GW501516 is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Updated 2026-08-01. Numbers and descriptions here follow the published literature rather than marketing material.
A common misconception is that cardarine has been proven safe for human use. In reality, human clinical data are limited, and long-term animal studies have raised concerns about cancer. Another misconception is that it is a supplement or vitamin-like compound. It is a synthetic research chemical with no approved medical indication. Scientific discussion often focuses on its mechanism and detection rather than therapeutic use. Regulatory and anti-doping literature treats it primarily as a prohibited substance.
Cardarine is explicitly prohibited by the World Anti-Doping Agency under the class of PPARδ agonists. Its presence in urine or blood samples can be detected using mass spectrometry-based methods, often liquid chromatography-tandem mass spectrometry. Athletes who test positive may face sanctions, including bans from competition. The compound is also regulated as a prescription-only or unapproved drug in many countries. Enforcement varies by jurisdiction, and some regions treat it as a controlled substance. Online sales may occur despite these restrictions, creating quality and legal risks.
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.
Safety discussions about cardarine frequently cite rodent carcinogenicity findings reported in the 2000s. In those studies, treated animals developed tumors at multiple sites, leading sponsors to discontinue clinical development. The relevance of these findings to humans has not been resolved, but they are a major reason the compound is not approved. Current literature emphasizes uncertainty about long-term effects and the risks of unregulated use. Regulators and health agencies have not established a safe human exposure level.
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.
| Property | Value | Notes |
|---|---|---|
| Regulatory status | Prohibited in sport | Listed by WADA as a PPARδ agonist. |
| Typical detection matrix | Urine | Most common sample for anti-doping analysis. |
| Common analytical method | LC-MS/MS | Liquid chromatography-tandem mass spectrometry. |
| Common synonyms | GW501516, GSK-516, endurobol | Names found in research and fitness contexts. |
| Typical detection window | Variable | Depends on dose, route, and individual metabolism. |
Cardarine is not approved for human therapeutic use in any major jurisdiction. It appears on the World Anti-Doping Agency Prohibited List as a PPARδ agonist within the hormone and metabolic modulators category. Sports organizations test for it because it has been detected in athlete samples and seized products. Regulatory actions against marketed research chemical versions have occurred in several countries, though enforcement varies. Availability through unregulated channels complicates oversight.
Analytical laboratories typically identify cardarine and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is a common matrix in anti-doping testing, while blood and tissue may be used in research settings. Detection windows depend on the assay, the sample matrix, and the compound's metabolism. Because cardarine is extensively metabolized, laboratories often target specific metabolites to improve sensitivity and confirmation. Reference standards are required for reliable quantification. Method validation includes checks for selectivity, linearity, and carryover.
GW501516 acts as a ligand for PPAR delta, a nuclear receptor that regulates transcription of genes involved in fatty acid oxidation and energy use. Activation of this receptor in skeletal muscle shifts metabolism toward fat burning in animal models. The compound does not burn fat directly; it changes gene expression over hours to days. Researchers study it to understand metabolic flexibility and exercise adaptation. Effects observed in rodents are not automatically expected in humans.
Preclinical research reported that GW501516 increased running endurance in mice and improved lipid profiles in some animal species. Early human trials explored effects on high-density lipoprotein cholesterol, triglycerides, and glucose handling, but the program was discontinued. Published human data are sparse and do not establish efficacy for any condition. Studies also examined PPAR delta in cancer biology, with conflicting findings across models. The relationship between receptor activation, tissue context, and disease risk remains an active area of investigation.
Anti-doping laboratories identify GW501516 and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is the usual matrix, and detection can occur after the parent compound has cleared from blood. The exact detection window depends on dose, formulation, individual metabolism, and assay sensitivity. Because the compound is prohibited at all times, athletes are subject to testing in and out of competition. Analytical methods continue to improve as new metabolites and designer analogs are characterized.
At the molecular level, GW501516 binds and activates PPARδ, a nuclear receptor that regulates transcription. Activation shifts expression of genes involved in fatty acid oxidation, energy expenditure, and lipid transport in skeletal muscle and liver. Animal studies report increased endurance and altered lipid profiles after exposure. Human data are limited to small trials and do not establish long-term safety or efficacy. PPARδ also has roles in cell proliferation, so the relationship between activation and cancer risk remains an open question.
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.
=== PDH dephosphorylation === Insulin stimulates the activity of pyruvate dehydrogenase phosphatase. The phosphatase removes the phosphate from pyruvate dehydrogenase activating it and allowing for conversion of pyruvate to acetyl-CoA. This mechanism leads to the increased rate of catalysis of this enzyme, so increases the levels of acetyl-CoA. Increased levels of acetyl-CoA will increase the flux through not only the fat synthesis pathway but also the citric acid cycle.
1993/3026) Value Added Tax (General) (Amendment) (No.7) Regulations 1993 (S.I. 1993/3027) Value Added Tax (Cash Accounting) (Amendment) (No. 2) Regulations 1993 (S.I. 1993/3028) Trade Marks and Service Marks (Fees) (Amendment) Rules 1993 (S.I. 1993/3029) Local Government Superannuation (Educational Institutions) Regulations 1993 (S.I. 1993/3030) Transfrontier Shipment of Radioactive Waste Regulations 1993 (S.I. 1993/3031) Gipsy Encampments (Metropolitan District of Salford) Order 1993 (S.I. 1993/3032) A564 Trunk Road Stoke—Derby Route (Doveridge Bypass and Slip Roads) Order 1993 (S.I. 1993/3033) A564 Trunk Road Stoke—Derby Route (Doveridge Bypass) (Detrunking) Order 1993 (S.I. 1993/3034) Local Government Act 1988 (Defined Activities) (Exemption) (Cambridge City Council) Order 1993 (S.I. 1993/3035) Sheep Annual Premium and Suckler Cow Premium Quotas (Amendment) Regulations 1993 (S.I. 1993/3036) Census of Production Order 1993 (S.I. 1993/3037) Licensing of Air Carriers (Second Amendment and Other Provisions) Regulations 1993 (S.I. 1993/3039) Access for Community Air Carriers to Intra-Community Air Routes (Amendment and Other Provisions) Regulations 1993 (S.I. 1993/3040) Air Fares (Second Amendment) Regulations 1993 (S.I. 1993/3041) Airports Slot Allocation (Amendment) Regulations 1993 (S.I. 1993/3042) Local Government Superannuation (Membership) Regulations 1993 (S.I. 1993/3043) Local Government Superannuation (Scotland) Amendment (No.3) Regulations 1993 (S.I. 1993/3044) Land Registration (Leasehold Reform) Rules 1993 (S.I.
== Further reading == 2012 CRE Toolkit - Guidance for Control of Carbapenem-resistant Enterobacteriaceae (CRE) CDC Healthcare-associated Infections, March 2013 Carbapenemase-producing Enterobacteriaceae (CPE) Affects Hospital Patients Manchester Royal Infirmary were discovered to have the superbug known as carbapenemase-producing enterobacteriaceae, known for short as CPE
=== Extended market indices === Russell 3000 Index: The Russell 3000 Index measures the performance of the largest 3,000 U.S. companies representing approximately 98% of the investable U.S. equity market.
Sources: en.wikipedia.org
=== Phenethylamines === Phenethylamines can be classified into ring-substituted and non-ring-substituted form. Ring-substituted Phenethylamines include 'D-series' and '2C-series' while common non-ring-substituted Phenethylamines contain Benzodifurans, PMMA, etc.
=== Primary ion source === Three types of ion source are used for SSIMS: electron-impact ionization, surface ionization, or liquid-metal ion sources. In the electron-impact ion source, electrons from a heated filament (cathode) are accelerated towards an anode by a voltage difference where they ionize supply-gas atoms on impact. This source usually operates with noble gases. Typically, the energy is variable from 0.1–5 keV, allowing spot sizes from ~50 μm to several millimeters. Surface ionization sources use Cs+ as the primary beam sources for TOF SIMS. Evaporation of caesium from a heated tungsten surface occurs both as atoms and ions. These ions are then accelerated away from the emitting surface. Since no collisions are involved, the ion beam is very pure, and since evaporation is by thermal means, the energy spread is very small, ~2kT (0.2 eV). The low energy spread and high intrinsic brightness of the ion sources offers the possibility of obtaining small spot sizes. Liquid-metal ion sources draw a liquid metal (usually gallium or bismuth) from a heated reservoir over a tip (radius ≈5 μm) of a needle. An electrostatic field is produced at the tip by an extraction electrode biased negatively in front of the tip. Opposing electrostatic and surface-tension forces acting on the liquid film produce a conical shape with a high-radius-of-curvature cusp (≈2 μm) protruding from the tip. From this cusp field, ion emission occurs, by means of the process of field evaporation.
Known colloquially as "Laborit's drug", chlorpromazine was released onto the market in 1953 by Rhône-Poulenc and given the trade name Largactil, derived from large "broad" and acti* "activity". Deniker then visited America, where the publication of their work alerted the American psychiatric community that the new treatment might represent a real breakthrough. Heinz Lehmann of the Verdun Protestant Hospital in Montreal trialled it in seventy patients and also noted its striking effects, with patients' symptoms resolving after many years of unrelenting psychosis. By 1954, chlorpromazine was being used in the United States to treat schizophrenia, mania, psychomotor excitement, and other psychotic disorders. Rhône-Poulenc licensed chlorpromazine to Smith Kline & French (today's GlaxoSmithKline) in 1953. In 1955 it was approved in the United States for the treatment of emesis (vomiting). The effect of this drug in emptying psychiatric hospitals has been compared to that of penicillin on infectious diseases. The popularity of the drug fell in the late 1960s as newer drugs came on the scene. From chlorpromazine several other similar antipsychotics were developed, leading to the discovery of antidepressants. Chlorpromazine largely replaced electroconvulsive therapy, hydrotherapy, psychosurgery, and insulin shock therapy. By 1964, about fifty million people worldwide had taken it. Chlorpromazine, in widespread use for fifty years, remains a "benchmark" drug in the treatment of schizophrenia, an effective drug although not a perfect one.
Sources: en.wikipedia.org
Fumarate, produced from the purine nucleotide cycle, is an intermediate of TCA cycle and enters the mitochondria by converting into malate and utilizing the malate shuttle where it is converted into oxaloacetic acid (OAA). During exercise, OAA either enters into TCA cycle or converts into aspartate in the mitochondria. As the purine nucleotide cycle produces ammonia (see below in ammonia synthesis), skeletal muscle needs to synthesize glutamate in a way that does not further increase ammonia, and as such the use of glutaminase to produce glutamate from glutamine would not be ideal. Also, plasma glutamine (released from the kidneys) requires active transport into the muscle cell (consuming ATP). Consequently, during exercise when the ATP reservoir is low (ADP>ATP), glutamate is produced from branch-chained amino acids (BCAAs) and α-ketoglutarate, as well as from alanine and α-ketoglutarate. Glutamate is then used to produce aspartate. The aspartate enters the purine nucleotide cycle, where it is used to convert IMP into S-AMP.
=== BASF refounded (1952) === On 28 July 1948, an explosion occurred at a BASF site in Ludwigshafen, killing 207 people and injuring 3818. In 1952, BASF was refounded under its name following the efforts of former Nazi Party member Carl Wurster, who served in Nazi Germany as Wehrwirtschaftsführer (war economy leader). With the German economic miracle in the 1950s, BASF added synthetics such as nylon to its product range. BASF developed Polystyrene in the 1930s and invented Styropor in 1951.
Application of a tourniquet to the bitten limb is generally not recommended. There is no convincing evidence that it is an effective first-aid tool as ordinarily applied. Tourniquets have been found to be completely ineffective in the treatment of Crotalus durissus bites, but some positive results have been seen with properly applied tourniquets for cobra venom in the Philippines. Uninformed tourniquet use is dangerous since reducing or cutting off circulation can lead to gangrene, which can be fatal. The use of a compression bandage is generally as effective, and much safer. Cutting open the bitten area, an action often taken before suction, is not recommended since it causes further damage and increases the risk of infection; the subsequent cauterization of the area with fire or silver nitrate (also known as infernal stone) is also potentially threatening. Sucking out venom, either by mouth or with a pump, does not work and may harm the affected area directly. Suction started after three minutes removes a clinically insignificant quantity—less than one-thousandth of the venom injected—as shown in a human study. In a study with pigs, suction not only caused no improvement but led to necrosis in the suctioned area. Suctioning by mouth presents a risk of further poisoning through the mouth's mucous tissues. The helper may also release bacteria into the person's wound, leading to infection.
Sources: en.wikipedia.org
Yes, WADA prohibits cardarine as a PPARδ agonist. It appears on the prohibited list and can be detected in urine or blood. Athletes using it risk sanctions.
Detection usually uses liquid chromatography-tandem mass spectrometry after sample cleanup. Laboratories look for the parent compound or metabolites. The method requires validated reference standards and controls.
Legality varies by country. In many places it is an unapproved drug and cannot be legally sold for human consumption. Purchasing from online vendors carries legal and quality risks.
Cardarine is an investigational synthetic compound that acts as a PPARδ agonist. It is also known as GW501516 and has been studied mainly in preclinical research. It is not an approved medicine.