Cardarine raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
This page was last updated on 2026-07-27 and is reviewed periodically as new material appears.
Published literature on cardarine includes in vitro assays, rodent experiments, and a small number of human studies. Reports describe effects on exercise capacity and lipid metabolism in animals, while human evidence is sparse. Many online descriptions present the compound as a proven endurance aid, a claim not supported by regulatory approval or large clinical trials. Analytical studies focus on identifying the parent compound and its metabolites in biological samples. Important uncertainties include species differences, dose-response relationships, and the relevance of rodent tumor findings to humans.
Cardarine is the common name for GW501516, a synthetic compound studied as a peroxisome proliferator-activated receptor delta agonist. Researchers developed it to explore treatments for lipid disorders and metabolic conditions. It is not an approved medicine in any country. Early clinical work examined changes in HDL cholesterol and triglycerides, but development was discontinued after animal studies raised concerns about cancer. The compound remains available as a research chemical and appears in discussions of performance enhancement.
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.
Clinical development stopped after rodent studies showed tumors at multiple sites. Whether those findings predict human cancer risk remains an open question, but they led sponsors to discontinue programs. Human safety data are limited to small, short-term studies that were not designed to assess cancer risk. Reported effects in those studies included changes in blood lipids, but the evidence is insufficient for medical use. Long-term consequences of nonmedical use are not well characterized. Questions about dose, duration, and individual susceptibility remain unresolved.
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.
| Property | Value | Notes |
|---|---|---|
| Common name | Cardarine | Also called GW501516 and endurobol. |
| Chemical formula | C21H18F3NO3S2 | Molecular weight about 453.5 g/mol. |
| Appearance | White to off-white solid | Form depends on synthesis and purity. |
| Solubility | Soluble in DMSO and ethanol | Low solubility in water. |
| Typical storage | -20 °C, desiccated, protected from light | Common for research chemicals. |
=== Treatment === Early administration (within 2–6 hours of bite) of antivenom and intubation for respiratory paralysis are keystones of management, but a chance of a hypersensivity reaction exists following antivenom administration. Neurotoxic symptoms may be irreversible once established due to the presynaptic nature of their pathology. The first taipan-specific antivenom was developed in 1954. Before this, tiger snake antivenom was used, though it was of little benefit in taipan envenomation.
=== Committee assignments === Committee on Armed Services (Vice Chair) Subcommittee on Tactical Air and Land Forces (Chair) Subcommittee on Seapower and Projection Forces Committee on Natural Resources Subcommittee on Fisheries, Wildlife, Oceans and Insular Affairs
Superoxide dismutase (or alternatively, myeloperoxidase) generates hydrogen peroxide from superoxide. Hydroxyl radicals are then generated via the Haber–Weiss reaction or the Fenton reaction, of which are both catalyzed by Fe2+. In the presence of halide ions, prominently chloride ions, myeloperoxidase uses hydrogen peroxide to produce hypochlorous acid. Nitric oxide synthase (the inducible isoform, iNOS, in immunity) catalyses the production of nitric oxide from L-arginine. Nitric oxide may react with superoxide anions to produce peroxynitrite anion.
The number of hydrogen bonds formed by a molecule of liquid water fluctuates with time and temperature. From TIP4P liquid water simulations at 25 °C, it was estimated that each water molecule participates in an average of 3.59 hydrogen bonds. At 100 °C, this number decreases to 3.24 due to the increased molecular motion and decreased density, while at 0 °C, the average number of hydrogen bonds increases to 3.69. Another study found a much smaller number of hydrogen bonds: 2.357 at 25 °C. Defining and counting the hydrogen bonds is not straightforward however. Because water may form hydrogen bonds with solute proton donors and acceptors, it may competitively inhibit the formation of solute intermolecular or intramolecular hydrogen bonds. Consequently, hydrogen bonds between or within solute molecules dissolved in water are almost always unfavorable relative to hydrogen bonds between water and the donors and acceptors for hydrogen bonds on those solutes. Hydrogen bonds between water molecules have an average lifetime of 10−11 seconds, or 10 picoseconds.
Sources: en.wikipedia.org
== Application in forensic science == The ability of the Coomassie dye to target amino acids with aromatic groups (phenylalanine, tyrosine, tryptophan) and basic side chains (lysine, arginine and histidine) allows the Bradford assay to be used for fingerprint analysis. The assay was successfully used to identify the biological sex of the fingerprint. Female samples were shown to have a higher absorbance than male samples when tested at similar wavelengths. This provides a simpler method for fingerprint analysis by reducing the number of amino acids needing to be analyzed from 23 to 6 and requires little to no assay preparation, in contrast to the ninhydrin chemical assay, which requires assay preparation such as heating and enzyme cascade.
After Banting's death, Best "claimed that the crucial innovation of using alcohol to remove toxic impurities had largely been his own", even though this had actually been Collip's key contribution. In 1972, an official history of the Nobel Committee declared that omitting Best might have been a mistake. In fact, Best was not considered because he was never nominated. Nomination for a Nobel Prize can only be made by certain individuals, including former recipients of the Prize, and his central role along with Banting was not known to those who had the ability to make nominations. Best was subsequently nominated for the 1950 Nobel Prize in physiology based on his work on choline and heparin. At the Centenary Celebration of the Nobel Prize for the Discovery of Insulin held by the Toronto Medical Society on November 27, 2023, Professor Erling Norrby, former chair of the Nobel Assembly at the Karolinska Institute, made a presentation - The Optimal Nobel Prize for Physiology or Medicine and presented the following information from the Nobel archives: “Best was nominated 14 times 1950-1954. The main nominator was Henry Dale who had been supervisor for Best’s Ph.D. work. The discovery proposed to be awarded was Best’s work on the lipotropic effect of choline, but Dale argued that separately that Best should have shared the 1923 prize to Banting. Best was subject to four evaluations by Ulf von Euler who gave support to Dale’s nomination. Although Best was declared worthy of a prize (1951, 1952, 1954) he never received it.”
The three substrates of this enzyme are D-glyceraldehyde 3-phosphate, phosphate (Pi), and oxidised nicotinamide adenine dinucleotide phosphate (NADP+). Its products are 1,3-bisphosphoglyceric acid, reduced NADPH, and a proton.
Sources: en.wikipedia.org
Cardarine is a common name for the investigational compound GW501516. It acts as a PPARδ agonist and is not approved for human use. It is prohibited in sport.
It activates PPARδ, a nuclear receptor that influences gene expression related to lipid and energy metabolism. Animal studies show changes in endurance and lipid levels. Human effects and risks are not well established.
No, cardarine is not a steroid. It belongs to a different chemical class, the PPARδ agonists. It is also not a selective androgen receptor modulator.
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.