If you have been reading about research chemical and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Updated 2026-03-24. 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.
Scientific discussion of SR9009 often separates animal evidence from human anecdote. Rodent studies provide controlled data on endurance, metabolism, and gene expression, but they use specific strains, doses, and treatment durations. Human reports are mostly uncontrolled and cannot establish cause and effect. Open questions include oral bioavailability, tissue distribution, metabolic stability, and long-term effects. Review articles generally call for more rigorous pharmacokinetic and safety research before any clinical use could be considered.
Analytical methods for SR9009 typically rely on liquid chromatography coupled with tandem mass spectrometry. The technique can separate the parent compound from related substances and detect low concentrations in biological matrices. Urine and blood are common samples in anti-doping testing, while in vitro studies may use cell culture media. Rapid metabolism and low expected concentrations make method validation important for reliable identification. Exact metabolite patterns can vary by species and are not fully mapped.
Regulatory treatment of SR9009 reflects its investigational status. The compound has no approved human therapeutic indication, and sports authorities prohibit its use. It appears on anti-doping lists as a non-approved substance or metabolic modulator, depending on the list version. Products sold online as research chemicals are not quality-controlled medicines, so their identity and purity can differ from the label. Such products may also contain unlisted compounds, which complicates both testing and safety assessment.
| 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. |
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.
Stability depends on physical form, temperature, light exposure, and solvent. Solid SR9009 is generally stored cold and dry, with protection from light to limit degradation. Dimethyl sulfoxide stocks are common for laboratory work, but repeated freeze-thaw cycles can reduce compound integrity. Aqueous solutions may be less stable than organic stocks, and the ethyl ester in the structure can be susceptible to hydrolysis under certain conditions. Researchers typically validate storage conditions and recheck purity before quantitative experiments, especially when using archived material.
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.
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.
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.
In laboratory settings, SR9009 is commonly identified by its molecular structure and its interaction with REV-ERB receptors. Vendors may list it under synonyms such as Stenabolic or REV-ERB agonist, but those names do not define purity or identity. Analytical confirmation typically uses high-performance liquid chromatography with ultraviolet detection or liquid chromatography–mass spectrometry. A reference standard is needed to compare retention time and mass spectrum, because the compound can be confused with related research chemicals.
Polycythemia (also spelt polycythaemia) is a medical condition suggested by a laboratory finding that the hematocrit (the volume percentage of red blood cells in the blood) and/or hemoglobin concentration are increased in the blood, although this finding is also present in capillary leak syndrome. Polycythemia is sometimes called erythrocytosis, and there is significant overlap in the two findings, but the terms are not the same: polycythemia describes any increase in hematocrit and/or hemoglobin, while erythrocytosis describes an increase specifically in the number of red blood cells in the blood. Polycythemia has many causes. It can describe an increase in the number of red blood cells ("absolute polycythemia") or a decrease in the volume of plasma ("relative polycythemia"). Absolute polycythemia can be due to genetic mutations in the bone marrow ("primary polycythemia"), physiological adaptations to one's environment, medications, and/or other health conditions. Laboratory studies such as serum erythropoeitin levels and genetic testing might be helpful to clarify the cause of polycythemia if the physical exam and patient history do not reveal a likely cause. Mild polycythemia on its own is often asymptomatic. Treatment for polycythemia varies, and typically involves treating its underlying cause. Treatment of primary polycythemia (see polycythemia vera) could involve phlebotomy, antiplatelet therapy to reduce risk of blood clots, and additional cytoreductive therapy to reduce the number of red blood cells produced in the bone marrow.
== Peroxisomal beta-oxidation == Fatty acid oxidation also occurs in peroxisomes when the fatty acid chains are too long to be processed by the mitochondria. The same enzymes are used in peroxisomes as in the mitochondrial matrix and acetyl-CoA is generated. Very long chain (greater than C-22) fatty acids, branched fatty acids, some prostaglandins and leukotrienes undergo initial oxidation in peroxisomes until octanoyl-CoA is formed, at which point it undergoes mitochondrial oxidation. One significant difference is that oxidation in peroxisomes is not coupled to ATP synthesis. Instead, the high-potential electrons are transferred to O2, which yields hydrogen peroxide. The enzyme catalase, found primarily in peroxisomes and the cytosol of erythrocytes (and sometimes in mitochondria), converts the hydrogen peroxide into water and oxygen. Peroxisomal β-oxidation also requires enzymes specific to the peroxisome and to very long fatty acids. There are four key differences between the enzymes used for mitochondrial and peroxisomal β-oxidation:
==== Checks and balances ==== In March 2025 Larson showed visible frustration at Elon Musk's failure to appear before the House Ways and Means Committee and answer DOGE data transparency questions. On April 6, 2026, Larson filed articles of impeachment against President Donald Trump.
=== Drug development === Tew's work on redox and pharmacogenetics focused on the discovery and development of drugs. Alongside colleagues, he introduced a novel zebrafish model with a glutathione S-transferase π1 (gstp1) knockout, revealing insights into redox homeostasis, reductive stress, and responses to drugs inducing endoplasmic reticulum stress and the unfolded protein response. His research has looked into the role of GTSP in cellular redox homeostasis and its over-expression in cancer drug resistance, particularly in the context of preclinical and clinical testing of the GSTP inhibitor TLK199 (Telintra) for treating myelodysplastic syndrome. He further revealed that the absence of microsomal glutathione transferase 1 (MGST1) impacts melanin biosynthesis and melanoma growth in mice and that, in numerous species, members of the GST family are involved in early hematopoiesis, and that the lack of GSTP in dendritic cells leads to increased proliferation, ROS levels and ERα levels, suggesting a role for GSTP in controlling ERα activity and dendritic cell function. Additionally, Tew and colleagues investigated how S-glutathionylation of the protein BiP, mediated by GSTP, contributes to acquired resistance to the multiple myeloma treatment bortezomib (Btz) by impacting BiP's foldase and ATPase activities.
==== Biomolecular mechanisms ==== Chronic use of amphetamine at excessive doses causes alterations in gene expression in the mesocorticolimbic projection, which arise through transcriptional and epigenetic mechanisms. The most important transcription factors that produce these alterations are Delta FBJ murine osteosarcoma viral oncogene homolog B (ΔFosB), cAMP response element binding protein (CREB), and nuclear factor-kappa B (NF-κB). ΔFosB is the most significant biomolecular mechanism in addiction because ΔFosB overexpression (i.e., an abnormally high level of gene expression which produces a pronounced gene-related phenotype) in the D1-type medium spiny neurons in the nucleus accumbens is necessary and sufficient for many of the neural adaptations and regulates multiple behavioral effects (e.g., reward sensitization and escalating drug self-administration) involved in addiction. Once ΔFosB is sufficiently overexpressed, it induces an addictive state that becomes increasingly more severe with further increases in ΔFosB expression. It has been implicated in addictions to alcohol, cannabinoids, cocaine, methylphenidate, nicotine, opioids, phencyclidine, propofol, and substituted amphetamines, among others. ΔJunD, a transcription factor, and G9a, a histone methyltransferase enzyme, both oppose the function of ΔFosB and inhibit increases in its expression. Sufficiently overexpressing ΔJunD in the nucleus accumbens with viral vectors can completely block many of the neural and behavioral alterations seen in chronic drug abuse (i.e., the alterations mediated by ΔFosB).
Sources: en.wikipedia.org
==== Drawbacks ==== This mechanism for resolving biological homochirality relies heavily on the prebiotic synthesis of RAO, and assumes that it is the prebiotic precursor to nucleic acids. The crystallization efficiency of compounds depends on their concentration, and RAO would need to be saturated in solution for enantioselective crystallization to occur. This could be achieved through frequent wet-dry cycles, which would also remove diastereomers of RAO which are also produced in prebiotic reactions and can modify its crystal habit.
== External links == Histology image: 00801ooa – Histology Learning System at Boston University - "Connective Tissue elastic fibers " UIUC Histology Subject 328 Anatomy photo: TermsCells&Tissues/connective/elastic/elastic2 - Comparative Organology at University of California, Davis - "Connective tissue, elastic (LM, High)"
is the nonlinear susceptibility tensor and X the direction of the filament (or main direction of the structure), Y orthogonal to X and Z the propagation of the excitation light. The orientation ϕ of the filaments in the plane XY of the image can also be extracted from p-SHG by FFT analysis, and put in a map.
The colon can be involved, and can cause pseudo-obstruction or ischemic colitis. Rarer complications include pneumatosis cystoides intestinalis, or gas pockets in the bowel wall, wide-mouthed diverticula in the colon and esophagus, and liver fibrosis. Patients with severe gastrointestinal involvement can become profoundly malnourished. Scleroderma may also be associated with gastric antral vascular ectasia, also known as "watermelon stomach". This is a condition in which atypical blood vessels proliferate, usually in a radially symmetric pattern around the pylorus of the stomach. It can be a cause of upper gastrointestinal bleeding or iron-deficiency anemia in patients with scleroderma.
== Gameplay == Sven Co-op is a first-person shooter based on Half-Life, using its GoldSrc game engine. The modification enables a server to be hosted, so many players can cooperate (along with any allied non-player characters) to complete levels against creatures and other enemies that are controlled by the computer. The modification was initially based around the levels from Half-Life, but since have expanded to include the other Half-Life games and user-made levels. Multiple levels may be connected to make a longer campaign by the level designer. The game can also be played in single-player mode, taking advantage of improvements over the original Half-Life that were made by the modifications, particularly the artificial intelligence used by non-player characters.
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.
No. It is an investigational compound without approved therapeutic indications. It is sold for research purposes only in many jurisdictions.