was invited to return to the United States by Philip A. Shaffer, whom he had known at Cornell. In 1922 Somogyi became an instructor in biochemistry at Washington University School of Medicine. There Somogyi worked with Shaffer and Edward Adelbert Doisy on insulin preparation and insulin's use in the treatment of diabetes. In 1926, Somogyi became the first biochemist on the staff of the new Jewish Hospital of St. Louis where he worked closely with physicians. He directed the hospital's clinical laboratory until he retired in 1957.

=== Phenylbutyrate therapy === Sodium phenylacetate/benzoate or sodium phenylbutyrate has been shown to reduce BCAA in a clinical trial done February 2011. Phenylbutyrate treatment reduced the blood concentration of BCAA and their corresponding BCKA in certain groups of MSUD patients and may be a possible adjunctive treatment.

Indigenous allies were crucial to conquest, as well as to creating and maintaining empire. Indigenous peoples in Colombia experienced a decline in population due to conquest as well as Eurasian diseases, such as smallpox, to which they had no immunity. Regarding the land as deserted, the Spanish Crown sold properties to all persons interested in colonized territories, creating large farms and possession of mines. In the 16th century, the nautical science in Spain reached a great development thanks to numerous scientific figures of the Casa de Contratación and nautical science was an essential pillar of the Iberian expansion. In 1542, the region of New Granada, along with all other Spanish possessions in South America, became part of the Viceroyalty of Peru, with its capital in Lima. In 1547, New Granada became a separate captaincy-general within the viceroyalty, with its capital at Santa Fe de Bogota. In 1549, the Royal Audiencia was created by a royal decree, and New Granada was ruled by the Royal Audience of Santa Fe de Bogotá, which at that time comprised the provinces of Santa Marta, Rio de San Juan, Popayán, Guayana and Cartagena. But important decisions were taken from the colony to Spain by the Council of the Indies.

== Causes == Heinz bodies are formed by damage to the hemoglobin component molecules, usually through oxidative damage by administered drugs, or from an inherited mutation (i.e. change of an internal amino acid residue). As a result, an electron from the hemoglobin is transferred to an oxygen molecule, which creates a reactive oxygen species (ROS) that can cause severe cell damage leading to premature cell lysis. Damaged cells are cleared by macrophages in the spleen, where the precipitate and damaged membrane are removed, leading to characteristic "bite cells". The denaturing process is irreversible and the continual elimination of damaged cells leads to Heinz body anemia. There are several pathways leading to the hemoglobin damage.

Sources: en.wikipedia.org

Supporting material

Estradiol patches have an extended duration and are available for twice-weekly (3–4-day) and once-weekly (7-day) application, while gels, emulsions, and sprays are administered daily. There are two types of estradiol patches: reservoir patches, which have been described as first-generation patches, and matrix patches, which are considered to be improved second-generation patches. Reservoir patches were designed for twice-weekly application, while matrix patches have been produced for both twice-weekly and once-weekly application. Reservoir patches of estradiol (e.g., Estraderm TTS) are mostly no longer used, with most estradiol patches available today being matrix patches (e.g., Alora, Climara, Esclim, Estradot, FemPatch, Menostar, Oesclim, Vivelle, Vivelle-Dot, and Estraderm MX).

=== Metabolism and body weight === As of 2017, reviews of clinical trials showed that using aspartame (or other non-nutritive sweeteners) in place of sugar reduces calorie intake and body weight in adults and children. A 2017 review of metabolic effects by consuming aspartame found that it did not affect blood glucose, insulin, total cholesterol, triglycerides, calorie intake, or body weight. While high-density lipoprotein levels were higher compared to control, they were lower compared to sucrose. In 2023, the World Health Organization recommended against the use of common non-sugar sweeteners (NSS), including aspartame, to control body weight or lower the risk of non-communicable diseases, stating: "The recommendation is based on the findings of a systematic review of the available evidence which suggests that use of NSS does not confer any long-term benefit in reducing body fat in adults or children. Results of the review also suggest that there may be potential undesirable effects from long-term use of NSS, such as an increased risk of type 2 diabetes, cardiovascular diseases, and mortality in adults."

== External links == History of Mass Spectrometry - Pioneers - University of New South Wales Sydney Five Mass Spectrometry Nobel Prize Pioneers - Bristol University History of Mass Spectrometry - Scripps Institute

Sources: en.wikipedia.org

Supporting material

We are giving them to the elected government of Palestine", adding that he would personally donate three cars and £25,000 to Hamas organisation "Prime Minister" Ismail Haniyeh. On 8 April 2009, Galloway joined Vietnam War veteran Ron Kovic to launch Viva Palestina US. A third Viva Palestina convoy began travelling at the end of 2009. On 8 January 2010, Galloway and his colleague Ron McKay were deported from Egypt immediately following their entry from Gaza. They had been attempting to help take about 200 aid trucks into the Gaza Strip. They were driven by the police to the airport and placed on a plane bound for London. The Foreign Ministry of Egypt released a statement reading: "George Galloway is considered persona non grata and will not be allowed to enter into Egypt again". Shortly after his deportation, Galloway said, "It is a badge of honour to be deported by a dictatorship" and "I've been thrown out of better joints than that." Viva Palestina was registered as a charity in April 2009 but, following its continued non-submission of accounts, ceased to be recognised as a charitable organisation in November 2013. It was taken over by the Charity Commission in October 2014, which appointed an accountant to oversee the group because of the concerns over its financial management.

== Strengths == Simple, fast and inexpensive: In COBRA, DNA methylation levels are easily and quickly measured without the need for laborious sub-cloning and sequencing, as with bisulfite sequencing. The assay is straightforward and can be done with standard inexpensive molecular biology reagents. High compatibility: Due to the PCR and purification steps, the method not only works with very small amounts of genomic DNA, but also samples that have been treated with paraffin, both of which can be problems in other DNA methylation quantification protocols such as Southern blotting and methylation-sensitive restriction enzyme digestion followed by PCR. Quantitative: This is in contrast to methylation-specific PCR, which is qualitative. With COBRA, DNA methylation levels can be directly quantified at a given locus, yielding more information per assay. Scalability for high-throughput sample processing: With COBRA, many regions of interest can be processed in parallel in separate samples digested with the same restriction enzyme. This is in contrast to bisulfite sequencing analysis, where each region needs to be examined rigorously by sequencing many clones per locus, costing more time. Multiple queries per assay: Methylation status can be interrogated at multiple CpG-containing restriction sites in a single digestion assay.

== Diagnosis == When an affected individual has fully developed the three clinical elements of uric acid overproduction, neurologic dysfunction, and cognitive and behavioral disturbances, diagnosis of LNS is easily made. Diagnosis is less easy in the early stages, when the three features are not yet obvious. Signs of self-injurious behavior (SIB), results of pedigree analysis and novel molecular biology with genetic testing (called as Diagnostic triad for LNS), often confirms the diagnosis. Suspicion often comes about when the developmental delay of the individual is associated with hyperuricemia. Otherwise, the diagnosis should be alleged when developmental delay is associated with kidney stones (nephrolithiasis) or blood in the urine (hematuria), caused by uric acid stones. For the most part, Lesch–Nyhan syndrome is first suspected when self-inflicted injury behavior develops. However, self-injurious behaviors occur in other conditions, including nonspecific intellectual disability, autism, Rett syndrome, Cornelia de Lange syndrome, Tourette syndrome, familial dysautonomia, choreoacanthocytosis, sensory neuropathy including hereditary sensory neuropathy type 1, and several psychiatric conditions. Of these, only individuals with Lesch–Nyhan syndrome, de Lange syndrome, and familial dysautonomia recurrently display loss of tissue as a consequence.

Sources: en.wikipedia.org

Frequently asked questions

What is SR9009?

SR9009 is a synthetic research compound that binds and modulates the nuclear receptors REV-ERBα and REV-ERBβ. It is used in laboratory studies of circadian biology and metabolism, not as an approved medicine. It is also known by the informal name Stenabolic.

Is SR9009 approved for human use?

No. SR9009 has not been approved as a therapeutic drug in the United States, European Union, or other major markets. Human safety and efficacy data are very limited. Its presence in consumer products does not imply regulatory approval.

Why is SR9009 banned in sport?

The World Anti-Doping Agency lists SR9009 as a prohibited substance because it can alter gene expression and metabolic pathways relevant to performance. The ban applies at all times, not only during competition. Detection relies on laboratory methods such as mass spectrometry.

Is SR9009 approved for human use?

No. It is an investigational compound without approved therapeutic indications. It is sold for research purposes only in many jurisdictions.

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