If you have been reading about GW501516 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 2026-07-03. Where a claim depends on a specific study, the study is described rather than over-claimed.
GW501516 acts as a ligand for PPAR delta, a nuclear receptor that regulates transcription of genes involved in fatty acid oxidation and energy use. Activation of this receptor in skeletal muscle shifts metabolism toward fat burning in animal models. The compound does not burn fat directly; it changes gene expression over hours to days. Researchers study it to understand metabolic flexibility and exercise adaptation. Effects observed in rodents are not automatically expected in humans.
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.
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.
Safety concerns emerged from long-term animal studies. In rodents given the compound for extended periods, researchers found an increased incidence of certain cancers, including liver and bladder tumors. These findings contributed to the discontinuation of clinical development. Whether similar risks apply to short-term or low-level exposure in humans is not established, and controlled human safety data are limited. The relevance of high-dose rodent carcinogenicity findings to human use remains a subject of debate.
| 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 GW501516, also GW-1516, a synthetic compound developed as a peroxisome proliferator-activated receptor delta (PPARδ) agonist. It belongs to a class of agents that modulate gene transcription related to lipid and energy metabolism. The compound was studied in preclinical and early clinical research for metabolic and cardiovascular conditions, but it did not progress to approved therapeutic use. Its name appears in fitness and sports contexts despite not being approved as a drug.
PPARδ is a nuclear receptor that influences transcription of genes involved in fatty acid oxidation, lipid transport, and energy homeostasis. GW501516 binds and activates this receptor with high selectivity relative to PPARα and PPARγ in laboratory assays. Activation alters expression of target genes in skeletal muscle, liver, and adipose tissue in animal models. The exact clinical consequences of these changes in humans remain incompletely characterized, and observed effects in animals do not establish therapeutic benefit or safety.
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.
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.
Als Karyorrhexis (aus dem Griechischen κάρυον karyon, „Kern“, und ῥῆξις rhexis, „Zerreissen“) wird in der Biologie ein endgültiger Zerfall, die destruktive Fragmentierung eines Zellkerns bezeichnet (Zellkernzerfall), der sich in absterbenden Zellen ereignen kann. Gewöhnlicherweise geht der Karyorrhexis die Schrumpfung und Verdichtung des Zellkerns, die Karyopyknose, voraus. Der Vorgang kann sowohl beim programmierten Zelltod (Apoptose) als auch im Rahmen des krankhaften Absterbens einzelner oder mehrerer Zellen stattfinden.
Der Karyotyp (altgriechisch κάρυον káryon ‚Nuss, Fruchtkern‘; altgriechisch τύπος týpos ‚Abdruck, Formel, Muster‘) bezeichnet die Gesamtheit mikroskopisch erkennbarer Merkmale der Chromosomen einer Zelle oder eines Individuums oder einer botanischen bzw. zoologischen Art. Zu diesen Merkmalen gehören die Anzahl der Chromosomen, ihre absoluten oder relativen Längen, die Lage der einzelnen Zentromere sowie weiterer Einschnürungen, die in mitotischen Chromosomen sichtbar werden. Bei letzteren handelt es sich um Regionen von Nukleolusorganisatoren. Eine solche Übersicht zeigt außerdem die Verteilung von Heterochromatin im Euchromatin sowie technisch hervorgerufene Bandenmuster. Ein Karyotyp wird mit Hilfe eines Karyogramms bestimmt. Die Erstellung des Karyogramms ist eine zytogenetische Aufgabe. Hierfür werden Chromosomen der mitotischen Metaphase präpariert, gefärbt und fotografiert, um sie schließlich paarweise anzuordnen. Die Reihe endet mit den Chromosomen, die das Geschlecht bestimmen (Gonosomen), sofern bei der jeweiligen Art welche existieren.
== Forschungsgeschichte == Von Theodor Boveri (1890) stammt der Grundsatz: “Für jede Spezies ist die Zahl der Chromosomen konstant.” Er untersuchte den kleinstmöglichen Karyotyp 2n = 2 beim Pferdespulwurm (Ascaris megalocephala univalens, nach Umbenennung heute Parascaris univalens).
Sources: de.wikipedia.org
== Humangenetische Diagnostik == Den diploiden Chromosomensatz des (gesunden) Menschen, 2n = 46, etablierte Joe Hin Tjio im Labor von Albert Levan aus embryonalen Lungenzellen. In der Humangenetik hat sich eine Schreibweise durchgesetzt, die die Gesamtzahl der Chromosomen und die Art der Geschlechtschromosomen (Gonosomen) wiedergibt. Dabei steht X für ein X-Chromosom und Y für ein Y-Chromosom. So bedeutet 2n = 46,XX den normalen, diploiden Chromosomensatz einer Frau, die Formel 2n = 46,XY das diploide Komplement eines Mannes. Die Analyse des Karyotyps zeigt außerdem chromosomale Anomalien als Kennzeichen von Erbkrankheiten sowie spontane Mutationen. Dazu gehören Veränderungen der Chromosomenzahl oder Chromosommutationen wie Brüche (Deletionen), Duplikationen eines Chromosomenabschnittes oder fehlerhafte Verschmelzungen (Translokationen). Besonderheiten unter den Autosomen werden mit einem Plus-Zeichen und der Nummer des betroffenen Chromosoms angegeben.
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.
Rodent studies reported increased endurance and fat oxidation after GW501516 exposure. Long-term studies also found higher rates of some tumors, which led to halted development.