PPARδ agonist is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Last reviewed on 2026-03-15. Where a claim depends on a specific study, the study is described rather than over-claimed.
Cardarine is a common name for GW501516, an investigational compound developed in the 1990s for metabolic conditions. It acts as an agonist at peroxisome proliferator-activated receptor delta, a nuclear receptor involved in lipid and energy metabolism. The compound is frequently mislabeled as a selective androgen receptor modulator, or SARM, but its molecular target is different. GW501516 reached early clinical testing before development was discontinued. It has no approved therapeutic use in any country. The name cardarine is not a formal international nonproprietary name.
Regulatory treatment varies, but cardarine is not approved as a medicine. Sports authorities list GW501516 as a prohibited substance, and it is banned at all times under the World Anti-Doping Agency code. Many countries restrict sales for human consumption, while online vendors market it as a research chemical. Such products may lack purity data, and their actual contents can differ from the label. Purchasing or possessing cardarine may carry legal consequences depending on jurisdiction. The compound is not a dietary supplement ingredient in regulated markets.
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.
| Property | Value | Notes |
|---|---|---|
| Common synonyms | GW501516; GW-1516; endurobol | GW501516 is the research code |
| Drug class | PPARδ agonist | Not a selective androgen receptor modulator |
| Molecular formula | C21H18F3NO3S2 | Established chemical formula |
| Molar mass | 453.5 g/mol | Calculated from the formula |
| Regulatory status | Prohibited in sport; not approved as medicine | Status varies by country |
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.
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.
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.
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.
== Limitations and advancements == While reporter gene technology has become an essential component of molecular biology, its application still has limitations. One primary concern is the influence of genomic context on reporter expression. Reporter genes integrated into the genome can be subject to position-effect variegation, where the surrounding chromatin structure influences transcriptional activity. This can lead to inconsistent expression and complicate the interpretation of results, especially in stable cell lines and transgenic organisms. Additionally, reporter expression may not always accurately reflect the activity of the endogenous gene of interest due to differences in post-transcriptional regulation, mRNA stability, or translational efficiency. Another common limitation is the cellular burden that reporter expression may impose. High levels of reporter protein production, such as fluorescent proteins or luciferases, can divert cellular resources, potentially impacting normal metabolism or physiology. This is particularly problematic in sensitive systems like stem cells or primary cell cultures, where even subtle changes in metabolism can influence cell behavior. Additionally, some reporter systems, like luciferase assays, require the addition of exogenous substrates (e.g., luciferin), adds complexity and may reduce reproducibility, particularly in live animal models where substrate availability can vary. To address these challenges, several innovations have improved the reliability and flexibility of reporter gene technologies.
Decrease in testosterone Decrease in serum DHT and 5-alpha reductase Decrease 3AAG, a peripheral marker of DHT metabolism Increase in SHBG Decrease in androgen receptors, 5-alpha reductase type I and II activity, and aromatase in the scalp This decrease in androgens and androgen receptors, and the increase in SHBG, are opposite to the increase in androgenic alopecia with aging. This is not intuitive, as testosterone and its peripheral metabolite, DHT, accelerate hair loss, and SHBG is thought to be protective. The ratio of T/SHBG, DHT/SHBG decreases by as much as 80% by age 80, in numeric parallel to hair loss, and approximates the pharmacology of antiandrogens such as finasteride. Free testosterone decreases in men by age 80 to levels double that of a woman at age 20. About 30% of the normal male testosterone level, the approximate level in females, is not enough to induce alopecia; 60%, closer to the amount found in elderly men, is sufficient. The testicular secretion of testosterone perhaps "sets the stage" for androgenic alopecia as a multifactorial diathesis stress model, related to hormonal predisposition, environment, and age. Supplementing eunuchs with testosterone during their second decade, for example, causes slow progression of androgenic alopecia over many years, while testosterone late in life causes rapid hair loss within a month. An example of premature age effect is Werner's syndrome, a condition of accelerated aging from low-fidelity copying of mRNA. Affected children display premature androgenic alopecia.
=== EC 1.8.3 With oxygen as acceptor === EC 1.8.3.1: sulfite oxidase EC 1.8.3.2: thiol oxidase EC 1.8.3.3: glutathione oxidase EC 1.8.3.4: methanethiol oxidase EC 1.8.3.5: prenylcysteine oxidase EC 1.8.3.6: farnesylcysteine lyase EC 1.8.3.7: formylglycine-generating enzyme
Static self-assembly is significantly slower compared to dynamic self-assembly as it depends on the random chemical interactions between particles. Self assembly can be directed in two ways. The first is by manipulating the intrinsic properties which includes changing the directionality of interactions or changing particle shapes. The second is through external manipulation by applying and combining the effects of several kinds of fields to manipulate the building blocks into doing what is intended. To do so correctly, a high level of direction and control is required and developing a simple, efficient method to organize molecules and molecular clusters into precise, predetermined structures is crucial.
Sources: en.wikipedia.org
in-frame 1. (of a gene or sequence) Read or transcribed in the same reading frame as another gene or sequence; not requiring a shift in reading frame to be intelligible or to result in a functional peptide. 2. (of a mutation) Not causing a frameshift.
Originally this research on alternative forms of DNA was driven by the question of how life evolved on earth and why RNA and DNA were selected by (chemical) evolution over other possible nucleic acid structures. Two hypotheses for the selection of RNA and DNA as life's backbone are either they are favored under life on Earth's conditions, or they were coincidentally present in pre-life chemistry and continue to be used now. Systematic experimental studies aiming at the diversification of the chemical structure of nucleic acids have resulted in completely novel informational biopolymers. So far a number of XNAs with new chemical backbones or leaving group of the DNA have been synthesized, e.g.: hexose nucleic acid (HNA); threose nucleic acid (TNA), glycol nucleic acid (GNA) cyclohexenyl nucleic acid (CeNA). The incorporation of XNA in a plasmid, involving 3 HNA codons, has been accomplished already in 2003. This XNA is used in vivo (E coli) as template for DNA synthesis. This study, using a binary (G/T) genetic cassette and two non-DNA bases (Hx/U), was extended to CeNA, while GNA seems to be too alien at this moment for the natural biological system to be used as template for DNA synthesis. Extended bases using a natural DNA backbone could, likewise, be transliterated into natural DNA, although to a more limited extent. Aside being used as extensions to template DNA strands, XNA activity has been tested for use as genetic catalysts.
A Ukrainian international law scholar, Alexander Merezhko, has developed a project called the International Convention on Prohibition of Cyberwar in Internet. According to this project, cyberwar is defined as the use of Internet and related technological means by one state against the political, economic, technological and information sovereignty and independence of another state. Professor Merezhko's project suggests that the Internet ought to remain free from warfare tactics and be treated as an international landmark. He states that the Internet (cyberspace) is a "common heritage of mankind". On the February 2017 RSA Conference Microsoft president Brad Smith suggested global rules – a "Digital Geneva Convention" – for cyber attacks that "ban the nation-state hacking of all the civilian aspects of our economic and political infrastructures". He also stated that an independent organization could investigate and publicly disclose evidence that attributes nation-state attacks to specific countries. Furthermore, he said that the technology sector should collectively and neutrally work together to protect Internet users and pledge to remain neutral in conflict and not aid governments in offensive activity and to adopt a coordinated disclosure process for software and hardware vulnerabilities. A fact-binding body has also been proposed to regulate cyber operations.
Sources: en.wikipedia.org
No. Cardarine is GW501516, a PPARδ agonist, while SARMs act on androgen receptors. The two classes are often grouped in informal discussions despite different mechanisms.
No. It has no approved medical indication in any country. Regulatory agencies have not cleared it for treatment or prevention of any condition.
Early clinical work stopped after rodent carcinogenicity findings. Those animal results raised concerns about long-term human risk, although direct human evidence is lacking. The human relevance of the tumors remains an open scientific question.
LC-MS/MS is common, often after sample cleanup. The assay targets GW501516 or its metabolites.