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Identity And Regulatory Status — Reference Sheet

By Editorial Desk · published 2026-04-06 · last reviewed 2026-05-11 · Data

anti-doping comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.

Updated 2026-05-11. Numbers and descriptions here follow the published literature rather than marketing material.

Identity and Regulatory Status

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.

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.

Mechanism and Detection Methods

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.

Cardarine at a glance

PropertyValueNotes
Common synonymsGW501516; GW-1516; endurobolGW501516 is the research code
Drug classPPARδ agonistNot a selective androgen receptor modulator
Molecular formulaC21H18F3NO3S2Established chemical formula
Molar mass453.5 g/molCalculated from the formula
Regulatory statusProhibited in sport; not approved as medicineStatus varies by country

Mechanism and Research Context

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.

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Regulation and Detection

Cardarine has no approved therapeutic indication and is not marketed as a medicine. The World Anti-Doping Agency lists GW501516 as a prohibited substance at all times, covering both in-competition and out-of-competition periods. National laws vary: some countries treat it as an unapproved drug subject to import controls, while others have specific restrictions on sale for human consumption. It is often sold as a research chemical, a label that does not imply safety or legality. Enforcement actions have targeted online vendors and shipments.

Anti-doping laboratories identify GW501516 and related metabolites using liquid chromatography coupled with tandem mass spectrometry. Urine is the most common matrix, though blood and dried blood spots may also be analyzed. The method targets the parent compound and phase I and phase II metabolites, which extend the detection window. Because the substance is prohibited at all times, athletes can be tested outside competition. Detection limits and windows depend on the assay, sample type, and individual metabolism.

Cardarine is frequently described as a fat-burning or endurance-enhancing supplement, but these claims exceed the available evidence. The compound is not a hormone, steroid, or selective androgen receptor modulator. Research articles discuss it as a tool compound for studying PPARδ biology, while anti-doping literature focuses on its abuse and detection. Quality of unapproved products is uncertain, and independent analyses have found impurities or incorrect labeling. Open questions include whether human cancer risk resembles that seen in rodents and how often non-athletes use the substance.

Regulatory Status and Detection Context

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.

Background and Research Context

Cardarine is a common name for GW501516, a synthetic compound developed in the 1990s through research collaborations involving GlaxoSmithKline. It belongs to a class of molecules known as peroxisome proliferator-activated receptor delta agonists. Early studies explored its effects on lipid metabolism and energy expenditure in animal models. The compound was never approved as a human medicine, and clinical development was discontinued. In the years since, it has appeared in fitness and bodybuilding communities as a performance-enhancing substance. Regulatory agencies classify it as an unapproved drug.

PPARδ is a nuclear receptor that regulates gene expression related to fatty acid oxidation, glucose homeostasis, and mitochondrial function. GW501516 binds to this receptor with high affinity and activates downstream signaling in skeletal muscle and other tissues. Animal studies reported increased endurance and altered fuel preference, but human data remain limited and inconsistent. The precise relationship between receptor activation and observed physiological changes is still an area of active investigation. Researchers have also examined whether the compound affects inflammation or cell proliferation. No approved therapeutic indication exists for cardarine.

Notes from published material

== Appearance and behaviour == Laboratory mice have retained many of the physical and behavioural characteristics of house mice; however, due to many generations of artificial selection, some of these characteristics now vary markedly. Due to the large number of strains of laboratory mice, it is impractical to comprehensively describe the appearance and behaviour of all of them; however, they are described below for two of the most commonly used strains.

When the USSR was dissolved in 1991, Moscow remained the capital of the Russian Federation. Since then, a market economy has emerged, producing a significant increase in Western-style retailing, services, architecture, and lifestyles. The city continued to grow during the 1990s and 2000s, its population rising from less than nine million to more than ten million. Scholars Mason and Nigmatullina argue that Soviet-era urban-growth controls produced controlled and sustainable metropolitan development, typified by the greenbelt built in 1935. Since then, however, low-density suburban sprawl has increased significantly, as a result of heavy demand for single-family dwellings (rather than multi-family apartments). In 1995–1997, the MKAD ring road was widened from an initial four lanes to ten lanes. In December 2002, Bulvar Dmitriya Donskogo became the first Moscow Metro station to open outside the MKAD. The Third Ring Road—intermediate between the early 19th-century Garden Ring and the Soviet-era outer ring road—was completed in 2004. The greenbelt is becoming more fragmented, and satellite cities are appearing at the fringe. Summer dachas are being converted into year-round residences; with the proliferation of automobiles, the city has heavy traffic congestion. Multiple old churches and other examples of architectural heritage that were demolished during the Stalin era have been restored, such as the Cathedral of Christ the Saviour. In the 2010s, Moscow's administration launched long-term projects such as the Moja Ulitsa (lit.

== Mechanisms of an alternative reaction route == These conformational changes also bring catalytic residues in the active site close to the chemical bonds in the substrate that will be altered in the reaction. After binding takes place, one or more mechanisms of catalysis lowers the energy of the reaction's transition state, by providing an alternative chemical pathway for the reaction. There are six possible mechanisms of "over the barrier" catalysis as well as a "through the barrier" mechanism:

Sources: en.wikipedia.org

Background from the literature

== Species distribution == Selenoproteins exist in all major domains of life, eukaryotes, bacteria and archaea. Among eukaryotes, selenoproteins appear to be common in animals, but rare or absent in other phyla—one has been identified in the green alga Chlamydomonas, but almost none in other plants or in fungi. The American cranberry (Vaccinium macrocarpon Ait.) is the only land plant known (as of 2014) to possess sequence-level machinery for producing selenocysteine (specifically in its mitochondrial genome), although its level of functionality is not yet determined. Among fungi, the order Harpellales was "particularly well represented" amongst fungal species found to possess selenocysteine, as 7 out of the 8 Harpellales species analyzed are believed to utilize selenoproteins Among bacteria and archaea, selenoproteins are only present in some lineages, while they are completely absent in many other phylogenetic groups. These observations have now been confirmed by whole genome analysis, which shows the presence or absence of selenoprotein genes and accessory genes for the synthesis of selenoproteins in the respective organism.

=== Legalization and regulated markets === Over 50 countries and the large majority of US states have legalized cannabis for medical use. In 2020, the CND acted on a recommendation from the WHO's ECDD by removing cannabis from the Single Convention's most restrictive Schedule IV category and recognized its medical value, while retaining it in the next most restrictive Schedule I. Addressing recreational use, the INCB in 2023 stated that "legalizing the non-medical use of cannabis ... contravenes the 1961 Single Convention on Narcotic Drugs" and that "the effects of cannabis use on individuals and societies should be studied further before Governments make long-term binding decisions", reminding governments that "the drug control conventions offer significant flexibility" for finding alternative solutions than legalization. In 2012, two US states, Colorado (Amendment 64) and Washington (Initiative 502), legalized cannabis by direct vote through ballot initiatives. The INCB had warned, "Implementing the decisions of popular votes held in the United States in Colorado and Washington to allow for the recreational use of cannabis would be a violation of international laws." In August 2013, the federal government announced it would not act against states opening cannabis stores, with the expectation that state regulations would be "tough in practice, not just on paper, and include strong, state-based enforcement efforts, backed by adequate funding." The UN did not propose sanctions against the US, in particular since there exists no applicable sanction for the UN to apply.

P-type calcium channels are voltage-dependent calcium channels that are classified under the high voltage activated class channel, along with L-, N-, Q- and R-type channels. These channels require a strong depolarization in order to be activated. They are found at axon terminals, as well as in somatodendritic areas of neurons within the central and peripheral nervous system. P-type calcium channels are also critical to vesicle release, specifically neurotransmitters and hormones at synaptic terminals of excitatory and inhibitory synapses. Voltage-gated P-type calcium channels consist of a main pore-forming α1 subunit (which is more specifically referred to as CaV2.1), an α2δ subunit and a β subunit. There can be γ subunits found in calcium channels of skeletal muscles. The α1 subunit is encoded specifically by the CACNA1A gene and is composed of four domains, each containing six transmembrane (S1-S6) spanning α helices. The S1-S2 loop and the S6 region are thought to be responsible for the channel's inactivation, the S4 region serves as the voltage sensor and S5-S6 loop forms the pore. There are seven subunits within the α1 subunit. The A subunit, called α1ACa2+, corresponds to what is functionally defined as the P-type and Q-type isoforms. P-type and Q-type calcium channels are closely related as they are produced from the same gene via alternative splicing. As a complication of the alternative splicing, P-type and Q-type channels may have different subunit compositions. The β subunit regulates the kinetics and expression of the channel, along with the α2δ subunit.

In the absence of suitable plate culture techniques, some microbes require culture within live animals. Bacteria such as Mycobacterium leprae and Treponema pallidum can be grown in animals, although serological and microscopic techniques make the use of live animals unnecessary. Viruses are also usually identified using alternatives to growth in culture or animals. Some viruses may be grown in embryonated eggs. Another useful identification method is Xenodiagnosis, or the use of a vector to support the growth of an infectious agent. Chagas disease is the most significant example, because it is difficult to directly demonstrate the presence of the causative agent, Trypanosoma cruzi in a patient, which therefore makes it difficult to definitively make a diagnosis. In this case, xenodiagnosis involves the use of the vector of the Chagas agent T. cruzi, an uninfected triatomine bug, which takes a blood meal from a person suspected of having been infected. The bug is later inspected for growth of T. cruzi within its gut.

Sources: en.wikipedia.org

Further detail

=== Overdose issues === In 2007, a nurse at Cedars-Sinai Medical Center mistakenly gave the 12-day-old twins of actor Dennis Quaid a dose of heparin that was 1,000 times the recommended dose for infants. The overdose allegedly arose because the labeling and design of the adult and infant versions of the product were similar. The Quaid family subsequently sued the manufacturer, Baxter Healthcare Corp., and settled with the hospital for $750,000. Prior to the Quaid accident, six newborn babies at Methodist Hospital in Indianapolis, Indiana, were given an overdose. Three of the babies died after the mistake. In July 2008, another set of twins born at Christus Spohn Hospital South, in Corpus Christi, Texas, died after an accidentally administered overdose of the drug. The overdose was due to a mixing error at the hospital pharmacy and was unrelated to the product's packaging or labeling. As of July 2008, the exact cause of the twins' death was under investigation. In March 2010, a two-year-old transplant patient from Texas was given a lethal dose of heparin at the University of Nebraska Medical Center. The exact circumstances surrounding her death are still under investigation.

The AQSIQ announced on 5 October that all tests showed all milk produced after 14 September were free from contamination. The General Administration of Quality Supervision, Inspection and Quarantine stated all dairy products made before 14 September will be tested for melamine. They gave notice to all supermarkets, shops, and all city, town and village-level vendors to urgently remove and seal up all powdered milk and liquid milk made before 14 September, pending further testing. Five government agencies, including the Ministry of Health, issued a joint statement on 9 October setting the legally acceptable level of melamine content in infant formula at 1 ppm (1 mg/kg), and at 2.5ppm in other dairy products (including milk) - in line with standards recognised by the World Health Organization and the UN Food and Agriculture Organization. A researcher at the Chinese Centre for Disease Control and Prevention said that any amount exceeding 1 ppm would give reason to suspect its presence was intentional.

Ma Bo mentioned hardtack as being a staple food of Chinese hard-labor workers in Inner Mongolia, during the Cultural Revolution. Hardtack was a staple of military servicemen in Japan and South Korea well into the late 20th century. It is known as Kanpan (乾パン) in Japan and geonbbang (geonppang, 건빵) in South Korea, meaning 'dry bread', and is still sold as a fairly popular snack food in both countries. (Canned kanpan is also distributed in Japan as emergency rations in case of earthquake, flood, or other disaster.) A harder hardtack than Kanpan, called Katapan (堅パン), is historically popular in Kitakyushu, Fukuoka, Japan as one of its regional specialty foods. In Korea, geonppang (hardtacks) mixed with byulsatang (star candy) as a medley is considered a popular snack.

Sources: en.wikipedia.org

Frequently asked questions

Is cardarine a SARM?

No. Cardarine is GW501516, a PPARδ agonist, while SARMs act on androgen receptors. The two classes are often grouped in informal discussions despite different mechanisms.

Is cardarine approved for human use?

No. It has no approved medical indication in any country. Regulatory agencies have not cleared it for treatment or prevention of any condition.

Why was its development discontinued?

Early clinical work stopped after rodent carcinogenicity findings. Those animal results raised concerns about long-term human risk, although direct human evidence is lacking. The human relevance of the tumors remains an open scientific question.

What receptor does cardarine target?

Cardarine targets PPARδ, a nuclear receptor involved in lipid and energy metabolism. It does not bind the androgen receptor in the way SARMs do.

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