This is a working overview of PPARδ agonist, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-05-12. Anything still debated is marked as such rather than presented as settled.
Anti-doping laboratories identify GW501516 and its metabolites using liquid chromatography-tandem mass spectrometry. Urine is the usual matrix, and detection can occur after the parent compound has cleared from blood. The exact detection window depends on dose, formulation, individual metabolism, and assay sensitivity. Because the compound is prohibited at all times, athletes are subject to testing in and out of competition. Analytical methods continue to improve as new metabolites and designer analogs are characterized.
GW501516 acts as a ligand for PPAR delta, a nuclear receptor that regulates transcription of genes involved in fatty acid oxidation and energy use. Activation of this receptor in skeletal muscle shifts metabolism toward fat burning in animal models. The compound does not burn fat directly; it changes gene expression over hours to days. Researchers study it to understand metabolic flexibility and exercise adaptation. Effects observed in rodents are not automatically expected in humans.
PPARδ is a nuclear receptor that influences transcription of genes involved in fatty acid oxidation, lipid transport, and energy homeostasis. GW501516 binds and activates this receptor with high selectivity relative to PPARα and PPARγ in laboratory assays. Activation alters expression of target genes in skeletal muscle, liver, and adipose tissue in animal models. The exact clinical consequences of these changes in humans remain incompletely characterized, and observed effects in animals do not establish therapeutic benefit or safety.
Published studies have examined GW501516 in animal models of obesity, insulin resistance, and exercise endurance. Early human trials reportedly ended, and development was discontinued after preclinical findings raised concerns about cancer in some rodent studies. Regulatory agencies have not approved cardarine for any medical use. Its availability through non-pharmaceutical channels raises questions about identity, purity, and legal status that are separate from its laboratory pharmacology. Those questions are often addressed through analytical testing rather than assumptions about product labels.
Cardarine is a common name for GW501516, also GW-1516, a synthetic compound developed as a peroxisome proliferator-activated receptor delta (PPARδ) agonist. It belongs to a class of agents that modulate gene transcription related to lipid and energy metabolism. The compound was studied in preclinical and early clinical research for metabolic and cardiovascular conditions, but it did not progress to approved therapeutic use. Its name appears in fitness and sports contexts despite not being approved as a drug.
| Property | Value | Notes |
|---|---|---|
| Molecular target | PPAR delta (NR1C2) | Ligand-activated nuclear receptor. |
| Primary tissues studied | Skeletal muscle, liver, adipose | Effects on fatty acid oxidation and energy use. |
| Typical detection matrix | Urine | Used in anti-doping analysis. |
| Common analytical method | LC-MS/MS | Detects parent compound and metabolites. |
| Sport regulatory class | Prohibited at all times | Listed as a metabolic modulator by WADA. |
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.
The pharmacological interest in cardarine centers on PPARδ activation and its downstream effects on lipid handling and mitochondrial function. In animal studies, PPARδ agonists have been associated with changes in exercise endurance and fatty acid utilization, though results vary by model and protocol. Human data remain sparse, and the absence of large controlled trials limits conclusions about efficacy. Researchers often describe the compound as a tool for probing PPARδ biology rather than a proven therapeutic agent.
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 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.
== Duty of care == In the UK, in April 2008, the Corporate Manslaughter Act was strengthened to target company directors as well as their drivers in cases of road deaths involving vehicles used on business. The Police have said they now treat every road death as 'an unlawful killing' and have the power to seize company records and computers during their investigations. They will bring prosecutions against company directors who fail to provide clear policies and guidance for their employees driving at work. Unfortunately, in the UK a number of businesses are failing to meet their duty of care. In particular prosecutions can be brought against company directors for failing to meet their duty of care and allowing HGV driver hours to exceed the legal limits. Failure to comply with EU rules can result in a fixed penalty of up to £300, a graduated deposit of up to £1500 or you could be summoned to court. Directors and business owners may not be aware that privately owned vehicles used for business journeys are treated exactly the same as company owned vehicles. Directors have an equal responsibility under the law to ensure these vehicles are also roadworthy and correctly insured. It is vital that every company has a 'Driving at Work' policy in place covering every element of their business vehicle operation, no matter how few vehicles are involved and who owns them. Every employee driving for business is required to sign up to the policy. In this way, the directors can reduce the risk of being prosecuted and a possible custodial sentence.
=== Depigmentation === In cases of extensive vitiligo, the option to depigment the unaffected skin with topical medications, such as monobenzone, mequinol, or hydroquinone may be considered to even out skin tone. The removal of all the skin pigment with monobenzone is permanent and vigorous. Lifelong sun safety is required to avoid severe sunburn and melanomas. Depigmentation takes about a year to complete.
== Purpose == The purpose of the GxP quality guidelines is to ensure a product is safe and meets its intended use. GxP guides quality manufacture in regulated industries including food, drugs, medical devices, and cosmetics. The most central aspects of GxP are good documentation practices (GDP), which are expected to be "ALCOA":
=== John B. Fenn Award for a Distinguished Contribution in Mass Spectrometry (since 1990) === 2024 Jennifer Brodbelt 2023 Carol Vivien Robinson 2017 Catherine E. Costello 2012 Catherine C. Fenselau 2009 Vicki H. Wysocki
Sources: en.wikipedia.org
In 1999, American scientists at the University of California, Berkeley, announced that they had succeeded in synthesizing three atoms of 293Og. These parent nuclei were reported to have successively emitted three alpha particles to form copernicium-281 nuclei, which were claimed to have undergone alpha decay, emitting alpha particles with decay energy 10.68 MeV and half-life 0.90 ms, but their claim was retracted in 2001 as it had been based on data fabricated by Ninov. This isotope was truly produced in 2010 by the same team; the new data contradicted the previous fabricated data. The missing isotopes 278Cn and 279Cn are too heavy to be produced by cold fusion and too light to be produced by hot fusion. They might be filled from above by decay of heavier elements produced by hot fusion, and indeed 280Cn and 281Cn were produced this way. The isotopes 286Cn and 287Cn could be produced by charged-particle evaporation, in the reaction 244Pu(48Ca,αxn) with x equalling 1 or 2.
=== Signaling pathways for mast cell activation === Specific signaling pathways of mast cells in different tissues provide mechanisms by which the immune system detects and is organized to deal with potential threats. Mast cells can be stimulated to degranulate by allergens through cross-linking with immunoglobulin E receptors (e.g., FcεRI), physical injury through pattern recognition receptors for damage-associated molecular patterns (DAMPs), microbial pathogens through pattern recognition receptors for pathogen-associated molecular patterns (PAMPs), and various compounds through their associated G-protein coupled receptors (e.g., morphine through opioid receptors) or ligand-gated ion channels. Complement proteins can activate membrane receptors on mast cells to exert various functions as well.
== Properties == Protolichesterinic acid is a member of the class of chemicals known as lactone fatty acids, a group that includes lichesterinic acid, alloprotolichesterinic acid, nephromopsinic acid, and nephrosterinic acid. In its purified form, protolichesterinic acid is a crystalline solid that forms lustrous plates when recrystallized from benzene or acetic acid at temperatures below 50 °C (122 °F). It has a melting point of 107.5 °C (225.5 °F). The compound exists in both enantiomeric forms, with the (+)-enantiomer showing an optical rotation of [α]D +12° in chloroform and the (-)-enantiomer showing [α]D -12° in chloroform. In ultraviolet–visible spectroscopy, it shows maximum absorption at 218 nm in methanol. Its infrared spectrum (KBr) shows characteristic peaks including those corresponding to carboxylic acid (3450 cm−1), alkene (3050 cm−1), and carbonyl (1720 cm−1) functionalities. Nuclear magnetic resonance spectroscopy confirms its structure, with distinctive signals in the 1H NMR spectrum including the terminal methyl group at δ 0.68 ppm and alkene protons at δ 6.03 and 6.39 ppm. The 13C NMR spectrum shows key resonances for the carboxylic acid (174.4 ppm), alkene (132.6 and 125.9 ppm), and lactone carbonyl (168.2 ppm) carbons.
=== Acid-base reactions === Carboxylic acids react with bases to form carboxylate salts, in which the hydrogen of the hydroxyl (–OH) group is replaced with a metal cation. For example, acetic acid found in vinegar reacts with sodium bicarbonate (baking soda) to form sodium acetate, carbon dioxide, and water:
== Mosher's method == Mosher's acid, via its acid chloride derivative, reacts readily with alcohols and amines to give esters and amides, respectively. The lack of an alpha-proton on the acid prevents loss of stereochemical fidelity under the reaction conditions. Thus, using an enantiomerically pure Mosher's acid allows for determination of the configuration of simple chiral amines and alcohols. For example, the (R)- and (S)-enantiomers of 1-phenylethanol react with (S)-Mosher acid chloride to yield (R,S)- and (S,S)-diastereomers, respectively, that are distinguishable in NMR.
Sources: en.wikipedia.org
When structures in different species are believed to exist and develop as a result of common adaptive responses to environmental pressure, those structures are termed convergent. For example, the fronds of Bryopsis plumosa and stems of Asparagus setaceus both have the same feathery branching appearance, even though one is an alga and one is a flowering plant. The similarity in overall structure occurs independently as a result of convergence. The growth form of many cacti and species of Euphorbia is very similar, even though they belong to widely distant families. The similarity results from common solutions to the problem of surviving in a hot, dry environment.
An inactive treatment or procedure that is intended to mimic as closely as possible a therapy in a clinical trial. Also called sham therapy. (NCI) The term also refers to psychotherapy that obtains its positive effect through the use of principles of social influence. Population study
==== Gastrointestinal and colorectal cancer ==== Reviews of preliminary clinical trials on people with colorectal or gastrointestinal cancer suggest that soy isoflavones may have a slight protective effect against such cancers.
=== Gambling === To help pay for his 2019 capital spending bill, Pritzker expanded gambling, allowing more casinos and legalized sports betting. This did not mean new casinos could be built and sports betting could begin right away: granting licenses for such activities is the job of the Illinois Gaming Board, and the process is a complex one, lasting several months or more and involving extensive criminal background checks, among other requirements. According to the governor's office, gambling will bring an additional $350 million in revenue each year. This gambling expansion bill extends to Chicago, something the city wanted. Chicago mayor Lori Lightfoot emphasized economic development in the city's South and West sides during her campaign. She has argued that a new casino, privately owned, and associated hospitality and entertainment venues will bring money into the city. On May 5, 2022, Lightfoot announced that she had selected Bally's Corporation's bid to construct a casino resort near the Chicago River.
Sources: en.wikipedia.org
It binds to and activates PPAR delta, a nuclear receptor that controls expression of genes related to fatty acid oxidation. This mechanism can alter energy metabolism in animal models. It is not a direct stimulant or fat-burning enzyme.
Early-stage trials examined lipid and glucose markers, but the development program was discontinued. Published human results are limited and do not support approved use for any indication. Claims of performance or health benefits remain unproven.
Yes. Laboratories use LC-MS/MS to detect GW501516 and its metabolites in urine. Detection depends on timing and sensitivity, but the substance is banned at all times.
Cardarine is commonly known as GW501516 or GW-1516. These names refer to the same synthetic compound. It is not a brand-name approved medicine.