GW501516 comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Updated 2026-05-17. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
Cardarine is not approved for human therapeutic use in any major jurisdiction. It appears on the World Anti-Doping Agency Prohibited List as a PPARδ agonist within the hormone and metabolic modulators category. Sports organizations test for it because it has been detected in athlete samples and seized products. Regulatory actions against marketed research chemical versions have occurred in several countries, though enforcement varies. Availability through unregulated channels complicates oversight.
Analytical laboratories typically identify cardarine and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is a common matrix in anti-doping testing, while blood and tissue may be used in research settings. Detection windows depend on the assay, the sample matrix, and the compound's metabolism. Because cardarine is extensively metabolized, laboratories often target specific metabolites to improve sensitivity and confirmation. Reference standards are required for reliable quantification. Method validation includes checks for selectivity, linearity, and carryover.
| Property | Value | Notes |
|---|---|---|
| Common synonyms | GW501516, GW-501516, GW 501516, endurobol | Names vary in research and anti-doping documents. |
| Chemical class | Synthetic PPARδ agonist | Small-molecule nuclear receptor ligand. |
| CAS Registry Number | 317318-70-0 | Identifier commonly associated with GW501516. |
| Appearance | White to off-white powder | Typical for purified research material. |
| Solubility | Low in water; soluble in DMSO and ethanol | Organic solvents are common for laboratory stock solutions. |
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.
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 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 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.
Laboratory studies indicate that GW501516 activates PPARδ, a nuclear receptor involved in fatty acid oxidation and energy metabolism. In rodent experiments, treated animals often showed increased endurance and reduced fat mass. These effects were observed under controlled conditions and do not establish safe or effective use in humans. The exact dose-response relationship in humans remains poorly characterized. Species differences in metabolism can affect how results translate across animals and people.
Safety concerns emerged from long-term animal studies. In rodents given the compound for extended periods, researchers found an increased incidence of certain cancers, including liver and bladder tumors. These findings contributed to the discontinuation of clinical development. Whether similar risks apply to short-term or low-level exposure in humans is not established, and controlled human safety data are limited. The relevance of high-dose rodent carcinogenicity findings to human use remains a subject of debate.
Human trials of GW501516 were small and short in duration. They examined lipid levels, glucose handling, and other metabolic markers, but the programs were halted after the animal cancer findings. No approved therapeutic product exists, and published human data are insufficient for establishing long-term safety. Reports of use for athletic performance come mainly from non-clinical settings and cannot be verified through controlled trials. Independent testing of products sold as cardarine has found inconsistent purity and labeling.
==== Ventral mesentery ==== The development of the septum transversum takes part in the formation of the diaphragm, while the caudal portion into which the liver grows forms the ventral mesentery. The part of the ventral mesentery that attaches to the stomach is known as the ventral mesogastrium. The lesser omentum is formed, by a thinning of the mesoderm or ventral mesogastrium, which attaches the stomach and duodenum to the anterior abdominal wall. By the subsequent growth of the liver, this leaf of mesoderm is divided into two parts – the lesser omentum between the stomach and liver, and the falciform and coronary ligaments between the liver and the abdominal wall and diaphragm. In the adult, the ventral mesentery is the part of the peritoneum closest to the navel.
== Safety/efficacy/controversy == There exists considerable controversy about the safety and/or efficacy of synephrine-containing preparations, which are often confused with synephrine alone, sometimes with m-synephrine. Furthermore, this body of literature deals with mixtures containing synephrine as only one of several biologically active components, even, in some cases, without explicit confirmation of the presence of synephrine.
Genetic code is a set of rules used by living cells to translate information encoded within genetic material (DNA or RNA sequences of nucleotide triplets or codons) into proteins. Translation is accomplished by the ribosome, which links proteinogenic amino acids in an order specified by messenger RNA (mRNA), using transfer RNA (tRNA) molecules to carry amino acids and to read the mRNA three nucleotides at a time. The genetic code is highly similar among all organisms and can be expressed in a simple table with 64 entries. The codons specify which amino acid will be added next during protein biosynthesis. With some exceptions, a three-nucleotide codon in a nucleic acid sequence specifies a single amino acid. The vast majority of genes are encoded with a single scheme (see the RNA codon table). That scheme is often called the canonical or standard genetic code, or simply the genetic code, though variant codes (such as in mitochondria) exist.
Sources: en.wikipedia.org
=== Pharmacogenetics === The dihydropyrimidine dehydrogenase (DPD) enzyme is responsible for the detoxifying metabolism of fluoropyrimidines, a class of drugs that includes 5-fluorouracil, capecitabine, and tegafur. Genetic variations within the DPD gene (DPYD) can lead to reduced or absent DPD activity, and individuals who are heterozygous or homozygous for these variations may have partial or complete DPD deficiency; an estimated 0.2% of individuals have complete DPD deficiency. Those with partial or complete DPD deficiency have a significantly increased risk of severe or even fatal drug toxicities when treated with fluoropyrimidines; examples of toxicities include myelosuppression, neurotoxicity and hand-foot syndrome.
=== Oxford debate walkout, 2013 === On 20 February 2013, Galloway walked out of a publicised debate when he found out that his opponent had Israeli citizenship. The debate, hosted by Oxford University's Christ Church, was on the topic "Israel should withdraw immediately from the West Bank". Galloway interrupted his opponent, Eylon Levy, a third-year PPE student, to ask whether he was an Israeli. When Levy acknowledged his joint British–Israeli nationality, Galloway stood up and stated "I don't recognise Israel and I don't debate with Israelis" and left the meeting. Explaining his actions on his Facebook page, Galloway wrote:
== Health effects == Gutter oil has been shown to be toxic, causing diarrhea and abdominal pain. Long-term consumption of gutter oil may cause many foodborne illnesses because the oil may contain excessive amounts of cholesterol, trans fats, toxic heavy metals and pathogens such as bacteria, and also carcinogenic substances such as polycyclic aromatic hydrocarbons and aflatoxins, and therefore lead to stomach and liver cancer. Zeng Jing of the Guangdong Armed Police Hospital said of gutter oil, "Animal and vegetable fat in refined waste oil will undergo rancidity, oxidation and decomposition after contamination. It will cause indigestion, insomnia, liver discomfort and other symptoms." Due to rumours and the fear of Chinese customers of restaurants using gutter oil in their cooking, it has been reported that some people in China have resorted to bringing their own cooking oil with them from home into restaurants and instructing chefs to use their home-brought oil in their kitchen when preparing their food instead of the restaurant's own cooking oil.
Sources: en.wikipedia.org
==== Other memorials ==== The northwest corner of Bryant Park, at Sixth Avenue and 42nd Street, contains the Heiskell Plaza, a stairway and entrance plaza paved with flagstones. It was placed in 1993 in honor of Andrew Heiskell, a cofounder of the BPC. The southwest corner of Bryant Park, at Sixth Avenue and 40th Street, is known as Nikola Tesla Corner. Tesla, an inventor, lived in the nearby New Yorker Hotel in his later years, and would feed pigeons in the park. The placement of the sign was due to the efforts of the Croatian Club of New York in cooperation with New York City officials, and Ljubo Vujovic of the Tesla Memorial Society of New York.
=== Ga–Go === Elmer L. Gaden (1923–2012). American biochemical engineer at the University of Virginia, known as the father of biochemical engineering. Michael H. Gelb (b. 1957). American biochemist at the University of Washington who studies study enzymatic processes of biomedical significance. Susan Gerbi, (b. 1944). American biochemist at Brown University working on RNA and DNA. Jonathan Gershenzon (b. 1955). American biochemist at the Max Planck Institute for Chemical Ecology in Jena, known for work on the biochemistry of secondary plant metabolites. Quentin Gibson FRS (1918–2011). British-American biochemist at Sheffield and later Cornell University who worked on haem proteins. Member Natl. Acad. Sci. USA. Walter Gilbert FRS (foreign member) (b. 1932). American biochemist at Harvard, awarded the Nobel Prize in Chemistry (1980) for work on DNA sequencing. Member Natl. Acad. Sci. USA. H. Bentley Glass (1906–2005). American biochemist at the State University of New York at Stony Brook. Member Natl. Acad. Sci. USA Joseph L. Goldstein (b. 1940). American biochemist at the University of Texas, awarded the Nobel Prize in Physiology or Medicine (1985) for studies of cholesterol. Member Natl. Acad. Sci. USA. Eugene Goldwasser (1922–2010). American biochemist at the University of Chicago, known for identifying the hormone erythropoietin. Michael M. Gottesman (b. 1946). American biochemist at the NIH, whose achievements includes the discovery of P-glycoprotein. Member Natl. Acad. Sci. USA. Alfred Gottschalk (1894–1973).
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==== Cancer ==== While traditional chemotherapy can effectively kill cancer cells, lack of specificity for discriminating normal cells and cancer cells in these treatments usually cause severe side effects. Numerous studies have demonstrated that RNAi can provide a more specific approach to inhibit tumor growth by targeting cancer-related genes (i.e., oncogene). It has also been proposed that RNAi can enhance the sensitivity of cancer cells to chemotherapeutic agents, providing a combinatorial therapeutic approach with chemotherapy. Another potential RNAi-based treatment is to inhibit cell invasion and migration. Compared with chemotherapy or other anti-cancer drugs, there are a lot of advantages of siRNA drug. SiRNA acts on the post-transcriptional stage of gene expression, so it does not modify or change DNA in a deleterious effect. SiRNA can also be used to produce a specific response in a certain type of way, such as by downgrading suppression of gene expression. In a single cancer cell, siRNA can cause dramatic suppression of gene expression with just several copies. This happens by silencing cancer-promoting genes with RNAi, as well as targeting an mRNA sequence. RNAi drugs treat cancer by silencing certain cancer promoting genes. This is done by complementing the cancer genes with the RNAi, such as keeping the mRNA sequences in accordance with the RNAi drug. Ideally, RNAi is should be injected and/or chemically modified so the RNAi can reach cancer cells more efficiently. RNAi uptake and regulation is controlled by the kidneys.
Sources: en.wikipedia.org
Cardarine is an investigational synthetic compound that acts as a PPARδ agonist. It is also known as GW501516 and has been studied mainly in preclinical research. It is not an approved medicine.
No. Cardarine is not a steroid hormone; it targets the nuclear receptor PPARδ. Its classification in anti-doping rules differs from anabolic steroids, though it remains prohibited in sport.
Early rodent studies reported tumor formation at multiple sites, which raised safety concerns. Sponsors stopped clinical development, and no approved human product exists.
No. Cardarine has not received approval for human therapeutic use in major jurisdictions. It remains an investigational compound.