A practical reference on SR9009: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
Reviewed 2026-02-28. Anything still debated is marked as such rather than presented as settled.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Common name | SR9009 | Also marketed informally as Stenabolic |
| Chemical class | Synthetic REV-ERB agonist | Binds REV-ERBα and REV-ERBβ |
| Molecular formula | C24H30ClN3O4S | Approximate molecular weight 492 g/mol |
| CAS Registry Number | 1379686-30-2 | Identifier for the parent compound |
| Regulatory status | Not approved for human use | Prohibited in sport by WADA |
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 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.
==== No small parameter ==== The competition between energy and entropy makes liquids difficult to model at the molecular level, as there is no idealized "reference state" that can serve as a starting point for tractable theoretical descriptions. Mathematically, there is no small parameter from which one can develop a systematic perturbation theory. This situation contrasts with both gases and solids. For gases, the reference state is the ideal gas, and the density can be used as a small parameter to construct a theory of real (nonideal) gases (see virial expansion). For crystalline solids, the reference state is a perfect crystalline lattice, and possible small parameters are thermal motions and lattice defects.
On 3 January 2026, the United States launched a military strike in Venezuela and captured incumbent Venezuelan president Nicolás Maduro and his wife, Cilia Flores. The US operation, codenamed Operation Absolute Resolve, began around 2 a.m. local time, when explosions were observed. The US Armed Forces bombed infrastructure across northern Venezuela to suppress air defenses as an apprehension force attacked Maduro's compound in Caracas. Approximately 80 people, including Venezuelan and Cuban military and civilians, died and seven American soldiers were wounded. Maduro and Flores were transported to New York City by US forces and were indicted on drug trafficking charges to which Maduro and Flores pleaded not guilty. US president Donald Trump and his administration justified the operation as a law-enforcement action with military support, saying that the president has "inherent constitutional authority" to undertake such an act. Venezuelan vice president Delcy Rodríguez denounced Maduro's "kidnapping". Venezuelan officials said at least 23 Venezuelan security officers were killed during the attack. The Cuban government said that 32 members of the Cuban military and intelligence agencies were killed. Officials in the United Nations (UN), the US, and other countries, as well as international law experts said the raid violated the UN Charter and Venezuela's sovereignty. Other reactions around the world included celebrations by the Venezuelan diaspora and protests against the attack.
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Sources: en.wikipedia.org
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Olaf College Elio Di Rupo (born 1951), Prime Minister of Belgium Israel Shahak (1933–2001), Israeli chemist and civil-rights activist Margaret Thatcher (1925–2013), Prime Minister of the United Kingdom (1979–1990), research chemist at BX Plastics
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Sources: en.wikipedia.org
==== Breakdown of blood-nerve barrier ==== Intraneural blood vessels, similar to other microvessels in the human body, increase their permeability in response to stress. During extended periods of metabolic stress, such as ischema caused by compression, the blood-nerve-barrier will increase in permeability. This increase in the permeability in the blood-nerve-barrier is the first pathological symptom observed during compression studies.
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Sources: en.wikipedia.org
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.
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.
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.
It is a synthetic REV-ERB agonist used mainly in preclinical research. It is not an approved medicine for human use.