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Sr9009 Identity And Mechanism — Research Overview

By Editorial Desk · published 2026-01-04 · last reviewed 2026-01-22 · Faq

This is a working overview of Stenabolic, written for readers who want more than a one-paragraph summary but less than a textbook.

Reviewed 2026-01-22. Anything still debated is marked as such rather than presented as settled.

SR9009 Identity and Mechanism

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.

REV-ERB proteins typically suppress gene expression by recruiting corepressor complexes to DNA response elements. SR9009 binds these receptors and strengthens that repressive action in cell-based assays. Studies in rodents have reported changes in lipid handling, mitochondrial function, and exercise capacity after treatment. Such findings are often cited as evidence for metabolic effects, but species differences and limited pharmacokinetic data make direct translation to humans uncertain. Researchers continue to examine which effects are robust and which depend on specific experimental conditions.

Regulation, Testing, and Storage

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 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

Handling Storage and Quality Control

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.

Related pages on this site

Background and Receptor Pharmacology

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.

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.

Supporting material

MC1R has a slightly different function in cold-blooded animals such as fish, amphibians, and reptiles. Here, α-MSH activation of MC1R results in the dispersion of eumelanin-filled melanosomes throughout the interior of pigment cells (called melanophores). This gives the skin of the animal a darker hue and often occurs in response to changes in mood or environment. Such a physiological color change implicates MC1R as a key mediator of adaptive cryptic coloration. The role of ASIP's binding to MC1R in regulating this adaptation is unclear; however, in teleost fish at least, functional antagonism is provided by melanin-concentrating hormone. This signals through its receptor to aggregate the melanosomes toward a small area in the centre of the melanophore, resulting in the animal's having a lighter overall appearance. Cephalopods generate a similar, albeit more dramatic, pigmentary effect using muscles to rapidly stretch and relax their pigmented chromatophores. MC1R does not appear to play a role in the rapid and spectacular colour changes observed in these invertebrates.

Wiskott–Aldrich syndrome (WAS) patients also present with eczema, autoimmune manifestations, recurrent bacterial infections, and lymphoma. In autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED), autoimmunity and infections coexist: organ-specific autoimmune manifestations (e.g., hypoparathyroidism and adrenocortical failure) and chronic mucocutaneous candidiasis. Finally, IgA deficiency is sometimes associated with developing autoimmune and atopic phenomena.

=== Corrosion === Ammonium carbamate solutions are highly corrosive to metallic construction materials – even to resistant forms of stainless steel – especially in the hottest parts of the synthesis plant such as the stripper. Historically corrosion has been minimized (although not eliminated) by continuous injection of a small amount of oxygen (as air) into the plant to establish and maintain a passive oxide layer on exposed stainless steel surfaces. Highly corrosion resistant materials have been introduced to reduce the need for passivation oxygen, such as specialized duplex stainless steels in the 1990s, and zirconium or zirconium-clad titanium tubing in the 2000s.

In December 2017 the company announced that in the summer of 2018 Geoffrey Babidge, who had been nearing retirement age, would step down and Jayne Hrdlicka would take over as CEO; at that time she was CEO of a subsidiary of Qantas. She took over in July 2018. At that time the company was experiencing strong growth via sales in China and had ramped up spending to further increase Chinese sales and to expand the US market. Hrdlicka resigned as CEO in December 2019, after her husband was found to have a kidney tumour. On her departure Geoffrey Babidge returned, as interim CEO. In August 2020 David Bortolussi was appointed CEO and managing director.

Sources: en.wikipedia.org

Notes from published material

== Therapeutic relevance == Fundamental discoveries uncovering the biology of ferroptosis and translational studies showing the disease relevance of ferroptosis have motivated efforts to develop therapeutics that modulate ferroptosis. For example, Kojin Therapeutics and PTC Therapeutics are exploring ferroptosis modulation for treatment of cancer and Friedrich's ataxia. Ferroptosis has been implicated in a range of different diseases including cancer, ischemia/reperfusion injury (IRI), inflammation, neurodegeneration, and kidney injury.

== Medical uses == Tiratricol is indicated for the treatment of peripheral thyrotoxicosis in people with monocarboxylate transporter 8 (MCT8) deficiency (Allan-Herndon-Dudley syndrome), from birth. Thyrotoxicosis in MCT8 deficiency is caused by a mutation (change) in the gene that provides instructions for making a protein called MCT8. This protein normally transports the thyroid hormone T3 into cells of various tissues and organs, including those of the brain. Due to the gene mutation, MCT8 does not work properly and so T3 cannot enter the brain cells, causing problems with brain and muscle development. It also leads to a buildup of T3 in other parts of the body, causing problems due to too much thyroid hormone (hyperthyroidism). Tiratricol, is very similar to T3 but it does not need MCT8 to move in and out of cells. Tiratricol is therefore expected to enter the body’s cells in people with MCT8 deficiency and replace the missing T3 hormone. This helps restore normal thyroid hormone activity in the body and reduce symptoms of peripheral thyrotoxicosis. MCT8 deficiency is a rare genetic disorder that primarily affects males. The condition is caused by a faulty gene that provides instructions for making the MCT8 transporter, a critical protein responsible for carrying thyroid hormone into the brain. Because thyroid hormone cannot cross the blood-brain barrier without the MCT8 transporter, the brain receives too little of this hormone, while excessive levels of the hormone build up in the bloodstream.

== Firebombing incident == In 2001, Rhéal Mathieu, a member of Front de libération du Québec (FLQ), who in 1967 had been sentenced to nine years in prison for terrorist activities including murder, was convicted of firebombing three Second Cup locations in Montreal. The responsibility for the bombings was claimed by the Brigade d'autodéfense du français (BAF) (translated as Self Defence Brigade of French). BAF claimed it had targeted the stores because the company used its incorporated English name, "Second Cup", demanding the inclusion of French in the name. After the media coverage of the fire bombings, many Second Cup locations in Quebec changed their signs to Les cafés Second Cup.

Sources: en.wikipedia.org

Further detail

== A new home for biochemistry in Liverpool == The world's first Biochemistry Department (originally employing the archaic term 'Bio-chemistry') opened its research doors in 1903 within the newly created Johnston Laboratories, forming an early biomedical hub with other buildings that homed the Nobel Prize winning neurophysiologist Sir Charles Sherrington, who coined the term synapse. The original buildings are still in use today by the university, although not for laboratory-based research. The public-health scientist and visionary Benjamin Moore, was the inaugural holder of the world's first chair in Biochemistry, named The Johnston Chair in honour of the local benefactor William Johnston, a prominent Liverpool businessman.

== Recent studies == Recently thermospray was also utilized for the production of semiconductor nanocrystals, analysis of bile acids, identification of dyes, and molecular weight determinations of proteins from multiply charged ions.

Complement component 1s (EC 3.4.21.42, C1 esterase, activated complement C1s, complement C overbar 1r, C1s) is a protein involved in the complement system. C1s is part of the C1 complex. In humans, it is encoded by the C1S gene. C1s cleaves C4 and C2, which eventually leads to the production of the classical pathway C3-convertase.

Mendeleev, reading de Boisbaudran's publication, sent a letter claiming that gallium was his predicted eka-aluminium. Although Lecoq de Boisbaudran was initially sceptical, and suspected that Mendeleev was trying to take credit for his discovery, he later admitted that Mendeleev was correct. In 1879, the Swedish chemist Lars Fredrik Nilson discovered a new element, which he named scandium: it turned out to be eka-boron. Eka-silicon was found in 1886 by German chemist Clemens Winkler, who named it germanium. The properties of gallium, scandium, and germanium matched what Mendeleev had predicted. In 1889, Mendeleev noted at the Faraday Lecture to the Royal Institution in London that he had not expected to live long enough "to mention their discovery to the Chemical Society of Great Britain as a confirmation of the exactitude and generality of the periodic law". Even the discovery of the noble gases at the close of the 19th century, which Mendeleev had not predicted, fitted neatly into his scheme as an eighth main group. Mendeleev nevertheless had some trouble fitting the known lanthanides into his scheme, as they did not exhibit the periodic change in valencies that the other elements did. After much investigation, the Czech chemist Bohuslav Brauner suggested in 1902 that the lanthanides could all be placed together in one group on the periodic table.

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 legal?

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.

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