Everything below concerns Nuclear receptor. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-07-05. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
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.
A persistent misconception is that cardarine is a fat-burning drug or a safe alternative to anabolic steroids. No approved therapeutic product exists, and human safety data are limited. The tumor findings in rodents remain a central concern in scientific reviews. Products sold online may contain inaccurate labels, impurities, or different compounds entirely, which complicates any assessment of effects. Independent testing of such products has reported frequent mislabeling. For these reasons, discussions in the literature emphasize risks and unknowns rather than benefits.
| Property | Value | Notes |
|---|---|---|
| Solubility | Soluble in dimethyl sulfoxide and some organic solvents; practically insoluble in water | Solvent choice affects laboratory handling |
| Typical storage | -20 °C, desiccated, protected from light | Common condition for research samples |
| Analytical method | Liquid chromatography–tandem mass spectrometry (LC-MS/MS) | Used for identification and quantification in biological or product samples |
| Common synonyms | GW501516, GW-501516, GSK-516, Endurobol | Names found in research and anti-doping literature |
| Regulatory status | Unapproved therapeutic; prohibited in competitive sport | Status can vary by country and context |
GW501516 acts as an agonist at the peroxisome proliferator-activated receptor delta, a nuclear receptor that regulates gene expression. Activation shifts transcription toward genes involved in fatty acid uptake, oxidation, and energy expenditure. The compound does not bind the androgen receptor and therefore differs from anabolic steroids and SARMs. In rodent models, this metabolic shift has been linked to increased running endurance and reduced fat accumulation. The exact downstream pathways in humans remain incompletely characterized.
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.
Cardarine can be detected in biological samples and product materials using liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). The method separates compounds by chromatography and identifies them by mass-to-charge transitions, allowing low-level detection in urine or blood. Sample preparation often involves enzymatic hydrolysis, solid-phase extraction, or protein precipitation. Certified reference materials and isotope-labeled internal standards improve quantification. Detection windows depend on metabolism, matrix, and assay sensitivity, so no single universal window applies.
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.
The capillaries are the smallest of the blood vessels and are part of the microcirculation. The microvessels have a width of a single cell in diameter to aid in the fast and easy diffusion of gasses, sugars and nutrients to surrounding tissues. Capillaries have no smooth muscle surrounding them and have a diameter less than that of red blood cells; a red blood cell is typically 7 micrometers outside diameter, capillaries typically 5 micrometers inside diameter. The red blood cells must distort in order to pass through the capillaries. These small diameters of the capillaries provide a relatively large surface area for the exchange of gasses and nutrients.
Injury: A mild form of myositis can occur with hard exercise. A more severe form of muscle injury, called rhabdomyolysis, is also associated with myositis. This is a condition where an injury to the patient's muscles causes them to quickly break down. Medicines: A variety of different medicines can cause myositis. One of the most common types of drugs that can cause myositis are statins, which are used to lower cholesterol levels. One of the most common side effects of statin therapy is muscle pain which, more rarely, can lead to myositis. Infection: The most common infectious cause of myositis is viral infections, such as the common cold. Other viruses, such as COVID-19, are also shown to be a rare cause of myositis. Benign acute childhood myositis has been described in children after prodromal viral infections with different viral agents. Bacterial, parasitic, and fungal infections are other infectious causes of myositis. Inherited muscle disease: Many inherited myopathies may have secondary myositis, including calpainopathy, dysferlinopathy, facioscapulohumeral muscular dystrophy, dystrophinopathy, and LMNA-associated myopathy. Autoimmune: Autoimmune disease is an abnormal immune response to specific body protein or other biomolecular target, such as one of the muscles. The three main types of idiopathic myositis (known as inflammatory myopathies) that typically test positive for autoantibodies are dermatomyositis, polymyositis, and inclusion body myositis. Other autoimmune diseases, such as systemic lupus erythematosus, can also cause myositis-like symptoms.
According to a survey investigation by the sociologist Jenny Hansson, Swedish national parliamentarians have an average workweek of 66 hours, including side responsibilities. Hansson's investigation further reports that the average Swedish national parliamentarian sleeps 6.5 hours per night.
=== Lower eyelid === The lower eyelid contains medial, central, and lateral fat compartments and transitions into the cheek at the tear trough. Supporting structures, including the canthal tendons, help maintain eyelid position. Fat protrusion and contour changes contribute to the appearance of under-eye “bags.”
Sources: en.wikipedia.org
The mine chose to send all ore to the crusher and to concentrate on copper production due to the rising price of copper on the world market. The price of natural untreated Sleeping Beauty turquoise has risen dramatically since the mine's closing. The Kingman Mine as of 2015 still operates alongside a copper mine outside of the city. Other mines include the Blue Bird mine, Castle Dome, and Ithaca Peak, but they are mostly inactive due to the high cost of operations and federal regulations. The Phelps Dodge Lavender Pit mine at Bisbee ceased operations in 1974 and never had a turquoise contractor. All Bisbee turquoise was "lunch pail" mined. It came out of the copper ore mine in miners' lunch pails. Morenci and Turquoise Peak are either inactive or depleted. Nevada is the country's other major producer, with more than 120 mines which have yielded significant quantities of turquoise. Unlike elsewhere in the US, most Nevada mines have been worked primarily for their gem turquoise and very little has been recovered as a byproduct of other mining operations. Nevada turquoise is found as nuggets, fracture fillings and in breccias as the cement filling interstices between fragments. Because of the geology of the Nevada deposits, a majority of the material produced is hard and dense, being of sufficient quality that no treatment or enhancement is required. While nearly every county in the state has yielded some turquoise, the chief producers are in Lander and Esmeralda counties.
==== 1.A α-type channels ==== 1.A.1 Voltage-gated ion channel superfamily 1.A.2 Inward-rectifier K+ channel family 1.A.3 Ryanodine-inositol-1,4,5-trisphosphate receptor Ca2+ channel family 1.A.4 Transient receptor potential Ca2+ channel family 1.A.5 Polycystin cation channel family 1.A.6 Epithelial Na+ channel family 1.A.7 ATP-gated P2X receptor cation channel family 1.A.8 Major intrinsic protein superfamily 1.A.9 Neurotransmitter receptor, Cys loop, ligand-gated ion channel family 1.A.10 Glutamate-gated ion channel family of neurotransmitter receptors 1.A.11 Ammonium channel transporter family 1.A.12 Intracellular chloride channel family 1.A.13 Epithelial chloride channel family 1.A.14 Testis-enhanced gene transfer family 1.A.15 Nonselective cation channel-2 family 1.A.16 Formate-nitrite transporter family 1.A.17 Calcium-dependent chloride channel family 1.A.18 Chloroplast envelope anion-channel-forming Tic110 family 1.A.19 Type A influenza virus matrix-2 channel family 1.A.20 BCL2/Adenovirus E1B-interacting protein 3 family 1.A.21 Bcl-2 family 1.A.22 Large-conductance mechanosensitive ion channel 1.A.23 Small-conductance mechanosensitive ion channel 1.A.24 Gap-junction-forming connexin family 1.A.25 Gap-junction-forming innexin family 1.A.26 Mg2+ transporter-E family 1.A.27 Phospholemman family 1.A.28 Urea transporter family 1.A.29 Urea/amide channel family 1.A.30 H+- or Na+-translocating bacterial MotAB flagellar motor/ExbBD outer-membrane transport energizer superfamily 1.A.31 Annexin family 1.A.32 Type B influenza virus NB channel family 1.A.33 Cation-channel-forming heat shock protein 70 family 1.A.34 Bacillus gap junction-like channel-forming complex family 1.A.35 CorA metal ion transporter family 1.A.36 Intracellular chloride channel family 1.A.37 CD20 Ca2+ channel family 1.A.38 Golgi pH regulator family 1.A.39 Type C influenza virus CM2 channel family 1.A.40 Human immunodeficiency virus type I Vpu channel family 1.A.41 Avian reovirus p10 Vvroporin family 1.A.42 HIV viral protein R family 1.A.43 Camphor resistance or fluoride exporter family 1.A.44 Pore-forming tail Tip pb2 protein of phage T5 family 1.A.45 Phage P22 injectisome family 1.A.46 Anion channel-forming bestrophin family 1.A.47 Nucleotide-sensitive anion-selective channel, ICln family 1.A.48 Anion channel Tweety family 1.A.49 Human coronavirus ns12.9 viroporin family 1.A.50 Phospholamban (Ca2+-channel and Ca2+-ATPase regulator) family 1.A.51 The Voltage-gated Proton Channel (VPC) Family 1.A.52 The Ca2+ Release-activated Ca2+ (CRAC) Channel (CRAC-C) Family 1.A.53 The Hepatitis C Virus P7 Viroporin Cation-selective Channel (HCV-P7) Family 1.A.54 The Presenilin ER Ca2+ Leak Channel (Presenilin) Family 1.A.55 The Synaptic Vesicle-Associated Ca2+ Channel, Flower (Flower) Family 1.A.56 The Copper Transporter (Ctr) Family 1.A.57 The Human SARS Coronavirus Viroporin (SARS-VP) 1.A.58 The Type B Influenza Virus Matrix Protein 2 (BM2-C) Family 1.A.59 The Bursal Disease Virus Pore-Forming Peptide, Pep46 (Pep46) Family 1.A.60 The Mammalian Reovirus Pre-forming Peptide, Mu-1 (Mu-1) Family 1.A.61 The Insect Nodavirus Channel-forming Chain F (Gamma-Peptide) Family 1.A.62 The Homotrimeric Cation Channel (TRIC) Family 1.A.63 The Ignicoccus Outer Membrane α-helical Porin (I-OMP Family 1.A.64 The Plasmolipin (Plasmolipin) Family 1.A.65 The Coronavirus Viroporin E Protein (Viroporin E) Family 1.A.66 The Pardaxin (Pardaxin) Family 1.A.67 The Membrane Mg2+ Transporter (MMgT) Family 1.A.68 The Viral Small Hydrophobic Viroporin (V-SH) Family 1.A.69 The Heteromeric Odorant Receptor Channel (HORC) Family 1.A.70 The Molecule Against Microbes A (MamA) Family 1.A.71 The Brain Acid-soluble Protein Channel (BASP1 Channel) Family 1.A.72 The Mer Superfamily 1.A.73 The Colicin Lysis Protein (CLP) Family 1.A.74 The Mitsugumin 23 (MG23) Family 1.A.75 The Mechanical Nociceptor, Piezo (Piezo) Family 1.A.76 The Magnesium Transporter1 (MagT1) Family 1.A.77 The Mg2+/Ca2+ Uniporter (MCU) Family 1.A.78 The K+-selective Channel in Endosomes and Lysosomes (KEL) Family 1.A.79 The Cholesterol Uptake Protein (ChUP) or Double Stranded RNA Uptake Family 1.A.80 The NS4a Viroporin (NS4a) Family 1.A.81 The Low Affinity Ca2+ Channel (LACC) Family 1.A.82 The Hair Cell Mechanotransduction Channel (HCMC) Family 1.A.83 The SV40 Virus Viroporin VP2 (SV40 VP2) Family 1.A.84 The Calcium Homeostasis Modulator Ca2+ Channel (CALHM-C) Family 1.A.85 The Poliovirus 2B Viroporin (2B Viroporin) Family 1.A.86 The Human Papilloma Virus type 16 (HPV16) L2 Viroporin (L2 Viroporin) Family 1.A.87 The Mechanosensitive Calcium Channel (MCA) Family 1.A.88 The Fungal Potassium Channel (F-Kch) Family 1.A.89 The Human Coronavirus 229E Viroporin (229E Viroporin) Family 1.A.90 The Human Metapneumovirus (HMPV) Viroporin (HMPV-Viroporin) Family 1.A.91 The Cytoadherence-linked Asexual Protein 3.2 of Plasmodium falciparum (Clag3) Family 1.A.92 The Reovirus Viroporin VP10 (RVP10) Family 1.A.93 The Bluetongue Virus Non-Structural Protein 3 Viroporin (NS3) Family 1.A.94 The Rotavirus Non-structural Glycoprotein 4 Viroporin (NSP4) Family 1.A.95 The Ephemerovirus Viroporin (EVVP) Family 1.A.96 The Human Polyoma Virus Viroporin (PVVP) Family 1.A.97 The Human Papillomavirus type 16 E5 Viroporin (HPV-E5) Family 1.A.98 Human T-Lymphotropic Virus 1 P13 protein (HTLV1-P13) Family 1.A.99 The Infectious Bronchitis Virus Envelope Small Membrane Protein E (IBV-E) Family 1.A.100 The Rhabdoviridae Putative Viroporin, U5 (RV-U5) Family 1.A.101 The Peroxisomal Pore-forming Pex11 (Pex11) Family 1.A.102 Influenza A viroporin PB1-F2 (PB1-F2) Family 1.A.103 The Simian Virus 5 (Parainfluenza Virus 5) SH (SV5-SH) Family 1.A.104 The Proposed Flagellar Biosynthesis Na+ Channel, FlaH (FlaH) Family 1.A.105 The Mixed Lineage Kinase Domain-like (MLKL) Family 1.A.106 The Calcium Load-activated Calcium Channel (CLAC) Family 1.A.107 The Pore-forming Globin (Globin) Family
==== Honorary appointments ==== Honorary General of the Swedish Army, 1888 Colonel-in-chief of the 1st King's Dragoon Guards, British Army, 25 March 1896 – 1914 Colonel-in-chief of the Kexholm Life Guards Grenadier Regiment, Russian Army, until 26 June 1914 Colonel-in-chief of the 12th Belgorod Lancer Regiment, Russian Army, until 26 June 1914 Colonel-in-chief of the 16th (Schleswig-Holstein) Hussars, German Army Colonel-in-chief of the 122nd (Emperor Francis Joseph of Austria, King of Hungary (4th Württemberg) Fusiliers Honorary Colonel of the 38th León Infantry Regiment, Spanish Army, 30 November 1905 Field Marshal of the British Army, 1 September 1903 – 1914
Sources: en.wikipedia.org
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.
No. It is not an anabolic-androgenic steroid; it is a synthetic PPARδ agonist. Because it is banned in sport, it is sometimes grouped with doping agents even though its chemical class differs from steroids.
Human data are limited and development was discontinued, so major effects and long-term risks are not well characterized. Some early studies examined metabolic markers, but they do not provide a basis for unsupervised use.
No. Cardarine has not received approval for human therapeutic use in major jurisdictions. It remains an investigational compound.