Nuclear receptor comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Updated 2026-05-09. 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.
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 | 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 the common name for GW501516, a synthetic compound studied as a peroxisome proliferator-activated receptor delta agonist. Researchers developed it to explore treatments for lipid disorders and metabolic conditions. It is not an approved medicine in any country. Early clinical work examined changes in HDL cholesterol and triglycerides, but development was discontinued after animal studies raised concerns about cancer. The compound remains available as a research chemical and appears in discussions of performance enhancement.
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.
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.
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.
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.
Subject to its constitutional principles and the basic concepts of its legal system, each Party shall adopt such measures as may be necessary to establish as a criminal offence under its domestic law, when committed intentionally, the possession, purchase or cultivation of narcotic drugs or psychotropic substances for personal consumption contrary to the provisions of the 1961 Convention, the 1961 Convention as amended or the 1971 Convention. Previous drug control treaties had targeted drug manufacturers and traffickers, rather than users. In their 2003 article, "The Mechanics and Dynamics of the UN System for International Drug Control," David Bewley-Taylor and Cindy Fazey explain that "[t]he 1988 Convention was an attempt to reach a political balance between consumer and producer countries. Consequently, it was not only the duty of producing countries (e.g. the developing countries of Asia and South America) to suppress illicit supply, but also the duty of consumer countries (e.g.
Injection of corticosteroids may or may not alleviate symptoms better than simulated (placebo) injections. There is no evidence that corticosteroid injection sustainably alters the natural history of the disease, which seems to be a gradual progression of neuropathy. Surgery to cut the transverse carpal ligament is the only known disease modifying treatment.
where k is a proportionality constant representing factors related to the instrument settings and characteristics. (9) reveals more clearly that the time of flight of the ion varies with the square root of its mass-to-charge ratio (m/q). Consider a real-world example of a MALDI time-of-flight mass spectrometer instrument which is used to produce a mass spectrum of the tryptic peptides of a protein. Suppose the mass of one tryptic peptide is 1000 daltons (Da). The kind of ionization of peptides produced by MALDI is typically +1 ions, so q = e in both cases. Suppose the instrument is set to accelerate the ions in a U = 15,000 volts (15 kilovolt or 15 kV) potential. And suppose the length of the flight tube is 1.5 meters (typical). All the factors necessary to calculate the time of flight of the ions are now known for (8), which is evaluated first of the ion of mass 1000 Da:
==== Metabolism ==== Scientists performed a study on NM-2-AI metabolism in silico and in vivo, in order to identify the main metabolites to be screened in the different biological samples. They performed the in silico metabolism prediction of NM-2-AI using MetaSiteTM software and subsequently verified the presence of metabolites in the blood, urine and hair of mice after NM-2-AI administration. LC-HRMS analysis identified seven main metabolites in the urine. They were identified, by their accurate masses and fragmentation patterns, as 2-aminoindane (2AI), two hydroxy-2-AI and four hydroxy-NM-2-AI; one of the hydroxy-NM-2-AI and one of the hydroxy-2-AI underwent also to conjugation. NM-2-AI and 2-AI were also detected by LC-HRMS in the hair and blood
Sources: en.wikipedia.org
The retention can be decreased by adding a less polar solvent (methanol, acetonitrile) into the mobile phase to reduce the surface tension of water. Gradient elution uses this effect by automatically reducing the polarity and the surface tension of the aqueous mobile phase during the course of the analysis. Structural properties of the analyte molecule can play an important role in its retention characteristics. In theory, an analyte with a larger hydrophobic surface area (C–H, C–C, and generally non-polar atomic bonds, such as S-S and others) can be retained longer as it does not interact with the water structure. On the other hand, analytes with higher polar surface area (as a result of the presence of polar groups, such as -OH, -NH2, COO− or -NH3+ in their structure) are less retained, as they are better integrated into water. The interactions with the stationary phase can also affected by steric effects, or exclusion effects, whereby a component of very large molecule may have only restricted access to the pores of the stationary phase, where the interactions with surface ligands (alkyl chains) take place. Such surface hindrance typically results in less retention. Retention time increases with more hydrophobic (non-polar) surface area of the molecules. For example, branched chain compounds can elute more rapidly than their corresponding linear isomers, because their overall surface area is lower.
In 1970, she established what was for nearly a decade the only protein crystallography laboratory in Israel. Then, from 1979 to 1984 she was a group leader with Heinz-Günter Wittmann at the Max Planck Institute for Molecular Genetics in Berlin. She was a visiting professor at the University of Chicago in 1977–78. She headed a Max-Planck Institute Research Unit at DESY in Hamburg, Germany (1986–2004) in parallel to her research activities at the Weizmann Institute. She focused on the mechanisms underlying protein biosynthesis, by ribosomal crystallography, a research line she pioneered over 20 years ago despite considerable skepticism of the international scientific community. Ribosomes translate RNA into protein and because they have slightly different structures in microbes, when compared to eukaryotes, such as human cells, they are often a target for antibiotics. In 1993, she visualized the path taken by the nascent proteins, namely the ribosomal tunnel, and recently revealed the dynamics elements enabling its involvement in elongation arrest, gating, intra-cellular regulation and nascent chain trafficking into their folding space. In 2000 and 2001, she determined the complete high-resolution structures of both ribosomal subunits and discovered within the otherwise asymmetric ribosome, the universal symmetrical region that provides the framework and navigates the process of polypeptide polymerization.
== Function == RTKs play a key role in the communication of cells with their microenvironment. These molecules are involved in the regulation of cell growth, differentiation, and metabolism. In several cases the biochemical mechanism by which RTKs transduce signals across the membrane has been shown to be ligand induced receptor oligomerization and subsequent intracellular phosphorylation. In the case of DDR2, the ligand is collagen which binds to its extracellular discoidin domain. This autophosphorylation leads to phosphorylation of cytosolic targets as well as association with other molecules, which are involved in pleiotropic effects of signal transduction. DDR2 has been associated with a number of diseases including fibrosis and cancer.
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 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.