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Identity And Pharmacological Classification — Research Overview

By Editorial Desk · published 2026-06-17 · last reviewed 2026-07-17 · Guide

A practical reference on prohibited list: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.

Reviewed 2026-07-17. Anything still debated is marked as such rather than presented as settled.

Identity and Pharmacological Classification

PPARδ is a nuclear receptor that influences transcription of genes involved in fatty acid oxidation, lipid transport, and energy homeostasis. GW501516 binds and activates this receptor with high selectivity relative to PPARα and PPARγ in laboratory assays. Activation alters expression of target genes in skeletal muscle, liver, and adipose tissue in animal models. The exact clinical consequences of these changes in humans remain incompletely characterized, and observed effects in animals do not establish therapeutic benefit or safety.

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.

Mechanism and Detection

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 at a glance

PropertyValueNotes
Chemical classPPARδ agonistNot an anabolic steroid.
Common synonymsGW501516, GW-1516Cardarine is an informal name.
AppearanceWhite to off-white powderTypical for research-grade solid.
Solubility classPoorly soluble in water; soluble in some organic solventsSuch as DMSO or ethanol in laboratory settings.
Typical storage temperatureCool, dry, protected from lightSpecific conditions vary by supplier and form.

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.

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Mechanism and Detection Methods

GW501516 acts as a selective agonist at PPARδ, a nuclear receptor that regulates transcription of genes involved in lipid handling and energy metabolism. Activation of PPARδ in preclinical models increases fatty acid oxidation, mitochondrial biogenesis, and exercise endurance in rodents. These effects have made the compound a subject of metabolic research and also a target for sport anti-doping rules. In humans, however, controlled studies are limited, and whether similar endurance or metabolic changes occur at tolerated exposures remains an open question. The receptor’s broad tissue distribution also means downstream effects may vary by organ and condition.

Detection of GW501516 in biological samples generally relies on liquid chromatography coupled with tandem mass spectrometry. Urine is a common matrix in anti-doping analysis, while blood or plasma may be used in research settings. Sample preparation can involve enzymatic hydrolysis, protein precipitation, or solid-phase extraction before instrumental analysis. Because the compound undergoes metabolism, assays may target the parent molecule, one or more metabolites, or both. Detection windows are not fixed; they depend on factors such as dose, route, individual metabolism, and assay sensitivity. Reference standards are required for accurate identification and quantification.

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 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.

Further detail

== Retirement == Heseltine stood down from his Henley constituency at the 2001 election, being succeeded by Spectator editor and future prime minister Boris Johnson, but he remained outspoken on British politics. He was created a life peer on 12 July 2001 taking the title Baron Heseltine, of Thenford in the County of Northamptonshire. In December 2002 Heseltine controversially called for Iain Duncan Smith to be replaced as leader of the Conservatives by the "dream-ticket" of Clarke as leader and Michael Portillo as deputy. He suggested the party's MPs vote on the matter rather than party members as currently required by party rules. Without the replacement of Duncan Smith, the party "has not a ghost of a chance of winning the next election" he said. Duncan Smith was removed the following year. In the 2005 party leadership election, Heseltine backed young moderniser David Cameron. Following Cameron's election to the leadership he set up a wide-ranging policy review. Chairmen of the various policy groups included ex-Chancellor Kenneth Clarke and other former Cabinet ministers John Redwood, John Gummer, Stephen Dorrell and Michael Forsyth as well as ex-leader Iain Duncan Smith. Heseltine was appointed to head the cities task force having been responsible for urban policy twice as Environment Secretary under Thatcher and Major. In 2008 Heseltine took part in the BBC Wales programme Coming Home about his Welsh family history. He said in this programme that he regarded Wales as his home and identified strongly with his Welsh ancestry.

Pea protein is a food product and protein supplement derived and extracted from yellow and green split peas, Pisum sativum. It can be used as a dietary supplement to increase an individual's protein or other nutrient intake, or as a substitute for other food products (e.g. the substitution of dairy milk by pea milk). As a powder, it is used as an ingredient in food manufacturing, such as a thickener, foaming agent, or an emulsifier. It is extracted in a powder form and can be processed and produced in different ways:

A free downloadable (PC) version — latest release AIDA v4.3b — which also works on Apple Macintosh computers running PC emulation software. A web-based version — called AIDA on-line — available to use via a standard web browser.

The use of adsorbent chemicals, such as zeolites, and other hemostatic agents are also used for sealing severe injuries quickly (such as in traumatic bleeding secondary to gunshot wounds). Thrombin and fibrin glue are used surgically to treat bleeding and to thrombose aneurysms. Hemostatic Powder Spray TC-325 is used to treated gastrointestinal bleeding. Desmopressin is used to improve platelet function by activating arginine vasopressin receptor 1A. Coagulation factor concentrates are used to treat hemophilia, to reverse the effects of anticoagulants, and to treat bleeding in people with impaired coagulation factor synthesis or increased consumption. Prothrombin complex concentrate, cryoprecipitate and fresh frozen plasma are commonly used coagulation factor products. Recombinant activated human factor VII is sometimes used in the treatment of major bleeding. Tranexamic acid and aminocaproic acid inhibit fibrinolysis and lead to a de facto reduced bleeding rate. Before its withdrawal, aprotinin was used in some forms of major surgery to decrease bleeding risk and the need for blood products.

Beginning in the 1st millennium BCE, groups of Amerindians including the Muisca, Zenú, Quimbaya, and Tairona developed the political system of cacicazgos with a pyramidal structure of power headed by caciques. The Muisca inhabited mainly the area of what is now the Departments of Boyacá and Cundinamarca high plateau (Altiplano Cundiboyacense) where they formed the Muisca Confederation. They farmed maize, potato, quinoa, and cotton, and traded gold, emeralds, blankets, ceramic handicrafts, coca and especially rock salt with neighboring nations. The Tairona inhabited northern Colombia in the isolated mountain range of Sierra Nevada de Santa Marta. The Quimbaya inhabited regions of the Cauca River Valley between the Western and Central Ranges of the Colombian Andes. Most of the Amerindians practiced agriculture and the social structure of each Indigenous community was different. Some groups of Indigenous people such as the Caribs lived in a state of permanent war, but others had less bellicose attitudes. During the 1200s, Malayo-Polynesians and Amerindians in Colombia made contact, thereby spreading Indigeous Amerindian genetics from Precolonial Colombia to some Pacific Ocean islands. The coconuts found in Colombia which originally come from the Philippines originate from this Precolombian exchange.

Sources: en.wikipedia.org

Background from the literature

== History == α-MSH was first isolated in the 1950s and its primary structure determined. By the 1960s, its role in promoting melanin diffusion was understood. In the 1980s, the University of Arizona synthesised more potent analogs of a-MSH, including afamelanotide. Afamelanotide was initially named melano-tan (or melanotan-I) due to its ability to tan skin with minimal sun exposure. Later, melanotan-II was synthesised. Following initial development at the University of Arizona as a sunless tanning agent, the Australian company Clinuvel conducted further clinical trials in that and other indications, and brought the drug to market in the European Union, the United States, and Australia. To pursue the tanning agent, melanotan-I was licensed by Competitive Technologies, a technology transfer company operating on behalf of University of Arizona, to an Australian startup called Epitan, which changed its name to Clinuvel in 2006. Early clinical trials showed that the peptide had to be injected about ten times a day due to its short half-life, so the company collaborated with Southern Research in the US to develop a depot formulation that would be injected under the skin, and release the peptide slowly. This was done by 2004. Multiple studies on the clinical effects of afamelanotide were conducted. According to ClinicalTrials.gov, Clinuvel sponsored several trials between 2007 and 2011 to explore its effects on erythropoietic protoporphyria, vitiligo, polymorphous light eruption, solar urticaria and acne vulgaris.

== Criminal trial == After being delayed for more than a year due to the COVID-19 pandemic, Vaught's trial began on March 21, 2022. Prosecutors portrayed the use of the override function as evidence of recklessness. On the other hand, defense experts testified that overrides were daily events at many hospitals, and Vaught testified that Vanderbilt's 2017 upgrade of its computer systems had caused such delays that nurses were instructed to use overrides to get medication that they needed. A Tennessee Bureau of Investigation agent testified that the medical center had a "heavy burden of responsibility" for the deadly medication error, but that the Bureau of Investigation only pursued criminal charges and penalties against the nurse, not the hospital. After Murphey's death, the hospital did not report the error to federal or state regulators (as required by law) and reported to the county medical examiner that Murphey died of natural causes with no mention of the vecuronium. The hospital also negotiated an out-of-court settlement with Murphey's family which prevents them from disclosing details of her death. On March 25, 2022, the jury convicted Vaught of gross neglect of an impaired adult and negligent homicide, which carries a maximum sentence of eight years in prison. She was acquitted of the more serious charge of reckless homicide. On May 13, 2022, Judge Jennifer Smith ruled that Vaught would not have to spend time in prison, sentencing her instead to three years' probation.

=== Post-independence (1946–1962) === The first elections after independence were the 1947 parliamentary election, with the People's Party winning a plurality in the Chamber of Deputies, but no absolute majority. In 1949, a series of military coups led to the dissolution of the Chamber of Deputies and constitutional suspensions. A Constituent Assembly elected in 1949 drafted the 1950 constitution, which strengthened parliamentary powers. Adib al-Shishakli's 1951 coup dissolved the Chamber of Deputies, and his 1953 election, with only 16% voter turnout, reconstituted the Chamber of Deputies as a 82-member legislative body under a presidential system. After his ouster in 1954, parliamentary rule was restored, with the People's Party and Ba'ath Party gaining influence. In 1958, the Chamber of Deputies was replaced by the UAR's National Assembly, where Syrians held one-third of the seats. Following Syria's withdrawal, the 1961 election restored parliamentary democracy.

=== Fosfomycin === Several antimicrobial drugs have been tested for the effective treatment of CRE. Fosfomycin is an antimicrobial agent that acts to inhibit UDP-N-acetylglucosamine enolpyruvyl transferase (MurA) which catalyzes one of the early steps of bacterial cell wall synthesis, and is effective against gram-negative and -positive aerobic bacteria, such as CRE. A meta-analysis of 17 studies investigating the clinical effectiveness of fosfomycin in four multidrug-resistant strains of Enterobacteriaceae found 11 which reported that over 90% of bacterial isolates were susceptible to fosfomycin. The elevated level of antimicrobial activity by fosfomycin can be attributed to the fact that resistance to this antibiotic in Enterobacteriaceae is chromosomally encoded and not plasmid-mediated. This causes a decreased capacity for survival in the bacteria. Bacteria that are naturally resistant to fosfomycin are less robust and less pathogenic.

Sources: en.wikipedia.org

Further detail

Agonists Cortagine Corticorelin Corticotropin-releasing hormone Sauvagine Stressin I Urocortin Antagonists Antalarmin Astressin-B CP-154,526 Emicerfont Hypericin LWH-234 NBI-27914 NBI-74788 Pexacerfont R-121919 TS-041 Verucerfont

The very large incentives given to pharmaceutical companies to produce orphan drugs have led to the impression that the financial support afforded to make these drugs possible is akin to abuse. Because drugs can be used to treat multiple conditions, companies can take drugs that were filed with their government agency as orphan drugs to receive financial assistance, and then market it to a wide population to increase their profit margin. For example AstraZeneca's cholesterol drug Crestor was filed as a treatment for the rare disease pediatric familial hypercholesterolemia. After the drug was approved for orphan drug designation, and AstraZeneca had received tax breaks and other advantages, AstraZeneca later applied and received FDA approval for the drug to be used to treat cholesterol in all diabetics.

These P450s are recruited by the X domain in the 7th NRPS module, which is unique to glycopeptide antibiotic biosynthesis. The cross-linked heptapeptide is then released by the action of the TE domain, and methyltransferase Vmt then N-methylates the terminal leucine residue. GtfE then joins D-glucose to the phenolic oxygen of residue 4, followed by the addition of vancosamine catalyzed by GtfD. Some of the glycosyltransferases capable of glycosylating vancomycin and related nonribosomal peptides display notable permissivity and have been used to generate libraries of differentially glycosylated analogs through glycorandomization.

Sources: en.wikipedia.org

Frequently asked questions

What is cardarine also known as?

Cardarine is commonly known as GW501516 or GW-1516. These names refer to the same synthetic compound. It is not a brand-name approved medicine.

Is cardarine a steroid?

No, cardarine is not a steroid. It is classified as a PPARδ agonist. Its structure and receptor target differ from anabolic steroids.

Has cardarine been approved for human use?

No regulatory agency has approved cardarine as a medicine. It was investigated in early research but development was discontinued. It is not available as a prescription drug.

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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