This is a working overview of Laboratory compound, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-01-24. Anything still debated is marked as such rather than presented as settled.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic PPARδ agonist | Not a steroid or a selective androgen receptor modulator. |
| Common synonyms | Cardarine, GW501516, GW-501516, endurobol | Names vary by supplier and literature source. |
| Appearance | White to off-white powder | Consistent with many small-molecule research chemicals. |
| Solubility | Low in water; soluble in DMSO and ethanol | Often prepared in organic solvent for laboratory work. |
| Primary target | PPARδ (NR1C2) | Nuclear receptor involved in lipid and energy metabolism. |
Safety concerns emerged from long-term animal studies. In rodents given the compound for extended periods, researchers found an increased incidence of certain cancers, including liver and bladder tumors. These findings contributed to the discontinuation of clinical development. Whether similar risks apply to short-term or low-level exposure in humans is not established, and controlled human safety data are limited. The relevance of high-dose rodent carcinogenicity findings to human use remains a subject of debate.
Human trials of GW501516 were small and short in duration. They examined lipid levels, glucose handling, and other metabolic markers, but the programs were halted after the animal cancer findings. No approved therapeutic product exists, and published human data are insufficient for establishing long-term safety. Reports of use for athletic performance come mainly from non-clinical settings and cannot be verified through controlled trials. Independent testing of products sold as cardarine has found inconsistent purity and labeling.
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.
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.
== Biomedical applications == DNA origami, being made of a natural biological polymer, is well suited to the biological environment when salt concentrations allow, and offers fine control over the positioning of molecules and structures in the system. This allows DNA origami to be applicable to a number of scenarios in biomedical engineering. Current biomedical applications include drug release with 0 order mechanisms, vaccines, cell signaling, and sensing applications. DNA is folded into an octahedron and coated with a single bilayer of phospholipid, mimicking the envelope of a virus particle. The DNA nanoparticles, each at about the size of a virion, are able to remain in circulation for hours after being injected into mice. It also elicits a much lower immune response than the uncoated particles. It presents a potential use in drug delivery, reported by researchers at the Wyss Institute at Harvard University. Researchers at the Harvard University Wyss Institute reported the self-assembling and self-destructing drug delivery vessels using the DNA origami in the lab tests. The DNA nanorobot they created is an open DNA tube with a hinge on one side which can be clasped shut. The drug filled DNA tube is held shut by a DNA aptamer, configured to identify and seek certain diseased related protein. Once the origami nanobots get to the infected cells, the aptamers break apart and release the drug. The first disease model the researchers used was leukemia and lymphoma.
=== Troll Center case === In January 2016, the El Diario de Hoy and La Prensa Gráfica newspapers reported that the Búnker digital-programming company had created mirror sites of the newspapers in June 2015 and posted false information in an attempt to damage their reputations; the newspapers described the incident as a cyberattack. In a subsequent investigation by the office of the attorney general (FGR), Bukele allegedly instructed a Twitter user to create the mirror sites. Bukele denied involvement in the creation of the mirror sites. The incident became known as the "Troll Center" case. Five people were charged in relation to the case, but the charges were dropped in December 2017. On 4 July 2017, Bukele sued La Prensa Gráfica for $6 million, alleging that the newspaper had defamed and slandered him in its reporting of the cyberattacks by "falsely" ("falsamente") connecting him to the Troll Center case and "damag[ing] [Bukele's] image" ("dañó la imagen del señor alcalde"). Later that month, a court dismissed Bukele's lawsuit and three other courts rejected his appeals. In December 2018, the FGR stated that it had reviewed information supposedly linking Bukele's cell phone to the cyberattacks.
=== Richard Keller === Dr. Richard Keller (voiced by Brice Armstrong) is a Black Mesa scientist, working with Colette and Gina. He appears in Half-Life: Decay. He is a 55-year-old, senior scientist in a wheel chair. He gives missions to Colette and Gina during the game. Keller also condemns Gordon Freeman and asks himself what Kleiner sees in him. His final fate is unknown.
Sources: en.wikipedia.org
== Pipeline == As of 31 December 2025, the company's pipeline consisted of ten drug candidates covering 14 indications across three platforms. Seven candidates are PDGF-based, with the remainder comprising mRNA, ASO, and Tβ4 candidates. Wound healing indications under development include thermal burns, diabetic foot ulcers (DFUs), fresh wounds, pressure ulcers, radiation ulcers, dry eye syndrome, corneal injury, photodermatitis, alopecia, haemorrhoids, and gastric ulcers.
18,000 hospitalizations 120 deaths (0.5 deaths per 100,000 inhabitants) 2.1 million lost days off work 1.2 million doctor consultations 300,000 prescriptions for antibiotics. Most foodborne disease outbreaks in Australia have been linked to raw or minimally cooked eggs or poultry. The Australian Food Safety Information Council estimates that one third of cases of food poisoning occur in the home.
Prolific in film since 1964, Freeman is known for his roles in genres ranging from dramas, historical epics, thrillers, action adventure, science fiction, and comedies. His most acclaimed and highest-grossing films, according to the review aggregate site Rotten Tomatoes, include the following:
=== Use in musical instruments === Birch wood is sometimes used as a tonewood for semiacoustic and acoustic guitar bodies, and occasionally for solid-body guitar bodies. It is also a common material used in mallets for keyboard percussion. Drum manufacturers, such as Gretsch and Yamaha, have been known to use birch wood in the construction of drum shells, owing to its strength and colour which takes stain in an appealing way, and which can also amber over very well, while also giving the drums an appealing tone which changes depending on the type of birch used.
Sources: en.wikipedia.org
The Treuhand's operations drew criticism for unnecessarily closing allegedly profitable businesses, misuse and waste of funds, and layoffs that were claimed to be unnecessary. It also drew substantial protest from the workforces affected, as 2.5 million employees in state-owned enterprises (out of 4 million in total) were laid off in the early 1990s. Supporters argued that not placing the former state-owned enterprises into private hands would have caused the loss of many more jobs and slowed economic recovery. On 1 April 1991, chairman of the Treuhand Detlev Karsten Rohwedder was shot dead by an unknown assassin (possibly the Red Army Faction). He was succeeded by Birgit Breuel. The trust itself was extraordinarily unprofitable, such that, when its operations ended in 1994, it had amassed 260 to 270 billion DM in debt, equal to around 350 billion United States dollars in 2025.
Ochronosis is a medical condition characterized by the accumulation of homogentisic acid in connective tissues, leading to pigmentation changes. The term derives from the yellowish-brown (ocher-like) discoloration observed in histological samples. However, macroscopically, the affected tissues often appear bluish-grey due to the Tyndall effect, a phenomenon in which scattered light gives deeper-lying pigments a blue hue. Ochronosis is most commonly associated with the rare metabolic disorder alkaptonuria, a genetic condition involving homogentisic acid oxidase deficiency. It may also occur as an acquired condition, known as exogenous ochronosis, resulting from prolonged topical application or systemic exposure to certain phenol derivatives, particularly hydroquinone. The condition was first described by German pathologist Rudolf Virchow in 1865.
One prominent case was the classification of ascolichen families by the structure of the ascus apex (the tip of the spore sac). Josef Hafellner (1984) reorganized many ascolichen families by ascus-apex staining (amyloid ring present vs. absent), treating that feature as primary. Later DNA work found several of those families to be polyphyletic: the ascus type had arisen independently in unrelated lineages. The results echoed Nylander's century-old warning against single-trait taxonomy. Leif Tibell (1998) urged that robust taxa rest on multiple, independent characters. Pier Luigi Nimis (1998) warned that elevating every apparent clade to genus rank risks "explosive inflation" and listed five tests—monophyly, formal analysis, ≥ 1 diagnostic trait, broad sampling, and demonstrable informational gain—before renaming species. Where those tests are not met, Nimis advised using subgeneric rank so that binomials remain stable. Tibell further separated goals: classification should provide a stable, useful scheme, whereas phylogeny seeks the full branching pattern. He argued that constant renaming for every new tree can undermine nomenclatural stability; revisions should await strong, multi-line evidence. These philosophical perspectives influenced how lichenologists handled emerging molecular results a few years later. By the late 1990s lichenologists, trained in data matrices and synapomorphy logic, were ready to fold DNA data into taxonomy.
There are 37 known isotopes of francium ranging in atomic mass from 197 to 233. Francium has seven metastable nuclear isomers. Francium-223 and francium-221 are the only isotopes that occur in nature, with the former being far more common. Francium-223 is the most stable isotope, with a half-life of 21.8 minutes, and it is highly unlikely that an isotope of francium with a longer half-life will ever be discovered or synthesized. Francium-223 is a fifth product of the uranium-235 decay series as a daughter isotope of actinium-227; thorium-227 is the more common daughter. Francium-223 then decays into radium-223 by beta decay (1.149 MeV decay energy), with a minor (0.006%) alpha decay path to astatine-219 (5.4 MeV decay energy). Francium-221 has a half-life of 4.8 minutes. It is the ninth product of the neptunium decay series as a daughter isotope of actinium-225. Francium-221 then decays into astatine-217 by alpha decay (6.457 MeV decay energy). Although all primordial 237Np is extinct, the neptunium decay series continues to exist naturally in tiny traces due to (n,2n) knockout reactions in natural 238U. Francium-222, with a half-life of 14 minutes, may be produced as a result of the beta decay of natural radon-222; this process has nonetheless not yet been observed, and it is unknown whether this process is energetically possible. The least stable ground state isotope is francium-215, with a half-life of 90 ns: it undergoes a 9.54 MeV alpha decay to astatine-211.
== GLP-1 and neuropeptide Y multi-agonists == In 2023, researchers disclosed the discovery of multiple peptides that activated the GLP-1 receptor, neuropeptide Y receptor Y1, and neuropeptide Y receptor Y2. Since neuropeptide Y receptors were a previous anti-obesity target, it is hoped that the combination might be more efficacious than GLP-1 receptor agonists.
Sources: en.wikipedia.org
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.
It binds to and activates PPARδ, a nuclear receptor that regulates genes related to fatty acid oxidation and energy use. This activation alters transcription in tissues such as skeletal muscle and liver. The full range of downstream effects in humans is not fully established.
No, cardarine is not known to occur naturally in plants, animals, or humans. It is a synthetic molecule produced for laboratory research. Products labeled as cardarine should therefore be treated as manufactured chemicals with variable purity.
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.