This is a working overview of regulatory status, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-08-01 and is reviewed periodically as new material appears.
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.
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, 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.
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 |
|---|---|---|
| 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 |
Cardarine is a synthetic compound also known as GW501516, GW-501516, and sometimes endurobol. It was developed as a selective agonist of peroxisome proliferator-activated receptor delta, a nuclear receptor involved in fatty acid oxidation and energy metabolism. The compound was studied in preclinical models for metabolic and cardiovascular conditions, but it did not become a marketed human medicine. In regulatory and anti-doping contexts, it is treated as a prohibited substance rather than a licensed medicine.
The pharmacological interest in cardarine centers on PPARδ activation and its downstream effects on lipid handling and mitochondrial function. In animal studies, PPARδ agonists have been associated with changes in exercise endurance and fatty acid utilization, though results vary by model and protocol. Human data remain sparse, and the absence of large controlled trials limits conclusions about efficacy. Researchers often describe the compound as a tool for probing PPARδ biology rather than a proven therapeutic agent.
GW501516 acts as an agonist at peroxisome proliferator-activated receptor delta, a nuclear receptor involved in transcription of genes related to lipid handling and energy use. Activation of PPARδ can shift skeletal muscle toward greater fatty acid oxidation in animal models, which is one reason it drew interest for metabolic disease and exercise research. The exact downstream effects depend on tissue, species, dose, and duration. Human data are sparse, so many proposed benefits remain hypotheses rather than established clinical outcomes.
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 April 1965, meprobamate was removed from the list of tranquilizers when experts ruled that the drug was a sedative, instead. The U.S. Pharmacopoeia published the ruling. At the same time, the Medical Letter disclosed that meprobamate could be addictive at doses not much above recommended. In December 1967, meprobamate was placed under abuse control amendments to the Food, Drug and Cosmetic Act. Records on production and distribution were required to be kept. Limits were placed on prescription duration and refills. On January 19, 2012, the European Medicines Agency withdrew marketing authorization in the European Union for all medicines containing meprobamate, "due to serious side effects seen with the medicine." The Agency's Committee for Medicinal Products for Human Use "concluded that the benefits of meprobamate do not outweigh its risks." In October 2013, Canada also withdrew marketing authorization.
== Determining quantity of carboamino in products == It is possible to determine how much carbamino is formed through the techniques of electron ionization and mass spectrometry. In determining the amount of product by mass spectrometry, a careful set of instructions are followed which allows for the carbamino adducts to be transferred to a vacuum for mass spectrometry. With the separation of the carbamino adducts in the ion sampling process, it should be that the pH does not change. Hence, mass spectrometry and electron ionization are a way to measure how much carbamino adduct there is in comparison to concentration of peptide in a solution.
The term behavioral addiction refers to a compulsion to engage in a natural reward despite adverse consequences. Addiction can exist without psychotropic drugs, an idea that was popularized by psychologist Stanton Peele. These are termed behavioral addictions. Such addictions may be passive or active, but they commonly contain reinforcing features, which are found in most addictions. Sexual behavior, eating, gambling, playing video games, and shopping are all associated with compulsive behaviors in humans and have been shown to activate the mesolimbic pathway and other parts of the reward system. Diagnostic manuals recognize only some of these as disorders. Gambling disorder is the only behavioral addiction classified as a clinical disorder in the DSM-5-TR, which lists internet gaming disorder as a condition requiring further study; the ICD-11 classifies both gambling disorder and gaming disorder as disorders due to addictive behaviors. Compulsive sexual behavior disorder, compulsive buying–shopping disorder, and problematic use of social media are discussed in the research literature as candidate addictive disorders, but are not classified as addictions in either manual.
Sources: en.wikipedia.org
=== Mechanism and antidote === NAPQI becomes toxic when GSH (glutathione) is depleted by an overdose of acetaminophen. Glutathione is an essential antidote to overdose. Glutathione conjugates to NAPQI and helps to detoxify it. In this capacity, it protects cellular protein thiol groups, which would otherwise become covalently modified; when all GSH has been spent, NAPQI begins to bind to certain enzymes like N-10 formyltetrahydrofolate dehydrogenase and glutamate dehydrogenase, reducing their activity and killing the cells in the process. This, along with the depletion of GSH which significantly impairs the function of mitochondria, plays a significant role in the development of paracetamol toxicity. The preferred treatment for an overdose of this painkiller is the administration of N-acetyl-L-cysteine (either via oral or IV administration), which is processed by cells to L-cysteine and used in the de novo synthesis of GSH.
=== Parasitic disease === Ivermectin has been researched in laboratory animals, as a potential treatment for trichinosis and trypanosomiasis. Ivermectin has also been tested on zebrafish infected with Pseudocapillaria tomentosa.
Therefore, surgical revision of transaxillary emplaced breast implants usually requires either an IMF incision or a periareolar incision. Transumbilical: a trans-umbilical breast augmentation (TUBA) is a less common implant-device emplacement technique wherein the incision is at the umbilicus (navel), and the dissection tunnels superiorly, up towards the bust. The TUBA approach allows emplacing the breast implants without producing visible scars upon the breast proper; but makes appropriate dissection and device-emplacement more technically difficult. A TUBA procedure is performed bluntly—without the endoscope's visual assistance—and is not appropriate for emplacing (pre-filled) silicone-gel implants, because of the great potential for damaging the elastomer silicone shell of the breast implant during its manual insertion through the short (~2.0 cm) incision at the navel, and because pre-filled silicone gel implants are incompressible, and cannot be inserted through so small an incision. Transabdominal: as in the TUBA procedure, in the transabdominoplasty breast augmentation (TABA), the breast implants are tunneled superiorly from the abdominal incision into bluntly dissected implant pockets, whilst the patient simultaneously undergoes an abdominoplasty.
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.
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.