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Identity And Regulatory Status — Hands-On Walkthrough

By Editorial Desk · published 2026-03-21 · last reviewed 2026-04-20 · News

This is a working overview of Cardarine, written for readers who want more than a one-paragraph summary but less than a textbook.

This page was last updated on 2026-04-20 and is reviewed periodically as new material appears.

Identity and Regulatory Status

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.

Mechanism and Detection

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.

Cardarine at a glance

PropertyValueNotes
Common synonymsGW501516; GW-1516; endurobolGW501516 is the research code
Drug classPPARδ agonistNot a selective androgen receptor modulator
Molecular formulaC21H18F3NO3S2Established chemical formula
Molar mass453.5 g/molCalculated from the formula
Regulatory statusProhibited in sport; not approved as medicineStatus varies by country

Identity and Pharmacological Mechanism

Activation of PPARδ changes transcription of genes involved in fatty acid transport, mitochondrial function, and skeletal muscle fuel preference. In rodent studies, pharmacological PPARδ activation was associated with increased endurance and altered body composition. These findings generated interest in performance enhancement, but species differences and study designs limit direct extrapolation to humans. Small human trials were conducted in the 2000s and later discontinued. The extent to which cardarine produces similar metabolic or performance effects in people remains an open question.

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.

Related pages on this site

Cardarine as Investigational PPARδ Agonist

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.

Further detail

A preservative is a substance or a chemical that is added to products such as food products, beverages, pharmaceutical drugs, paints, biological samples, cosmetics, wood, and many other products to prevent decomposition by microbial growth or by undesirable chemical changes. In general, preservation is implemented in two modes, chemical and physical. Chemical preservation entails adding chemical compounds to the product. Physical preservation entails processes such as refrigeration or drying. Preservative food additives reduce the risk of foodborne infections, decrease microbial spoilage, and preserve fresh attributes and nutritional quality. Some physical techniques for food preservation include dehydration, UV-C radiation, freeze-drying, and refrigeration. Chemical preservation and physical preservation techniques are sometimes combined.

Idrees Kahloon, "Border Control: The economics of immigration vs. the politics of immigration", The New Yorker, 12 June 2023, pp. 65–69. "The limits of immigration are not set by economics but by political psychology – by backlash unconcerned with net benefits." (p. 65.) Susan Harbage Page & Inéz Valdez (17 April 2011). "Residues of Border Control", Southern Spaces James, Paul (2014). "Faces of Globalization and the Borders of States: From Asylum Seekers to Citizens". Citizenship Studies. 18 (2): 208–23. doi:10.1080/13621025.2014.886440. S2CID 144816686. Philippe Legrain (2007). Immigrants: Your Country Needs Them, Little Brown, ISBN 0-316-73248-6 Aristide Zolberg (2006). A Nation by Design: Immigration Policy in the Fashioning of America, Harvard University Press, ISBN 0-674-02218-1 Philippe Legrain (2007). Immigrants: Your Country Needs Them, Little Brown, ISBN 0-316-73248-6 Ruben Rumbaut & Walter Ewing (Spring 2007). "The Myth of Immigrant Criminality and the Paradox of Assimilation: Incarceration Rates among Native and Foreign-Born Men", The Immigration Policy Center. Bryan Balin (2008). State Immigration Legislation and Immigrant Flows: An Analysis The Johns Hopkins University Douglas S. Massey (September 2005). "Beyond the Border Buildup: Towards a New Approach to Mexico-U.S. Migration", Immigration Policy Center, the American Immigration Law Foundation IPC Special Report (November 2005). "Economic Growth & Immigration: Bridging the Demographic Divide", Immigration Policy Center, the American Immigration Law Foundation American Immigration Council (April 2014).

Indoors ozone (O3) is produced by certain high-voltage electric devices (such as air ionizers), and as a by-product of other types of pollution. It appears in lower concentrations indoors than outdoors, usually at 0.2–0.7 of the outdoor concentration. Typically, most ozone is lost to surface reactions indoors, rather than to reactions in air, due to the large surface to volume ratios found indoors. Outdoor air used for ventilation may have sufficient ozone to react with common indoor pollutants as well as skin oils and other common indoor air chemicals or surfaces. Particular concern is warranted when using "green" cleaning products based on citrus or terpene extracts, because these chemicals react rapidly with ozone to form toxic and irritating chemicals as well as fine and ultrafine particles. Ventilation with outdoor air containing elevated ozone concentrations may complicate remediation attempts. The WHO standard for ozone concentration is 60 μg/m3 for long-term exposure and 100 μg/m3 as the maximum average over an 8-hour period. The EPA standard for ozone concentration is 0.07 ppm average over an 8-hour period.

Sources: en.wikipedia.org

Background from the literature

Antibodies have antigen-binding fragment (Fab) regions and constant fragment (Fc) regions. The Neutralization of virus infection occurs when the Fab regions of antibodies binds to virus antigen(s) in a manner that blocks infection. Antibodies are also able to "kill" virus particles directly and/or kill infected cells using antibody-mediated "effector functions" such as opsonization, complement-dependent cytotoxicity, antibody-dependent cell-mediated cytotoxicity and antibody-dependent phagocytosis. These effector functions are contained in the Fc region of antibodies, but is also dependent on binding of the Fab region to antigen. Effector functions also require the use of complement proteins in serum or Fc-receptor on cell membranes. Ansuvimab has been found to be capable of killing cells by antibody-dependent cell-mediated cytotoxicity.

DNA nanotechnology uses the unique molecular recognition properties of DNA and other nucleic acids to create self-assembling branched DNA complexes with useful properties. DNA is thus used as a structural material rather than as a carrier of biological information. This has led to the creation of two-dimensional periodic lattices (both tile-based and using the DNA origami method) and three-dimensional structures in the shapes of polyhedra. Nanomechanical devices and algorithmic self-assembly have also been demonstrated, and these DNA structures have been used to template the arrangement of other molecules such as gold nanoparticles and streptavidin proteins. DNA and other nucleic acids are the basis of aptamers, synthetic oligonucleotide ligands for specific target molecules used in a range of biotechnology and biomedical applications.

=== Detection in body fluids === Concentrations of midazolam or its major metabolite, 1-hydroxymidazolam glucuronide, may be measured in plasma, serum, or whole blood to monitor for safety in those receiving the drug therapeutically, to confirm a diagnosis of poisoning in hospitalized patients, or to assist in a forensic investigation of a case of fatal overdosage. Patients with renal dysfunction may exhibit prolongation of elimination half-life for both the parent drug and its active metabolite, with accumulation of these two substances in the bloodstream and the appearance of adverse depressant effects.

Following ISIL's successful Anbar campaign and June 2014 offensive, the Badr Organization mobilized and won a series of battles against ISIL, including the Liberation of Jurf Al Sakhr and the Lifting of the Siege of Amirli. In early February 2015, the group, operating from its base at Camp Ashraf, fought in Diyala Governorate against ISIL. Over 100 militia were killed in the fighting, including 25 in Al Mansouryah. Badr's leader, Hadi al-Amiri, said his militiamen were committed to the safety of Sunnis, but deep mutual suspicions remained in the light of recent sectarian killings and the suspicion that some Sunni tribes were allied with IS. A leaked US diplomatic cable cited sources alleging that Hadi al-Amiri had personally ordered attacks on Sunnis.

Sources: en.wikipedia.org

Further detail

==== Peripheral and autonomic nervous systems ==== An alternative hypothesis to nociplastic pain views fibromyalgia as a stress-related dysautonomia with neuropathic pain features. This view highlights the role of autonomic and peripheral nociceptive nervous systems in the generation of widespread pain, fatigue, and insomnia. The description of small fiber neuropathy in a subgroup of fibromyalgia patients supports the disease neuropathic-autonomic underpinning. However, others claim that small fiber neuropathy occurs only in small groups of those with fibromyalgia. Some suggest that fibromyalgia is caused or maintained by decreased vagal tone, as indicated by low heart rate variability, signaling a heightened sympathetic response. Accordingly, several studies show that clinical improvement is associated with an increase in heart rate variability. Some examples of interventions that increase the heart rate variability and vagal tone are meditation, yoga, mindfulness, and exercise.

Abbreviations are used very frequently in medicine, despite being widely discouraged by the Institute of Safe Medicine Practices and other organizations concerned about patient safety. Abbreviations are especially discouraged when healthcare providers are communicating with patients and when there is a possibility of confusion between similar abbreviations. Some facilities maintain a list of acceptable abbreviations. Abbreviations are sometimes specific to a facility, which means that newer staff may be unfamiliar with them; this becomes a potential source of preventable medical errors. The Joint Commission and other organizations maintain lists of certain medical abbreviations that should be avoided to prevent mistakes, according to best practices (and in some cases regulatory requirements); these are flagged in the list of abbreviations used in medical prescriptions.

== Use and effects == In his book PiHKAL (Phenethylamines I Have Known and Loved), Alexander Shulgin lists DOPR's dose as 2.5 to 5 mg orally and its duration as 20 to 30 hours. It is said to have a very slow onset. The effects of DOPR have been reported to include closed-eye imagery, visuals, thinking changes, and insomnia and sleep disruption, among others. In one of the reports, it was described as a "heavy duty psychedelic", including strong and unignorable visuals.

Sources: en.wikipedia.org

Frequently asked questions

Is cardarine a SARM?

No. Cardarine is GW501516, a PPARδ agonist, while SARMs act on androgen receptors. The two classes are often grouped in informal discussions despite different mechanisms.

Is cardarine approved for human use?

No. It has no approved medical indication in any country. Regulatory agencies have not cleared it for treatment or prevention of any condition.

Why was its development discontinued?

Early clinical work stopped after rodent carcinogenicity findings. Those animal results raised concerns about long-term human risk, although direct human evidence is lacking. The human relevance of the tumors remains an open scientific question.

How does cardarine work in the body?

It binds to and activates PPAR delta, a nuclear receptor that controls expression of genes related to fatty acid oxidation. This mechanism can alter energy metabolism in animal models. It is not a direct stimulant or fat-burning enzyme.

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