This is a working overview of Cardarine, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2025-09-25. Anything still debated is marked as such rather than presented as settled.
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.
Clinical development stopped after rodent studies showed tumors at multiple sites. Whether those findings predict human cancer risk remains an open question, but they led sponsors to discontinue programs. Human safety data are limited to small, short-term studies that were not designed to assess cancer risk. Reported effects in those studies included changes in blood lipids, but the evidence is insufficient for medical use. Long-term consequences of nonmedical use are not well characterized. Questions about dose, duration, and individual susceptibility remain unresolved.
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.
Cardarine is the common name for GW501516, a synthetic compound studied as a peroxisome proliferator-activated receptor delta agonist. Researchers developed it to explore treatments for lipid disorders and metabolic conditions. It is not an approved medicine in any country. Early clinical work examined changes in HDL cholesterol and triglycerides, but development was discontinued after animal studies raised concerns about cancer. The compound remains available as a research chemical and appears in discussions of performance enhancement.
At the molecular level, GW501516 binds and activates PPARδ, a nuclear receptor that regulates transcription. Activation shifts expression of genes involved in fatty acid oxidation, energy expenditure, and lipid transport in skeletal muscle and liver. Animal studies report increased endurance and altered lipid profiles after exposure. Human data are limited to small trials and do not establish long-term safety or efficacy. PPARδ also has roles in cell proliferation, so the relationship between activation and cancer risk remains an open question.
| Property | Value | Notes |
|---|---|---|
| Common synonyms | GW501516; GW-1516; endurobol | GW501516 is the research code |
| Drug class | PPARδ agonist | Not a selective androgen receptor modulator |
| Molecular formula | C21H18F3NO3S2 | Established chemical formula |
| Molar mass | 453.5 g/mol | Calculated from the formula |
| Regulatory status | Prohibited in sport; not approved as medicine | Status varies by country |
"On January 22, the perverse Brown woke up anchored near the mouth of the Rimac River with the greatest insolence imaginable, as if he knew that there was no gunboat or armed ship in the port. His forces were composed of four ships and a pailebot. Three of them went ahead until they anchored in the same bay, fired a few cannon shots as if to mock them, they were answered by the castles, they raised anchor again and kept looking around until midnight, when they returned to shoot at the port, and They managed to do the damage by sinking one of the ships that remained at anchor, the frigate Fuente-Hermosa." Such was the hostility of the Argentine corsairs towards the Peruvian population, that it has been recorded that several travelers from Peru to Europe (especially friars of the Catholic Church), at the moment of undertaking the return from the Brazilian coast to Peru, arrived in to prefer the land route, from Goiás and Mato Grosso, to reach Peru via the Amazon, "rather than run the risk of falling into the hands of corsairs from La Plata at sea." On the other hand, some historians, with indigenist, Hispanist or revisionist orientations of the nationalist current, have wanted to affirm that the Argentine Liberator himself, Don José de San Martin, could have been an anti-Peruvian figure, questioning whether a foreigner would arrive (San Martín) to proclaim independence.
=== Natural populations of Drosophila === In the 1930s, Dobzhansky and his coworkers collected Drosophila pseudoobscura and D. persimilis from wild populations in California and neighboring states. Using Painter's technique they studied the polytene chromosomes and discovered that the wild populations were polymorphic for chromosomal inversions. All the flies look alike whatever inversions they carry: this is an example of a cryptic polymorphism. Evidence rapidly accumulated to show that natural selection was responsible. Using a method invented by L'Héritier and Teissier, Dobzhansky bred populations in population cages, which enabled feeding, breeding and sampling whilst preventing escape. This had the benefit of eliminating migration as a possible explanation of the results. Stocks containing inversions at a known initial frequency can be maintained in controlled conditions. It was found that the various chromosome types do not fluctuate at random, as they would if selectively neutral, but adjust to certain frequencies at which they become stabilised. By the time Dobzhansky published the third edition of his book in 1951 he was persuaded that the chromosome morphs were being maintained in the population by the selective advantage of the heterozygotes, as with most polymorphisms.
== Society and culture == Pantopon gave its name to the poem "Pantopon Rose" by the American writer William Burroughs and to a song with the same name by the Northern Ireland alternative metal band Therapy? on their 1994 album Troublegum. Pantopon also gave its name to the 1996 Mexican documentary Rosa Pantopon.
Sources: en.wikipedia.org
== History == The company was founded in 1854 in Peru by William Russell Grace at the age of 22. Grace left Ireland during the Great Famine and traveled to South America with his family. He went first to Peru to work for the firm of Bryce and Company as a ship chandler to the merchantmen harvesting guano, which was used as a fertilizer and gunpowder ingredient due to its high levels of phosphorus and nitrogen. His brother, Michael P. Grace, joined the business, and in 1865 the company name was changed to Grace Brothers & Co. The company established headquarters in New York City in 1865. Working in fertilizer and machinery, the company was chartered in 1872 and incorporated in 1895. From 1904 to 1907, Edward Eyre served as president after the death of William Grace. In 1907, Joseph Peter Grace, the son of William Russell Grace, became president of the company. In 1914, the company created Grace National Bank.
According to the American Association of Sleep Medicine, daytime sleepiness is determined as mild, moderate and severe depending on its impact on social life. Daytime sleepiness can be assessed with the Epworth Sleepiness Scale (ESS), a self-reported questionnaire on the propensity to fall asleep or doze off during daytime. Screening tools for OSA comprise the STOP questionnaire, the Berlin questionnaire and the STOP-BANG questionnaire which has been reported as being a powerful tool to detect OSA.
=== Severe MTHFR deficiency === Severe MTHFR deficiency is rare (about 50 cases worldwide) and caused by mutations resulting in 0–20% residual enzyme activity. Patients exhibit developmental delay, motor and gait dysfunction, seizures, and neurological impairment and have extremely high levels of homocysteine in their plasma and urine as well as low to normal plasma methionine levels. This deficiency and mutations in MTHFR have also been linked to recessive spastic paraparesis with complex I deficiency. A study on the Chinese Uyghur population indicated that rs1801131 polymorphism in MTHFR was associated with nsCL/P in Chinese Uyghur population. Given the unique genetic and environmental characters of the Uyghur population, these findings may be helpful for exploring the pathogenesis of this complex disease.
== Mechanism of action == AOD9604 appears to enhance lipolysis in mice by upregulating beta-3 adrenergic receptors. Beta-3 adrenergic receptor knockout mice are unresponsive to the lipolytic effects of AOD9604.
Sources: en.wikipedia.org
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.
No. It has no approved medical indication in any country. Regulatory agencies have not cleared it for treatment or prevention of any condition.
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.
Cardarine is a common name for the investigational compound GW501516. It acts as a PPARδ agonist and is not approved for human use. It is prohibited in sport.