This is a working overview of unapproved substance, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-01-09 and is reviewed periodically as new material appears.
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.
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.
| Property | Value | Notes |
|---|---|---|
| IUPAC name | {4-[({4-methyl-2-[4-(trifluoromethyl)phenyl]-1,3-thiazol-5-yl}methyl)sulfanyl]phenoxy}acetic acid | Systematic name for GW501516 |
| CAS Registry Number | 317318-70-0 | Unique identifier for the parent compound |
| Molecular formula | C21H18F3NO3S2 | Includes carbon, hydrogen, fluorine, nitrogen, oxygen, and sulfur |
| Molecular weight | 453.5 g/mol | Approximate value for the neutral form |
| Appearance | White to off-white powder | Typical description for purified laboratory material |
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.
GW501516 binds and activates PPARδ, a nuclear receptor that influences transcription of genes involved in fatty acid oxidation and energy use. Activation shifts some metabolic pathways in preclinical models, which is why the compound has been studied for lipid disorders and exercise-related endpoints. The exact downstream effects in humans are incompletely mapped. PPARδ is expressed in many tissues, including skeletal muscle, liver, and adipose tissue, so broad activation may have varied consequences. Researchers continue to examine how selective or partial activation might alter the balance between benefits and risks.
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.
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.
National Semiconductor microprocessors NS320xx NE2000 Hitachi Data Systems Bob Pease, designer of the LM331 and LM337 among others Bob Widlar inventor of the Widlar current source List of LM-series integrated circuits List of semiconductor fabrication plants EE Power
of stoichiometric iron pyrite FeS2 amounts to 541.87 pm. The unit cell is composed of a Fe face-centered cubic sublattice into which the S2 ions are embedded. (Note though that the iron atoms in the faces are not equivalent by translation alone to the iron atoms at the corners.) The pyrite structure is also seen in other MX2 compounds of transition metals M and chalcogens X = O, S, Se and Te. Certain dipnictides with X standing for P, As and Sb etc. are also known to adopt the pyrite structure. The Fe atoms are bonded to six S atoms, giving a distorted octahedron. The material is a semiconductor. The Fe ions are usually considered to be low spin divalent state (as shown by Mössbauer spectroscopy as well as XPS). The material as a whole behaves as a Van Vleck paramagnet, despite its low-spin divalency. The sulfur centers occur in pairs, described as S2−2. Reduction of pyrite with potassium gives potassium dithioferrate, KFeS2. This material features ferric ions and isolated sulfide (S2−) centers. The S atoms are tetrahedral, being bonded to three Fe centers and one other S atom. The site symmetry at Fe and S positions is accounted for by point symmetry groups C3i and C3, respectively. The missing center of inversion at S lattice sites has important consequences for the crystallographic and physical properties of iron pyrite. These consequences derive from the crystal electric field active at the sulfur lattice site, which causes a polarization of S ions in the pyrite lattice.
=== Inhibition === One means of caspase inhibition is through the IAP (inhibitor of apoptosis) protein family, which includes c-IAP1, c-IAP2, XIAP, and ML-IAP. XIAP binds and inhibits initiator caspase-9, which is directly involved in the activation of executioner caspase-3. During the caspase cascade, however, caspase-3 functions to inhibit XIAP activity by cleaving caspase-9 at a specific site, preventing XIAP from being able to bind to inhibit caspase-9 activity.
Cardiovascular–kidney–metabolic syndrome (CKM syndrome) is a multisystem disorder of the metabolic, renal and cardiovascular systems. (The term CKM syndrome was first introduced by the American Heart Association in 2023.) This syndrome is the result of interactions between metabolic risk factors, e.g., prediabetes, type 2 diabetes, insulin resistance in normally insulin-sensitive tissues, systemic inflammation, metabolic dysfunction–associated steatotic liver disease (i.e., non-alcoholic fatty liver disease due to the accumulation of excessive fat levels in the liver), dyslipidemia, and obesity. Acting alone or interacting with each other, these abnormalities can promote chronic kidney and cardiovascular disorders and thereby lead to increases in morbidity and mortality rates.
Sources: en.wikipedia.org
Research mainly focuses on polymers that show thermoresponsivity in aqueous solution. Promising areas of application are tissue engineering, liquid chromatography, drug delivery and bioseparation. Only a few commercial applications exist, for example, cell culture plates coated with an LCST-polymer.
The definition can easily be extended to include any number of reagents. The reagents need not always be a metal and a ligand but can be any species which form a complex. Stability constants defined in this way, are association constants. This can lead to some confusion as pKa values are dissociation constants. In general purpose computer programs it is customary to define all constants as association constants. The relationship between the two types of constant is given in association and dissociation constants.
Grafting, in the context of polymer chemistry, refers to the addition of polymer chains onto a surface. In the so-called 'grafting onto' mechanism, a polymer chain adsorbs onto a surface out of solution. In the more extensive 'grafting from' mechanism, a polymer chain is initiated and propagated at the surface. Because pre-polymerized chains used in the 'grafting onto' method have a thermodynamically favored conformation in solution (an equilibrium hydrodynamic volume), their adsorption density is self-limiting. The radius of gyration of the polymer therefore is the limiting factor in the number of polymer chains that can reach the surface and adhere. The 'grafting from' technique circumvents this phenomenon and allows for greater grafting densities. The processes of grafting "onto", "from", and "through" are all different ways to alter the chemical reactivity of the surface they attach with. Grafting onto allows a preformed polymer, generally in a "mushroom regime", to adhere to the surface of either a droplet or bead in solution. Due to the larger volume of the coiled polymer and the steric hindrance this causes, the grafting density is lower for 'onto' in comparison to 'grafting from'. The surface of the bead is wetted by the polymer and the interaction in the solution caused the polymer to become more flexible. The 'extended conformation' of the polymer grafted, or polymerized, from the surface of the bead means that the monomer must be in the solution and there for lyophilic.
There are many different biosynthesis pathways to ascorbic acid in plants. Most proceed through products of glycolysis and other metabolic pathways. For example, one pathway uses plant cell wall polymers. The principal plant ascorbic acid biosynthesis pathway seems to be via l-galactose. The enzyme l-galactose dehydrogenase catalyzes the overall oxidation to the lactone and isomerization of the lactone to the C4-hydroxyl group, resulting in l-galactono-1,4-lactone. l-Galactono-1,4-lactone then reacts with the mitochondrial flavoenzyme l-galactonolactone dehydrogenase to produce ascorbic acid. l-Ascorbic acid has a negative feedback on l-galactose dehydrogenase in spinach. Ascorbic acid efflux by embryos of dicot plants is a well-established mechanism of iron reduction and a step obligatory for iron uptake. All plants synthesize ascorbic acid. Ascorbic acid is a cofactor for enzymes involved in photosynthesis, synthesis of plant hormones, as an antioxidant and regenerator of other antioxidants. Plants use multiple pathways to synthesize vitamin C. The major pathway starts with glucose, fructose or mannose (all simple sugars) and proceeds to l-galactose, l-galactonolactone and ascorbic acid. This biosynthesis is regulated following a diurnal rhythm. Enzyme expression peaks in the morning to supporting biosynthesis for when mid-day sunlight intensity demands high ascorbic acid concentrations.
=== Treatment approaches for primary glaucoma === Primary angle closure glaucoma: Once any symptoms have been controlled, the first line (and often definitive) treatment is laser iridotomy. This may be performed using either Nd:YAG or argon lasers, or in some cases by conventional incisional surgery. The goal of treatment is to reverse and prevent contact between the iris and the trabecular meshwork. In early to moderately advanced cases, iridotomy is successful in opening the angle in around 75% of cases. In the other 25%, laser iridoplasty, medication (pilocarpine), or incisional surgery may be required. Primary open-angle glaucoma: Prostaglandin agonists work by opening uveoscleral passageways. Beta-blockers, such as timolol, work by decreasing aqueous formation. Carbonic anhydrase inhibitors decrease bicarbonate formation from ciliary processes in the eye, thus decreasing the formation of aqueous humor. Parasympathetic analogs are drugs that work on the trabecular outflow by opening up the passageway and constricting the pupil. Alpha 2 agonists (brimonidine, apraclonidine) both decrease fluid production (via inhibition of AC) and increase drainage. A review of people with primary open-angle glaucoma and ocular hypertension concluded that medical IOP-lowering treatment slowed down the progression of visual field loss.
Sources: en.wikipedia.org
No. Major drug regulators have not approved GW501516 for treating any medical condition. Products sold as cardarine are typically unapproved research chemicals or supplements, so their contents and safety are not assured.
It is prohibited by the World Anti-Doping Agency as a hormone and metabolic modulator. Athletes who test positive for GW501516 can face sanctions, including suspensions and loss of results.
Cardarine is a common or trade-style name, while GW501516 is the research code for the same chemical entity. Some sources also use Endurobol or GSK-516. The names refer to the same compound, not distinct drugs.
Cardarine targets PPARδ, a nuclear receptor involved in lipid and energy metabolism. It does not bind the androgen receptor in the way SARMs do.