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Cardarine As Investigational Pparδ Agonist — Quick Reference

By Editorial Desk · published 2026-01-24 · last reviewed 2026-03-11 · Wiki

GW501516 is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.

Updated 2026-03-11. Numbers and descriptions here follow the published literature rather than marketing material.

Cardarine as Investigational PPARδ Agonist

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.

Regulation and Detection

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 at a glance

PropertyValueNotes
Common synonymsGW501516, GW-501516, GW 501516, endurobolNames vary in research and anti-doping documents.
Chemical classSynthetic PPARδ agonistSmall-molecule nuclear receptor ligand.
CAS Registry Number317318-70-0Identifier commonly associated with GW501516.
AppearanceWhite to off-white powderTypical for purified research material.
SolubilityLow in water; soluble in DMSO and ethanolOrganic solvents are common for laboratory stock solutions.

Identity and Pharmacological Classification

Published studies have examined GW501516 in animal models of obesity, insulin resistance, and exercise endurance. Early human trials reportedly ended, and development was discontinued after preclinical findings raised concerns about cancer in some rodent studies. Regulatory agencies have not approved cardarine for any medical use. Its availability through non-pharmaceutical channels raises questions about identity, purity, and legal status that are separate from its laboratory pharmacology. Those questions are often addressed through analytical testing rather than assumptions about product labels.

Cardarine is a common name for GW501516, also GW-1516, a synthetic compound developed as a peroxisome proliferator-activated receptor delta (PPARδ) agonist. It belongs to a class of agents that modulate gene transcription related to lipid and energy metabolism. The compound was studied in preclinical and early clinical research for metabolic and cardiovascular conditions, but it did not progress to approved therapeutic use. Its name appears in fitness and sports contexts despite not being approved as a drug.

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Regulation and Analytical Detection

Products sold as cardarine have been found to contain incorrect compounds, variable amounts, or no active ingredient at all. Independent testing is required to verify identity and purity. Common analytical approaches include high-performance liquid chromatography, mass spectrometry, and nuclear magnetic resonance for structural confirmation. These methods can distinguish GW501516 from related PPAR agonists and from unrelated steroids. For regulators and researchers, such verification is central to interpreting both biological results and adverse event reports.

Cardarine is prohibited in competitive sport under the World Anti-Doping Agency code, where it is classified as a metabolic modulator. It is not approved as a prescription medicine in the United States, European Union, or other major markets. Regulatory action has focused on its presence in sports and in products marketed as research chemicals. Because it has no accepted medical indication, supply is often unregulated. This status creates legal and safety uncertainties for anyone who encounters the substance.

Background and Regulatory History

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 the investigational chemical GW501516, also written GW-1516. It was developed as a peroxisome proliferator-activated receptor delta agonist for metabolic conditions such as dyslipidemia. Early research focused on lipid handling and energy use in skeletal muscle and other tissues. The compound was never approved as a medicine. In public discussion, it is often grouped with performance-enhancing substances, although its receptor target differs from that of anabolic steroids or selective androgen receptor modulators. Regulatory and health authorities have issued warnings about its use.

Notes from published material

== Varieties == Glass noodles are made from a variety of starches. In China, glass noodles are usually made of mung bean starch or sweet potato starch. Chinese varieties made from mung bean starch are called Chinese vermicelli, bean threads, or bean thread noodles. Chinese varieties made from sweet potato starch are called fentiao or hongshufen. Thicker Korean varieties made with sweet potato starch are called sweet potato noodles or dangmyeon. Glass noodles are available in various thicknesses. Wide, flat glass noodle sheets called mung bean sheets are also produced in China. In Korea, napjak-dangmyeon (literally "flat dangmyeon") refers to flat sweet potato noodles.

=== Peripheral edema and hypoalbuminemia === Kwashiorkor is a form of protein deficiency, which can result in both osmotic imbalances and irregularities in the lymphatic system. Kwashiorkor is most notable for peripheral edema. The presence of edema in kwashiorkor is correlated with very low albumin concentration (hypoalbuminemia). Edema results from a loss of fluid balance between the hydrostatic and oncotic pressures across the capillary blood vessel walls due to the lack of protein which affects the body's ability to draw fluid from the tissues into the bloodstream. Low albumin concentration influences negatively the strength of oncotic pressure. Failure leads to fluid buildup in the abdomen, resulting in edema and belly distension. Furthermore, the release of antidiuretic hormone is stimulated by hypovolemia, also leading to the development of peripheral edema. Plasma renin is also stimulated, promoting sodium retention. It is important to distinguish the pathophysiology of marasmus and kwashiorkor when it comes to treating malnourished children who may have hypovolemic shock that is caused by an acute loss of salt and water. Children with severe albumin deficiency struggle physiologically to maintain their blood volume.

=== Mechanism of action === Phentolamine acts as a reversible dual or non-selective α1- and α2-adrenergic receptor antagonist. Its primary action is vasodilation due to α1-adrenergic receptor blockade. Reportedly, phentolamine may also stimulate β-adrenergic receptors. Non-selective α-blockers can cause a much more pronounced reflex tachycardia than the selective α1 blockers. Like the selective α1 blockers, phentolamine causes a relaxation of systemic vasculature, leading to hypotension. This hypotension is sensed by the baroreceptor reflex, which results in increased sympathetic nerve firing on the heart, releasing norepinephrine. In response, the β1 adrenergic receptors on the heart increase their rate, contractility, and dromotropy, which help to offset the decrease in systemic blood pressure. Unlike the α1 selective blockers, phentolamine also inhibits the α2 receptors, which function predominantly as presynaptic negative feedback for norepinephrine release. By abolishing this negative feedback phentolamine leads to even less regulated norepinephrine release, which results in a more drastic increase in heart rate.

West Coast sites replaced the steel lattice towers with simpler guy-stayed masts, although they retained the same wooden towers for reception. East Coast sites had transmitter and receiver blocks protected with earth mounds and blast walls, along with separate reserve transmitter and receivers in small bunkers with attached 120 ft aerial masts. These reserves were in close proximity to the respective transmitter/receiver sites, often in a neighbouring field. West Coast sites relied on site dispersal for protection, duplicating the entire transmitter and receiver buildings.

Sources: en.wikipedia.org

Background from the literature

Amy M. Barrios is an American medicinal chemist working as a professor of Medicinal Chemistry and the Associate Dean for Postdoctoral Affairs for the University of Utah. Barrios' research lab focuses on developing probes to study protein tyrosine phosphatase (PTP) activity and regulation.

The evolutionary role of opioid signalling in these behaviours was confirmed in dogs, chicks, and rats. Opioid receptors also have a role in mating behaviors. However, mu-opioid receptors do not just control social behaviour because they also make individuals feel relaxed in a wide range of other situations. Kappa- and delta-opioid receptors may be less associated with relaxation and analgesia because kappa-opioid receptor suppresses mu-opioid receptor activation, and delta-opioid receptor interacts differently with agonists and antagonists. Kappa-opioid receptors are involved in chronic anxiety's perceptual mobilization, whereas delta-opioid receptors induce action initiation, impulsivity, and behavioural mobilization. These differences led some researches to suggest that up- or down-regulations within three opioid receptors families are the basis of different dispositional emotionality seen in psychiatric disorders. Human-specific opioid-modulated cognitive features are not attributable to coding differences for receptors or ligands, which share 99% similarity with primates, but to regulatory changes in expression levels.

== Early life and career == Kennedy was born in Centreville, Mississippi, and raised in Zachary, Louisiana. He graduated from Zachary High School as co-valedictorian in 1969. He then attended Vanderbilt University, where he majored in philosophy, political science, and economics. He graduated in 1973 with a Bachelor of Arts, magna cum laude, and was elected president of his class and to Phi Beta Kappa. Kennedy received a Juris Doctor degree in 1977 from the University of Virginia School of Law. There, he was an executive editor of the Virginia Law Review and, graduating in the top ten percent of his class, he was elected to the Order of the Coif. In 1979, he earned a Bachelor of Civil Law, an advanced degree, with first class honours from Oxford University, where he was a member of Magdalen College and studied under Rupert Cross and J. H. C. Morris. Kennedy was a partner in the New Orleans and Baton Rouge law firm Chaffe McCall from 1985 to 1987 and 1992 to 1996. He also served as an adjunct professor at Louisiana State University's Paul M. Hebert Law Center in Baton Rouge from 2002 to 2016.

=== Expansion === Due to the success of the Selous Scouts, Walls directed in mid-1974 that it be expanded from three to six troops. This process was completed by December 1974, and included 50 former insurgents being added to the unit. A Reconnaissance Troop was formed in the second half of 1976 to conduct scouting operations in Mozambique and Zambia; this unit had a peak strength of twelve men. As part of the expansion of the Selous Scouts, the Rhodesian Army's Tracking Wing and Tracker Combat Unit were merged into it during 1974. The Tracking Wing became the Selous Scouts' Training Troop. The Selous Scouts continued to deliver training in tracking and trackers for the remainder of the war, with this forming a cover for the unit's actual role. The Tracker Combat Unit was made up of white reservists; while these men were not suitable for Selous Scouts operations, they were retained to help provide cover. These changes reduced the effectiveness of the Rhodesian Army's tracking capabilities. The size of the Selous Scouts increased further over time, and eventually reached 1,800 men. Many of these were territorial soldiers who were not permanently attached. The rapid expansion of the Selous Scouts led to a drop in the quality of its personnel, which reduced the effectiveness of pseudo operations. This in turn caused the unit to increasingly undertake offensive operations where it directly attacked insurgents rather than gathered intelligence on them.

In 2026 Song and colleagues described Eoceras shaanxiense, a siphuncle-bearing cephalopod, based on fossils from the Early Cambrian Shuijingtuo Formation of China, making it the earliest known definitive cephalopod at the time of its discovery. Early cephalopods were likely predators near the top of the food chain. After the late Cambrian extinction led to the disappearance of many radiodonts, predatory niches became available for other animals. During the Ordovician period, the primitive cephalopods underwent pulses of diversification to become diverse and dominant in the Paleozoic and Mesozoic seas. In the Early Palaeozoic, their range was far more restricted; they were mainly confined to sublittoral regions of shallow shelves of the low latitudes, and usually occurred in association with thrombolites. A more pelagic habit was gradually adopted as the Ordovician progressed. Deep-water cephalopods, whilst rare, have been found in the Lower Ordovician – but only in high-latitude waters. The mid-Ordovician saw the first cephalopods with septa strong enough to cope with the pressures associated with deeper water, and could inhabit depths greater than 100–200 m. The direction of shell coiling would prove to be crucial to the future success of the lineages; endogastric coiling would only permit large size to be attained with a straight shell, whereas exogastric coiling – initially rather rare – permitted the spirals familiar from the fossil record to develop, with their corresponding large size and diversity.

Sources: en.wikipedia.org

Further detail

== Development == The world's first major one-place study is believed to have been an attempt started in Austria in 1920 by Konrad Brandner to chart a complete genealogy of the population of the Steiermark region. After the Nazi takeover of Germany, the Nazi farming authority Reichsnährstand began a nationwide campaign in 1937 to document the "Aryan blood" of countryfolk by documenting the ancestry of every village in a Dorfsippenbuch. 30 such books were published by 1940. Nazi schoolteachers led the copying of parish registers onto index cards, and boasted that 30,000 Heimat histories would be written, but the Second World War brought this project to a halt. Though genealogy in Germany was to take decades to shake off this evil association, some enthusiasts resumed work on the card indexes or typewritten lists left from before the war, and the first new one-place study, now renamed an Ortssippenbuch, appeared in 1956. Later the term was changed yet again, to de:Ortsfamilienbuch. More than 3,000 have appeared, with a trend away from print to electronic publication.

Further adjustments variations on BARAC to produce DIBAC/ADIBO were performed to add distal ring strain and reduce sterics around the alkyne to further increase reactivity. Keto-DIBO, in which the hydroxyl group has been converted to a ketone, has a three-fold increase in rate due to a change in ring conformation. Attempts to make a difluorobenzocyclooctyne (DIFBO) were unsuccessful due to the instability. Problems with DIFO with in vivo mouse studies illustrate the difficulty of producing bioorthogonal reactions. Although DIFO was extremely reactive in the labeling of cells, it performed poorly in mouse studies due to binding with serum albumin. Hydrophobicity of the cyclooctyne promotes sequestration by membranes and serum proteins, reducing bioavailable concentrations. In response, DIMAC (dimethoxyazacyclooctyne) was developed to increase water solubility, polarity, and pharmacokinetics, although efforts in bioorthogonal labeling of mouse models is still in development.

== Criticism and news media portrayal == Since 2013, the term has been adopted by feminists and the media to refer to a misogynist culture within an organization or community. In a New York Magazine article in September 2013, Ann Friedman wrote: "Bro once meant something specific: a self-absorbed young white guy in board shorts with a taste for cheap beer. But it’s become a shorthand for the sort of privileged ignorance that thrives in groups dominated by wealthy, white, straight men." Vox referred to Silicon Valley's "bro culture problem" in its review of Emily Chang's book Brotopia. In 2014 and 2017, Inc published articles on bro culture in business. In its coverage of the 2019 Telegramgate scandal, in which investigative journalists published text messages written by the governor of Puerto Rico, The New York Times referred to "an arrogant 'bro' culture of elites who joked about making chumps out of even their own supporters." The term Bernie Bro, an epithet directed at supporters of Bernie Sanders has been criticized as a reductive smear tactic used by political opponents. The term was widely used because the concept of "bro" itself was vague.

=== Genetics === In MCTD, major histocompatibility complex (MHC) and non-MHC genes have been linked to disease vulnerability. HLA-DR4 in the MHC is linked to both anti-RNP antibody responses and MCTD. The HLA class II phenotype/genotype most closely connected with scleroderma, HLA-DR5, and its subgroups, has been demonstrated to have a negative connection with MCTD. Another genetic feature of MCTD is the presence of anti-RNP antibodies. However, these antibodies are not present in all patients. Genome-wide association studies have revealed that there are parts of a patient’s genetic material that cause production of these anti-RNP antibodies. The mechanism is not yet thoroughly defined.

Many of the key psychoactive compounds in M. speciosa are indole alkaloids related to mitragynine, which is a tetracyclic relative of the pentacyclic indole alkaloids, yohimbine and voacangine. In particular, mitragynine and 7-hydroxymitragynine (7-HMG) compose significant proportions of the natural products isolable from M. speciosa; e.g., in one study, mitragynine was 12% by weight from Malaysian leaf sources, versus 66% from Thai sources, and 7-hydroxymitragynine constituted ~2% by weight. At least 40 other compounds have been isolated from M. speciosa leaves, including ~25 additional alkaloids, including raubasine/ajmalicine (originally isolated from Rauvolfia serpentina), corynantheidine (also found in Corynanthe johimbe), as well as mitraphylline, mitragynine pseudoindoxyl, and rhynchophylline. In addition to alkaloids, M. speciosa produces many other secondary metabolites. These include various saponins, iridoids and other monoterpenoids, triterpenoids such as ursolic acid and oleanic acid, as well as various polyphenols including the flavonoids apigenin and quercetin. Although some of these compounds possess antinociceptive, anti-inflammatory, gastrointestinal, antidepressant, antioxidant, and antibacterial effects in cells and non-human animals, there is no sufficient evidence to support the clinical use of kratom in humans.

Sources: en.wikipedia.org

Frequently asked questions

What is cardarine?

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.

Is cardarine a steroid?

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.

Why was cardarine not developed further?

Early rodent studies reported tumor formation at multiple sites, which raised safety concerns. Sponsors stopped clinical development, and no approved human product exists.

Is cardarine legal?

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.

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