Everything below concerns REV-ERB agonist. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2025-09-05. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Common name | SR9009 | Also referred to as Stenabolic in non-scientific contexts. |
| Chemical class | Synthetic small molecule | Not a steroid or peptide hormone. |
| Receptor target | REV-ERBα and REV-ERBβ | Nuclear receptor agonist in preclinical studies. |
| Development status | Investigational | No approved human therapeutic indication. |
| Regulatory attention | Prohibited in sport | Listed by anti-doping authorities. |
For long-term storage, SR9009 is typically kept as a solid at low temperature, protected from moisture and light. Desiccated conditions limit hydrolysis, while opaque containers reduce photochemical breakdown. Solutions are less stable than solids and are often stored frozen in aliquots to avoid repeated freeze-thaw cycles. Stability data are not standardized across all suppliers, so users should rely on certificate-of-analysis information when available. Degradation may appear as color change, precipitate, or decreased chromatographic purity.
Laboratory identification of SR9009 typically relies on chromatographic separation coupled to mass spectrometry, often with ultraviolet detection as a secondary check. Nuclear magnetic resonance spectroscopy can confirm molecular structure when a reference standard is available. Because many suppliers sell the compound as a research chemical, independent identity testing is important for experimental reproducibility. A single retention time is not sufficient proof of identity, especially when related compounds may be present. Purity assessments usually report a percentage based on area normalization.
SR9009 is generally described as poorly soluble in water and more soluble in organic solvents such as dimethyl sulfoxide and ethanol. Stock solutions are commonly prepared in an organic solvent before dilution into an aqueous buffer or vehicle. Precipitation can occur if the organic fraction is reduced too quickly or if the final concentration exceeds the compound's solubility limit. Sonication or gentle warming may aid dissolution in some protocols, but excessive heat can promote degradation. Container material and pH can also influence observed solubility.
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.
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.
This phenomenon was used in the design of light meters and similar devices. Selenium's semiconductor properties found numerous other applications in electronics. The development of selenium rectifiers began during the early 1930s, and these replaced copper oxide rectifiers because they were more efficient. These lasted in commercial applications until the 1970s, following which they were replaced with less expensive and even more efficient silicon rectifiers. Selenium came to medical notice later because of its toxicity to industrial workers. Selenium was also recognized as an important veterinary toxin, which is seen in animals that have eaten high-selenium plants. In 1954, the first hints of specific biological functions of selenium were discovered in microorganisms by biochemist, Jane Pinsent. It was discovered to be essential for mammalian life in 1957. In the 1970s, it was shown to be present in two independent sets of enzymes. This was followed by the discovery of selenocysteine in proteins. During the 1980s, selenocysteine was shown to be encoded by the codon UGA. The recoding mechanism was worked out first in bacteria and then in mammals (see SECIS element).
The metabolism of drugs is often divided into the following three phases. Phase I: modification, phase II: conjugation, and phase III: excretion. These phases act in concert to detoxify drugs and remove them from cells and eventually from the body. The purpose of phase I is to introduce polar groups that either themselves directly facilitate excretion or to create reactive functional groups. These reactive groups can be conjugated in a phase II reaction with molecules that are recognized by transport proteins. In the last step, transport proteins eliminate the drug conjugate from the body. In phase I, enzymes such as Cytochrome P450 oxidases introduce reactive or polar groups into xenobiotics. These modified compounds are then conjugated to polar compounds in phase II reactions. These reactions are catalyzed by transferase enzymes such as glutathione S-transferases. Finally, in phase III, the conjugated xenobiotics may be further processed, before being recognized by efflux transporters and pumped out of cells. Drug metabolism often converts lipophilic compounds into hydrophilic products that are more readily excreted.
== External links == Pathway at biocarta.com Nosek, Thomas M. "Section 6/6ch2/s6ch2_34". Essentials of Human Physiology. Archived from the original on 2016-03-24. Overview of all the structural information available in the PDB for UniProt: P01282 (VIP peptides) at the PDBe-KB.
Myelofibrosis can be a late complication of other myeloproliferative disorders, such as polycythemia vera, and less commonly, essential thrombocythemia. In these cases, myelofibrosis occurs as a result of somatic evolution of the abnormal hematopoietic stem cell clone that caused the original disorder. In some cases, the development of myelofibrosis following these disorders may be accelerated by the oral chemotherapy drug hydroxyurea.
== Prognosis == Studies of the life expectancy of patients with Alport syndrome are rare, but one 2012 study found that Alport patients receiving renal replacement therapy (dialysis or kidney transplantation) exhibited, on average, better survival compared with matched controls who had other kidney diseases (and who also received renal replacement therapy).
Sources: en.wikipedia.org
== History == Was first partially isolated and purified from a serum that contained chondrocytes from chick embryos in 1981 by scientists/researchers A. Tyl Hewitt, Hugh H. Varner, Michael H. Silver, Waltraud Dessau, Charlotte M. Wilkes, and George R. Martin. This group would later go on in the study and deem this attachment factor that they found to be chondronectin.[7] It was then found in human fetal cartilage and human serum. Early scientists focused on proving that chondronectin was its own separate protein. They needed to show that it was not just another molecule that had already been identified. By the 1980s, newer studies gave researchers more evidence about its role in supporting cartilage and surrounding cells. Finding it in many biological samples also showed that it exists in different species. It is not limited to only one type of tissue. In 1987, chondronectin was isolated from articular cartilage from a canine by researchers Nancy Burton-Wurster, Valerie J. Horn, and George Lust. It was then reported to be in human synovial fluid in a 1988 study done by Steven Carsons and Valerie J. Horn. How they did this was by using a monoclonal antibody that was used in a linked immunosorbent assay (ELISA), along with a Western blot assay to observe the protein in synovial fluid. Scientist found chondronectin in both joint fluid and cartilage. This find made researchers wonder if it helps keep joints healthy. In the past, experts used it as a simple tool to help cells stick to a surface. Now they see it as a vital part of connective tissue research.
=== Platyspondylic lethal skeletal dysplasia, Torrance type === Fewer than 10 COL2A1 mutations have been identified in people with platyspondylic lethal skeletal dysplasia, Torrance type. Most result in a single amino acid change in the pro-alpha1(II) chain, producing an abnormal chain that cannot be incorporated into collagen fibers. This leads to reduced collagen production and skeletal abnormalities such as short limbs, small chest, flattened vertebrae, and short fingers and toes.
Both of these reported discoveries were shown to be erroneous because the spectrum line that "corresponded" to element 61 was identical to that of didymium; the lines thought to belong to element 61 turned out to belong to a few impurities (barium, chromium, and platinum). In 1934, Josef Mattauch finally formulated the isobar rule. One of the indirect consequences of this rule was that element 61 was unable to form stable isotopes. From 1938, a nuclear experiment was conducted by H. B. Law et al. at the Ohio State University. Nuclides were produced in 1941 which were not radioisotopes of neodymium or samarium, and the name "cyclonium" was proposed, but there was a lack of chemical proof that element 61 was produced and the discovery was not largely recognized.
== Natural alpha glucosidase inhibitors == There are a large number of natural products with alpha-glucosidase inhibitor action. In fact, the prototypic drug of this class (acarbose) is discovered from soil bacteria. For example, research has shown the culinary mushroom Maitake (Grifola frondosa) has a hypoglycemic effect. The reason Maitake lowers blood sugar is because the mushroom naturally contains an alpha glucosidase inhibitor. All cinnamon species show acarbose-like activity. A single dose of raw cinnamon before a meal containing complex carbohydrates decreases the postprandial hyperglycemia (higher than 140 mg/dL; >7.8 mmol/L) in patients with type II diabetes. Another plant attracting a lot of attention is Salacia oblonga.
Former Yemeni president Ali Abdullah Saleh had accused the Houthis of having ties to external backers, in particular the Iranian government; Saleh stated in an interview with The New York Times,The real reason they received unofficial support from Iran was because they repeat same slogan that is raised by Iran – death to America, death to Israel. We have another source for such accusations. The Iranian media repeats statements of support for these [Houthi] elements. They are all trying to take revenge against the USA on Yemeni territories. Such backing has been reported by diplomatic correspondents of major news outlets (e.g., Patrick Wintour of The Guardian), and has been the reported perspective of Yemeni governmental leaders militarily and politically opposing Houthi efforts (e.g., as of 2017, the UN-recognized, deposed Yemeni President Abd Rabbu Mansour Hadi, who referred to the "Houthi rebels... as 'Iranian militias'". The Houthis in turn accused the Saleh government of being backed by Saudi Arabia and of using Al-Qaeda to repress them. Under the next President Hadi, Gulf Arab states accused Iran of backing the Houthis financially and militarily, though Iran denied this, and they were themselves backers of President Hadi. Despite confirming statements by Iranian and Yemeni officials in regards to Iranian support in the form of trainers, weaponry, and money, the Houthis denied reception of substantial financial or arm support from Iran.
Sources: en.wikipedia.org
It is a synthetic compound studied as an agonist of REV-ERB nuclear receptors. It is not an approved medicine and has mainly been examined in laboratory and animal research.
No. It is a small molecule that binds nuclear receptors involved in circadian regulation. Its classification differs from anabolic steroids or peptide hormones.
Published human clinical trial data are lacking. Most safety and activity information comes from preclinical models, so effects in people remain uncertain.
SR9009 is a synthetic compound investigated as an agonist of the nuclear receptors REV-ERBα and REV-ERBβ. It is used in preclinical research on circadian rhythm and metabolism. It is not an approved drug.