Everything below concerns WADA Prohibited List. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-05-19. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Regulatory status | Not approved for human therapeutic use | No marketing authorization identified in major jurisdictions. |
| Anti-doping class | PPARδ agonist; hormone and metabolic modulators | Listed on the WADA Prohibited List. |
| Common test matrix | Urine | Also blood and tissue in research settings. |
| Typical analytical method | LC-MS/MS | Targets parent compound and metabolites. |
| Major safety signal | Tumor findings in rodents | Human relevance not established; limited human data. |
Early clinical research explored GW501516 for lipid disorders, obesity, and diabetes. Some short-term human studies reported changes in HDL cholesterol, LDL cholesterol, and triglycerides. The development program was discontinued after rodent studies showed dose-dependent tumor formation in multiple tissues, including liver, bladder, stomach, and skin. These findings raised concerns about long-term cancer risk in humans. Because human exposure data are limited, the clinical significance of the rodent tumors remains uncertain.
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.
Cardarine is prohibited in competitive sport under the World Anti-Doping Agency code, where it is classified as a metabolic modulator. It is not approved as a prescription medicine in the United States, European Union, or other major markets. Regulatory action has focused on its presence in sports and in products marketed as research chemicals. Because it has no accepted medical indication, supply is often unregulated. This status creates legal and safety uncertainties for anyone who encounters the substance.
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.
==== Metabolites ==== Desmetramadol is metabolized in the liver into the active metabolite N,O-didesmethyltramadol via CYP3A4 and CYP2B6. The inactive tramadol metabolite N-desmethyltramadol is metabolized into the active metabolite N,O-didesmethyltramadol by CYP2D6.
Gemtuzumab ozogamicin, sold under the brand name Mylotarg, is an antibody-drug conjugate (a drug-linked monoclonal antibody) that is used to treat acute myeloid leukemia (AML). The most common side effects include infection, febrile neutropenia, decreased appetite, hyperglycemia, mucositis, hypoxia, hemorrhage, increased transaminase, diarrhea, nausea, and hypotension. However, the addition of gemtuzumab ozogamicin to standard chemotherapy regimens does not increase infection rates.
Excitatory amino acid transporter 2 (EAAT2) also known as solute carrier family 1 member 2 (SLC1A2) and glutamate transporter 1 (GLT-1) is a protein that in humans is encoded by the SLC1A2 gene. Alternatively spliced transcript variants of this gene have been described, but their full-length nature is not known.
Sources: en.wikipedia.org
Since the ligand is responsible for cellular interaction, it is chosen for the application depending on the target site. The target site contains binding sites that the ligand targets to deliver the LTL to the desired area. Favorable target site characteristics are determined by what is commonly expressed by tissues of the pathology of interest. Determinants can include histones, basement membrane fibrinogen, selectins, adhesion molecules, and other ligand targets. For example, in some human cancer tumors such as ovarian carcinomas, folate is over-expressed. LTLs for targeting cancer often use a ligand that targets this over-expression of folate to localize drug delivery to the desired area. The tumor microenvironment of solid tumor cancers is also a unique targeting site. Tumor endothelial cells are important for angiogenesis, which is key to tumor growth; therefore, using LTLs to target these cells can limit the growth and vascularization of a tumor.
=== Secondary ion mass spectrometry (SIMS) procedure === In case of measuring the hydration rim using the depth profiling ability of the secondary ion mass spectrometry technique, the sample is mounted on a holder without any preparation or cutting. This method of measurement is non-destructive. There are two general SIMS modes: static mode and dynamic mode, depending on the primary ion current density, and three different types of mass spectrometers: magnetic sector, quadrupole and time-of-flight (TOF). Any mass-spectrometer can work in static mode (very low ion current, a top mono-atomic layer analysis), and dynamic mode (a high ion current density, in-depth analysis). Although relatively infrequent the use of SIMS on obsidian surface investigations has produced great progress in OHD dating. SIMS in general refers to four instrumental categories according to their operation; static, dynamic, quadrupole, and time-of-flight, TOF. In essence it is a technique with a large resolution on a plethora of chemical elements and molecular structures in an essentially non destructive manner. An approach to OHD with a completely new rationale suggests that refinement of the technique is possible in a manner which improves both its accuracy and precision and potentially expands the utility by generating reliable chronological data. Anovitz et al. presented a model which relied solely on compositionally-dependent diffusion, following numerical solutions (finite difference (FD), or finite element) elaborating on the H+ profile acquired by SIMS.
== Toxicity == The recommended therapeutic dose is 80-100 mg/m2 body area. Optimal dosage is determined based on measurements of unbound platinum concentration following intravenous infusion, combined with rate of creatine clearance as an assessment of renal function using Ishibashi’s formula: DoseNDP = AUC × CLNDP, where CLNDP = 0.0738 × creatinine clearance + 4.47 The exact mechanism of uptake into the cell is unknown, with information being considerably less available compared to cisplatin. What is known is that nedaplatin does not interact with the Oct2 or apical multidrug and toxin extrusion transporter (MATE) transporters, potentially explaining the difference in nephrotoxicity due to reduced accumulation in the proximal tubules of the kidney. Toxicogenomics has helped elucidate some of the mechanisms behind nephrotoxicity, where oxidative stress has been shown to deregulate gene expression via Hmox1 and other genes.
It could possibly be extended to 10 days and prevent substantial cell damage by low temperature preservation methods. On the same day, a separate study reports new cryoprotectant solvents, tested with cells, that could preserve organs by the latter methods for much longer with substantially reduced damage.
Sources: en.wikipedia.org
No. Cardarine has not received approval for human therapeutic use in major jurisdictions. It remains an investigational compound.
It is classified as a PPARδ agonist on the WADA Prohibited List. Anti-doping laboratories can detect it and its metabolites in urine. Its use is banned in competition and usually out of competition.
Rodent studies reported increased tumor incidence at multiple sites. The human relevance remains uncertain, but the findings contributed to discontinuation of development. No long-term human cancer data are available.
Cardarine is a common name for GW501516, a synthetic PPARδ agonist developed for research. It has not been approved as a medication in any country. It is classified as an unapproved drug and a prohibited substance in sport.