Everything below concerns LC-MS/MS. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-03-22. Where a claim depends on a specific study, the study is described rather than over-claimed.
GW501516 acts as an agonist at peroxisome proliferator-activated receptor delta, a nuclear receptor involved in transcription of genes related to lipid handling and energy use. Activation of PPARδ can shift skeletal muscle toward greater fatty acid oxidation in animal models, which is one reason it drew interest for metabolic disease and exercise research. The exact downstream effects depend on tissue, species, dose, and duration. Human data are sparse, so many proposed benefits remain hypotheses rather than established clinical outcomes.
Laboratory studies have examined GW501516 in cell cultures and rodents for conditions such as dyslipidemia, insulin resistance, and obesity. Some trials in humans were initiated, but development was discontinued after preclinical findings raised concerns about cancer in certain models. Those findings do not prove that the compound causes cancer in people, but they contributed to regulatory caution. Later reviews often describe the evidence as preliminary and insufficient for assessing long-term safety.
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.
Cardarine is a common name for GW501516, a synthetic compound developed in the 1990s through research collaborations involving GlaxoSmithKline. It belongs to a class of molecules known as peroxisome proliferator-activated receptor delta agonists. Early studies explored its effects on lipid metabolism and energy expenditure in animal models. The compound was never approved as a human medicine, and clinical development was discontinued. In the years since, it has appeared in fitness and bodybuilding communities as a performance-enhancing substance. Regulatory agencies classify it as an unapproved drug.
| Property | Value | Notes |
|---|---|---|
| Solubility | Soluble in dimethyl sulfoxide and some organic solvents; practically insoluble in water | Solvent choice affects laboratory handling |
| Typical storage | -20 °C, desiccated, protected from light | Common condition for research samples |
| Analytical method | Liquid chromatography–tandem mass spectrometry (LC-MS/MS) | Used for identification and quantification in biological or product samples |
| Common synonyms | GW501516, GW-501516, GSK-516, Endurobol | Names found in research and anti-doping literature |
| Regulatory status | Unapproved therapeutic; prohibited in competitive sport | Status can vary by country and context |
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.
Regulatory treatment of cardarine differs by context and jurisdiction. In competitive sport, the World Anti-Doping Agency lists PPARδ agonists, including GW501516, as prohibited at all times. Outside sport, it lacks approval as a prescription medicine in major drug markets, and products sold for human consumption may be treated as unapproved drugs. Some countries also restrict importation or sale through general consumer protection and medicines laws. These classifications affect availability, testing, and legal risk without establishing therapeutic value.
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 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.
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.
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.
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.
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.
Preclinical research reported that GW501516 increased running endurance in mice and improved lipid profiles in some animal species. Early human trials explored effects on high-density lipoprotein cholesterol, triglycerides, and glucose handling, but the program was discontinued. Published human data are sparse and do not establish efficacy for any condition. Studies also examined PPAR delta in cancer biology, with conflicting findings across models. The relationship between receptor activation, tissue context, and disease risk remains an active area of investigation.
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.
Ahmedin Muktar Jemal is an American cancer epidemiologist who serves as senior vice president of the Surveillance & Health Equity Science Department of the American Cancer Society. He has been researching racial differences in lung cancer rates since the mid-1990s, when he was a fellow at the National Cancer Institute.
Clematis ispahanica Bioss Clematis × jackmanii T.Moore – Jackman's clematis Clematis koreana Kom. – Korean clematis Clematis lanuginosa Lindl. & Paxton Clematis lasiantha Nutt. – pipestem clematis Clematis leptophylla (F.Muell. ex Benth.) H.Eichler Clematis ligusticifolia Nutt. – western white clematis, hierba de chivo Clematis linearifolia Steud. Clematis macropetala Ledeb. – downy clematis Clematis mandshurica Clematis marmoraria Sneddon – New Zealand dwarf clematis Clematis microphylla DC. – small-leaved clematis Clematis montana Buch.-Ham. ex DC. – anemone clematis Clematis morefieldii Kral – Huntsville vasevine Clematis napaulensis DC. Clematis occidentalis (Hornem.) DC. – western blue virginsbower Clematis ochroleuca Ait. – curlyheads Clematis orientalis L. – Chinese clematis Clematis palmeri Rose – Palmer clematis Clematis paniculata J.F.Gmel. – puawhananga Clematis patens C.Morren & Decne. Clematis pauciflora Nutt. – ropevine clematis Clematis pickeringii A.Gray Clematis pitcheri Torr. & A.Gray – bluebill Clematis pubescens Hügel ex Endl. – common clematis Clematis recta L. – ground clematis Clematis reticulata Walter – netleaf leather flower Clematis rhodocarpa Rose Clematis smilacifolia Wall. Clematis socialis Kral – Alabama leather flower Clematis stans Siebold & Zucc. – kusabotan Clematis tangutica (Maxim.) Korsh. – golden clematis Clematis terniflora DC. – sweet autumn clematis Clematis texensis Buckley – scarlet leather flower Clematis urophylla Clematis versicolor – manycolored leather flower Clematis verticillaris – purple virgins bower Clematis viorna L.
Impact factor data ... have a strong influence on the scientific community, affecting decisions on where to publish, whom to promote or hire, the success of grant applications, and even salary bonuses. More targeted research has begun to provide firm evidence of how deeply the impact factor is embedded within formal and informal research assessment processes. A review in 2019 studied how often the JIF featured in documents related to the review, promotion, and tenure of scientists in US and Canadian universities. It concluded that 40% of universities focused on academic research specifically mentioned the JIF as part of such review, promotion, and tenure processes. A 2017 study of how researchers in the life sciences behave concluded that "everyday decision-making practices as highly governed by pressures to publish in high-impact journals." It has been argued that the deeply embedded nature of such indicators not only affects research assessment, but the more fundamental issue of what research is actually undertaken: "Given the current ways of evaluation and valuing research, risky, lengthy, and unorthodox project rarely take center stage."
Sublingual administration of medications that are subject to a high first-pass effect with oral administration can result in improved bioavailability because the first pass through the intestines and liver is bypassed. As a result, sublingual estradiol has been found to result in estradiol levels and a ratio of estradiol to estrone that are substantially higher than oral estradiol. Maximal circulating levels of estradiol are as much as 10-fold higher with sublingual administration than with oral administration, and the absolute bioavailability of estradiol is approximately 5-fold higher. On the other hand, levels of estradiol fall rapidly with sublingual administration, whereas they remain elevated for a prolonged period of time with oral administration. This is due to the large circulating pool of hormonally inert estrogen conjugates with long half-lives that is reversibly generated with oral estradiol during first-pass metabolism, which serves as a metabolism-resistant and long-lasting reservoir for continuous reconversion back into estradiol. It is also responsible for the differences in ratios between sublingual estradiol and oral estradiol in terms of maximal estradiol levels (10:1) achieved and absolute bioavailability (5:1). A study in marmoset monkeys found that the bioavailability of sublingual estradiol was 10% of that of estradiol administered by intramuscular injection. After a dose of sublingual estradiol, levels of estrone start to slowly but progressively rise within 10 minutes.
Sources: en.wikipedia.org
In October 2016, he was selected as a "full member" of the Royal College of Physicians of Edinburgh, one of only a handful of Turkish nationals to receive that honor, marked by a ceremony in which Okan's membership diploma was bestowed upon him by then-President of the Royal College, and later director of the National Institute for Health Research, Derek Bell. In November 2020, he was awarded an FRCP from the Royal College of Physicians of London, and in January 2021 awarded an FRCP from the Royal College of Physicians of Ireland. In his early days, he started his career as a dermatologist at Acibadem Bakirkoy Hospital and later worked Medical Park Hospital and Memorial Bahcelievler Hospital as an associate professor and also as a skin diseases specialist. He founded and chaired the Dermatology Department at Istanbul Kemerburgaz University in 2013. He volunteered with Health Volunteers Overseas as part of the Dermatology program at Preah Kossamak Hospital, Phnom Penh, Cambodia. He assisted in the training of dermatology students, provided continuing education regarding current and new trends of dermatologic diagnosis and treatment and provided training to nurses and physicians involved in dermatologic care. In 2021, Okan and his team reported their findings that psoriasis patients had unusually high levels of neurofilament and Tau protein, which act as a skeleton in the nerve cells in these patients. These levels were higher than those of non-sick individuals, especially when compared to the levels of those with severe psoriasis under the age of 40.
== Pharmacology == The drug is a selective KOR antagonist and shows approximately 10- to 20-fold higher affinity for the KOR (Ki = 1–3 nM) over the μ-opioid receptor (MOR) (Ki = 10–64 nM) and has negligible affinity for the δ-opioid receptor (DOR) (Ki > 4,000 nM). It is a "short-acting" or non-inactivating antagonist of the KOR (as opposed to irreversible antagonists like JDTic). Although originally characterized as a KOR neutral antagonist however, subsequent research revealed in 2020 that PF-04455242 is actually only a moderately efficacious partial antagonist of the KOR (Imax ≈ 50%). In any case, the drug reversed the analgesic and prolactin-elevating effects of the KOR agonist spiradoline in animals, showed efficacy in animal models predictive of antidepressant activity, and reversed stress-induced reinstatement of cocaine-seeking behavior. However, PF-04455242 also showed a variety of other weak off-target activities.
Ewan Gordon McGregor ( YOO-ən; born 31 March 1971) is a Scottish actor and filmmaker. His accolades include a Golden Globe Award and a Primetime Emmy Award. In 2013, he was appointed Officer of the Order of the British Empire (OBE) for his service to drama and charity. While studying drama at the Guildhall School of Music and Drama, McGregor began his career with a leading role in the British series Lipstick on Your Collar (1993). He gained international recognition for starring as drug addict Mark Renton in Trainspotting (1996), and as Obi-Wan Kenobi in the Star Wars prequel trilogy (1999–2005). His career progressed with starring roles in the musical Moulin Rouge! (2001) for which he was nominated for the AACTA Award for Best Actor in a Leading Role, action film Black Hawk Down (2001), fantasy film Big Fish (2003), and thriller Angels and Demons (2009). He was praised for his performances in the thriller The Ghost Writer (2010) and the romantic comedy Salmon Fishing in the Yemen (2011). McGregor made his directorial debut with the crime film American Pastoral (2016), in which he also starred. For his dual role as brothers Ray and Emmit Stussy in the third season of the anthology series Fargo (2017), he won the Golden Globe Award for Best Actor – Miniseries or Television Film. He portrayed and voiced Lumière in Beauty and the Beast (2017), and played the title role in Christopher Robin (2018), Dan Torrance in Doctor Sleep (2019), and Black Mask in Birds of Prey (2020).
Sources: en.wikipedia.org
It binds and activates PPARδ, a nuclear receptor that influences gene expression related to fatty acid metabolism and energy balance. This mechanism has been studied mainly in animals and cell models, not established as a safe human therapy.
No. It is not an anabolic-androgenic steroid; it is a synthetic PPARδ agonist. Because it is banned in sport, it is sometimes grouped with doping agents even though its chemical class differs from steroids.
Human data are limited and development was discontinued, so major effects and long-term risks are not well characterized. Some early studies examined metabolic markers, but they do not provide a basis for unsupervised use.
Cardarine is a common name for GW501516, a synthetic PPARδ agonist developed for research. It has not been approved as a medication in any country. It is classified as an unapproved drug and a prohibited substance in sport.