PPAR delta is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Last reviewed on 2025-09-27. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
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.
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.
| 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 |
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.
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.
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 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.
Because cardarine is not an approved medicine, no pharmacopeial monograph defines its identity, purity, or storage requirements. Laboratories typically rely on in-house methods and reference standards when testing materials labeled as GW501516. Certificates of analysis may report purity and identity for a specific batch, but their scope varies and they do not guarantee safety or legal status. Independent verification can include high-performance liquid chromatography, mass spectrometry, nuclear magnetic resonance, and elemental analysis. The distinction between research chemical labeling and human use is significant because quality standards and oversight differ.
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.
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.
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.
=== First mammals === The Permian–Triassic extinction event about 252 million years ago, which was a prolonged event due to the accumulation of several extinction pulses, ended the dominance of carnivorous therapsids. In the early Triassic, most medium to large land carnivore niches were taken over by archosaurs which, over an extended period (35 million years), came to include the crocodylomorphs, the pterosaurs and the dinosaurs; however, large cynodonts like Trucidocynodon and traversodontids still occupied large sized carnivorous and herbivorous niches respectively. By the Jurassic, the dinosaurs had come to dominate the large terrestrial herbivore niches as well. The first mammals (in Kemp's sense) appeared in the Late Triassic epoch (about 225 million years ago), 40 million years after the first therapsids. They expanded out of their nocturnal insectivore niche from the mid-Jurassic onwards; the Jurassic Castorocauda, for example, was a close relative of true mammals that had adaptations for swimming, digging and catching fish. Most, if not all, are thought to have remained nocturnal (the nocturnal bottleneck), accounting for much of the typical mammalian traits. The majority of the mammal species that existed in the Mesozoic Era were multituberculates, eutriconodonts and spalacotheriids. The earliest-known fossil of the Metatheria ("changed beasts") is Sinodelphys, found in 125-million-year-old Early Cretaceous shale in China's northeastern Liaoning Province. The fossil is nearly complete and includes tufts of fur and imprints of soft tissues.
Prolyl 3-hydroxylase 2 is an enzyme that in humans is encoded by the gene P3H2 (formally LEPREL1). This enzyme is involved in the assembly of collagen. Pathogenic mutations in the gene are associated with severe nearsightedness (myopia) and cataracts.
China's Atomic Energy Authority rates the China Experimental Fast Reactor at 65 MW thermal and 20 MW electrical. It first reached criticality in 2010 and supplied electricity to the grid in 2011. China initiated a research and development project in thorium molten-salt thermal breeder-reactor technology (liquid fluoride thorium reactor), formally announced at the Chinese Academy of Sciences annual conference in 2011. Its ultimate target was to investigate and develop a thorium-based molten salt nuclear system over about 20 years. In November 2025, the Chinese Academy of Sciences reported thorium-to-uranium fuel conversion in an experimental molten-salt reactor built by its Shanghai Institute of Applied Physics. The institute described a goal of demonstrating a 100-megawatt project by 2035.
For example, in 1890, Serbia introduced a royal government directive which ordered patients to be treated at the Pasteur Institute in Budapest. Despite the increased availability of vaccines, in practice they were often restricted to the wealthy upper classes, since access commonly required complicated procedures, such as traveling long distances to access treatment and arranging for an extended stay to receive the treatment which involved several weeks of injections, which many people could not afford. The Pasteur-Roux vaccine attenuated the harvested virus samples by allowing them to dry for five to ten days. Similar nerve tissue-derived vaccines are still used in some countries, and while they are much cheaper than modern cell culture vaccines, they are not as effective. Neural tissue vaccines also carry a certain risk of neurological complications. Since the 1980s, countries have increasingly abandoned the use of nerve tissue-derived vaccines, replacing them with modern vaccines. The use of nerve tissue-derived vaccines was phased out in China in 1990, Thailand in 1992, Sri Lanka in 1995, Indonesia in 1996, Philippines in 1997, Laos in 2005, Cambodia in 2005, India in 2005, Nepal in 2006, Vietnam in 2007 and Bangladesh in 2011.
Liu Wenhui's role in the Long March is described differently by various sources. According to one account, during the fight with Communist forces while the Long March was in process, Chiang Kai-shek repeatedly ordered Liu to bring his troops against the Communists, but Liu made excuses, while secretly allowing safe passage for the Chinese Red Army in a non-aggression pact. Thus, the engagements around Xiakou Village in 1934 did not involve Liu's 24th Army, but the 21st Army of KMT troops garrisoned just across the Sichuan border in Mingshan. However, a contradictory account of his engagement with the Communists is given by the communist-aligned Guangming Daily, which states that during May 1935 Liu Wenhui was supposedly forced by Chiang Kai-shek to oversee the battle with the Red Army at Hanyuan. Liu's 24th Army suffered heavy losses during the battles of Dadu River and Luding Bridge. Another report in his 1990 biography, also written in mainland China by the communist revolutionaries Peng and Shu, instead states that in May 1935 Chiang ordered Liu, as well as general Li Yunheng (李韞珩) of the 16th Army, to block the communist advance. Li's army had stationed at Kangding, and Li supposedly had ambitions to replace Liu's role as head of Xikang. To avoid expending his forces, Liu had his army stage a battle with the communists, firing into the air when necessary and faking reports to Chiang, letting the Red Army pass through Luding Bridge with minimal engagement.
Sources: en.wikipedia.org
== Immune function == Platelets have a central role in innate immunity, initiating and participating in multiple inflammatory processes, directly binding and even destroying pathogens. Clinical data show that many patients with serious bacterial or viral infections have thrombocytopenia, thus reducing their contribution to inflammation. Platelet-leukocyte aggregates (PLAs) found in circulation are typical in sepsis or inflammatory bowel disease, showing the connection between thrombocytes and immune cells. The platelet cell membrane has receptors for collagen. Following rupture of the blood vessel wall, platelets are exposed and adhere to the collagen in the surrounding tissue.
Nonetheless, for Westad the Wall's demise carried significance well beyond the symbolic, since it reopened what had been, since the earliest years of the Cold War, an unresolved German question—one that the postwar division had sustained against the wishes of the German population itself—even as European leaders, Thatcher foremost among them, regarded the prospect of a reunified and economically formidable Germany with considerable unease.
Trump administration officials stated in a July 2026 court filing that the cancellations were "based solely on the political identity" of the grant recipient's state. In October 2025, the US used trade and visa threats to sabotage an agreement for cleaner international shipping at the International Maritime Organization. In December 2025, Russel Vought announced plans to dismantle the National Center for Atmospheric Research. The Department of Energy issued several emergency orders in 2025 directing coal power plants to continue operating. The cost to ratepayers to maintain and run these aging plants was estimated at $3 billion per year. On January 7, 2026, Trump announced that the United States would be withdrawing from the 1992 United Nations Framework Convention on Climate Change (UNFCC), the UN's Intergovernmental Panel on Climate Change (IPCC), and 65 other international organizations—alleging the treaties "no longer serve American interests". The next day, Trump's administration announced that the country would be withdrawing from the Green Climate Fund, which since 2010 has provided funds to help poorer nations deal with the effects of climate change. On January 14, 2026, the EPA revised its regulations on air pollution so as to no longer consider the dollar value of pollution's impact on human health when determining acceptable levels of polluted air for public health. In June 2026, the Trump administration announced dismantlement of the Ocean Observatories Initiative that includes 900 deep-sea instruments.
=== 1973 Antitrust case over griseofulvin === In the 1960s, Glaxo Group Ltd. (Glaxo) and Imperial Chemical Industries (ICI) each owned patents covering various aspects of the antifungal drug griseofulvin. They created a patent pool by cross-licensing their patents, subject to express licensing restrictions that the chemical from which the "finished" form of the drug (tablets and capsules) was made must not be resold in bulk form, and they licensed other drug companies to sell the drug in finished form and subject to similar restrictions. The effect and intent of the bulk-sale restriction was to keep the drug chemical out of the hands of small companies that might act as price-cutters, and the effect was to maintain stable, uniform prices. The United States brought an antitrust suit against the two companies—United States v. Glaxo Group Ltd.—charging them with violation of the Sherman Act and also seeking to have the patents declared invalid. The trial court found that the defendants had engaged in several unlawful conspiracies, but dismissed the part of the suit seeking invalidation of patents and refused to grant as relief mandatory sales of the bulk drug chemical and compulsory licensing of the patents. The government appealed to the Supreme Court, which reversed, in United States v. Glaxo Group Ltd., 410 U.S. 52 (1973).
Heavy ions can also be generated with an ion gun which typically uses the thermionic emission of electrons to ionize a substance in its gaseous state. Such instruments are typically used for surface analysis. Gas flows through the ion source between the anode and the cathode. A positive voltage is applied to the anode. This voltage, combined with the high magnetic field between the tips of the internal and external cathodes allow a plasma to start. Ions from the plasma are repelled by the anode's electric field. This creates an ion beam.
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.
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.