Anti-doping 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.
Last reviewed on 2026-02-15. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Sporting authorities added GW501516 to prohibited lists after it appeared in athlete samples and online markets. The World Anti-Doping Agency classifies it as a hormone and metabolic modulator, and its use can lead to an anti-doping rule violation. Some early laboratory work suggested effects on fatty acid oxidation and endurance-related metabolism in animals, but those findings do not establish safe or effective use in people. Reports of adverse events in humans are scarce and often anecdotal, which complicates risk assessment.
Legal status varies by country. In some places, cardarine is controlled under medicines or psychoactive substances laws; in others, it may be sold with minimal oversight as a research chemical. Customs agencies have intercepted shipments, and several national health agencies have issued warnings about products marketed for bodybuilding or performance enhancement. The lack of a standardized pharmaceutical supply means identity, purity, and contamination levels can differ widely between samples. These factors make cardarine a regulatory and public health concern rather than a conventional prescription drug.
Cardarine is a common name for GW501516, a synthetic compound first described in the 1990s as a selective agonist of the peroxisome proliferator-activated receptor delta. It was studied in preclinical models for metabolic and cardiovascular conditions, but it has not been approved as a medicine in the United States, Europe, or other major jurisdictions. Retail products labeled as cardarine are generally research chemicals or supplements, not pharmaceutical formulations. Because human safety and efficacy data remain limited, regulatory agencies treat it as an unapproved substance rather than a therapeutic product.
| 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 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.
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.
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.
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.
== Mögliche Nebenwirkungen == Blutdruckabfall, Herzinsuffizienz, Herzrhythmusstörungen (Bradykardie, AV-Block, ventrikuläre Extrasystolen, Kammerflattern), Sehstörungen (Doppelbilder), Schwindel, Kopfschmerzen, Verwirrtheitszustand, Übelkeit, Transaminasenanstieg, cholestatische Hepatitis, Kurzatmigkeit und Verdauungsstörungen. Selten Müdigkeit und vermehrte Schweißneigung. Sehr selten Mundtrockenheit, Fieber, Muskel- oder Gelenkschmerzen, Angstzustände, allergische Hautreaktionen und vorübergehende Potenzstörungen. Bereits 1991 wurde in der CAST-Studie gezeigt, dass bei Patienten mit koronarer Herzkrankheit Medikamente wie Flecainid trotz nachgewiesener Wirksamkeit gegen die ventrikulären Arrhythmien das Risiko des plötzlichen Herztodes erhöhen. Das wird dadurch erklärt, dass das Flecainid selbst gefährliche (maligne) Rhythmusstörungen auslösen kann (proarrhythmischer Effekt). Diese proarrhythmischen Effekte scheinen auch genetisch mitbestimmt zu sein.
== Literatur == Anne Paschen: Herz. In: Jörg Braun, Roland Preuss (Hrsg.): Klinikleitfaden Intensivmedizin. 9. Auflage. Elsevier, München 2016, ISBN 978-3-437-23763-8, S. 185–283, hier: S. 253 f. (Flecainid).
== Eigenschaften == Es gibt verschiedene Fleckfieberimpfstoffe, die allesamt keine Immunität vermitteln. Fleckfieberimpfstoffe sind entweder Formalin-inaktivierte oder attenuierte Rickettsien. Während der inaktivierte Fleckfieberimpfstoff nur einen kurzen und unvollständigen Impfschutz vermittelt, kommen beim attenuierten Impfstoff (Impfstamm Madrid-E) gelegentliche Reversionen zu einer virulenten Form (Evir) vor. Die Reversion basiert auf einer Punktmutation. Der inaktivierte Impfstoff wird meistens zweimal in vierwöchigem Abstand verabreicht und bewirkt eine sechsmonatige begrenzte Schutzwirkung. Einer der ersten Fleckfieberimpfstoffe wurden 1924 von R. Spencer und R. Parker entwickelt. Dieser Impfstoff wurde aus Zecken isoliert, die zuvor bei infizierten Meerschweinchen Blut gesaugt hatten, die Rickettsien wurden anschließend mit Phenol und Formalin inaktiviert. Ein weiterer früher Impfstoff wurde in embryonierten Hühnereiern erzeugt (Cox-Impfstoff). Beide Impfstoffe wurden 1973 getestet und bei beiden Impfstoffen entwickelten alle Geimpften eine Erkrankung. Bei erneuter Exposition verlief die Erkrankung in beiden Fällen milder. Ein weiterer inaktivierter Fleckfieberimpfstoff wurde ab 1970 vom US-Militär (USAMRIID) entwickelt und in Zellkulturen von embryonalen Hühner-Fibroblasten erzeugt. Ebenfalls 1924 entwickelte der polnische Biologe Rudolf Weigl einen Impfstoff aus Rickettsia-Suspensionen, die er aus dem Verdauungstrakt von Läusen gewann (Weigl-Impfstoff).
Damit konnte zwar keine Immunität erreicht werden, aber Geimpfte hatten einen deutlich milderen Verlauf im Falle einer Infektion. Es wird geschätzt, dass in den 1930er Jahren acht Millionen Polen und Russen den Impfstoff erhielten. Weitere Fleckfieberimpfstoffe sind der Castaneda-Impfstoff aus Lungengewebe von infizierten Kaninchen und ein früher Impfstoff von Hans Zinsser.
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.
No. Major drug regulators have not approved GW501516 for treating any medical condition. Products sold as cardarine are typically unapproved research chemicals or supplements, so their contents and safety are not assured.