This is a working overview of SR9009, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-04-05. 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.
Handling practices for SR9009 focus on minimizing degradation and contamination. The solid is generally stored desiccated at or below -20 °C, protected from light and moisture. Stock solutions are often prepared in dimethyl sulfoxide or ethanol, then aliquoted to avoid repeated freeze–thaw cycles. Aqueous solubility is low, so formulations for animal studies may require cosolvents or suspending agents. Personnel should follow institutional chemical safety procedures, because toxicological data for humans are incomplete.
Regulatory status varies by country and intended use. Major drug agencies have not granted marketing authorization for SR9009 as a medicine, and it is not listed as a controlled substance in many jurisdictions. It is often sold as a research chemical, a category that may fall outside pharmaceutical manufacturing rules. Buyers should verify local laws and supplier documentation, including certificates of analysis. The lack of standardized quality controls raises concerns about identity, purity, and actual content in products marketed online.
| 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 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.
Regulatory agencies have not approved SR9009 for human therapeutic use. It is typically sold as a research chemical with labels stating that it is not for human consumption. The World Anti-Doping Agency prohibits the substance in sport, generally under the category of non-approved substances. Customs and national laws may restrict importation, sale, or possession. Product quality and legal status can vary by country and vendor, and therapeutic claims are not permitted in regulated advertising because the compound lacks approval.
Several misconceptions surround SR9009. It is often described as a SARM, a steroid, or an exercise pill, but its known target is the REV-ERB receptor family. Rodent studies have examined exercise capacity and metabolic markers, yet human outcomes remain unproven. Oral bioavailability appears low in animals, and human pharmacokinetics are not well characterized. Online products may contain impurities or different compounds, so identity and purity testing are important for research use.
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.
Regulatory treatment of SR9009 varies by country and region. It is not approved as a pharmaceutical, and several jurisdictions restrict its sale for human consumption. Some authorities classify it as a research chemical, a prescription-only substance, or a prohibited performance-enhancing agent in sport. Purchasers may encounter certificates of analysis, but these documents do not guarantee identity, purity, or legality. In research settings, institutional safety reviews and controlled procurement help ensure that materials are handled under appropriate oversight. The absence of harmonized rules means that legal status can change and requires verification.
Analytical identification of SR9009 typically relies on liquid chromatography coupled with tandem mass spectrometry. In biological samples, researchers first separate the compound from matrix components using protein precipitation, liquid-liquid extraction, or solid-phase extraction. High-performance liquid chromatography with ultraviolet detection and nuclear magnetic resonance spectroscopy can support structural confirmation of reference materials. Because SR9009 is a small, relatively lipophilic molecule, reverse-phase columns and acidic mobile phases are common. Laboratories often include isotope-labeled internal standards to improve quantification and to correct for ion suppression.
In order to regulate the secretion of ACTH, many substances secreted within this axis exhibit slow/intermediate and fast feedback-loop activity. Glucocorticoids secreted from the adrenal cortex work to inhibit CRH secretion by the hypothalamus, which in turn decreases anterior pituitary secretion of ACTH. Glucocorticoids may also inhibit the rates of POMC gene transcription and peptide synthesis. The latter is an example of a slow feedback loop, which works on the order of hours to days, whereas the former works on the order of minutes. The half-life of ACTH in human blood is reported to be between ten and 30 minutes. ACTH consists of 39 amino acids, the first 13 of which (counting from the N-terminus) may be cleaved to form α-melanocyte-stimulating hormones (α-MSH) (this common structure is responsible for excessively tanned skin in Addison's disease). After a short period of time, ACTH is cleaved into α-melanocyte-stimulating hormone (α-MSH) and CLIP, a peptide with unknown activity in humans. In the human body, total weight ACTH is 4540 Da.
15-Oxo-ETE). Other eicosanoid oxoreductases that use NAD+ and NADH as co-factors include: 12-hydroxyicosatetraenoate dehydrogenase which metabolizes 12-hydroxyeicosatetraenoic acid (12-HETE) and LTB4 to their corresponding 12-oxo analogs and 11-hydroxy-TXB2 dehydrogenase, which metabolizes TXB2 to its 11-oxo analog; and 15-hydroxyprostaglandin dehydrogenase (NAD+) which metabolizes (5Z,13E)-(15S)-11alpha,15-dihydroxy-9-oxoprost-13-enoate to its 15-oxo analog. Other eicosanoid oxireductases that use NADP+ and NADPH as cofactors include LTB4 12-hydroxy dehydrogenase which metabolizes LTB4 to its 12-oxo analog, and 15-hydroxyprostaglandin-D dehydrogenase (NADP+), 15-hydroxyprostaglandin-I dehydrogenase (NADP+), and 15-hydroxyprostaglandin dehydrogenase (NADP+) which metabolize PGD2, PGI2, and (13E)-(15S)-11alpha,15-dihydroxy-9-oxoprost-13-enoate, respectively, to their corresponding 15-oxo analogs.
In the first decade of the 21st century, what was called "age management medicine" was considered a field of alternative medicine, and, as of 2007, was not recognized by the American Medical Association. Other names at this time included "antiaging medicine" and "regenerative medicine". Age management medicine is controversial. The field is underregulated and supported by insufficient scientific evidence. People who practice it open themselves up to legal liability on grounds of negligence–malpractice, warranty issues, and product liability. The use of growth hormone has been frequently recommended; however, such use is associated with cancer. Age management medicine is often promoted by anti-aging practitioners specializing in nutritional supplements and hormone-replacement, a practice that may lead to harmful side-effects.
Alexandra C. Newton is a Canadian and American biochemist. She is a Distinguished Professor of pharmacology at the University of California, San Diego. Newton runs a multidisciplinary Protein kinase C and Cell signaling biochemistry and cell biology research group in the School of Medicine, investigating molecular mechanisms of signal transduction in the Phospholipase C (PLC) and Phosphoinositide 3-kinase (PI3 kinase, or PI3-K) signaling pathways. She has been continuously funded by the US National Institutes of Health since 1988. Newton was born in Cape Town, South Africa, and was schooled in Vancouver, Athens, and Aix-en-Provence. She graduated in 1980 from the Simon Fraser University in Canada, where she was awarded a 1st-class honours degree in biochemistry and French literature. She received her PhD in chemistry in 1986 from Stanford University, working with Wray H. Huestis on a thesis examining band 3, a red cell membrane protein.
Sources: en.wikipedia.org
Ketone bodies can be used as fuels, yielding 22 ATP and 2 GTP molecules per acetoacetate molecule when oxidized in the mitochondria. Ketone bodies are transported from the liver to other tissues, where acetoacetate and beta-hydroxybutyrate can be reconverted to acetyl-CoA to produce reducing equivalents (NADH and FADH2), via the citric acid cycle. Ketone bodies cannot be used as fuel by the liver, because the liver lacks the enzyme β-ketoacyl-CoA transferase, also called thiolase. Acetoacetate in low concentrations is taken up by the liver and undergoes detoxification through the methylglyoxal pathway which ends with lactate. Acetoacetate in high concentrations is absorbed by cells other than those in the liver and enters a different pathway via 1,2-propanediol. Though the pathway follows a different series of steps requiring ATP, 1,2-propanediol can be turned into pyruvate.
Viral induction of apoptosis occurs when one or several cells of a living organism are infected with a virus, leading to cell death. Cell death in organisms is necessary for the normal development of cells and the cell cycle maturation. It is also important in maintaining the regular functions and activities of cells. Viruses can trigger apoptosis of infected cells via a range of mechanisms including:
Subfamily ABCC contains thirteen members and nine of these transporters are referred to as the Multidrug Resistance Proteins (MRPs). The MRP proteins are found throughout nature and they mediate many important functions. They are known to be involved in ion transport, toxin secretion, and signal transduction. Of the nine MRP proteins, four of them, MRP4, 5, 8, 9, (ABCC4, 5, 11, and 12), have a typical ABC structure with four domains, comprising two membrane spanning domains, with each spanning domain followed by a nucleotide binding domain. These are referred to as short MRPs. The remaining 5 MRP's (MRP1, 2, 6, 7) (ABCC1, 2, 3, 6 and 10) are known as long MRPs and feature an additional fifth domain at their N terminus. CFTR, the transporter involved in the disease cystic fibrosis, is also considered part of this subfamily. Cystic fibrosis occurs upon mutation and loss of function of CFTR. The sulfonylurea receptors (SUR), involved in insulin secretion, neuronal function, and muscle function, are also part of this family of proteins. Mutations in SUR proteins are a potential cause of Neonatal diabetes mellitus. SUR is also the binding site for drugs such as sulfonylureas and potassium-channel openers activators such as diazoxide.
Before amylin deposition was associated with diabetes, already in 1901, scientists described the phenomenon of "islet hyalinization", which could be found in some cases of diabetes. A thorough study of this phenomenon was possible much later. In 1986, the isolation of an aggregate from an insulin-producing tumor was successful, a protein called IAP (Insulinoma Amyloid Peptide) was characterized, and amyloids were isolated from the pancreas of a diabetic patient, but the isolated material was not sufficient for full characterization. This was achieved only a year later by two research teams whose research was a continuation of the work from 1986.
This 1686-amino acid protein belongs to the ADAMTS family and is one of 19 members known in humans. It is a large, multi-domain enzyme that undergoes extensive post-translational modifications, including N- and O-linked glycosylation, chondroitin sulfate attachment, and potential C-mannosylation and O-fucosylation of the thrombospondin (TSP) type 1 domains. The domain structure from the N-terminus to the C-terminus consists of:
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.
Liquid chromatography–mass spectrometry is common for identity and purity checks. High-performance liquid chromatography with ultraviolet detection can also be used. Both methods require a suitable reference standard.