The short version of WADA Prohibited List fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2026-08-01 and is reviewed periodically as new material appears.
GW501516 acts as an agonist at the peroxisome proliferator-activated receptor delta, a nuclear receptor that regulates gene expression. Activation shifts transcription toward genes involved in fatty acid uptake, oxidation, and energy expenditure. The compound does not bind the androgen receptor and therefore differs from anabolic steroids and SARMs. In rodent models, this metabolic shift has been linked to increased running endurance and reduced fat accumulation. The exact downstream pathways in humans remain incompletely characterized.
Early clinical research explored GW501516 for lipid disorders, obesity, and diabetes. Some short-term human studies reported changes in HDL cholesterol, LDL cholesterol, and triglycerides. The development program was discontinued after rodent studies showed dose-dependent tumor formation in multiple tissues, including liver, bladder, stomach, and skin. These findings raised concerns about long-term cancer risk in humans. Because human exposure data are limited, the clinical significance of the rodent tumors remains uncertain.
Preclinical research reported that GW501516 increased running endurance in mice and improved lipid profiles in some animal species. Early human trials explored effects on high-density lipoprotein cholesterol, triglycerides, and glucose handling, but the program was discontinued. Published human data are sparse and do not establish efficacy for any condition. Studies also examined PPAR delta in cancer biology, with conflicting findings across models. The relationship between receptor activation, tissue context, and disease risk remains an active area of investigation.
Anti-doping laboratories identify GW501516 and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is the usual matrix, and detection can occur after the parent compound has cleared from blood. The exact detection window depends on dose, formulation, individual metabolism, and assay sensitivity. Because the compound is prohibited at all times, athletes are subject to testing in and out of competition. Analytical methods continue to improve as new metabolites and designer analogs are characterized.
GW501516 acts as a ligand for PPAR delta, a nuclear receptor that regulates transcription of genes involved in fatty acid oxidation and energy use. Activation of this receptor in skeletal muscle shifts metabolism toward fat burning in animal models. The compound does not burn fat directly; it changes gene expression over hours to days. Researchers study it to understand metabolic flexibility and exercise adaptation. Effects observed in rodents are not automatically expected in humans.
| Property | Value | Notes |
|---|---|---|
| Primary target | PPARδ | Nuclear receptor; not androgen receptor |
| Studied indications | Dyslipidemia; obesity; diabetes | Early clinical research; development discontinued |
| Rodent toxicity | Tumor formation in multiple tissues | Dose-dependent findings in some studies |
| Human approval | None | No approved therapeutic use |
| Typical analytical method | LC-MS/MS | Used for identity and quantification |
Cardarine can be detected in biological samples and product materials using liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). The method separates compounds by chromatography and identifies them by mass-to-charge transitions, allowing low-level detection in urine or blood. Sample preparation often involves enzymatic hydrolysis, solid-phase extraction, or protein precipitation. Certified reference materials and isotope-labeled internal standards improve quantification. Detection windows depend on metabolism, matrix, and assay sensitivity, so no single universal window applies.
Regulatory treatment of cardarine differs by context and jurisdiction. In competitive sport, the World Anti-Doping Agency lists PPARδ agonists, including GW501516, as prohibited at all times. Outside sport, it lacks approval as a prescription medicine in major drug markets, and products sold for human consumption may be treated as unapproved drugs. Some countries also restrict importation or sale through general consumer protection and medicines laws. These classifications affect availability, testing, and legal risk without establishing therapeutic value.
Because cardarine is not an approved medicine, no pharmacopeial monograph defines its identity, purity, or storage requirements. Laboratories typically rely on in-house methods and reference standards when testing materials labeled as GW501516. Certificates of analysis may report purity and identity for a specific batch, but their scope varies and they do not guarantee safety or legal status. Independent verification can include high-performance liquid chromatography, mass spectrometry, nuclear magnetic resonance, and elemental analysis. The distinction between research chemical labeling and human use is significant because quality standards and oversight differ.
Cardarine is a common name for the investigational chemical GW501516, also written GW-1516. It was developed as a peroxisome proliferator-activated receptor delta agonist for metabolic conditions such as dyslipidemia. Early research focused on lipid handling and energy use in skeletal muscle and other tissues. The compound was never approved as a medicine. In public discussion, it is often grouped with performance-enhancing substances, although its receptor target differs from that of anabolic steroids or selective androgen receptor modulators. Regulatory and health authorities have issued warnings about its use.
GW501516 acts on PPARδ, a nuclear receptor that helps regulate fatty acid oxidation and energy homeostasis. In animal studies, activation of this receptor was associated with increased endurance and changes in lipid metabolism. Human trials examined effects on blood lipids and other metabolic markers, but the compound did not advance to approval. Rodent studies later reported tumors in multiple tissues at doses used in those experiments. Whether those findings translate to human risk remains uncertain, and the clinical relevance of the animal data is still debated.
Regulatory bodies treat GW501516 as a prohibited substance in competitive sport. The World Anti-Doping Agency added it to the prohibited list, and it falls under classes covering metabolic modulators and hormone-related agents. It is not approved by drug regulators for human use, and it is not a lawful dietary supplement. Products sold under the cardarine name may contain unlisted ingredients or different compounds. Because no approved product exists, quality and identity are not guaranteed by pharmaceutical manufacturing standards.
Cardarine is the common name for GW501516, a synthetic compound studied as a peroxisome proliferator-activated receptor delta agonist. Researchers developed it to explore treatments for lipid disorders and metabolic conditions. It is not an approved medicine in any country. Early clinical work examined changes in HDL cholesterol and triglycerides, but development was discontinued after animal studies raised concerns about cancer. The compound remains available as a research chemical and appears in discussions of performance enhancement.
At the molecular level, GW501516 binds and activates PPARδ, a nuclear receptor that regulates transcription. Activation shifts expression of genes involved in fatty acid oxidation, energy expenditure, and lipid transport in skeletal muscle and liver. Animal studies report increased endurance and altered lipid profiles after exposure. Human data are limited to small trials and do not establish long-term safety or efficacy. PPARδ also has roles in cell proliferation, so the relationship between activation and cancer risk remains an open question.
GW501516 acts as a selective agonist at PPARδ, a nuclear receptor that regulates transcription of genes involved in lipid handling and energy metabolism. Activation of PPARδ in preclinical models increases fatty acid oxidation, mitochondrial biogenesis, and exercise endurance in rodents. These effects have made the compound a subject of metabolic research and also a target for sport anti-doping rules. In humans, however, controlled studies are limited, and whether similar endurance or metabolic changes occur at tolerated exposures remains an open question. The receptor’s broad tissue distribution also means downstream effects may vary by organ and condition.
Detection of GW501516 in biological samples generally relies on liquid chromatography coupled with tandem mass spectrometry. Urine is a common matrix in anti-doping analysis, while blood or plasma may be used in research settings. Sample preparation can involve enzymatic hydrolysis, protein precipitation, or solid-phase extraction before instrumental analysis. Because the compound undergoes metabolism, assays may target the parent molecule, one or more metabolites, or both. Detection windows are not fixed; they depend on factors such as dose, route, individual metabolism, and assay sensitivity. Reference standards are required for accurate identification and quantification.
== Other controversies == Other proceedings are active before Australian courts regarding Dank's supply of thymosin beta on sportsmen. Findings were made that he supplied the drug to a Mr Earl by the Administrative Appeals Tribunal in 2015; these proceedings are subject to appeal, but were noted by the Court of Arbitration for Sport in their findings regarding the Essendon Football Club doping scandal. In July 2016, Dank was targeted by a drive-by shooting attack that injured him. In 2017, it was reported that Dank entered bankruptcy.
Elizabeth Broadbent; Keith J Petrie; Jodie Main; John Weinman (2006). "The brief illness perception questionnaire". Journal of Psychosomatic Research. 60 (6): 631–637. doi:10.1016/j.jpsychores.2005.10.020. PMID 16731240. Wikidata Q50936509. Elizabeth Broadbent; Carissa Wilkes; Heidi Koschwanez; John Weinman; Sam Norton; Keith J Petrie (2015). "A systematic review and meta-analysis of the Brief Illness Perception Questionnaire". Psychology & Health. 30 (11): 1361–1385. doi:10.1080/08870446.2015.1070851. PMID 26181764. Wikidata Q38548518. E. Broadbent; R. Stafford; B. MacDonald (2009). "Acceptance of Healthcare Robots for the Older Population: Review and Future Directions". International journal of social robotics. 1 (4): 319–330. doi:10.1007/s12369-009-0030-6. Wikidata Q115258302. Hayley Robinson; Bruce Macdonald; Ngaire Kerse; Elizabeth Broadbent (2013). "The psychosocial effects of a companion robot: a randomized controlled trial". Journal of the American Medical Directors Association. 14 (9): 661–667. doi:10.1016/j.jamda.2013.02.007. PMID 23545466. Wikidata Q45166572. Elizabeth Broadbent; Liesje Donkin; Julia C Stroh (2011). "Illness and treatment perceptions are associated with adherence to medications, diet, and exercise in diabetic patients". Diabetes Care. 34 (2): 338–340. doi:10.2337/dc10-1779. PMC 3024345. PMID 21270191. Wikidata Q34507111.
== Metabolism == cADPR and ADPR are synthesized from NAD+ by the bifunctional ectoenzymes of the CD38 family (also includes the GPI-anchored CD157 and the specific, monofunctional ADP ribosyl cyclase of the mollusc Aplysia). The same enzymes are also capable of hydrolyzing cADPR to ADPR. Catalysis proceeds via a covalently bound intermediate. The hydrolysis reaction is inhibited by ATP, and cADPR may accumulate. Synthesis and degradation of cADPR by enzymes of the CD38 family involve, respectively, the formation and the hydrolysis of the N1-glycosidic bond. In 2009, the first enzyme able to hydrolyze the phosphoanhydride linkage of cADPR, i.e. the one between the two phosphate groups, was reported. SARM1 and other TIR domain-containing proteins also catalyze the formation of cADPR from NAD+.
The German Democratic Republic (East Germany) was a Marxist-Leninist communist state that utilised a planned economy based on economic policies set by the ruling Socialist Unity Party of Germany (SED). The vast majority of the economy belonged to state-owned enterprises known as Volkseigene Betriebe (VEBs), which were under the control of the State Planning Commission of the Council of Ministers. The SED allocated investment into certain industries based on its economic policies, rather than based on the supply and demand of the market. While East Germany was able to maintain a modest economic growth and an increase in living standards, it was unable to keep pace with the spending growth of the welfare state needed to maintain those living standards. A growing proportion of investment funds were consumed by the ever-expanding and costly welfare state. The SED attempted to fuel economic growth with foreign loans, but the economy actually headed towards stagnation and led to a severe debt crisis that only starved East German industries even further. By the time of Die Wende and the fall of the SED regime in 1989, East Germany's industries were significantly labour intensive and underdeveloped compared to those in the Federal Republic of Germany (West Germany), which made many of them unprofitable and indebted. The de Maizière cabinet, the first non-socialist government of East Germany, decided on a mass privatisation of these industries.
Sources: en.wikipedia.org
Based on his own experience as a Rhodes Scholar, Florey created a version for European students. The European Studentship scheme provided support for graduates from eleven western European and Scandinavian countries with an annual stipend of £1,100 (equivalent to £16,000 in 2025) for two years. Florey raised the money for nine studentships. Florey did not live to see the first studentship awarded in 1969, and without him additional funding was not forthcoming and the money was exhausted by 1980. By then 76 students had benefited from the scheme, and they had published 15 books and 250 articles in peer-reviewed journals. During his term as provost, there was a major construction program to provide enough accommodation for all undergraduates to be able to spend at least two years in residence. This involved three developments, the largest of which was Florey's personal project: the construction of a new building on the River Cherwell at St Clement's, Oxford. The cost was substantial—the purchase price of the site alone was £500,000 (equivalent to £9,133,000 in 2025)—but Florey was accustomed to raising large sums of money. It was designed by the British architect Sir James Stirling. Florey died the day that construction work was scheduled to begin. When the building was opened in 1971, it was named the Florey Building in his honour. Buildings were also named after Florey in Adelaide, Melbourne, and Canberra, where his refurbished original John Curtin School of Medicine Building was renamed the Florey Building in 2015.
The prevalence of abdominal obesity is increasing in Western populations, possibly due to a combination of low physical activity and high-calorie diets, and also in developing countries, where it is associated with the urbanization of populations. Other environmental factors, such as maternal smoking, estrogenic compounds in the diet, and endocrine-disrupting chemicals may be important also. Hypercortisolism, such as in Cushing's syndrome, also leads to central obesity. Many prescription drugs, such as dexamethasone and other steroids, can also have side effects resulting in central obesity, especially in the presence of elevated insulin levels. There are various ways of measuring abdominal obesity including: Absolute waist circumference (>102 cm (40 in) in men and >88 cm (35 in) in women) Waist–hip ratio (the circumference of the waist divided by that of the hips of >0.9 for men and >0.85 for women) Waist-stature ratio (waist circumference divided by their height, >0.5 for adults under 40 and >0.6 for adults over 50) Sagittal Abdominal Diameter
Uranium (92U) is a naturally occurring radioactive element (radioelement) with no stable isotopes. It has two primordial isotopes, uranium-238 and uranium-235, that have long half-lives and are found in appreciable quantity in Earth's crust. The decay product uranium-234 is also found. Other isotopes such as uranium-233 have been produced in breeder reactors. In addition to isotopes found in nature or nuclear reactors, many isotopes with far shorter half-lives have been produced, ranging from 214U to 242U (except for 220U). The standard atomic weight of natural uranium is 238.02891(3). Natural uranium consists of three main isotopes, 238U (99.2739–99.2752% natural abundance), 235U (0.7198–0.7202%), and 234U (0.0050–0.0059%). All three isotopes are radioactive (i.e., they are radioisotopes), and the most abundant and stable is uranium-238, with a half-life of 4.463×109 years (about the age of the Earth). Uranium-238 is an alpha emitter, decaying through the 18-member uranium series into lead-206. The decay series of uranium-235 (historically called actino-uranium) has 15 members and ends in lead-207. The constant rates of decay in these series makes comparison of the ratios of parent-to-daughter elements useful in radiometric dating. Uranium-233 is made from thorium-232 by neutron bombardment.
Sources: en.wikipedia.org
It targets PPARδ, a nuclear receptor involved in lipid and energy metabolism. It does not act primarily on androgen receptors. This distinction separates it from SARMs.
Rodent studies found dose-dependent tumors in several organs. The sponsor discontinued the program over cancer concerns. Human risk from long-term use remains unknown.
Controlled human endurance trials are lacking. Animal studies show increased exercise capacity under some conditions. Anecdotal reports are not equivalent to clinical evidence.
It binds to and activates PPAR delta, a nuclear receptor that controls expression of genes related to fatty acid oxidation. This mechanism can alter energy metabolism in animal models. It is not a direct stimulant or fat-burning enzyme.