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Background And Mechanism Of Sr9009 — Deep Dive

By Editorial Desk · published 2026-07-15 · last reviewed 2026-08-01 · Info

SR9009 raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.

This page was last updated on 2026-08-01 and is reviewed periodically as new material appears.

Background and Mechanism of SR9009

SR9009 is a synthetic small molecule studied as a REV-ERB agonist. REV-ERBα and REV-ERBβ are nuclear receptors that help regulate circadian rhythms and metabolic gene expression. The compound was identified in academic screening efforts to find synthetic ligands for these receptors. In cell and animal studies, SR9009 alters transcription of genes involved in lipid and glucose metabolism, and it can shift circadian behavior. It is not an approved therapeutic agent.

Mechanistically, SR9009 binds the ligand-binding domain of REV-ERBα/β and enhances recruitment of corepressor complexes. This represses target genes rather than activating them. Because REV-ERB proteins normally compete with ROR proteins at shared response elements, the net effect depends on tissue and timing. Researchers use SR9009 to probe how nuclear receptor signaling links the clock to metabolism, inflammation, and muscle biology. Findings are largely preclinical, and the precise contribution of each receptor subtype remains under study.

Background and Receptor Mechanism

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.

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.

Sr9009 at a glance

PropertyValueNotes
Chemical classSynthetic REV-ERB agonistSmall-molecule ligand; not a hormone or peptide
Molecular formulaC20H24ClN3O4SReported for the free base
CAS Registry Number1379686-30-2Unique chemical identifier
Common synonymsSR9009; stenabolicStenabolic is informal and not an official name
Reported targetsREV-ERBα and REV-ERBβNuclear receptors linked to circadian and metabolic regulation

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.

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.

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Background and Receptor Pharmacology

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.

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.

Background and Mechanism

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.

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.

Notes from published material

The ideal relationship between products and reactants in a chemical reaction can be obtained by using a chemical reaction equation. Stoichiometry is used to run calculations about chemical reactions, for example, the stoichiometric mole ratio between reactants and products. The stoichiometry of a chemical reaction is based on chemical formulas and equations that provide the quantitative relation between the number of moles of various products and reactants, including yields. Stoichiometric equations are used to determine the limiting reagent or reactant—the reactant that is completely consumed in a reaction. The limiting reagent determines the theoretical yield—the relative quantity of moles of reactants and the product formed in a chemical reaction. Other reactants are said to be present in excess. The actual yield—the quantity physically obtained from a chemical reaction conducted in a laboratory—is often less than the theoretical yield. The theoretical yield is what would be obtained if all of the limiting reagent reacted to give the product in question. A more accurate yield is measured based on how much product was actually produced versus how much could be produced. The ratio of the theoretical yield and the actual yield results in a percent yield. When more than one reactant participates in a reaction, the yield is usually calculated based on the amount of the limiting reactant, whose amount is less than stoichiometrically equivalent (or just equivalent) to the amounts of all other reactants present.

Hiroaki Suga (菅 裕明, born February 21, 1963) is a Japanese biochemist and businessman. He is best known for his work on artificial ribozymes (flexizymes) and their application in mRNA display (RaPID, random nonstandard peptide integrated discovery). Suga was awarded the 2023 Wolf Prize in Chemistry, jointly with Chuan He and Jeffery W. Kelly, "for pioneering discoveries that illuminate the functions and pathological dysfunctions of RNA and proteins and for creating strategies to harness the capabilities of these biopolymers in new ways to ameliorate human diseases."

immortalization The natural or artificial changing of a cell population with a normally finite lifespan into one with a hypothetically infinite lifespan, capable of dividing indefinitely without cellular senescence as long as essential nutrients are available and conditions are conducive for cell division. Cells that undergo such a change are said to be immortalized. Mutations that cause immortalization occur naturally in the neoplasms that cause cancer but can also be induced artificially, which makes it possible to culture certain cell lines in vitro for prolonged periods. Immortalized cell lines are thus broadly useful for experimental purposes and in many biotechnology applications. Immortalized eukaryotic cells are commonly obtained by isolating them from a naturally occurring neoplasm (as with the human HeLa cell line), or may be generated from normal cells by introducing viral genes (as with HEK 293 cells), by artificially overexpressing proteins required for immortality such as telomerase, or by fusing normal cells with cancer cells (as in the hybridoma technologies used in the commercial production of antibodies). Though stem cells are also capable of continuous self-renewal and are thus technically 'immortal', their immortalization is not abnormal because they are an ordinary part of the development of multicellular organisms.

Uptake into the postsynaptic compartment, Re-uptake into the presynaptic compartment, or Uptake into a third, nonneuronal compartment. Postsynaptic neurons remove little glutamate from the synapse. There is active reuptake into presynaptic neurons, but this mechanism appears to be less important than astrocytic transport. Astrocytes could dispose of transported glutamate in two ways. They could export it to blood capillaries, which abut the astrocyte foot processes. However, this strategy would result in a net loss of carbon and nitrogen from the system. An alternate approach would be to convert glutamate into another compound, preferably a non-neuroactive species. The advantage of this approach is that neuronal glutamate could be restored without the risk of trafficking the transmitter through extracellular fluid, where glutamate would cause neuronal depolarization. Astrocytes readily convert glutamate to glutamine via the glutamine synthetase pathway and released into the extracellular space. The glutamine is taken into the presynaptic terminals and metabolized into glutamate by the phosphate-activated glutaminase (a mitochondrial enzyme). The glutamate that is synthesized in the presynaptic terminal is packaged into synaptic vesicles by the glutamate transporter, VGLUT. Once the vesicle is released, glutamate is removed from the synaptic cleft by excitatory amino-acid transporters (EAATs).

Sources: en.wikipedia.org

Background from the literature

= 0.0546. Next, multiply this value of "K" by the time elapsed between the first and second measures of radioactivity, 19 hours: (0.0546 x 19) = 1.0368. Change the sign, to make it -1.0368, then find the "inverse Ln"; in this case 0.3546. This value is in the denominator of the decay correcting fraction, so it is the same as multiplying the numerator by its inverse (

==== Complex and Function of Membrane Protein in Cholesterol Homeostasis ==== As mentioned before, scientists Monika Suchanek, Anna Radzikowski, and Christoph Thiele wanted to study protein-protein interaction in their natural environment. Specifically, the membrane proteins (in a complex and are SCAP, Insig-1, and SREBP) that regulate cholesterol homeostasis so they wanted to know what their function was and the complex structure. What they had found was that using this photo-reactive amino acid was incorporated efficiently into the protein by mammalian cells, but did not need to use modified tRNAs (transfer RNA's) or AARS's (aminoacyl tRNA syntheses) which that allowed the specific cross-linking needed. This cross-linking could be determined by western blotting and they had discovered a direct interaction between Insig-1 and PGRMC1 (a progesterone-binding membrane protein). All four of the membrane proteins are found in the endoplasmic reticulum and the complex responds to low cholesterol levels. Cells (COS7) that had HA (hemagglutinin tagged PGRMC1) and Myc tagged Insig-1 were grown with and without photo-Met. In the presence of photo-Met, Insig-1 and SCAP had cross-linked with PGRMC1; specifically, Insig-1 cross-linked had a strong band. The cross-linking was detected by immunoprecipitating detergent-extracts with an antibody to HA then the precipitant was tested for Insig-1 using western blotting with the antibody for Myc.

June 25 2026 Utah wildfires: Utah Governor Spencer Cox announces a state of emergency and temporary restrictions on fireworks through the Fourth of July weekend until July 5 due to ongoing wildfires in the state, including the Cottonwood Fire. In Mullin v. Al Otro Lado, the U.S. Supreme Court rules 6–3 that migrants stopped on the Mexican side of the U.S.–Mexico border have not "arrived in the United States" for the purposes of federal immigration law, allowing the federal government to revive its "metering" policy for asylum seekers at border crossings. Florida Governor Ron DeSantis confirms that the Alligator Alcatraz detention center in Ochopee, Florida, will close operations, a year after it opened. June 26 Iran war: Trump accuses Iran of violating the truce with the US by launching drone attacks on ships in the Hormuz. The United States Central Command later announces that in retaliation to the alleged truce violations, the US hit Iranian missile and drone storage facilities, as well as coastal radar stations. Former national security adviser John Bolton pleads guilty to improperly retaining classified material. Flash floods hit Kentucky, leaving four dead. June 27 Iran war: The US military announces that it struck Iranian military surveillance infrastructure, communication systems, air defense sites, drone storage facilities, and minelayer capabilities at the commander-in-chief's direction in retaliation for an alleged Iranian attack against a ship in the Hormuz.

Sources: en.wikipedia.org

Further detail

== Personal life == Guillaume was married twice; first to Marlene Williams in 1955, with whom he had two sons. Guillaume's daughter was born in 1980. They divorced in 1984. He married Donna Brown in 1986. The couple had a daughter. He also fathered a daughter by a different mother, who was born in 1950. In 1999, Guillaume suffered a stroke while working on Sports Night at Walt Disney Studios in Burbank, California. The stroke was minor, causing relatively slight damage and little effect on his speech. After six weeks in the hospital, he underwent therapy consisting of walks and gym sessions.

Diacetyldihydromorphine (also known as Paralaudin, dihydroheroin, acetylmorphinol) is a potent opiate derivative developed in Germany in 1928 which is rarely used in some countries for the treatment of severe pain such as that caused by terminal cancer, as another form of diacetylmorphine (also commonly known as Heroin). Diacetyldihydromorphine is fast-acting and longer-lasting than diamorphine, with a duration of action of around 4–7 hours. As an ester/analogue of dihydromorphine, diacetyldihydromorphine is presumably a Schedule I/Narcotic controlled substance in the United States but does not have its own ACSCN or annual production quota. It does appear in the German Betäubungsmittelgesetz and other European controlled-substances laws. Diacetyldihydromorphine is quickly metabolized by plasma esterase enzymes into dihydromorphine, in the same way that diamorphine is metabolized into morphine. Diacetyldihydromorphine is roughly equipotent to morphine, where as diamorphine (heroin) is 1.50–1.80 times the potency of morphine. It shares with other opioids the risk of overdose or (potentially life-threatening) respiratory depression. When strong narcotics are required, and morphine and diamorphine are not an option, it is more common to use better known drugs such as nicomorphine, hydromorphone, levorphanol, oxymorphone or fentanyl which doctors will be more familiar with, and which do not share the stigma associated with either heroin or morphine.

In mid-January, Trump posted on his website Truth Social "NATO: Tell Denmark to get them out of here, NOW!" and reiterated false claims that the Danish Defence forces protecting Greenland consists of "two dogsleds". He said he would impose tariffs on countries that participated in Operation Arctic Endurance; a 10% import tariff would be imposed on Denmark, Norway, Sweden, France, Germany, the United Kingdom, the Netherlands, and Finland starting 1 February 2026, and it would increase to a 25% tariff on 1 June unless Denmark agreed to sell Greenland to the US. In a message to the Norwegian prime minister Jonas Gahr Støre, that Trump asked be shared widely with world leaders, Trump reiterated his demand for "Complete and Total Control of Greenland [sic]" and ascribed his own attitude therein to not being awarded the 2025 Nobel Peace Prize, writing that he no longer feels an "obligation to think purely of Peace". Støre said that "I have several times clearly explained to Trump what is well known, namely that it is an independent Nobel Committee, and not the Norwegian government, that awards the prize." The prize is awarded for laureates' work in the preceding year; Trump was not in office in 2024. On 19 January, Trump again refused to rule out invading Greenland and reiterated his tariff threats. On 20 January, Trump reiterated threats, stating that there is "no going back" on his plan to annex Greenland, claiming "Greenland is imperative for national and world security".

Sources: en.wikipedia.org

Frequently asked questions

What is SR9009?

SR9009 is a synthetic compound investigated as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is used in preclinical research on circadian rhythm and metabolism. It is not an approved drug.

Is SR9009 approved for human use?

No. It has no approved medical indication, and human safety and efficacy data are limited. It appears in research chemical markets and is banned by some sports authorities.

How does SR9009 differ from natural REV-ERB ligands?

Natural ligands include heme and certain metabolites; SR9009 is a synthetic small molecule with higher potency and selectivity in some assays. Its effects depend on cell type and timing. It is not a naturally occurring compound.

What is SR9009?

SR9009 is a synthetic research compound that activates the REV-ERBα and REV-ERBβ nuclear receptors. It is not an approved drug and has no established human therapeutic use. Most published biological data come from cell and rodent studies.

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