Metabolite is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Updated 2025-10-28. 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.
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.
| 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 |
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.
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.
Preclinical research reported that GW501516 increased running endurance in mice and improved lipid profiles in some animal species. Early human trials explored effects on high-density lipoprotein cholesterol, triglycerides, and glucose handling, but the program was discontinued. Published human data are sparse and do not establish efficacy for any condition. Studies also examined PPAR delta in cancer biology, with conflicting findings across models. The relationship between receptor activation, tissue context, and disease risk remains an active area of investigation.
Anti-doping laboratories identify GW501516 and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is the usual matrix, and detection can occur after the parent compound has cleared from blood. The exact detection window depends on dose, formulation, individual metabolism, and assay sensitivity. Because the compound is prohibited at all times, athletes are subject to testing in and out of competition. Analytical methods continue to improve as new metabolites and designer analogs are characterized.
GW501516 acts as a ligand for PPAR delta, a nuclear receptor that regulates transcription of genes involved in fatty acid oxidation and energy use. Activation of this receptor in skeletal muscle shifts metabolism toward fat burning in animal models. The compound does not burn fat directly; it changes gene expression over hours to days. Researchers study it to understand metabolic flexibility and exercise adaptation. Effects observed in rodents are not automatically expected in humans.
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.
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.
2-Aminoisobutyric acid (Aib) is the non-proteinogenic amino acid with the structural formula H2N-C(CH3)2-COOH. The Aib residue is a component of tirzepatide, a commonly prescribed antidiabetic medication for treatment of type 2 diabetes. Although uncommon, it is also found in some natural products
Sertraline, sold under the brand name Zoloft among others, is an antidepressant medication of the selective serotonin reuptake inhibitor (SSRI) class used to treat major depressive disorder, generalized anxiety disorder, social anxiety disorder, obsessive–compulsive disorder (OCD), panic disorder, and premenstrual dysphoric disorder. Although also having approval for post-traumatic stress disorder (PTSD), findings indicate it leads to only modest improvements in symptoms associated with this condition. The drug shares the common side effects and contraindications of other SSRIs, with high rates of nausea, diarrhea, headache, insomnia, mild sedation, dry mouth, and sexual dysfunction, but it appears not to lead to much weight gain, and its effects on cognitive performance are mild. In some patients, sexual dysfunction may persist even after the drug is discontinued, a condition known as post-SSRI sexual dysfunction; regulatory agencies including the European Medicines Agency and Health Canada have recommended that sertraline's product labeling warn of this risk. Similar to other antidepressants, the use of sertraline for depression may be associated with a mildly elevated rate of suicidal thoughts in people under the age of 25 years old. It should not be used together with monoamine oxidase inhibitors (MAOIs): this combination may cause serotonin syndrome, which can be life-threatening in some cases. Sertraline taken during pregnancy is associated with an increase in congenital heart defects in newborns.
Flucytosine: The toxicity of flucytosine is increased and allows for a lower dose of amphotericin B. Amphotericin B may also facilitate entry of flucytosine into the fungal cell by interfering with the permeability of the fungal cell membrane. Diuretics or cisplatin: Increased renal toxicity and increased risk of hypokalemia Corticosteroids: Increased risk of hypokalemia Imidazole antifungals: Amphotericin B may antagonize the activity of ketoconazole and miconazole. The clinical significance of this interaction is unknown. Neuromuscular-blocking agents: Amphotericin B–induced hypokalemia may potentiate the effects of certain paralytic agents. Foscarnet, ganciclovir, tenofovir, adefovir: The risk of hematological and kidney side effects of amphotericin B is increased Zidovudine: Increased the risk of kidney and hematological toxicity. Other nephrotoxic drugs (such as aminoglycosides): Increased risk of serious renal damage Cytostatic drugs: Increased risk of kidney damage, low blood pressure, and airway spasms Transfusion of leukocytes: There is a risk that pulmonary (lung) damage may occur. Space the intervals between the application of amphotericin B and the transfusion, and monitor pulmonary function
Glycolysis is the metabolic pathway that converts glucose (C6H12O6) into pyruvate and, in most organisms, occurs in the liquid part of cells (the cytosol). The free energy released in this process is used to form the high-energy molecules adenosine triphosphate (ATP) and reduced nicotinamide adenine dinucleotide (NADH). Glycolysis is a sequence of ten reactions catalyzed by enzymes.
Sources: en.wikipedia.org
== 20th Century == 1901: Florence Bascom became the first female geologist to present a paper before the Geological Survey of Washington. 1903: Marie Curie became the first woman to win the Nobel Prize, awarded in Physics, and went on to also win the Nobel Prize in Chemistry. She performed pioneering research in radioactivity, and discovered two elements (polonium and radium). 1912: Henrietta Swan Leavitt studied the bright-dim cycle periods of Cepheid stars, then found a way to calculate the distance from such stars to Earth. 1924: Florence Bascom became the first woman elected to the Council of the Geological Society of America. 1925: Florence Sabin became the first woman elected to the National Academy of Sciences. 1928: Alice Evans became the first woman elected president of the Society of American Bacteriologists. 1936: Edith Patch became the first female president of the Entomological Society of America.
In Situ and Ex Situ NMR Techniques NMR technology can be divided into two main experimental approaches in battery research: In Situ NMR and Ex Situ NMR. Each offers unique advantages depending on the research goals.
Blood-thinning agents are divided into two groups, antiplatelet drugs and anticoagulants. They are indicated to facilitate smooth blood flow within blood vessels by preventing the formation of blood clots and retarding their growth. Blood clots are formed to prevent an injured blood vessel from excessive bleeding by a mechanism called hemostasis. The body has intrinsic mechanisms to dissolve the blood clot as the injury heals. However, it can be dangerous when clots do not dissolve naturally and develop within vessels, also known as thrombosis. Hence, blood-thinning medications can be prescribed to reduce the risk of cardiovascular diseases led by blood clots, such as myocardial infarction (heart attack), ischemic stroke, and venous thromboembolism. Haemorrhage (internal bleeding) is the most prominent side effect of blood-thinning therapy. Concomitant use of drugs that increase the risk of bleeding is not recommended. Meanwhile, patients should receive education about proper management of cuts, bruises and nosebleeds. The agents can be classified according to different mechanisms of action.
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.
No. Cardarine is a PPARδ agonist, while selective androgen receptor modulators act on androgen receptors. The two classes differ in receptor target and downstream effects.