A practical reference on Reference standard: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2025-12-28 and is reviewed periodically as new material appears.
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.
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.
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.
| 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 |
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.
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.
Analytical laboratories typically identify cardarine and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is a common matrix in anti-doping testing, while blood and tissue may be used in research settings. Detection windows depend on the assay, the sample matrix, and the compound's metabolism. Because cardarine is extensively metabolized, laboratories often target specific metabolites to improve sensitivity and confirmation. Reference standards are required for reliable quantification. Method validation includes checks for selectivity, linearity, and carryover.
A persistent misconception is that cardarine is a fat-burning drug or a safe alternative to anabolic steroids. No approved therapeutic product exists, and human safety data are limited. The tumor findings in rodents remain a central concern in scientific reviews. Products sold online may contain inaccurate labels, impurities, or different compounds entirely, which complicates any assessment of effects. Independent testing of such products has reported frequent mislabeling. For these reasons, discussions in the literature emphasize risks and unknowns rather than benefits.
Cardarine is not approved for human therapeutic use in any major jurisdiction. It appears on the World Anti-Doping Agency Prohibited List as a PPARδ agonist within the hormone and metabolic modulators category. Sports organizations test for it because it has been detected in athlete samples and seized products. Regulatory actions against marketed research chemical versions have occurred in several countries, though enforcement varies. Availability through unregulated channels complicates oversight.
== Biological functions == Vitamin B3 has several vitamers that can act in place of each other, including nicotinic acid and nicotinamide. It is precursor of the coenzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). These compounds are coenzymes for many dehydrogenases, participating in many hydrogen transfer processes. NAD is important in catabolism of fat, carbohydrate, protein, and alcohol, as well as cell signaling and DNA repair, and NADP mostly in anabolism reactions such as fatty acid and cholesterol synthesis. Vitamin intake recommendations made by several countries are that intakes of 14–18 mg/day are sufficient to meet the needs of healthy adults. Nicotinic acid and nicotinamide are both used for prevention and treatment of pellagra, a disease caused by lack of the vitamin.
Diagnosis is made with reasonable certainty based on history and clinical examination. X-rays may confirm the diagnosis. The typical changes seen on X-ray include: joint space narrowing, subchondral sclerosis (increased bone formation around the joint), subchondral cyst formation, and osteophytes. The combination of knee pain and osteophytes on x-ray or hip pain and osteophytes on x-ray, has good sensitivity and specificity for the diagnosis of osteoarthritis of those joints. X-rays may not correlate with the findings on physical examination or with the degree of pain, especially in the early course of osteoarthritis, where imaging findings may be relatively normal. In 1990, the American College of Rheumatology, using data from a multi-center study, developed a set of criteria for the diagnosis of hand osteoarthritis based on hard tissue enlargement and swelling of certain joints. These criteria were found to be 92% sensitive and 98% specific for hand osteoarthritis versus other entities such as rheumatoid arthritis and spondyloarthropathies.
Nicotinamide adenine dinucleotide (NAD+) is a coenzyme central to metabolism. Found in all living cells, NAD is called a dinucleotide because it consists of two nucleotides joined through their phosphate groups. One nucleotide contains an adenine nucleobase and the other, nicotinamide. NAD exists in two forms: an oxidized and reduced form, abbreviated as NAD+ and NADH (H for hydrogen), respectively. In cellular metabolism, NAD is involved in redox reactions, carrying electrons from one reaction to another, so it is found in two forms: NAD+ is an oxidizing agent, accepting electrons from other molecules and becoming reduced; with H+, this reaction forms NADH, which can be used as a reducing agent to donate electrons. These electron transfer reactions are the main function of NAD. It is also used in other cellular processes, most notably as a substrate of enzymes in adding or removing chemical groups to or from proteins, in posttranslational modifications. Because of the importance of these functions, the enzymes involved in NAD metabolism are targets for drug discovery. In organisms, NAD can be synthesized from simple building-blocks (de novo) from either tryptophan or aspartic acid, each a case of an amino acid. Alternatively, more complex components of the coenzymes are taken up from nutritive compounds such as vitamin B3 (also called niacin, or (nicotinic acid, hence the name "nicotinamide"). Similar compounds are produced by reactions that break down the structure of NAD, providing a salvage pathway that recycles them back into their respective active form.
== Systemic diseases == Myopathies in systemic disease results from several different disease processes including endocrine, inflammatory, paraneoplastic, infectious, drug- and toxin-induced, critical illness myopathy, metabolic, collagen-related, and myopathies with other systemic disorders. Patients with systemic myopathies often present acutely or subacutely. On the other hand, familial myopathies or dystrophies generally present in a chronic fashion with exceptions of metabolic myopathies, in which symptoms on occasion can be precipitated acutely. Metabolic myopathies, which affect the production of ATP within the muscle cell, typically present with dynamic (exercise-induced) rather than static symptoms. Most of the inflammatory myopathies can have a chance association with malignant lesion; the incidence appears to be specifically increased only in patients with dermatomyositis. There are many types of myopathy. ICD-10 codes are provided here where available.
BASF is an acronym for Badische Anilin- und Sodafabrik (German for 'Baden Aniline and Soda Factory'). It was founded by Friedrich Engelhorn on 6 April 1865 in Mannheim, in the German-speaking state of Baden. Engelhorn had been responsible for setting up a gasworks and street lighting for the town council in 1861. The gasworks produced tar as a by-product from coal, and Engelhorn used this to extract aniline for the production of dyes. BASF was set up in 1865, to produce other chemicals necessary for dye production, notably soda and acids. The plant, however, was erected on the other side of the Rhine river at Ludwigshafen because the town council of Mannheim was afraid that the air pollution from the chemical plant could bother the inhabitants of the town. In 1866, the dye production processes were also moved to the BASF site.
Sources: en.wikipedia.org
Selenoprotein I (SELENOI/EPT1), a CDP-ethanolamine:diacylglycerol ethanolamine-phosphotransferase. Selenoprotein K and Selenoprotein S are small transmembrane proteins found on the ER menbrane. Selenoprotein M and Selenoprotein F, thioredoxin-like proteins found in the endoplasmic reticulum (ER). Selenoprotein N, a large transmembran proteins found on the ER menbrane. Selenoprotein O, protein found in the mitochondrial, probably with a redox function. Selenoprotein P is an extracellular glycoprotein, unusually with more than one Sec residue (usually several), found in eukaryotes including humans. The precise number of residues vary and appears linked to the selenium needs of the organism. Selenoprotein R (MSRB1) is a peptide-methionine (R)-S-oxide reductase. It has two non-selenoprotein relatives in humans, also of the same catalytic activity. Families only existing as non-seleno-proteins in mammals:
=== Solubility === Legumin proteins are insoluble in water because of their hydrophobic units. Legumins are soluble in very weak acids and alkalies. This protein is not coagulated by heat. Due to their important storage function legumin proteins and another important storage protein vicilin have been found be to the most abundant water and alkali soluble proteins within cottonseed.
List of largest empires List of military conflicts spanning multiple wars List of countries by number of military and paramilitary personnel List of militaries by country List of ongoing armed conflicts Interwar period Post–Cold War era
== Instant noodle consumption == World Instant Noodle Association: Of 43 nations, Thailand is the eighth biggest consumer of instant noodles, consuming three billion packet/cups in 2014. The Bangkok Post reported in 2018 that Thais consume 49 packages of instant noodles per year per capita, more than three times the global average of 13.3 packages.
== In cancer research == In Cullen's paper "Granzymes in Cancer and Immunity" he describes the process of "immune surveillance [as] the process whereby precancerous and malignant cells are recognized by the immune system as damaged and are consequently targeted for elimination". For a tumor to progress it requires conditions within the body and surrounding area to be growth-promoting. Almost all people have suitable immune cells to fight off tumors in the body. Studies have shown that the immune system even has the ability to prevent precancerous cells from growing and arbitrate the regression of established tumors. The dangerous thing about cancer cells is they have the ability to inhibit the function of the immune system. Although a tumor may be in its beginning stage and very weak, it may be giving off chemicals that inhibit the function of the immune system allowing it to grow and become harmful. Tests have shown that mice without granzymes and perforins are at high risk to have tumors spread throughout their body. Tumors have the ability to escape from immune surveillance by secreting immunosuppressive TGF-β. This inhibits proliferation and activation of T cells. TGF-β production is the most potent mechanism of immune avoidance used by tumors. TGF-β inhibits expression of five different cytotoxic genes including perforin, granzyme A, and granzyme B, which then inhibits T cell-mediated tumor clearance.
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.