This is a working overview of GW501516, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-06-13 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 a synthetic compound also known as GW501516, GW-501516, and sometimes endurobol. It was developed as a selective agonist of peroxisome proliferator-activated receptor delta, a nuclear receptor involved in fatty acid oxidation and energy metabolism. The compound was studied in preclinical models for metabolic and cardiovascular conditions, but it did not become a marketed human medicine. In regulatory and anti-doping contexts, it is treated as a prohibited substance rather than a licensed medicine.
The pharmacological interest in cardarine centers on PPARδ activation and its downstream effects on lipid handling and mitochondrial function. In animal studies, PPARδ agonists have been associated with changes in exercise endurance and fatty acid utilization, though results vary by model and protocol. Human data remain sparse, and the absence of large controlled trials limits conclusions about efficacy. Researchers often describe the compound as a tool for probing PPARδ biology rather than a proven therapeutic agent.
Safety discussions about cardarine frequently cite rodent carcinogenicity findings reported in the 2000s. In those studies, treated animals developed tumors at multiple sites, leading sponsors to discontinue clinical development. The relevance of these findings to humans has not been resolved, but they are a major reason the compound is not approved. Current literature emphasizes uncertainty about long-term effects and the risks of unregulated use. Regulators and health agencies have not established a safe human exposure level.
| 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. |
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.
Anti-doping laboratories detect GW501516 and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is the most common matrix, though blood and dried blood spots may also be used in some programs. Detection depends on factors such as dose, timing, metabolism, and the sensitivity of the assay. Published methods describe limits of detection in the low nanogram per milliliter range for related compounds. Exact detection windows are not fixed for all situations and remain an area of ongoing study.
Products sold as cardarine have been found to contain incorrect compounds, variable amounts, or no active ingredient at all. Independent testing is required to verify identity and purity. Common analytical approaches include high-performance liquid chromatography, mass spectrometry, and nuclear magnetic resonance for structural confirmation. These methods can distinguish GW501516 from related PPAR agonists and from unrelated steroids. For regulators and researchers, such verification is central to interpreting both biological results and adverse event reports.
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.
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.
Human serum albumin is the main protein of human blood plasma. It makes up around 50% of human plasma proteins. It binds water, cations (such as Ca2+, Na+ and K+), fatty acids, hormones, bilirubin, thyroxine (T4) and pharmaceuticals (including barbiturates). Its main function is to regulate the oncotic pressure of blood. The isoelectric point of albumin is 4.7. Alpha-fetoprotein is a fetal plasma protein that binds various cations, fatty acids and bilirubin. Vitamin D-binding protein binds to vitamin D and its metabolites, as well as to fatty acids. Afamin binds vitamin E. It seems to carry lipidated Wnt proteins and Vitamin E around. Extracellular matrix protein 1 is a less canonical albumin. It regulates bone mineralization. The four canonical human albumins are arranged on chromosome 4 region 4q13.3 in a tandem manner.
VIP is highly localised in lungs (70%) and binds with alveolar type II (AT II) cells via VPAC1. The biological (vasodilator) activity of vasoactive intestinal peptide (VIP) was discovered in the lungs before the peptide was isolated and chemical identity characterized from intestine. VIP levels are also considerably high in the brain and the gut. It is localized in key sites in the lung, has potent activities on its major functions, and appears to play an important role in pulmonary physiology and disease. The principal localization of VIP-containing neurons in the tracheobronchial tree is in the smooth muscle layer, around submucosal mucous glands and in the walls of pulmonary and bronchial arteries. Immunoreactive VIP is also present in neuronal cell bodies forming microglia that provide a source of intrinsic innervation of pulmonary structures.
The F1 fraction derives its name from the term "Fraction 1" and FO (written as a subscript letter "o", not "zero") derives its name from being the binding fraction for oligomycin, a type of naturally derived antibiotic that is able to inhibit the FO unit of ATP synthase. These functional regions consist of different protein subunits — refer to tables. This enzyme is used in synthesis of ATP through aerobic respiration. Located within the thylakoid membrane and the inner mitochondrial membrane, ATP synthase consists of two regions FO and F1. FO causes rotation of F1 and is made of c-ring and subunits a, two b, F6. F1 is made of α, β, γ, and δ subunits. F1 has a water-soluble part that can hydrolyze ATP. FO on the other hand has mainly hydrophobic regions. FO F1 creates a pathway for protons movement across the membrane.
Sources: en.wikipedia.org
TNF is a cytokine produced mainly by activated macrophages, and is the major extrinsic mediator of apoptosis. Most cells in the human body have two receptors for TNF: TNFR1 and TNFR2. The binding of TNF to TNFR1 has been shown to initiate the pathway that leads to caspase activation via the intermediate membrane proteins TNF receptor-associated death domain (TRADD) and Fas-associated death domain protein (FADD). cIAP1/2 can inhibit TNF signaling by binding to TRAF2. FLIP inhibits the activation of caspase-8. Binding of this receptor can also indirectly lead to the activation of transcription factors involved in cell survival and inflammatory responses. However, signalling through TNFR1 might also induce apoptosis in a caspase-independent manner. The link between TNF and apoptosis shows why an abnormal production of TNF plays a fundamental role in several human diseases, especially in autoimmune diseases. The TNF receptor superfamily also includes death receptors (DRs), such as DR4 and DR5. These receptors bind to the protein TRAIL and mediate apoptosis. Apoptosis is known to be one of the primary mechanisms of targeted cancer therapy. Luminescent iridium complex-peptide hybrids (IPHs) have recently been designed, which mimic TRAIL and bind to death receptors on cancer cells, thereby inducing their apoptosis.
A lab-on-a-chip is a device that integrates one or several laboratory functions on a single chip that deals with handling particles in hollow microfluidic channels. It has been developed for over a decade. Advantages in handling particles at such a small scale include lowering fluid volume consumption (lower reagents costs, less waste), increasing portability of the devices, increasing process control (due to quicker thermo-chemical reactions) and decreasing fabrication costs. Additionally, microfluidic flow is entirely laminar (i.e., no turbulence). Consequently, there is virtually no mixing between neighboring streams in one hollow channel. In cellular biology convergence, this rare property in fluids has been leveraged to better study complex cell behaviors, such as cell motility in response to chemotactic stimuli, stem cell differentiation, axon guidance, subcellular propagation of biochemical signaling and embryonic development.
Serum, suspected to contain IgE antibodies, is drawn from the allergic (atopic) patient. This serum is injected intradermally into a non-allergic person. The suspected antigens are then intradermally injected into the non-allergic person 24–48 hours later. If the person being tested for an allergy has made antibodies for the antigen, this will cause a local reaction in the non-allergic person when the antibodies mix with the antigen. This demonstrates a type I hypersensitivity reaction, and the allergic reaction to the injected antigen is confirmed for the patient being tested. A positive PK test usually appears as a wheal and flare. The test was developed by Otto Prausnitz and Heinz Küstner. The first PK test occurred in 1921 when Prausnitz injected Küstner's serum into his abdominal skin. Küstner had previously noted that he developed allergic symptoms after eating fish. After eating some fish, Prausnitz's skin became hot, red, and swollen at the site of the serum injection, confirming their hypothesis that Küstner was allergic to fish.
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.
Cardarine is an investigational synthetic compound that acts as a PPARδ agonist. It is also known as GW501516 and has been studied mainly in preclinical research. It is not an approved medicine.