The short version of reference standard fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2026-04-16. Anything still debated is marked as such rather than presented as settled.
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.
Physicochemical behavior influences handling. SR9009 is described as a solid with limited aqueous solubility, so organic solvents such as dimethyl sulfoxide or ethanol are common in research stock solutions. Aqueous dilution can produce precipitates if the organic content is too low. Light, heat, and repeated freeze-thaw cycles may affect stability. Storage recommendations usually specify a desiccated freezer environment protected from light, but exact stability data depend on the formulation and matrix.
Detection in biological samples can be complicated by rapid metabolism and low circulating concentrations. Some studies report phase I and phase II metabolites, and analytical methods may need to target those species in addition to the parent compound. Immunoassays are not broadly available, so mass spectrometry remains the main confirmatory approach. For anti-doping testing, laboratories look for SR9009 and its metabolites using validated LC-MS methods. Open questions include how long metabolites remain detectable and how different routes of administration alter detection windows.
In laboratory settings, SR9009 is typically characterized by liquid chromatography–mass spectrometry (LC-MS) or high-performance liquid chromatography with ultraviolet detection (HPLC-UV). These methods can confirm identity and estimate purity, but they require reference standards for accurate quantification. Because SR9009 is not a licensed pharmaceutical, no harmonized pharmacopeial monograph exists. Laboratories often validate in-house methods for matrices such as plasma, urine, or cell culture media. Sample preparation may involve protein precipitation or liquid-liquid extraction before analysis.
| 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 |
Preclinical reports describe effects on exercise endurance, mitochondrial content, and lipid profiles in rodents, but these findings come from specific experimental conditions. Many studies use high doses or delivery methods that may not translate directly to human use. SR9009 has been reported to have low oral bioavailability and a short half-life, which complicates interpretation of oral dosing studies. It is not established as safe or effective for any indication. Literature discussions often separate its pharmacological mechanism from unverified claims made in fitness and supplement markets.
SR9009 is a synthetic small molecule studied as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is not an approved medicine and has no established human therapeutic use. The compound appears in scientific literature as a tool for probing circadian and metabolic regulation. Online sellers often label it as a research chemical, sometimes using the nickname Stenabolic. Its chemical identity is distinct from selective androgen receptor modulators, stimulants, and peroxisome proliferator-activated receptor delta agonists. Researchers use it mainly in cell and animal experiments.
At the molecular level, SR9009 binds REV-ERBα and REV-ERBβ and alters their repressive activity on target genes. These nuclear receptors help regulate the circadian clock, lipid synthesis, glucose metabolism, and inflammatory pathways. By changing transcription, the compound can shift the timing or magnitude of downstream metabolic processes in model systems. It does not act through androgen receptors or adenosine receptors, which distinguishes it from several substances sold for athletic performance. Whether the same transcriptional changes occur in humans at tolerable exposures remains an open question because controlled human studies are lacking.
Californium is produced in nuclear reactors and particle accelerators. Californium-250 is made by bombarding berkelium-249 (249Bk) with neutrons, forming berkelium-250 (250Bk) via neutron capture (n,γ) which, in turn, quickly beta decays (β−) to californium-250 (250Cf) in the following reaction:
== Safety and side effects == Some anti-obesity medications can have severe, even lethal side effects, fen-phen being a famous example. Fen-phen was reported through the FDA to cause abnormal echocardiograms, heart valve problems, and rare valvular diseases. Out of 25 anti-obesity medications withdrawn from the market between 1964 and 2009, 23 acted by altering the functions of chemical neurotransmitters in the brain. The most common side effects of these drugs that led to withdrawals were mental disturbances, cardiac side effects, and drug abuse or drug dependence. GLP-1 receptor agonists are known to have common side effects including nausea and vomiting. Deaths were associated with seven products. Ephedra was removed from the US market in 2004 over concerns that it raises blood pressure and could lead to strokes and death.
== Tissue distribution == EAAT1 is expressed throughout the CNS, and is highly expressed in astrocytes and Bergmann glia in the cerebellum. In the retina, EAAT1 is expressed in Muller cells. EAAT1 is also expressed in a number of other tissues including cardiac myocytes.
Aside from cheap clothing stores that catered to the derelict and down-and-out population of men, commercial activity along the Bowery became specialized in used restaurant supplies and lighting fixtures. In the 1930s and again in 1947, there were efforts to change the name of the Bowery to something more "dignified and prosaic", such as "Fourth Avenue South".
Sources: en.wikipedia.org
=== Excessive release from cells === Metabolic acidosis can cause hyperkalemia as the elevated hydrogen ions in the cells can displace potassium, causing the potassium ions to leave the cell and enter the bloodstream. However, in respiratory acidosis or organic acidosis such as lactic acidosis, the effect on serum potassium is much less significant, although the mechanisms are not completely understood. Insulin deficiency can cause hyperkalemia as the hormone insulin increases the uptake of potassium into the cells. Hyperglycemia can also contribute to hyperkalemia by causing hyperosmolality in extracellular fluid, increasing water diffusion out of the cells, and causing potassium to move alongside water out of the cells. The co-existence of insulin deficiency, hyperglycemia, and hyperosmolality is often seen in those affected by diabetic ketoacidosis. Apart from diabetic ketoacidosis, other causes that reduce insulin levels, such as the use of the medication octreotide, and fasting, which can also cause hyperkalemia. Increased tissue breakdown such as rhabdomyolysis, burns, or any cause of rapid tissue necrosis, including tumor lysis syndrome can cause the release of intracellular potassium into blood, causing hyperkalemia. Beta2-adrenergic agonists act on beta-2 receptors to drive potassium into the cells. Therefore, beta blockers can raise potassium levels by blocking beta-2 receptors. However, the rise in potassium levels is not marked unless other co-morbidities are present.
==== Rise in oxygen levels theory for multicellularity ==== Despite the fact that organisms had the potential to become multicellular it is likely that it was not actually possible until the late Neoproterozoic. This is because multicellularity requires oxygen, and before the late Neoproterozoic there was very limited oxygen availability. After the melting of the “Snowball Earth” during the mid Neoproterozoic, nutrients that were trapped in the ice flooded the oceans. Surviving bacteria flourished due to the increased nutrient levels. Among these microbes were cyanobacteria and other oxygen producing bacteria, which led to the massive rise in oxygen levels. The increased oxygen availability allowed it to be used by cells in order to manufacture collagen. Collagen is the key component for cell aggregation, It is a rope-like molecule that “ties” cells together. Oxygen is required for collagen synthesis because ascorbic acid (Vitamin C) is essential for this process to occur. A key component in the ascorbic acid molecule is oxygen (chemical formula C6H8O6). Therefore, it is evident that the rise in oxygen is a crucial step to the rise of multicellularity since it is essential for the synthesis of collagen.
=== Other causes === Cranial CSF leaks result from intracranial hypertension in the vast majority of cases. The increased pressure causes a rupture of the cranial dura mater, leading to a CSF leak and intracranial hypotension. Patients with a nude nerve root, where the root sleeve is absent, are at increased risk for developing recurrent CSF leaks. Lumbar disc herniation has been reported to cause CSF leaks in at least one case. Degenerative spinal disc diseases cause a disc to pierce the dura mater, leading to a CSF leak. CSF leaks can result from a lumbar puncture procedure.
However, the reduction of seizure threshold could be attributed to tramadol's putative inhibition of GABAA receptors at high doses (significant inhibition at 100 μM). In addition, desmetramadol is a high-affinity ligand of the DOR, and activation of this receptor could be involved in tramadol's ability to provoke seizures in some individuals, as DOR agonists are well known for inducing seizures. Nausea and vomiting caused by tramadol are thought to be due to activation of the 5-HT3 receptor via increased serotonin levels. In accordance, the 5-HT3 receptor antagonist ondansetron can be used to treat tramadol-associated nausea and vomiting. Tramadol and desmetramadol themselves do not bind to the 5-HT3 receptor.
At the time of the K-Pg extinction, the Deccan Traps flood basalts of India were actively erupting. The eruptions can be separated into three phases around the K-Pg boundary, two prior to the boundary and one after. The second phase, which occurred very close to the boundary, would have extruded 70 to 80% of the volume of these eruptions in intermittent pulses that occurred around 100,000 years apart. Greenhouse gases such as carbon dioxide and sulfur dioxide would have been released by this volcanic activity, resulting in climate change through temperature perturbations of roughly 3 °C (5.4 °F) but possibly as high as 7 °C (13 °F). Like the Chicxulub impact, the eruptions may also have released sulfate aerosols, which would have caused acid rain and global cooling. However, due to large error margins in the dating of the eruptions, the role of the Deccan Traps in the K-Pg extinction remains unclear. Before 2000, arguments that the Deccan Traps eruptions—as opposed to the Chicxulub impact—caused the extinction were usually linked to the view that the extinction was gradual. Prior to the discovery of the Chicxulub crater, the Deccan Traps were used to explain the global iridium layer; even after the crater's discovery, the impact was still thought to only have had a regional, not global, effect on the extinction event. In response, Luis Alvarez rejected volcanic activity as an explanation for the iridium layer and the extinction as a whole.
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 usually detected by LC-MS or HPLC-UV against a reference standard. In biological matrices, metabolite targeting can improve detection. No universal immunoassay is widely available.