Everything below concerns Chromatographic purity. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2025-10-08. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
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.
| 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 |
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.
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.
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.
== Risk factors == The most prominent risk factors for myocardial infarction are older age, actively smoking, high blood pressure, diabetes mellitus, and total cholesterol and high-density lipoprotein levels. Many risk factors of myocardial infarction are shared with coronary artery disease, the primary cause of myocardial infarction, with other risk factors including male sex, low levels of physical activity, a past family history, obesity, and alcohol use. Risk factors for myocardial disease are often included in risk factor stratification scores, such as the Framingham Risk Score. At any given age, men are more at risk than women for the development of cardiovascular disease. High levels of blood cholesterol is a known risk factor, particularly high low-density lipoprotein, low high-density lipoprotein, and high triglycerides. Many risk factors for myocardial infarction are potentially modifiable, with the most important being tobacco smoking (including secondhand smoke). Smoking appears to be the cause of about 36% and obesity the cause of 20% of coronary artery disease. Lack of physical activity has been linked to 7–12% of cases. Less common causes include stress-related causes such as job stress, which accounts for about 3% of cases, and chronic high stress levels.
The two substrates of this enzyme are shikimate and oxidised nicotinamide adenine dinucleotide phosphate (NADP+). Its products are 3-dehydroshikimate, reduced NADPH, and a proton. This enzyme participates in phenylalanine, tyrosine and tryptophan biosynthesis.
== Pathophysiology == Scleroderma is characterised by increased synthesis of collagen (leading to the sclerosis), damage to small blood vessels, activation of T lymphocytes, and production of altered connective tissue. Its proposed pathogenesis is the following:
Excess post-exercise oxygen consumption (EPOC, informally called afterburn) is a measurably increased rate of oxygen intake following strenuous activity. In historical contexts the term "oxygen debt" was popularized to explain or perhaps attempt to quantify anaerobic energy expenditure, particularly as regards lactic acid/lactate metabolism; in fact, the term "oxygen debt" is still widely used to this day. However, direct and indirect calorimeter experiments have definitively disproven any association of lactate metabolism as causal to an elevated oxygen uptake. In recovery, oxygen (EPOC) is used in the processes that restore the body to a resting state and adapt it to the exercise just performed. These include: hormone balancing, replenishment of fuel stores, cellular repair, innervation, and anabolism. Post-exercise oxygen consumption replenishes the phosphagen system. New ATP is synthesized and some of this ATP donates phosphate groups to creatine until ATP and creatine levels are back to resting state levels again. Another use of EPOC is to fuel the body’s increased metabolism from the increase in body temperature which occurs during exercise. EPOC is accompanied by an elevated consumption of fuel. In response to exercise, fat stores are broken down and free fatty acids (FFA) are released into the blood stream. In recovery, the direct oxidation of free fatty acids as fuel and the energy consuming re-conversion of FFAs back into fat stores both take place.
Sources: en.wikipedia.org
== Etymology and pronunciation == The word synovium is related to the word synovia in its sense meaning "synovial fluid". The latter was coined by Paracelsus. More information is given at Synovial fluid § Etymology and pronunciation.
Studies show that the EPOC effect exists after both aerobic exercise and anaerobic exercise. In a 1992 Purdue study, results showed that high intensity, anaerobic type exercise resulted in a significantly greater magnitude of EPOC than aerobic exercise of equal work output. For exercise regimens of comparable duration and intensity, aerobic exercise burns more calories during the exercise itself, but the difference is partly offset by the higher increase in caloric expenditure that occurs during the EPOC phase after anaerobic exercise. Anaerobic exercise in the form of high-intensity interval training was also found in one study to result in greater loss of subcutaneous fat, even though the subjects expended fewer than half as many calories during exercise. Whether this result was caused by the EPOC effect has not been established, and the caloric content of the participants' diet was not controlled during this particular study period. Most researchers use a measure of EPOC as a natural part of the quantification or measurement of exercise and recovery energy expenditure; to others this is not deemed necessary. After a single bout or set of weight lifting, Scott et al. found considerable contributions of EPOC to total energy expenditure. In their 2004 survey of the relevant literature, Meirelles and Gomes found: "In summary, EPOC resulting from a single resistance exercise session (i.e., many lifts) does not represent a great impact on energy balance; however, its cumulative effect may be relevant".
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.
Sources: en.wikipedia.org
June 29 – July 6: 2019 Men's U20 European Lacrosse Championship in Prague (debut event) England defeated Germany, 9–8, to win the inaugural Men's U20 European Lacrosse Championship title. The Czech Republic took third place. July 16 – 25: 2019 Women's European Lacrosse Championship in Netanya England defeated Israel, 10–7, to win their third consecutive and seventh overall Women's European Lacrosse Championship title. Wales took third place. August 1 – 10: 2019 FIL Women's Under-19 World Lacrosse Championships in Peterborough The United States defeated Canada, 13–3, to win their fifth Women's Under-19 World Lacrosse Championships title. Australia took third place. September 19 – 28: 2019 World Indoor Lacrosse Championship in Langley Canada defeated Haudenosaunee, 19–12, to win their fifth consecutive World Indoor Lacrosse Championship title. United States took third place.
Sunflower trypsin inhibitor (SFTI) is a small, circular peptide produced in sunflower seeds, and is a potent inhibitor of trypsin. It is the smallest known member of the Bowman-Birk family of serine protease inhibitors. One example of Sunflower trypsin inhibitor is Sunflower trypsin inhibitor-1 (SFTI-1). Sunflower trypsin inhibitor-1 is a potent Bowman-Birk inhibitor. Sunflower trypsin inhibitor-1 is the simplest cysteine-rich peptide scaffold because it is a bicyclic 14 amino acid peptide and only has one disulfide bond. The disulfide bond divides the peptide into a primary trypsin inhibitory loop (Thr4-Ile10) and a cyclisation loop (Phe12-Arg2). The cyclisation loop can be replaced by a foregin bioactive loop without disrupting the scaffold's fold. It is extracted from a seed of a sunflower called Helianthus annuus. The synthesis of SFTI is not known however, it can evolutionarily linked to a gene-coded product from classic Bowman-Birk inhibitors. STFI is used in radiopharmaceutical, antimicrobial, and pro-angiogenic peptides.
Calcium isotope fractionation during mineral formation has led to several applications of calcium isotopes. In particular, the 1997 observation by Skulan and DePaolo that calcium minerals are isotopically lighter than the solutions from which the minerals precipitate is the basis of analogous applications in medicine and in paleoceanography. In animals with skeletons mineralised with calcium, the calcium isotopic composition of soft tissues reflects the relative rate of formation and dissolution of skeletal mineral. In humans, changes in the calcium isotopic composition of urine have been shown to be related to changes in bone mineral balance. When the rate of bone formation exceeds the rate of bone resorption, the 44Ca/40Ca ratio in soft tissue rises and vice versa. Because of this relationship, calcium isotopic measurements of urine or blood may be useful in the early detection of metabolic bone diseases like osteoporosis. A similar system exists in seawater, where 44Ca/40Ca tends to rise when the rate of removal of Ca2+ by mineral precipitation exceeds the input of new calcium into the ocean. In 1997, Skulan and DePaolo presented the first evidence of change in seawater 44Ca/40Ca over geologic time, along with a theoretical explanation of these changes. More recent papers have confirmed this observation, demonstrating that seawater Ca2+ concentration is not constant, and that the ocean is never in a "steady state" with respect to calcium input and output. This has important climatological implications, as the marine calcium cycle is closely tied to the carbon cycle.
== Interactions == Combining ertugliflozin with insulin or insulin secretagogues (such as sulfonylureas) may result in an increased risk for low blood sugar. Combination with diuretics may result in a higher risk for dehydration and low blood pressure. No clinically relevant pharmacokinetic interactions have been found in studies.
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.
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.