The short version of Metabolite fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2025-07-22 and is reviewed periodically as new material appears.
Laboratory studies have examined GW501516 in cell cultures and rodents for conditions such as dyslipidemia, insulin resistance, and obesity. Some trials in humans were initiated, but development was discontinued after preclinical findings raised concerns about cancer in certain models. Those findings do not prove that the compound causes cancer in people, but they contributed to regulatory caution. Later reviews often describe the evidence as preliminary and insufficient for assessing long-term safety.
In the fitness and bodybuilding literature, cardarine is frequently discussed as an endurance agent or fat-loss compound, although such claims are not supported by robust clinical evidence. Online descriptions often mix animal data, user anecdotes, and marketing language. Researchers who study PPARδ agonists distinguish between receptor activation in controlled experiments and unsupervised use of unverified products. The latter introduces unknown purity, dose, and interactions, making reported experiences difficult to interpret scientifically.
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.
| Property | Value | Notes |
|---|---|---|
| Solubility | Soluble in dimethyl sulfoxide and some organic solvents; practically insoluble in water | Solvent choice affects laboratory handling |
| Typical storage | -20 °C, desiccated, protected from light | Common condition for research samples |
| Analytical method | Liquid chromatography–tandem mass spectrometry (LC-MS/MS) | Used for identification and quantification in biological or product samples |
| Common synonyms | GW501516, GW-501516, GSK-516, Endurobol | Names found in research and anti-doping literature |
| Regulatory status | Unapproved therapeutic; prohibited in competitive sport | Status can vary by country and context |
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.
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.
Legal status varies by country. In some places, cardarine is controlled under medicines or psychoactive substances laws; in others, it may be sold with minimal oversight as a research chemical. Customs agencies have intercepted shipments, and several national health agencies have issued warnings about products marketed for bodybuilding or performance enhancement. The lack of a standardized pharmaceutical supply means identity, purity, and contamination levels can differ widely between samples. These factors make cardarine a regulatory and public health concern rather than a conventional prescription drug.
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.
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.
Cardarine is explicitly prohibited by the World Anti-Doping Agency under the class of PPARδ agonists. Its presence in urine or blood samples can be detected using mass spectrometry-based methods, often liquid chromatography-tandem mass spectrometry. Athletes who test positive may face sanctions, including bans from competition. The compound is also regulated as a prescription-only or unapproved drug in many countries. Enforcement varies by jurisdiction, and some regions treat it as a controlled substance. Online sales may occur despite these restrictions, creating quality and legal risks.
Edgar Degas's 1876 painting The Absinthe Drinker or Glass of Absinthe (L'Absinthe) can be seen at the Musée d'Orsay epitomising the popular view of absinthe addicts as sodden and benumbed, and Émile Zola described its effects in his novel L'Assommoir. In 1905, Swiss farmer Jean Lanfray murdered his wife and two children and then attempted to kill himself after drinking absinthe. Lanfray had drunk a lot of wine and brandy before the killings, but that was overlooked or ignored, and blame for the murders was placed solely on his consumption of two glasses of absinthe. The Lanfray murders were the tipping point in this hotly debated topic, and a subsequent petition collected more than 82,000 signatures to ban it in Switzerland. A referendum was held on 5 July 1908. It was approved by voters, and the prohibition of absinthe was written into the Swiss constitution. In 1906, Belgium and Brazil banned the sale and distribution of absinthe although these were not the first countries to take such action. It had been banned as early as 1898 in the colony of the Congo Free State. The Netherlands banned it in 1909, Switzerland in 1910, the United States in 1912, and France in 1914. The prohibition of absinthe in France eventually led to the popularity of pastis, and to a lesser extent, ouzo, and other anise-flavoured spirits that do not contain wormwood.
Ring strain and electron deficiency in the oxanorbornadiene increase reactivity towards the cycloaddition rate-limiting step. The retro-Diels Alder reaction occurs quickly afterwards to form the stable 1,2,3 triazole. Problems include poor tolerance for substituents which may change electronics of the oxanorbornadiene and low rates (second order rate constants on the order of 10−4).
=== On bone formation === Due to myostatin's ability to inhibit muscle growth, it can indirectly inhibit bone formation by decreasing the load on the bone. It has a direct signalling effect on bone formation as well as degradation. Knockdown of myostatin has been shown to reduce formation of osteoclasts (multinucleated cells responsible for the breakdown of bone tissue) in mice modeling rheumatoid arthritis. Rheumatoid arthritis is an autoimmune disorder that, among other effects, leads to the degradation of the bone tissue in affected joints. Myostatin has not, however, been shown to be solely sufficient for the formation of mature osteoclasts from macrophages, only an enhancer. Myostatin expression is increased around the site of a fracture. Suppression of myostatin at the fracture site leads to increased callus and overall bone size, further supporting the inhibitory effect of myostatin on bone formation. One study by Berno Dankbar et al., 2015 found that myostatin deficiency leads to a notable reduction in inflammation around a fracture site. Myostatin affects osteoclastogenesis by binding to receptors on osteoclastic macrophages and causing a signalling cascade. The downstream signalling cascade enhances the expression of RANKL-dependent integrin αvβ3, DC-STAMP, calcitonin receptors, and NFATc1 (which is part of the initial intracellular complex that starts the signaling cascade, along with R-Smad2 and ALK4 or ALK5).
== Epidemiology == Up to 90% of UCTD cases are females between 32 and 44 years old. In the United States, up to 78% of patients were female, against 93 to 95% in Italy and 94% in Hungary. Higher female prevalence is common in autoimmune diseases. In the United States, up to 72% of patients diagnosed with UCTD had white skin. The prevalence of UCTD has been estimated at 2 people per 100,000 per year. Annual incidence has been estimated as varying from 41 to 149 per 100,000 adults. It has also been suggested that UCTD is a relatively common condition seen in rheumatology practice, making up 10–20% of referrals to tertiary care clinics. Classical epidemiological data for UCTD are not available due to the limited literature exploring the disease. Also, differences in patient selection criteria in existing studies make comparisons between them difficult.
== Persons influential in relation to diabetes mellitus == Paul Langerhans Joseph von Mering Oskar Minkowski Edward Albert Sharpey-Schafer Frederick Banting Charles Best James Collip Harold Percival Himsworth Thorburn Brailsford Robertson
Sources: en.wikipedia.org
The four substrates of this enzyme are anthranilic acid, reduced nicotinamide adenine dinucleotide (NADH), oxygen, and a proton. Its products are catechol, carbon dioxide, oxidised NAD+, and ammonia. The enzyme can also use nicotinamide adenine dinucleotide phosphate as a cofactor. This enzyme is an oxidoreductase which uses molecular oxygen as oxidant and incorporates its atoms into the product. The systematic name of this enzyme class is anthranilate,NAD(P)H:oxygen oxidoreductase (1,2-hydroxylating, deaminating, decarboxylating). Other names in common use include anthranilate hydroxylase, anthranilic hydroxylase, and anthranilic acid hydroxylase. It participates in three metabolic pathways: benzoate degradation via hydroxylation, carbazole degradation, and nitrogen metabolism. It requires ferrous iron.
=== Traditional medicine === Xanthoria parietina has a long history of use in traditional medicine across several cultures. In Andalucia, Spain, this lichen was known as flor de piedra ('stone flower') or rompepiedra ('stone breaker'). Spanish traditional healers employed it for several purposes: treating menstrual complaints when prepared as a decoction in wine, addressing kidney disorders and toothaches when made into water-based decoctions, and serving as a general analgesic. They also incorporated it into cough syrups along with various plant ingredients. In European traditional medicine during the early modern era, X. parietina was boiled with milk to treat jaundice, often alongside Polycauliona candelaria. This application exemplifies the Doctrine of signatures – a belief system that plants resembling parts of the body could treat ailments of those parts – as the yellow-orange color of the lichen was thought to indicate its efficacy against the yellowing of the skin in jaundice. In Traditional Chinese medicine, it was known as Chinese: shí huáng yī ('stone yellow clothes') and valued for its antibacterial properties. The widespread medicinal use of lichens, including X. parietina, had been mostly abandoned by 1800, and these applications represent historical folk remedies rather than evidence-based treatments.
==== Gloucester Marine Genomics Institute ==== Founded in 2013, the nonprofit Gloucester Marine Genomics Institute to study marine genomes for potential therapeutic compounds and to advance fisheries science. He is also the founder and director of the Gloucester Biotechnology Academy, which is providing technical training in the life science industry to high school graduates in Gloucester, MA, USA.
"Whereas, for all time since the creation of mankind, no king whosoever had destroyed Armanum and Ebla, the god Nergal, by means of (his) weapons opened the way for Naram-Sin, the mighty, and gave him Armanum and Ebla. Further, he gave to him the Amanus, the Cedar Mountain, and the Upper Sea. By means of the weapons of the god Dagan, who magnifies his kingship, Naram-Sin, the mighty, conquered Armanum and Ebla."
There are no stable nuclides having an equal number of protons and neutrons in their nuclei with atomic number greater than 20 (i.e. calcium) as can be readily observed from the chart. Nuclei of greater atomic number require an excess of neutrons for stability. The only stable nuclides having an odd number of protons and an odd number of neutrons are hydrogen-2 (deuterium), lithium-6, boron-10, nitrogen-14 and (observationally) tantalum-180m. This is because the mass–energy of such atoms is usually higher than that of their neighbors on the same isobaric chain, so most of them are unstable to beta decay. There are no stable nuclides with mass number 5 or 8. There are stable nuclides with all other mass numbers up to 208 with the exceptions of 147 and 151, which are represented by the very long-lived samarium-147 and europium-151. (Bismuth-209 was found to be radioactive in 2003, but with a half-life of 2.01×1019 years.) With the exception of the pair tellurium-123 and antimony-123, odd mass numbers are never represented by more than one stable nuclide. This is because the mass–energy is a convex function of atomic number, so all nuclides on an odd isobaric chain except one have a lower-energy neighbor to which they can decay by beta decay. See Mattauch isobar rule.
Sources: en.wikipedia.org
It binds and activates PPARδ, a nuclear receptor that influences gene expression related to fatty acid metabolism and energy balance. This mechanism has been studied mainly in animals and cell models, not established as a safe human therapy.
No. It is not an anabolic-androgenic steroid; it is a synthetic PPARδ agonist. Because it is banned in sport, it is sometimes grouped with doping agents even though its chemical class differs from steroids.
Human data are limited and development was discontinued, so major effects and long-term risks are not well characterized. Some early studies examined metabolic markers, but they do not provide a basis for unsupervised use.
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.