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Cardarine As Investigational Pparδ Agonist — Reference Sheet

By Editorial Desk · published 2025-07-28 · last reviewed 2025-09-14 · News

If you have been reading about LC-MS/MS and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.

Updated 2025-09-14. Numbers and descriptions here follow the published literature rather than marketing material.

Cardarine as Investigational PPARδ Agonist

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.

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.

Mechanism and Detection Methods

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.

Handling and quality assessment of cardarine reference material follow general laboratory practices for poorly characterized compounds. It typically appears as a white to off-white powder and is sparingly soluble in water but soluble in organic solvents such as dimethyl sulfoxide and ethanol. Storage recommendations usually specify a cool, dry, dark place, with long-term storage at low temperature and desiccation. Purity may be checked by high-performance liquid chromatography with ultraviolet detection, while identity is confirmed by mass spectrometry and nuclear magnetic resonance. No pharmacopeial monograph exists, so reported purity and stability depend on the supplier’s methods.

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.

Cardarine at a glance

PropertyValueNotes
Common synonymsGW501516, GW-501516, GW 501516, endurobolNames vary in research and anti-doping documents.
Chemical classSynthetic PPARδ agonistSmall-molecule nuclear receptor ligand.
CAS Registry Number317318-70-0Identifier commonly associated with GW501516.
AppearanceWhite to off-white powderTypical for purified research material.
SolubilityLow in water; soluble in DMSO and ethanolOrganic solvents are common for laboratory stock solutions.

Notes from published material

Silicon nanoparticles strength and hardness are four times more than the value of the bulk material. The resistance to pressure applied can be attributed to the line defects inside the particles as well as a dislocation that provides strengthening of the mechanical properties of the nanomaterial. Furthermore, the addition of nanoparticles strengthens a matrix because the pinning of particles inhibits grain growth. This refines the grain, and hence improves the mechanical properties. However, not all additions of nanomaterials lead to an increase in properties for example nano-Cu. But this is attributed to the inherent properties of the material being weaker than the matrix. Nonmetallic nanoparticles and nanomaterials: Size-dependent behavior of mechanical properties is still not clear in the case of polymer nanomaterials however, in one research by Lahouij they found that the compressive moduli of polystyrene nanoparticles were found to be less than that of the bulk counterparts. This can be associated with the functional groups being hydrated. Furthermore, nonmetallic nanomaterials can lead to agglomerates forming inside the matrix they are being added to and hence decrease the mechanical properties by leading to fracture under even low mechanical loads, such as the addition of CNTs. The agglomerates will act as slip planes as well as planes in which cracks can easily propagate (9). However, most organic nanomaterials are flexible and these and the mechanical properties such as hardness etc. are not dominant.

==== Cell-based scheme of coagulation ==== A newer model of coagulation mechanism explains the intricate combination of cellular and biochemical events that occur during the coagulation process in vivo. Along with the procoagulant and anticoagulant plasma proteins, normal physiologic coagulation requires the presence of two cell types for formation of coagulation complexes: cells that express tissue factor (usually extravascular) and platelets. The coagulation process occurs in two phases. First is the initiation phase, which occurs in tissue-factor-expressing cells. This is followed by the propagation phase, which occurs on activated platelets. The initiation phase, mediated by the tissue factor exposure, proceeds via the classic extrinsic pathway and contributes to about 5% of thrombin production. The amplified production of thrombin occurs via the classic intrinsic pathway in the propagation phase; about 95% of thrombin generated will be during this second phase.

== Eukaryotic == The process of transcriptional termination is less understood in eukaryotes, which have extensive post-transcriptional RNA processing, and each of the three types of eukaryotic RNA polymerase have a different termination system. In RNA polymerase I, Transcription termination factor, RNA polymerase I binds downstream of the pre-rRNA coding regions, causing the dissociation of the RNA polymerase from the template and the release of the new RNA strand. In RNA polymerase II, the termination occurs via a polyadenylation/cleaving complex. The 3' tail on the ending of the strand is bound at the polyadenylation site, but the strand will continue to code. The newly synthesised ribonucleotides are removed one at a time by the cleavage factors CSTF and CPSF, in a process that is still not fully understood. The remainder of the strand is disengaged by a 5′-exonuclease when the transcription is finished. RNA polymerase III terminates after a series of uracil polymerization residues in the transcribed mRNA. Unlike in bacteria and in polymerase I, the termination RNA hairpin needs to be upstream to allow for correct cleaving.

=== In silico screening === T cell epitope content, which is one of the factors that contributes to the risk of immunogenicity can now be measured relatively accurately using in silico tools. Immunoinformatics algorithms for identifying T-cell epitopes are now being applied to triage protein therapeutics into higher risk and low risk categories. These categories refer to assessing and analyzing whether an immunotherapy or vaccine will cause unwanted immunogenicity. One approach is to parse protein sequences into overlapping nonamer (that is, 9 amino acid) peptide frames, each of which is then evaluated for binding potential to each of six common class I HLA alleles that "cover" the genetic backgrounds of most humans worldwide. By calculating the density of high-scoring frames within a protein, it is possible to estimate a protein's overall "immunogenicity score". In addition, sub-regions of densely packed high scoring frames or "clusters" of potential immunogenicity can be identified, and cluster scores can be calculated and compiled. Using this approach, the clinical immunogenicity of a novel protein therapeutics can be calculated. Consequently, a number of biotech companies have integrated in silico immunogenicity into their pre-clinical process as they develop new protein drugs.

Sources: en.wikipedia.org

Related pages on this site

Background from the literature

=== Microtox Omni software === The Microtox Omni software was developed by Azur Environmental and allows users of the Microtox Model 500 analyser to run tests, visualize data, calculate statistics and generate reports. This program contains a set of templates for all of the commonly used toxicity tests and allows you to modify or add to the provided templates. The modification of these templates allows for the production of new test formats not originally included with the software. The test templates that are included in this software define all of the parameters for a particular test method. This program calculates the most efficient way of setting up the desired test on the Model 500 Analyser. A test tutor is also included with Microsoft Omni that gives listed instructions on how to set up and run the test of interest. This software allows users to load files from previous versions of the Microtox DOS Software and also gives users the ability to save new data in that original format. A database is included in this software that grants users to access data from a number of other users and test sites, allowing for a comparison of data and trend changes over time. Microtox Omni can be used with any number of databases.

Pulmonary arterial hypertension (PAH) is a syndrome in which the blood pressure in the pulmonary arteries and pulmonary arterioles (the blood vessels located proximal to the capillary bed, the site of oxygen exchange in the lungs) is elevated. This pre-capillary pulmonary artery pressure being elevated is essential, and by definition a mean pulmonary artery pressure greater than 20 mmHg as measured by a right heart catheterization is required for the diagnosis. This pre-capillary pulmonary hypertension is confirmed with measuring pulmonary vascular resistance being greater than 3 Woods Units. A pulmonary artery wedge pressure being less than 15 mmHg (also measured by right heart catheterization) excludes post-capillary bed (in the veins distal to the capillary bed) pulmonary hypertension. Pulmonary arterial hypertension is a subgroup of pulmonary hypertension and is categorized as World Health Organization as group 1. PAH is further subdivided into various categories based on the cause, including idiopathic, heritable, drug and toxin induced, PAH associated with specific diseases (such as connective tissue disorders, portal hypertension or HIV), PAH that is responsive to vasodilators, PAH with venous or capillary involvement, and persistent PAH in the newborn period. If left untreated, the increased pulmonary vascular resistance will eventually lead to right heart failure and death. In the 1980s (before disease specific treatments became available) the 5 year survival rate was 34%.

Difficulty with walking Tingling or loss of sensation (numbness) in hands and feet Loss of tendon reflexes Loss of muscle function or paralysis of the lower legs Mental confusion/speech difficulties Pain Involuntary eye movements (nystagmus) Vomiting A selective impairment of the large proprioceptive sensory fibers without motor impairment can occur and present as a prominent sensory ataxia, which is a loss of balance and coordination due to loss of the proprioceptive inputs from the periphery and loss of position sense.

Leucine is a branched-chain amino acid (BCAA) since it possesses an aliphatic side chain that is not linear. Racemic leucine had been subjected to circularly polarized synchrotron radiation to better understand the origin of biomolecular asymmetry. An enantiomeric enhancement of 2.6% had been induced, indicating a possible photochemical origin of biomolecules' homochirality.

== Sample preparation and extraction == The bioanalyst deals with complex biological samples containing the analyte alongside a diverse range of chemicals that can have an adverse impact on the accurate and precise quantification of the analyte. As such, a wide range of techniques are applied to extract the analyte from its matrix. These include:

Sources: en.wikipedia.org

Reference notes

Most players accepted the provisional suspensions immediately; Dustin Fletcher and Jobe Watson both participated in the 2014 International Rules Series test match on 22 November before beginning their suspensions; Alwyn Davey and Leroy Jetta, neither of whom was on the Essendon list any longer, both opted to play the 2014/15 Northern Territory Football League season (which runs over the Australian summer), and did not begin their provisional suspensions until February 2015. After the tribunal hearings were complete, it was announced that a final decision was expected in late March. This meant that the thirty-four players, including seventeen still at Essendon, would be under provisional suspension during the 2015 NAB Challenge pre-season matches. All twenty-five Essendon players who were at the club during the supplements program received permission to miss the series, including eight players who were not facing charges but were permitted to stand aside to protect their teammates' anonymity; of those eight players, four elected to play. Essendon was given permission to field VFL-listed players from its reserves team, and to sign players from state leagues to temporary contracts to serve as top-up players during the NAB Challenge. On 31 March, the week before the opening of the 2015 AFL season, the tribunal announced that it had found the 34 players not guilty. The tribunal confirmed that Thymosin beta-4 was a banned substance during the program, but that it was not comfortably satisfied that the players had been administered the substance.

Space pharmacology is the application of biomedical engineering that studies the use and dynamics of drugs or pharmaceuticals in space environments. Falling in the realm of space medicine, outer space drug delivery is the practical application of using drugs to treat disorders that may arise due to space's extreme conditions, such as microgravity, radiation, and other physiological and psychological risks. The physical conditions and hazards posed by outer space conditions can result in space-related disorders to the human body, posing a necessity to manufacture, modify, and test drugs to work in outer space.

=== Anti-mitotic agent === Moroidin has shown to have anti-mitotic properties, chiefly by inhibiting the polymerization of tubulin. Tubulin protein polymers are the major component of microtubules. During mitosis, microtubules form the organizing structure called the mitotic apparatus, which captures, aligns, and separates chromosomes. The proper alignment and separation of chromosomes is critical to ensure that cells divide their genetic material equally between daughter cells. Failure to attach chromosomes to the mitotic apparatus activates the mitotic checkpoint, preventing cells from entering anaphase to proceed with cell division. Agents that disrupt microtubules therefore inhibit mitosis through activation of this checkpoint. Moroidin and its related compounds, the celogentins, inhibit tubulin polymerization. Of this family, celogentin C is the most potent (IC50 0.8×10−6 M), and it is more potent than the anti-mitotic agent vinblastine (IC50 3.0×10−6). Moroidin has the same potency as vinblastine. Because of this biological activity, compounds in this family have potential as anti-cancer agents. The mechanism of tubulin disruption is not known, but the degree of biological activity has been linked to the structure of the right-hand ring containing the Trp-His linkage. Moroidin and the celogentins can be divided into three groups according to structural similarity of the right-hand ring. Celogentin C, the most potent compound, has a unique right-hand ring containing a proline residue.

== Notable people == Michael Dunn, Oscar- and Tony-nominated American actor, The Wild Wild West, Star Trek Warwick Davis, English actor and TV presenter, Willow, Return of the Jedi, Leprechaun film series. His two children also have SED. Lenny Rush, English actor, Am I Being Unreasonable? Natalia Grace, Ukrainian-born American with dwarfism, The Curious Case of Natalia Grace Alexander Katan, Dutch Jewish accountant, teacher, and translator who was murdered by the Nazis during the Holocaust, photos of him were notoriously on display in various museums.

Of the 90 patients, four required surgical intervention due to nodules in the lips. Gore-Tex implants. In medical uses, Gore-Tex is known as EPTFE, or expanded polytetrafluoroethylene and, commercially as Advanta, UltraSoft, and SoftForm. The EPTFE is delivered to surgeons in strips that are 1⁄16 inch (1.6 mm) and 3⁄16 inch (4.8 mm) diameter tubes.

Sources: en.wikipedia.org

Frequently asked questions

What is cardarine?

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.

Is cardarine a steroid?

No. Cardarine is not a steroid hormone; it targets the nuclear receptor PPARδ. Its classification in anti-doping rules differs from anabolic steroids, though it remains prohibited in sport.

Why was cardarine not developed further?

Early rodent studies reported tumor formation at multiple sites, which raised safety concerns. Sponsors stopped clinical development, and no approved human product exists.

What receptor does cardarine target?

Cardarine targets PPARδ, a nuclear receptor involved in lipid and energy metabolism. It does not bind the androgen receptor in the way SARMs do.

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