Laboratory compound comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Updated 2026-04-08. Numbers and descriptions here follow the published literature rather than marketing material.
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.
Human trials of GW501516 were small and short in duration. They examined lipid levels, glucose handling, and other metabolic markers, but the programs were halted after the animal cancer findings. No approved therapeutic product exists, and published human data are insufficient for establishing long-term safety. Reports of use for athletic performance come mainly from non-clinical settings and cannot be verified through controlled trials. Independent testing of products sold as cardarine has found inconsistent purity and labeling.
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.
| Property | Value | Notes |
|---|---|---|
| Primary target | PPARδ (NR1C2) | Nuclear receptor involved in lipid metabolism |
| Preclinical effect | Increased fatty acid oxidation | Observed in rodent studies |
| Key safety signal | Tumors in rodents after long-term exposure | Contributed to halted clinical development |
| Human trial status | No approved product; development stopped | Limited short-term metabolic data |
| Sport regulatory status | Prohibited at all times | WADA hormone and metabolic modulators class |
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.
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.
Published human data are sparse and mostly come from early-phase trials. Those studies examined short-term changes in lipids, glucose, and exercise capacity, but they were not large enough to establish efficacy or long-term safety. Some animal experiments reported increased running endurance, yet such findings do not prove a performance benefit in people. Anti-doping laboratories detect GW501516 and its metabolites in urine or blood using liquid chromatography-tandem mass spectrometry. Detection windows depend on dose, sample type, and individual metabolism. The method is sensitive enough to identify trace residues in tested samples.
Laboratory handling focuses on identity, purity, and stability. Reference standards are typically stored cold and dry, protected from light, because solutions can degrade over time. Analytical checks may use high-performance liquid chromatography with ultraviolet detection or mass spectrometry. Impurities and related substances can be separated chromatographically and compared with a known standard. Because cardarine is not an approved drug, compendial monographs are absent, and laboratories often rely on in-house methods. Reported purity varies among unregulated products and should not be assumed from a label.
GW501516 binds and activates PPARδ, a nuclear receptor that influences transcription of genes involved in fatty acid oxidation and energy use. Activation shifts some metabolic pathways in preclinical models, which is why the compound has been studied for lipid disorders and exercise-related endpoints. The exact downstream effects in humans are incompletely mapped. PPARδ is expressed in many tissues, including skeletal muscle, liver, and adipose tissue, so broad activation may have varied consequences. Researchers continue to examine how selective or partial activation might alter the balance between benefits and risks.
Laboratory detection of GW501516 commonly uses liquid chromatography coupled with tandem mass spectrometry. The method can identify the parent compound or its metabolites in urine and blood after sample cleanup. Protein precipitation, solid-phase extraction, or enzymatic hydrolysis may precede analysis, depending on the matrix. Reference standards are required for accurate quantification and confirmation. Because the compound is not approved, testing often occurs in anti-doping, forensic, or research settings rather than routine clinical care. Results are reported with limits of detection and quantification.
Stability of GW501516 depends on form, temperature, light exposure, and moisture. Solid reference material is typically stored frozen or refrigerated in a desiccator and protected from light. Solutions in organic solvents such as dimethyl sulfoxide are often kept frozen in aliquots to reduce freeze-thaw cycling. Aqueous solubility is low, so aqueous stock solutions can be difficult to prepare without cosolvents. Degradation may appear as changes in chromatographic purity or mass spectral signal. Stability studies are needed to establish shelf life for any specific preparation.
Quality assessment for cardarine samples usually combines identity, purity, and impurity testing. Nuclear magnetic resonance spectroscopy and mass spectrometry can confirm molecular structure, while high-performance liquid chromatography estimates purity. Certificates of analysis from testing laboratories may list these results, but they do not establish safety or legality. In the absence of approved manufacturing, products sold online may contain the wrong compound, variable amounts, or unlisted contaminants. Independent verification is therefore central to analytical work and to interpreting any reported biological activity.
=== Protein divergence === C3orf52 is evolving more quickly than other common proteins including cytochrome c and fibrinogen alpha chain. This would suggest some sort of selective pressure on the protein driving its rapid evolution.
=== Control strategies === There is no known method of eradication or control for invasive Cercopagis pengoi. Containing the spread to new areas is the only form of management. Stricter ballast water regulations and awareness would prevent the spread. The C. pengoi invasion of the Great Lakes occurred after the United States passed a regulation requiring ships exchange freshwater ballast water with ocean water to kill off potential invaders. This means that either the resting eggs remain viable even after boats filled with ballast water switch out their ballast water in the ocean, or the required ballast water regulations are not being followed, or the species was brought into the Great Lakes in no-ballast-on-board (NOBOB) vessels (the most like possibility). NOBOB vessels carry only residual water (<50000L) but were not required to exchange ballast water at the time of Cercopagis' invasion. Locally C. pengoi spread can be limited by only releasing bait or bait water into the water body where the bait was originally collected. Boat owners should wash their boats and equipment with high pressure and hot water (above 40 °C) to limit the spread of adult C. pengoi. Alternatively boats and equipment should be allowed to dry for at least five days before moving to another body of water.
A synergy of two mechanisms, stabilization of closed conformation and exclusion of catalytic water by the tightly juxtaposed GAMEN loop was proposed as the mechanism of inhibition. Moreover, M1 aminopeptidases use a tyrosine residue in the active site to stabilize the transition state. In the case of IRAP, the catalytic Tyr549 is found in different orientations in the open and closed conformations. For example, in the case of phosphinic pseudopeptide inhibitors, which mimic the transition state of peptide substrates, Tyr549 changes orientation upon ligand binding to interact with one of the oxygen atoms of the phosphinic group, which is equivalent to the oxygen atoms of the substrate in the transition state.
Copper IUDs acts as a spermicide. Copper ions released from the IUD damage sperm and disrupt their ability to move, preventing sperm from traveling through the cervical mucus or destroying them as they pass through so that they never meet the egg. They also start a local inflammatory reaction that causes the uterus and fallopian tubes to produce a fluid that contains white blood cells, enzymes, and prostaglandins, which are toxic to sperm. While not the main mechanism of action, studies have found that copper can also alter the endometrial (uterine) lining. This alteration can prevent implantation of a fertilized egg ("blastocyst"), but it cannot disrupt a fertilized egg that has already been implanted in the uterine lining.
Sources: en.wikipedia.org
== Background == Found in several fungal species such as Fusarium graminearum NRRL 2903 (formerly misidentified as Dactylium dendroides), and other species of Fusarium and Aspergillus genera, galactose oxidase was first isolated in 1959. This enzyme is secreted by fungi to function in extracellular space. Although the oxidation reaction of D-galactose gives galactose oxidase its name, the coupled reduction of dioxygen to hydrogen peroxide is believed to have greater physiological significance in yeasts. Hydrogen peroxide which can be produced by yeasts in this way is possibly a bacteriostatic agent.
=== International Union of Pure and Applied Chemistry (IUPAC) === In its 2012 proposed terminology for biologically related polymers, the IUPAC defined a nanoparticle as "a particle of any shape with dimensions in the 1 × 10−9 and 1 × 10−7 m range". This definition evolved from one given by IUPAC in 1997. In the same 2012 publication, the IUPAC extends the term to include tubes and fibers with only two dimensions below 100 nm.
== Mutations == Y184F – Abolishes phosphorylation. Y304F – Decreases activity by two-thirds and alters conformation. S364A – Strong decrease of phosphorylation by PRKACA (the catalytic subunit of protein kinase A).
Sources: en.wikipedia.org
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.
Small short-term human trials examined metabolic markers such as lipids and glucose. The trials did not continue after rodent cancer findings, so long-term human safety is unknown.
Controlled human trials have not established a performance benefit. Anecdotal reports exist, but they are not reliable evidence.
Cardarine is commonly known as GW501516 or GW-1516. These names refer to the same synthetic compound. It is not a brand-name approved medicine.