If you have been reading about research chemical and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Updated 2026-05-25. Numbers and descriptions here follow the published literature rather than marketing material.
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.
Sporting authorities added GW501516 to prohibited lists after it appeared in athlete samples and online markets. The World Anti-Doping Agency classifies it as a hormone and metabolic modulator, and its use can lead to an anti-doping rule violation. Some early laboratory work suggested effects on fatty acid oxidation and endurance-related metabolism in animals, but those findings do not establish safe or effective use in people. Reports of adverse events in humans are scarce and often anecdotal, which complicates risk assessment.
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.
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.
| Property | Value | Notes |
|---|---|---|
| IUPAC name | {4-[({4-methyl-2-[4-(trifluoromethyl)phenyl]-1,3-thiazol-5-yl}methyl)sulfanyl]phenoxy}acetic acid | Systematic name for GW501516 |
| CAS Registry Number | 317318-70-0 | Unique identifier for the parent compound |
| Molecular formula | C21H18F3NO3S2 | Includes carbon, hydrogen, fluorine, nitrogen, oxygen, and sulfur |
| Molecular weight | 453.5 g/mol | Approximate value for the neutral form |
| Appearance | White to off-white powder | Typical description for purified laboratory material |
Products sold as cardarine have been found to contain incorrect compounds, variable amounts, or no active ingredient at all. Independent testing is required to verify identity and purity. Common analytical approaches include high-performance liquid chromatography, mass spectrometry, and nuclear magnetic resonance for structural confirmation. These methods can distinguish GW501516 from related PPAR agonists and from unrelated steroids. For regulators and researchers, such verification is central to interpreting both biological results and adverse event reports.
Cardarine is prohibited in competitive sport under the World Anti-Doping Agency code, where it is classified as a metabolic modulator. It is not approved as a prescription medicine in the United States, European Union, or other major markets. Regulatory action has focused on its presence in sports and in products marketed as research chemicals. Because it has no accepted medical indication, supply is often unregulated. This status creates legal and safety uncertainties for anyone who encounters the substance.
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.
Literature on cardarine often separates receptor pharmacology from toxicology. Mechanistic papers describe PPARδ activation and gene expression changes, while safety assessments focus on carcinogenicity and species differences. Questions remain about whether rodent tumors arise through PPARδ-dependent or off-target mechanisms. Another open area is how human metabolism and exposure compare with those in animal studies. Analytical methods such as liquid chromatography–mass spectrometry are used to confirm identity in biological and product samples.
== Pathology == VIP is overproduced in VIPoma. In addition to VIPoma, VIP has a role in osteoarthritis (OA). While there is existing conflict in whether down-regulation or up-regulation of VIP contributes to OA, VIP has been shown to prevent cartilage damage in animals.
The intracellular KOR signaling axis involves continued Gi/o coupling on late endosomal membranes, sustained suppression of adenylyl cyclase and cAMP production, and prolonged recruitment of ERK pathway components through Gβγ-dependent mechanisms, thereby establishing a biochemical niche for chronic dynorphin signaling distinct from acute plasma membrane responses. This signaling permits differential integration of intracellular second messenger systems and transcriptional responses compared to plasma membrane-restricted coupling.
Hence, although DOM-NBOMe could still be an active psychedelic in humans, it may have attenuated hallucinogenic effects compared to non-25-NB DOx psychedelics. The doses of DOM-NBOMe producing the head-twitch response were not reported.
=== Discovery === Copernicium was first created on 9 February 1996, at the Gesellschaft für Schwerionenforschung (GSI) in Darmstadt, Germany, by Sigurd Hofmann, Victor Ninov et al. This element was created by firing accelerated zinc-70 nuclei at a target made of lead-208 nuclei in a heavy ion accelerator. A single atom of copernicium was produced with a mass number of 277. (A second was originally reported, but was found to have been based on data fabricated by Ninov, and was thus retracted.)
Sources: en.wikipedia.org
The Cabinet approved a 50,000-square-foot (4,600 m2) building at £3 per square foot in 1947 (equivalent to A$229 in 2022), but the design Florey and Sanders agreed upon was a 235,000-square-foot (21,800 m2) building at £4 per square foot (equivalent to A$306 in 2022). In 1950, the Cabinet approved £810,000 (equivalent to A$47,137,000 in 2022) for the building and £200,000 (equivalent to $11,639,000 in 2022) for equipment. People were also important, and Florey had a fairly free hand hiring his professors. He recruited Hugh Ennor as his professor of biochemistry, Adrien Albert as professor of medical chemistry, and Frank Fenner as professor of microbiology. A. F. Bunker was appointed the laboratory manager, and he outfitted the building. Florey visited Canberra in March 1953, but he made it clear that he did not wish to continue as acting director of the John Curtin School of Medical Research, nor take up the position of director, although he reluctantly agreed to continue as an advisor. He was pessimistic about the project, writing home to Jennings that "it will be a miracle if this place can be given a real university atmosphere". By this time the project was in jeopardy; while the prime minister, Robert Menzies, supported it, a faction in the Cabinet led by Richard Casey and Wilfrid Kent Hughes did not; they were chagrined that it was named after a man they despised, and that it called itself a school when it would not train doctors. Changing the name required amending the act, and this did not occur.
=== Protactinium-234m === Protactinium-234m is a member of the uranium series with a half-life of 1.17 minutes. It was discovered in 1913 by Kazimierz Fajans and Oswald Helmuth Göhring, who named it brevium for its short half-life. It is now believed that all decays of the parent thorium-234 produce this isomer and the ground state is observed because of (invisible) IT decay. Protactinium-234m has the same mass (same number of protons and neutrons) as protactinium-234, the difference merely visible in their non-identical half-life, with protactinium-234m having a noticeably shorter lifespan. This phenomenon is called nuclear isomerism.
=== Anticarcinogenic activity === The anticancer activity of bovine lactoferrin (bLF) has been demonstrated in experimental lung, bladder, tongue, colon, and liver carcinogeneses on rats, possibly by suppression of phase I enzymes, such as cytochrome P450 1A2 (CYP1A2). Also, in another experiment done on hamsters, bovine lactoferrin decreased the incidence of oral cancer by 50%. Currently, bLF is used as an ingredient in yogurt, chewing gums, infant formulas, and cosmetics.
Contrary to popular belief, nicotine itself does not cause cancer in humans, although it is unclear whether it functions as a tumor promoter as of 2012. A 2018 report by the US National Academies of Sciences, Engineering, and Medicine concludes, "[w]hile it is biologically plausible that nicotine can act as a tumor promoter, the existing body of evidence indicates this is unlikely to translate into increased risk of human cancer." Although nicotine is classified as a non-carcinogenic substance, it can still theoretically promote tumor growth and metastasis as evidenced from alterations. Nicotine induces several processes, some of them via nicotine's effects on immune function, that contribute to cancer progression in both smoking-related and non-smoking-related cancers, including cell cycle progression, epithelial-to-mesenchymal transition, migration, invasion, angiogenesis, and evasion of apoptosis. These effects are primarily mediated through nicotinic acetylcholine receptors (nAChRs), particularly the α7 subtype, and to a lesser extent, β-adrenergic receptors (β-ARs). Activation of these receptors triggers several signaling cascades crucial in cancer biology, notably the MAPK/ERK pathway, PI3K/AKT pathway, and JAK-STAT signaling. Nicotine potentially promotes lung cancer development by enhancing proliferation, angiogenesis, migration, invasion, and epithelial–mesenchymal transition (EMT) via nAChRs, which are present in lung cancer cells. Additionally, nicotine-induced EMT contributes to drug resistance in cancer cells.
Interestingly, this contact inhibition of locomotion among NC cells is coupled with chemical coattraction between NC cells, which allows the cells to keep in motion for efficient migration as well as to stay together, respectively, leading to collective migration. Cells are most often influenced by surrounding cells towards collective migration in development, such as polster cells which are the first to internalize at the start of gastrulation in zebrafish. Unlike neural crest cells, these cells don't exhibit contact inhibition of locomotion or coattraction, but instead migrate collectively due to E-cadherin interactions between leading cells and following cells. The following polster cells are polarized and migrate towards the animal pole of the embryo for unknown reasons, reaching their actin-rich protrusions towards the leading cells and inducing interactions between E-cadherin proteins located on following cell protrusion membranes and leading cell membranes. The interactions between E-cadherins create tension, which causes internal a-catenin (bridging extracellular E-cadherin with intracellular actin) to be stretched into an open configuration, leading to the recruitment of vinculin and eventually the orientation of actin towards the same direction of migration as the following cells. Without these E-cadherin interactions, leading cells will exhibit non-directional migration.
Sources: en.wikipedia.org
No. Major drug regulators have not approved GW501516 for treating any medical condition. Products sold as cardarine are typically unapproved research chemicals or supplements, so their contents and safety are not assured.
It is prohibited by the World Anti-Doping Agency as a hormone and metabolic modulator. Athletes who test positive for GW501516 can face sanctions, including suspensions and loss of results.
Cardarine is a common or trade-style name, while GW501516 is the research code for the same chemical entity. Some sources also use Endurobol or GSK-516. The names refer to the same compound, not distinct drugs.
Anti-doping laboratories typically use LC-MS/MS to detect GW501516 and its metabolites in urine. The method is sensitive and can identify the compound at low concentrations. Detection depends on sample timing, metabolism, and the specific assay.