A practical reference on GW501516: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
Reviewed 2026-05-11. Anything still debated is marked as such rather than presented as settled.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Regulatory status | Prohibited in sport; not approved as medicine | Listed by WADA at all times. |
| Common synonyms | GW501516, GW-501516, endurobol | Cardarine is a colloquial name. |
| Typical analytical method | LC-MS/MS | Detects parent compound and metabolites. |
| Common test matrix | Urine | Blood and dried blood spots also possible. |
| Legal classification | Varies by country | Often treated as unapproved drug or research chemical. |
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.
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.
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 compound is typically described as a laboratory compound rather than a therapeutic product. Published reports have explored its role in lipid disorders, insulin sensitivity, and exercise metabolism, yet no major drug regulator has approved it for medical use. Commercial samples sold under the cardarine name may vary in purity and identity. Analytical confirmation is therefore necessary when the material is discussed in scientific or regulatory contexts. Its classification as a prohibited substance in sport further shapes how it is studied and reported.
=== Workplace safety === In 2023, an Oregon employee lost three fingers when the rotors of an ice cream machine pulled the towel she was using and her hand into the machine's blades. In response, the employees reportedly immediately quit their jobs. In a similar incident in 2007, also involving a rag and an ice cream machine, an employee lost one finger.
== Career == King joined Massachusetts Institute of Technology in 1959 as an assistant professor of chemical engineering to become director of the School of Chemical Engineering Practice station at the Exxon (then Esso) Bayway refinery in New Jersey. In 1963, King joined University of California, Berkeley as assistant professor of chemical engineering, becoming associate professor in 1966 and full professor in 1969. From 1967 to 1972, he served as the vice chairman of Department of Chemical Engineering. He then served as the chairman of the department from 1972 to 1981. In 1981, King was appointed as the dean of College of Chemistry and later in 1987 as the provost of the Professional Schools and Colleges, a position in which he served until 1994. At the time of his appointment, King was the first chemical engineer to become dean of the College of Chemistry at Berkeley. King was appointed the vice provost for research for the entire nine-campus University of California in 1994. In 1995 he became provost and senior vice president for academic affairs, again university-wide. During his time as UC provost, King helped launch the new, tenth UC campus at Merced, the California Digital Library, and eScholarship, the University of California's open access, electronic repository for publications by UC authors. He returned to UC Berkeley in 2004 as the director of Center for Studies in Higher Education, serving in this position for a full decade until 2014.
==== Photolithography ==== Ultraviolet radiation is used for very fine resolution photolithography, a procedure wherein a chemical called a photoresist is exposed to UV radiation that has passed through a mask. The exposure causes chemical reactions to occur in the photoresist. After removal of unwanted photoresist, a pattern determined by the mask remains on the sample. Steps may then be taken to "etch" away, deposit on or otherwise modify areas of the sample where no photoresist remains. Photolithography is used in the manufacture of semiconductors, integrated circuit components, and printed circuit boards. Photolithography processes used to fabricate electronic integrated circuits presently use 193 nm UV and are experimentally using 13.5 nm UV for extreme ultraviolet lithography.
Sources: en.wikipedia.org
=== Post-translational regulation === Interactions of cMyBP-C with its binding partners vary with its posttranslational modification status. At least three extensively characterized phosphorylation sites (Ser273, 282 and 302; numbering refers to the mouse sequence) are localized in the M motif of cMyBP-C and are targeted by protein kinases in a hierarchical order of events. In its dephosphorylated state, cMyBP-C binds predominantly to myosin S2 and brakes crossbridge formation, however, when phosphorylated in response to β-adrenergic stimulation through activating cAMP-dependent protein kinase (PKA), it favours binding to actin, then accelerating crossbridge formation, enhancing force development and promoting relaxation. Protein kinases identified thus far to phosphorylate cMyBP-C in the M motif are PKA, Ca2+/calmodulin-dependent kinase II (CaMKII), ribosomal s6 kinase (RSK), protein kinase D (PKD), and protein kinase C (PKC). Furthermore, GSK3β was described as another protein kinase to phosphorylate cMyBP-C outside the M-domain in the proline-alanine-rich actin-binding site at Ser133 in human myocardium (mouse Ser131). Phosphorylation is required for normal cardiac function and cMyBP-C stability, and overall phosphorylation levels of cMyBP-C are reduced in human and experimental heart failure. Other posttranslational modifications of cMyBP-C exist, which occur throughout the protein and are not thoroughly characterised yet, such as acetylation, citrullination, S-glutathiolation, S-nitrosylation and carbonylation.
"There's no way Rush will ever exist again because Neil's not here to be a part of it... that's not to say that we can't do other things and we can't do things that benefit our communities and all of that. I have lots of plans for that sort of thing that don't necessarily include Geddy. I get asked this all the time—are we gonna do this, or are we gonna do that? Who knows? All I know is we still love each other and we're still very, very good friends, and we always will be."
=== Training === Brigadier General William P. Burnham, who had previously commanded the 164th Brigade, led the division during most of its training and movement to Europe. In early April 1918, the division embarked from the ports in Boston, New York City and Brooklyn to Liverpool, England, where the division fully assembled by mid-May 1918. From there, the division moved to Continental Europe, leaving Southampton and arriving at Le Havre, France. The 82nd Division then moved to the British-controlled sector of the Somme, where it began sending small numbers of troops and officers to the front lines to gain combat experience. On 16 June, it moved by rail to the French sector. The division was briefly assigned to I Corps before falling under the command of IV Corps until late August. It was then moved to the Woëvre front.
Sources: en.wikipedia.org
Legal status varies by country. It is not approved as a medicine, and it is prohibited in sport. Some jurisdictions restrict import, sale, or possession.
Laboratories use liquid chromatography-tandem mass spectrometry to detect GW501516 and its metabolites. Urine is commonly tested, and testing can occur in and out of competition.
No, cardarine is not a SARM. It is a PPARδ agonist, which acts on a different receptor. The two classes are often confused in online discussions.
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.