If you have been reading about LC-MS/MS 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.
Last reviewed on 2026-05-07. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Activation of PPARδ changes transcription of genes involved in fatty acid transport, mitochondrial function, and skeletal muscle fuel preference. In rodent studies, pharmacological PPARδ activation was associated with increased endurance and altered body composition. These findings generated interest in performance enhancement, but species differences and study designs limit direct extrapolation to humans. Small human trials were conducted in the 2000s and later discontinued. The extent to which cardarine produces similar metabolic or performance effects in people remains an open question.
The compound is typically described as a laboratory compound rather than a therapeutic product. Published reports have explored its role in lipid disorders, insulin sensitivity, and exercise metabolism, yet no major drug regulator has approved it for medical use. Commercial samples sold under the cardarine name may vary in purity and identity. Analytical confirmation is therefore necessary when the material is discussed in scientific or regulatory contexts. Its classification as a prohibited substance in sport further shapes how it is studied and reported.
| Property | Value | Notes |
|---|---|---|
| Regulatory status | Prohibited in sport; not approved as medicine | Listed by WADA at all times. |
| Common synonyms | GW501516, GW-501516, endurobol | Cardarine is a colloquial name. |
| Typical analytical method | LC-MS/MS | Detects parent compound and metabolites. |
| Common test matrix | Urine | Blood and dried blood spots also possible. |
| Legal classification | Varies by country | Often treated as unapproved drug or research chemical. |
In laboratory settings, cardarine is studied as a tool compound for probing PPARδ biology. Published experiments often use cell cultures, rodent models, or isolated tissues. Some investigations focus on metabolic effects, while others assess potential risks such as carcinogenicity observed in long-term animal studies. Because human trials are sparse, most knowledge comes from preclinical work and adverse event reports. Scientific literature frequently notes the gap between animal findings and human outcomes. The compound is not a dietary supplement and is not intended for human consumption.
Cardarine is a common name for GW501516, a synthetic compound developed in the 1990s through research collaborations involving GlaxoSmithKline. It belongs to a class of molecules known as peroxisome proliferator-activated receptor delta agonists. Early studies explored its effects on lipid metabolism and energy expenditure in animal models. The compound was never approved as a human medicine, and clinical development was discontinued. In the years since, it has appeared in fitness and bodybuilding communities as a performance-enhancing substance. Regulatory agencies classify it as an unapproved drug.
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.
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.
Anti-doping laboratories detect GW501516 and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is the most common matrix, though blood and dried blood spots may also be used in some programs. Detection depends on factors such as dose, timing, metabolism, and the sensitivity of the assay. Published methods describe limits of detection in the low nanogram per milliliter range for related compounds. Exact detection windows are not fixed for all situations and remain an area of ongoing study.
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.
Laboratory detection of cardarine typically involves sample preparation followed by chromatographic separation and mass spectrometric identification. Urine is the most common matrix for anti-doping tests, though blood and hair have also been explored. Methods can target the parent compound or its metabolites, depending on the expected window of detection. Reference standards are required for accurate quantification. Matrix effects and dilution can influence results, so laboratories use internal standards and validation protocols. The exact detection window varies with dose, route, and individual metabolism.
The botched embalming of Pope Pius XII (1876–1958; pope 1939–1958) by a charlatan doctor – which only sped up the rate of decomposition – led to his body turning black and his nose falling off while lying in state, and the body disintegrated in the coffin. The Swiss Guards stationed around Pius XII's body were forced to change shifts every 10 to 15 minutes, since the body's odor caused some guards to pass out. The doctor who performed the embalming had also taken photos of the pontiff in his death throes, intending to sell them to tabloids. The Italian tabloids refused to buy the photos, and the doctor was banned from entering the Vatican City-State by John XXIII, who furthermore prohibited any photography of a deceased pope until the body is properly vested and laid out. Charles XII (1682–1718) is one of several Swedish kings to have been embalmed. When Charles XII's sarcophagus was opened in 1917, his features were still recognizable, almost 200 years after his death. Photographs of his remains clearly show the gunshot wound to his head leading to his death. The body of Pope John XXIII (1881–1963; pope 1958–1963) is on display on an altar on the main floor of the Basilica of Saint Peter after having been exhumed from the grottoes beneath the main altar and has retained an extremely well-preserved state. If a body's remains do not decompose, contrary to expectations, it is often treated as a miracle. However, the case of John XXIII's body did not enjoy the same acclamation, as it was held to have been due to embalming and adipocere formation.
Tyrphostins such as AG538 and AG1024. These are in early pre-clinical testing. They are not thought to be ATP-competitive, although they are when used in EGFR as described in QSAR studies. These show some selectivity towards IGF-1R over IR. Pyrrolo(2,3-d)-pyrimidine derivatives such as NVP-AEW541, invented by Novartis, which show far greater (100 fold) selectivity towards IGF-1R over IR. Monoclonal antibodies are probably the most specific and promising therapeutic compounds. Teprotumumab is a novel therapy showing significant benefit for Thyroid Eye Disease.
== Characterization == Several qualitative tests are used to detect the presence of reducing sugars. Two of them use solutions of copper(II) ions: Benedict's reagent (Cu2+ in aqueous sodium citrate) and Fehling's solution (Cu2+ in aqueous sodium tartrate). The reducing sugar reduces the copper(II) ions in these test solutions to copper(I), which then forms a brick red copper(I) oxide precipitate. Reducing sugars can also be detected with the addition of Tollens' reagent, which consist of silver ions (Ag+) in aqueous ammonia. When Tollens' reagent is added to an aldehyde, it precipitates silver metal, often forming a silver mirror on clean glassware. 3,5-dinitrosalicylic acid is another test reagent, one that allows quantitative detection. It reacts with a reducing sugar to form 3-amino-5-nitrosalicylic acid, which can be measured by spectrophotometry to determine the amount of reducing sugar that was present. Some sugars, such as sucrose, do not react with any of the reducing-sugar test solutions. However, a non-reducing sugar can be hydrolyzed using dilute hydrochloric acid. After hydrolysis and neutralization of the acid, the product may be a reducing sugar that gives normal reactions with the test solutions. All carbohydrates are converted to aldehydes and respond positively in Molisch's test. But the test has a faster rate when it comes to monosaccharides.
=== Cardiogenesis === Development of heart is involved in several rounds of EMT and MET. While development splanchnopleure undergo EMT and produce endothelial progenitors, these then form the endocardium through MET. Pericardium is formed by sinus venosus mesenchymal cells that undergo MET. Quite similar processes occur also while regeneration in the injured heart. Injured pericardium undergoes EMT and is transformed into adipocytes or myofibroblasts which induce arrhythmia and scars. MET than leads to the formation of vascular and epithelial progenitors that can differentiate into vasculogenic cells which lead to regeneration of heart injury.
Sources: en.wikipedia.org
The three substrates of this enzyme are hydroxy-1,4-benzoquinone, reduced nicotinamide adenine dinucleotide (NADH), and a proton. Its products are hydroxyquinol and oxidised NAD+. This enzyme participates in the metabolism of 2,4,5-trichlorophenoxyacetic acid in the bacteria Burkholderia cepacia.
The same equations can be applied to the dual of current in an inductor. Furthermore, the particular case of a capacitor or inductor changing through several parallel resistors makes an interesting example of multiple decay processes, with each resistor representing a separate process. In fact, the expression for the equivalent resistance of two resistors in parallel mirrors the equation for the half-life with two decay processes. Geophysics: Atmospheric pressure decreases approximately exponentially with increasing height above sea level, at a rate of about 12% per 1000m. Heat transfer: If an object at one temperature is exposed to a medium of another temperature, the temperature difference between the object and the medium follows exponential decay (in the limit of slow processes; equivalent to "good" heat conduction inside the object, so that its temperature remains relatively uniform through its volume). See also Newton's law of cooling. Luminescence: After excitation, the emission intensity – which is proportional to the number of excited atoms or molecules – of a luminescent material decays exponentially. Depending on the number of mechanisms involved, the decay can be mono- or multi-exponential. Pharmacology and toxicology: It is found that many administered substances are distributed and metabolized (see clearance) according to exponential decay patterns. The biological half-lives "alpha half-life" and "beta half-life" of a substance measure how quickly a substance is distributed and eliminated.
Growth hormone secretagogues or GH secretagogues (GHSs) are a class of drugs which act as secretagogues (i.e., induce the secretion) of growth hormone (GH). They include agonists of the ghrelin/growth hormone secretagogue receptor (GHSR), such as ghrelin (lenomorelin), pralmorelin (GHRP-2), GHRP-6, examorelin (hexarelin), ipamorelin, and ibutamoren (MK-677), and agonists of the growth hormone-releasing hormone receptor (GHRHR), such as growth hormone-releasing hormone (GHRH, somatorelin), CJC-1295, sermorelin, and tesamorelin. Many of them also induce the secretion of insulin-like growth factor 1 (IGF-1), as well as of other hypothalamic-pituitary hormones such as prolactin and cortisol. The main clinical application of these agents is the treatment of growth hormone deficiency.
NS Otto Hahn, the only European nuclear-powered civilian ship (1964); a crater on the Moon (shared with his namesake Friedrich von Hahn); and the asteroid 19126 Ottohahn; the Otto Hahn Prize of both the German Chemical and Physical Societies and the city of Frankfurt/Main; the Otto Hahn Medal – An Incentive for Young Scientists – and the Otto Hahn Award of the Max Planck Society; and the Otto Hahn Peace Medal in Gold of the United Nations Association of Germany (DGVN) in Berlin (1988). Proposals were made at various times, first in 1971 by American chemists, that the newly synthesised element 105 should be named hahnium in Hahn's honour, but in 1997 the IUPAC named it dubnium, after the Russian research centre in Dubna. In 1992 element 108 was discovered by a German research team, and they proposed the name hassium (after Hesse). In spite of the long-standing convention to give the discoverer the right to suggest a name, a 1994 IUPAC committee recommended that it be named hahnium. After protests from the German discoverers, the name hassium (Hs) was adopted internationally in 1997.
== Cause == The cause of PAH is unknown. Idiopathic PAH (WHO group 1.1) is not associated with an underlying disease or exposure. It is estimated that 39-46% of those with PAH have the idiopathic variant. Group 1.2 PAH includes the variants that are heritable. Genetic variants or mutations in bone morphogenic protein receptor 2 (BMPR2) account for approximately 75-80% of cases of heritable PAH. BMPR2 mutations are also seen in 20% of idiopathic PAH. BMPR2 is a protein involved in endothelial cell (cells that line blood vessels) proliferation and remodeling. Other types of genes coding for proteins involved in BMPR2 signaling have also been implicated as causes of heritable PAH, such as activin A receptor type-2-like-1 ACVRL1, Endoglin (ENG), SMAD genes encoding for SMAD transcription factors involved in downstream BMPR2 signaling and cell growth including Smad1, Smad4 and Smad9. KCNK3 encodes for a potassium channel which regulates membrane potential across cells thus controlling vascular tone. Eukaryotic translation initiation factor 2 alpha kinase 4 (E1F2AK4) is mutated causes heritable pulmonary veno-occlusive disease and pulmonary capillary hemangiomatosis. Group 1.3 PAH includes disease that is due to drug or toxin exposures. Methamphetamines, the chemotherapeutic dasatinib and the appetite suppressant and diet drug fenfluramine are associated with PAH. Group 1.4 PAH is disease that is associated with underlying disease.
Sources: en.wikipedia.org
Legal status varies by country. It is not approved as a medicine, and it is prohibited in sport. Some jurisdictions restrict import, sale, or possession.
Laboratories use liquid chromatography-tandem mass spectrometry to detect GW501516 and its metabolites. Urine is commonly tested, and testing can occur in and out of competition.
No, cardarine is not a SARM. It is a PPARδ agonist, which acts on a different receptor. The two classes are often confused in online discussions.
Cardarine is a common name for GW501516, a synthetic PPARδ agonist. It is not a steroid or a selective androgen receptor modulator. It was developed and studied as a research compound for metabolic pathways.