The short version of GW501516 fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2025-12-11. Anything still debated is marked as such rather than presented as settled.
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.
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.
| 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 |
Handling and quality assessment of cardarine reference material follow general laboratory practices for poorly characterized compounds. It typically appears as a white to off-white powder and is sparingly soluble in water but soluble in organic solvents such as dimethyl sulfoxide and ethanol. Storage recommendations usually specify a cool, dry, dark place, with long-term storage at low temperature and desiccation. Purity may be checked by high-performance liquid chromatography with ultraviolet detection, while identity is confirmed by mass spectrometry and nuclear magnetic resonance. No pharmacopeial monograph exists, so reported purity and stability depend on the supplier’s 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.
Anti-doping laboratories detect GW501516 and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is the most common matrix, though blood and dried blood spots may also be used in some programs. Detection depends on factors such as dose, timing, metabolism, and the sensitivity of the assay. Published methods describe limits of detection in the low nanogram per milliliter range for related compounds. Exact detection windows are not fixed for all situations and remain an area of ongoing study.
Products sold as cardarine have been found to contain incorrect compounds, variable amounts, or no active ingredient at all. Independent testing is required to verify identity and purity. Common analytical approaches include high-performance liquid chromatography, mass spectrometry, and nuclear magnetic resonance for structural confirmation. These methods can distinguish GW501516 from related PPAR agonists and from unrelated steroids. For regulators and researchers, such verification is central to interpreting both biological results and adverse event reports.
Bully: Tyler Height: 6'1" Weight: 250 lbs Victim(s): Joe and Dylan Fighter: Daniel Cormier Height: 5'11" Weight: 247 lbs Money earned by Bully: $0 Money earned by victim(s): $10,000 Original airing: This episode aired on MTV2 on September 29, 2012. In MTV Latin America, this is run as the first episode of season 3, followed by the "Michael" episode, thus omitting the episode where Mayhem fights Andy.
Stem cell-based therapies: Mesenchymal stem cells or induced pluripotent stem cells (iPSCs) can be differentiated into tenocytes in vitro. These cells offer an almost unlimited source for expanding tendon-like cells, which could be used for tendon repair and regeneration. However, their differentiation protocols still require optimization to achieve functional tenocytes that closely mimic the native tendon environment. Tendon tissue engineering: Combining tenocytes (or stem cells) with biomaterials, such as scaffolds, that mimic the natural tendon extracellular matrix is a promising avenue for tendon repair. These scaffolds can provide structural support and guide the differentiation and organization of tendon cells. Gene editing: Techniques like CRISPR-Cas9 could be used to enhance the tenogenic properties of stem cells or to correct defects in autologous tenocytes derived from the patient's own tissue. This approach could allow for more controlled and efficient tendon regeneration.
== In animals == Naturally occurring myophosphorylase deficiency (GSD-V; McArdle disease) has been found in Charolais cattle and Merino sheep. The cattle were asymptomatic at rest, but when forced to exercise, would become noticeably fatigued and recumbent (having to lie down) for approximately 10 minutes before being able to resume exercise (the second wind phenomenon). Artificially-induced myophosphorylase deficiency was created in mice, by altering their embryonic DNA, for use in laboratory experiments.
Many countries have restrictions on cigarette advertising, promotion, sponsorship, and marketing. For example, in the Canadian provinces of British Columbia, Saskatchewan and Alberta, the retail store display of cigarettes is completely prohibited if persons under the legal age of consumption have access to the premises. In the Canadian provinces of Ontario, Manitoba, Newfoundland and Labrador, and Quebec, as well as the Australian Capital Territory, the display of tobacco is prohibited for everyone, regardless of age, as of 2010. This retail display ban includes noncigarette products such as cigars and blunt wraps.
Sources: en.wikipedia.org
Demon Copperhead is a 2022 novel by Barbara Kingsolver. It was a co-recipient of the 2023 Pulitzer Prize for Fiction, and won the 2023 Women's Prize for Fiction. Kingsolver was inspired by the Charles Dickens novel David Copperfield. While Kingsolver's novel is similarly about a boy who experiences poverty, Demon Copperhead is set in Appalachia and explores contemporary issues. The book touches on themes of the social and economic stratification in Appalachia, child poverty in rural America, and drug addiction with a focus on the opioid crisis.
== The leading research groups, producers and applications == One of the leading groups in academy for creating ion-trap MMS is Prof. Graham Cooks with his associate Professor Zheng Ouyang at Purdue University. They have built a series of mini mass spectrometer based on quadrupole ion trap called Mini 10, Mini 11, Mini 12. The group used Mini 10 mass spectrometer weighing 10 kg to analyze proteins, peptides and alkaloids in complex plant materials with electrospray ionization ESI and paperspray ionization. The group used low radio frequency of resonant ion ejection to increase mass range up to 17,000 Da proteins. For interfacing ESI source with MMS, a 10 cm stainless steel capillary was fabricated to transfer the ions directly into the vacuum manifold. The resulting high pressure of 20 mTorr, which is several orders of magnitude higher than that used in lab-scale mass spectrometers is compensated by using the pressure-tolerant rectilinear ion trap. One of the key component of this MMS is the commercial turbo-bump and the MS can be operated at 10−3 torr. To overcome the problem of continuous sample introduction because of the small size of the pump, the group developed a technique called discontinuous atmospheric pressure introduction (DAPI). This technique performs direct chemical analysis without sample pretreatment and enables the coupling of miniature mass spectrometers to atmospheric pressure ionization sources, including ESI, atmospheric pressure chemical ionization (APCI), and various ambient ionization sources.
== Adverse effects == Nephrotoxicity: Like cisplatin, nephrotoxicity, harm to the kidneys, is the primary dose-limiting factor. However, the nephrotoxicity of nedaplatin has been shown to be less severe than cisplatin. In rats, nedaplatin primarily affected the renal papilla, with papillary necrosis in severe cases. Neurotoxicity: Nedaplatin is widely reported to be neurotoxic, especially to the nerves of the ear. Causing symptoms like numbness and tingling in mild cases, or sensory ataxia in more severe cases. Nausea and vomiting: The emetogenic effects of nedaplatin are commonly managed with prophylactic antiemetics, such as duplex dexamethasone and ondansetron or triplex dexamethasone, ondansetron and aprepitant. Ototoxicity: Nedaplatin is toxic to the nerve and hair cells in the cochlea. In rats, nedaplatin was severely toxic to the nerve cells at a concentration of 10 μM, with damage to hair cells becoming more severe exceeding 100 μM. Neutropenia, leukopenia, anemia and thrombocytopenia (see "Aqupla アクプラ" in External Links): Nedaplatin is toxic to the hemopoietic cells of the bone marrow, combined with reduced levels of erythropoietin, leads to elevated incidence of bone marrow suppression compared to cisplatin. Incidence of severe grades of leukopenia and neutropenia are reported to be higher than cisplatin in treatment combined with radiotherapy. These haematological adverse effects are common in general.
It could possibly be extended to 10 days and prevent substantial cell damage by low temperature preservation methods. On the same day, a separate study reports new cryoprotectant solvents, tested with cells, that could preserve organs by the latter methods for much longer with substantially reduced damage.
The body is able to substantially reduce the amount of iron it absorbs across the mucosa. It does not seem to be able to entirely shut down the iron transport process. Also, in situations where excess iron damages the intestinal lining itself (for instance, when children eat a large quantity of iron tablets produced for adult consumption), even more iron can enter the bloodstream and cause a potentially deadly syndrome of iron overload. Large amounts of free iron in the circulation will cause damage to critical cells in the liver, the heart and other metabolically active organs. Iron toxicity results when the amount of circulating iron exceeds the amount of transferrin available to bind it, but the body is able to vigorously regulate its iron uptake. Thus, iron toxicity from ingestion is usually the result of extraordinary circumstances like iron tablet over-consumption[1] rather than variations in diet. The type of acute toxicity from iron ingestion causes severe mucosal damage in the gastrointestinal tract, among other problems. Excess iron has been linked to higher rates of disease and mortality. For example, breast cancer patients with low ferroportin expression (leading to higher concentrations of intracellular iron) survive for a shorter period of time on average, while high ferroportin expression predicts 90% 10-year survival in breast cancer patients. Similarly, genetic variations in iron transporter genes known to increase serum iron levels also reduce lifespan and the average number of years spent in good health.
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 commonly known as GW501516 or GW-1516. These names refer to the same synthetic compound. It is not a brand-name approved medicine.