LC-MS/MS is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Last reviewed on 2025-09-21. Where a claim depends on a specific study, the study is described rather than over-claimed.
GW501516 acts on PPARδ, a nuclear receptor that helps regulate fatty acid oxidation and energy homeostasis. In animal studies, activation of this receptor was associated with increased endurance and changes in lipid metabolism. Human trials examined effects on blood lipids and other metabolic markers, but the compound did not advance to approval. Rodent studies later reported tumors in multiple tissues at doses used in those experiments. Whether those findings translate to human risk remains uncertain, and the clinical relevance of the animal data is still debated.
Regulatory bodies treat GW501516 as a prohibited substance in competitive sport. The World Anti-Doping Agency added it to the prohibited list, and it falls under classes covering metabolic modulators and hormone-related agents. It is not approved by drug regulators for human use, and it is not a lawful dietary supplement. Products sold under the cardarine name may contain unlisted ingredients or different compounds. Because no approved product exists, quality and identity are not guaranteed by pharmaceutical manufacturing standards.
Cardarine is a common name for the investigational chemical GW501516, also written GW-1516. It was developed as a peroxisome proliferator-activated receptor delta agonist for metabolic conditions such as dyslipidemia. Early research focused on lipid handling and energy use in skeletal muscle and other tissues. The compound was never approved as a medicine. In public discussion, it is often grouped with performance-enhancing substances, although its receptor target differs from that of anabolic steroids or selective androgen receptor modulators. Regulatory and health authorities have issued warnings about its use.
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.
| Property | Value | Notes |
|---|---|---|
| Common name | Cardarine | Common internet and media name. |
| Research code | GW501516 | Also written GW-1516. |
| Drug class | PPARδ agonist | Not a selective androgen receptor modulator. |
| Development status | Discontinued | Clinical development halted after rodent cancer findings. |
| Regulatory status | Prohibited in sport | Listed by WADA; not approved as medicine. |
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.
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.
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.
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.
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.
When dried for eating, pine nuts are 2% water, 13% carbohydrates, 14% protein, and 68% fat (table). In a 100-gram (3+1⁄2-ounce) reference serving, dried pine nuts supply 2,815 kilojoules (673 kilocalories) of food energy and are a rich source (20% or more of the Daily Value, DV) of numerous dietary minerals, particularly manganese, copper, magnesium, and zinc, with substantial amounts of vitamin E, vitamin K, and the B vitamins, thiamin and niacin (table).
A mismatch between the circadian rhythm and the meals schedule, such as in circadian rhythm disorders, may increase insulin resistance. Insufficient sleep has been shown to cause insulin resistance, and also increases the risk of developing metabolic diseases such as type 2 diabetes and obesity.
== Further reading == Andersen, O.M. (2006). Flavonoids: Chemistry, Biochemistry and Applications. Boca Raton FL: CRC Press. ISBN 978-0-8493-2021-7. Gould, K.; Davies, K.; Winefield, C., eds. (2008). Anthocyanins: Biosynthesis, Functions, and Applications. Springer. ISBN 978-0-387-77334-6.
Sources: en.wikipedia.org
corrosion An irreversible interfacial chemical reaction of a material, especially a metal, with its environment, which results in consumption of the material or dissolution into the material of an external component of the environment.
in the range of 108 – 1010 M−1 s−1. These enzymes are so efficient they effectively catalyse a reaction each time they encounter a substrate molecule and have thus reached an upper theoretical limit for efficiency (diffusion limit); and are sometimes referred to as kinetically perfect enzymes. But most enzymes are far from perfect: the average values of
Congenital tracheomalacia often improves without specific intervention; when required, interventions may include beta agonists and muscarinic agonists, which enhance the tone of the smooth muscle surrounding the trachea; positive pressure ventilation, or surgery, which may include the placement of a stent, or the removal of the affected part of the trachea. In dogs, particularly miniature dogs and toy dogs, tracheomalacia, as well as bronchomalacia, can lead to tracheal collapse, which often presents with a honking goose-like cough.
Sources: en.wikipedia.org
=== EC 1.14.99 Miscellaneous === EC 1.14.99.1: prostaglandin-endoperoxide synthase EC 1.14.99.2: kynurenine 7,8-hydroxylase EC 1.14.99.3: Now EC 1.14.14.18, heme oxygenase (biliverdin-producing) EC 1.14.99.4: progesterone monooxygenase EC 1.14.99.5: Now EC 1.14.19.1, stearoyl-CoA 9-desaturase EC 1.14.99.6: Now EC 1.14.19.2, acyl-[acyl-carrier-protein] desaturase EC 1.14.99.7: Transferred to EC 1.14.13.132, squalene monooxygenase EC 1.14.99.8: Now included with EC 1.14.14.1 unspecific monooxygenase EC 1.14.99.9: Now classified as EC 1.14.14.19, steroid 17α-monooxygenase EC 1.14.99.10: Now EC 1.14.14.16, steroid 21-monooxygenase EC 1.14.99.11: estradiol 6β-monooxygenase EC 1.14.99.12: 4-androstene-3,17-dione monooxygenase EC 1.14.99.13: Now EC 1.14.13.23, 3-hydroxybenzoate 4-monooxygenase EC 1.14.99.14: Now EC 1.14.14.197, progesterone 11α-monooxygenase EC 1.14.99.15: 4-methoxybenzoate monooxygenase (O-demethylating) EC 1.14.99.16: Now EC 1.14.13.72, methylsterol monooxygenase EC 1.14.99.17: Now EC 1.14.16.5, glyceryl-ether monooxygenase EC 1.14.99.18: deleted EC 1.14.99.19: Now classified as EC 1.14.19.77, plasmanylethanolamine desaturase EC 1.14.99.20: phylloquinone monooxygenase (2,3-epoxidizing) EC 1.14.99.21: Latia-luciferin monooxygenase (demethylating) EC 1.14.99.22: ecdysone 20-monooxygenase EC 1.14.99.23: 3-hydroxybenzoate 2-monooxygenase EC 1.14.99.24: steroid 9α-monooxygenase EC 1.14.99.25: Now EC 1.14.19.3, linoleoyl-CoA desaturase EC 1.14.99.26: 2-hydroxypyridine 5-monooxygenase EC 1.14.99.27: Now classified as EC 1.17.3.4, juglone 3-monooxygenase EC 1.14.99.28: Now EC 1.14.14.84, linalool 8-monooxygenase EC 1.14.99.29: deoxyhypusine monooxygenase EC 1.14.99.30: Now EC 1.3.5.6, 9,9′-dicis-ζ-carotene desaturase. EC 1.14.99.31: Now classified as EC 1.14.19.24, myristoyl-CoA 11-(E) desaturase EC 1.14.99.32: Now classified as EC 1.14.19.5, acyl-CoA 11-(Z)-desaturase EC 1.14.99.33: Now EC 1.14.19.39, acyl-lipid Δ12-acetylenase EC 1.14.99.34: monoprenyl isoflavone epoxidase EC 1.14.99.35: thiophene-2-carbonyl-CoA monooxygenase EC 1.14.99.36: Now classified as EC 1.13.11.63, β-carotene 15,15′-dioxygenase EC 1.14.99.37: Now EC 1.14.14.176, taxadiene 5α-hydroxylase EC 1.14.99.38: cholesterol 25-hydroxylase EC 1.14.99.39: ammonia monooxygenase EC 1.14.99.40: Now EC 1.13.11.79, 5,6-dimethylbenzimidazole synthase EC 1.14.99.41: Now EC 1.13.11.75, all-trans-8′-apo-β-carotenal 15,15′-oxygenase EC 1.14.99.42: Now EC 1.13.11.84, crocetin dialdehyde synthase EC 1.14.99.43: Now EC 1.14.14.134, β-amyrin 24-hydroxylase EC 1.14.99.44: diapolycopene oxygenase EC 1.14.99.45: Now EC 1.14.14.158, carotene ε-monooxygenase EC 1.14.99.46: pyrimidine oxygenase EC 1.14.99.47: (+)-larreatricin hydroxylase EC 1.14.99.48: heme oxygenase (staphylobilin-producing) EC 1.14.99.49: Now EC 1.14.15.31, 2-hydroxy-5-methyl-1-naphthoate 7-hydroxylase EC 1.14.99.50: γ-glutamyl hercynylcysteine S-oxide synthase EC 1.14.99.51: hercynylcysteine S-oxide synthase EC 1.14.99.52: L-cysteinyl-L-histidinylsulfoxide synthase EC 1.14.99.53: lytic chitin monooxygenase EC 1.14.99.54: lytic cellulose monooxygenase (C1-hydroxylating) EC 1.14.99.55: lytic starch monooxygenase EC 1.14.99.56: lytic cellulose monooxygenase (C4-dehydrogenating) EC 1.14.99.57: heme oxygenase (mycobilin-producing) EC 1.14.99.58: heme oxygenase (biliverdin-IX-β and δ-forming) EC 1.14.99.59: tryptamine 4-monooxygenase EC 1.14.99.60: 3-demethoxyubiquinol 3-hydroxylase EC 1.14.99.61: cyclooctat-9-en-7-ol 5-monooxygenase EC 1.14.99.62: cyclooctatin synthase EC 1.14.99.63: β-carotene 4-ketolase EC 1.14.99.64: zeaxanthin 4-ketolase EC 1.14.99.65: 4-amino-L-phenylalanyl-[CmlP-peptidyl-carrier-protein] 3-hydroxylase EC 1.14.99.66: [histone H3]-N6,N6-dimethyl-L-lysine4 FAD-dependent demethylase EC 1.14.99.67: α-N-dichloroacetyl-p-aminophenylserinol N-oxygenase EC 1.14.99.68: 4-aminobenzoate N-oxygenase EC 1.14.99.69: tRNA 2-(methylsulfanyl)-N6-isopentenyladenosine37 hydroxylase
=== Blood supply === Branches of the internal pudendal arteries are the main arterial supply. The dorsal arteries of the penis run alongside the dorsal vein between the corpora cavernosa and supply the fibrous tissue surrounding them, the corpus spongiosum, the spongy urethra and the penile skin. The deep arteries of the penis run in the centre of each corpus cavernosum and supply the erectile tissue; their branches, the helicine arteries, are coiled when the penis is flaccid. The penile skin is also supplied by superficial and deep branches of the external pudendal arteries. The deep dorsal vein of the penis receives blood from a venous plexus draining the cavernous spaces, while the superficial dorsal vein drains the skin and subcutaneous tissue.
== Definition == The classifications of substances as performance-enhancing substances are not entirely clear-cut and objective. As in other types of categorization, certain prototype performance enhancers are universally classified as such (like anabolic steroids), whereas other substances (like vitamins and protein supplements) are virtually never classified as performance enhancers despite their effects on performance. As is usual with categorization, there are borderline cases; caffeine, for example, is considered a performance enhancer by some but not others.
Both Takin' It to the Streets and Livin' on the Fault Line reflected Johnston's diminished role in the group following his illness. Restored to fitness and briefly back in the fold, he contributed one original song to Takin' It to the Streets ("Turn It Loose"), and also sang a verse on Simmons' tune "Wheels of Fortune". He also made live appearances with the band in 1976 (documented in a concert filmed that year at the Winterland in San Francisco, excerpts of which appear occasionally on VH1 Classic) but was sidelined once again that fall due to exhaustion. The Doobie Brothers recorded five new Johnston compositions for Livin' on the Fault Line, but Johnston decided the band's direction had strayed too far from their original sound. He left the band he co-founded, withdrew permission for the Doobie Brothers to use the five songs he contributed to Livin' on the Fault Line, and embarked on a solo career that eventually yielded one modestly successful 1979 Warner Brothers album, Everything You've Heard is True, which featured the single "Savannah Nights", and the less successful album Still Feels Good in 1981. Regardless, he received credit for guitars and vocals on Livin' on the Fault Line and was pictured on the album's inner sleeve band photo. During this period of transition, the band also elevated former roadie Bobby LaKind to onstage backup vocalist and percussionist. In the studio, LaKind first contributed percussion to Takin' It to the Streets but had been a member of the band's lighting crew since 1974.
Sources: en.wikipedia.org
No. Cardarine is a PPARδ agonist, while selective androgen receptor modulators act on androgen receptors. The two classes differ in receptor target and downstream effects.
Preclinical rodent studies reported cancers, including liver and bladder tumors, at tested doses. The human relevance of those findings is uncertain, but development was discontinued. No approved human product resulted.
No. It remains an investigational compound without approved therapeutic labeling. Sports regulators prohibit its use, and health agencies have warned against consuming it.
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.