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 2025-11-24 and is reviewed periodically as new material appears.
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.
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.
Laboratory detection of cardarine typically involves sample preparation followed by chromatographic separation and mass spectrometric identification. Urine is the most common matrix for anti-doping tests, though blood and hair have also been explored. Methods can target the parent compound or its metabolites, depending on the expected window of detection. Reference standards are required for accurate quantification. Matrix effects and dilution can influence results, so laboratories use internal standards and validation protocols. The exact detection window varies with dose, route, and individual metabolism.
A common misconception is that cardarine has been proven safe for human use. In reality, human clinical data are limited, and long-term animal studies have raised concerns about cancer. Another misconception is that it is a supplement or vitamin-like compound. It is a synthetic research chemical with no approved medical indication. Scientific discussion often focuses on its mechanism and detection rather than therapeutic use. Regulatory and anti-doping literature treats it primarily as a prohibited substance.
| Property | Value | Notes |
|---|---|---|
| Common synonyms | GW501516, GW-501516, GW 501516, endurobol | Names vary in research and anti-doping documents. |
| Chemical class | Synthetic PPARδ agonist | Small-molecule nuclear receptor ligand. |
| CAS Registry Number | 317318-70-0 | Identifier commonly associated with GW501516. |
| Appearance | White to off-white powder | Typical for purified research material. |
| Solubility | Low in water; soluble in DMSO and ethanol | Organic solvents are common for laboratory stock solutions. |
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.
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.
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.
GW501516 acts on PPARδ, a nuclear receptor that helps regulate fatty acid oxidation and energy homeostasis. In animal studies, activation of this receptor was associated with increased endurance and changes in lipid metabolism. Human trials examined effects on blood lipids and other metabolic markers, but the compound did not advance to approval. Rodent studies later reported tumors in multiple tissues at doses used in those experiments. Whether those findings translate to human risk remains uncertain, and the clinical relevance of the animal data is still debated.
Regulatory bodies treat GW501516 as a prohibited substance in competitive sport. The World Anti-Doping Agency added it to the prohibited list, and it falls under classes covering metabolic modulators and hormone-related agents. It is not approved by drug regulators for human use, and it is not a lawful dietary supplement. Products sold under the cardarine name may contain unlisted ingredients or different compounds. Because no approved product exists, quality and identity are not guaranteed by pharmaceutical manufacturing standards.
Cardarine is a common name for the investigational chemical GW501516, also written GW-1516. It was developed as a peroxisome proliferator-activated receptor delta agonist for metabolic conditions such as dyslipidemia. Early research focused on lipid handling and energy use in skeletal muscle and other tissues. The compound was never approved as a medicine. In public discussion, it is often grouped with performance-enhancing substances, although its receptor target differs from that of anabolic steroids or selective androgen receptor modulators. Regulatory and health authorities have issued warnings about its use.
uridine monophosphate (UMP)), usually to tyrosine propionylation pyroglutamate formation S-glutathionylation S-nitrosylation S-sulfenylation, reversible covalent addition of one oxygen atom to the thiol group of a cysteine residue to form a sulfenic acid S-sulfinylation, normally irreversible covalent addition of two oxygen atoms to the thiol group of a cysteine residue to form a sulfinic acid S-sulfonylation, normally irreversible covalent addition of three oxygen atoms to the thiol group of a cysteine residue, resulting in the formation of a cysteic acid residue sulfation, the addition of a sulfate group to a tyrosine.
Noodles (Chinese: 面/麵 miàn) were invented in China over 4,000 years ago and have since spread across the world. Chinese noodles come dry or fresh in a variety of sizes, shapes and textures and are often served in soups or fried as toppings. Some varieties, such as Shou Mian (寿面, literally noodles of longevity), is an avatar of long life and good health according to Chinese traditions. Noodles can be served hot or cold with different toppings, with broth, and occasionally dry (as is the case with mi-fen). Noodles are commonly made with rice flour or wheat flour, but other flours such as soybean are also used in minor groups. Some noodles names describe their methods of creation, such as the hand-pulled noodle.
== Education == Sereti received a M.D. from the University of Athens in 1991. She did research for one year in Gregory Spear's laboratory at Rush University Medical Center. Sereti completed an internship, residency, and chief residency in medicine at Northwestern University.
Mining of an active deep sea hydrothermal vent ecosystem would depend on the recolonization of chemosynthetic bacteria, and therefore the continuation of the hydrothermal vent fluid as it is the main hydrothermal energy source. It is very difficult to get an idea of the effects of mining on the hydrothermal vent fluid because there have been no large scale studies done. However, there have been studies on the recolonization of these vent ecosystems after volcanic destruction. From these we can develop insight on the potential effects of mining destruction, and have learned it took 3–5 years for bacteria to recolonize the area, and around 10 years for megafauna to return. It was also found that there was a shift in the composition of species in the ecosystem compared to before the destruction, and the presence of immigrant species. This shift in biodiversity poses issues to certain critically endangered species that thrive in harsh deep sea environment, like mollusks. Though further research into the effects of sustained seafloor SMS mining on species recolonization is needed. Shallow hydrothermal vents have also been proposed as a potential model for climate change in extreme environments, specifically by tracking changes to highly specialized organisms local to the vent. Major impacts of climate change such as ocean acidification, increasing temperature and heavy metal deposition, on local hydrothermal vent ecosystems are areas of interest for these models. Deep sea mining's impact on efficacy of these models is an area of future interest.
Sources: en.wikipedia.org
==== Phosphorylated tau ==== Alzheimer's disease is also considered a tauopathy due to the abnormal aggregation of the tau protein within cells. Every neuron has a cytoskeleton, an internal support structure partly made up of organelles called microtubules. These microtubules act like tracks, guiding nutrients and molecules from the body of the cell to the ends of the axon and back. The tau protein stabilises the microtubules when phosphorylated, and it is therefore called a microtubule-associated protein. In Alzheimer's disease, tau undergoes chemical changes, becoming hyperphosphorylated; it then begins to pair with other threads, creating neurofibrillary tangles and disintegrating the neuron's transport system. Pathogenic tau can also cause neuronal death through transposable element dysregulation. Necroptosis has also been reported as a mechanism of cell death in brain cells affected with tau tangles.
Elevated creatine kinase (CK) levels in the blood (at most ~10 times normal) are typical in sIBM but affected individuals can also present with normal CK levels. Electromyography (EMG) studies display variable abnormalities such as increased insertional activity, increased spontaneous activity (fibrillation potentials and sharp waves), and large/broad or short/narrow motor unit potentials. On EMG, recruitment patterns can be reduced or increased. Findings can vary even within the same muscle of an affected individual. Muscle biopsy may display several common findings including inflammatory cells invading muscle cells, vacuolar degeneration, and inclusion bodies of aggregations of multiple proteins. sIBM is a challenge to the pathologist and even with a biopsy, diagnosis can be ambiguous. A diagnosis of inclusion body myositis was historically dependent on muscle biopsy results. Antibodies to cytoplasmic 5'-nucleotidase (cN1A; NT5C1A) have been strongly associated with the condition. However, other inflammatory conditions, such as lupus, can have a positive anti-NT5C1A. As of 2019, it remains to be established whether a positive anti-NT5C1A antibody test can make muscle biopsy unneeded.
=== Triggers === Several environmental factors have been postulated to modify illness susceptibility or induce disease; the most persuasive of these is the role of female sex hormones, as evidenced by the disease's significant female-to-male ratio and other data. Furthermore, investigations indicate that Epstein–Barr virus, retroviruses, or other viruses may play a role in causing disease in some patients. Cytomegalovirus has also been proposed as capable of eliciting anti-RNP antibody responses in the absence of illness. Environmental exposure to vinyl chloride has been linked to the development of an MCTD-like condition.
=== Other tumors === In a few people, acromegaly is caused by tumors of the pancreas, lungs, and adrenal glands. These tumors also lead to an excess of GH, either because they produce GH themselves or, more frequently, because they produce GHRH (growth hormone-releasing hormone), the hormone that stimulates the pituitary to make GH. When these nonpituitary tumors are surgically removed, GH levels fall and the symptoms of acromegaly improve.
The National Liberals, as they were called by then, were gradually absorbed into the Conservative Party, finally merging in 1968. The official Liberals found themselves a tiny minority within a government committed to protectionism. Slowly they found this issue to be one they could not support. In early 1932 it was agreed to suspend the principle of collective responsibility to allow the Liberals to oppose the introduction of tariffs. Later in 1932 the Liberals resigned their ministerial posts over the introduction of the Ottawa Agreement on Imperial Preference. However, they remained sitting on the government benches supporting it in Parliament, though in the country local Liberal activists bitterly opposed the government. Finally in late 1933 the Liberals crossed the floor of the House of Commons and went into complete opposition. By this point their number of MPs was severely depleted. In the 1935 general election, just 17 Liberal MPs were elected, along with Lloyd George and three followers as independent Liberals. Immediately after the election the two groups reunited, though Lloyd George declined to play much of a formal role in his old party. Over the next ten years there would be further defections as MPs deserted to either the Liberal Nationals or Labour. Yet there were a few recruits, such as Clement Davies, who had deserted to the National Liberals in 1931 but now returned to the party during World War II and who would lead it after the war.
Sources: en.wikipedia.org
=== International === Cooperation with international NGOs including Pesticide Action Network UK and Greenpeace started soon after the tragedy. One of the earliest reports is the Trade Union report from ILO 1985. In 1992, a session of the Permanent Peoples' Tribunal on Industrial Hazards and Human Rights took place in Bhopal, and in 1996, the "Charter on Industrial Hazards and Human Rights" was adopted. In 1994, the International Medical Commission on Bhopal (IMCB) met in Bhopal. Their work contributed to long-term health effects being officially recognised.
In eukaryotes, ribosomes are present in mitochondria (sometimes called mitoribosomes) and in plastids such as chloroplasts (also called plastoribosomes). They also consist of large and small subunits bound together with proteins into one 70S particle. These ribosomes are similar to those of bacteria and these organelles are thought to have originated as symbiotic bacteria. Of the two, chloroplastic ribosomes are closer to bacterial ones than mitochondrial ones are. Many pieces of ribosomal RNA in the mitochondria are shortened, and in the case of 5S rRNA, replaced by other structures in animals and fungi. In particular, Leishmania tarentolae has a minimalized set of mitochondrial rRNA. In contrast, plant mitoribosomes have both extended rRNA and additional proteins as compared to bacteria, in particular, many pentatricopetide repeat proteins. The cryptomonad and chlorarachniophyte algae may contain a nucleomorph that resembles a vestigial eukaryotic nucleus. Eukaryotic 80S ribosomes may be present in the compartment containing the nucleomorph.
=== 19th century === Mary Watson (1856–1933), one of the first two female chemistry students at the University of Oxford Margaret Seward (1864–1929), one of the first two female chemistry students at the University of Oxford; signed the 1904 petition to the Chemical Society Vera Bogdanovskaia (1868–1897), one of the first female Russian chemists Martina Casiano y Mayor (1881–1958), first female member of the Spanish Society of Physics and Chemistry Gerty Cori (1896–1957) Jewish Czech-American biochemist who was the first American to win a Nobel Prize in science Margot Dorenfeldt (1895–1986) First woman to graduate from Norwegian Institute of Technology (1919) Ida Freund (1863–1914), first woman to be a university chemistry lecturer in the United Kingdom Ellen Gleditsch (1879–1968), Norwegian radiochemist; Norway's second female professor Louise Hammarström (1849–1917), Swedish mineral chemist, first formally educated female Swedish chemist Edith Humphrey (1875–1978), Inorganic chemist, probably the first British woman to gain a doctorate in chemistry Julia Lermontova (1846–1919), Russian chemist, first Russian female doctorate in chemistry Laura Linton (1853–1915), American chemist, teacher, and physician Rachel Lloyd (1839–1900), First American female to earn a doctorate in chemistry, first regularly admitted female member of the American Chemical Society, studied sugar beets Muriel Wheldale Onslow (1880–1932), British biochemist Marie Pasteur (1826–1910), French chemist and bacteriologist Mary Engle Pennington (1872–1952), American chemist Agnes Pockels (1862–1935), German chemist Anna Sundström (1785–1871), Swedish chemist Clara Immerwahr (1870–1915), First woman to get her doctorate in chemistry in Germany Ellen Swallow Richards (1842–1911), American industrial and environmental chemist Anna Volkova (1800–1876), Russian chemist Nadezhda Olimpievna Ziber-Shumova (died 1914), Russian chemist Fanny Rysan Mulford Hitchcock (1851–1936), one of thirteen (American) women to graduate with a degree in chemistry in the 1800s, and the first to graduate with a doctorate in philosophy of chemistry. Her areas of focus were in entomology, fish osteology, and plant pathology.
=== Immunity-related === TCTP caused histamine release from the human basophils of a subpopulation of donors, and this release was dependent on IgE. The expression of TCTP is regulated at two distinct levels, depletion of the ER calcium causes an increase in TCTP mRNA abundance, increased cytosolic calcium concentrations regulate gene expression at the post-transcriptional level. Downregulation of the protein levels by siRNA in HTR-8/SVneo (Homo sapiens placenta cells) was associated with a reduced cellular calcium-uptake activity and buffering capacity.
Function-Spacer-Lipid (FSL) Kode constructs (Kode Technology) are amphiphatic, water dispersible biosurface engineering constructs that can be used to engineer the surface of cells, viruses and organisms, or to modify solutions and non-biological surfaces with bioactives. FSL Kode constructs spontaneously and stably incorporate into cell membranes. FSL Kode constructs with all these aforementioned features are also known as Kode Constructs. The process of modifying surfaces with FSL Kode constructs is known as "koding" and the resultant "koded" cells, viruses and liposomes are respectively known as kodecytes, and kodevirions.
Sources: en.wikipedia.org
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.
No. Cardarine is not a steroid hormone; it targets the nuclear receptor PPARδ. Its classification in anti-doping rules differs from anabolic steroids, though it remains prohibited in sport.
Early rodent studies reported tumor formation at multiple sites, which raised safety concerns. Sponsors stopped clinical development, and no approved human product exists.
Yes, WADA prohibits cardarine as a PPARδ agonist. It appears on the prohibited list and can be detected in urine or blood. Athletes using it risk sanctions.