This is a working overview of Cardarine, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2025-09-27. Anything still debated is marked as such rather than presented as settled.
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.
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 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.
| Property | Value | Notes |
|---|---|---|
| Common name | Cardarine | Common internet and media name. |
| Research code | GW501516 | Also written GW-1516. |
| Drug class | PPARδ agonist | Not a selective androgen receptor modulator. |
| Development status | Discontinued | Clinical development halted after rodent cancer findings. |
| Regulatory status | Prohibited in sport | Listed by WADA; not approved as medicine. |
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.
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.
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.
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.
The thrifty gene hypothesis (also called the famine hypothesis) states that in some populations the body would be more efficient at retaining fat in times of plenty, thereby endowing greater resistance to starvation in times of food scarcity. This hypothesis, originally advanced in the context of glucose metabolism and insulin resistance, has been discredited by physical anthropologists, physiologists, and the original proponent of the idea himself with respect to that context, although according to its developer it remains "as viable as when [it was] first advanced" in other contexts. In 1995, Jeffrey Friedman, in his residency at the Rockefeller University, together with Rudolph Leibel, Douglas Coleman et al. discovered the protein leptin that the genetically obese mouse lacked. Leptin is produced in the white adipose tissue and signals to the hypothalamus. When leptin levels drop, the body interprets this as a loss of energy, and hunger increases. Mice lacking this protein eat until they are four times their normal size. Leptin, however, plays a different role in diet-induced obesity in rodents and humans. Because adipocytes produce leptin, leptin levels are elevated in the obese. However, hunger remains, and—when leptin levels drop due to weight loss—hunger increases. The drop of leptin is better viewed as a starvation signal than the rise of leptin as a satiety signal. However, elevated leptin in obesity is known as leptin resistance. The changes that occur in the hypothalamus to result in leptin resistance in obesity are currently the focus of obesity research.
== External links == Creatine+Kinase,+BB+Form at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Human CKB genome location and CKB gene details page in the UCSC Genome Browser. This article incorporates text from the United States National Library of Medicine, which is in the public domain.
== Medical uses == Hydroxychloroquine treats rheumatic disorders such as systemic lupus erythematosus, rheumatoid arthritis, and porphyria cutanea tarda, and certain infections such as Q fever and certain types of malaria. It is considered the first-line treatment for systemic lupus erythematosus. Certain types of malaria, resistant strains, and complicated cases require different or additional medication. Hydroxychloroquine blocks the effects of some chemicals released in autoimmune diseases, and is used to treat inflammatory conditions. It is widely used to treat primary Sjögren syndrome but does not appear to be effective. Hydroxychloroquine is widely used in the treatment of post-Lyme arthritis. It may have both an anti-spirochete activity and an anti-inflammatory activity, similar to the treatment of rheumatoid arthritis.
Sources: en.wikipedia.org
== References == Cinefantastique, Vol. 24, #6/Vol. 25, #1, February 1994 (special double-issue, with multiple articles on the Fox Network run). "Batman: The Animated Series Original Airdate and episode list". worldsfinestonline.com. Retrieved April 15, 2007. "Batman: The Animated Series Writers". Worldsfinestonline.com. Retrieved April 18, 2007. "Batman: The Animated Series Directors". Worldsfinestonline.com. Retrieved April 18, 2007. "Batman – Mask of the Phantasm". Worldsfinestonline.com. Retrieved April 18, 2007. "Batman & Mr. Freeze: Sub-Zero". Worldsfinestonline.com. Retrieved April 18, 2007. "Batman: The Animated Series Official Website". batmantas.com. Retrieved April 18, 2007.
Isotope masses from: Audi, Georges; Bersillon, Olivier; Blachot, Jean; Wapstra, Aaldert Hendrik (2003), "The NUBASE evaluation of nuclear and decay properties", Nuclear Physics A, 729: 3–128, Bibcode:2003NuPhA.729....3A, doi:10.1016/j.nuclphysa.2003.11.001 Isotopic compositions and standard atomic masses from: de Laeter, John Robert; Böhlke, John Karl; De Bièvre, Paul; Hidaka, Hiroshi; Peiser, H. Steffen; Rosman, Kevin J. R.; Taylor, Philip D. P. (2003). "Atomic weights of the elements. Review 2000 (IUPAC Technical Report)". Pure and Applied Chemistry. 75 (6): 683–800. doi:10.1351/pac200375060683. Wieser, Michael E. (2006). "Atomic weights of the elements 2005 (IUPAC Technical Report)". Pure and Applied Chemistry. 78 (11): 2051–2066. doi:10.1351/pac200678112051. "News & Notices: Standard Atomic Weights Revised". International Union of Pure and Applied Chemistry. 19 October 2005. Half-life, spin, and isomer data selected from the following sources. G. Audi; A. H. Wapstra; C. Thibault; J. Blachot; O. Bersillon (2003). "The NUBASE evaluation of nuclear and decay properties" (PDF). Nuclear Physics A. 729 (1): 3–128. Bibcode:2003NuPhA.729....3A. doi:10.1016/j.nuclphysa.2003.11.001. Archived from the original (PDF) on 2011-07-20. National Nuclear Data Center. "NuDat 3.0 database". Brookhaven National Laboratory. Holden, Norman E. (2004). "11. Table of the Isotopes". In Lide, David R. (ed.). CRC Handbook of Chemistry and Physics (85th ed.). Boca Raton, Florida: CRC Press. ISBN 978-0-8493-0485-9.
=== Stolle methodology === The Stolle procedure is considered the best alternative to Sandmeyer methodology for the synthesis of both substituted and unsubstituted isatins. In this case primary or secondary arylamines are condensed with oxalyl chloride to form a chlorooxalylanilide intermediate which can then cyclize in the presence of a Lewis acid (e.g. aluminium trichloride, titanium tetrachloride, boron trifluoride, etc.).
Sources: en.wikipedia.org
NAD and its precursors nicotinic acid (NA) and nicotinamide (NAM) have been shown to be vital cofactors in cellular oxidation/reduction reactions and ATP synthesis. Classic NAD synthesis pathways characterized in eukaryotes include an eight-step de novo pathway from Trp and two pathways using the NAD precursors NA and NAM: a three-step NA-based pathway known as the Preiss-Handler pathway; and an NAM-based pathway involving the enzyme Nicotinamide phosphoribosyltransferase (NAMPT) and the formation of nicotinamide mononucleotide (NMN). In 2004, a previously unknown pathway was reported when nicotinamide riboside (NR) was identified as an additional NAD precursor in eukaryotes. NR is now recognized as a form of vitamin B3 which can be found in both cow and human milk. Once internalized into a cell, NR is rapidly phosphorylated by the activity of nicotinamide riboside kinase enzymes (NRK1 and NRK2) to form nicotinamide mononucleotide (NMN), bypassing the previously known biosynthetic routes to NAD production. NMN is then converted to NAD by NMN-adenylyltransferase (NMNAT). Research in mammals indicates that NRK1 is a cytosolic protein, encoded by the Nmrk1 gene. It is found in most tissues but predominantly in the liver and kidney. The NRK2 protein may be related to muscle tissue including cardiac muscle. It is encoded by the Nmrk2 gene and appears to be more highly expressed in cases of metabolic stress or cellular damage. Since different types of tissues display differing concentrations of NR and NRKs, it is likely that NR utilization will vary in different tissues.
== Licences == SIRIUS is developed by the group of Sebastian Böcker at the FSU Jena in close collaboration with the Bright Giant GmbH. SIRIUS is provided as a software-as-a-service solution. The client software is open-source and installed on the users' computers. Molecular formula annotation using fragmentation trees and isotope pattern analysis is performed on your local computer without subscription requirement. The SIRIUS web services for structural elucidation, including molecular fingerprint prediction, structure database search, confidence score assessment and compound class prediction, require a user account. The web services are free for academic/non-commercial use provided/hosted by the FSU Jena. Academic institutions are identified by their email domain and access will be granted automatically. In some cases, further validation might be required. Bright Giant GmbH offers subscription-based access to the SIRIUS web services for structural elucidation for commercial users.
Similar effects are known for related androgenic progestins like medroxyprogesterone acetate and megestrol acetate. CPA has also been reported to lower HDL cholesterol levels, another effect associated with androgens. Accordingly, CPA shows weak androgenic effects in the liver in rodents which can be blocked by flutamide.
A gunshot wound to the neck can be particularly dangerous because of the high number of vital anatomical structures contained within a small space. The neck contains the larynx, trachea, pharynx, esophagus, vasculature (carotid, subclavian, and vertebral arteries; jugular, brachiocephalic, and vertebral veins; thyroid vessels), and nervous system anatomy (spinal cord, cranial nerves, peripheral nerves, sympathetic chain, brachial plexus). Gunshots to the neck can thus cause severe bleeding, airway compromise, and nervous system injury. Initial assessment of a gunshot wound to the neck involves non-probing inspection of whether the injury is a penetrating neck injury (PNI), classified by violation of the platysma muscle. If the platysma is intact, the wound is considered superficial and only requires local wound care. If the injury is a PNI, surgery should be consulted immediately while the case is being managed. Of note, wounds should not be explored on the field or in the emergency department given the risk of exacerbating the wound. Due to the advances in diagnostic imaging, management of PNI has been shifting from a "zone-based" approach, which uses anatomical site of injury to guide decisions, to a "no-zone" approach which uses a symptom-based algorithm. The no-zone approach uses a hard signs and imaging system to guide next steps. Hard signs include airway compromise, unresponsive shock, diminished pulses, uncontrolled bleeding, expanding hematoma, bruits/thrill, air bubbling from wound or extensive subcutaneous air, stridor/hoarseness, neurological deficits.
Sources: en.wikipedia.org
No. Cardarine is a PPARδ agonist, while selective androgen receptor modulators act on androgen receptors. The two classes differ in receptor target and downstream effects.
Preclinical rodent studies reported cancers, including liver and bladder tumors, at tested doses. The human relevance of those findings is uncertain, but development was discontinued. No approved human product resulted.
No. It remains an investigational compound without approved therapeutic labeling. Sports regulators prohibit its use, and health agencies have warned against consuming it.
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.