Everything below concerns Anti-doping. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-02-03. 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.
The compound is typically described as a laboratory compound rather than a therapeutic product. Published reports have explored its role in lipid disorders, insulin sensitivity, and exercise metabolism, yet no major drug regulator has approved it for medical use. Commercial samples sold under the cardarine name may vary in purity and identity. Analytical confirmation is therefore necessary when the material is discussed in scientific or regulatory contexts. Its classification as a prohibited substance in sport further shapes how it is studied and reported.
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.
| 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 |
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.
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.
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.
GW501516 acts as an agonist at peroxisome proliferator-activated receptor delta, a nuclear receptor involved in transcription of genes related to lipid handling and energy use. Activation of PPARδ can shift skeletal muscle toward greater fatty acid oxidation in animal models, which is one reason it drew interest for metabolic disease and exercise research. The exact downstream effects depend on tissue, species, dose, and duration. Human data are sparse, so many proposed benefits remain hypotheses rather than established clinical outcomes.
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.
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.
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.
Cardarine is the common name for GW501516, a synthetic compound studied as a peroxisome proliferator-activated receptor delta agonist. Researchers developed it to explore treatments for lipid disorders and metabolic conditions. It is not an approved medicine in any country. Early clinical work examined changes in HDL cholesterol and triglycerides, but development was discontinued after animal studies raised concerns about cancer. The compound remains available as a research chemical and appears in discussions of performance enhancement.
At the molecular level, GW501516 binds and activates PPARδ, a nuclear receptor that regulates transcription. Activation shifts expression of genes involved in fatty acid oxidation, energy expenditure, and lipid transport in skeletal muscle and liver. Animal studies report increased endurance and altered lipid profiles after exposure. Human data are limited to small trials and do not establish long-term safety or efficacy. PPARδ also has roles in cell proliferation, so the relationship between activation and cancer risk remains an open question.
α2-Macroglobulin is known to bind zinc, as well as copper in plasma, even more strongly than albumin, and such it is also known as transcuprein. 10 to 15% of copper in human plasma is chelated by α2-macroglobulin.
== Properties and production == The characteristics of dark meat from poultry (such as its color, low plasticity, and high fat content) are caused by myoglobin, a pigmented chemical compound found in muscle tissue that undergoes frequent use. Because domestic poultry rarely fly, the flight muscles in the breast contain little myoglobin and appear white. Dark meat which is high in myoglobin is less useful in industry, especially fast food, because it is difficult to mold into shapes. Processing dark meat into a slurry makes it more like white meat, easier to prepare. The meat is first finely ground and mixed with water. The mixture is then used in a centrifuge or with an emulsifier to separate the fats and myoglobin from the muscle. The product is then allowed to settle into three layers: meat, excess water, and fat. The remaining liquefied meat is then flash-frozen and packaged.
Additionally, low levels of cortisol cause a dysregulated renin-angiotensin system, as cortisol interacts with the renin-angiotensin system, which regulates blood pressure through vasoconstriction and fluid balance. Low cortisol levels can disrupt this system, leading to altered angiotensin production, reduced aldosterone secretion, and subsequently lower blood pressure. Conversely, high levels of cortisol lead to increased vascular tone, enhanced sodium retention, and increased sympathetic activity. Stress-induced release of high-level glucocorticoids such as cortisol activates the sympathetic nervous system (SNS). The SNS controls heart rate, cardiac output, and vasomotor tone, causing constriction, and thereby increasing peripheral arterial resistance, resulting in an increase in blood pressure. In 11β-hydroxylase deficiency, 11-deoxycortisol can also be converted to androstenedione in a pathway that could explain the increase in androstenedione levels this condition. In 21-hydroxylase deficiency, 11-deoxycortisol levels are low.
Flutamide has been used to prevent the effects of the testosterone flare at the start of GnRH agonist therapy in men with prostate cancer. The combination of flutamide with an estrogen such as ethinylestradiol sulfonate has been used as a form of combined androgen blockade and as an alternative to the combination of flutamide with surgical or medical castration.
== Function == As an isocitrate dehydrogenase, IDH1 catalyzes the reversible oxidative decarboxylation of isocitrate to yield α-ketoglutarate (α-KG) as part of the TCA cycle in glucose metabolism. IDH1 interacts with isocitrate and a divalent metal ion cofactor, typically Mg2+ or Mn2+, which plays a crucial role in stabilizing the negatively charged intermediates formed during the enzymatic reaction. It undergoes oxidation at the hydroxyl group on the C2 carbon, a reaction that removes electrons and produces oxalosuccinate. During this step, NAD(P)+ acts as an electron acceptor, transforming into NAD(P)H by gaining these electrons. Subsequently, oxalosuccinate undergoes decarboxylation, meaning it loses a carbon dioxide molecule, resulting in the formation of α-ketoglutarate. This step also allows for the concomitant reduction of nicotinamide adenine dinucleotide phosphate (NADP+) to reduced nicotinamide adenine dinucleotide phosphate (NADPH). Since NADPH and α-KG function in cellular detoxification processes in response to oxidative stress, IDH1 also indirectly participates in mitigating oxidative damage. In addition, IDH1 is key to β-oxidation of unsaturated fatty acids in the peroxisomes of liver cells. IDH1 also participates in the regulation of glucose-induced insulin secretion. Notably, IDH1 is the primary producer of NADPH in most tissues, especially in brain. Within cells, IDH1 has been observed to localize to the cytoplasm, peroxisome, and endoplasmic reticulum.
Sources: en.wikipedia.org
The club's reserve team, formerly the SC Freiburg Amateure, now SC Freiburg II, has, for the most part of its history played in the lower amateur leagues. It made a three-season appearance in the tier four Verbandsliga Südbaden from 1983 to 1986, but then took until 1994 to return to this league. In 1998 the team won promotion to the Oberliga Baden-Württemberg after a league championship in the Verbandsliga. Freiburg II spent the next ten seasons at this level as an upper table side before another league championship took the team to the Regionalliga Süd. After four seasons at this league the team became part of the new Regionalliga Südwest in 2012. After a seventh place in its first season in the league the team finished runner-up in 2013–14. A South Baden Cup win in 2001 qualified it for the first round of the 2001–02 DFB-Pokal, the German Cup, where it lost to Schalke 04.
== Former supermarket chains == Carrefour (Taken over by AEON Group to become AEON BiG) Emporium Supermarket & Departmental Store Fajar Supermarket Hiong Kong Supermarket Jaya Supermarket Kimisawa Supermarket Makro (Taken over by Tesco to become Tesco Extra) Ngiu Kee Pasaraya Greatwall Pasaraya Ocean Rich Supermarket Senyum Supermarket Costco Sri Kota Supermarket Tesco (Taken over by Lotus's) Tesco Extra Tops Yaohan Supermarket Kedai Runcit Usaha Kami Yuyi Supermarket
Uncompetitive antagonist of the NMDA receptor via the MK-801/PCPTooltip phencyclidine site SERTTooltip Serotonin transporter and NETTooltip norepinephrine transporter blocker (cf. serotonin–norepinephrine reuptake inhibitor) Sigma σ1 receptor agonist Negative allosteric modulator of nicotinic acetylcholine receptors Ligand of the serotonin 5-HT1B/1D, histamine H1, α2-adrenergic, and muscarinic acetylcholine receptors Dextromethorphan is a prodrug of dextrorphan, which is the actual mediator of most of its dissociative effects through acting as a more potent NMDA receptor antagonist than dextromethorphan itself. What role, if any, (+)-3-methoxymorphinan, dextromethorphan's other major metabolite, plays in its effects is not entirely clear.
=== Tests === Thyroid function tests include a battery of blood tests, including the measurement of the thyroid hormones, as well as the measurement of thyroid stimulating hormone (TSH). They may reveal hyperthyroidism (high T3 and T4), hypothyroidism (low T3, T4), or subclinical hyperthyroidism (normal T3 and T4 with a low TSH). TSH levels are considered the most sensitive marker of thyroid dysfunction. They are however not always accurate, particularly if the cause of hypothyroidism is thought to be related to insufficient thyrotropin releasing hormone (TRH) secretion, in which case it may be low or falsely normal. In such a case a TRH stimulation test, in which TRH is given and TSH levels are measured at 30 and 60-minutes after, may be conducted. T3 and T4 can be measured directly. However, as the two thyroid hormones travel bound to other molecules, and it is the "free" component that is biologically active, free T3 and free T4 levels can be measured. T3 is preferred, because in hypothyroidism T3 levels may be normal. The ratio of bound to unbound thyroid hormones is known as the thyroid hormone binding ratio (THBR). It is also possible to measure directly the main carriers of the thyroid hormones, thyroglobulin and throxine-binding globulin. Thyroglobulin will also be measurable in a healthy thyroid, and will increase with inflammation, and may also be used to measure the success of thyroid removal or ablation. If successful, thyroglobulin should be undetectable.
== Demographics == The homeland was set up to house Setswana-speaking peoples. In 1983, it had more than 1,430,000 inhabitants; in 1990, it had an estimated population of 2,352,296. Only 10% of Bophuthatswana's total land area was arable, and much of that was covered with scrub bush. Though the majority of its population was Tswana-speaking, Tswana, English, and Afrikaans were all designated as official languages by the Constitution of Bophuthatswana.
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.
Cardarine is a common name for GW501516, a synthetic PPARδ agonist. It is not a steroid or a selective androgen receptor modulator. It was developed and studied as a research compound for metabolic pathways.