The short version of GW501516 fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2025-11-30 and is reviewed periodically as new material appears.
Human trials of GW501516 were small and short in duration. They examined lipid levels, glucose handling, and other metabolic markers, but the programs were halted after the animal cancer findings. No approved therapeutic product exists, and published human data are insufficient for establishing long-term safety. Reports of use for athletic performance come mainly from non-clinical settings and cannot be verified through controlled trials. Independent testing of products sold as cardarine has found inconsistent purity and labeling.
Laboratory studies indicate that GW501516 activates PPARδ, a nuclear receptor involved in fatty acid oxidation and energy metabolism. In rodent experiments, treated animals often showed increased endurance and reduced fat mass. These effects were observed under controlled conditions and do not establish safe or effective use in humans. The exact dose-response relationship in humans remains poorly characterized. Species differences in metabolism can affect how results translate across animals and people.
Safety concerns emerged from long-term animal studies. In rodents given the compound for extended periods, researchers found an increased incidence of certain cancers, including liver and bladder tumors. These findings contributed to the discontinuation of clinical development. Whether similar risks apply to short-term or low-level exposure in humans is not established, and controlled human safety data are limited. The relevance of high-dose rodent carcinogenicity findings to human use remains a subject of debate.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Primary target | PPARδ (NR1C2) | Nuclear receptor involved in lipid metabolism |
| Preclinical effect | Increased fatty acid oxidation | Observed in rodent studies |
| Key safety signal | Tumors in rodents after long-term exposure | Contributed to halted clinical development |
| Human trial status | No approved product; development stopped | Limited short-term metabolic data |
| Sport regulatory status | Prohibited at all times | WADA hormone and metabolic modulators class |
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.
Anti-doping laboratories identify GW501516 and related metabolites using liquid chromatography coupled with tandem mass spectrometry. Urine is the most common matrix, though blood and dried blood spots may also be analyzed. The method targets the parent compound and phase I and phase II metabolites, which extend the detection window. Because the substance is prohibited at all times, athletes can be tested outside competition. Detection limits and windows depend on the assay, sample type, and individual metabolism.
Cardarine is frequently described as a fat-burning or endurance-enhancing supplement, but these claims exceed the available evidence. The compound is not a hormone, steroid, or selective androgen receptor modulator. Research articles discuss it as a tool compound for studying PPARδ biology, while anti-doping literature focuses on its abuse and detection. Quality of unapproved products is uncertain, and independent analyses have found impurities or incorrect labeling. Open questions include whether human cancer risk resembles that seen in rodents and how often non-athletes use the substance.
Cardarine has no approved therapeutic indication and is not marketed as a medicine. The World Anti-Doping Agency lists GW501516 as a prohibited substance at all times, covering both in-competition and out-of-competition periods. National laws vary: some countries treat it as an unapproved drug subject to import controls, while others have specific restrictions on sale for human consumption. It is often sold as a research chemical, a label that does not imply safety or legality. Enforcement actions have targeted online vendors and shipments.
Laboratory detection of GW501516 commonly uses liquid chromatography coupled with tandem mass spectrometry. The method can identify the parent compound or its metabolites in urine and blood after sample cleanup. Protein precipitation, solid-phase extraction, or enzymatic hydrolysis may precede analysis, depending on the matrix. Reference standards are required for accurate quantification and confirmation. Because the compound is not approved, testing often occurs in anti-doping, forensic, or research settings rather than routine clinical care. Results are reported with limits of detection and quantification.
Stability of GW501516 depends on form, temperature, light exposure, and moisture. Solid reference material is typically stored frozen or refrigerated in a desiccator and protected from light. Solutions in organic solvents such as dimethyl sulfoxide are often kept frozen in aliquots to reduce freeze-thaw cycling. Aqueous solubility is low, so aqueous stock solutions can be difficult to prepare without cosolvents. Degradation may appear as changes in chromatographic purity or mass spectral signal. Stability studies are needed to establish shelf life for any specific preparation.
Quality assessment for cardarine samples usually combines identity, purity, and impurity testing. Nuclear magnetic resonance spectroscopy and mass spectrometry can confirm molecular structure, while high-performance liquid chromatography estimates purity. Certificates of analysis from testing laboratories may list these results, but they do not establish safety or legality. In the absence of approved manufacturing, products sold online may contain the wrong compound, variable amounts, or unlisted contaminants. Independent verification is therefore central to analytical work and to interpreting any reported biological activity.
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.
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.
== Horse racing scandals == Show jumping horse killings – from 1975 to 1995, wealthy owners and trainers of show jumping horses conspired to electrocute and otherwise kill over-valued as well as under-performing animals in a 20-year-long scheme to defraud insurance companies. Crimes also committed during this equestrian sports scandal include extortion, mail fraud, animal cruelty and the murder of at least one human being. Fine Cotton/Bold Personality ring-in – a 1984 betting scam in which the conspirators, which included some elite figures in Australian Thoroughbred racing, substituted the far more talented Bold Personality for Fine Cotton in a low-class race. The scheme was discovered immediately after the race and the investigation led to lifetime bans for six individuals and bans of more than a decade for at least two more. 2020 Horse racing doping scam – the scam was revealed in March 2020, when the FBI cracked down several top names in American horse racing. Initially, 27 people (trainers and veterinarians) were charged with doping, which later increased to 29 people.
==== Name and country change, convicted of drug smuggling ==== On 10 October 1991, Olofsson was released, changed his name to Daniel Demuynck, and moved to the Belgian countryside, 80 km outside Brussels. In July 1996, Olofsson was arrested outside a bank in Oslo when the police thought he was preparing a robbery. He was released after 24 hours. On a stormy November night, he was rescued by a sea rescue helicopter off the coast of Halland after his wooden boat was smashed against the rocks. A few weeks later, he was taken into custody for drunk driving in Stockholm. On 15 April 1998, he was arrested in Tenerife as the head of drug smuggling after being wanted internationally via Interpol for several months. He was extradited to Denmark and after a high-profile trial in Frederikssund, he was sentenced in 1999 to fourteen years in prison for smuggling 49 kilos of amphetamine into Denmark. It was then the most severe punishment for drug offenses ever handed out in Danish legal history. While in Denmark, he was held in the isolation ward at Vestre Prison in Copenhagen. He was released on parole on 9 May 2005.
Amine reactive: aminoallyl nucleotides contain a primary amine group on a linker that reacts with the amino-reactive dye such as cyanine or Alexa Fluor dyes, which contain a reactive leaving group like succinimidyl ester (NHS). Base-pairing amino groups are not affected. Thiol reactive: thiol-containing nucleotides react with the fluorophore linked to a reactive leaving group like maleimide. Biotin-linked nucleotides rely on the same indirect labelling principle (and fluorescent streptavidin) and are used in Affymetrix DNAchips. Fluorophores find a variety of uses in medicine and biochemistry. The most commonly used and commercially available fluorescent base analogue, 2-aminopurine (2-AP), has a high-fluorescence quantum yield free in solution (0.68) that is considerably reduced (appr. 100 times but highly dependent on base sequence) when incorporated into nucleic acids. The emission sensitivity of 2-AP to immediate surroundings is shared by other promising and useful fluorescent base analogues like 3-MI, 6-MI, 6-MAP, pyrrolo-dC (also commercially available), modified and improved derivatives of pyrrolo-dC, furan-modified bases and many other ones (see recent reviews). This sensitivity to the microenvironment has been utilized in studies of e.g. structure and dynamics within both DNA and RNA, dynamics and kinetics of DNA-protein interaction and electron transfer within DNA.
== History == Etoperidone was discovered by scientists at Angelini, who also discovered trazodone. Its development names have included ST-1191 and McN-A-2673-11. The INNTooltip International Nonproprietary Name etoperidone was proposed in 1976 and recommended in 1977. The drug was given brand names in Spain (Centren (Esteve) and Depraser (Lepori)) and Italy (Staff (Sigma Tau)) and was also given the brand names Axiomin and Etonin, but it is not entirely clear if it was actually marketed; the Pharmaceutical Manufacturing Encyclopedia provides no dates for commercial introduction. According to Micromedex's Index Nominum: International Drug Directory, etoperidone was indeed previously marketed in Spain and Italy.
Sources: en.wikipedia.org
== Pathophysiology == The primary characteristic of MASLD is the accumulation of lipids in the liver, largely in the form of triglycerides. However, the mechanisms by which triglycerides accumulate and the reasons that accumulation can lead to liver dysfunction are complex and incompletely understood. MASLD can include steatosis along with varied signs of liver injury: either lobular or portal inflammation (a form of liver injury) or ballooning degeneration. Similarly, MASH can include histological features such as portal inflammation, polymorphonuclear cell infiltrates, Mallory bodies, apoptotic bodies, clear vacuolated nuclei, microvesicular steatosis, megamitochondria, and perisinusoidal fibrosis. Hepatocyte death via apoptosis or necroptosis is increased in MASH compared with simple steatosis, and inflammation is a hallmark of MASH. The degree of inflammation can be correlated to the number of inflammatory foci. Various definitions exist for an inflammatory focus, but one defines it as the presence of more than four mononuclear cells in proximity within the hepatic parenchyma. One debated mechanism proposes that hepatic steatosis progresses to steatosis with inflammation following some further injury, or second hit. Oxidative stress, hormonal imbalances, and mitochondrial abnormalities are potential causes of this "second hit" phenomenon. A further nutrigenomics model named multiple hit extends the second hit model, suggesting that multiple disease biomarkers and factors such as genes and nutrition influence MASLD and MASH progression.
Many catabolic biochemical processes, such as glycolysis, the citric acid cycle, and beta oxidation, produce the reduced coenzyme NADH. This coenzyme contains electrons that have a high transfer potential; in other words, they will release a large amount of energy upon oxidation. However, the cell does not release this energy all at once, as this would be an uncontrollable reaction. Instead, the electrons are removed from NADH and passed to oxygen through a series of enzymes that each release a small amount of the energy. This set of enzymes, consisting of complexes I through IV, is called the electron transport chain and is found in the inner membrane of the mitochondrion. In eukaryotes, the enzymes in this electron transport system use the energy released from O2 by NADH to pump protons across the inner membrane of the mitochondrion. This causes protons to build up in the intermembrane space, and generates an electrochemical gradient across the membrane. The energy stored in this potential is then used by ATP synthase to produce ATP. Oxidative phosphorylation in the eukaryotic mitochondrion is the best-understood example of this process. The mitochondrion is present in almost all eukaryotes, with the exception of anaerobic protozoa such as Trichomonas vaginalis that instead reduce protons to hydrogen in a remnant mitochondrion called a hydrogenosome.
The new government naively assumed that the insurgents were fighting for Spanish liberalism and that the Spanish Constitution could still be the basis of reconciliation between the two sides. The government implemented the Constitution and held elections in the overseas provinces, just as in Spain. It also ordered military commanders to begin armistice negotiations with the insurgents with the promise that they could participate in the restored representative government.
Sources: en.wikipedia.org
Chick-fil-A has donated over $5 million, via the WinShape Foundation, to groups that oppose same-sex marriage. In response, students at several colleges and universities worked to ban or remove the company's restaurants from their campuses. In June and July 2012, Chick-fil-A's chief operating officer Dan T. Cathy made several public statements about same-sex marriage, saying that those who "have the audacity to define what marriage is about" were "inviting God's judgment on our nation". Several prominent politicians expressed disapproval. Boston Mayor Thomas Menino and Chicago Alderman Proco "Joe" Moreno said they hoped to block franchise expansion into their areas. The proposed local bans drew criticism from liberal pundits, legal experts, and the American Civil Liberties Union. The Jim Henson Company, which had a Pajanimals kids' meal toy licensing arrangement with Chick-fil-A, said it would cease its business relationship, and donate the payment to the Gay & Lesbian Alliance Against Defamation. Chick-fil-A stopped distributing the toys, claiming that unrelated safety concerns had arisen before the controversy. Chick-fil-A released a statement on July 31, 2012, saying, "We are a restaurant company focused on food, service, and hospitality; our intent is to leave the policy debate over same-sex marriage to the government and political arena." In response to the controversy, former Arkansas Governor Mike Huckabee initiated a Chick-fil-A Appreciation Day movement to counter a boycott of Chick-fil-A launched by same-sex marriage activists.
==== Slovak ==== First Catholic Slovak Ladies Association - Founded January 1, 1892, at St. Ladislaus Church in Cleveland as the First Catholic Slovak Ladies Union. Adopted the current name in the late 1960s. Absorbed some smaller fraternals over the years, including the Cleveland Slovak Union in 1945, the Slovak Catholic Cadets Union, the Catholic Slovak Benefit Organization of Cleveland, and the Catholic Slovak Brotherhood from Braddock, Pennsylvania. In 1969 it absorbed the Catholic Slovak Union, which had 1,500 members. Had 102,000 members in 1965, 95,000 in 1979 and 87,000 in 1994 Headquarters in Beachwood, Ohio. Locals called "Branches", present in 12 states and two Canadian provinces. National convention meets quadrennially. Gives aid to convents, monasteries, a theological seminary in Rome, and a "priest scholarship" underwritten by the Cleveland diocese. Awards $10,000 in nursing and college scholarships annually; maintains home for the aged in Beachwood. Organizes biannual youth conferences for people 16-20 which emphasizes the fraternal benefit system. Those who have been with the group for 25 years receive a pin, and 50 years a cash reward. First Catholic Slovak Union of the United States of America and Canada - Slovak name Prva Katolicka Slovenska Jednota Originally organized as the St. Joseph Society for Slovak Catholics in Cleveland, May 5, 1889. On April 9, 1890, they voted to form a union of all Slovak Catholic societies in the US. A union convention took place in Cleveland on September 4, 1890, and united seven Slovak Catholic societies.
The normal concentration of fibrinogen in blood plasma is 150–400 mg/dl, with levels appreciably below or above this range associated with pathological bleeding and/or thrombosis. Fibrinogen has a circulating half-life of ~4 days.
NAD(P)+ + a hydroquinone The 4 substrates of this enzyme are NADH, NADPH, H+, and quinone, whereas its 3 products are NAD+, NADP+, and hydroquinone. This enzyme belongs to the family of oxidoreductases, specifically those acting on NADH or NADPH with a quinone or similar compound as acceptor. The systematic name of this enzyme class is NAD(P)H:quinone oxidoreductase. Other names in common use include menadione reductase, phylloquinone reductase, quinone reductase, dehydrogenase, reduced nicotinamide adenine dinucleotide (phosphate,, quinone), DT-diaphorase, flavoprotein NAD(P)H-quinone reductase, menadione oxidoreductase, NAD(P)H dehydrogenase, NAD(P)H menadione reductase, NAD(P)H-quinone dehydrogenase, NAD(P)H-quinone oxidoreductase, NAD(P)H: (quinone-acceptor)oxidoreductase, NAD(P)H: menadione oxidoreductase, NADH-menadione reductase, naphthoquinone reductase, p-benzoquinone reductase, reduced NAD(P)H dehydrogenase, viologen accepting pyridine nucleotide oxidoreductase, vitamin K reductase, diaphorase, reduced nicotinamide-adenine dinucleotide (phosphate) dehydrogenase, vitamin-K reductase, NAD(P)H2 dehydrogenase (quinone), NQO1, QR1, and NAD(P)H:(quinone-acceptor) oxidoreductase. This enzyme participates in biosynthesis of steroids. It employs one cofactor, FAD. At least one compound, Dicumarol is known to inhibit this enzyme.
Sources: en.wikipedia.org
Rodent studies reported increased endurance and fat oxidation after GW501516 exposure. Long-term studies also found higher rates of some tumors, which led to halted development.
Small short-term human trials examined metabolic markers such as lipids and glucose. The trials did not continue after rodent cancer findings, so long-term human safety is unknown.
Controlled human trials have not established a performance benefit. Anecdotal reports exist, but they are not reliable evidence.
Cardarine is a common name for GW501516, a synthetic PPARδ agonist developed for research. It has not been approved as a medication in any country. It is classified as an unapproved drug and a prohibited substance in sport.