If you have been reading about NR1D1 and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Last reviewed on 2025-11-11. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C20H24ClN3O4S | Reported for the free base |
| Molecular weight | 437.9 g/mol | Calculated from the formula |
| Primary target | REV-ERBα and REV-ERBβ | Nuclear receptors involved in circadian regulation |
| Solubility | Soluble in DMSO and ethanol | Poorly soluble in water |
| Typical storage | -20 °C, desiccated | Protect from light and moisture |
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.
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.
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.
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.
Laboratory samples of SR9009 are typically handled as research chemicals rather than pharmaceuticals. Suppliers usually state that the material is for research use only and not for human or veterinary administration. Storage recommendations generally call for a freezer at approximately −20 °C, protection from light, and a desiccated environment. The solid is often described as a white to off-white powder. Solubility is commonly reported in organic solvents such as dimethyl sulfoxide and ethanol, with low solubility in water.
Analytical identification and purity assessment often use high-performance liquid chromatography with ultraviolet detection or mass spectrometry. Liquid chromatography–tandem mass spectrometry is used to detect and quantify SR9009 in biological matrices, including urine and blood, for anti-doping or pharmacokinetic studies. Nuclear magnetic resonance spectroscopy can confirm molecular structure. Stability depends on form and storage: the solid is generally more stable than solutions, and repeated freeze–thaw cycles may degrade samples. Purity is typically reported as a percentage from a certificate of analysis.
=== Advancements in fluid flow analysis === Inviscid flow was further analyzed by various mathematicians (Jean le Rond d'Alembert, Joseph Louis Lagrange, Pierre-Simon Laplace, Siméon Denis Poisson) and viscous flow was explored by a multitude of engineers including Jean Léonard Marie Poiseuille and Gotthilf Hagen. Further mathematical justification was provided by Claude-Louis Navier and George Gabriel Stokes in the Navier–Stokes equations, and boundary layers were investigated (Ludwig Prandtl, Theodore von Kármán), while various scientists such as Osborne Reynolds, Andrey Kolmogorov, and Geoffrey Ingram Taylor advanced the understanding of fluid viscosity and turbulence.
Fifteen minutes later Faith 7 landed just four miles (6 km) from the prime recovery ship, the carrier USS Kearsarge. This was the most accurate landing to date, despite the lack of automatic controls. Faith 7 landed 70 nautical miles (130 km) southeast of Midway Island, in the Pacific Ocean. This would be near 27°30′N 176°15′W. Splashdown was at 34 hours 19 minutes 49 seconds after liftoff. The spacecraft tipped over in the water momentarily, then righted itself. Helicopters dropped rescue swimmers and relayed Cooper's request of an Air Force officer for permission to be hoisted aboard the Navy's carrier. Permission was granted. Forty minutes later the explosive hatch blew open on the deck of Kearsarge. Cooper stepped out of Faith 7 to a warm greeting.
=== Toxicity evaluation === BPF is under preliminary research to determine its potential toxicity, which may include airway irritation if BPF dust is inhaled, and an allergic reaction if it is in contact with the skin.
Galloway told Ahmadinejad: "I have police protection in London from the Iranian opposition because of my support for your election campaign" in 2009. "I mention this so you know where I'm coming from." In May 2025, Galloway was awarded the Ismail Haniyeh Prize at the Iranian state-organized Sobh International Media Festival, named after the assassinated former chairman of Hamas. In his acceptance speech, he praised Iranian Supreme Leader Ali Khamenei, stating: "I thank the revolutionary people of Iran, your leadership, your heroes, and your martyrs for standing firm in support of the Palestinian people."
The mdx mouse has been at the forefront of CRISPR-Cas9 gene editing research for Duchenne muscular dystrophy. In 2014, the first successful correction of the dystrophin mutation using CRISPR-Cas9 was demonstrated directly in mdx mice, marking a historic milestone in gene editing therapy. In 2018, researchers used AAV-delivered CRISPR-Cas9 to restore dystrophin expression in mdx mice following a single systemic injection, demonstrating the remarkable potential of this approach. These results in mdx mice directly led to the first CRISPR-based clinical trials for DMD in human patients, representing a direct translation from mouse model to human medicine.
Sources: en.wikipedia.org
=== Kla Tham Party === Deputy Prime Minister Thamanat Prompow first noted that the results exceeded expectations, especially in northern Thailand. He remained confident that the party would surpass more than 50 seats, emphasizing how the ministers and candidates of the Kla Tham Party were actively working in their respective constituencies throughout the campaign. Thamanat remarked that the party was still waiting for an invitation from Bhumjaithai to renew their past coalition. The party finished with 58 seats, ahead of his forecast, but no invitation came and Kla Tham was left out of the government.
Angiogenesis, the formation of new blood vessels, is often critical for tumour cells to survive and grow in nutrient-depleted conditions. Akt is activated downstream of vascular endothelial growth factor (VEGF) in endothelial cells in the lining of blood vessels, promoting survival and growth. Akt also contributes to angiogenesis by activating endothelial nitric oxide synthase (eNOS), which increases production of nitric oxide (NO). This stimulates vasodilation and vascular remodelling. Signaling through the PI3K-Akt pathway increases translation of hypoxia-inducible factor α (HIF1α and HIF2α) transcription factors via mTOR. HIF promotes gene expression of VEGF and glycolytic enzymes, allowing metabolism in oxygen-depleted environments.
== Sodium-23 == Sodium-23 is the sole natural isotope of sodium, with an atomic mass of 22.98976928. Because of this, sodium-23 is used in nuclear magnetic resonance in various research fields, including materials science and battery research. Sodium-23 relaxation has applications in studying cation-biomolecule interactions, intracellular and extracellular sodium, ion transport in batteries, and quantum information processing.
== Neurodegeneration == Inhibition of Hsp90 leads to Hsp70 and Hsp40 upregulation, which can channel misfolded protein for proteasome degradation, which can potentially inhibit the progression of neurodegenerative diseases. For example, Hsp70 overexpression in human neuroglioma cells transfected with mutant alpha-synuclein led to 50% less oligomeric alpha-synuclein species, pointing towards the possibility that increasing its expression could diminish the spread of Parkinson's disease. Similarly, Hsp70 overexpression suppressed poly-Q dependent aggregation and neurodegeneration in cell cultures, yeast, fly, and mouse models, and deletion of hsp70 increased the size of polyQ inclusion bodies, suggesting that increasing its expression could help to prevent Huntington's disease. Similarly, reductions in Hsp70 have been shown in transgenic mouse models of ALS and patients with sporadic ALS. Lastly, increased expression or activity of Hsp70 has been proposed as a method to prevent the progression of Alzheimer's disease, because knock down of Hsp70 promoted A-beta toxicity, and Hsp70 was shown to promote tau stability, while Hsp70 levels are decreased in tauopathies like Alzheimer's disease. Given the complex interplay between the different chaperone proteins, therapeutic development in this field is aimed at investigating how the chaperone network as a whole can be manipulated and the effect of this manipulation on the progression of neurodegenerative disease, but the balance of Hsp70 and Hsp90 levels appears to be central in this pathophysiology.
=== Crack tip plastic zone === In theory the stress at the crack tip where the radius is nearly zero, would tend to infinity. This would be considered a stress singularity, which is not possible in real-world applications. For this reason, in numerical studies in the field of fracture mechanics, it is often appropriate to represent cracks as round tipped notches, with a geometry dependent region of stress concentration replacing the crack-tip singularity. In actuality, the stress concentration at the tip of a crack within real materials has been found to have a finite value but larger than the nominal stress applied to the specimen. Nevertheless, there must be some sort of mechanism or property of the material that prevents such a crack from propagating spontaneously. The assumption is, the plastic deformation at the crack tip effectively blunts the crack tip. This deformation depends primarily on the applied stress in the applicable direction (in most cases, this is the y-direction of a regular Cartesian coordinate system), the crack length, and the geometry of the specimen. To estimate how this plastic deformation zone extended from the crack tip, Irwin equated the yield strength of the material to the far-field stresses of the y-direction along the crack (x direction) and solved for the effective radius. From this relationship, and assuming that the crack is loaded to the critical stress intensity factor, Irwin developed the following expression for the idealized radius of the zone of plastic deformation at the crack tip:
Sources: en.wikipedia.org
It is a synthetic REV-ERB agonist used mainly in preclinical research. It is not an approved medicine for human use.
It binds to REV-ERBα and REV-ERBβ, nuclear receptors involved in circadian and metabolic gene regulation. This can alter transcription of genes related to lipid and glucose metabolism in experimental models.
No controlled human trials have established that effect. Endurance findings come primarily from rodent studies, and human responses remain unknown.
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.