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 2026-07-12 and is reviewed periodically as new material appears.
Sporting authorities added GW501516 to prohibited lists after it appeared in athlete samples and online markets. The World Anti-Doping Agency classifies it as a hormone and metabolic modulator, and its use can lead to an anti-doping rule violation. Some early laboratory work suggested effects on fatty acid oxidation and endurance-related metabolism in animals, but those findings do not establish safe or effective use in people. Reports of adverse events in humans are scarce and often anecdotal, which complicates risk assessment.
Legal status varies by country. In some places, cardarine is controlled under medicines or psychoactive substances laws; in others, it may be sold with minimal oversight as a research chemical. Customs agencies have intercepted shipments, and several national health agencies have issued warnings about products marketed for bodybuilding or performance enhancement. The lack of a standardized pharmaceutical supply means identity, purity, and contamination levels can differ widely between samples. These factors make cardarine a regulatory and public health concern rather than a conventional prescription drug.
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 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.
| Property | Value | Notes |
|---|---|---|
| IUPAC name | {4-[({4-methyl-2-[4-(trifluoromethyl)phenyl]-1,3-thiazol-5-yl}methyl)sulfanyl]phenoxy}acetic acid | Systematic name for GW501516 |
| CAS Registry Number | 317318-70-0 | Unique identifier for the parent compound |
| Molecular formula | C21H18F3NO3S2 | Includes carbon, hydrogen, fluorine, nitrogen, oxygen, and sulfur |
| Molecular weight | 453.5 g/mol | Approximate value for the neutral form |
| Appearance | White to off-white powder | Typical description for purified laboratory material |
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.
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.
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.
=== Occupational monitoring === A medical surveillance program must be established. In case of exposure, occupational health professionals need to ask for a detailed history and do a thorough physical exam. They should test the urine of the potentially exposed worker by doing a urine dipstick or microscopic examination, mainly looking for blood, as several antineoplastic drugs are known to cause bladder damage. Urinary mutagenicity is a marker of exposure to antineoplastic drugs that was first used by Falck and colleagues in 1979 and uses bacterial mutagenicity assays. Apart from being nonspecific, the test can be influenced by extraneous factors such as dietary intake and smoking and is, therefore, used sparingly. However, the test played a significant role in changing the use of horizontal flow cabinets to vertical flow biological safety cabinets during the preparation of antineoplastic drugs because the former exposed health care workers to high levels of drugs. This changed the handling of drugs and effectively reduced workers' exposure to antineoplastic drugs. Biomarkers of exposure to antineoplastic drugs commonly include urinary platinum, methotrexate, urinary cyclophosphamide and ifosfamide, and urinary metabolite of 5-fluorouracil. In addition to this, there are other drugs used to measure the drugs directly in the urine, although they are rarely used. A measurement of these drugs directly in one's urine is a sign of high exposure levels and that an uptake of the drugs is happening either through inhalation or dermally.
A sequence-controlled polymer is a macromolecule, in which the sequence of monomers is controlled to some degree. This control can be absolute but not necessarily. In other words, a sequence-controlled polymer can be uniform (its dispersity Ð is equal to 1) or non-uniform (Ð>1). For example, an alternating copolymer synthesized by radical polymerization is a sequence-controlled polymer, even if it is also a non-uniform polymer, in which chains have different chain-lengths and slightly different compositions. A biopolymer (for example a protein) with a perfectly defined primary structure is also a sequence-controlled polymer. However, in the case of uniform macromolecules, the term sequence-defined polymer can also be used. With comparison to traditional polymers, the composition of sequence-controlled polymers can be precisely defined via chemical synthetic methods, such as multicomponent reactions, click reactions etc. Such tunable polymerizing manner endows sequence-controlled polymers with particular properties and thereby, sequence-controlled polymers-based applications (e.g. information storage, biomaterials, nanomaterials etc.) are developed. In nature, DNA, RNA, proteins and other macromolecules can also be recognized as sequence-controlled polymers for their well-ordered structural skeletons. DNA, based on A-T, C-G base pairs, are formed in well-aligned sequences. Through precise sequences of DNA, 20 amino acids are able to generate sequential peptide chains with three-dimensional structures by virtue of transcription and translation process.
=== Selective norepinephrine reuptake inhibitors === Noradrenergic neurons are located in two major regions in the brain, the locus coeruleus and lateral tegmental. With administration of SNRIs, neuronal activity in the locus coeruleus is induced because of increased concentration of norepinephrine in the synaptic cleft. This results in activation of α2 adrenergic receptors, as discussed previously. Assays have shown that SNRIs have insignificant penchant for mACh, α1 and α2 adrenergic, or H1 receptors.
=== Plant isoforms === Plant BCATs have also been identified, but vary between species in terms of number and sequence. In studies of Arabidopsis thaliana (thale cress), six BCAT isoforms have been identified that share between 47.5-84.1% homology with each other. These isoforms also share around 30% sequence homology to the human and yeast (Saccharomyces cerevisiae) isoforms. BCAT1 is located in the mitochondria, BCAT2, 3, and 5 are located in chloroplasts, and BCAT4 and 6 are located in the cytoplasm of A. thaliana. However, studies of BCATs in Solanum tuberosum (potato) revealed two isoforms that are 683 (BCAT1) and 746 (BCAT2) bp long located primarily in chloroplasts.
== Signs and symptoms == Symptoms include chest pain or angina, shortness of breath, and fatigue. A completely blocked coronary artery will cause a heart attack. Common heart attack symptoms include chest pain or angina, pain or discomfort that spreads to the shoulder, arm, back, neck jaw, teeth or the upper belly, cold sweats, fatigue, heartburn, nausea, shortness of breath, or lightheadedness.
Sources: en.wikipedia.org
== Clinical significance == Inherited deficiency of urocanase leads to elevated levels of urocanic acid in the urine, a condition known as urocanic aciduria. An important role for the onset of atopic dermatitis and asthma has been attributed to filaggrin, a skin precursor of urocanic acid. Urocanic acid is thought to be a significant attractant of the nematode parasite Strongyloides stercoralis, in part because of relatively high levels in the plantar surfaces of the feet, the site through which this parasite often enters the body.
DFMDA, also known as F2-MDA or as 3,4-(difluoromethylenedioxy)amphetamine, is a chemical compound of the phenethylamine, amphetamine, and MDxx families related to the entactogen and psychedelic drug MDA. It is the derivative of MDA in which the two hydrogen atoms on the carbon atom of the 3,4-methylenedioxy ring have been replaced with fluorine atoms. Daniel Trachsel tested DFMDA in humans and found that it was inactive at doses of up to 250 mg orally. Higher doses were not tested. For comparison, he listed MDA's dose as 80 to 160 mg orally. DFMDA was active at the serotonin transporter (SERT) similarly to MDA and MDMA and with intermediate affinity between the two. It was developed with the aim of finding a non-neurotoxic drug able to be used as a less harmful substitute for entactogens such as MDMA. Since a major route of the normal metabolism of these compounds is scission of the methylenedioxy ring, producing neurotoxic metabolites such as α-methyldopamine, it was hoped that the difluoromethylenedioxy bioisostere would show increased metabolic stability and less toxicity. These compounds have not yet been tested in animals to verify whether they show similar pharmacological activity to the non-fluorinated parent compounds. It is also now generally accepted that MDMA neurotoxicity results from a variety of different causes and is not solely due to accumulation of α-methyldopamine, making it unclear how much less neurotoxic DFMDA and related drugs would be in practice. The chemical synthesis of DFMDA has been described.
=== Executive committee === The management of the Society is vested in an Executive Committee made up of Officers and General Members, they also act as Trustees of the Society. There are currently 10 officers of the Society namely the Chair, Vice-Chair, Treasurer, General Secretary, Meetings Secretary, Papers Secretary, Education Officer, Publicity Secretary, Special Interest Group Co-ordinator, and Digital Communications Officer.
=== Lawsuits === In April 2012, Johnson & Johnson (J&J) and its subsidiary Janssen Pharmaceuticals Inc. were fined $1.2 billion for downplaying multiple risks associated with risperidone. The verdict was later reversed by the Arkansas state supreme court. In August 2012, J&J agreed to pay $181 million to 36 US states to settle claims that it had promoted risperidone and paliperidone for off-label uses including for dementia, anger management, and anxiety. In November 2013, J&J was fined $2.2 billion for illegally marketing risperidone for use in people with dementia and paying kickbacks to prescribing physicians and nursing home pharmacies. In 2015, Steven Brill wrote an investigative journalism piece about J&J in The Huffington Post focused on J&J's marketing of risperidone. J&J has faced numerous civil lawsuits on behalf of children who were prescribed risperidone who grew breasts (a condition called gynecomastia); as of July 2016 there were about 1,500 cases in Pennsylvania state court in Philadelphia, and there had been a February 2015 verdict against J&J with $2.5 million awarded to a man from Alabama, a $1.75 million verdict against J&J that November, and in 2016 a $70 million verdict against J&J. In October 2019, a jury ordered J&J to pay $8 billion in punitive damages to a Pennsylvania man who had grown breasts during adolescence. This verdict amount chosen by the jury was reduced more than 1,000-fold by a judge in January 2020, with the new punitive damages being $6.8 million.
Sources: en.wikipedia.org
No. Major drug regulators have not approved GW501516 for treating any medical condition. Products sold as cardarine are typically unapproved research chemicals or supplements, so their contents and safety are not assured.
It is prohibited by the World Anti-Doping Agency as a hormone and metabolic modulator. Athletes who test positive for GW501516 can face sanctions, including suspensions and loss of results.
Cardarine is a common or trade-style name, while GW501516 is the research code for the same chemical entity. Some sources also use Endurobol or GSK-516. The names refer to the same compound, not distinct drugs.
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.