The short version of GW501516 fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2025-11-11. 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.
Laboratory handling focuses on identity, purity, and stability. Reference standards are typically stored cold and dry, protected from light, because solutions can degrade over time. Analytical checks may use high-performance liquid chromatography with ultraviolet detection or mass spectrometry. Impurities and related substances can be separated chromatographically and compared with a known standard. Because cardarine is not an approved drug, compendial monographs are absent, and laboratories often rely on in-house methods. Reported purity varies among unregulated products and should not be assumed from a label.
GW501516 binds and activates PPARδ, a nuclear receptor that influences transcription of genes involved in fatty acid oxidation and energy use. Activation shifts some metabolic pathways in preclinical models, which is why the compound has been studied for lipid disorders and exercise-related endpoints. The exact downstream effects in humans are incompletely mapped. PPARδ is expressed in many tissues, including skeletal muscle, liver, and adipose tissue, so broad activation may have varied consequences. Researchers continue to examine how selective or partial activation might alter the balance between benefits and risks.
Published human data are sparse and mostly come from early-phase trials. Those studies examined short-term changes in lipids, glucose, and exercise capacity, but they were not large enough to establish efficacy or long-term safety. Some animal experiments reported increased running endurance, yet such findings do not prove a performance benefit in people. Anti-doping laboratories detect GW501516 and its metabolites in urine or blood using liquid chromatography-tandem mass spectrometry. Detection windows depend on dose, sample type, and individual metabolism. The method is sensitive enough to identify trace residues in tested samples.
| 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 |
Literature on cardarine often separates receptor pharmacology from toxicology. Mechanistic papers describe PPARδ activation and gene expression changes, while safety assessments focus on carcinogenicity and species differences. Questions remain about whether rodent tumors arise through PPARδ-dependent or off-target mechanisms. Another open area is how human metabolism and exposure compare with those in animal studies. Analytical methods such as liquid chromatography–mass spectrometry are used to confirm identity in biological and product samples.
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.
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 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.
Stability of GW501516 depends on form, temperature, light exposure, and moisture. Solid reference material is typically stored frozen or refrigerated in a desiccator and protected from light. Solutions in organic solvents such as dimethyl sulfoxide are often kept frozen in aliquots to reduce freeze-thaw cycling. Aqueous solubility is low, so aqueous stock solutions can be difficult to prepare without cosolvents. Degradation may appear as changes in chromatographic purity or mass spectral signal. Stability studies are needed to establish shelf life for any specific preparation.
Quality assessment for cardarine samples usually combines identity, purity, and impurity testing. Nuclear magnetic resonance spectroscopy and mass spectrometry can confirm molecular structure, while high-performance liquid chromatography estimates purity. Certificates of analysis from testing laboratories may list these results, but they do not establish safety or legality. In the absence of approved manufacturing, products sold online may contain the wrong compound, variable amounts, or unlisted contaminants. Independent verification is therefore central to analytical work and to interpreting any reported biological activity.
Laboratory detection of GW501516 commonly uses liquid chromatography coupled with tandem mass spectrometry. The method can identify the parent compound or its metabolites in urine and blood after sample cleanup. Protein precipitation, solid-phase extraction, or enzymatic hydrolysis may precede analysis, depending on the matrix. Reference standards are required for accurate quantification and confirmation. Because the compound is not approved, testing often occurs in anti-doping, forensic, or research settings rather than routine clinical care. Results are reported with limits of detection and quantification.
== Complications == LA-ICP-MS function optimally with gold particles greater than 60 μm in diameter to avoid any contamination during measurements. Although LA-ICP-MS has a lower detection limit, its overall precision was lower than other analysis techniques for trace element concentrations such as field emission-electron probe microanalysis (FE-EPMA) and synchrotron micro X-ray fluorescence spectroscopy (SR-l-XRF). Due to the small size of gold (<5μm-250μm) small fragments of minerals need to be separated from the gold before analysis can occur. Gold fingerprinting has limitations including elemental fractionation (the non-sample related analyte) and calibration requires matrix-matched standards. A few other problems exist that limit actual sourcing or provencancing of gold in relation to manufactured art objects. These problems include: a lack of an extensive database of elemental profiles in gold ores, the natural differences that coexist in ore geology and the difficulties of accurately analyzing trace elements. Also, trading, looting and re-melting of so called “precious” metal objects add to the problem of sourcing.
. However, away from this reference point, errors will accumulate over time thus convergence test is needed to find an optimal time step for more accurate results. Among these three reproduction numbers,
=== Career === After earning his MDiv, and before returning for his PhD, Humphreys was ordained as an Episcopal priest. He served in a number of parishes and advocated for the Civil Rights Movement, which put him in tension with a number of the parishes in which he served. In 1965, Humphreys returned to study for a PhD which he earned in 1968. Afterwards, Humphreys was an assistant professor of sociology at Southern Illinois University in Edwardsville, Illinois, from 1968 to 1970. He was associate professor of sociology at the School of Criminal Justice, State University of New York in Albany from 1970 to 1972. He was associate professor of sociology at Pitzer College, in Claremont, California, from 1972 to 1975; he earned full professorship at Pitzer in 1975, where he worked until about 1980, when he began to focus on his psychotherapist practice. However, he did not retire from Pitzer until 1986, two years before his death. Humphreys belonged to several sociological professional organizations, including the American Sociological Association (ASA), the Society for the Study of Social Problems, the Pacific Sociological Association, and the Academy of Criminal Justice Sciences. He was a charter member of the International Academy of Sex Research. During his academic career, he served on a number of editorial boards and served as chair of multiple professional society committees. He was an invited speaker at more than a dozen symposia and other events, and was a guest on four TV shows.
An alternative picoinjection method involves utilizing the injection reagent as the conductor of an electric field where a voltage applied to the fluid stimulates injection. Such a method also allows for greater control of injection as the voltage applied corresponds to the volume of reagent fluid injected. Droplet-to-droplet contamination is a challenge of many injection methods. To combat this, Doonan et al. developed a multifunctional K-channel, which flows reagent streams opposite the path of the droplet stream. Utilizing an interface between the two channels, injection is achieved similarly to picoinjection, but any bilateral contamination washed away through continuous reagent flow. Contamination is avoided at the expense of potentially wasting precious reagent.
=== Legacy === A research center that was planned in the 1970s was opened in 1975 (CBM) in the Autonomous University of Madrid (UAM). After his death, it was named the Centro de Biología Molecular Severo Ochoa. In Leganés, Madrid, a hospital bears his name, as does the Madrid Metro station serving it, Hospital Severo Ochoa. The asteroid 117435 Severochoa is also named in his honor. In 2003, the Spanish General Post Office (Correos) issued a €0,76 postage stamp honoring Ochoa, as one of a pair featuring Spanish medical Nobel Prize winners alongside Santiago Ramón y Cajal. In June 2011, the United States Postal Service issued a stamp honoring him, as part of the American Scientists collection, along with Melvin Calvin, Asa Gray, and Maria Goeppert-Mayer. This was the third volume in the series. The main road in to the tourist resort Benidorm is named Avenida Dr. Severo Ochoa in his honor.
Sources: en.wikipedia.org
=== Alzheimer's disease === The ATP-binding cassette protein ABCC1 has received attention in the last decade due to its possible connection with Alzheimer's disease. One of the more prominent signs of Alzheimer's disease is the accumulation of β-amyloid proteins in the brain. As these proteins accumulate, they begin to form plaques that interfere with signaling between cells of the nervous system found within the brain. Due to its presence in the choroid plexus and blood-brain barrier and its ability to transport multiple kinds of molecules out of cells, ABCC1 has been a point of interest in many Alzheimer's disease studies. The transporter protein has been shown to decrease β-amyloid accumulation by nearly 80 percent when activated, leading researchers to further investigation on its use in future treatments of Alzheimer's and other neurological disorders.
=== External factors === External factors may involve mechanical trauma (physical damage to the body which causes cellular breakdown), electric shock, damage to blood vessels (which may disrupt blood supply to associated tissue), and ischemia. Thermal effects (extremely high or low temperature) can often result in necrosis due to the disruption of cells, especially in bone cells. Necrosis can also result from chemical trauma, with alkaline and acidic compounds causing liquefactive and coagulative necrosis, respectively, in affected tissues. The severity of such cases varies significantly based on multiple factors, including the compound concentration, type of tissue affected, and the extent of chemical exposure. In frostbite, crystals form, increasing the pressure of remaining tissue and fluid causing the cells to burst. Under extreme conditions tissues and cells may die through an unregulated process of membrane and cytosol destruction.
=== Early prototypes and barriers to entry: 1920s–1990s === In 1927, Joseph Robinson applied for a patent for an electronic vaporizer to be used with medicinal compounds. The patent was approved in 1930 but the device was never marketed. In 1930, the United States Patent and Trademark Office reported a patent stating, "for holding medicinal compounds which are electrically or otherwise heated to produce vapors for inhalation." In 1934 and 1936, further similar patents were applied for. The earliest e-cigarette can be traced to American Herbert A. Gilbert. In 1963, Gilbert applied for a patent for "a smokeless non-tobacco cigarette" that involved "replacing burning tobacco and paper with heated, moist, flavored air". This device produced flavored steam without nicotine. The patent was granted in 1965. Gilbert's invention was ahead of its time. However, it received little attention and was never commercialized because smoking was still fashionable at that time. Gilbert said in 2013 that today's electric cigarettes follow the basic design set forth in his original patent. The Favor cigarette, introduced in 1986 by public company Advanced Tobacco Products, was another early noncombustible product promoted as an alternative nicotine-based tobacco product. Favor was conceptualized by Phil Ray, one of the founders of Datapoint Corporation and inventors of the microprocessor. Development started in 1979 by Phil Ray and Norman Jacobson.
=== Nanoparticle drug delivery === Delivering medications to the brain has long been a significant challenge in treating neurological diseases. The main reason lies in the blood-brain barrier (BBB), a highly selective, protective layer that shields the brain from toxins and pathogens in the bloodstream. While the BBB is crucial for maintaining brain health, it also makes it difficult for most therapeutic drugs to reach their target, especially in conditions like Alzheimer's and Parkinson's disease. As a result, conventional drug delivery methods often fall short, either causing unwanted side effects or failing to deliver a high enough concentration to be effective. To address this, researchers have turned to nanoparticles, tiny engineered carriers designed to sneak past the BBB and deliver drugs directly to the brain tissue These particles can be tailored to take advantage of the body's own transport systems. For example, by attaching certain molecules to their surfaces, nanoparticles can trigger receptor-mediated transcytosis, a natural process that allows them to pass through cells lining the BBB and enter the brain. This kind of targeted delivery helps reduce the drug's exposure to the rest of the body, lowering the risk of side effects and increasing concentration where it matters most. So far, this strategy has shown promise in delivering treatments to the brain for conditions like Alzheimer's and Parkinson's disease. Several types of nanoparticles are being studied for this purpose.
Between her second and third flights, Caldwell Dyson continued to work inside Houston’s Mission Control Center as CAPCOM for both space shuttle and space station operations, serving as the lead CAPCOM for various ISS missions, including the lead and development of the CAPCOM cadre for Boeing Starliner Mission Operations team. She was also the ground IV for US EVA 32, performed by Scott Kelly and Kjell Lindgren. Caldwell Dyson initiated and led several projects to improve training and operations aboard the ISS, most notably developing the EVA Qualification training flow (EVQ) for astronaut candidates. After her third trip to space, she served as the ground IV for US EVA 95, performed by Jessica Meir and Christopher Williams in March 2026. She also worked as one of the CAPCOM for the Artemis II mission, working during 3 separate shifts. During the summer 2026 with the European Space Agency, she participated in the CAVES training program with her NASA astronaut colleague, Ben Bailey and astronauts from other agencies John McFall, Ayu Yoneda and Rosemary Coogan. As Tracy Dyson, she is the host of a series on NASA TV called StationLife, which focuses on facets of life aboard the International Space Station. On March 21, 2017, Caldwell Dyson stood behind President Trump as he signed a bill for NASA to send humans to Mars in the 2030s and receive $19.5 billion in 2018 funding. Caldwell Dyson and fellow NASA astronaut Chris Cassidy presented Trump with an official flight jacket during the ceremony.
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.
Anti-doping and clinical laboratories commonly use liquid chromatography-tandem mass spectrometry. The method can identify GW501516 and its metabolites in urine or blood. Detection depends on sample timing and the amount present.