Carcinogenicity comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Updated 2025-08-26. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Primary target | PPARδ | Nuclear receptor; not androgen receptor |
| Studied indications | Dyslipidemia; obesity; diabetes | Early clinical research; development discontinued |
| Rodent toxicity | Tumor formation in multiple tissues | Dose-dependent findings in some studies |
| Human approval | None | No approved therapeutic use |
| Typical analytical method | LC-MS/MS | Used for identity and quantification |
== External links == "Sofpironium Bromide (Code C152384)". NCI Thesaurus. Clinical trial number NCT03836287 for "Safety and Efficacy Study of Sofpironium Bromide in Subjects With Axillary Hyperhidrosis (BBI-4000-CL-301) (CardiganI)" at ClinicalTrials.gov Clinical trial number NCT03948646 for "Safety and Efficacy Study of Sofpironium Bromide in Subjects With Axillary Hyperhidrosis (BBI-4000-CL-302) (CARDIGANII)" at ClinicalTrials.gov
Second Cup agreed to transform some of its western Canada locations into recreational cannabis dispensaries, with no cannabis-related products to be sold at its cafés. The company stated that this alliance would allow it to leverage its real estate assets to drive value for the franchisees without affecting plans for new product innovation and opening new cafés across Canada. In August 2018, the company was already considering which of its locations in Ontario might be suitable as cannabis retail stores as an alternative to their current use, in conjunction with National Access Cannabis. On November 8, 2019, Second Cup announced plans to change its name to Aegis Brands Inc. (TSX: AEG), pending stockholder approval the following year. The company was scheduled to open two cannabis stores in Calgary in early 2020 and planned expansion into Ontario. On December 5, 2019, Aegis Brands announced its acquisition of Ottawa-based coffeehouse chain Bridgehead Coffee for $11 million. In February 2021, Aegis Brands agreed to sell Second Cup to Quebec-based Foodtastic Inc. for an undisclosed sale price that included $14 million in cash. Foodtastic chief executive Peter Mammas said that the company intended to expand the brand to 300 locations by 2025, from the existing store count of 190. In May 2025, Second Cup's international division filed for creditor protection under the Companies' Creditors Arrangement Act in Canada. This comes after the company was unable to pay nearly $10 million to its creditors.
Dyson favoured the dual origin theory: that life first formed as cells, then enzymes, and finally, much later, genes. This was first propounded by the Russian biochemist, Alexander Oparin. J. B. S. Haldane developed the same theory independently. In Dyson's version of the theory, life evolved in two stages, widely separated in time. Because of the biochemistry, he regards it as too unlikely that genes could have developed fully blown in one process. Current cells contain adenosine triphosphate or ATP and adenosine 5'-monophosphate or AMP, which greatly resemble each other but have completely different functions. ATP transports energy around the cell, and AMP is part of RNA and the genetic apparatus. Dyson proposed that in a primitive early cell containing ATP and AMP, RNA and replication came into existence only because of the similarity between AMP and RNA. He suggested that AMP was produced when ATP molecules lost two of their phosphate radicals, and then one cell somewhere performed Eigen's experiment and produced RNA. There is no direct evidence for the dual origin theory, because once genes developed, they took over, obliterating all traces of the earlier forms of life. In the first origin, the cells were probably just drops of water held together by surface tension, teeming with enzymes and chemical reactions, and having a primitive kind of growth or replication. When the liquid drop became too big, it split into two drops.
===== MeSH D08.811.520.224 – carbon-carbon lyases (EC 4.1) ===== MeSH D08.811.520.224.062 – aldehyde lyases MeSH D08.811.520.224.062.250 – 2-dehydro-3-deoxyphosphoheptonate aldolase MeSH D08.811.520.224.062.400 – fructose-bisphosphate aldolase MeSH D08.811.520.224.125 – carboxy-lyases MeSH D08.811.520.224.125.050 – adenosylmethionine decarboxylase MeSH D08.811.520.224.125.100 – aromatic-L-amino-acid decarboxylase MeSH D08.811.520.224.125.100.500 – dopa decarboxylase MeSH D08.811.520.224.125.250 – glutamate decarboxylase MeSH D08.811.520.224.125.300 – histidine decarboxylase MeSH D08.811.520.224.125.350 – indole-3-glycerol-phosphate synthase MeSH D08.811.520.224.125.387 – methylmalonyl-coa decarboxylase MeSH D08.811.520.224.125.425 – ornithine decarboxylase MeSH D08.811.520.224.125.450 – orotidine-5'-phosphate decarboxylase MeSH D08.811.520.224.125.500 – phosphoenolpyruvate carboxykinase (atp) MeSH D08.811.520.224.125.550 – phosphoenolpyruvate carboxykinase (gtp) MeSH D08.811.520.224.125.650 – phosphoenolpyruvate carboxylase MeSH D08.811.520.224.125.750 – pyruvate decarboxylase MeSH D08.811.520.224.125.800 – ribulose-bisphosphate carboxylase MeSH D08.811.520.224.125.875 – tyrosine decarboxylase MeSH D08.811.520.224.125.900 – uroporphyrinogen decarboxylase MeSH D08.811.520.224.187 – deoxyribodipyrimidine photo-lyase MeSH D08.811.520.224.600 – oxo-acid-lyases MeSH D08.811.520.224.600.200 – anthranilate synthase MeSH D08.811.520.224.600.700 – isocitrate lyase MeSH D08.811.520.224.800 – tryptophanase MeSH D08.811.520.224.900 – tyrosine phenol-lyase
Sources: en.wikipedia.org
He beat Andrey Rublev for the 17th title of his career and the fourth of the season, in 59 minutes, the shortest match in the tournament history. At the US Open, Zverev sought to claim his first major title following his run to the final the previous year. He reached the semifinals following wins over Jack Sock and Lloyd Harris. There, he lost to Novak Djokovic in five sets despite taking the first set, ending his career-high 16-match win streak stretching back to the Olympics. Zverev was seeded 3rd at the 2021 BNP Paribas Open, where he reached the quarterfinals. On the way, he defeated Jenson Brooksby, Andy Murray and Gaël Monfils. He lost to Taylor Fritz, despite having two match points. At the Erste Bank Open in Vienna, seeded second, he defeated Filip Krajinović and Alex de Minaur to reach the quarterfinals. The victory over De Minaur gave Zverev his 300th ATP tour match win. He then beat Félix Auger-Aliassime and Carlos Alcaraz to reach the final where he won his fifth title of the year and 18th overall, defeating Frances Tiafoe in straight sets. Zverev was the fourth seed at the 2021 Rolex Paris Masters. He received a bye into the second round, where he defeated Dušan Lajović. He defeated next sixteenth seed Grigor Dimitrov in the third round and sixth seed Casper Ruud in the quarterfinals. He lost in the semifinals to second seed Daniil Medvedev in straight sets. As a result of this run he equaled his singles career-high ranking of World No. 3 on 8 November 2021. For a fifth successive season, Zverev qualified for the 2021 ATP Finals in Turin, as the third seed.
The search for the cause of this condition was enhanced considerably in 1968, when the Hereditary Disease Foundation (HDF) was created by Milton Wexler, a psychoanalyst based in Los Angeles, California, whose wife Leonore Sabin had been diagnosed earlier that year with Huntington's disease. Sabin's three brothers also had this disease. The foundation was involved in the recruitment of more than 100 scientists in the US-Venezuela Huntington's Disease Collaborative Project, which over a 10-year period from 1979, worked to locate the genetic cause. This was achieved in 1983 when a causal gene was approximately located, and in 1993, the gene was precisely located at chromosome 4 (4p16.3). The study had focused on the populations of two isolated Venezuelan villages, Barranquitas and Lagunetas, where there was an unusually high prevalence of HD, and involved over 18,000 people, mostly from a single extended family, and resulted in making HD the first autosomal disease locus found using genetic linkage analysis. Among other innovations, the project developed DNA-marking methods which were an important step in making the Human Genome Project possible. In the same time, key discoveries concerning the mechanisms of the disorder were being made, including the findings by Anita Harding's research group on the effects of the gene's length. Modeling the disease in various types of animals, such as the transgenic mouse developed in 1996, enabled larger-scale experiments.
By the end of 2017, it was announced that Catherine Keener would star opposite Carrey in Kidding. The series lasted two seasons. Carrey was also the subject of two documentaries in 2017. The first, a short subject entitled I Needed Color about his lifelong passion for art, was released online in the summer. Later that year another documentary, Jim & Andy: The Great Beyond—Featuring a Very Special, Contractually Obligated Mention of Tony Clifton, premiered at The Venice Film Festival and was later picked up by Netflix. The film chronicles the behind-the-scenes drama during the shooting of Man on the Moon, when he never broke character as Andy Kaufman. It incorporates footage that was shot for the film's electronic press kit but ultimately pulled by Universal as they felt that it was too damaging.
Sources: en.wikipedia.org
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.
Rodent studies found dose-dependent tumors in several organs. The sponsor discontinued the program over cancer concerns. Human risk from long-term use remains unknown.
Controlled human endurance trials are lacking. Animal studies show increased exercise capacity under some conditions. Anecdotal reports are not equivalent to clinical evidence.
Rodent studies reported increased endurance and fat oxidation after GW501516 exposure. Long-term studies also found higher rates of some tumors, which led to halted development.