If you have been reading about GW501516 and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Last reviewed on 2025-12-10. Where a claim depends on a specific study, the study is described rather than over-claimed.
Cardarine is a common name for GW501516, a synthetic compound first described in the 1990s as a selective agonist of the peroxisome proliferator-activated receptor delta. It was studied in preclinical models for metabolic and cardiovascular conditions, but it has not been approved as a medicine in the United States, Europe, or other major jurisdictions. Retail products labeled as cardarine are generally research chemicals or supplements, not pharmaceutical formulations. Because human safety and efficacy data remain limited, regulatory agencies treat it as an unapproved substance rather than a therapeutic product.
Sporting authorities added GW501516 to prohibited lists after it appeared in athlete samples and online markets. The World Anti-Doping Agency classifies it as a hormone and metabolic modulator, and its use can lead to an anti-doping rule violation. Some early laboratory work suggested effects on fatty acid oxidation and endurance-related metabolism in animals, but those findings do not establish safe or effective use in people. Reports of adverse events in humans are scarce and often anecdotal, which complicates risk assessment.
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.
| Property | Value | Notes |
|---|---|---|
| IUPAC name | {4-[({4-methyl-2-[4-(trifluoromethyl)phenyl]-1,3-thiazol-5-yl}methyl)sulfanyl]phenoxy}acetic acid | Systematic name for GW501516 |
| CAS Registry Number | 317318-70-0 | Unique identifier for the parent compound |
| Molecular formula | C21H18F3NO3S2 | Includes carbon, hydrogen, fluorine, nitrogen, oxygen, and sulfur |
| Molecular weight | 453.5 g/mol | Approximate value for the neutral form |
| Appearance | White to off-white powder | Typical description for purified laboratory material |
GW501516 binds and activates PPARδ, a nuclear receptor that influences transcription of genes involved in fatty acid oxidation and energy use. Activation shifts some metabolic pathways in preclinical models, which is why the compound has been studied for lipid disorders and exercise-related endpoints. The exact downstream effects in humans are incompletely mapped. PPARδ is expressed in many tissues, including skeletal muscle, liver, and adipose tissue, so broad activation may have varied consequences. Researchers continue to examine how selective or partial activation might alter the balance between benefits and risks.
Published human data are sparse and mostly come from early-phase trials. Those studies examined short-term changes in lipids, glucose, and exercise capacity, but they were not large enough to establish efficacy or long-term safety. Some animal experiments reported increased running endurance, yet such findings do not prove a performance benefit in people. Anti-doping laboratories detect GW501516 and its metabolites in urine or blood using liquid chromatography-tandem mass spectrometry. Detection windows depend on dose, sample type, and individual metabolism. The method is sensitive enough to identify trace residues in tested samples.
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.
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.
The debate continued for two days, mostly between TheJosh and Justin27. It narrowed down to a disagreement over if a week constitutes seven or eight days; Justin27 defined it as seven, from Sunday to Saturday, while TheJosh defined it as eight, from Sunday to the next Sunday. It then hinged on if Sunday was a "real day". English dictionaries universally define a week as having seven days, including Sunday. The two users' rhetoric intensified to where they were posting harsh insults, such as when Justin27 told TheJosh: "You are the dumbest boy alive. Jump off a bridge." After 120 posts across five web pages, the thread was locked by moderators, without the two coming to an agreement. TheJosh ended the debate by saying they had only been trolling, which SB Nation writer Jon Bois theorized was an attempt to maintain their dignity after being publicly embarrassed. As of 2016, the thread had 3 million page views since its creation. It had gone viral after being posted on Reddit in 2015. However, the debate "had been raging in the minds of" Bodybuilding.com's users since 2008. It was the subject of a 2016 SB Nation documentary titled The Dumbest Boy Alive by Bois, who referred to it as the "perhaps the dumbest argument in the history of the Internet". Deadspin writer Albert Burneko claimed it was "the least essential discussion ever had", and Chris Person said it was "the stuff of legends". In 2015, Vice magazine contacted U.S.-based mathematician Joanna Nelson for a resolution to the debate.
== Occurrence == Dimethyl trisulfide has been found in volatiles emitted from cooked onion, leek and other Allium species, from broccoli and cabbage, as well as from Limburger cheese, and is involved in the unpalatable aroma of aged beer and stale Japanese sake. It is a product of bacterial decomposition, including the early stages of human decomposition, and is a major attractant for blowflies looking for hosts. Dimethyl trisulfide along with dimethyl sulfide and dimethyl disulfide have been confirmed as volatile compounds given off by the fly-attracting plant known as dead-horse arum (Helicodiceros muscivorus). These flies are attracted to the odor of fetid meat and help pollinate this plant. DMTS contributes to the foul odor given off by the fungus Phallus impudicus, also known as the common stinkhorn. DMTS causes the characteristic malodorous smell of a fungating lesion, e.g., from cancer wounds, and contributes to the odor of human feces. DMTS can be synthesized by the reaction of methanethiol with hydrogen sulfide (in the presence of copper (II)) and with sulfur dichloride, among other methods:
Other diseases can also be triggers of renal dysfunction, for example infections, autoimmune diseases, poisonings or tumors. Virtually any infection or even lupus erythematosus can lead to the deposition of antigen-antibody complexes in the basal membrane of the renal corpuscles and thus to their damage. Many lily species, ethylene glycol, melamine, cyanuric acid and some heavy metals (cadmium, lead, mercury) have a strong toxic effect on the kidneys (renal toxicity) in cats. But also many drugs such as amphotericin B, cholecalciferol, doxorubicin, polymyxins, aminoglycosides and numerous non-steroidal anti-inflammatory drugs (→ analgesic nephropathy) can cause kidney damage.
Sources: en.wikipedia.org
== Wife of the heir to Austrian throne == At this time, Archduke Charles was in his twenties and did not expect to become emperor for some time, especially while Franz Ferdinand remained in good health. This changed on 28 June 1914 when the heir and his wife Sophie were assassinated in Sarajevo by Bosnian Serb nationalists. Charles and Zita received the news by telegram that day. She said of her husband, "Though it was a beautiful day, I saw his face go white in the sun." In the war that followed, Charles was promoted to General in the Austro-Hungarian army, taking command of the 20th Corps for an offensive in Tyrol. The war was personally difficult for Zita, as several of her brothers fought on opposing sides in the conflict (Prince Felix and Prince René had joined the Austrian army, while Prince Sixtus and Prince Xavier lived in France before the war and enlisted in the Belgian army.) Also her country of birth, Italy, joined the war against Austria in 1915, and so rumours of the 'Italian' Zita began to be muttered. Even as late as 1917, the German ambassador in Vienna, Count Botho von Wedel-Jarlsberg, would write to Berlin saying "The Empress is descended from an Italian princely house... People do not entirely trust the Italian and her brood of relatives." At Franz Joseph's request, Zita and her children left their residence at Schloss Hetzendorf and moved into a suite of rooms at Schönbrunn Palace. Here, Zita spent many hours with the old Emperor on both formal and informal occasions, where Franz Joseph confided in her his fears for the future.
=== Synthetic alizarin 1868 – 1873 === The development of synthetic alizarin opened up a huge market that was formerly served by natural dye makers. Alizarin was the first dye whose structure chemist determined, and they quickly set it as a target of synthesis, succeeding by 1868. Other chemical components of natural madder were identified and applied by the mid-19th century, including purpurin, which produced a delicate lilac colour, and green alizarin, which was patented in Britain and famously displayed at the 1867 Paris International Exhibition. Similar to aniline dyes, the precursors for Synthetic Alizarin were easily obtainable from coal tar. Germany dominated the synthetic alizarin market, however foreign competition was not non-extant, for example the British Alizarine Company Ltd.
=== Historical sites === Lebanon is the home of the Historic Cragun House. Built in 1893, it was once the home of Strange Nathaniel Cragun and his family. The family travelled the world, and their house is now a living history museum full of the pieces they collected from their travels as well as original furniture from the dwelling. This Victorian home is owned and maintained by the Boone County Historical Society and serves as headquarters for the organization. The Cragun House has been added to the National Register of Historic Places. Also listed on the National Register of Historic Places are the Boone County Courthouse and Oak Hill Cemetery.
Sources: en.wikipedia.org
20,000, 11 December 2007- On 29 October 2007, the SENSEX crossed the 20,000 mark for the first time with a massive 734.5-point gain, but closed below the 20,000 mark. The SENSEX would close above the 20,000 mark for the first time on 11 December 2007. It took 42 days after reaching the 19,000 milestone to close above 20,000 points for the first time. The journey of the last 10,000 points was covered in just 483 sessions, compared to 7,297 sessions taken to touch the 10,000 mark from its base value of 100 points. In the second half of 2007 alone, the SENSEX reached six 1,000-point milestones.
== External links == Jane Higdon, "Vitamin A", Micronutrient Information Center, Linus Pauling Institute, Oregon State University NIH Office of Dietary Supplements – Vitamin A Vitamin A Deficiency at the Merck Manual of Diagnosis and Therapy
== Clinical trials == Innovation Pharmaceuticals advanced brilacidin through early stage human clinical trials to a completed Phase 2a proof-of-concept clinical trial. Since acquisition, brilacidin was entered into a Phase 2b clinical trial. Brilacidin was granted the Qualified Infectious Disease Product (QIDP) designation by the FDA under the Generating Antibiotic Incentives Now Act of 2011 (GAIN Act).
Sources: en.wikipedia.org
No. Major drug regulators have not approved GW501516 for treating any medical condition. Products sold as cardarine are typically unapproved research chemicals or supplements, so their contents and safety are not assured.
It is prohibited by the World Anti-Doping Agency as a hormone and metabolic modulator. Athletes who test positive for GW501516 can face sanctions, including suspensions and loss of results.
Cardarine is a common or trade-style name, while GW501516 is the research code for the same chemical entity. Some sources also use Endurobol or GSK-516. The names refer to the same compound, not distinct drugs.
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.