Everything below concerns anti-doping. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-08-01. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
Cardarine is a common name for GW501516, a synthetic compound studied for its effects on lipid and glucose metabolism. It functions as an agonist at peroxisome proliferator-activated receptor delta, or PPARδ, a nuclear receptor that influences gene expression. The molecule is not a steroid, nor is it a selective androgen receptor modulator. It is also known in research and sports literature as GW-501516 and endurobol. Early laboratory work examined its metabolic activity in cell cultures and animal models.
| 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. |
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.
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.
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.
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.
GW501516 acts as an agonist at the peroxisome proliferator-activated receptor delta, a nuclear receptor that regulates gene expression. Activation shifts transcription toward genes involved in fatty acid uptake, oxidation, and energy expenditure. The compound does not bind the androgen receptor and therefore differs from anabolic steroids and SARMs. In rodent models, this metabolic shift has been linked to increased running endurance and reduced fat accumulation. The exact downstream pathways in humans remain incompletely characterized.
Early clinical research explored GW501516 for lipid disorders, obesity, and diabetes. Some short-term human studies reported changes in HDL cholesterol, LDL cholesterol, and triglycerides. The development program was discontinued after rodent studies showed dose-dependent tumor formation in multiple tissues, including liver, bladder, stomach, and skin. These findings raised concerns about long-term cancer risk in humans. Because human exposure data are limited, the clinical significance of the rodent tumors remains uncertain.
Through modulation of liver protein synthesis, conjugated oral estrogen increases the risk of blood clots, increases circulating levels of a variety of binding proteins including thyroid binding globulin (TBG), cortisol binding globulin (CBG), sex hormone binding globulin (SHBG), growth hormone binding protein (GHBP), insulin-like growth factor-binding proteins (IGFBPs), and copper binding protein (CBP), suppresses growth hormone (GH)-mediated insulin-like growth factor 1 (IGF-1) production, and produces positive blood lipid changes, among a variety of other effects. In contrast to oral estradiol, transdermal estradiol has relatively minimal impact on liver protein synthesis. As an example, a study found that 1 mg/day oral estradiol significantly increased SHBG levels by 45%, while 50 μg/day transdermal estradiol increased SHBG levels non-significantly by only 12%. In the circulation, approximately 38% of estradiol is reversibly bound to SHBG and 60% is reversibly bound to albumin in women under normal physiological circumstances, with 2 to 3% of total estradiol circulating free or unbound at any given time. Only estradiol that is free or unbound is able to be enter target cells and hence is biologically active. The increase in SHBG levels with oral estradiol (e.g., +50%) can result in a clinically meaningful increase in the fractions of sex hormones like estradiol and testosterone that are bound to SHBG, whereas this is not the case with typical clinical dosages of transdermal estradiol.
== External links == CD98+Antigens at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Large+Neutral+Amino+Acid-Transporter+1 at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Amino+Acid+Transport+System+L at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
Field desorption ionization was first reported by Beckey in 1969. In field ionization, a high-potential electric field is applied to an emitter with a sharp surface, such as a razor blade, or more commonly, a filament from which tiny "whiskers" have been grown. This produces a very high electric field in which electron tunneling can result in ionization of gaseous analyte molecules. FI produces mass spectra with little or no fragmentation, dominated by molecular radical cations M+. and occasionally protonated molecules
where the denominator includes only covalently bound H2CO3 and does not include hydrated CO2(aq). The much smaller and often-quoted value near 4.16 × 10−7 (or pKa1 = 6.38) is an apparent value calculated on the (incorrect) assumption that all dissolved CO2 is present as carbonic acid, so that
A method of providing experimental therapeutics prior to final FDA approval for use in humans. This procedure is used with very sick individuals who have no other treatment options. Often, case-by-case approval must be obtained from the FDA for "compassionate use" of a drug or therapy. (NLM) Compassionate use trial
Sources: en.wikipedia.org
The trial judge did not accept this defence, noting that comments such as Galloway being guilty of "treason", "in Saddam's pay", and being "Saddam's little helper" caused him [the judge] to conclude that "the newspaper was not neutral but both embraced the allegations with relish and fervour and went on to embellish them"; additionally, the judge ruled, Galloway had not been given a fair or reasonable opportunity to make inquiries or meaningful comment upon the documents before they were published.
Isaria cicadae Miq. 1838, which is the same as Cordyceps cicadae (Miq.) Massee 1895 and Paecilomyces cicadae. The preferred name for this species appears to be Cordyceps cicadae (Miq.) Massee 1895, especially since Isaria has proven to be polyphyletic. Cordyceps cicadae Shing 1975, which is now properly known as Tolypocladium dujiaolongae Y.P. Cao & C.R. Li after its local name in TCM ("Du Jiao Long"). Some Chinese sources believe that it is the teleomorph of "Chan Hua", which is now proven false with the discovery of its true teleomorph. Cordyceps sobolifera (now Ophiocordyceps sobolifera). Japanese sources incorrectly believe that this is the teleomorph of "Chan Hua", but it is in reality another TCM material known as "Xiao Chan Hua" (small cicada flower). The error has spread to Korean, Taiwanese, and Chinese sources. Cordyceps kobayasii, another purported teleomorph of "Chan Hua". Cordyceps chanhua Z.Z. Li et al., which is the correct name of "Chan Hua". In traditional medicine-related papers, each of the names have been used to describe the material known as "Chan Hua". C. cicadae and I. cicadae used to be very common in sources written by Chinese researchers, though they have largely adopted the corrected C. chanhua name. Japanese, Korean, and Taiwanese sources still use C. sobolifera. Other reported synonyms include Cordyceps zhejiangensis and C. sinclairii.
antisense RNA (asRNA) Also antisense transcript and antisense oligonucleotide (ASO). A single-stranded non-coding RNA molecule containing an antisense sequence that is complementary to a sense strand, such as a messenger RNA, with which it readily hybridizes, thereby inhibiting the sense strand's further activity (e.g. translation into protein). Many different classes of naturally occurring RNA such as siRNA function by this principle, making them potent gene silencers in various gene regulation mechanisms. Synthetic antisense RNA has also found widespread use in gene knockdown studies, and in practical applications such as antisense therapy.
If a mutation is present in a germ cell, it can give rise to offspring that carries the mutation in all of its cells. This is the case in hereditary diseases. In particular, if there is a mutation in a DNA repair gene within a germ cell, humans carrying such germline mutations may have an increased risk of cancer. A list of 34 such germline mutations is given in the article DNA repair-deficiency disorder. An example of one is albinism, a mutation that occurs in the OCA1 or OCA2 gene. Individuals with this disorder are more prone to many types of cancers, other disorders and have impaired vision. DNA damage can cause an error when the DNA is replicated, and this error of replication can cause a gene mutation that, in turn, could cause a genetic disorder. DNA damages are repaired by the DNA repair system of the cell. Each cell has a number of pathways through which enzymes recognize and repair damages in DNA. Because DNA can be damaged in many ways, the process of DNA repair is an important way in which the body protects itself from disease. Once DNA damage has given rise to a mutation, the mutation cannot be repaired.
Sources: en.wikipedia.org
On 24 June 2013, while the Essendon Football Club was being investigated by the Australian Sports Anti-Doping Authority (ASADA) over the legality of its supplements program during the 2012 AFL season, Watson admitted on the Fox Footy program On the Couch that he believed he was given the substance AOD-9604 during the 2012 season with the assistance of the club. The World Anti-Doping Agency (WADA) released a statement clarifying that AOD-9604 fell into the "S0. Non-Approved Substances" category in their List of Prohibited Substances and Methods. ASADA also stated that the use of AOD-9604 is prohibited for use by athletes in any circumstances. During the investigation, Watson was among the thirty-four present and former Essendon players issued show cause notices by ASADA and infraction notices by the AFL, alleging the use of the banned peptide Thymosin beta-4 during the 2012 season. On 31 March 2015, the AFL Anti-Doping Tribunal found all thirty-four players not guilty of all charges. In January 2016, following an appeal by WADA against the AFL Tribunal's not-guilty finding, Watson, along with the other thirty-three players, had their not-guilty verdict overturned. All thirty-four players were suspended for two years, backdated to November 2016, causing him to miss the entire 2016 AFL season. As Watson had won the 2012 Brownlow Medal, during the season that the supplements program took place, the AFL Commission reviewed the award.
The Sinaloa Cartel began to contest the Gulf Cartel's domination of the southwest Texas corridor following the arrest of Gulf Cartel leader Osiel Cárdenas in March 2003. In 2006, it formalized "the Federation," an alliance of criminal groups in Sinaloa under Joaquín "El Chapo" Guzmán, who became Mexico's most-wanted trafficker, with an estimated net worth of US$1 billion.
Atrial natriuretic peptide (natriuretic polypeptide (ANP) or atrial natriuretic factor (ANF) is a natriuretic peptide hormone secreted from the cardiac atria that in humans is encoded by the NPPA gene. Natriuretic peptides (ANP, BNP, and CNP) are a family of hormone/paracrine factors that are structurally related. The main function of ANP is causing a reduction in expanded extracellular fluid (ECF) volume by increasing renal sodium excretion. ANP is synthesized and secreted by cardiac muscle cells in the walls of the atria in the heart. These cells contain volume receptors which respond to increased stretching of the atrial wall due to increased atrial blood volume. Reduction of blood volume by ANP can result in secondary effects such as reduction of extracellular fluid (ECF) volume, improved cardiac ejection fraction with resultant improved organ perfusion, decreased blood pressure, and increased serum potassium. These effects may be blunted or negated by various counter-regulatory mechanisms operating concurrently on each of these secondary effects. Brain natriuretic peptide (BNP) – a misnomer; it is secreted by cardiac muscle cells in the heart ventricles – is similar to ANP in its effect. It acts via the same receptors as ANP does, but with 10-fold lower affinity than ANP. The biological half-life of BNP, however, is twice as long as that of ANP, and that of NT-proBNP is even longer, making these peptides better choices than ANP for diagnostic blood testing.
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.
Cardarine is a common name for GW501516, a synthetic PPARδ agonist. It is not a steroid or a selective androgen receptor modulator. It was developed and studied as a research compound for metabolic pathways.