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Sr9009 Identity And Mechanism — Quick Reference

By Editorial Desk · published 2026-07-06 · last reviewed 2026-08-01 · Blog

REV-ERB agonist 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 2026-08-01. Where a claim depends on a specific study, the study is described rather than over-claimed.

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.

Mechanism and Preclinical Findings

Preclinical reports have linked SR9009 to improved endurance and altered energy expenditure in rodents. Such findings have prompted interest in whether REV-ERB activation can influence skeletal muscle metabolism. However, the reported effects depend on dose, route, and experimental model, and replication across laboratories is limited. Human trials have not established comparable outcomes, so claims about exercise performance remain speculative. The absence of controlled human data is a central limitation in interpreting these observations.

The mechanism of action involves binding to REV-ERB receptors and recruiting corepressor complexes, which represses target gene transcription. This contrasts with many nuclear receptor agonists that activate transcription. Downstream effects may include changes in autophagy, mitochondrial biogenesis, and lipid handling, but the precise pathways remain an active area of study. Whether these molecular events translate into meaningful physiological effects in humans is unresolved. Most evidence comes from cultured cells and rodent models rather than human participants.

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 Pharmacological Mechanism

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.

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.

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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.

SR9009 is frequently discussed in fitness and research-chemical contexts, yet it has no approved medical indication. Regulatory agencies have not authorized it for human use, and it is not a standard prescription drug. Some sports organizations list it as a prohibited substance because of its potential performance-enhancing properties. Published human data are sparse, so claims about its effects in people often rely on animal models or anecdotal reports. Quality and identity of online materials can vary widely.

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.

Supporting material

==== History ==== Initially the countercurrent exchange mechanism and its properties were proposed in 1951 by professor Werner Kuhn and two of his former students who called the mechanism found in the loop of Henle in mammalian kidneys a Countercurrent multiplier and confirmed by laboratory findings in 1958 by Professor Carl W. Gottschalk. The theory was acknowledged a year later after a meticulous study showed that there is almost no osmotic difference between liquids on both sides of nephrons. Homer Smith, a considerable contemporary authority on renal physiology, opposed the model countercurrent concentration for 8 years, until conceding ground in 1959. Ever since, many similar mechanisms have been found in biologic systems, the most notable of these: the rete mirabile in fish.

(1886), lawyer and stockbroker, grandfather of Jacqueline Kennedy Onassis, Lee Radziwill and Edith Bouvier Beale Benjamin Cardozo (1889), associate justice of the U.S. Supreme Court William Bondy (1890), judge on the United States District Court for the Southern District of New York Irving Lehman (1896), chief judge of the New York Court of Appeals, son of Mayer Lehman and member of the Lehman family Joseph M. Proskauer (1896), lawyer, judge, co-founder of international law firm Proskauer Rose Frederic Kimber Seward (1899), corporate lawyer and Titanic survivor Arthur Garfield Hays (1902), counsel for the American Civil Liberties Union and lawyer in the Scopes Trial Benjamin Kaye (1904), lawyer, playwright, co-founder of international law firm Kaye Scholer George Z. Medalie (1905), United States Attorney for the Southern District of New York 1931–1933; Republican nominee for the United States Senate in New York in 1932 Irwin Untermyer (1907), jurist, civic leader, son of Samuel Untermyer Alexander Holtzoff (1908), judge on the United States District Court for the District of Columbia Paul Windels (1908), former Corporation Counsel of New York City and co-founder of the Lycée Français de New York Emil N. Baar (1913), New York Supreme Court justice and former chairman of the Union of American Hebrew Congregations Albert Levitt (1913), judge on the District Court of the Virgin Islands Peter I. B. Lavan (1915), lawyer and philanthropist and namesake of Stroock & Stroock & Lavan Raymond L.

The CAP Foundation is the philanthropic arm of the organization and is classified as a 501(c)(3) charitable entity. Its flagship program, See, Test & Treat, partners with hospitals and clinicians to provide free cancer and HPV screening, as well as educational events, to underserved communities. The program served over 900 women in 2017.

== Safety == TCFH does not irritate skin but is a potent eye irritant. The sensitization potential of TCFH was shown to be low compared to other amide bond forming agents, which can be used in the context of peptide synthesis (it is non-sensitizing at 1% in the local lymph node assay according to OECD 429). The major by-product of using TCFH is tetramethylurea, which has demonstrated teratogenic activity in several laboratory animal species.

Sources: en.wikipedia.org

Notes from published material

The condition, or types of it, has had various other names over the years and in different nations; "osteogenesis imperfecta" has, however, been the most widely accepted name for the condition since the late 20th century. Among some of the most common alternatives are "fragilitas ossium"; "Ekman–Lobstein syndrome", and "Vrolik syndrome", both eponyms; and, the colloquialism, "brittle bone disease".

== Research == Research studying the safety and efficacy of corneal cross-linking is ongoing. Transepithelial or epithelium-on (epi-on) cross-linking is a technique which was first performed in 2004 in the U.S., the corneal epithelium layer is left intact. in this technique, because the epithelium is not removed, riboflavin loading requires more time than with epi-off techniques, and may be less effective, as keratoconus progression may be more likely in epi-on procedures. Contact lens-assisted cross-linking (CACXL) may be performed for people with corneal stromal thickness between 350 μm to 400 μm after epithelial removal. in this method a pre-corneal riboflavin film, a riboflavin-soaked UV barrier-free soft contact lens of negligible power and a pre-contact lens riboflavin film are used to decrease UV irradiance to safe levels at the level of the endothelium. Topography-guided crosslinking relies on an active eye tracker to allow a patterned delivery of UV light. Both the power and pattern can be programmed into the unit based on the topography of the individual's eyes. Accelerated crosslinking allows a shorter treatment time by delivering the same energy more quickly, compared to the standard crosslinking procedure, which involves 3 mW of UV-A exposure for 30 minutes. Some hospitals are using this accelerated CXL technique delivering a similar amount of UV-A energy in eight to ten minutes, following research showing the cornea may better tolerate this shorter burst of UV-A.

=== Osteocyte === Osteocytes are cells of mesenchymal origin and originate from osteoblasts that have migrated into and become trapped and surrounded by a bone matrix that they themselves produced. The spaces the cell body of osteocytes occupy within the mineralized collagen type I matrix are known as lacunae, while the osteocyte cell processes occupy channels called canaliculi. The many processes of osteocytes reach out to meet osteoblasts, osteoclasts, bone lining cells, and other osteocytes probably for the purposes of communication. Osteocytes remain in contact with other osteocytes in the bone through gap junctions—coupled cell processes which pass through the canalicular channels.

Sources: en.wikipedia.org

Background from the literature

Osavampator (developmental code names TAK-653 and NBI-1065845) is an experimental drug being investigated as a treatment for treatment-resistant depression. It is being developed by Neurocrine Biosciences and Takeda Pharmaceuticals (Millennium Pharmaceuticals, Inc.). Takeda Pharmaceuticals discovered the molecule originally, and holds exclusive right to market the drug in Japan, while Neurocrine Biosciences holds the right to market it to the rest of the world.

21 May The WHO informs about the international 2022 monkeypox outbreak in non-endemic countries – an unprecedented number of cases detected outside of Africa after the first of these cases was detected on 6 May. On 24 May, the WHO states that the outbreak can be contained. The main method used for the early containment is 'ring vaccination' – vaccinating close contacts of positive cases via existing vaccines. 23 May Researchers report that CRISPR-Cas9 gene editing has been used to boost vitamin D in tomatoes. A study shows why decarbonization must be accompanied by strategies to reduce the levels of short-lived climate pollutants with near-term effects for climate goals. 24 May Scientists report the first 3D-printed lab-grown wood. It is unclear if it could ever be used on a commercial scale (e.g. with sufficient production efficiency and quality). A CDC study based on electronic health records shows that "one in five COVID-19 survivors aged 18–64 years and one in four survivors aged ≥65 years experienced at least one incident condition that might be attributable to previous COVID-19" or long COVID. On 18 May, an analysis of private healthcare claims shows that of 78,252 patients diagnosed with 'long COVID', 75.8% had not been hospitalized for COVID-19. 25 May – The world's smallest remote-controlled walking robot, measuring just half a millimetre wide, is demonstrated. Potential applications include the clearing of blocked arteries.

=== Marriage and family === In 1937, Dorothy Crowfoot married Thomas Lionel Hodgkin, an historian's son, who was then teaching an adult-education class in mining and industrial communities in the north of England after he resigned from the Colonial Office. He was an intermittent member of the Communist Party and later wrote several major works on African politics and history, becoming a well-known lecturer at Balliol College in Oxford. As his health was too poor for active military service, he continued working throughout World War II, returning to Oxford on the weekends, where his wife remained working on penicillin. The couple had three children: Luke (1938 – October 2020), Elizabeth (born 1941) and Toby (born 1946). The oldest son, Luke, became a mathematics instructor at the new University of Warwick. Their daughter, Elizabeth, followed her father's career as a historian. Their younger son, Toby, studied botany and agriculture. Overall, Thomas Hodgkin spent extended periods of time in West Africa, where he was an enthusiastic supporter and chronicler of the emerging postcolonial states. Thomas Hodgkin died in Greece on 25 March 1982.

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 compound that acts as an agonist at REV-ERBα and REV-ERBβ. It is used mainly as a research chemical to study circadian and metabolic pathways. It is not approved for human therapeutic use.

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