This is a working overview of WADA Prohibited List, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2025-11-25 and is reviewed periodically as new material appears.
Laboratory studies indicate that GW501516 activates PPARδ, a nuclear receptor involved in fatty acid oxidation and energy metabolism. In rodent experiments, treated animals often showed increased endurance and reduced fat mass. These effects were observed under controlled conditions and do not establish safe or effective use in humans. The exact dose-response relationship in humans remains poorly characterized. Species differences in metabolism can affect how results translate across animals and people.
Safety concerns emerged from long-term animal studies. In rodents given the compound for extended periods, researchers found an increased incidence of certain cancers, including liver and bladder tumors. These findings contributed to the discontinuation of clinical development. Whether similar risks apply to short-term or low-level exposure in humans is not established, and controlled human safety data are limited. The relevance of high-dose rodent carcinogenicity findings to human use remains a subject of debate.
Human trials of GW501516 were small and short in duration. They examined lipid levels, glucose handling, and other metabolic markers, but the programs were halted after the animal cancer findings. No approved therapeutic product exists, and published human data are insufficient for establishing long-term safety. Reports of use for athletic performance come mainly from non-clinical settings and cannot be verified through controlled trials. Independent testing of products sold as cardarine has found inconsistent purity and labeling.
Laboratory detection of cardarine typically involves sample preparation followed by chromatographic separation and mass spectrometric identification. Urine is the most common matrix for anti-doping tests, though blood and hair have also been explored. Methods can target the parent compound or its metabolites, depending on the expected window of detection. Reference standards are required for accurate quantification. Matrix effects and dilution can influence results, so laboratories use internal standards and validation protocols. The exact detection window varies with dose, route, and individual metabolism.
A common misconception is that cardarine has been proven safe for human use. In reality, human clinical data are limited, and long-term animal studies have raised concerns about cancer. Another misconception is that it is a supplement or vitamin-like compound. It is a synthetic research chemical with no approved medical indication. Scientific discussion often focuses on its mechanism and detection rather than therapeutic use. Regulatory and anti-doping literature treats it primarily as a prohibited substance.
| Property | Value | Notes |
|---|---|---|
| Primary target | PPARδ (NR1C2) | Nuclear receptor involved in lipid metabolism |
| Preclinical effect | Increased fatty acid oxidation | Observed in rodent studies |
| Key safety signal | Tumors in rodents after long-term exposure | Contributed to halted clinical development |
| Human trial status | No approved product; development stopped | Limited short-term metabolic data |
| Sport regulatory status | Prohibited at all times | WADA hormone and metabolic modulators class |
Cardarine is a common name for GW501516, an investigational compound developed in the 1990s for metabolic conditions. It acts as an agonist at peroxisome proliferator-activated receptor delta, a nuclear receptor involved in lipid and energy metabolism. The compound is frequently mislabeled as a selective androgen receptor modulator, or SARM, but its molecular target is different. GW501516 reached early clinical testing before development was discontinued. It has no approved therapeutic use in any country. The name cardarine is not a formal international nonproprietary name.
Regulatory treatment varies, but cardarine is not approved as a medicine. Sports authorities list GW501516 as a prohibited substance, and it is banned at all times under the World Anti-Doping Agency code. Many countries restrict sales for human consumption, while online vendors market it as a research chemical. Such products may lack purity data, and their actual contents can differ from the label. Purchasing or possessing cardarine may carry legal consequences depending on jurisdiction. The compound is not a dietary supplement ingredient in regulated markets.
Clinical development stopped after rodent studies showed tumors at multiple sites. Whether those findings predict human cancer risk remains an open question, but they led sponsors to discontinue programs. Human safety data are limited to small, short-term studies that were not designed to assess cancer risk. Reported effects in those studies included changes in blood lipids, but the evidence is insufficient for medical use. Long-term consequences of nonmedical use are not well characterized. Questions about dose, duration, and individual susceptibility remain unresolved.
Laboratory studies have examined GW501516 in cell cultures and rodents for conditions such as dyslipidemia, insulin resistance, and obesity. Some trials in humans were initiated, but development was discontinued after preclinical findings raised concerns about cancer in certain models. Those findings do not prove that the compound causes cancer in people, but they contributed to regulatory caution. Later reviews often describe the evidence as preliminary and insufficient for assessing long-term safety.
In the fitness and bodybuilding literature, cardarine is frequently discussed as an endurance agent or fat-loss compound, although such claims are not supported by robust clinical evidence. Online descriptions often mix animal data, user anecdotes, and marketing language. Researchers who study PPARδ agonists distinguish between receptor activation in controlled experiments and unsupervised use of unverified products. The latter introduces unknown purity, dose, and interactions, making reported experiences difficult to interpret scientifically.
GW501516 acts as an agonist at peroxisome proliferator-activated receptor delta, a nuclear receptor involved in transcription of genes related to lipid handling and energy use. Activation of PPARδ can shift skeletal muscle toward greater fatty acid oxidation in animal models, which is one reason it drew interest for metabolic disease and exercise research. The exact downstream effects depend on tissue, species, dose, and duration. Human data are sparse, so many proposed benefits remain hypotheses rather than established clinical outcomes.
Cardarine is not approved for human therapeutic use in any major jurisdiction. It appears on the World Anti-Doping Agency Prohibited List as a PPARδ agonist within the hormone and metabolic modulators category. Sports organizations test for it because it has been detected in athlete samples and seized products. Regulatory actions against marketed research chemical versions have occurred in several countries, though enforcement varies. Availability through unregulated channels complicates oversight.
Analytical laboratories typically identify cardarine and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is a common matrix in anti-doping testing, while blood and tissue may be used in research settings. Detection windows depend on the assay, the sample matrix, and the compound's metabolism. Because cardarine is extensively metabolized, laboratories often target specific metabolites to improve sensitivity and confirmation. Reference standards are required for reliable quantification. Method validation includes checks for selectivity, linearity, and carryover.
A persistent misconception is that cardarine is a fat-burning drug or a safe alternative to anabolic steroids. No approved therapeutic product exists, and human safety data are limited. The tumor findings in rodents remain a central concern in scientific reviews. Products sold online may contain inaccurate labels, impurities, or different compounds entirely, which complicates any assessment of effects. Independent testing of such products has reported frequent mislabeling. For these reasons, discussions in the literature emphasize risks and unknowns rather than benefits.
=== Legal status === United States: During clinical trials a small number of users (~4%) reported euphoria after use, which led to its control in the US. The Drug Enforcement Administration (DEA) classified pregabalin as a depressant and placed pregabalin, including its salts, and all products containing pregabalin into Schedule V of the Controlled Substances Act. Norway: Pregabalin is in prescription Schedule B, alongside benzodiazepines. United Kingdom: On January 14, 2016, the Advisory Council on the Misuse of Drugs (ACMD) recommended that pregabalin, along with gabapentin, be controlled under the Misuse of Drugs Act 1971. In October 2018, it was announced that pregabalin would be reclassified as a Class C controlled substance, effective April 2019. As a Class C drug, pregabalin now requires a prescription in the UK, and the prescription must clearly specify the dose. Australia: Pregabalin has been classified as Schedule 4 (prescription only) since its registration in Australia in 2005. Despite this classification, concerns about misuse and deaths led the Therapeutic Goods Administration (TGA) to add boxed warnings regarding abuse and dependence to pregabalin's prescribing information in 2021. Data from the National Coronial Information System showed pregabalin-related deaths rose from 16 in 2013 to 121 in 2016, and a 2019 study in the Medical Journal of Australia found over a tenfold increase in pregabalin-related ambulance attendances in Victoria between 2012 and 2017. Pregabalin is subject to real-time prescription monitoring in all states and territories.
=== Synthetic organic chemistry === BCATs have been used in the synthesis of some pharmaceutical drugs as an alternative to heavy metal catalysts, which can be expensive/environmentally unfriendly. Aminotransferases (transaminases) in general have been used to create unnatural amino acids, important building blocks for peptidomimetic drugs and agricultural products. BCAT from E. coli is typically engineered to be overexpressed and extracted from whole cells to be used for chemical synthesis. Aminotransferases are used because they can accomplish a typically multi-step reaction in one step, can perform reactions on a wide range of substrates, and have high regioselectivity and enantioselectivity. In synthetic organic chemistry, BCATs are typically used for the conversion of L-Leucine to 2-ketoglutarate.
The maximum life span of transgenic mice has been extended about 20% by overexpression of human catalase targeted to mitochondria A comparison of 7 non-primate mammals (mouse, hamster, rat, guinea-pig, rabbit, pig and cow) showed that the rate of mitochondrial superoxide and hydrogen peroxide production in heart and kidney were inversely correlated with maximum life span A study of 8 non-primate mammals showed an inverse correlation between maximum life span and oxidative damage to mtDNA (mitochondrial DNA) in heart & brain A study of several species of mammals and a bird (pigeon) indicated a linear relationship between oxidative damage to protein and maximum life span There is a direct correlation between DNA repair and maximum life span for mammalian species Drosophila (fruit-flies) bred for 15 generations by only using eggs that were laid toward the end of reproductive life achieved maximum life spans 30% greater than that of controls Overexpression of the enzyme which synthesizes glutathione in long-lived transgenic Drosophila (fruit-flies) extended maximum lifespan by nearly 50% A mutation in the age−1 gene of the nematode worm Caenorhabditis elegans increased mean life span 65% and maximum life span 110%. However, the degree of lifespan extension in relative terms by both the age-1 and daf-2 mutations is strongly dependent on ambient temperature, with ≈10% extension at 16 °C and 65% extension at 27 °C. Fat-specific Insulin Receptor KnockOut (FIRKO) mice have reduced fat mass, normal calorie intake and an increased maximum life span of 18%.
== Overview == Dependent origination is a philosophically complex concept, subject to a large variety of explanations and interpretations. As the interpretations often involve specific aspects of dependent origination, they are not necessarily mutually exclusive to each other. Dependent origination can be contrasted with the classic Western concept of causation in which an action by one thing is said to cause a change in another thing. Dependent origination instead views the change as being caused by many factors, not just one or even a few. The principle of dependent origination has a variety of philosophical implications.
Sources: en.wikipedia.org
== Misattributed == Teleny, or The Reverse of the Medal (Paris, 1893) has been attributed to Wilde, but its authorship is unclear. One theory is that it was a combined effort by several of Wilde's friends, which he may have edited. Constance – On September 14, 2011, Wilde's grandson Merlin Holland contested Wilde's claimed authorship of this play entitled Constance, scheduled to open that week in the King's Head Theatre. It was not, in fact, "Oscar Wilde's final play," as its producers were claiming. Holland said Wilde did sketch out the play's scenario in 1894, but "never wrote a word" of it, and that "it is dishonest to foist this on the public." The artistic director Adam Spreadbury-Maher of the King's Head Theatre and producer of Constance pointed out that Wilde's son, Vyvyan Holland, wrote, in 1954, "a significant amount of the dialogue (of Constance) bears the authentic stamp of my father's hand". There is further proof that the developed scenario that Constance was reconstituted from was written by Wilde between 1897 and his death in 1900, rather than the 1894 George Alexander scenario which Merlin Holland quotes.
On 10 December 2009, Mgr Yves Le Saux, Bishop of Le Mans, France, opened the diocesan process for the beatification of Zita. Zita was in the habit of spending several months each year in the diocese of Le Mans at St. Cecilia's Abbey, Solesmes, where three of her sisters were nuns. The actor is the French Association pour la Béatification de l'Impératrice Zita. The postulator for the cause is Alexander Leonhardt. Vice postulator for Hungary is Catholic theologian Norbert Nagy. The judge of the tribunal is Bruno Bonnet. The promoter of justice is François Scrive. With the opening of her cause, the late Empress has been named Servant of God.
The capacity to store retinol in the liver means that well-nourished humans can go months on a vitamin A deficient diet without manifesting signs and symptoms of deficiency. Two liver cell types are responsible for storage and release: hepatocytes and hepatic stellate cells (HSCs). Hepatocytes take up the lipid-rich chylomicrons, bind retinol to retinol-binding protein 4 (RBP4), and transfer the retinol-RBP4 to HSCs for storage in lipid droplets as retinyl esters. Mobilization reverses the process: retinyl ester hydrolase releases free retinol which is transferred to hepatocytes, bound to RBP4, and put into blood circulation. Other than either after a meal or when consumption of large amounts exceeds liver storage capacity, more than 95% of retinol in circulation is bound to RBP4.
Sources: en.wikipedia.org
== History == In the 18th century, young British chimney sweeps who climbed into chimneys suffered from chimney sweeps' carcinoma, a scrotal cancer peculiar to their profession, and this was connected to the effects of soot in 1775, in the first work of occupational cancer epidemiology and also the first connection of any chemical mixture to cancer formation. Frequent skin cancers were noted among fuel industry workers in the 19th century. In 1933, BaP was determined to be the compound responsible for these cases, and its carcinogenicity was demonstrated when skin tumors occurred in laboratory animals repeatedly painted with coal tar. BaP has since been identified as a prime carcinogen in cigarette smoke. Public health authorities distinguish between the addictive effects of nicotine and the carcinogenic substances present in cigarette smoke, such as BaP.
=== Myopathies with fiber size variation === Myopathies with varying fiber size, such as congenital fiber type disproportion, occurs when type 1 fibers, the slow twitch fibers involved in sustaining activity, are smaller than type 2 fibers, the fast twitch fibers involved in quick activity. Since smaller type 1 fibers is not associated with nemaline myopathy, the most common type of congenital myopathy, it has not been studied in as great detail as many of the others. However, the smaller type 1 fibers explains why patients typically can participate in activities for shorter periods of time, but struggle with extended activity.
The courts give the EU a wide discretion to implement policy, so judicial review is possible only if agricultural measures are 'manifestly inappropriate'. EU law does not yet have a systematic plan or subsidies to rewild depleted environments, and to move to complete clean energy infrastructure.
== Skin contracture == Wound contraction, where the edges of the skin are pulled together to close the wound, is a normal part of wound healing. However, large wounds and abnormal wound healing cause skin contractures by excessively tightening the skin and limiting movement. A skin contracture due to a burn is known as a burn scar contracture. Large areas of missing skin (such as large burns, grazes, and gouges) drastically reduce the area of skin causing it to become tight when pulled together during wound healing. Scars initially lack elasticity with synthesis of elastic tissue fibres (elastogenesis) being a function of duration and site of the scar. Deep wounds and abnormal wound healing causes abnormal scarring such as hypertrophic scars. Studies on hypertrophic scars have shown a lack of improvement to both elasticity and stiffness suggesting a prolonged healing phase without amelioration seen in a normal wound-healing curve. Surgery can help alleviate skin contractures in the form of skin grafts and removal of hypertrophic scars. For hypertrophic scars, timing is important when considering surgery, as over time scars will mature and may show decreased contractures along with flattening, softening, and repigmentation without surgical intervention.
Sources: en.wikipedia.org
Rodent studies reported increased endurance and fat oxidation after GW501516 exposure. Long-term studies also found higher rates of some tumors, which led to halted development.
Small short-term human trials examined metabolic markers such as lipids and glucose. The trials did not continue after rodent cancer findings, so long-term human safety is unknown.
Controlled human trials have not established a performance benefit. Anecdotal reports exist, but they are not reliable evidence.
Yes, WADA prohibits cardarine as a PPARδ agonist. It appears on the prohibited list and can be detected in urine or blood. Athletes using it risk sanctions.