GW501516 comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Updated 2026-07-28. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic PPARδ agonist | Not a steroid or a selective androgen receptor modulator. |
| Common synonyms | Cardarine, GW501516, GW-501516, endurobol | Names vary by supplier and literature source. |
| Appearance | White to off-white powder | Consistent with many small-molecule research chemicals. |
| Solubility | Low in water; soluble in DMSO and ethanol | Often prepared in organic solvent for laboratory work. |
| Primary target | PPARδ (NR1C2) | Nuclear receptor involved in lipid and energy metabolism. |
GW501516 acts as an agonist at the peroxisome proliferator-activated receptor delta, a nuclear receptor that regulates gene expression. Activation shifts transcription toward genes involved in fatty acid uptake, oxidation, and energy expenditure. The compound does not bind the androgen receptor and therefore differs from anabolic steroids and SARMs. In rodent models, this metabolic shift has been linked to increased running endurance and reduced fat accumulation. The exact downstream pathways in humans remain incompletely characterized.
Early clinical research explored GW501516 for lipid disorders, obesity, and diabetes. Some short-term human studies reported changes in HDL cholesterol, LDL cholesterol, and triglycerides. The development program was discontinued after rodent studies showed dose-dependent tumor formation in multiple tissues, including liver, bladder, stomach, and skin. These findings raised concerns about long-term cancer risk in humans. Because human exposure data are limited, the clinical significance of the rodent tumors remains uncertain.
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.
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.
Although PI3K is the major mode of Akt activation, other tyrosine or serine/threonine kinases have been shown to activate Akt directly, in response to growth factors, inflammation or DNA damage. These can function even when PI3K activity is inhibited. Other studies have shown Akt can be activated in response to heat shock or increases in cellular Ca2+ concentration, via Ca2+/Calmodulin-dependent protein kinase kinase (CAMKK).
Parker was born in March 1938, and was the only daughter of Frederick and Hilda Witcomb (née Linscott). She was married to Joseph Parker, a Post Office engineer, and lived in the Kings Norton area of Birmingham. After several years as a police photographer, she joined the University of Birmingham Medical School, where she was employed as a medical photographer in the Anatomy Department. She often worked in a darkroom above the laboratory where research on smallpox viruses was being conducted.
ASQ provides its members with certification, training, publications, conferences, and other services. ASQ is a founding partner of the American Customer Satisfaction Index (ACSI), a quarterly economic indicator. Since 1989, ASQ has administered the annual Malcolm Baldrige National Quality Award. The ASQ also gives the Dorian Shainin Medal, which is awarded annually for the "Development and Application of Creative or Unique Statistical Approaches in the Solving of Problems Relative to the Quality of Product or Service".
5-HT2C receptor agonists reduce appetite by working on serotonin receptors in a region of the brain called the hypothalamus. Lorcaserin (Belviq) was FDA approved for weight loss but was withdrawn from the market because a safety clinical trial shows an increased occurrence of cancer. Cannabinoid receptor antagonists were developed to treat obesity because researchers noticed that cannabinoid agonists (such as THC, the main pharmacologically active component of cannabis), increased appetite. However, some drugs in this class such as rimonabant were withdrawn or ceased development due to concerns about mental health and suicide. More selective drugs—some are in development that act only in peripheral tissues, not the brain—may be able to achieve this result with fewer adverse effects. GLP-1 agonists such as tirzepatide, semaglutide, and liraglutide slow gastric emptying and also have neurologically driven effects on appetite. It is unknown if GLP-1 agonists or dual/triple agonists of GLP-1 and/or the glucagon or GIP receptors act solely by reducing energy intake or if they also increase energy expenditure. Setmelanotide is an agonist of the melanocortin 4 receptor and is used in people with certain rare genetic conditions that cause obesity. It is less effective and not approved for general obesity.
Sources: en.wikipedia.org
In a few people, acromegaly is caused by tumors of the pancreas, lungs, and adrenal glands. These tumors also lead to an excess of GH, either because they produce GH themselves or, more frequently, because they produce GHRH (growth hormone-releasing hormone), the hormone that stimulates the pituitary to make GH. When these nonpituitary tumors are surgically removed, GH levels fall and the symptoms of acromegaly improve. Diagnosis is by measuring growth hormone after a person has consumed a glucose solution, or by measuring insulin-like growth factor I in the blood. After diagnosis, medical imaging of the pituitary is carried out to determine if an adenoma is present. If excess growth hormone is produced during childhood, the result is the condition gigantism rather than acromegaly, and it is characterized by excessive height. An MRI of the brain focusing on the sella turcica after gadolinium administration allows for clear delineation of the pituitary and the hypothalamus and the location of the tumor.
Scleroderma, polymyositis, and dermatomyositis elicit little or no CRP response. CRP levels also tend to remain low despite inflammatory activity in systemic lupus erythematosus (SLE) unless serositis or synovitis is present. This may be explained by increased levels of type I IFN in SLE, since type I IFN (i.e IFN alpha) inhibits hepatic CRP production. A polymorphisms of the CRP gene which cause lower CRP levels is also more frequent in SLE patients compared with controls. Elevations of CRP in the absence of clinically significant inflammation can occur in kidney failure. CRP level is an independent risk factor for atherosclerotic disease. Patients with high CRP concentrations are more likely to develop stroke, myocardial infarction, and severe peripheral vascular disease. Elevated level of CRP can also be observed in inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis. High levels of CRP has been associated to point mutation Cys130Arg in the APOE gene, coding for apolipoprotein E, establishing a link between lipid values and inflammatory markers modulation.
Two species of AAV were recognised by the International Committee on Taxonomy of Viruses in 2013: adeno-associated dependoparvovirus A (formerly AAV-1, −2, −3 and −4) and adeno-associated dependoparvovirus B (formerly AAV-5). Until the 1990s, virtually all AAV biology was studied using AAV serotype 2. However, AAV is highly prevalent in humans and other primates and several serotypes have been isolated from various tissue samples. Serotypes 2, 3, 5, and 6 were discovered in human cells, AAV serotypes 1, 4, and 7–11 in nonhuman primate samples. As of 2006 there have been 11 AAV serotypes described, the 11th in 2004. AAV capsid proteins contain 12 hypervariable surface regions, with most variability occurring in the threefold proximal peaks, but the parvovirus genome in general presents highly conserved replication and structural genes across serotypes. All of the known serotypes can infect cells from multiple diverse tissue types.
Sources: en.wikipedia.org
In the European Union, a biological medicinal product is one of the active substance(s) produced from or extracted from a biological (living) system, and requires, in addition to physicochemical testing, biological testing for full characterisation. The characterisation of a biological medicinal product is a combination of testing the active substance and the final medicinal product together with the production process and its control. For example: Production process – it can be derived from biotechnology or from other technologies. It may be prepared using more conventional techniques as is the case for blood or plasma-derived products and a number of vaccines. Active substance – consisting of entire microorganisms, mammalian cells, nucleic acids, proteinaceous, or polysaccharide components originating from a microbial, animal, human, or plant source. Mode of action – therapeutic and immunological medicinal products, gene transfer materials, or cell therapy materials.
An analytical ultracentrifuge has a light source and optical detectors. To allow the light to pass through the analyte during the ultracentrifuge run, specialized cells are required which have to meet high optical standards as well as to resist the centrifugal forces. Each cell consists of a housing, two windows made from optically pure quartz glass, and a centrepiece with one or two sectors and filling holes for the sector(s), closed with a screw plug in the housing. These cell are placed into a rotor cavity with a continuous bore, with a collar at the bottom to retain the cell. By applying specific equipment and adapting measurement parameters several types of experiments can be performed. Most common AUC experiments are sedimentation velocity and sedimentation equilibrium experiments.
Greater emphasis on risk management Introduces “Special Requirements” Introduces “Critical Items” Measure: Requirements conformance Measure: Delivery performance Adopt proven product development processes Eliminate “recurring corrective actions” AS9100 Revision C was released in January, 2009, with considerable delay in application of the new version in audits, largely due to the delay in the release of AS9101 Revision D and auditor training to the increased auditing rigor of that update. AS9100 Revision D (2016), Quality Management System – Requirements for Aviation, Space and Defense Organizations The update of AS9100 from revision C to D includes the full text of ISO 9001:2015. In addition to aligning the structure of the aviation, space and defense requirements to the new structure of ISO 9001:2015, the following key changes were implemented:
Sources: en.wikipedia.org
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.
It binds to and activates PPARδ, a nuclear receptor that regulates genes related to fatty acid oxidation and energy use. This activation alters transcription in tissues such as skeletal muscle and liver. The full range of downstream effects in humans is not fully established.
No, cardarine is not known to occur naturally in plants, animals, or humans. It is a synthetic molecule produced for laboratory research. Products labeled as cardarine should therefore be treated as manufactured chemicals with variable purity.
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.