This is a working overview of Cardarine, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-01-20. Anything still debated is marked as such rather than presented as settled.
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.
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.
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 |
|---|---|---|
| Common synonyms | GW501516; GW-1516; endurobol | GW501516 is the research code |
| Drug class | PPARδ agonist | Not a selective androgen receptor modulator |
| Molecular formula | C21H18F3NO3S2 | Established chemical formula |
| Molar mass | 453.5 g/mol | Calculated from the formula |
| Regulatory status | Prohibited in sport; not approved as medicine | Status varies by country |
Cardarine is a common name for GW501516, a synthetic compound studied for its effects on lipid and glucose metabolism. It functions as an agonist at peroxisome proliferator-activated receptor delta, or PPARδ, a nuclear receptor that influences gene expression. The molecule is not a steroid, nor is it a selective androgen receptor modulator. It is also known in research and sports literature as GW-501516 and endurobol. Early laboratory work examined its metabolic activity in cell cultures and animal models.
Activation of PPARδ changes transcription of genes involved in fatty acid transport, mitochondrial function, and skeletal muscle fuel preference. In rodent studies, pharmacological PPARδ activation was associated with increased endurance and altered body composition. These findings generated interest in performance enhancement, but species differences and study designs limit direct extrapolation to humans. Small human trials were conducted in the 2000s and later discontinued. The extent to which cardarine produces similar metabolic or performance effects in people remains an open question.
The pharmacological interest in cardarine centers on PPARδ activation and its downstream effects on lipid handling and mitochondrial function. In animal studies, PPARδ agonists have been associated with changes in exercise endurance and fatty acid utilization, though results vary by model and protocol. Human data remain sparse, and the absence of large controlled trials limits conclusions about efficacy. Researchers often describe the compound as a tool for probing PPARδ biology rather than a proven therapeutic agent.
Safety discussions about cardarine frequently cite rodent carcinogenicity findings reported in the 2000s. In those studies, treated animals developed tumors at multiple sites, leading sponsors to discontinue clinical development. The relevance of these findings to humans has not been resolved, but they are a major reason the compound is not approved. Current literature emphasizes uncertainty about long-term effects and the risks of unregulated use. Regulators and health agencies have not established a safe human exposure level.
Cardarine is a synthetic compound also known as GW501516, GW-501516, and sometimes endurobol. It was developed as a selective agonist of peroxisome proliferator-activated receptor delta, a nuclear receptor involved in fatty acid oxidation and energy metabolism. The compound was studied in preclinical models for metabolic and cardiovascular conditions, but it did not become a marketed human medicine. In regulatory and anti-doping contexts, it is treated as a prohibited substance rather than a licensed medicine.
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.
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.
In laboratory settings, cardarine is studied as a tool compound for probing PPARδ biology. Published experiments often use cell cultures, rodent models, or isolated tissues. Some investigations focus on metabolic effects, while others assess potential risks such as carcinogenicity observed in long-term animal studies. Because human trials are sparse, most knowledge comes from preclinical work and adverse event reports. Scientific literature frequently notes the gap between animal findings and human outcomes. The compound is not a dietary supplement and is not intended for human consumption.
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.
=== Chemical composition === Tear film was described in 1946 by Wolff using a slit lamp to have a three-layered structure: lipid, aqueous, and mucous. Tears are composed of water, salts, antibodies, and lysozymes (antibacterial enzymes). The composition of each layer determines its function. For example, the diverse lipid classes in the tear film lipid layer (TFLL) confer unique physicochemical properties that support roles such as enabling thin film formation and preventing its collapse onto the ocular surface. More recently, Mazyar Yazdani at Oslo University Hospital proposed that the TFLL may also contribute to corneal oxygenation, based on its composition-driven properties. The composition varies among different tear types. The composition of tears caused by an emotional reaction differs from that of tears as a reaction to irritants, such as onion fumes, dust, or allergens. Emotional tears contain higher concentrations of stress hormones such as adrenocorticotropic hormone and leucine enkephalin (a natural pain killer), which suggests that emotional tears play a biological role in balancing stress hormone levels.
Depending on the venue's climate, the turf used was either a hybrid of 84% Kentucky bluegrass and 16% perennial ryegrass (for cooler temperatures), or Bermuda grass (for warmer temperatures). Four venues (Atlanta, Dallas, Houston, and Vancouver) were indoor stadiums that used retractable roof systems, all equipped with climate control, while a fifth, SoFi Stadium in Los Angeles, was open-air but had a translucent roof and no climate control. The host of the final match—MetLife Stadium in East Rutherford, New Jersey—was announced by FIFA on February 4, 2024. Although there were soccer-specific stadiums in Canada and the United States, the largest soccer-specific stadium in the U.S., Geodis Park in Nashville, Tennessee, seated 30,000, fell short of FIFA's minimum requirement of 40,000 seats (Toronto's BMO Field was expanded from 30,000 to 45,500 for this tournament). Stadiums including Mercedes-Benz Stadium in Atlanta; Gillette Stadium in Foxborough, Massachusetts; and Lumen Field in Seattle have been used by both National Football League (NFL) and Major League Soccer (MLS) teams. Although the Canadian and American stadiums were primarily used for gridiron football, they were also designed to accommodate soccer matches. Mexico City was the only capital of the three host nations chosen as a venue site; Ottawa and Washington, D.C., joined Bonn (West Germany, 1974) and Tokyo (Japan, 2002) as the only capital cities not selected to host World Cup matches.
Rudolf Schoenheimer (May 10, 1898 – September 11, 1941) was a German-American biochemist who developed the technique of isotope labelling of biomolecules, enabling detailed study of metabolism. This work revealed that all the constituents of an organism are in a constant state of chemical renewal. Born in Berlin, after graduating in medicine from the Friedrich Wilhelm University there, he learned further organic chemistry at the University of Leipzig and then studied biochemistry at the University of Freiburg where he rose to be Head of Physiological Chemistry. He spent the 1930-31 academic year at the University of Chicago. In 1933, following the rise of the Nazis to power he emigrated from Germany to the Columbia University to join the department of Biological Chemistry. Working with David Rittenberg, from the radiochemistry laboratory of Harold C. Urey and later together with Konrad Bloch, they used stable isotopes to tag foodstuffs and trace their metabolism within living things. He further established that cholesterol is a risk factor in atherosclerosis. He suffered from manic depression all of his life, which led to him in 1941 committing suicide using sodium cyanide. He had been honoured with the request to give the Dunham Lecture at Harvard before his death. It was read for him following his death.
==== Coffee ==== The world's primary source of caffeine is the coffee "bean" (the seed of the coffee plant), from which coffee is brewed. Caffeine content in coffee varies widely depending on the type of coffee bean and the method of preparation used; even beans within a given bush can show variations in concentration. In general, one serving of coffee ranges from 80 to 100 milligrams, for a single shot (30 milliliters) of arabica-variety espresso, to approximately 100–125 milligrams for a cup (120 milliliters) of drip coffee. Arabica coffee typically contains half the caffeine of the robusta variety. In general, dark-roast coffee has slightly less caffeine than lighter roasts because the roasting process reduces caffeine content of the bean by a small amount.
Sources: en.wikipedia.org
Further separation was carried out in the presence of a citric acid/ammonium buffer solution in a weakly acidic medium (pH ≈ 3.5), using ion exchange at elevated temperature. The chromatographic separation behavior was unknown for element 97 at the time but was anticipated by analogy with terbium. The first results were disappointing because no alpha-particle emission signature could be detected from the elution product. With further analysis, searching for characteristic X-rays and conversion electron signals, a berkelium isotope was eventually detected. Its mass number was uncertain between 243 and 244 in the initial report, but was later established as 243.
=== Competition === There are currently two products approved as maintenance therapy following treatment of inoperable locoregional Stage III NSCLC with induction chemotherapy: Tarceva (erlotinib), a targeted small molecule from Genentech, a member of the Roche Group, and Alimta (pemetrexed), a chemotherapeutic from Eli Lilly and Company. Tecemotide has not been tested in combination with or in comparison to these products. It is possible that other existing or new agents will be approved for this indication. In addition, there are at least two vaccines in development for the treatment of NSCLC, including GSK's MAGE A3 vaccine in Phase 3 and Transgene's TG-4010 in Phase 2/3. TG-4010 also targets MUC1, although using technology different from tecemotide.
The earliest known compilation of medicinal substances was the Sushruta Samhita, an Indian Ayurvedic treatise attributed to Sushruta in the 6th century BC. However, the earliest text as preserved dates to the 3rd or 4th century AD. Many Sumerian (4th millennium BC – early 2nd millennium BC) cuneiform clay tablets record prescriptions for medicine. Ancient Egyptian pharmacological knowledge was recorded in various papyri such as the Ebers Papyrus of 1550 BC, and the Edwin Smith Papyrus of the 16th century BC.
Sources: en.wikipedia.org
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.
No. It has no approved medical indication in any country. Regulatory agencies have not cleared it for treatment or prevention of any condition.
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.
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.