A practical reference on GW501516: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2025-10-19 and is reviewed periodically as new material appears.
Cardarine has no approved therapeutic indication and is not marketed as a medicine. The World Anti-Doping Agency lists GW501516 as a prohibited substance at all times, covering both in-competition and out-of-competition periods. National laws vary: some countries treat it as an unapproved drug subject to import controls, while others have specific restrictions on sale for human consumption. It is often sold as a research chemical, a label that does not imply safety or legality. Enforcement actions have targeted online vendors and shipments.
Anti-doping laboratories identify GW501516 and related metabolites using liquid chromatography coupled with tandem mass spectrometry. Urine is the most common matrix, though blood and dried blood spots may also be analyzed. The method targets the parent compound and phase I and phase II metabolites, which extend the detection window. Because the substance is prohibited at all times, athletes can be tested outside competition. Detection limits and windows depend on the assay, sample type, and individual metabolism.
Cardarine is frequently described as a fat-burning or endurance-enhancing supplement, but these claims exceed the available evidence. The compound is not a hormone, steroid, or selective androgen receptor modulator. Research articles discuss it as a tool compound for studying PPARδ biology, while anti-doping literature focuses on its abuse and detection. Quality of unapproved products is uncertain, and independent analyses have found impurities or incorrect labeling. Open questions include whether human cancer risk resembles that seen in rodents and how often non-athletes use the substance.
Analytical laboratories typically identify cardarine and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is a common matrix in anti-doping testing, while blood and tissue may be used in research settings. Detection windows depend on the assay, the sample matrix, and the compound's metabolism. Because cardarine is extensively metabolized, laboratories often target specific metabolites to improve sensitivity and confirmation. Reference standards are required for reliable quantification. Method validation includes checks for selectivity, linearity, and carryover.
A persistent misconception is that cardarine is a fat-burning drug or a safe alternative to anabolic steroids. No approved therapeutic product exists, and human safety data are limited. The tumor findings in rodents remain a central concern in scientific reviews. Products sold online may contain inaccurate labels, impurities, or different compounds entirely, which complicates any assessment of effects. Independent testing of such products has reported frequent mislabeling. For these reasons, discussions in the literature emphasize risks and unknowns rather than benefits.
Cardarine is not approved for human therapeutic use in any major jurisdiction. It appears on the World Anti-Doping Agency Prohibited List as a PPARδ agonist within the hormone and metabolic modulators category. Sports organizations test for it because it has been detected in athlete samples and seized products. Regulatory actions against marketed research chemical versions have occurred in several countries, though enforcement varies. Availability through unregulated channels complicates oversight.
| Property | Value | Notes |
|---|---|---|
| Regulatory status | Prohibited in sport; not approved as medicine | Listed by WADA at all times. |
| Common synonyms | GW501516, GW-501516, endurobol | Cardarine is a colloquial name. |
| Typical analytical method | LC-MS/MS | Detects parent compound and metabolites. |
| Common test matrix | Urine | Blood and dried blood spots also possible. |
| Legal classification | Varies by country | Often treated as unapproved drug or research chemical. |
In laboratory settings, cardarine is studied as a tool compound for probing PPARδ biology. Published experiments often use cell cultures, rodent models, or isolated tissues. Some investigations focus on metabolic effects, while others assess potential risks such as carcinogenicity observed in long-term animal studies. Because human trials are sparse, most knowledge comes from preclinical work and adverse event reports. Scientific literature frequently notes the gap between animal findings and human outcomes. The compound is not a dietary supplement and is not intended for human consumption.
Cardarine is a common name for GW501516, a synthetic compound developed in the 1990s through research collaborations involving GlaxoSmithKline. It belongs to a class of molecules known as peroxisome proliferator-activated receptor delta agonists. Early studies explored its effects on lipid metabolism and energy expenditure in animal models. The compound was never approved as a human medicine, and clinical development was discontinued. In the years since, it has appeared in fitness and bodybuilding communities as a performance-enhancing substance. Regulatory agencies classify it as an unapproved drug.
PPARδ is a nuclear receptor that regulates gene expression related to fatty acid oxidation, glucose homeostasis, and mitochondrial function. GW501516 binds to this receptor with high affinity and activates downstream signaling in skeletal muscle and other tissues. Animal studies reported increased endurance and altered fuel preference, but human data remain limited and inconsistent. The precise relationship between receptor activation and observed physiological changes is still an area of active investigation. Researchers have also examined whether the compound affects inflammation or cell proliferation. No approved therapeutic indication exists for cardarine.
Literature on cardarine often separates receptor pharmacology from toxicology. Mechanistic papers describe PPARδ activation and gene expression changes, while safety assessments focus on carcinogenicity and species differences. Questions remain about whether rodent tumors arise through PPARδ-dependent or off-target mechanisms. Another open area is how human metabolism and exposure compare with those in animal studies. Analytical methods such as liquid chromatography–mass spectrometry are used to confirm identity in biological and product samples.
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.
== Function == Vitellogenin provides the major egg yolk protein that is a source of nutrients during early development of egg-laying (oviparous) vertebrates and invertebrates. Although vitellogenin also carries some lipid for deposition in the yolk, the primary mechanism for deposition of yolk lipid is instead via VLDLs, at least in birds and reptiles. Vitellogenin precursors are multi-domain apolipoproteins (proteins that bind to lipids to form lipoproteins), that are cleaved into distinct yolk proteins. Different vitellogenin proteins exist, which are composed of variable combinations of yolk protein components; however, the cleavage sites are conserved.
== Application == Microtox has a variety of environmental and industrial applications. Common applications are for testing the toxicity of both marine and freshwater, as well as sediments for pesticides and other inorganic and organic chemicals. Drinking water: Microtox is used to test drinking water sources in many areas where either accidental or deliberate contamination is possible. Toxic contaminants in drinking water are indicated by a change in the color or intensity of light, or by a change in the rate of oxygen use. Lakes and rivers: Microtox is used to test the toxicity of lake and river sediments contaminated by metals or nonspecific contaminants. The Solid-Phase test is used for sediments, while either the Basic test or the 100% test is used for pore water. Sediment testing: Microtox is used to test and evaluate the toxicity of various marine and freshwater sediments contaminated by metals and organics. Aqueous extracts of contaminated soils, drilling muds, and sludge. Microtox data may be used to establish apparent effects threshold (AET), sediment quality standards and used for NPDES permits, as well as Superfund cleanup levels. Industrial: This bioassay is used in the assessment of the toxicity of complex industrial effluent sources. It is a cost-effective way for monitoring and testing large numbers of samples. Microtox can also be applied as an early warning system (EWS) and aid in detecting the presence of toxic materials, as well as predict the outcomes of other bioassays and tests.
== Etymology == The term hyaluronic acid is derived from hyalos (Greek for vitreous, meaning 'glass-like') and uronic acid because it was first isolated from the vitreous humour and possesses a high uronic acid content. The term hyaluronate refers to the conjugate base of hyaluronic acid. Since the molecule typically exists in vivo in its polyanionic form, it is most commonly referred to as hyaluronan.
=== Metabolism and excretion === Docetaxel is mainly metabolised in the liver by the cytochrome P450 CYP3A4 and CYP3A5 subfamilies of isoenzymes. Metabolism is principally oxidative and at the tert-butylpropionate side chain, resulting first in an alcohol docetaxel (M2), which is then cyclised to three further metabolites (M1, M3 and M4). M1 and M3 are two diastereomeric hydroxyoxazolidinones and M4 is an oxazolidinedione. Phase II trials of 577 patients showed docetaxel clearance is related to body surface area and to hepatic enzyme and alpha1 acid glycoprotein plasma levels. The following model represents docetaxel clearance in humans:
Sources: en.wikipedia.org
== Format == A formal, distinct, and unique 6-part name is given to each term for test or observation identity. The database currently has over 71,000 observation terms that can be accessed and understood universally. Each database record includes six fields for the unique specification of each identified single test, observation, or measurement:
=== Approved drugs === Escitalopram (Cipralex; Entact; Lexapro; LU-26054; MLD-55; (S)-citalopram; Seroplex; Sipralex; Sipralexa) – selective serotonin reuptake inhibitor (SSRI) [14] Fluoxetine (LY-110140; Prozac; Reneuron; Sarafem) – selective serotonin reuptake inhibitor (SSRI) [15] Fluoxetine (Fluoxetine Tablets) – selective serotonin reuptake inhibitor (SSRI) [16] Paroxetine (Aropax; BRL-29060; Deroxat; Divarius; FG-7051; Frosinor; Motivan; NNC-207051; Paxil; Seroxat; SI-211103; Tagonis) – selective serotonin reuptake inhibitor (SSRI) [17] Paroxetine (Dropax; Dropaxin; Serestill) – selective serotonin reuptake inhibitor (SSRI) [18] Sertraline (Aremis; Besitran; CP-51974; Gladem; Lustral; Serad; Serlain; Tatig; Zoloft) – selective serotonin reuptake inhibitor (SSRI) [19] Venlafaxine (Dobupal; Efexor XR; Effexor; Effexor XR; Elafax; WY-45030; WY-45651; WY-45655) – serotonin–norepinephrine reuptake inhibitor (SNRI) [20]
=== Graft-versus-host disease === Due to its immunosuppressant activity, rapamycin has been assessed as prophylaxis or treatment agent of graft-versus-host disease (GVHD), a complication of hematopoietic stem cell transplantation. While contrasted results were obtained in clinical trials, pre-clinical studies have shown that rapamycin can mitigate GVHD by increasing the proliferation of regulatory T cells, inhibiting cytotoxic T cells and lowering the differentiation of effector T cells.
The other route uses glutathione (GSH) to conjugate with arsenic (III) to form an arsenic (GS) 3 complex. This complex can form a monomethylated arsenic (III) GS complex, using Cyt19 arsenic methyltransferase, and this monomethylated GS complex is in equilibrium with the monomethylated arsenic (III). Cyt19 arsenic methyltransferase can methylate the complex one more time, and this forms a dimethylated arsenic GS complex, which is in equilibrium with a dimethyl arsenic (III) complex. Both of the mono-methylated and di-methylated arsenic compounds can readily be excreted in urine. However, the monomethylated compound was shown to be more reactive and more toxic than the inorganic arsenic compounds to human hepatocytes (liver), keratinocytes in the skin, and bronchial epithelial cells (lungs). Studies in experimental animals and humans show that both inorganic arsenic and methylated metabolites cross the placenta to the fetus, however, there is evidence that methylation is increased during pregnancy and that it could be highly protective for the developing organism. Enzymatic methylation of arsenic is a detoxification process; it can be methylated to methylarsenite, dimethylarsenite or trimethylarsenite, all of which are trivalent. The methylation is catalyzed by arsenic methyltransferase (AS3MT) in mammals, which transfers a methyl group on the cofactor S-adenomethionine (SAM) to arsenic (III). An orthologue of AS3MT is found in bacteria and is called CmArsM. This enzyme was tested in three states (ligand free, arsenic (III) bound and SAM bound).
=== First endosymbiosis === Eukaryotic algae are polyphyletic thus their origin cannot be traced back to a single hypothetical common ancestor. It is thought that they came into existence when photosynthetic coccoid cyanobacteria got phagocytized by a unicellular heterotrophic eukaryote (a protist), giving rise to double-membranous primary plastids. Such symbiogenic events (primary symbiogenesis) are believed to have occurred more than 1.5 billion years ago during the Calymmian period, early in Boring Billion, but it is difficult to track the key events because of so much time gap. Primary symbiogenesis gave rise to three divisions of archaeplastids, namely the Viridiplantae (green algae and later plants), Rhodophyta (red algae) and Glaucophyta ("grey algae"), whose plastids further spread into other protist lineages through eukaryote-eukaryote predation, engulfments and subsequent endosymbioses (secondary and tertiary symbiogenesis). This process of serial cell "capture" and "enslavement" explains the diversity of photosynthetic eukaryotes. The oldest undisputed fossil evidence of eukaryotic algae is Bangiomorpha pubescens, a red alga found in rocks around 1047 million years old.
Sources: en.wikipedia.org
Legal status varies by country. It is not approved as a medicine, and it is prohibited in sport. Some jurisdictions restrict import, sale, or possession.
Laboratories use liquid chromatography-tandem mass spectrometry to detect GW501516 and its metabolites. Urine is commonly tested, and testing can occur in and out of competition.
No, cardarine is not a SARM. It is a PPARδ agonist, which acts on a different receptor. The two classes are often confused in online discussions.
No. Cardarine has not received approval for human therapeutic use in major jurisdictions. It remains an investigational compound.