research chemical raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
This page was last updated on 2025-11-22 and is reviewed periodically as new material appears.
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.
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.
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.
| 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.
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.
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.
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.
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.
David Baker (born October 6, 1962) is an American biochemist and computational biologist who has pioneered methods to design proteins and predict their three-dimensional structures. He is the Henrietta and Aubrey Davis Endowed Professor in Biochemistry, an investigator with the Howard Hughes Medical Institute, and an adjunct professor of genome sciences, bioengineering, chemical engineering, computer science, and physics at the University of Washington. He was awarded the shared 2024 Nobel Prize in Chemistry for his work on computational protein design. Baker is a member of the United States National Academy of Sciences and of the United States National Academy of Engineering, and is the director of the University of Washington's Institute for Protein Design. He has co-founded more than a dozen biotechnology companies and was included in Time magazine's inaugural list of the 100 Most Influential People in health in 2024.
Diffuse expression of E cadherin, Thy-1 and CD4 has not been observed in HS or MH in skin or other sites; this together with cytomorphology assists in the distinction of MH and HS from histiocytoma and reactive histiocytosis (such as cutaneous and systemic histiocytosis). In histiocytoma, the phenotype is quite similar to that of HS except for the expression of E-cadherin which occurs in histiocytoma especially in the cellular infiltrate immediately adjacent to the epidermis. In reactive histiocytosis, infiltration and proliferation of activated interstitial (dermal) DC which consistently express CD4 and Thy-1 occurs. In hemophagocytic HS, histiocytes express CD11d instead of CD11c, and MHC II. Expression of CD1 molecules is uniformly low or occasionally moderate but with a patchy distribution. This phenotype is consistent with macrophage differentiation rather than DC differentiation in which abundant expression of CD1 and CD11c is expected. The exact sublineage of DC involved in HS has not been determined in most instances. The most likely candidates include interdigitating DC in lymphoid tissues and perivascular interstitial DC in other involved tissues. Immunophenotyping and careful morphological assessment should also avoid confusion of HS and MH with the large cell form of cutaneous T cell lymphoma, and poorly differentiated mast cell tumors.
=== Cardiac arrest === While intravenous calcium has been used in cardiac arrest, its general use is not recommended. Cases of cardiac arrest in which it is still recommended include high blood potassium, low blood calcium such as may occur following blood transfusions, and calcium channel blocker overdose. There is the potential that general use could worsen outcomes. If calcium is used, calcium chloride is generally the recommended form.
=== 20th century === Elly Agallidis (1914–2006), Greek physical chemist Nancy Allbritton, American analytical and biochemist Marianne Angermann (1904-1977), German-Spanish-New Zealand biochemist Valerie Ashby, American chemist Barbara Askins (born 1939), American chemist Kim K. Baldridge, American computational chemist Alice Ball (1892–1916), American chemist Carolyn Bertozzi (born 1966), American biochemist Cynthia Burrows, American physical organic chemist Asima Chatterjee (1917–2006), Indian organic chemist Ecaterina Ciorănescu-Nenițescu (1909–2000), Romanian chemist Astrid Cleve (1875–1968), Swedish chemist Mildred Cohn (1913–2009), American chemist Janine Cossy (born 1950), French organic chemist Maria Skłodowska-Curie (1867–1934), Polish-French physicist and chemist (discoverer of polonium and radium, pioneer in radiology); Nobel laureate in physics 1903, and in chemistry 1911 Jillian Lee Dempsey (born 1983), American chemist Vy M. Dong, American organic chemist Abigail Doyle (born 1980), American organic chemist Odile Eisenstein (born 1949), French, theoretical chemist Gertrude B. Elion (1918–1999), American biochemist (Nobel prize in Physiology or Medicine 1988 for drug development) Margaret Faul, Irish/American organic chemist Mary Peters Fieser (1909–1997), American organic chemist Marye Anne Fox (1947–2021), American physical organic chemist Rosalind Franklin (1920–1957), British physical chemist and crystallographer Helen Murray Free (1923–2021), American chemist Gunda I.
Sources: en.wikipedia.org
== Pump operation == The pump can operate in manual mode if certain parameters such as basal rates are programmed by the user. In automated mode, the SmartGuard algorithm requires a CGM to operate. Out of the box, the algorithm also requires a 48-hour warm-up period in manual mode to collect insulin usage data. The algorithm is based on historical trends of insulin doses such as total daily dose. Directly before entering automated mode, the algorithm requires a blood glucose reading from a meter to confirm the proper operation of the CGM. The 780G algorithm adapts by updating itself to the individual user every night at midnight. The insulin delivery amount and timing of both automated basal rates and automated boluses are then precisely controlled by the controller. While in SmartGuard mode, the user can bolus for a meal, change the glucose target, and adjust the active insulin time.
== External links == "État civil de Paris en ligne" [Paris civil status online] (in French). Archived from the original on January 5, 2020. "Commission de reconstitution de l'état civil parisien (1875-1897)" [Commission for the reconstitution of Parisian civil status (1875-1897)] (PDF) (in French). Archived from the original (PDF) on January 1, 2022. "Inventaire des registres de catholicité de baptêmes, mariages et sépultures des églises parisiennes de 1792 à 1909 conservés aux archives de Paris (collection de l'archevêché) et dans les paroisses" [Inventory of Catholic registers of baptisms, marriages and burials in Paris churches from 1792 to 1909 held by the Archives de Paris (archbishop's collection) and parishes.] (PDF) (in French). Archived from the original (PDF) on February 21, 2024. "Diocèse de Paris, formulaire de recherche pour trouver la paroisse dont dépend une adresse parisienne" [Diocese of Paris, search form to find the parish of a Paris address] (in French). Archived from the original on March 9, 2014. "Registre de relevés d'actes de baptêmes, mariages et sépultures de l'église Saint-Sulpice de Paris pour la période 1537-1748" [Register of records of baptisms, marriages and burials from the Saint-Sulpice church in Paris for the period 1537-1748] (in French). Archived from the original on December 4, 2013. "Archives numérisées de l'AP-HP Assistance Publique Hôpitaux de Paris" [Digital archives of AP-HP Assistance Publique Hôpitaux de Paris] (in French). Archived from the original on October 22, 2013.
Additionally, the regulation of sulfur plays an interconnected role with other nutrient cycles like carbon, nitrogen, and iron. For example, if MetR is impaired, the management of iron homeostasis is at risk. In plants, under sulfur-limiting conditions they optimize nitrogen assimilation to maintain metabolic homeostasis. In animals, since sulfur uptake is primarily obtained through the diet in the form of cysteine or methionine, the regulation of sulfur metabolism is done via the transsulfuration pathway. In this pathway, methionine is converted to homocysteine and then later converted to cysteine via the enzymes Cystathionine Beta-synthase (CBS) and Cystathionine gamma-lyase (CGL). Cysteine is utilized for glutathione production, and high levels of glutathione feedback negatively to downregulate the enzymes CBS and CGL. Regulation of sulfur assimilation is tightly controlled to ensure balanced production of sulfur-compounds like cysteine, methionine, and glutathione. These are key molecules that play a role in redox balance, and protein synthesis. Sulfur levels are also interconnected with other nutrient cycles to maintain an overall metabolic balance in plants, animals, and fungi.
Sources: en.wikipedia.org
== Lysis buffer in DNA and RNA studies == In studies like DNA fingerprinting the lysis buffer is used for DNA isolation. Dish soap can be used in a pinch to break down the cell and nuclear membranes, allowing the DNA to be released. Other such lysis buffers include the proprietary Qiagen product Buffer P2.
=== Schizophrenic behavior of UCST-LCST diblock copolymers === A more complex scenario can be found in the case of diblock copolymers that feature two orthogonally thermo-responsive blocks, i.e., an UCST and an LCST-type block. By applying a temperature stimulus, the individual polymer blocks show different phase transitions, e.g. by increasing the temperature, the UCST-type block features an insoluble-soluble transition, while the LCST-type block undergoes a soluble-insoluble transition. The order of the individual phase transitions depends on the relative positions of the UCST and LCST. Thus, upon temperature change the roles of the soluble and insoluble polymer blocks are reversed and this structural inversion is typically called 'schizophrenic' in the literature. Besides the fundamental interest in the mechanism of this behavior, such block copolymers have been proposed for application in smart emulsification, drug delivery, and rheology control. Schizophrenic diblock copolymer have also been applied as thin films for potential use as sensors, smart coatings or nanoswitches, and soft robotics.
Chymopapain is one of the substracts used in chemonucleolysis (a type of percutaneous discectomy). This method was a new proposal to treat primary lumbar intervertebral disc disease using a nonsurgical method. As a matter of fact, the treatment consists on an injection of proteolytic enzymes to dissolve the herniated nucleus pulposus of the intervertebral discs. Purified chymopapain is the main component of the injection, composed basically of 20 mg in five millilitres. It is provided in vials containing 10.000 units of the lyophilized agent with 0.37 mg of disodium edetate, 3.5 mg of cysteine hydrochloride monohydrate and 1.0 mg of bisulfide. All of them work as stabilisers and activators. Sodium hydroxide is in charge of adjusting the PH of the solution. Then, the injection is rehydrated with 5 milliliters of sterile water. A surgeon injects the solution directly into the herniated disc on the spine to dissolve part of it and ease the pain. This process is under fluoroscopic control. Chymopapain is responsible for catalysis, both in vivo and in vitro, a rapid reduction in the viscosity and, as a consequence, the weight of the nucleus pulposus. In fact, it is a depolymerization of the chondromucoprotein and a decrease in the ability of a disk to imbibe fluid. The dose for a single intervertebral disc is 2 to 4 nanokatals, with a maximum dose per patient of 8 nanokatals. Chymopapain injections are normally given under local, rather than general, anaesthesia. This enzyme has been studied by universities departments around the world.
This is a list of investigational anxiety disorder drugs, or drugs that are currently under development for clinical use in the treatment of anxiety disorders (type unspecified) but are not yet approved. Chemical/generic names are listed first, with developmental code names, synonyms, and brand names in parentheses. The format of list items is "Name (Synonyms) – Mechanism of Action [Reference]". This list was last comprehensively updated in September 2025. It is likely to become outdated with time.
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.