LC-MS/MS raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
Reviewed 2026-07-17. Anything still debated is marked as such rather than presented as settled.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | PPARδ agonist | Not an anabolic steroid. |
| Common synonyms | GW501516, GW-1516 | Cardarine is an informal name. |
| Appearance | White to off-white powder | Typical for research-grade solid. |
| Solubility class | Poorly soluble in water; soluble in some organic solvents | Such as DMSO or ethanol in laboratory settings. |
| Typical storage temperature | Cool, dry, protected from light | Specific conditions vary by supplier and form. |
Legal status varies by country. In some places, cardarine is controlled under medicines or psychoactive substances laws; in others, it may be sold with minimal oversight as a research chemical. Customs agencies have intercepted shipments, and several national health agencies have issued warnings about products marketed for bodybuilding or performance enhancement. The lack of a standardized pharmaceutical supply means identity, purity, and contamination levels can differ widely between samples. These factors make cardarine a regulatory and public health concern rather than a conventional prescription drug.
Cardarine is a common name for GW501516, a synthetic compound first described in the 1990s as a selective agonist of the peroxisome proliferator-activated receptor delta. It was studied in preclinical models for metabolic and cardiovascular conditions, but it has not been approved as a medicine in the United States, Europe, or other major jurisdictions. Retail products labeled as cardarine are generally research chemicals or supplements, not pharmaceutical formulations. Because human safety and efficacy data remain limited, regulatory agencies treat it as an unapproved substance rather than a therapeutic product.
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.
Anti-doping laboratories identify GW501516 and related metabolites using liquid chromatography coupled with tandem mass spectrometry. Urine is the most common matrix, though blood and dried blood spots may also be analyzed. The method targets the parent compound and phase I and phase II metabolites, which extend the detection window. Because the substance is prohibited at all times, athletes can be tested outside competition. Detection limits and windows depend on the assay, sample type, and individual metabolism.
Cardarine is frequently described as a fat-burning or endurance-enhancing supplement, but these claims exceed the available evidence. The compound is not a hormone, steroid, or selective androgen receptor modulator. Research articles discuss it as a tool compound for studying PPARδ biology, while anti-doping literature focuses on its abuse and detection. Quality of unapproved products is uncertain, and independent analyses have found impurities or incorrect labeling. Open questions include whether human cancer risk resembles that seen in rodents and how often non-athletes use the substance.
Cardarine has no approved therapeutic indication and is not marketed as a medicine. The World Anti-Doping Agency lists GW501516 as a prohibited substance at all times, covering both in-competition and out-of-competition periods. National laws vary: some countries treat it as an unapproved drug subject to import controls, while others have specific restrictions on sale for human consumption. It is often sold as a research chemical, a label that does not imply safety or legality. Enforcement actions have targeted online vendors and shipments.
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.
Some GSDs have different forms, e.g. infantile, juvenile, adult (late-onset). Some GSDs have different subtypes, e.g. GSD1a / GSD1b, GSD9A1 / GSD9A2 / GSD9B / GSD9C / GSD9D. GSD type 0: Although glycogen synthase deficiency does not result in storage of extra glycogen in the liver, it is classified with the GSDs as type 0 because it is another defect of glycogen storage and can cause similar problems. GSD type VIII (GSD 8): In the past, liver phosphorylase-b kinase deficiency was considered a distinct condition, however it has been classified with GSD type VI and GSD IXa1; it has been described as X-linked recessive inherited. GSD IX has become the dominant classification for this disease, grouped with the other isoenzymes of phosphorylase-b kinase deficiency. GSD type XI (GSD 11): Fanconi-Bickel syndrome (GLUT2 deficiency), hepatorenal glycogenosis with renal Fanconi syndrome, no longer considered a glycogen storage disease, but a defect of glucose transport. The designation of GSD type XI (GSD 11) has been repurposed for muscle lactate dehydrogenase deficiency (LDHA). GSD type XIV (GSD 14): No longer classed as a GSD, but as a congenital disorder of glycosylation type 1T (CDG1T), affects the phosphoglucomutase enzyme (gene PGM1). Phosphoglucomutase 1 deficiency is both a glycogenosis and a congenital disorder of glycosylation. Individuals with the disease have both a glycolytic block as muscle glycogen cannot be broken down, as well as abnormal serum transferrin (loss of complete N-glycans).
It decomposes back to its elements at a temperature of above 523 K (250 °C; 482 °F), and is reduced by water to radon gas and hydrogen fluoride: it may also be reduced back to its elements by hydrogen gas. It has a low volatility and was thought to be RnF2. Because of the short half-life of radon and the radioactivity of its compounds, it has not been possible to study the compound in any detail. Theoretical studies on this molecule predict that it should have a Rn–F bond distance of 2.08 ångströms (Å), and that the compound is thermodynamically more stable and less volatile than its lighter counterpart xenon difluoride (XeF2). The octahedral molecule RnF6 was predicted to have an even lower enthalpy of formation than the difluoride. The [RnF]+ ion is believed to form by the following reaction:
Scanning Electron Microscope (SEM) Transmission electron Microscope (TEM) Fourier Transform Infrared Spectroscopy (FTIR) Atomic force microscopy Contact angle meter Zeta potential (streaming potential) X-ray Diffraction (XRD) Liquid–Liquid Displacement Porosimetry (LLDP)
==== Na+,K+-ATPase and Insect resistance to cardiotonic steroids ==== Many examples of convergent evolution exist in insects in terms of developing resistance at a molecular level to toxins. One well-characterized example is the evolution of resistance to cardiotonic steroids (CTSs) via amino acid substitutions at well-defined positions of the α-subunit of Na+,K+-ATPase (ATPalpha). Variation in ATPalpha has been surveyed in various CTS-adapted species spanning six insect orders. Among 21 CTS-adapted species, 58 (76%) of 76 amino acid substitutions at sites implicated in CTS resistance occur in parallel in at least two lineages. 30 of these substitutions (40%) occur at just two sites in the protein (positions 111 and 122). CTS-adapted species have also recurrently evolved neo-functionalized duplications of ATPalpha, with convergent tissue-specific expression patterns.
Sources: en.wikipedia.org
=== Phylogenetics and modern definition === By the early 21st century, vertebrate paleontologists were beginning to adopt phylogenetic taxonomy, in which all groups are defined in such a way as to be monophyletic; that is, groups which include all descendants of a particular ancestor. The reptiles as historically defined are paraphyletic, since they exclude both birds and mammals. These respectively evolved from dinosaurs and from early therapsids, both of which were traditionally called "reptiles". Birds are more closely related to crocodilians than the latter are to the rest of extant reptiles. Colin Tudge wrote:
Banting was born on November 14, 1891, in his family's farmhouse 3.2 km (2 mi) from Alliston, Ontario. He was the youngest of five children of William Thompson Banting, a farmer in New Tecumseth, and Margaret Grant, the daughter of a mill manager. The Bantings were a financially stable family of British and Northern Irish origin. Banting's distant relative, the London-based undertaker William Banting, popularised a weight-loss diet in 1864, and the word "Banting" entered the Oxford English Dictionary as its description. His mother's relatives, the Grants, were of Scottish descent. With his family being located within a secure rural community, Banting was raised in prosperous circumstances. He was often called "Fred" or "Freddie." Farm life largely defined most of his boyhood. He felt excluded from his siblings, all multiple years his senior, and recalled that "my older brothers could not be bothered with me for the most part." When he began schooling at the age of seven, Banting was a shy, asocial boy who tired of the attendance and was bullied frequently. Early difficulties with spelling ensured poor marks in exams: "I simply could not spell. Every word seemed to have about three ways of spelling. It was a guess and I invariably guessed wrong." He later attributed these experiences as being the product of an inferiority complex. During his childhood, Banting devoted himself to farmwork, grew close with his mother, and sympathised with animals in the absence of other company.
=== Essendon === Thompson played for Essendon Football Club from 1983 until 1996, playing a total number of 202 games and kicked a total of 50 goals. Thompson played most of his football in the backline, gaining a reputation as a fierce competitor. He won the club award for "Most Determined Player" in 1984 and 1986, "Most Improved Player" and "Best Clubman" in 1985, and best-and-fairest awards in 1987 and 1990. He also finished in the top five in the best-and-fairest on four other occasions. Thompson played in the 1984 and 1985 premiership sides and captained the 1993 premiership team. In 2002, Thompson's contribution to the club was recognised when he was voted the 20th best Essendon player of all time in the "Champions of Essendon" list.
=== Lead poisoning === Magnesium sulfate was historically used as a treatment for lead poisoning. Prior to the development of chelation therapy, cases of accidental lead ingestion were often immediately treated with magnesium sulfate, which would cause the lead to be precipitated out and, with a high enough dose, literally purged from the digestive system as insoluble lead(II) sulfate. In this application, magnesium sulfate saw particular use in veterinary medicine of the early-to-mid 20th century; Epsom salt was already available on many farms for agricultural purposes, and it was often prescribed in the treatment of farm animals which inadvertently ingested lead.
Bush and Mikhail Gorbachev meet in Helsinki, Finland and issue a joint declaration condemning the invasion of Kuwait. October 1: The Rwandan Civil War begins, between the RPF and the Rwandan government. October 3: Germany is reunified. October 4: The Mozambican Civil War ends with the defeat of the anti-communist RENAMO, allowing the ruling Marxist party, FRELIMO, to remain in power. October 15: Mikhail Gorbachev is awarded the Nobel Peace Prize. October 25: The Kazakhstan Soviet Socialist Republic issues a declaration on state sovereignty which gives republic's operations precedence over all others. It is later renamed the following year on December 10, 1991, to the Republic of Kazakhstan. November 2: The Transnistria War begins in Moldova. November 21: The Paris Charter is ratified by the Organization for Security and Co-operation in Europe. December 23: Slovenia holds an independence referendum with a majority voting in favor.
Sources: en.wikipedia.org
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.
No, cardarine is not a steroid. It is classified as a PPARδ agonist. Its structure and receptor target differ from anabolic steroids.
No regulatory agency has approved cardarine as a medicine. It was investigated in early research but development was discontinued. It is not available as a prescription drug.
It binds and activates PPARδ, a nuclear receptor that influences gene expression related to fatty acid metabolism and energy balance. This mechanism has been studied mainly in animals and cell models, not established as a safe human therapy.