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Identity And Pharmacological Mechanism — Quick Reference

By Editorial Desk · published 2025-09-05 · last reviewed 2025-09-19 · Data

The short version of GW501516 fits in a sentence. The long version — which is the one that helps — is below.

Reviewed 2025-09-19. Anything still debated is marked as such rather than presented as settled.

Identity and Pharmacological Mechanism

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.

Cardarine as Investigational PPARδ Agonist

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 at a glance

PropertyValueNotes
Chemical classSynthetic PPARδ agonistNot a steroid or a selective androgen receptor modulator.
Common synonymsCardarine, GW501516, GW-501516, endurobolNames vary by supplier and literature source.
AppearanceWhite to off-white powderConsistent with many small-molecule research chemicals.
SolubilityLow in water; soluble in DMSO and ethanolOften prepared in organic solvent for laboratory work.
Primary targetPPARδ (NR1C2)Nuclear receptor involved in lipid and energy metabolism.

Detection, Regulation, and Quality Context

Cardarine can be detected in biological samples and product materials using liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). The method separates compounds by chromatography and identifies them by mass-to-charge transitions, allowing low-level detection in urine or blood. Sample preparation often involves enzymatic hydrolysis, solid-phase extraction, or protein precipitation. Certified reference materials and isotope-labeled internal standards improve quantification. Detection windows depend on metabolism, matrix, and assay sensitivity, so no single universal window applies.

Regulatory treatment of cardarine differs by context and jurisdiction. In competitive sport, the World Anti-Doping Agency lists PPARδ agonists, including GW501516, as prohibited at all times. Outside sport, it lacks approval as a prescription medicine in major drug markets, and products sold for human consumption may be treated as unapproved drugs. Some countries also restrict importation or sale through general consumer protection and medicines laws. These classifications affect availability, testing, and legal risk without establishing therapeutic value.

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Background and Research Context

Cardarine is a common name for GW501516, a synthetic compound developed in the 1990s through research collaborations involving GlaxoSmithKline. It belongs to a class of molecules known as peroxisome proliferator-activated receptor delta agonists. Early studies explored its effects on lipid metabolism and energy expenditure in animal models. The compound was never approved as a human medicine, and clinical development was discontinued. In the years since, it has appeared in fitness and bodybuilding communities as a performance-enhancing substance. Regulatory agencies classify it as an unapproved drug.

PPARδ is a nuclear receptor that regulates gene expression related to fatty acid oxidation, glucose homeostasis, and mitochondrial function. GW501516 binds to this receptor with high affinity and activates downstream signaling in skeletal muscle and other tissues. Animal studies reported increased endurance and altered fuel preference, but human data remain limited and inconsistent. The precise relationship between receptor activation and observed physiological changes is still an area of active investigation. Researchers have also examined whether the compound affects inflammation or cell proliferation. No approved therapeutic indication exists for cardarine.

In laboratory settings, cardarine is studied as a tool compound for probing PPARδ biology. Published experiments often use cell cultures, rodent models, or isolated tissues. Some investigations focus on metabolic effects, while others assess potential risks such as carcinogenicity observed in long-term animal studies. Because human trials are sparse, most knowledge comes from preclinical work and adverse event reports. Scientific literature frequently notes the gap between animal findings and human outcomes. The compound is not a dietary supplement and is not intended for human consumption.

Mechanism and Research Context

GW501516 acts as an agonist at peroxisome proliferator-activated receptor delta, a nuclear receptor involved in transcription of genes related to lipid handling and energy use. Activation of PPARδ can shift skeletal muscle toward greater fatty acid oxidation in animal models, which is one reason it drew interest for metabolic disease and exercise research. The exact downstream effects depend on tissue, species, dose, and duration. Human data are sparse, so many proposed benefits remain hypotheses rather than established clinical outcomes.

Laboratory studies have examined GW501516 in cell cultures and rodents for conditions such as dyslipidemia, insulin resistance, and obesity. Some trials in humans were initiated, but development was discontinued after preclinical findings raised concerns about cancer in certain models. Those findings do not prove that the compound causes cancer in people, but they contributed to regulatory caution. Later reviews often describe the evidence as preliminary and insufficient for assessing long-term safety.

Background and Regulatory History

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.

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.

Reference notes

With its large size and geographic variety, the United States includes most climate types. East of the 100th meridian, the climate ranges from humid continental in the north to humid subtropical in the south. The western Great Plains are semi-arid. Many mountainous areas of the American West have an alpine climate. The climate is arid in the Southwest, Mediterranean in coastal California, and oceanic in coastal Oregon, Washington, and southern Alaska. Most of Alaska is subarctic or polar. Hawaii, the southern tip of Florida and U.S. territories in the Caribbean and Pacific are tropical. The United States receives more high-impact extreme weather incidents than any other country. States bordering the Gulf of Mexico are prone to hurricanes, and most of the world's tornadoes occur in the country, mainly in Tornado Alley. Due to climate change, extreme weather has become more frequent in the U.S. in the 21st century, with three times the number of reported heat waves compared to the 1960s. Since the 1990s, droughts in the American Southwest have become more persistent and more severe. The regions considered as the most attractive to the population are the most vulnerable.

=== Faulty paternity tests === Labcorp has been criticized over faulty paternity tests, many of which have resulted in lawsuits. The most notable case was the 2005 false accusation of Washington hairdresser Andre Chreky, who spent $200,000 and years in court proving, despite a false-positive test, that he was not the father. In the trial, it was determined that only five people at Labcorp reviewed data and made paternity determinations, including during 10 hour shifts that required making determinations every 4 minutes.

=== Name === Within the INN, USAN, BAN, and AAN naming systems this drug is known as butorphanol, while within JAN it is named torbugesic. As the tartrate salt, butorphanol is known as butorphanol tartrate (USAN, BAN).

=== Cancer === The antiproliferative effects of sirolimus may have a role in treating cancer. When dosed appropriately, sirolimus can enhance the immune response to tumor targeting or otherwise promote tumor regression in clinical trials. Sirolimus seems to lower the cancer risk in some transplant patients. Sirolimus was shown to inhibit the progression of dermal Kaposi's sarcoma in patients with renal transplants. Other mTOR inhibitors, such as temsirolimus (CCI-779) or everolimus (RAD001), are being tested for use in cancers such as glioblastoma multiforme and mantle cell lymphoma. However, these drugs have a higher rate of fatal adverse events in cancer patients than control drugs. A combination therapy of doxorubicin and sirolimus has been shown to drive Akt-positive lymphomas into remission in mice. Akt signalling promotes cell survival in Akt-positive lymphomas and acts to prevent the cytotoxic effects of chemotherapy drugs, such as doxorubicin or cyclophosphamide. Sirolimus blocks Akt signalling and the cells lose their resistance to the chemotherapy. Bcl-2-positive lymphomas were completely resistant to the therapy; eIF4E-expressing lymphomas are not sensitive to sirolimus.

Sources: en.wikipedia.org

Notes from published material

Certain countries and trade blocs establish programmes for high-frequency and/or low-risk travellers to expedite border controls, subjecting them to lighter or automated checks or priority border-control facilities. In some countries, citizens or residents have access to automated facilities not available to foreigners. The following expedited border control programmes are currently in effect:

The term flourishing, in positive psychology, refers to optimal human functioning. It comprises four parts: goodness, generativity, growth, and resilience (Fredrickson, 2005). According to Fredrickson (2005), goodness is made up of: happiness, contentment, and effective performance; generativity is about making life better for future generations, and is defined by "broadened thought-action repertoires and behavioral flexibility"; growth involves the use of personal and social assets; and resilience reflects survival and growth after enduring a hardship. A flourishing life stems from mastering all four of these parts. Two contrasting ideologies are languishing and psychopathology. On the mental health continuum, these are considered intermediate mental health disorders, reflecting someone living an unfulfilled and perhaps meaningless life. Those who languish experience more emotional pain, psychosocial deficiency, restrictions in regular activities, and missed workdays. Fredrickson & Losada (2005) conducted a study on university students, operationalizing positive and negative affect. Based on a mathematical model which has been strongly criticized, and now been formally withdrawn by Fredrickson as invalid, Fredrickson & Losada claimed to have discovered a critical positivity ratio, above which people would flourish and below which they would not.

A large proportion of commercial drugs (e.g. aspirin, ivermectin, cyclosporin, taxol) are derived from natural products that evolved due to their involvement in ecological interactions. While it has been proposed that the study of natural history could contribute to the discovery of new drug leads, most drugs derived from natural products were not discovered due to prior knowledge of their ecological functions. However, many fundamental biological discoveries have been facilitated by the study of plant toxins. For example, the characterization of the nicotinic acetylcholine receptor, the first neurotransmitter receptor to be identified, ensued from investigations into the mechanisms of action of curare and nicotine. Similarly, the muscarinic acetylcholine receptor takes its name from the fungal toxin muscarine. Whereas aquatic fungi provide specialized metabolites of interest for antibiotics, e.g. pestalone. Pestalone inhibits the growth of marine bacteria, the pathway to produce pestalone by marine fungi was found not to work when the bacteria is absent. The compound pestalone was derived from a marine fungus located in the Bahamas Islands on the surface of a brown alga, Rosenvingea sp. Development in biotechnology focuses on aquatic fungi in the pursuit of new antibiotics was inspired by terrestrial fungi, the cross over is not equivalent as demands in aquatic fungi are not exact to their terrestrial counter parts. Some aquatic fungi have shown changes to sphingolipid production under stressors such as acid resulting in the inhibition of biofilm formation.

Sources: en.wikipedia.org

Further detail

Personalized Dosing of Dichloroacetate Using GSTZ1 Clinical Genotyping Assay. Langaee T, Wagner R, Horne LP, Lawson LA, Becker C, Shahin M, Starostik P, Stacpoole PW. Genet Test Mol Biomarkers. 2018 Apr;22(4):266-269. doi: 10.1089/gtmb.2017.0261. Epub 2018 Mar 19. PMID: 29641284 Variation in the GSTZ1 haplotype is the principal variable influencing DCA kinetics and dynamics in humans. We aimed to develop a sensitive and rapid clinical genetic screening test for determining GSTZ1 haplotype status in individuals who would be treated with DCA, …

As with animal findings, both TMPAA and NAM have been said to be inactive based on human tests. It has also been noted that metabolites like TMPA and TMPE are rapidly metabolized. As such, metabolites of mescaline like TMPA, TMPE, TMPAA, and NAM do not appear to be involved in the drug's psychedelic-related effects. 3,4,5-Trimethoxyamphetamine (TMA), the α-methyl analogue of mescaline and an MAO-resistant psychedelic, is only about twice as potent as mescaline as a psychedelic in humans despite having similar serotonin receptor affinity. This suggests that the deamination of mescaline has a relatively limited impact on its potency, compared to for example the 2C series of psychedelics. Another analogue of mescaline, the deuterated isotopologue Alpha-D (α,α-dideuteromescaline), has been reported to be roughly one-third more potent than mescaline as a psychedelic in humans, albeit based on limited testing. This is consistent with findings of about one-third of a dose of mescaline being metabolized via deamination.

RNA-editing processes show great molecular diversity, and some appear to be evolutionarily recent acquisitions that arose independently. The diversity of RNA editing phenomena includes nucleobase modifications such as cytidine (C) to uridine (U) and adenosine (A) to inosine (I) deaminations, as well as non-template nucleotide additions and insertions. RNA editing in mRNAs effectively alters the amino acid sequence of the encoded protein so that it differs from that predicted by the genomic DNA sequence.

Sources: en.wikipedia.org

Frequently asked questions

What is cardarine?

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.

How does cardarine interact with the body?

It binds to and activates PPARδ, a nuclear receptor that regulates genes related to fatty acid oxidation and energy use. This activation alters transcription in tissues such as skeletal muscle and liver. The full range of downstream effects in humans is not fully established.

Is cardarine found naturally?

No, cardarine is not known to occur naturally in plants, animals, or humans. It is a synthetic molecule produced for laboratory research. Products labeled as cardarine should therefore be treated as manufactured chemicals with variable purity.

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.

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