Prohibited list 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 2026-05-27. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
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.
Cardarine is a common name for GW501516, a synthetic compound studied for its effects on lipid and glucose metabolism. It functions as an agonist at peroxisome proliferator-activated receptor delta, or PPARδ, a nuclear receptor that influences gene expression. The molecule is not a steroid, nor is it a selective androgen receptor modulator. It is also known in research and sports literature as GW-501516 and endurobol. Early laboratory work examined its metabolic activity in cell cultures and animal models.
| Property | Value | Notes |
|---|---|---|
| Common name | Cardarine | Also called GW501516 and endurobol. |
| Chemical formula | C21H18F3NO3S2 | Molecular weight about 453.5 g/mol. |
| Appearance | White to off-white solid | Form depends on synthesis and purity. |
| Solubility | Soluble in DMSO and ethanol | Low solubility in water. |
| Typical storage | -20 °C, desiccated, protected from light | Common for research chemicals. |
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.
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 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 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.
== Redoxpotentiale in der Biochemie == Für biochemische Vorgänge rechnet man mit den auf pH 7 bezogenen Potentialen Eo'. Für Reaktionen, an denen Protonen beteiligt sind, ergibt sich somit eine Potentialdifferenz von 0,413 V, wie in der nachfolgenden Tabelle angegeben.
Bitte beachten: Werden Redoxpotentiale als Eo oder Eo' angegeben (Tabelle), so bezeichnen sie formal das Potential relativ zur Normal-Wasserstoffelektrode. Das Redoxpotential eines Halbelements relativ zu einer anderen Bezugselektrode als Normalwasserstoff ergibt sich durch vorzeichenrichtige Addition bzw. Subtraktion zweier Werte aus nachstehender Tabelle: dem Wert für die betrachtete Halbzelle und dem Wert für die betrachtete Bezugselektrode. Das n bezeichnet die Anzahl der Elektronen, die während der Redoxreaktion übertragen werden. Nach allgemeiner Konvention bezieht sich das Formalpotential E0 bzw. E0' auf das Reduktionspotential. Daher steht auf der linken Seite der Tabelle die Reduktionsreaktion.
Homoglutathion ist ein dem Glutathion strukturverwandtes Thiol. Das Tripeptid (γ-L-Glutamyl-L-cysteinyl-β-alanin) ist aus den Aminosäuren Glutaminsäure, Cystein und β-Alanin aufgebaut. Es unterscheidet sich von Glutathion damit nur durch seine C-terminale Aminosäure. Homoglutathion ersetzt teilweise oder vollständig Glutathion in Leguminosen. Während in der Familie der Fabaceae die meisten Vertreter der Fabeae und Trifolieae beide homologe Tripeptide enthalten, bilden die Phaseoleae nur Homoglutathion. Homoglutathion übernimmt in den Phaseoleae viele Funktionen, die in anderen Pflanzen Glutathion zukommen. So dient Homoglutathion im Pflanzenkörper der Phaseoleae als Haupttransportform reduzierten Schwefels. Homoglutathion ist die Vorstufe der Homophytochelatine, die in den Phaseoleae zur Bindung und Entgiftung von Schwermetallen dienen. Auch ist Homoglutathion in Homologie zum Glutathion an der Entgiftung von Herbiziden über die Homoglutathion-Sulfotransferase-Reaktion beteiligt. Zusätzlich spielt Homoglutathion eine Rolle als Reduktionsmittel bei der lichtabhängigen Wasserstoffperoxid-Entgiftung in den Chloroplasten der Phaseoleae.
Homoglutathion wird in den Leguminosen aus den Aminosäuren L-Glutaminsäure, L-Cystein und β-Alanin in einem zweistufigen Prozess synthetisiert. Unter ATP-Verbrauch wird aus Glutaminsäure und Cystein γ-Glutamylcystein durch die Ligase γ-Glutamylcysteinsynthetase gebildet. Im zweiten Schritt der Synthesekette wird unter ATP-Verbrauch β–Alanin mithilfe des Enzyms Homoglutathionsynthetase an das terminale Kohlenstoffatom addiert.
Sources: de.wikipedia.org
Cardarine is a common name for the investigational compound GW501516. It acts as a PPARδ agonist and is not approved for human use. It is prohibited in sport.
It activates PPARδ, a nuclear receptor that influences gene expression related to lipid and energy metabolism. Animal studies show changes in endurance and lipid levels. Human effects and risks are not well established.
No, cardarine is not a steroid. It belongs to a different chemical class, the PPARδ agonists. It is also not a selective androgen receptor modulator.
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.