If you have been reading about anti-doping 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.
Last reviewed on 2025-10-17. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Analytical chemists detect SR9009 with liquid chromatography-tandem mass spectrometry, commonly abbreviated LC-MS/MS. Sample preparation may involve protein precipitation, liquid-liquid extraction, or solid-phase extraction before analysis. Laboratories can target the parent compound or its metabolites, depending on the matrix and the purpose of testing. Anti-doping methods require sensitive and specific assays because concentrations in biological samples can be low. Reference standards and validated methods are essential for reliable identification and quantification.
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.
In rodent studies, SR9009 has been reported to increase mitochondrial content in skeletal muscle and improve exercise endurance under some conditions. These findings led to popular descriptions such as an exercise mimetic, although that term oversimplifies the biology. Effects vary by dose, timing, tissue, and model. The compound's influence on circadian pathways means that time of administration can matter in experiments. Whether similar metabolic changes occur in humans remains largely unexplored in controlled published trials.
Pharmacokinetic data for SR9009 are limited in published literature. Some reports indicate low oral bioavailability and rapid clearance in animals, which complicates interpretation of exposure and effect. Researchers often use injected routes in preclinical work to achieve measurable systemic levels. Analytical studies rely on mass spectrometry to detect the parent compound and its metabolites. Questions about tissue distribution, active metabolites, and long-term consequences remain open. Species differences in metabolism can affect observed half-life and target engagement.
| Property | Value | Notes |
|---|---|---|
| Regulatory status | Not approved for human use | Research-use-only status in many markets |
| WADA status | Prohibited in sport | Generally listed as a non-approved substance |
| Detection technique | LC-MS/MS | Common for urine and blood analysis |
| Common alias | Stenabolic | Informal market nickname, not a pharmacopoeial name |
| Purity check | HPLC or LC-UV | Independent certificate of analysis is typical |
SR9009 is not approved as a medicine by major regulatory agencies. It is commonly sold as a research chemical, a category that may fall outside customary drug approval and quality rules. In sports, the World Anti-Doping Agency lists SR9009 as a prohibited substance. Athletes who use it can face sanctions if it is detected in a sample. Legal status varies by country, and importation may be restricted. Enforcement practices differ across borders.
Detection of SR9009 in biological samples usually employs liquid chromatography coupled with tandem mass spectrometry. This method can identify the parent compound and sometimes metabolites in urine or blood. Because exposure can be low and clearance may be rapid, sample timing and limits of detection matter. Laboratories validate assays for sensitivity and specificity. Results are interpreted alongside chain-of-custody and quality-control records. Urine is the common matrix for anti-doping analysis, while blood may be used in research settings.
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.
Silver salts have antiseptic properties. In 1881 Credé introduced a method known as Credé's prophylaxis, which used of dilute (2%) solutions of silver nitrate in newborn babies' eyes at birth to prevent contraction of gonorrhea from the mother, which could cause blindness via ophthalmia neonatorum. (Modern antibiotics are now used instead). Fused silver nitrate, shaped into sticks, was traditionally called "lunar caustic". It is used as a cauterizing agent, for example to remove granulation tissue around a stoma. General Sir James Abbott noted in his journals that in India in 1827 it was infused by a British surgeon into wounds in his arm resulting from the bite of a mad dog to cauterize the wounds and prevent the onset of rabies. Silver nitrate is used to cauterize superficial blood vessels in the nose to help prevent nosebleeds. Dentists sometimes use silver nitrate-infused swabs to heal oral ulcers. Silver nitrate is used by some podiatrists to kill cells located in the nail bed. The Canadian physician C. A. Douglas Ringrose researched the use of silver nitrate for sterilization procedures, believing that silver nitrate could be used to block and corrode the fallopian tubes. The technique was ineffective.
The blue mackerel is found in tropical to subtropical waters of the Indian and Pacific Oceans. In the Indo-West Pacific, there is a population in the Red Sea and western Arabian Sea, one in the Northwest Pacific (Japan, China, and Taiwan), and another one in the Southwest Pacific (Australia and New Zealand). Furthermore, the blue mackerel also occur in the eastern Pacific (Hawaii and Revillagigedo Islands, Mexico). It occurs in surface waters down to 300 m (980 ft).
Diabetes is a chronic disease, i.e. it cannot be cured, but symptoms and complications can be minimized with proper treatment. Diabetes can lead to elevated blood sugar levels, which in turn can lead to damage to the heart, blood vessels, kidneys, eyes and nerves. There are very few studies on how to treat LADA, specifically, which is probably due to difficulties in classifying and diagnosing the disease. LADA patients often do not need insulin treatment immediately after being diagnosed because their own insulin production decreases more slowly than T1D patients, but in the long run they will need it. About 80% of all LADA patients initially misdiagnosed with type 2 (and who have GAD antibodies) will become insulin-dependent within 3 to 15 years (according to differing LADA sources). The treatment for Type 1 diabetes/LADA is exogenous insulin to control glucose levels, prevent further destruction of residual beta cells, reduce the possibility of diabetic complications, and prevent death from diabetic ketoacidosis (DKA). Although LADA may appear to initially respond to similar treatment (lifestyle and medications) as type 2 diabetes, this will not halt or slow the progression of beta cell destruction; people with LADA will eventually become insulin-dependent. People with LADA have insulin resistance comparable to long-term type 1 diabetes; some studies found that people with LADA have less insulin resistance than those with type 2 diabetes, but others found no difference.
=== Chronic exposures === The long-term toxicity of copper has not been well studied in humans, but it is infrequent in normal populations that do not have a hereditary defect in copper homeostasis. There is little evidence to indicate that chronic human exposure to copper results in systemic effects other than liver injury. Chronic copper poisoning leading to liver failure was reported in a young adult male with no known genetic susceptibility who consumed 30–60 mg/d of copper as a mineral supplement for 3 years. Individuals residing in U.S. households supplied with tap water containing >3 mg/L of copper exhibited no adverse health effects. No effects of copper supplementation on serum liver enzymes, biomarkers of oxidative stress, and other biochemical endpoints have been observed in healthy young human volunteers given daily doses of 6 to 10 mg/d of copper for up to 12 weeks. Infants aged 3–12 months who consumed water containing 2 mg Cu/L for 9 months did not differ from a concurrent control group in gastrointestinal tract (GIT) symptoms, growth rate, morbidity, serum liver enzyme and bilirubin levels, and other biochemical endpoints.) Serum ceruloplasmin was transiently elevated in the exposed infant group at 9 months and similar to controls at 12 months, suggesting homeostatic adaptation and/or maturation of the homeostatic response. Dermal exposure has not been associated with systemic toxicity but anecdotal reports of allergic responses may be a sensitization to nickel and cross-reaction with copper or a skin irritation from copper.
Sources: en.wikipedia.org
=== Monk === On February 14, 2025, Jonathan Monk became the third offender of the case to stand trial for the 2017 Pasquotank County prison murders. Jury selection lasted from February to March 2025. On March 18, 2025, the jury found Monk guilty of all 13 criminal charges, including four counts of first degree murder. During the sentencing phase, the defence sought to seek mercy for Monk and implored the jury to sentence Monk to life without parole, on account of Monk's troubled childhood, caused by his mother's neglect and that his early exposure to abuse caused long-lasting psychological issues to him while growing up. On March 27, 2025, 38-year-old Jonathan Monk was sentenced to death by Judge Jeffery B. Foster upon the jury's unanimous recommendation for capital punishment. Apart from the four death sentences, Monk also received 60 to 81 years in prison for attempted first degree murder, felony burning a public building, felony attempted escape, and felony riot. Monk was transferred into the Federal Bureau of Prisons system and was held at USP Lee briefly before joining Brady and Buckman at ADX Florence on December 23, 2025.
Historically, red blood cell transfusion was considered when the hemoglobin level fell below 100g/L or hematocrit fell below 30%. Because each unit of blood given carries risks, a trigger level lower than that, at 70 to 80g/L, is now usually used, as it has been shown to have better patient outcomes. The administration of a single unit of blood (approximately 450ml) is the standard for hospitalized people who are not bleeding, with this treatment followed with re-assessment and consideration of symptoms and hemoglobin concentration. Patients with poor oxygen saturation may need more blood. The advisory caution to use blood transfusion only with more severe anemia is in part due to evidence that outcomes are worsened if larger amounts are given. One may consider transfusion for people with symptoms of cardiovascular disease such as chest pain or shortness of breath. In cases where patients have low levels of hemoglobin due to iron deficiency, but are cardiovascularly stable, oral or parenteral iron is a preferred option based on both efficacy and safety. Other blood products are given where appropriate, e.g., fresh frozen plasma to treat clotting deficiencies and platelets to treat or prevent bleeding in thrombocytopenic patients.
Neuropathic pain is a recognized symptom of Charcot–Marie–Tooth disease, although its presence and severity can vary greatly among individuals, and not all patients experience pain. For some, it can be moderate to severe and significantly interfere with daily activities and overall quality of life. When it presents, the pain experienced in CMT is often similar in character to that observed in other forms of peripheral neuropathy, including postherpetic neuralgia and complex regional pain syndrome. Addressing this symptom typically requires an individualized treatment plan, which may include pharmacological interventions, physical therapy, and other supportive strategies to manage and alleviate discomfort. Charcot–Marie–Tooth disease type 1A (CMT1A) can also include mild enlargement or hypertrophy of leg muscles, particularly the calves, alongside typical symptoms of distal muscle weakness and atrophy. However, this muscle enlargement typically represents pseudohypertrophy due to fatty tissue infiltration rather than actual muscle growth. This hypertrophic type of CMT is not caused by the muscles enlarging directly, but by pseudohypertrophy of the legs as fatty tissue enters the leg muscles.
Sources: en.wikipedia.org
Legality depends on the country and the intended use. In many places it is not approved as a medicine and may be sold only as a research chemical. Importation or possession can be restricted, and sports organizations prohibit it.
Anti-doping laboratories typically use LC-MS/MS to detect SR9009 or its metabolites in urine or blood. The exact assay depends on the laboratory and the testing program. Detection can be challenging because the compound may be rapidly metabolized and present at low levels.
Stenabolic is an informal nickname used in online fitness and research-chemical markets, not an official drug name. It likely references reported effects on endurance in rodent studies. The nickname does not imply approval or proven human benefit.
It is a synthetic research compound that activates REV-ERB nuclear receptors. It is not an approved drug or dietary supplement. Most information comes from cell and animal studies.