This is a working overview of PPARδ agonist, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-07-10 and is reviewed periodically as new material appears.
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.
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.
| 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 |
Published literature on cardarine includes in vitro assays, rodent experiments, and a small number of human studies. Reports describe effects on exercise capacity and lipid metabolism in animals, while human evidence is sparse. Many online descriptions present the compound as a proven endurance aid, a claim not supported by regulatory approval or large clinical trials. Analytical studies focus on identifying the parent compound and its metabolites in biological samples. Important uncertainties include species differences, dose-response relationships, and the relevance of rodent tumor findings to humans.
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.
Published studies have examined GW501516 in animal models of obesity, insulin resistance, and exercise endurance. Early human trials reportedly ended, and development was discontinued after preclinical findings raised concerns about cancer in some rodent studies. Regulatory agencies have not approved cardarine for any medical use. Its availability through non-pharmaceutical channels raises questions about identity, purity, and legal status that are separate from its laboratory pharmacology. Those questions are often addressed through analytical testing rather than assumptions about product labels.
Cardarine is a common name for GW501516, also GW-1516, a synthetic compound developed as a peroxisome proliferator-activated receptor delta (PPARδ) agonist. It belongs to a class of agents that modulate gene transcription related to lipid and energy metabolism. The compound was studied in preclinical and early clinical research for metabolic and cardiovascular conditions, but it did not progress to approved therapeutic use. Its name appears in fitness and sports contexts despite not being approved as a drug.
PPARδ is a nuclear receptor that influences transcription of genes involved in fatty acid oxidation, lipid transport, and energy homeostasis. GW501516 binds and activates this receptor with high selectivity relative to PPARα and PPARγ in laboratory assays. Activation alters expression of target genes in skeletal muscle, liver, and adipose tissue in animal models. The exact clinical consequences of these changes in humans remain incompletely characterized, and observed effects in animals do not establish therapeutic benefit or safety.
Heseltine was disappointed not to receive the support of old allies on the second ballot; these included Secretary of State for Defence Tom King (whom he asked in vain to second his nomination, but who was angry at a leadership contest when British troops were soon to go to war in Kuwait and supported Douglas Hurd), Cecil Parkinson and Norman Lamont (who managed John Major's campaign). Over the weekend on 24–25 November, many Conservative MPs were faced with the anger of their local party members who overwhelmingly supported Thatcher but did not at that time have a vote in leadership elections, and opinion polls showed that chancellor John Major would also boost Conservative support if leader (previously Heseltine's unique selling-point). Heseltine had never done much to court support among younger MPs the way Major had, and was seen as aloof even by his own supporters. In the second ballot, a week after the first, Heseltine's vote actually fell to 131 (just over 35%) as some MPs had voted for him in the first ballot as a protest against or to try to oust Thatcher but preferred to vote for other candidates now that they had a wider choice. John Major, with 185 votes, was only two votes short of an overall majority. Heseltine immediately and publicly conceded defeat, announcing that he would vote for Major if the third ballot went ahead (it did not, as Hurd, who had finished a distant third, also conceded).
Deregulated kinase activity is a frequent cause of disease, in particular cancer, wherein kinases regulate many aspects that control cell growth, movement and death. Drugs that inhibit specific kinases are being developed to treat several diseases, and some are currently in clinical use, including Gleevec (imatinib) and Iressa (gefitinib).
== History == The concept of electrostatically trapping ions in an orbit around a central spindle was developed by Kenneth Hay Kingdon in the early 1920s. The Kingdon trap consists of a thin central wire and an outer cylindrical electrode. A static applied voltage results in a radial logarithmic potential between the electrodes. In 1981, Knight introduced a modified outer electrode that included an axial quadrupole term that confines the ions on the trap axis. Neither the Kingdon nor the Knight configurations were reported to produce mass spectra. In 1986, Professor Yuri Konstantinovich Golikov in USSR developed theory of ion motion in quadro-logarithmic potential, and filed for patents in USSR for its use in a time-of-flight analyzer. Golikov, leading a team at the St. Petersburg State Pedagogical University's Radiophysics Faculty, laid the theoretical groundwork for Orbitrap technology as one of inventors in USSR Inventor's certificate No. 1247973 in 1986. Golikov later remarked "Based on my ideas, analytical instruments with record parameters were built, but unfortunately not in Russia, but abroad." Contrary to popular belief, Alexander Makarov is not the original inventor of quadro-logarithmic potential which was known since 1950s. Reflecting on his early interaction with Golikov, Alexander Makarov recalled, "As a fifth-year student at MIPT, I entered one of the numerous rooms at the Polytechnic Institute, where I was met by Yuri Konstantinovich Golikov.
== Awards and honors == 1976–1981 - N.I.H. Research Career Development Award 1975, 1992 - Kaiser Permanente Award for Excellence in Teaching 1996–1997 - President, Biophysical Society 1997 - Distinguished Lecturer, Beckman Center, University of Illinois at Urbana-Champaign 1999 - Distinguished Service Award, Biophysical Society 2000 - Athalie Clarke Research Achievement Award, Outstanding Researcher, UCI College of Medicine 2001 - Fellow, Biophysical Society 2002 - César Milstein Plenary Lecture, XIVth International Biophysics Congress 2006 - Keynote Lecture, Gordon Research Conference on Biopolymers 2008 - Ph.D. honoris causa, Stockholm University 2009 - Avanti Award in Lipids, Biophysical Society 2009 - Bioengineering Distinguished Speaker, University of California at Riverside 2010 - Matrone Distinguished Lecture in Biochemistry, North Carolina State University 2010 - Cátedra de Investigación Científica, Autonomous University of San Luis Potosí 2010 - Frederic M. Richards Lecture, Yale 2011 - O'Malley Lectures in Chemical Biology, Boston College 2014 - Carl Brändén Award, The Protein Society 2016 - Fellow, Neutron Scattering Society of America 2018 - Fellow, American Association for the Advancement of Science 2019 - University of Kansas Newmark Award Lecture 2022 - UCI School of Medicine, Lifetime Research Achievement Award for Excellence in Basic Science research.
The xanthophyll cycle involves the enzymatic removal of epoxy groups from xanthophylls (e.g. violaxanthin, antheraxanthin, diadinoxanthin) to create so-called de-epoxidised xanthophylls (e.g. diatoxanthin, zeaxanthin). These enzymatic cycles were found to play a key role in stimulating energy dissipation within light-harvesting antenna proteins by non-photochemical quenching- a mechanism to reduce the amount of energy that reaches the photosynthetic reaction centers. Non-photochemical quenching is one of the main ways of protecting against photoinhibition. In higher plants, there are three carotenoid pigments that are active in the xanthophyll cycle: violaxanthin, antheraxanthin, and zeaxanthin. During light stress, violaxanthin is converted, i.e. reduced, to zeaxanthin via the intermediate antheraxanthin, which plays a direct photoprotective role acting as a lipid-protective anti-oxidant and by stimulating non-photochemical quenching within light-harvesting proteins. This conversion of violaxanthin to zeaxanthin is done by the enzyme violaxanthin de-epoxidase (EC 1.23.5.1), while the reverse reaction, i.e. oxidation, is performed by zeaxanthin epoxidase (EC 1.14.15.21). In diatoms and dinoflagellates, the xanthophyll cycle consists of the pigment diadinoxanthin, which is transformed into diatoxanthin (diatoms) or dinoxanthin (dinoflagellates) under high-light conditions. Wright et al.
Sources: en.wikipedia.org
The prime recovery ship was USS Wasp. The recovery was supported by 10,249 U.S. Department of Defense personnel, 134 aircraft, and 26 ships. Postflight medical examination found the astronauts to be in good health, and no significant physiological changes were found.
=== Insulin === When levels of blood sugar rise, whether as a result of glycogen conversion, or from digestion of a meal, a different hormone is released from beta cells found in the islets of Langerhans in the pancreas. This hormone, insulin, causes the liver to convert more glucose into glycogen (this process is called glycogenesis), and to force about 2/3 of body cells (primarily muscle and fat tissue cells) to take up glucose from the blood through the GLUT4 transporter, thus decreasing blood sugar. When insulin binds to the receptors on the cell surface, vesicles containing the GLUT4 transporters come to the plasma membrane and fuse together by the process of endocytosis, thus enabling a facilitated diffusion of glucose into the cell. As soon as the glucose enters the cell, it is phosphorylated into glucose-6-phosphate in order to preserve the concentration gradient so glucose will continue to enter the cell. Insulin also provides signals to several other body systems, and is the chief regulator of metabolic control in humans. There are also several other causes for an increase in blood sugar levels. Among them are the 'stress' hormones such as epinephrine (also known as adrenaline), several of the steroids, infections, trauma, and of course, the ingestion of food. Diabetes mellitus type 1 is caused by insufficient or non-existent production of insulin, while type 2 is primarily due to a decreased response to insulin in the tissues of the body (insulin resistance).
A steroid hormone is a steroid that acts as a hormone. Steroid hormones can be grouped into two classes: corticosteroids (typically made in the adrenal cortex, hence cortico-) and sex steroids (typically made in the gonads or placenta). Within those two classes are five types according to the receptors to which they bind: glucocorticoids and mineralocorticoids (both corticosteroids) and androgens, estrogens, and progestogens (sex steroids). Vitamin D derivatives are a sixth closely related hormone system with homologous receptors. They have some of the characteristics of true steroids as receptor ligands. Steroid hormones help control metabolism, inflammation, immune functions, salt and water balance, development of sexual characteristics, and the ability to withstand injury and illness. The term steroid describes both hormones produced by the body and artificially produced medications that duplicate the action for the naturally occurring steroids.
=== DCVJ, rigidity sensitive dyes === 4-(dicyanovinyl)julolidine (DCVJ) is a molecular rotor probe with fluorescence that is strongly dependent on the rigidity of its environment. When protein denatures, DCVJ increases in fluorescence. It has been reported to work with 40 mg/ml of antibody.
=== Biofilm formation === Pseudomonas syringae produces polysaccharides which allow it to adhere to the surface of plant cells. It also releases quorum sensing molecules, which allows it to sense the presence of other bacterial cells nearby. If these molecules pass a threshold level, the bacteria change their pattern of gene expression to form a biofilm and begin expression of virulence-related genes. The bacteria secrete highly viscous compounds such as polysaccharides and DNA to create a protective environment in which to grow.
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.
Cardarine is a common name for GW501516, a synthetic PPARδ agonist developed for research. It has not been approved as a medication in any country. It is classified as an unapproved drug and a prohibited substance in sport.