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Sr9009 Identity And Mechanism — Reference Sheet

By Editorial Desk · published 2026-04-06 · last reviewed 2026-04-23 · Blog

Everything below concerns circadian rhythm. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.

Updated 2026-04-23. Numbers and descriptions here follow the published literature rather than marketing material.

SR9009 Identity and Mechanism

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.

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.

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 is a synthetic small molecule developed as an agonist of the nuclear receptors REV-ERBα (NR1D1) and REV-ERBβ (NR1D2). These receptors help regulate circadian rhythms and metabolic gene expression. In cell and animal studies, SR9009 alters transcription of genes involved in lipid metabolism, inflammation, and mitochondrial function. It is not an approved medicine, and its pharmacological profile in humans remains largely uncharacterized. The compound is frequently discussed in the context of circadian biology and metabolic research rather than clinical 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

Background and Pharmacological Mechanism

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 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.

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Background and Mechanism of SR9009

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.

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.

Background and Receptor Mechanism

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.

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.

SR9009 Background and Mechanism

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.

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.

Background from the literature

Military AI usage attempts to enhance command and control, communications, sensors, integration and interoperability. Intelligence collection and analysis, logistics, cyber operations, information operations, and semiautonomous and autonomous vehicles are being researched. AI technologies are used in coordination of sensors and effectors, threat detection and identification, marking of enemy positions, target acquisition, coordination and deconfliction of distributed Joint Fires between networked combat vehicles, both human-operated and autonomous. AI has been used in military operations in Iraq, Syria, Israel and Ukraine.

(2026) study the morphology of hominin limb bones from the Salawusu site (China), finding no evidence of diagnostic features of the Neanderthal lineage, and reporting morphological evidence consistent with affinities with modern humans. Li et al. (2026) report evidence from the study of the palynological record from the East China Sea continental shelf spanning the past 71,000 years indicative of presence of a cool, dry temperate grassland biome during the lowstand intervals (including the Last Glacial Maximum), as well as evidence of presence of an open-forest landscape during the milder conditions of the Marine Isotope Stage 3, and interpret their findings as supporting the interpretation of the exposed East China Sea continental shelf as a habitat facilitating the initial dispersal of early modern humans into East Asia. Zhang et al. (2026) study the features of stone tools from the Nwya Devu site (China), reporting evidence of differences from stone tool assemblages from northern Initial Upper Paleolithic sites, and interpret tools from the Nwya Devu site as either representing a regional variant of Initial Upper Paleolithic technology or resulting from a separate dispersal of blade technologies into East Asia. Totsuka et al. (2026) reconstruct the chronology of early Upper Paleolithic sites in Japan, and report evidence of rapid increase in the number of sites between 36,000 and 34,000 years ago that was likely linked to growth of the human population size. Oktaviana et al.

The hydrocarbon-generating potential and thermal maturity of petroleum source rocks are commonly evaluated using Rock-Eval pyrolysis and vitrinite reflectance measurements, which provide quantitative indicators of organic matter type, maturation level, and the likelihood of oil or gas generation. Catagenesis was pyrolytic despite the fact that it happened at relatively low temperatures (when compared to commercial pyrolysis plants) of 60 to several hundred °C. Pyrolysis was possible because of the long reaction times involved. Heat for catagenesis came from the decomposition of radioactive materials of the crust, especially 40K, 232Th, 235U and 238U. The heat varied with geothermal gradient and was typically 10–30 °C per km of depth from the Earth's surface. Unusual magma intrusions, however, could have created greater localized heating.

==== Member of the Order of the British Empire (MBE) ==== Civil Division Harcourt Thomas Bastian. For services to the economic development of the country. Fannie Suzanne Bethel, . For services to education and the community. Wilton Eric Darville. For services as a public officer and a trade unionist. Loretta Minnis. For services to education. Lamour Rolle. For community service to the Island of Bimini. Felix Nathaniel Stubbs. For services to the community, especially to youth.

Sources: en.wikipedia.org

Reference notes

June 9, 2010: Law on the creation of childcare assistant centers and various provisions relating to childcare assistants. July 9, 2010: Law on violence specifically against women, domestic violence, and the impact of such violence on children. September 28, 2010: Law aimed at combating school absenteeism. October 11, 2010: Law banning the concealment of the face in public spaces. November 9, 2010: Pension reform law. January 27, 2011: Law on the balanced representation of women and men on boards of directors and supervisory boards, and on professional equality. May 24, 2011: Decree establishing a Commission on the image of women in the media. July 7, 2011: Law on bioethics. March 12, 2012: Law on access to permanent employment and improving working conditions for contract agents in the civil service, combating discrimination, and various civil service provisions. May 24, 2012: Decree on the responsibilities of the Minister for Women's Rights. August 6, 2012: Law on sexual harassment. September 28, 2012: Decree on the Interministerial Committee on Women's Rights and Gender Equality. November 30, 2012: The Interministerial Committee on Women's Rights establishes a 4-year action plan, prioritizing women's rights in public policies. December 17, 2012: Social Security Financing Law for 2013, including provisions on paternity leave. December 18, 2012: Decree on the implementation of corporate obligations regarding professional equality between women and men.

In both meetings, according to him, "the good relations between Brazil and the Holy See and the harmonious collaboration between Church and State in favour of the promotion of moral values and the common good" were highlighted.

The decreased oxytocin receptor levels were associated with behavioral changes including increased aggression and anxiety-like behavior, hyperactivity, and diminished social behaviors and memory. Exogenous administration of oxytocin receptor agonists like oxytocin or TGOT was able to partially reverse the behavioral changes. Fecal microbiota transplant from people with social anxiety disorder into rodents caused selective social anxiety-like symptoms in the rodents. This was associated with brain oxytocinergic abnormalities, including decreased expression of the oxytocin receptor. Lactobacillus reuteri has been found to increase oxytocinergic signaling in rodents, with its metabolite ergothioneine reducing social avoidance behavior. Conversely, propionic acid (propionate), which is produced by certain gut bacteria and is increased by social isolation, has been found to induce social deficits and anxiety in rodents, with this being associated with decreased oxytocin receptor expression. In some mammals, oxytocin receptors are also found in the kidney and heart.

== History == Amanita muscaria has been used by humans as a psychoactive drug since ancient times. Muscimol was isolated from Amanita muscaria independently by three different research groups in 1964 and 1965. It was synthesized by Gagneux and colleagues in 1965. The chemical structure of muscimol, along with that of ibotenic acid, was published by Conrad Eugster at the University of Zurich in 1967. Its structural similarity to the neurotransmitter γ-aminobutyric acid (GABA) was quickly recognized and muscimol was shown to have GABA-like actions by Graham Johnston and colleagues in 1968. Subsequently, its actions were shown to be reversed by the GABA receptor antagonist bicuculline in 1971. The effects of muscimol in humans were studied and described by Waser in 1967. Later, ethnobotanist Jonathan Ott further described the effects of muscimol, via Amanita pantherina consumption, in 1976. Danish medicinal chemist Povl Krogsgaard-Larsen and colleagues studied muscimol and synthetic analogues over several decades starting in the 1970s. Other GABAA receptor ligands, such as gaboxadol (THIP) and 4-PIOL, and GABA transporter modulators, such as nipecotic acid and tiagabine, have been derived from muscimol. Many muscimol analogues were developed by Krogsgaard-Larsen and colleagues. Muscimol was encountered online as a novel designer drug in 2023.

== Background == Degeneracy of the genetic code was identified by Lagerkvist. For instance, codons GAA and GAG both specify glutamic acid and exhibit redundancy; but, neither specifies any other amino acid and thus are not ambiguous or demonstrate no ambiguity. The codons encoding one amino acid may differ in any of their three positions; however, more often than not, this difference is in the second or third position. For instance, the amino acid glutamic acid is specified by GAA and GAG codons (difference in the third position); the amino acid leucine is specified by UUA, UUG, CUU, CUC, CUA, CUG codons (difference in the first or third position); and the amino acid serine is specified by UCA, UCG, UCC, UCU, AGU, AGC (difference in the first, second, or third position). Degeneracy results because there are more codons than encodable amino acids. For example, if there were two bases per codon, then only 16 amino acids could be coded for (4²=16). Because at least 21 codes are required (20 amino acids plus stop) and the next largest number of bases is three, then 4³ gives 64 possible codons, meaning that some degeneracy must exist.

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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