Everything below concerns circadian rhythm. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2025-10-26. 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.
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.
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.
SR9009 is a synthetic small molecule studied as an agonist of REV-ERB nuclear receptors. REV-ERB alpha and REV-ERB beta help regulate circadian rhythms and metabolic gene expression. In laboratory research, SR9009 has been used to probe how these receptors affect skeletal muscle, liver, and adipose tissue. The compound was identified in academic drug-discovery work and is often described in scientific literature by its chemical name and research code. It is not an approved medicine, and human clinical data remain limited or absent.
SR9009 binds REV-ERB receptors and alters their repressive activity on target genes. This action can change transcription of genes involved in lipid handling, glucose metabolism, and mitochondrial function. In rodent studies, treated animals have shown changes in muscle oxidative capacity and exercise performance, though effects vary by dose, duration, and model. The precise molecular steps connecting receptor binding to whole-body outcomes are still an active area of investigation. Findings in animals do not automatically translate to humans.
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.
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.
The two substrates of this enzyme are 14-demethyllanosterol and oxidised nicotinamide adenine dinucleotide phosphate (NADP+). Its products are 4,4-dimethyl-5α-cholesta-8,14,24-trien-3β-ol, reduced NADPH, and a proton. This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-CH group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is 4,4-dimethyl-5alpha-cholesta-8,24-dien-3beta-ol:NADP+ Delta14-oxidoreductase. This enzyme participates in biosynthesis of steroids.
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The optimal ranges for estrogen apply only to individuals taking estradiol (or an ester of estradiol), and not to those taking synthetic or other non-bioidentical preparations (e.g., conjugated estrogens or ethinylestradiol). Physicians also recommend broader medical monitoring, including complete blood counts; tests of renal function, liver function, and lipid and glucose metabolism; and monitoring of prolactin levels, body weight, and blood pressure. If prolactin levels are greater than 100 ng/mL, estrogen therapy should be stopped and prolactin levels should be rechecked after 6 to 8 weeks. If prolactin levels remain high, an MRI scan of the pituitary gland to check for the presence of a prolactinoma should be ordered. Otherwise, estrogen therapy may be restarted at a lower dosage. Cyproterone acetate is particularly associated with elevated prolactin levels, and discontinuation of cyproterone acetate lowers prolactin levels. In contrast to cyproterone acetate, estrogen and spironolactone therapy is not associated with increased prolactin levels.
Committee for Revolutionary International Regroupment (CRIR), founded by groups originating from the USFI and IWL-FI Liaison Committee for the Reconstruction of the Fourth International (CERCI), founded by the Bolivian party POR which broke off with the original Fourth International in the 1950s. International Revolutionary Workers' Current – Fourth International (CORI-QI) International Committee for the Reconstruction of the LIT of Nahuel Moreno (CIR) La Marx International, founded by the Nuevo PST in Argentina Socialism or Barbarism, founded by the Nuevo MAS in Argentina. Partido Obrero affiliated International Debates website Organizing Committee for the Reconstitution of the Fourth International (CORQI) COI-IWC
Haematoxylin and eosin staining is frequently used in histology to examine thin tissue sections. Haematoxylin stains cell nuclei blue, while eosin stains cytoplasm, connective tissue and other extracellular substances pink or red. Eosin is strongly absorbed by red blood cells, colouring them bright red. In a skillfully made H&E preparation the red blood cells are almost orange, and collagen and cytoplasm (especially muscle) acquire different shades of pink.
Sources: en.wikipedia.org
== Target and molecular mechanism == When U7-CNTX-Pn1a was tested on HEK 293 cells that were transfected with rTRPV1, capsaicin receptor, induced inward Ca2+ currents were blocked. U7-CNTX-Pn1a inhibited the release of glutamate from the trigeminal ganglion. This together suggests that the toxin blocks TRPV1 receptors. In comparison to SB-366791, which is a selective TRPV1 blocker, the toxin was found to exert greater inhibitory potency as a much lower concentration was needed of the U7-CNTX-Pn1a, with an IC50 of 47 ± 0.18nM, 45 ± 1.18nM and 390 ± 5.1nM for the native, recombinant U7-CNTX-Pn1a and SB-366791, respectively. Additionally, in a neuropathic pain model the toxin was discovered to target L-type voltage-gated calcium channels (VGCCs) using L-type VGCC blockers. The mild antinociceptive effect reversed when U7-CNTX-Pn1a was administered to the mice (30 fmol/site, i.t.), however, the exact underlying mechanism was not discovered yet.
Buttenwieser (1958), educator, Democratic Party fundraiser, member of the Lehman family Allen Rosenshine (1959), founder of the Omnicom Group, chairman and CEO of BBDO Doug Morris (1960), CEO of Sony Music Entertainment and former CEO of Universal Music Group Bernard Selz (1960), fund manager, philanthropist and anti-vaccination supporter Frank Lorenzo (1961), former chairman of Eastern Airlines, Texas Air Corporation and Texas International Airlines Douglas H. McCorkindale (1961), former chairman and CEO of Gannett William Campbell (1962), chairman of the board of Intuit, former board director of Apple Inc.; founder of Claris Sanford Greenberg (1962), investor, author and philanthropist Kenneth Lipper (1962), financier and deputy mayor of New York City; Academy Award-winning producer of The Holocaust documentary The Last Days Jerry Speyer (1962), billionaire, founding partner, chairman and CEO of Tishman Speyer and chairman of the Museum of Modern Art Robert Kraft (1963), chairman and CEO of The Kraft Group; owner of the New England Patriots Mark H.
== Criticism == The AIOCD (All India organization of Chemists & Druggists) called for a nationwide strike on 14 October 2015 against online sale of drugs and criticized ePharmacies like MedPlusMart.com as illegal and a threat to the interests of around 8.5 lakhs chemists around India. MedPlus defended its online sales policy as being in compliance with the current drug act and as a valuable service to its customers.
=== Elderly === A 2006 review regarding the management of insomnia and the elderly found that considerable evidence of the effectiveness and lasting benefits of nondrug treatments for insomnia exist. Compared with the benzodiazepines, the nonbenzodiazepine sedative-hypnotics offer few if any advantages in efficacy or tolerability in elderly persons. Other agents such as the melatonin receptor agonists may be more suitable and effective for the management of chronic insomnia in elderly people. Long-term use of sedative-hypnotics for insomnia lacks an evidence base and is discouraged for reasons that include concerns about such potential adverse drug effects as cognitive impairment (anterograde amnesia), daytime sedation, motor incoordination, and increased risk of motor vehicle accidents and falls.
In humans, maintenance from sexual maturity on (–)-deprenyl (1mg daily) is, for the time being, the most promising prophylactic treatment to fight against the age related decay of behavioral performances, prolonging life, and preventing or delaying the onset of age-related neurodegenerative diseases such as Parkinson's and Alzheimer's. The mechanism of selegiline's longevity-promoting effect has been researched by several groups, including Knoll and his associates at Semmelweis University, Budapest. The drug has been determined to be a catecholaminergic activity enhancer when present in minuscule concentrations far below those at which monoamine oxidase inhibitory activity can be observed, thereby potentiating the release of catecholamine neurotransmitters in response to stimuli. Knoll maintains that micro-doses of selegiline act as a synthetic analogue to a known or unknown trace amine in order to preserve the brain catecholaminergic system, which he perceives as integral to the organism's ability to function in an adaptive, goal-directed and motivated manner during advancing physical age:
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.