The short version of Carcinogenicity fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2025-08-23. Anything still debated is marked as such rather than presented as settled.
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.
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.
Early clinical research explored GW501516 for lipid disorders, obesity, and diabetes. Some short-term human studies reported changes in HDL cholesterol, LDL cholesterol, and triglycerides. The development program was discontinued after rodent studies showed dose-dependent tumor formation in multiple tissues, including liver, bladder, stomach, and skin. These findings raised concerns about long-term cancer risk in humans. Because human exposure data are limited, the clinical significance of the rodent tumors remains uncertain.
Literature on cardarine often separates receptor pharmacology from toxicology. Mechanistic papers describe PPARδ activation and gene expression changes, while safety assessments focus on carcinogenicity and species differences. Questions remain about whether rodent tumors arise through PPARδ-dependent or off-target mechanisms. Another open area is how human metabolism and exposure compare with those in animal studies. Analytical methods such as liquid chromatography–mass spectrometry are used to confirm identity in biological and product samples.
GW501516 acts as an agonist at the peroxisome proliferator-activated receptor delta, a nuclear receptor that regulates gene expression. Activation shifts transcription toward genes involved in fatty acid uptake, oxidation, and energy expenditure. The compound does not bind the androgen receptor and therefore differs from anabolic steroids and SARMs. In rodent models, this metabolic shift has been linked to increased running endurance and reduced fat accumulation. The exact downstream pathways in humans remain incompletely characterized.
| Property | Value | Notes |
|---|---|---|
| Common synonyms | GW501516, GW-501516, GW 501516, endurobol | Names vary in research and anti-doping documents. |
| Chemical class | Synthetic PPARδ agonist | Small-molecule nuclear receptor ligand. |
| CAS Registry Number | 317318-70-0 | Identifier commonly associated with GW501516. |
| Appearance | White to off-white powder | Typical for purified research material. |
| Solubility | Low in water; soluble in DMSO and ethanol | Organic solvents are common for laboratory stock solutions. |
Handling and quality assessment of cardarine reference material follow general laboratory practices for poorly characterized compounds. It typically appears as a white to off-white powder and is sparingly soluble in water but soluble in organic solvents such as dimethyl sulfoxide and ethanol. Storage recommendations usually specify a cool, dry, dark place, with long-term storage at low temperature and desiccation. Purity may be checked by high-performance liquid chromatography with ultraviolet detection, while identity is confirmed by mass spectrometry and nuclear magnetic resonance. No pharmacopeial monograph exists, so reported purity and stability depend on the supplier’s methods.
GW501516 acts as a selective agonist at PPARδ, a nuclear receptor that regulates transcription of genes involved in lipid handling and energy metabolism. Activation of PPARδ in preclinical models increases fatty acid oxidation, mitochondrial biogenesis, and exercise endurance in rodents. These effects have made the compound a subject of metabolic research and also a target for sport anti-doping rules. In humans, however, controlled studies are limited, and whether similar endurance or metabolic changes occur at tolerated exposures remains an open question. The receptor’s broad tissue distribution also means downstream effects may vary by organ and condition.
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.
Laboratory studies indicate that GW501516 activates PPARδ, a nuclear receptor involved in fatty acid oxidation and energy metabolism. In rodent experiments, treated animals often showed increased endurance and reduced fat mass. These effects were observed under controlled conditions and do not establish safe or effective use in humans. The exact dose-response relationship in humans remains poorly characterized. Species differences in metabolism can affect how results translate across animals and people.
Nitrate reductase (NAD(P)H) (EC 1.7.1.2, assimilatory nitrate reductase, assimilatory NAD(P)H-nitrate reductase, NAD(P)H bispecific nitrate reductase, nitrate reductase (reduced nicotinamide adenine dinucleotide (phosphate)), nitrate reductase NAD(P)H, NAD(P)H-nitrate reductase, nitrate reductase [NAD(P)H2], NAD(P)H2:nitrate oxidoreductase) is an enzyme with systematic name nitrite:NAD(P)+ oxidoreductase. This enzyme catalises the following chemical reaction
==== Phycoerythrin-like proteins ==== Phycobiliproteins are water soluble light-capturing proteins, produced by cyanobacteria, and several algae. These pigments have been explored as fluorescent tags, food coloring agents, cosmetics, and immunological diagnostic agents. Most of these pigments are synthesized and accumulated intracellularly. As an exception, the cyanobacteria Oscillatoria and Scytonema sp. release an extracellular phycoerythrin-like 250 kDa protein. This pigment inhibits the growth of the green algae Chlorella fusca and Chlamydomonas and can be potentially used as an algicide.
As noted above, in radioactive decay the half-life is the length of time after which there is a 50% chance that an atom will have undergone nuclear decay. It varies depending on the atom type and isotope, and is usually determined experimentally. See List of nuclides. The current flowing through an RC circuit or RL circuit decays with a half-life of ln(2)RC or ln(2)L/R, respectively. For this example the term half time tends to be used rather than "half-life", but they mean the same thing. In a chemical reaction, the half-life of a species is the time it takes for the concentration of that substance to fall to half of its initial value. In a first-order reaction the half-life of the reactant is ln(2)/λ, where λ (also denoted as k) is the reaction rate constant.
==== Chronic fatigue syndrome ==== Chronic fatigue syndrome is debilitating illness of unknown cause that often follows an acute viral infection. According to one research study, 95% of CFS patients have anti-cardiolipin antibodies.
Sources: en.wikipedia.org
== Biography == Partha Mitra received his PhD in theoretical physics from Harvard University under the guidance of Bertrand Halperin in 1993. He was a member of the Theoretical Physics Department at Bell Laboratories from 1993 to 2003, and an assistant professor in Theoretical Physics at Caltech from 1996 before moving to Cold Spring Harbor Laboratory in 2003 where he is a Crick-Clay professor of biomathematics. Professor Mitra also holds adjunct positions in the NYU School of Medicine and Weill Cornell Medical College.
Trimipramine is a weak but significant antagonist of the dopamine D1 and D2 receptors, and also binds to the D4 receptor (Ki = 275 nM). Its affinities for various monoamine receptors including the D2 and 5-HT2A receptors closely resemble those of the atypical antipsychotic clozapine. In accordance, high doses of trimipramine have been found to have antipsychotic effects in schizophrenic patients, notably without causing extrapyramidal symptoms, and trimipramine has recently been found to be effective in reducing psychotic symptoms in patients with delusional depression. The lack of extrapyramidal symptoms with trimipramine may be related to its affinity for the D4 receptor, these both being properties it shares with clozapine. Unlike other TCAs, but reminiscent of antipsychotics, trimipramine has been found to markedly increase plasma prolactin levels (a marker of D2 receptor antagonism) at a dose of 75 mg/day and to increase nocturnal prolactin secretion at doses of 75 and 200 mg/day. These findings are suggestive of important antidopaminergic actions of trimipramine. Unlike various other TCAs, trimipramine shows marked antagonism of presynaptic dopamine autoreceptors, potentially resulting in increased dopaminergic neurotransmission. This effect has also been observed with low-potency tricyclic antipsychotics like thioridazine and chlorprothixene. Notably, these two antipsychotics have been claimed many times to also possess antidepressant effects.
St. John's wort affects the clearance of numerous drugs, including cyclosporin, SSRI antidepressants, digoxin, indinavir, and phenprocoumon. It may also interact with the anti-cancer drugs irinotecan and imatinib. Salvia miltiorrhiza may enhance anticoagulation and bleeding among people taking warfarin. Allium sativum has been found to decrease the plasma concentration of saquinavir, and may cause hypoglycemia when taken with chlorpropamide. Ginkgo biloba can cause bleeding when combined with warfarin or aspirin. Concomitant Ephedra and caffeine use has been reported to, in rare cases, cause fatalities.
An "official" label was announced on November 8 for notable accounts. Hours after the label began rolling out, Musk tweeted that he "killed" the label. Accounts that had been verified through the previous system were renamed to "legacy verified", with Musk calling the previous system "corrupt and nonsensical" in a tweet, and stating the blue checkmarks on those accounts would be removed "in a few months". Musk claimed that the impersonation issue was resolved by manually reviewing all applications, but The Washington Post tech columnist Geoffrey A. Fowler was able to create an impersonation account of senator Ed Markey, which was promptly verified after subscribing to Twitter Blue and only suspended after Fowler's story was published. On December 12, 2022, Twitter Blue was relaunched again with some changes, including an increased price of $11 for users who sign up through iOS devices to compensate for the 30% cut imposed by Apple. Twitter stated that only Twitter accounts older than 90 days and with a confirmed phone number are able to subscribe and Blue checkmarks are issued once Twitter reviews the account, and any changes to the profile "will result in the loss of the blue checkmark" until Twitter can review the account again.
Features of the Established Lesion: Predominance of plasma cells without bone loss Presence of extravascular immunoglobulins in the connective tissue and junctional epithelium Continuing loss of collagen Proliferation, apical migration and lateral extension of the junctional epithelium, with or without pocket formation
Sources: en.wikipedia.org
=== Chemistry === Capensinidin (Cp), a blue-red plant dye Carbon monophosphide, a diatomic radical chemical compound Cassiopium (Cp), a name formerly used for the chemical element Lutetium Chlorinated paraffins (CPs), complex mixtures of polychlorinated n-alkanes Copernicium, a chemical element, with proposed symbol Cp Counterpoise method, a way to correct for basis set superposition error in quantum chemistry Cross-polarization Cyclopentadienyl complex (Cp), read as "C P", the cyclic C5H5 fragment in a coordination complex The similar symbol Cp* ("C P star") represents pentamethylcyclopentadienyl, the C5Me5 ligand
The colonization of Tahiti occurred in a time of rivalry for resources of the Pacific by colonizing European nations including the French and the British. It was also a time of rivalry and fighting between the people of Tahiti and neighbouring islands. It is unclear which is the first European ship to arrive at the island of Tahiti but it is often recognised as being HMS Dolphin captained by British Captain Samuel Wallis on 18 June 1767. He met a welcoming party of Tahitians who traded with him. Cultural differences leading to grave communication errors that resulted in a battle in Matavai Bay between three hundred war canoes and HMS Dolphin which fired on the war canoes with muskets, quarterdeck guns and then cannons. The Tahitian chief Obera (Purea) ordered peace offerings from her people after this battle and Wallis and the Tahitians departed on amicable terms when he left on 27 July 1767. A few months later the French arrived on 2 April 1768 with the ships Boudeuse and Etoile captained by Louis-Antoine de Bougainville.
4.A.1 The PTS Glucose-Glucoside (Glc) Family 4.A.2 The PTS Fructose-Mannitol (Fru) Family 4.A.3 The PTS Lactose-N,N'-Diacetylchitobiose-β-glucoside (Lac) Family 4.A.4 The PTS Glucitol (Gut) Family 4.A.5 The PTS Galactitol (Gat) Family 4.A.6 The PTS Mannose-Fructose-Sorbose (Man) Family 4.A.7 The PTS L-Ascorbate (L-Asc) Family
=== Witnesses === Afraid of being kidnapped and missing Mendonça, one of the boy's friend at school tried to commit suicide, two months after the disappearance. In the crime's reconstitution, Dias could not explain what he did between 14 (2 P.M) and 18 (6 P.M) hours on the day Mendonça disappeared. With the reconstitution it was proven that the investigation let leads and important witnesses slip by. The inspectors did not want to explain to the press the reason why they devalued Alcina Dias' testimony. A man that worked in a gas station guaranteed that at the time of the disappearance he saw Mendonça, in the centre of the village of Lousada, walking next to two other boys. The court questioned the witness about his statements to the GNR the day following the disappearance, where he said he saw two children passed by on bikes, but that neither was Mendonça. The witness insisted that he could not remember giving the testimony to GNR, even thought his signature was in the records. They also heard a witness that said they saw Mendonça's bicycle at 16 (4 P.M) hours. Without being identified, a boy that was 14 at the time of the disappearance, told RTP that PJ did not value the different testimonies given to the police. The witness, along with four other young people, was waiting for Mendonça to arrive to play football. When Mendonça got there he said he was not going to play anymore, hid his bike and got in the car. In 2003, in the Casa Pia Process, a man said that he was with Mendonça in a pension for sexual meetings, in the end of January 2001.
=== Microscopic features === A hymenium is a layer of microscopic spore-bearing cells that covers the surface of gills. In the nongilled mushrooms, the hymenium lines the inner surfaces of the tubes of boletes and polypores, or covers the teeth of spine fungi and the branches of corals. In the Ascomycota, spores develop within microscopic elongated, sac-like cells called asci, which typically contain eight spores in each ascus. The Discomycetes, which contain the cup, sponge, brain, and some club-like fungi, develop an exposed layer of asci, as on the inner surfaces of cup fungi or within the pits of morels. The Pyrenomycetes, tiny dark-colored fungi that live on a wide range of substrates including soil, dung, leaf litter, and decaying wood, as well as other fungi, produce minute, flask-shaped structures called perithecia, within which the asci develop. In the basidiomycetes, usually four spores develop on the tips of thin projections called sterigmata, which extend from club-shaped cells called a basidia. The fertile portion of the Gasteromycetes, called a gleba, may become powdery as in the puffballs or slimy as in the stinkhorns. Interspersed among the asci are threadlike sterile cells called paraphyses. Similar structures called cystidia often occur within the hymenium of the Basidiomycota. Many types of cystidia exist, and assessing their presence, shape, and size is often used to verify the identification of a mushroom. Cystidia on the faces of gills are called pleurocystidia, while cystidia on the edges of the gills are called cheilocystidia.
Sources: en.wikipedia.org
Cardarine is an investigational synthetic compound that acts as a PPARδ agonist. It is also known as GW501516 and has been studied mainly in preclinical research. It is not an approved medicine.
No. Cardarine is not a steroid hormone; it targets the nuclear receptor PPARδ. Its classification in anti-doping rules differs from anabolic steroids, though it remains prohibited in sport.
Early rodent studies reported tumor formation at multiple sites, which raised safety concerns. Sponsors stopped clinical development, and no approved human product exists.
It targets PPARδ, a nuclear receptor involved in lipid and energy metabolism. It does not act primarily on androgen receptors. This distinction separates it from SARMs.