The short version of Nuclear receptor fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2026-01-05 and is reviewed periodically as new material appears.
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.
The compound is typically described as a laboratory compound rather than a therapeutic product. Published reports have explored its role in lipid disorders, insulin sensitivity, and exercise metabolism, yet no major drug regulator has approved it for medical use. Commercial samples sold under the cardarine name may vary in purity and identity. Analytical confirmation is therefore necessary when the material is discussed in scientific or regulatory contexts. Its classification as a prohibited substance in sport further shapes how it is studied and reported.
Cardarine is a common name for GW501516, a synthetic compound studied for its effects on lipid and glucose metabolism. It functions as an agonist at peroxisome proliferator-activated receptor delta, or PPARδ, a nuclear receptor that influences gene expression. The molecule is not a steroid, nor is it a selective androgen receptor modulator. It is also known in research and sports literature as GW-501516 and endurobol. Early laboratory work examined its metabolic activity in cell cultures and animal models.
Activation of PPARδ changes transcription of genes involved in fatty acid transport, mitochondrial function, and skeletal muscle fuel preference. In rodent studies, pharmacological PPARδ activation was associated with increased endurance and altered body composition. These findings generated interest in performance enhancement, but species differences and study designs limit direct extrapolation to humans. Small human trials were conducted in the 2000s and later discontinued. The extent to which cardarine produces similar metabolic or performance effects in people remains an open question.
| 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. |
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 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.
Because cardarine is not an approved medicine, no pharmacopeial monograph defines its identity, purity, or storage requirements. Laboratories typically rely on in-house methods and reference standards when testing materials labeled as GW501516. Certificates of analysis may report purity and identity for a specific batch, but their scope varies and they do not guarantee safety or legal status. Independent verification can include high-performance liquid chromatography, mass spectrometry, nuclear magnetic resonance, and elemental analysis. The distinction between research chemical labeling and human use is significant because quality standards and oversight differ.
Cardarine can be detected in biological samples and product materials using liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). The method separates compounds by chromatography and identifies them by mass-to-charge transitions, allowing low-level detection in urine or blood. Sample preparation often involves enzymatic hydrolysis, solid-phase extraction, or protein precipitation. Certified reference materials and isotope-labeled internal standards improve quantification. Detection windows depend on metabolism, matrix, and assay sensitivity, so no single universal window applies.
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.
While being branded, ten blood samples were collected, heart rate measurements were taken, and vocalizations recorded with the microphone. These samplings occurred at uneven intervals during a 25-minute period, from five minutes before to twenty minutes after branding. This study determined that mean concentrations of plasma epinephrine were higher for hot branded calves than for both freeze branded calves and sham branded calves. Epinephrine levels peaked at 30 seconds for hot branded calves and at 1 minute for freeze branded calves. Heart rates, hormone concentrations, and epinephrine levels, the study's primary pain proxy, were all elevated in hot-branded calves. In terms of vocalization, one hot-branded and two freeze-branded calves expressed distress during branding, although this may have been due to the absence of other cattle in the calf's field of view. Calves branded in the presence of other calves were more likely to vocalize, as would be expected from herd animals. Another study also using calves monitored their escape-avoidance reaction. The vertical movement of a calf during branding was used as an operational definition to measure avoidance of the brand. The experimenters concluded that hot-branded calves tried harder to escape their branding irons than either the freeze-branded or sham-branded calves.
=== Mental health === Women with PMOS are far more likely to have depression than women without PMOS. Symptoms of depression might be heightened by certain symptoms of the condition, such as hirsutism or obesity, that can lead to low self-esteem or poor body image. Screening for depression and anxiety disorders is recommended using validated questionnaires, for instance, at diagnosis as well as afterwards, based on clinical judgement. For eating disorders and body image distress, screening is only recommended when clinically indicated. For sexually active women who give permission to discuss it, psychosexual dysfunction can be assessed too. Treatment of PMOS shows no to moderate effect on depression or anxiety, and standard therapies (such a psychotherapy and antidepressants) are recommended instead. Cognitive behaviour therapy can be used for girls and women with low self-esteem, poor body image, disordered eating or psychosexual dysfunction.
=== In other vertebrates === The primary function of prolactin in fish is osmoregulation, i.e., controlling the movement of water and salts between the tissues of the fish and the surrounding water. Like mammals, however, prolactin in fish also has reproductive functions, including promoting sexual maturation and inducing breeding cycles, as well as brooding and parental care. In the South American discus, prolactin may also regulate the production of a skin secretion that provides food for larval fry. An increase in brooding behaviour caused by prolactin has been reported in hens. Prolactin and its receptor are expressed in the skin, specifically in the hair follicles, where they regulate hair growth and moulting in an autocrine fashion. Elevated levels of prolactin can inhibit hair growth, and knock-out mutations in the prolactin gene cause increased hair length in cattle and mice. Conversely, mutations in the prolactin receptor can cause reduced hair growth, resulting in the "slick" phenotype in cattle. Additionally, prolactin delays hair regrowth in mice. Analogous to its effects on hair growth and shedding in mammals, prolactin in birds controls the moulting of feathers, as well as the age at onset of feathering in both turkeys and chickens. Pigeons, flamingos and male emperor penguins feed their young a cheese-like secretion from the upper digestive tract called crop milk, whose production is regulated by prolactin. In rodents, pseudopregnancy can occur when a female is mated with a sterile male.
It has been shown that certain surfactants, upon reaching a critical concentration, begin to self-assemble into micelles, which then compete with nanocrystal surfaces for other surfactant molecules. With fewer surface molecules interacting with the nanocrystal surface, crystal growth and aggregation is reported to occur at increased amounts. Use of surfactant at optimal concentrations reportedly allows for higher stability, larger drug capacity as a carrier, and sustained drug release. In a study using PEG as a stabilizer was found that nanocrystals treated with PEG enhanced accumulation at tumor sites and had greater blood circulation, than those not treated with PEG. Amorphization can occur in top-down methods of production. With different intramolecular arrangements, amorphization of nanocrystals leads to different thermodynamic and kinetic properties that affect drug delivery and kinetics. Transition to amorphous structures is reported to occur through production practices such as spray drying, lyophilization, and mechanical mechanisms, such as milling. This amorphization has been reportedly observed with or without the presence of stabilizer in a dry milling process. Using a wet milling process with surfactant, however significantly reduced amorphization, suggesting that solvent, in this case water, and surfactant could inhibit amorphization for some top-down production methods that otherwise reportedly facilitate amorphization.
=== Metabolism === Bacillus cereus has mechanisms for both aerobic and anaerobic respiration, making it a facultative anaerobe. Its aerobic pathway consists of three terminal oxidases: cytochrome aa3, cytochrome caa3, and cytochrome bd, the use of each dependent on the amount of oxygen present in the environment. The B. cereus genome encodes genes for metabolic enzymes including NADH dehydrogenases, succinate dehydrogenase, complex III, and cytochrome c oxidase, as well as others. Bacillus cereus can metabolize several different compounds to create energy, including carbohydrates, proteins, peptides, and amino acids. The Embden-Meyerhof pathway is the predominant pathway used by Bacillus cereus to catabolize glucose at every stage of the cell's development, according to estimates of a radiorespirometric method of glucose catabolism. This is true at times of germinative phases, as well as sporogenic phases. At the filamentous, granular, forespore, and transitional stages, the Embden-Meyerhof pathway was responsible for the catabolism of 98% of the cell's glucose. The remainder of the glucose was catabolized by the hexose monophosphate oxidative pathway. Analysis of the core genome of B. cereus reveals a limited presence of enzymes meant for breakdown of polysaccharides and a prevalence of proteases and amino acid degradation and transport pathways, indicating that their preferred diet consists of proteins and their breakdown products. An isolate of a bacterium found to produce PHBs was identified as B.
Sources: en.wikipedia.org
Noribogaine is a hERG inhibitor and appears at least as potent as ibogaine. The inhibition of the hERG potassium channel delays the repolarization of cardiac action potentials, resulting in QT interval prolongation and, subsequently, in arrhythmias and sudden cardiac arrest. Ibogaine and the structurally related hallucinogen harmaline are tremorigenic, whereas noribogaine is not or is much less so. Noribogaine, but not ibogaine, produces potent psychoplastogenic effects in vitro in preclinical research. This can be blocked by the serotonin 5-HT2A receptor antagonist ketanserin, by the mTOR inhibitor rapamycin, and by a TrkB antagonist.
== Interactions == Like other fluoroquinolones, delafloxacin chelates metals including aluminum, magnesium, sucralfate, iron, zinc, and divalent and trivalent cations like didanosine; using this drugs with antacids, some dietary supplements, or drugs buffered with any of these ions will interfere with available amounts of delafloxacin.
Regulation This pathway undergoes transcriptional regulation by FadR and FabR. FadR is the more extensively studied protein and has been attributed bifunctional characteristics. It acts as an activator of fabA and fabB transcription and as a repressor for the β-oxidation regulon. In contrast, FabR acts as a repressor for the transcription of fabA and fabB.
The Rockefeller Foundation continued funding German eugenics research even after it was clear that it was being used to rationalize discrimination against Jewish people and other groups, after the Nuremberg laws in 1935. In 1936, Rockefeller fulfilled pledges of $655,000 to Kaiser Wilhelm Institute, even though several distinguished Jewish scientists had been dropped from the institute at the time. The Rockefeller Foundation did not alert the world about the racist implications of Nazi ideology, but furthered and funded eugenic research through the 1930s. Even into the 1950s, Rockefeller continued to provide some funding for research borne out of German eugenics. The foundation also funded the relocation of scholars threatened by the Nazis to America in the 1930s, known as the Refugee Scholar Program and the Emergency Committee in Aid of Displaced Foreign Scholars. Some of the notable figures relocated or saved, among a total of 303 scholars, were Thomas Mann, Claude Lévi-Strauss and Leó Szilárd. The foundation helped The New School provide a haven for scholars threatened by the Nazis.
Sources: en.wikipedia.org
==== Extraction ==== Extraction of polyphenols can be performed using a solvent like water, hot water, methanol, methanol/formic acid, methanol/water/acetic or formic acid. Liquid–liquid extraction can be also performed or countercurrent chromatography. Solid phase extraction can also be made on C18 sorbent cartridges. Other techniques are ultrasonic extraction, heat reflux extraction, microwave-assisted extraction, critical carbon dioxide, high-pressure liquid extraction or use of ethanol in an immersion extractor. The extraction conditions (temperature, extraction time, ratio of solvent to raw material, particle size of the sample, solvent type, and solvent concentrations) for different raw materials and extraction methods have to be optimized. Mainly found in the fruit skins and seeds, high levels of polyphenols may reflect only the measured extractable polyphenol (EPP) content of a fruit which may also contain non-extractable polyphenols. Black tea contains high amounts of polyphenol and makes up for 20% of its weight. Concentration can be made by ultrafiltration. Purification can be achieved by preparative chromatography.
Proteases are a group of enzymes that show a broad range of cleavage specificities. Promiscuous proteases as digestive enzymes unspecifically degrade peptides, whereas highly specific proteases are involved in signaling cascades.
=== Later life and death === William H. Stein and his wife traveled around the world and hosted many prominent scientists in their own home in New York City throughout his scientific career. In addition to Stein's long-term professorship at Rockefeller Institute, he served as a visiting professor to the University of Chicago in 1961 and Harvard University in 1964. Stein also lectured at the Washington University in St. Louis and Haverford College. In 1969, Stein experienced sudden paralysis, diagnosed as Guillain–Barré syndrome, after developing a fever several days prior during a symposium in Copenhagen. Despite remaining quadriplegic the rest of his life, Stein's colleagues alleged that his spirit and sense of humor endured. He continued to be a guiding presence at the Rockefeller Institute to his younger colleagues and their work on the study of RNase. At the age of sixty-eight, Stein experienced unexpected heart failure. William H. Stein died February 2, 1980 in New York City.
== Stigma == A 2016 report on stigma concluded "there is no country, society or culture where people with mental illness have the same societal value as people without mental illness". It is also important to comprehend that there are different types of stigmas: the most commonly understood is public stigma, which involves the negative or discriminatory attitudes that others may have about mental illness; it often leads to a more structural stigma, which involves policies of government and private organizations that intentionally or unintentionally limit opportunities for people with mental illness (examples include lower budgets for mental illness research or fewer mental health services in comparison to other types health care); finally, it is unavoidable to not talk about self-stigma, which refers to the negative attitudes, including internalized shame, that people with mental illness may have about their own condition. And stigma about mental illnesses seems to be widely endorsed as well as many misconceptions, the more common being: people with mental illness are homicidal maniacs who need to be feared; they have childlike perceptions of the world that should be marveled; or they are responsible for their illness because they have weak character. Indeed, the public seems to disapprove of people with psychiatric disabilities significantly more than people with related conditions such as physical illness. Severe mental illness has been likened to drug addiction, prostitution, and criminality.
===== Post-market safety surveillance ===== After NDA approval, the sponsor must then review and report to the FDA every single patient adverse drug experience it learns of. They must report unexpected serious and fatal adverse drug events within 15 days, and other events on a quarterly basis. The FDA also receives directly adverse drug event reports through its MedWatch program. These reports are called "spontaneous reports" because reporting by consumers and health professionals is voluntary. While this remains the primary tool of post-market safety surveillance, FDA requirements for post-marketing risk management are increasing. As a condition of approval, a sponsor may be required to conduct additional clinical trials, called Phase IV trials. In some cases, the FDA requires risk management plans called Risk Evaluation and Mitigation Strategies (REMS) for some drugs that require actions to be taken to ensure that the drug is used safely. For example, thalidomide can cause birth defects, but has uses that outweigh the risks if men and women taking the drugs do not conceive a child; a REMS program for thalidomide mandates an auditable process to ensure that people taking the drug take action to avoid pregnancy; many opioid drugs have REMS programs to avoid addiction and diversion of drugs. The drug isotretinoin has a REMS program called iPLEDGE.
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 a common name for GW501516, a synthetic PPARδ agonist. It is not a steroid or a selective androgen receptor modulator. It was developed and studied as a research compound for metabolic pathways.