GW501516 raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
This page was last updated on 2026-07-23 and is reviewed periodically as new material appears.
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.
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.
GW501516 acts as a selective agonist at PPARδ, a nuclear receptor that regulates transcription of genes involved in lipid handling and energy metabolism. Activation of PPARδ in preclinical models increases fatty acid oxidation, mitochondrial biogenesis, and exercise endurance in rodents. These effects have made the compound a subject of metabolic research and also a target for sport anti-doping rules. In humans, however, controlled studies are limited, and whether similar endurance or metabolic changes occur at tolerated exposures remains an open question. The receptor’s broad tissue distribution also means downstream effects may vary by organ and condition.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic PPARδ agonist | Not a steroid or a selective androgen receptor modulator. |
| Common synonyms | Cardarine, GW501516, GW-501516, endurobol | Names vary by supplier and literature source. |
| Appearance | White to off-white powder | Consistent with many small-molecule research chemicals. |
| Solubility | Low in water; soluble in DMSO and ethanol | Often prepared in organic solvent for laboratory work. |
| Primary target | PPARδ (NR1C2) | Nuclear receptor involved in lipid and energy metabolism. |
Because cardarine is not an approved medicine, no pharmacopeial monograph defines its identity, purity, or storage requirements. Laboratories typically rely on in-house methods and reference standards when testing materials labeled as GW501516. Certificates of analysis may report purity and identity for a specific batch, but their scope varies and they do not guarantee safety or legal status. Independent verification can include high-performance liquid chromatography, mass spectrometry, nuclear magnetic resonance, and elemental analysis. The distinction between research chemical labeling and human use is significant because quality standards and oversight differ.
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.
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.
Published studies have examined GW501516 in animal models of obesity, insulin resistance, and exercise endurance. Early human trials reportedly ended, and development was discontinued after preclinical findings raised concerns about cancer in some rodent studies. Regulatory agencies have not approved cardarine for any medical use. Its availability through non-pharmaceutical channels raises questions about identity, purity, and legal status that are separate from its laboratory pharmacology. Those questions are often addressed through analytical testing rather than assumptions about product labels.
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.
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 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.
== History == The safety and effectiveness of eladocagene exuparvovec were demonstrated in an open-label, single-arm clinical study in 13 children with confirmed diagnosis of aromatic L-amino acid decarboxylase deficiency. At the start of the study, all participants had no gross motor function (the most severe presentation of aromatic L-amino acid decarboxylase deficiency) and decreased aromatic L-amino acid decarboxylase activity in the plasma. Participants treated with eladocagene exuparvovec were compared to untreated participants (natural history). Motor milestone assessments were completed for 12 of the 13 participants at week 48 after receiving the treatment. The efficacy of eladocagene exuparvovec was demonstrated based on gross motor function improvement in 8 of 12 treated participants, which has not been reported in untreated participants with the severe presentation of aromatic L-amino acid decarboxylase deficiency.
Potassium, in the form of potassium chloride is used as a medication to treat and prevent low blood potassium. Low blood potassium may occur due to vomiting, diarrhea, or certain medications. It is given by slow injection into a vein or by mouth.
== Career == Ciulli remained in Cambridge University to conduct post-doctoral research on fragment-based drug discovery with Professor Abell and Professor Tom L. Blundell, under a College Junior Research Fellowship. Between February and June 2009, Ciulli went to Yale University as Human Frontier Science Programme visiting fellow to visit the laboratory of Professor Craig Crews before returning to Cambridge University to start his independent research career. While at Cambridge, Ciulli was the group leader in the Department of Chemistry, Director of Studies in Chemistry and BBSRC David Phillis Fellow at Christ's College. In April 2013, he took up a Readership in Chemical & Structural Biology as a principal investigator within the Division of Biological Chemistry and Drug Discovery in the University of Dundee. Ciulli was promoted as the Professor of Chemical & Structural Biology in the same division in October 2016. In 2017, he co-founded Amphista Therapeutics, a company that focuses on developing drugs based on targeted protein degradation. He was elected to the Fellowship of the Royal Society of Edinburgh in 2023.
== Applications == A SILAC approach involving incorporation of tyrosine labeled with nine carbon-13 atoms (13C) instead of the normal carbon-12 (12C) has been utilized to study tyrosine kinase substrates in signaling pathways. SILAC has emerged as a very powerful method to study cell signaling, post translation modifications such as phosphorylation, protein–protein interaction and regulation of gene expression. In addition, SILAC has become an important method in secretomics, the global study of secreted proteins and secretory pathways. It can be used to distinguish between proteins secreted by cells in culture and serum contaminants. It has also been adapted as a 'forward+reverse' SILAC method for simultaneous labeling of host and microbe, which enables the study of host-microbe interactions. Standardized protocols of SILAC for various applications have also been published.
=== RISC activation and catalysis === Exogenous dsRNA is detected and bound by an effector protein, known as RDE-4 in C. elegans and R2D2 in Drosophila, that stimulates Dicer activity. This protein only binds long dsRNAs, but the mechanism producing this length specificity is unknown. This RNA-binding protein then facilitates the transfer of cleaved siRNAs to the RISC complex. In C. elegans this initiation response is amplified through the synthesis of a population of 'secondary' siRNAs during which the Dicer-produced initiating or 'primary' siRNAs are used as templates. These 'secondary' siRNAs are structurally distinct from Dicer-produced siRNAs and appear to be produced by an RNA-dependent RNA polymerase (RdRP).
Sources: en.wikipedia.org
Within a protein, phosphorylation can occur on several amino acids. Phosphorylation on serine is thought to be the most common, followed by threonine. Tyrosine phosphorylation is relatively rare but lies at the head of many protein phosphorylation signalling pathways (e.g. in tyrosine kinase-linked receptors) in most of the eukaryotes. Phosphorylation on amino acids, such as serine, threonine, and tyrosine results in the formation of a phosphoprotein, when the phosphate group of the phosphoprotein reacts with the -OH group of a Ser, Thr, or Tyr sidechain in an esterification reaction. However, since tyrosine phosphorylated proteins are relatively easy to purify using antibodies, tyrosine phosphorylation sites are relatively well understood. Histidine and aspartate phosphorylation occurs in prokaryotes as part of two-component signaling and in some cases in eukaryotes in some signal transduction pathways. The analysis of phosphorylated histidine using standard biochemical and mass spectrometric approaches is much more challenging than that of Ser, Thr or Tyr. and In prokaryotes, archaea, and some lower eukaryotes, histidine's nitrogen act as a nucleophile and binds to a phosphate group. Once histidine is phosphorylated the regulatory domain of the response regulator catalyzes the transfer of the phosphate to aspartate.
==== MPP salary increase and pension re-introduction ==== In 2025, Ford's government introduced legislation to grant MPPs a 35 per cent pay raise. Previously, an MPP earned $116,550 annually, which had not changed since 2009. With support from the other parties, the Legislature enacted the MPP Pension and Compensation Act, 2025, which increased MPPs' salaries to $157,350, ministers from $165,851 to $223,909, and the premier from $208,974 to $282,129. The change also re-introduced pensions for MPPs.
The meanings of the various colors are standardized by the Clinical and Laboratory Standards Institute and are the same across manufacturers. The term order of draw refers to the sequence in which tubes should be filled. The needle which pierces the tubes can carry additives from one tube into the next, so the sequence is standardized so that any cross-contamination of additives will not affect laboratory results.
=== Phase 3 === Fasedienol (Aloradine; AM-005; PH-94B; 4-androstadienol) – vomeropherine Soclenicant (BNC-210; IW-2143) – α7 nicotinic acetylcholine receptor negative allosteric modulator (abandoned after failed phase 3 trials. See [1].) VQW-765 (VQW765; AQW051; AQW-051; JQH481R778) – α7 nicotinic acetylcholine receptor partial agonist [2]
In relation to its selectivity for the AR, unlike steroidal antiandrogens (SAAs) such as CPA and megestrol acetate (MGA), bicalutamide does not interact importantly with other steroid hormone receptors (including the ERsTooltip estrogen receptors, PRsTooltip progesterone receptors, GRTooltip glucocorticoid receptor, or MRTooltip mineralocorticoid receptor), and in accordance, has no clinically relevant additional, off-target hormonal activity (estrogenic or antiestrogenic, progestogenic or antiprogestogenic, glucocorticoid or antiglucocorticoid, or mineralocorticoid or antimineralocorticoid). However, it has been reported that bicalutamide has weak affinity for the progesterone receptor (PR) (~100- to 500-fold lower than for the AR), where it acts as an antagonist (with only ~12-fold lower functional inhibition relative to the AR in one study). Hence, bicalutamide may have some antiprogestogenic activity, although the clinical relevance of this is unknown. Bicalutamide does not inhibit 5α-reductase and is not known to inhibit other enzymes involved in androgen steroidogenesis (e.g., CYP17A1). Although bicalutamide does not bind to the ERs, it can increase estrogen levels secondarily to blockade of the AR when used as a monotherapy in males, and for this reason, the medication can indirectly activate the ERs to a degree and hence have some indirect estrogenic effects in men.
Sources: en.wikipedia.org
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.
It binds to and activates PPARδ, a nuclear receptor that regulates genes related to fatty acid oxidation and energy use. This activation alters transcription in tissues such as skeletal muscle and liver. The full range of downstream effects in humans is not fully established.
No, cardarine is not known to occur naturally in plants, animals, or humans. It is a synthetic molecule produced for laboratory research. Products labeled as cardarine should therefore be treated as manufactured chemicals with variable purity.
Cardarine targets PPARδ, a nuclear receptor involved in lipid and energy metabolism. It does not bind the androgen receptor in the way SARMs do.