Everything below concerns anti-doping. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-03-17. Numbers and descriptions here follow the published literature rather than marketing material.
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.
Anti-doping laboratories identify GW501516 and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is the usual matrix, and detection can occur after the parent compound has cleared from blood. The exact detection window depends on dose, formulation, individual metabolism, and assay sensitivity. Because the compound is prohibited at all times, athletes are subject to testing in and out of competition. Analytical methods continue to improve as new metabolites and designer analogs are characterized.
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 |
|---|---|---|
| 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, 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.
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 first described in the 1990s as a selective agonist of the peroxisome proliferator-activated receptor delta. It was studied in preclinical models for metabolic and cardiovascular conditions, but it has not been approved as a medicine in the United States, Europe, or other major jurisdictions. Retail products labeled as cardarine are generally research chemicals or supplements, not pharmaceutical formulations. Because human safety and efficacy data remain limited, regulatory agencies treat it as an unapproved substance rather than a therapeutic product.
Sporting authorities added GW501516 to prohibited lists after it appeared in athlete samples and online markets. The World Anti-Doping Agency classifies it as a hormone and metabolic modulator, and its use can lead to an anti-doping rule violation. Some early laboratory work suggested effects on fatty acid oxidation and endurance-related metabolism in animals, but those findings do not establish safe or effective use in people. Reports of adverse events in humans are scarce and often anecdotal, which complicates risk assessment.
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.
Palumbo et al. (1990) distinguish three cell types from osteoblast to mature osteocyte: type I preosteocyte (osteoblastic osteocyte), type II preosteocyte (osteoid osteocyte), and type III preosteocyte (partially surrounded by mineral matrix). The embedded "osteoid-osteocyte" must do two functions simultaneously: regulate mineralization and form connective dendritic processes, which requires cleavage of collagen and other matrix molecules. The transformation from motile osteoblast to entrapped osteocyte takes about three days, and during this time, the cell produces a volume of extracellular matrix three times its own cellular volume, which results in 70% volume reduction in the mature osteocyte cell body compared to the original osteoblast volume. The cell undergoes a dramatic transformation from a polygonal shape to a cell that extends dendrites toward the mineralizing front, followed by dendrites that extend to either the vascular space or bone surface. As the osteoblast transitions to an osteocyte, alkaline phosphatase is reduced, and casein kinase II is elevated, as is osteocalcin. Osteocytes appear to be enriched in proteins that are resistant to hypoxia, which appears to be due to their embedded location and restricted oxygen supply. Oxygen tension may regulate the differentiation of osteoblasts into osteocytes, and osteocyte hypoxia may play a role in disuse-mediated bone resorption.
Only two SSRIs are licensed for use with children in the UK, sertraline (Zoloft) and fluvoxamine (Luvox), for the treatment of obsessive–compulsive disorder. Fluoxetine is not licensed for this use. A 2007 comparison of aggression and hostility occurring during treatment with fluoxetine to placebo in children and adolescents found that no significant difference between the fluoxetine group and the placebo group. There is also evidence that higher rates of SSRI prescriptions are associated with lower rates of suicide in children, though since the evidence is correlational, the true nature of the relationship is unclear. A 2021 Swedish study, using a within-individual design, also found that young people (as well as adults) who have both attempted suicide and been prescribed SSRIs most commonly make the attempt before, rather than after, starting their SSRI prescription.
== History == Results of a Phase I clinical trial were reported in 2016. In December 2019, enfortumab vedotin was approved in the United States for the treatment of adult patients with locally advanced or metastatic urothelial cancer who had previously received a programmed cell death receptor-1 (PD-1) or programmed death ligand 1 (PD-L1) inhibitor and a platinum-containing chemotherapy. The approval was based on the results of a clinical trial of 125 such patients. The overall response rate, reflecting the percentage of patients who had a certain amount of tumor shrinkage, was 44%; specifically, 12% had a complete response and 32% a partial response. The median duration of response was 7.6 months. The U.S. Food and Drug Administration (FDA) granted the application for enfortumab vedotin accelerated approval, priority review designation, and breakthrough therapy designation. The FDA granted the approval of Padcev to Astellas Pharma US Inc. In July 2021, the FDA approved enfortumab vedotin for adults with locally advanced or metastatic urothelial cancer who have previously received a PD-1 or PD-L1 inhibitor and platinum-containing chemotherapy, or who are ineligible for cisplatin-containing chemotherapy and have previously received therapy.
Sources: en.wikipedia.org
=== GPI-anchor === Bioinformatic analysis predicts the addition of a GPI-anchor on many AGPs. The early synthesis of the GPI moiety occurs on the ER cytoplasmic surface and subsequent assembly take place in the lumen of the ER. These include the assembly of tri-mannose (Man), galactose, non-N-acetylated glucosamine (GlcN) and ethanolamine phosphate to form the mature GPI moiety. AGPs undergo GPI-anchor addition while co-translationally migrating into the ER and these two processes finally converge. Subsequently, a transamidase complex simultaneously cleaves the core protein at the C-terminus when it recognizes the ω cleavage site and transfers the fully assembled GPI-anchor onto the amino acid residue at the C-terminus of the protein. These events occur prior to prolyl hydroxylation and glycosylation. The core glycan structure of GPI anchors is Man-α-1,2-Man-α-1,6-Man-α-1,4-GlcN-inositol (Man: mannose, GlcN: glucosaminyl), which is conserved in many eukaryotes. The only plant GPI anchor structure characterized to date is the GPI-anchored AGP from Pyrus communis suspension-cultured cells. This showed a partially modified glycan moiety compared to previously characterized GPI anchors as it contained β-1,4-Gal. The GPI anchor synthesis and protein assembly pathway is proposed to be conserved in mammals and plants. The integration of a GPI-anchor enables the attachment of the protein to the membrane of the ER transiting to the GA leading to secretion to the outer leaflet of the plasma membrane facing the wall.
=== Suppressing information on health effects === Since the 1970s, DuPont and 3M were aware that PFAS was "highly toxic when inhaled and moderately toxic when ingested". Producers used several strategies to influence science and regulation – most notably, suppressing unfavorable research and distorting public discourse. In 2018, under the first presidency of Donald Trump, White House staff and the EPA pressured the U.S. Agency for Toxic Substances and Disease Registry to suppress a study that showed PFAS to be more dangerous than previously thought.
=== Clinical marker === Genome-wide association studies identified ADAMTS7 as a risk locus for coronary artery disease. Studies have been carried on classification of ADAMTS7 binding site, which may serve as the first step toward developing a new therapeutic target for coronary artery disease. Significant associations for coronary artery calcification with SNPs in ADAMTS7 has also been found in Hispanics. Additionally, a multi-locus genetic risk score study based on a combination of 27 loci, including the ADAMTS7 gene, identified individuals at increased risk for both incident and recurrent coronary artery disease events, as well as an enhanced clinical benefit from statin therapy. The study was based on a community cohort study (the Malmo Diet and Cancer study) and four additional randomized controlled trials of primary prevention cohorts (JUPITER and ASCOT) and secondary prevention cohorts (CARE and PROVE IT-TIMI 22).
Sources: en.wikipedia.org
Drug development is the process of bringing a new drug to the market once a lead compound has been identified through the process of drug discovery. It includes pre-clinical research (microorganisms/animals) and clinical trials (on humans) and may include the step of obtaining regulatory approval to market the drug. Drug Development Process Discovery: The Drug Development process starts with Discovery, a process of identifying a new medicine. Development: Chemicals extracted from natural products are used to make pills, capsules, or syrups for oral use. Injections for direct infusion into the blood drops for eyes or ears. Preclinical research: Drugs go under laboratory or animal testing, to ensure that they can be used on Humans. Clinical testing: The drug is used on people to confirm that it is safe to use. FDA Review: drug is sent to FDA before launching the drug into the market. FDA post-Market Review: The drug is reviewed and monitored by FDA for the safety once it is available to the public.
== M == MIKES – Mass-analyzed ion kinetic energy spectrometry MS – Mass spectrometer MS – Mass spectrometry MS2 – Mass spectrometry/mass spectrometry, i.e. tandem mass spectrometry MS/MS – Mass spectrometry/mass spectrometry, i.e. tandem mass spectrometry MALDESI – Matrix-assisted laser desorption electrospray ionization MALDI – Matrix-assisted laser desorption/ionization MAII – Matrix-assisted inlet ionization MAIV – Matrix-assisted ionization vacuum MIMS – Membrane introduction mass spectrometry, membrane inlet mass spectrometry, membrane interface mass spectrometry MCP – Microchannel plate MSn – Multiple-stage mass spectrometry MCP – Microchannel plate MPI – Multiphoton ionization MRM – Multiple reaction monitoring
=== Economics === In 2003, Abbott (AbbVie, Inc.) raised the price of a Norvir course from US$1.71 per day to US$8.57 per day, leading to claims of price gouging by patients' groups and some members of Congress. Consumer group Essential Inventions petitioned the NIH to override the Norvir patent, but the NIH announced on August 4, 2004, that it lacked the legal right to allow generic production of Norvir.
Sources: en.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.
Cardarine targets PPARδ, a nuclear receptor involved in lipid and energy metabolism. It does not bind the androgen receptor in the way SARMs do.