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Sr9009 Identity And Mechanism — 2026 Update

By Editorial Desk · published 2025-11-03 · last reviewed 2025-11-30 · Blog

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

This page was last updated on 2025-11-30 and is reviewed periodically as new material appears.

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.

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.

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.

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

Background and Receptor Mechanism

SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ, also called NR1D1 and NR1D2. These receptors help regulate circadian rhythms and metabolic gene programs. The compound was developed for laboratory research, not as an approved therapeutic. Its identity is distinct from steroid hormones and selective androgen receptor modulators. Scientific interest centers on how REV-ERB activation changes gene expression in cells and animal models.

At the molecular level, SR9009 binds the ligand-binding domain of REV-ERB and strengthens recruitment of corepressor proteins such as NCoR and HDAC3. This increases repression of target genes, including Bmal1 and other clock-controlled and metabolic genes. In rodent studies, such changes have been linked to altered lipid handling, glucose metabolism, and energy expenditure. The precise chain of events between receptor binding and whole-body effects remains an active area of research. Findings in animals do not automatically translate to humans.

Laboratory studies often administer SR9009 by injection because oral absorption appears poor in rodents. Reported pharmacokinetic properties include rapid metabolism and low systemic exposure after oral dosing. Human pharmacokinetic data are sparse, so absorption, distribution, metabolism, and excretion in people are not well defined. Some research explores related REV-ERB compounds with improved drug-like properties. Regulatory approval for any REV-ERB agonist as a human medicine has not been granted to date.

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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.

Background and Research Status

Most published work on SR9009 consists of preclinical studies. It is widely sold as a research chemical, a category that does not imply safety, efficacy, or pharmaceutical-grade quality. Sports anti-doping organizations have listed SR9009 as a prohibited substance, and its presence in an athlete sample can lead to sanctions. Legal status differs by country; in several jurisdictions it is not approved for human consumption and may be treated as an unapproved new drug.

SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not a steroid, peptide, or natural hormone. In scientific literature, it appears under the code SR9009 and in non-scientific contexts as Stenabolic. The compound was identified through chemical screening efforts aimed at targeting circadian clock components. Its status remains investigational, and no regulatory agency has approved it as a human medicine.

REV-ERB proteins help regulate daily cycles in gene expression, including genes tied to lipid and glucose metabolism. SR9009 binds these receptors and alters their activity in cell and animal experiments. Consequences observed in rodents include changes in skeletal muscle oxidative capacity, blood lipid levels, and exercise performance. The precise chain from receptor occupancy to whole-body effects is still an active area of study. Human responses cannot be assumed from rodent data.

Background from the literature

Irene Hirano, fundraiser for charitable causes and second wife of Daniel Inouye Leicester City footballer Keith Weller, who made over 300 appearances for the Foxes, scoring 47 goals, made four appearances for England, scoring one goal. Katie Price Canadian public-health physician Sheela Basrur (1956–2008) developed uterine leiomyosarcoma in 2006. American actress Diana Sands The first year of treatment for leiomyosarcoma of Canadian comedian Irwin Barker was the subject of a 2008 television documentary, That's My Time; he died in 2010. Linda Uttley (1966–2009), English rugby union footballer in the Women's England Team, was diagnosed with leiomyosarcoma in 2007 and died in 2009 at the age of 43. Deborah Finck (1967–2025), TikToker and Nanny 911 star, was diagnosed with leiomyosarcoma in 2020 and died on January 14, 2025, at the age of 57. Loni Anderson (1945–2025), American actress, died from metastatic uterine leiomyosarcoma on August 3, 2025, at the age of 79.

For example, the pattern may be 10 press ups, then two minutes rest, 10 press ups, then two minutes rest etc. The ability to recover during an exercise (active recovery), during a training session, and resting between training sessions are all of fundamental importance in strength training. If recovery cannot take place then fatigue may occur leading to worse performance and an increased chance of injury.

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== Toxicity == The β-glycosidic bond between glucose and the hydroxyl group at C5 on the pyrimidine ring are hydrolysed to yield the aglycone of vicine, divicine (2,6-diamino-4,5-dihydroxypyrimidine). These aglycones have a strong oxidising capacity for glutathione. In healthy individuals, this is not a problem, as glutathione can be reduced quickly enough to regenerate it. In individuals with a deficiency for glucose 6-phosphate dehydrogenase (G6PD) however, this results in haemolytic anaemia.

Sources: en.wikipedia.org

Further detail

ECD devices can be of two forms. It can trap analyte ions during the ECD stage or can undergo flow through mode where dissociation takes place as analyte ions flows continuously through the ECD region. Flow through mode has advantage over other mode because nearly all the analyte ion beam is used. However, that decreases the efficiency of ECD for flow through mode. ECD produces significantly different types of fragment ions (although primarily c- and z-type, b-ions have been identified in ECD) than other MS/MS fragmentation methods such as electron-detachment dissociation (EDD) (primarily a and x types), collision-induced dissociation (CID) (primarily b and y type) and infrared multiphoton dissociation. CID and IRMPD introduce internal vibrational energy in some way or another, causing loss of post-translational modifications during fragmentation. In ECD, unique fragments (and complementary to CID) are observed, and the ability to fragment whole macromolecules effectively has been promising. Although ECD is primarily used in Fourier transform ion cyclotron resonance mass spectrometry, investigators have indicated that it has been successfully used in an ion-trap mass spectrometer. ECD can also do rapid integration of multiple scans in FTICR-MS if put in a combination with external accumulation. ECD is a recently introduced MS/MS fragmentation technique and is still being investigated.

=== Commercial Engineers & Body Builders Company Ltd (CEBBCO) === Commercial Engineers & Body Builders Company Ltd (CEBBCO), a Madhya Pradesh based manufacturer of tipplers, trailers, and specialized defence vehicles, was acquired by Jupiter Wagons Limited in a buyout of its organization in 2019 under a National Company Law Tribunal (NCLT) governed stressed asset sale. JWL latter on 29 June 2022, announced its reverse merger with CEBBCO. Therefore, with this, the company completed its listing on the bourses.

==== Freeze-drying ==== This method is the most expensive out of all dehydration methods but provides the advantage of long stable shelf life at room temperature and an excellent retention of soluble nutrients (nitrogen protein and other solids). The product undergoes quick freeze at 10 °C (50 °F) and is then dried at a moderate temperature inside a strong vacuum. Due to the expensive nature of the equipment, the final product price is higher than tempeh preserved through other methods.

Sources: en.wikipedia.org

Background from the literature

== Inhibition of glycolytic pathway == The impairment of glucose metabolism by fatty acid oxidation is mediated by the short-term inhibition of several glycolytic processes. The extent of inhibition increases along the glycolytic pathway, being most severe at the level of pyruvate dehydrogenase and less severe at the level of glucose uptake and 6-phosphofructo-1-kinase (PFK-1). This sequence occurs because of the initial event, triggered by fatty acid oxidation, is an increase in the mitochondrial ratios of [acetyl-CoA]/[CoA] and [NADH]/[NAD+]. These both serve to inhibit pyruvate dehydrogenase activity. It has been proposed that these changes lead to an accumulation of cytosolic citrate, which in turn inhibits PFK-1, followed by an increase in glucose 6-phosphate, which eventually inhibits hexokinase.

Over the shah's indifference, Domantovich and his Cossacks worked hard on training the Cossack Brigade, which became the only disciplined unit in the entire Persian Army, and thus of considerable importance in maintaining the shah's authority.

=== Regulation === Glucose-6-phosphate dehydrogenase is the rate-controlling enzyme of this pathway. It is allosterically stimulated by NADP+ and strongly inhibited by NADPH. The ratio of NADPH:NADP+ is the primary mode of regulation for the enzyme and is normally about 100:1 in liver cytosol. This makes the cytosol a highly-reducing environment. An NADPH-utilizing pathway forms NADP+, which stimulates Glucose-6-phosphate dehydrogenase to produce more NADPH. This step is also inhibited by acetyl CoA. G6PD activity is also post-translationally regulated by cytoplasmic deacetylase SIRT2. SIRT2-mediated deacetylation and activation of G6PD stimulates oxidative branch of PPP to supply cytosolic NADPH to counteract oxidative damage or support de novo lipogenesis.

== Function == HIV-1 PR serves a dual purpose. Precursor HIV-1 PR is responsible for catalyzing its own production into mature PR enzymes via PR auto-processing. Mature protease is able to hydrolyze peptide bonds on the Gag-Pol polyproteins at nine specific sites, processing the resulting subunits into mature, fully functional proteins. These cleaved proteins, including reverse transcriptase, integrase, and RNaseH, are encoded by the coding region components necessary for viral replication.

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.

What is SR9009?

It is a synthetic REV-ERB agonist used mainly in preclinical research. It is not an approved medicine for human use.

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