PPARδ agonist 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 2025-10-01. Where a claim depends on a specific study, the study is described rather than over-claimed.
Preclinical research reported that GW501516 increased running endurance in mice and improved lipid profiles in some animal species. Early human trials explored effects on high-density lipoprotein cholesterol, triglycerides, and glucose handling, but the program was discontinued. Published human data are sparse and do not establish efficacy for any condition. Studies also examined PPAR delta in cancer biology, with conflicting findings across models. The relationship between receptor activation, tissue context, and disease risk remains an active area of investigation.
Anti-doping laboratories identify GW501516 and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is the usual matrix, and detection can occur after the parent compound has cleared from blood. The exact detection window depends on dose, formulation, individual metabolism, and assay sensitivity. Because the compound is prohibited at all times, athletes are subject to testing in and out of competition. Analytical methods continue to improve as new metabolites and designer analogs are characterized.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular target | PPAR delta (NR1C2) | Ligand-activated nuclear receptor. |
| Primary tissues studied | Skeletal muscle, liver, adipose | Effects on fatty acid oxidation and energy use. |
| Typical detection matrix | Urine | Used in anti-doping analysis. |
| Common analytical method | LC-MS/MS | Detects parent compound and metabolites. |
| Sport regulatory class | Prohibited at all times | Listed as a metabolic modulator by WADA. |
Cardarine is a common name for the investigational chemical GW501516, also written GW-1516. It was developed as a peroxisome proliferator-activated receptor delta agonist for metabolic conditions such as dyslipidemia. Early research focused on lipid handling and energy use in skeletal muscle and other tissues. The compound was never approved as a medicine. In public discussion, it is often grouped with performance-enhancing substances, although its receptor target differs from that of anabolic steroids or selective androgen receptor modulators. Regulatory and health authorities have issued warnings about its use.
GW501516 acts on PPARδ, a nuclear receptor that helps regulate fatty acid oxidation and energy homeostasis. In animal studies, activation of this receptor was associated with increased endurance and changes in lipid metabolism. Human trials examined effects on blood lipids and other metabolic markers, but the compound did not advance to approval. Rodent studies later reported tumors in multiple tissues at doses used in those experiments. Whether those findings translate to human risk remains uncertain, and the clinical relevance of the animal data is still debated.
Regulatory bodies treat GW501516 as a prohibited substance in competitive sport. The World Anti-Doping Agency added it to the prohibited list, and it falls under classes covering metabolic modulators and hormone-related agents. It is not approved by drug regulators for human use, and it is not a lawful dietary supplement. Products sold under the cardarine name may contain unlisted ingredients or different compounds. Because no approved product exists, quality and identity are not guaranteed by pharmaceutical manufacturing standards.
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.
Detection of GW501516 in biological samples generally relies on liquid chromatography coupled with tandem mass spectrometry. Urine is a common matrix in anti-doping analysis, while blood or plasma may be used in research settings. Sample preparation can involve enzymatic hydrolysis, protein precipitation, or solid-phase extraction before instrumental analysis. Because the compound undergoes metabolism, assays may target the parent molecule, one or more metabolites, or both. Detection windows are not fixed; they depend on factors such as dose, route, individual metabolism, and assay sensitivity. Reference standards are required for accurate identification and quantification.
Handling and quality assessment of cardarine reference material follow general laboratory practices for poorly characterized compounds. It typically appears as a white to off-white powder and is sparingly soluble in water but soluble in organic solvents such as dimethyl sulfoxide and ethanol. Storage recommendations usually specify a cool, dry, dark place, with long-term storage at low temperature and desiccation. Purity may be checked by high-performance liquid chromatography with ultraviolet detection, while identity is confirmed by mass spectrometry and nuclear magnetic resonance. No pharmacopeial monograph exists, so reported purity and stability depend on the supplier’s methods.
== Literatur == Kim, I. et al. (2007): Selective degradation of mitochondria by mitophagy. In: Arch Biochem Biophys. 462(2); 245–253; PMID 17475204; PMC 2756107 (freier Volltext) H. Abeliovich, M. Zarei, K.T.G. Rigbolt, R.J. Youle, J. Dengjel (2013) Involvement of mitochondrial dynamics in the segregation of mitochondrial matrix proteins during stationary phase mitophagy. In: Nature Communications 4, Nr. 2789 doi:10.1038/ncomms3789
Erika L. Pearce (geboren 1972 in New York City) ist eine US-amerikanische Zellbiologin und Immunologin. Pearce war von 2015 bis 2020 Direktorin am Max-Planck-Institut für Immunbiologie und Epigenetik in Freiburg im Breisgau. Seit 2021 ist Bloomberg Distinguished Professor an der Johns-Hopkins-Universität in Baltimore. 2018 erhielt sie den Gottfried Wilhelm Leibniz-Preis für ihre Arbeiten auf dem Gebiet der Stoffwechsel- und Entzündungsforschung, wobei sie sich vor allem auf die T-Lymphozyten konzentriert. 2026 wurde Pearce zum Mitglied der National Academy of Sciences gewählt.
== Leben und Werk == Erika L. Pearce wurde 1972 in New York City geboren. Sie studierte Biologie an der Cornell University und bekam dort ihren Bachelor of Arts 1998. Danach beschäftigte sie sich mit der Identifizierung der Rolle eines Schlüsseltranskriptionsfaktors für die CD8-T-Zell-Effektorfunktionen und die metabolische Reprogrammierung, die für die Entwicklung von T-Speicherzellen wichtig ist. Im Jahr 2005 wurde sie in Zell- und Molekularbiologie an der University of Pennsylvania promoviert. Ihre Dissertation hatte den Titel Developement of CD8 T cell responses. Von 2009 bis 2011 arbeitete sie am Trudeau Institute in Saranac Lake, New York, danach ging sie an die Washington University School of Medicine in St. Louis, wo sie ab 2011 erst Assistant Professor und später Associate Professor war. Von 2015 bis 2020 war Erika Pearce Direktorin am Max-Planck-Institut für Immunbiologie und Epigenetik in Freiburg im Breisgau und leitete dort die Abteilung des Instituts für Immunmetabolismus. Seit 2020 ist sie Bloomberg Distinguished Professor an der Johns-Hopkins-Universität in Baltimore, wo sie in der Abteilung für Onkologie der Medizinischen Fakultät und am Bloomberg-Kimmel-Institut für Krebsimmuntherapie tätig ist sowie eine Stelle in der Abteilung für Biochemie und Molekularbiologie an der Bloomberg School of Public Health innehat. Nach ihren eigenen Angaben konzentriert sich ihre Forschung auf das Verständnis der zellulären und molekularen Mechanismen, die die Immunreaktionen steuern, mit besonderem Schwerpunkt auf der Frage, wie der Stoffwechsel diesen Prozess steuert.
Sources: de.wikipedia.org
Sie ist Mitglied im Advisory Editorial Board des Journal of Experimental Medicine sowie Mitglied des Editorial Board der Zeitschriften Cell und Cell Metabolism. Zudem ist sie im Steering Committee für Immunometabolism bei Janssen Pharmaceuticals, externes Mitglied des Aufsichtsrats des Immunology Network von GlaxoSmithKline und im wissenschaftlichen Beirat von ImmunoMet Therapeutics.
Sources: de.wikipedia.org
It binds to and activates PPAR delta, a nuclear receptor that controls expression of genes related to fatty acid oxidation. This mechanism can alter energy metabolism in animal models. It is not a direct stimulant or fat-burning enzyme.
Early-stage trials examined lipid and glucose markers, but the development program was discontinued. Published human results are limited and do not support approved use for any indication. Claims of performance or health benefits remain unproven.
Yes. Laboratories use LC-MS/MS to detect GW501516 and its metabolites in urine. Detection depends on timing and sensitivity, but the substance is banned at all times.
Anti-doping laboratories typically use LC-MS/MS to detect GW501516 and its metabolites in urine. The method is sensitive and can identify the compound at low concentrations. Detection depends on sample timing, metabolism, and the specific assay.