Cardarine 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 2026-01-15. Numbers and descriptions here follow the published literature rather than marketing material.
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.
Published studies have examined GW501516 in animal models of obesity, insulin resistance, and exercise endurance. Early human trials reportedly ended, and development was discontinued after preclinical findings raised concerns about cancer in some rodent studies. Regulatory agencies have not approved cardarine for any medical use. Its availability through non-pharmaceutical channels raises questions about identity, purity, and legal status that are separate from its laboratory pharmacology. Those questions are often addressed through analytical testing rather than assumptions about product labels.
Cardarine is a common name for GW501516, also GW-1516, a synthetic compound developed as a peroxisome proliferator-activated receptor delta (PPARδ) agonist. It belongs to a class of agents that modulate gene transcription related to lipid and energy metabolism. The compound was studied in preclinical and early clinical research for metabolic and cardiovascular conditions, but it did not progress to approved therapeutic use. Its name appears in fitness and sports contexts despite not being approved as a drug.
| 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 |
Published literature on cardarine includes in vitro assays, rodent experiments, and a small number of human studies. Reports describe effects on exercise capacity and lipid metabolism in animals, while human evidence is sparse. Many online descriptions present the compound as a proven endurance aid, a claim not supported by regulatory approval or large clinical trials. Analytical studies focus on identifying the parent compound and its metabolites in biological samples. Important uncertainties include species differences, dose-response relationships, and the relevance of rodent tumor findings to humans.
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.
In laboratory settings, cardarine is studied as a tool compound for probing PPARδ biology. Published experiments often use cell cultures, rodent models, or isolated tissues. Some investigations focus on metabolic effects, while others assess potential risks such as carcinogenicity observed in long-term animal studies. Because human trials are sparse, most knowledge comes from preclinical work and adverse event reports. Scientific literature frequently notes the gap between animal findings and human outcomes. The compound is not a dietary supplement and is not intended for human consumption.
Cardarine is a common name for GW501516, a synthetic compound developed in the 1990s through research collaborations involving GlaxoSmithKline. It belongs to a class of molecules known as peroxisome proliferator-activated receptor delta agonists. Early studies explored its effects on lipid metabolism and energy expenditure in animal models. The compound was never approved as a human medicine, and clinical development was discontinued. In the years since, it has appeared in fitness and bodybuilding communities as a performance-enhancing substance. Regulatory agencies classify it as an unapproved drug.
PPARδ is a nuclear receptor that regulates gene expression related to fatty acid oxidation, glucose homeostasis, and mitochondrial function. GW501516 binds to this receptor with high affinity and activates downstream signaling in skeletal muscle and other tissues. Animal studies reported increased endurance and altered fuel preference, but human data remain limited and inconsistent. The precise relationship between receptor activation and observed physiological changes is still an area of active investigation. Researchers have also examined whether the compound affects inflammation or cell proliferation. No approved therapeutic indication exists for cardarine.
Alfred Ellis Wilhelmi (1910–1994) was an American endocrinologist recognized for contributing to the understanding of anterior pituitary hormones. Born in Lakewood, Ohio, Wilhelmi attended Cleveland public schools. Wilhelmi earned a B.S. degree in premedical sciences from Western Reserve University in 1933. He then attended Oxford University as a Rhodes Scholar, where he obtained a B.A. in 1933 and Ph.D. in animal physiology in 1937. He then joined Yale University's Biochemistry Department, rising to the position of Professor in 1950. Wilhelmi chaired the Department of Biochemistry at Emory University School of Medicine from 1950 to 1977. In 1960, he was named Charles Howard Candler Professor of Biochemistry. In 1979, he received Emory's Thomas Jefferson award for service to the university and community. Wilhelmi also was President of the Endocrine Society from 1968 to 1969. During his career, he published over 80 articles in scientific journals.
Announced on 8 May 2024, AlphaFold 3 was co-developed by Google DeepMind and Isomorphic Labs, both subsidiaries of Alphabet. AlphaFold 3 is not limited to proteins, as it can also predict the structures of protein complexes with DNA, RNA, post-translational modifications and selected ligands and ions. AlphaFold 3 introduces the "Pairformer," a deep learning architecture inspired by the transformer, which is considered similar to, but simpler than, the Evoformer used in AlphaFold 2. The Pairformer module's initial predictions are refined by a diffusion model. This model begins with a cloud of atoms and iteratively refines their positions, guided by the Pairformer's output, to generate a 3D representation of the molecular structure. The AlphaFold server was created to provide free access to AlphaFold 3 for non-commercial research. As of November 2025, the AlphaFold 3 research paper has been directly cited more than 9,000 times.
From the 17th century, and before modern developments in organic chemistry nomenclature, acetone was given many different names. They included "spirit of Saturn", which was given when it was thought to be a compound of lead and, later, "pyro-acetic spirit" and "pyro-acetic ester". Prior to the name "acetone" being coined by French chemists, it was named "mesit" (from the Greek μεσίτης, meaning mediator) by Carl Reichenbach, who also said that methyl alcohol consisted of mesit and ethyl alcohol. Names derived from mesit include mesitylene and mesityl oxide which were first synthesised from acetone. In 1839, the name "acetone" began to be used, because it was obtained from acetic acid. Unlike many compounds with the acet- prefix which have a 2-carbon chain, acetone has a 3-carbon chain. That has caused confusion because there can not be a ketone with 2 carbons. The prefix refers to acetone's relation to vinegar (acetum in Latin, also the source of the words "acid" and "acetic"), rather than its chemical structure.
The structure of prolactin is similar to that of growth hormone and placental lactogen. The molecule is folded due to the activity of three disulfide bonds. Significant heterogeneity of the molecule has been described, thus bioassays and immunoassays can give different results due to differing glycosylation, phosphorylation and sulfation, as well as degradation. The non-glycosylated form of prolactin is the dominant form that is secreted by the pituitary gland. The three different sizes of prolactin are:
The sulfur cycle is a biogeochemical cycle in which the sulfur moves between rocks, waterways and living systems. It is important in geology as it affects many minerals and in life because sulfur is an essential element (CHNOPS), being a constituent of many proteins and cofactors, and sulfur compounds can be used as oxidants or reductants in cellular respiration. The global sulfur cycle involves the transformations of sulfur species through different oxidation states, which play an important role in both geological and biological processes. Steps of the sulfur cycle are: Mineralization of organic sulfur into inorganic forms, such as hydrogen sulfide (H2S), elemental sulfur, as well as sulfide minerals. Incorporation of sulfide into organic compounds (including metal-containing derivatives). Oxidation of hydrogen sulfide, sulfide, and elemental sulfur (S) to sulfate (SO2−4). Reduction of sulfate and sulfite to sulfide. Disproportionation of sulfur compounds (elemental sulfur, sulfite, thiosulfate) into sulfate and hydrogen sulfide. These are often termed as follows:
Sources: en.wikipedia.org
Many pathways and signals lead to apoptosis, but these converge on a single mechanism that actually causes the death of the cell. After a cell receives stimulus, it undergoes organized degradation of cellular organelles by activated proteolytic caspases. In addition to the destruction of cellular organelles, mRNA is rapidly and globally degraded by a mechanism that is not yet fully characterized. mRNA decay is triggered very early in apoptosis. A cell undergoing apoptosis shows a series of characteristic morphological changes. Early alterations include:
The binding of S-arrestin to rhodopsin is specific and involves changes that occur in rhodopsin after activation. Important serine (Ser) and threonine (Thr) residues in rhodopsin's tail, particularly Thr-340 and Ser-343, are phosphorylated by enzymes called GRKs. These phosphorylated residues strongly attract S-arrestin, helping it bind tightly and effectively shut down rhodopsin's signaling. Additionally, studies of the protein structure have shown that during activation, rhodopsin's transmembrane helix 7 (TM7) and helix 8 change shape. These changes expose a binding site that interacts with a specific part of arrestin called the "finger loop." This interaction, clearly seen in the crystal structure (PDB ID: 4ZWJ), shows how arrestin fits precisely onto activated and phosphorylated rhodopsin, efficiently stopping the visual signal. Arrestin at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
NETA metabolizes into ethinylestradiol at a rate of 0.20 to 0.33% across a dose range of 10 to 40 mg. Peak levels of ethinylestradiol with a 10, 20, or 40 mg dose of NETA were 58, 178, and 231 pg/mL, respectively. For comparison, a 30 to 40 μg dose of oral ethinylestradiol typically results in a peak ethinylestradiol level of 100 to 135 pg/mL. As such, in terms of ethinylestradiol exposure, 10 to 20 mg NETA may be equivalent to 20 to 30 μg ethinylestradiol and 40 mg NETA may be similar to 50 μg ethinylestradiol. In another study however, 5 mg NETA produced an equivalent of 28 μg ethinylestradiol (0.7% conversion rate) and 10 mg NETA produced an equivalent of 62 μg ethinylestradiol (1.0% conversion rate). Due to its estrogenic activity via ethinylestradiol, high doses of NETA have been proposed for add-back in the treatment of endometriosis without estrogen supplementation. Generation of ethinylestradiol with high doses of NETA may increase the risk of venous thromboembolism but may also decrease menstrual bleeding relative to progestogen exposure alone.
Pandey has the Human Proteome Organization(HUPO)'s Discovery in Proteomic Sciences Award. The Wellcome Trust/DBT India Alliance named him a Margdarshi Fellow, and he established a Center for Molecular Medicine at NIMHANS in Bangalore as a result. He is an Associate Editor of Clinical Proteomics and a member of the Editorial Boards of Molecular and Cellular Proteomics, Proteomics, and the Journal of Clinical Investigation. He has received the Howard Temin Award from the National Cancer Institute, the Experimental Pathologist-In-Training Award from the American Society for Investigative Pathology, and the Sidney Kimmel Scholar Award from the Sidney Kimmel Foundation for Cancer Research. The United States Department of Defense also bestowed upon him the Era of Hope Scholar Award.
The first definition of the term bioinformatics was coined by Paulien Hogeweg and Ben Hesper in 1970, to refer to the study of information processes in biotic systems. This definition placed bioinformatics as a field parallel to biochemistry (the study of chemical processes in biological systems). Bioinformatics and computational biology involved the analysis of biological data, particularly DNA, RNA, and protein sequences. The field of bioinformatics experienced explosive growth starting in the mid-1990s, driven largely by the Human Genome Project and by rapid advances in DNA sequencing technology. Analyzing biological data to produce meaningful information involves writing and running software programs that use algorithms from graph theory, artificial intelligence, soft computing, data mining, image processing, and computer simulation. The algorithms in turn depend on theoretical foundations such as discrete mathematics, control theory, system theory, information theory, and statistics.
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 commonly known as GW501516 or GW-1516. These names refer to the same synthetic compound. It is not a brand-name approved medicine.