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Sr9009 Identity And Mechanism — Hands-On Walkthrough

By Editorial Desk · published 2025-12-07 · last reviewed 2026-01-03 · Guide

The short version of REV-ERB agonist fits in a sentence. The long version — which is the one that helps — is below.

Reviewed 2026-01-03. 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.

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.

Detection, Regulation, and Misconceptions

Regulatory agencies have not approved SR9009 for human therapeutic use. It is typically sold as a research chemical with labels stating that it is not for human consumption. The World Anti-Doping Agency prohibits the substance in sport, generally under the category of non-approved substances. Customs and national laws may restrict importation, sale, or possession. Product quality and legal status can vary by country and vendor, and therapeutic claims are not permitted in regulated advertising because the compound lacks approval.

Several misconceptions surround SR9009. It is often described as a SARM, a steroid, or an exercise pill, but its known target is the REV-ERB receptor family. Rodent studies have examined exercise capacity and metabolic markers, yet human outcomes remain unproven. Oral bioavailability appears low in animals, and human pharmacokinetics are not well characterized. Online products may contain impurities or different compounds, so identity and purity testing are important for research use.

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 Receptor Mechanism

Because REV-ERB receptors are core clock components, SR9009 has been examined for effects on daily rhythms as well as metabolism. Research has explored whether the compound can shift or reinforce circadian gene expression in tissues such as liver and muscle. Some studies report improved metabolic markers in obese or diabetic mice, while others show context-dependent responses. Questions remain about which effects are direct, which are secondary to timing, and how they might differ across species.

SR9009 is a synthetic small molecule studied as an agonist of REV-ERB nuclear receptors. REV-ERB alpha and REV-ERB beta help regulate circadian rhythms and metabolic gene expression. In laboratory research, SR9009 has been used to probe how these receptors affect skeletal muscle, liver, and adipose tissue. The compound was identified in academic drug-discovery work and is often described in scientific literature by its chemical name and research code. It is not an approved medicine, and human clinical data remain limited or absent.

SR9009 binds REV-ERB receptors and alters their repressive activity on target genes. This action can change transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. In rodent studies, treated animals have shown changes in muscle oxidative capacity and exercise performance, though effects vary by dose, duration, and model. The precise molecular steps connecting receptor binding to whole-body outcomes are still an active area of investigation. Findings in animals do not automatically translate to humans.

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Background and Mechanism of SR9009

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.

Analytical Detection and Stability

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.

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.

Further detail

7027/2022, which raises to ₲ 7000 million the reward for information on the whereabouts of the kidnapped citizens Edelio Morínigo, Félix Urbieta, and Óscar Denis. The decree authorizes the Ministry of the Interior to make partial or total payments, depending on the quality and truthfulness of the information, through confidential funds. The rule establishes that any citizen may provide useful information, except public officials of security and justice institutions, or their relatives up to the fifth degree of consanguinity. Confidentiality of sources is guaranteed, and false information is to be reported to the Public Ministry.

== Bibliography == Kardashian, Kim; Kardashian, Kourtney; Kardashian, Khloé (2010). Kardashian Konfidential. St. Martin's Press. ISBN 978-0-312-62807-9. Kardashian, Kim; Kardashian, Kourtney; Kardashian, Khloé (2011). Dollhouse. William Morrow. ISBN 9780062063847. Kardashian, Khloe (2015). Strong Looks Better Naked. Regan Arts. ISBN 9781682450772.

=== 1950–2000 === In the 1950s, thiazide diuretics were developed by Merck scientists Karl H. Beyer, James M. Sprague, John E. Baer, and Frederick C. Novello and led to the marketing of the first drug of this class, chlorothiazide, under the trade name Diuril in 1958. The research leading to the discovery of chlorothiazide, leading to "the saving of untold thousands of lives and the alleviation of the suffering of millions of victims of hypertension" was recognized by a special Public Health Award from the Lasker Foundation in 1975. In 1953, Merck & Co. merged with Philadelphia-based Sharp & Dohme, Inc., becoming the largest U.S. drugmaker. Sharp and Dohme had acquired H. K. Mulford Company in 1929, adding smallpox vaccines to its portfolio. The combined company kept the trade name Merck in the United States and Canada, and as Merck Sharp & Dohme (MSD) outside these two countries. In 1965, Merck & Co. acquired Charles Frosst Ltd. of Montreal (founded 1899), creating Merck-Frosst Canada, Inc., as its Canadian subsidiary and pharmaceutical research facility. Merck & Co. closed this facility in July 2010 but reemerged in 2011 as Merck Canada. Maurice Hilleman, a scientist at Merck, developed the first mumps vaccine in 1967, the first rubella vaccine in 1969, and the first trivalent measles, mumps, rubella (MMR vaccine) in 1971. The incidence of rubella-associated birth defects fell from up to 10,000 per year in the U.S. to zero in the aftermath of the rubella vaccine's development.

== Abundance == Reversible phosphorylation of proteins is abundant in both prokaryotic and even more so in eukaryotic organisms. For instance, in bacteria 5–10% of all proteins are thought to be phosphorylated. By contrast, it is estimated that one third of all human proteins is phosphorylated at any point in time, with 230,000, 156,000, and 40,000 unique phosphorylation sites existing in human, mouse, and yeast, respectively. In yeast, about 120 kinases (out of ~6,000 proteins total) cause 8,814 known regulated phosphorylation events, generating about 3,600 phosphoproteins (about 60% of all yeast proteins). Hence, phosphorylation is a universal regulatory mechanism that affects a large portion of proteins. Even if a protein is not phosphorylated itself, its interactions with other proteins may be regulated by phosphorylation of these interacting proteins.

Sources: en.wikipedia.org

Background from the literature

DDP-116 – the first of the Series 16 DDP-124 – part of a trio of 24-bit systems: DDP-24, 124, 224. Honeywell bought the company after the 24 trio, and built the balance of the Series 16. The Honeywell 516 was used in the NPL network for the first implementation of packet switching in early 1969. The 516 and later the 316 were also used as Interface Message Processors (IMP) for the ARPANET. In addition, it was later configured as a Terminal IMP (TIP), which added support for up to 63 teletype machines through a multi-line controller. The H-316 was used by Charles H. Moore to develop the first complete, stand-alone implementation of Forth at NRAO in 1971. The original Prime computers were designed to be compatible with the Series-16 minicomputers. The Honeywell 316 also had industrial applications. A 316 was used at Bradwell nuclear power station in Essex as the primary reactor temperature-monitoring computer until summer 2000, when the internal 160k disk failed. Two PDP-11/70s, which had previously been secondary monitors, were moved to primary.

== Early life and education == Balalaie was born on 26 September 1965 in Rasht, Gilan Province, Iran. He completed his undergraduate studies in Chemistry at the University of Tehran (1984–1989), followed by a Master of Science degree in Organic Chemistry from Shahid Beheshti University (1989–1991). He earned his Ph.D. in Organic Chemistry from Sharif University of Technology (1992–1996), where he worked on "Photooxygenation of organic compounds by singlet oxygen" under the supervision of Professor Mohammad Mahmoudi Hashemi. During his doctoral studies, he spent six months as a visiting researcher in Germany working with Professor Junes Ipaktschi.

=== Modifiable === Western pattern diet Abdominal obesity Diabetes Dyslipidemia High blood cholesterol High blood pressure Elevated concentrations of apolipoprotein B (ApoB)-containing lipoproteins (such as LDL particles), for which LDL-cholesterol (LDL-C) is the most commonly used surrogate marker High saturated fat diet Trans fat Tobacco smoking Bacterial infections HIV/AIDS Psychological stress Sedentary lifestyle

Natural fibers are also used in composite materials, much like synthetic or glass fibers. These composites, called biocomposites, are a natural fiber in a matrix of synthetic polymers. One of the first biofiber-reinforced plastics in use was a cellulose fiber in phenolics in 1908. Usage includes applications where energy absorption is important, such as insulation, noise absorbing panels, or collapsable areas in automobiles. Natural fibers can have different advantages over synthetic reinforcing fibers. Most notably they are biodegradable and renewable. Additionally, they often have low densities and lower processing costs than synthetic materials. Design issues with natural fiber-reinforced composites include poor strength (natural fibers are not as strong as glass fibers) and difficulty with actually bonding the fibers and the matrix. Hydrophobic polymer matrices offer insufficient adhesion for hydrophilic fibers.

=== Arthrochalasia === Arthrochalasia EDS (aEDS; formerly categorized as types 7A and B) is characterized by severe joint hypermobility and congenital hip dislocation. Other common features include fragile, elastic skin with easy bruising, hypotonia, kyphoscoliosis (kyphosis and scoliosis), and mild osteopenia. Type-I collagen is usually affected. It is very rare, with about 30 cases reported. It is more severe than the hypermobility type. Variations in the genes COL1A1 and COL1A2 cause it.

Sources: en.wikipedia.org

Reference notes

=== Barbiturates === Barbiturates are powerful anxiolytics but the risk of abuse and addiction is high. Many experts consider these drugs obsolete for treating anxiety but valuable for the short-term treatment of severe insomnia, though only after benzodiazepines or non-benzodiazepines have failed.

== Research == Metreleptin is being investigated for the treatment of diabetes and/or hypertriglyceridemia, in patients with rare forms of lipodystrophy, syndromes characterized by abnormalities in adipose tissue distribution, and severe metabolic abnormalities. The FDA approved Metreleptin injection for treating complications of leptin deficiency in February 2014. In a three-year study of metreleptin in patients with lipodystrophy organized by the National Institute of Diabetes and Digestive and Kidney Diseases at the National Institutes of Health, metreleptin treatment was associated with a significant decrease in blood glucose (A1c decreased from 9.4% at baseline to 7.0% at study end) and triglyceride concentration (from 500 mg/dl at baseline to 200 mg/dl at study end). Metreleptin is effective in most patients with generalized lipodystrophy where circulating leptin levels are extremely low. Analogous to insulin replacement for patients with type 1 diabetes, metreleptin restores the function of a deficient hormone. However, in patients with partial lipodystrophy where there is only a relative leptin deficiency, the response to metreleptin is not universal. This may or may not be due to anti-leptin antibodies. Metreleptin is undergoing research for its potential benefit in the treatment of anorexia nervosa. It is hypothesized that the gradual loss of body fat mass, and more specifically the ensuing low leptin levels, escalate the preexisting drive for thinness into an obsessive-compulsive-like and addictive-like state.

After a fire at the Washington National Records Center, unclassified, non-privacy-protected, water-damaged records were frozen on site and vacuum freeze-dried off site; most of the paper-based records looked essentially the same after drying.

== Pathology == The main activity of activation of the insulin receptor is inducing glucose uptake. For this reason "insulin insensitivity", or a decrease in insulin receptor signaling, leads to diabetes mellitus type 2 – the cells are unable to take up glucose, and the result is hyperglycemia (an increase in circulating glucose), and all the sequelae that result from diabetes. Patients with insulin resistance may display acanthosis nigricans. A few patients with homozygous mutations in the INSR gene have been described, which causes Donohue syndrome or Leprechaunism. This autosomal recessive disorder results in a totally non-functional insulin receptor. These patients have low-set, often protuberant, ears, flared nostrils, thickened lips, and severe growth retardation. In most cases, the outlook for these patients is extremely poor, with death occurring within the first year of life. Other mutations of the same gene cause the less severe Rabson-Mendenhall syndrome, in which patients have characteristically abnormal teeth, hypertrophic gingiva (gums), and enlargement of the pineal gland. Both diseases present with fluctuations of the glucose level: After a meal the glucose is initially very high, and then falls rapidly to abnormally low levels. Other genetic mutations to the insulin receptor gene can cause Severe Insulin Resistance.

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 to buy?

Legality depends on the country and the intended use. In many places it is not approved as a medicine and may be sold only as a research chemical. Importation or possession can be restricted, and sports organizations prohibit it.

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