Classification explainer

Cardarine (GW501516): not a SARM, and the carcinogenicity data

By the Decadewise team Education only Last updated 3 August 2026 No dosing table on this page

Short answer

The classification: GW501516, sold as cardarine, is a peroxisome proliferator-activated receptor delta agonist, not a selective androgen receptor modulator, with no androgen receptor activity.

Where it came from: discovery work published in 2001 on reverse cholesterol transport in cells and monkeys.

The human record: six published papers report the compound given to people, five measuring lipids and metabolism, none athletic performance. The largest randomized 268 patients across three amounts and placebo for 12 weeks (Olson, 2012).

Why development ended: the anti-doping agency's 2013 alert says the drug was withdrawn from research when serious toxicities were discovered in pre-clinical studies.

What the cancer claim rests on: two 104-week daily oral carcinogenicity studies, in rats and mice, run by the developer's own safety-assessment group and published only as meeting abstracts (Geiger, 2009; Newsholme, 2009). Both reported test-article-related tumors at every amount tested.

Where it sits: the 2026 WADA Prohibited List names GW1516 at S4.4.1, metabolic modulators, prohibited at all times, and no approved medicine anywhere contains it.

On this page

Short answer What is GW501516? Where the endurance claim starts The human data The carcinogenicity record Is cardarine a SARM? Does cardarine cause cancer? Why was it abandoned? Is cardarine legal? What is unsettled The safety picture How this is sourced Related pages The disclaimer

What is GW501516?

The molecule: a synthetic agonist selective for the delta subtype of the peroxisome proliferator-activated receptor family, built with combinatorial chemistry and structure-based design and first described in 2001 (Oliver, 2001).

What that receptor family does: the three subtypes are lipid sensors that regulate fatty acid and carbohydrate metabolism. Fibrates work through the alpha subtype and glitazones through the gamma subtype; the delta subtype had no selective ligand until this compound.

The original target: reverse cholesterol transport. In cells the compound raised expression of the cholesterol transporter ABCA1, and in insulin-resistant middle-aged obese rhesus monkeys it produced a dose-dependent rise in HDL cholesterol while lowering small dense LDL, fasting triglycerides and fasting insulin.

What it is not: anything to do with the androgen receptor. The retail category it is sold in has no bearing on where it binds.

Where the endurance claim starts

The paper everyone quotes: a 2008 mouse study testing pathway-specific drugs on treadmill running (Narkar, 2008). It reported that a PPAR-beta/delta agonist together with exercise training raised oxidative muscle fibers and running endurance in adult mice, and that the two acted together rather than the drug acting alone.

The number that gets misattributed: the headline 44 percent endurance increase in sedentary mice came from four weeks of AICAR, an AMPK agonist, not from GW501516. Two different compounds, one paper, one figure that travels under the wrong name.

What the paper did not do: it did not run in humans, and it did not measure endurance in humans. Every endurance claim aimed at a person is an extrapolation from mice on a treadmill.

The published human record

What happened when it reached people

How to read this: six published papers report GW501516 given to people. Five are metabolic or lipid studies and they are the table below, each with the amount administered, the duration, and the endpoint measured. The sixth is an anti-doping excretion study, described under the table. None measured athletic performance, and none was designed to look for tumors.

GW501516 in published human studies

Source	Population	What the study gave	Reported result
Sprecher, 2007	24 healthy volunteers allocated, hospitalized and sedentary	2.5mg (9 people) or 10mg (9 people) by mouth once daily for 2 weeks, against placebo (6 people)	HDL cholesterol rose in both arms while it fell 11.5 percent on placebo; serum triglycerides trended down at the higher arm; clearance of triglyceride after a fat meal improved
Risérus, 2008	healthy moderately overweight subjects, six per group in three parallel groups	10mg by mouth once daily for 2 weeks, against a PPAR-alpha comparator and placebo	fasting triglycerides down 30 percent, apolipoprotein B down 26 percent, LDL cholesterol down 23 percent, insulin down 11 percent, liver fat content down 20 percent, urinary isoprostanes down 30 percent
Christodoulides, 2009	six healthy, overweight or obese male volunteers, one arm of a three-group study	10mg by mouth daily for 2 weeks	circulating fibroblast growth factor 21 rose 32 percent
Ooi, 2011	13 dyslipidemic men with central obesity	2.5mg by mouth daily for two 6-week periods, randomized double-blind crossover against placebo with a 2-week washout between them	plasma triglycerides, fatty acid, apoB-100 and apoB-48 concentrations fell; HDL cholesterol, apoA-II and LpA-I:A-II rose; cholesteryl ester transfer protein activity fell
Olson, 2012	268 patients with HDL cholesterol below 1.16 mmol/L, plus a second exploratory study in 37	2.5mg, 5.0mg or 10.0mg, or placebo, for 12 weeks	HDL cholesterol up to 16.9 percent higher and apoA-I up to 6.6 percent higher; LDL cholesterol down 7.3 percent, triglycerides down 16.9 percent, apoB down 14.9 percent, free fatty acids down 19.4 percent

The 2007 report describes itself as the first administration of a PPAR-delta agonist to man. The 2008 and 2009 papers come from the same center and describe a two-week course at the same daily amount in groups of six, so the participant figures cannot simply be added across the five papers above.

The sixth paper, and why it is not in the table: a 2012 anti-doping excretion study gave a single 15mg oral dose and then followed the urine, reporting the sulfone metabolite still detectable up to 40 days later (Sobolevsky, 2012). Its endpoint is how long a doping test can still catch the compound, not a health outcome, so it has no result to place in the columns above. It is counted because people did receive the compound, and the amount it gave is higher than any amount in the table. One dose does not extend the longest exposure on record, which is still 12 weeks, and the paper says nothing about whether any of this is safe.

The scale of the human record: the largest published trial randomized 268 patients across three amounts and placebo, and ran for 12 weeks. That is the longest published human exposure we could retrieve. The 2011 crossover is next, at two 6-week periods separated by a washout.

What the record still does not contain: a performance trial, a study designed to look for tumors, or any exposure beyond 12 weeks. The endpoints were cholesterol, triglycerides, apolipoproteins and fat oxidation, in populations selected for metabolic problems rather than for athletic ability. An earlier version of this page understated both the number of these studies and their size and length. The table above is the corrected record.

The carcinogenicity record, and what it is made of

Why this section is careful: the cancer claim is the load-bearing fact about this compound, and it circulates without anyone naming the document. Here is the document trail as we found it.

The carcinogenicity trail, source by source

Source	What kind of record	What it states
Geiger, 2009	meeting abstract 895, Society of Toxicology, from the developer's safety-assessment group	104-week daily oral gavage carcinogenicity study in Han Wistar rats. Test-article-related neoplastic findings in multiple tissues at every amount given. The organs named are liver, urinary bladder, thyroid, tongue, stomach, skin, Harderian gland, testis, ovary and uterus, each with its own threshold. Mortality rose in females at every amount, with uterine endometrial adenocarcinoma contributing to death in a high proportion of them
Newsholme, 2009	meeting abstract 896, Society of Toxicology, same group	104-week daily oral gavage carcinogenicity study in CD1 mice. Squamous cell carcinoma of the stomach and combined squamous cell tumors at every amount given, liver adenoma from the lowest amount upward and hepatocellular carcinoma from the second amount upward, and reduced survival above the lowest amount. The abstract states the results do not support a role for this receptor in colon carcinogenesis
Mitchell and Bishop-Bailey, 2019	peer-reviewed letter, Pulmonary Circulation	states the compound causes cancer in rats and in mice after 104 weeks of dosing, citing the two abstracts above, and notes that neither has been published as a full peer-reviewed paper
Pollock, 2010	peer-reviewed full paper, PPAR Research	in mice given a carcinogen first, the compound drove metastatic squamous cell carcinoma of the forestomach within two months
WADA alert, 21 March 2013	anti-doping agency alert	the drug was withdrawn from research and terminated when serious toxicities were discovered in pre-clinical studies. The alert links those studies directly to the 2009 abstract book, by page and by abstract number

Both 2009 abstracts are readable in full in the Society of Toxicology's published abstract book, on page 185, which is the document the anti-doping agency's own alert points to. An earlier version of this page reported that these abstracts could not be retrieved. They can be, and the findings above are taken from them directly.

What that trail supports: two 104-week rodent carcinogenicity studies were run by the developer, both reported tumors related to the compound at every amount given, and the peer-reviewed literature repeats that finding by citation. That is a real and serious record.

What it does not support: a quantified human risk. The rodent figures are milligrams per kilogram of body weight per day, by gavage, for two years, which is a toxicology screening design rather than a human exposure. Neither abstract carries incidence tables or control comparisons, and neither study reached full peer review.

The one full paper's limit: the 2010 mouse model gave a carcinogen first and the compound afterwards, so it describes tumor promotion in a sensitised animal. It is strong evidence of a mechanism and it is not a two-year carcinogenicity study.

Is cardarine a SARM?

No. A SARM binds the androgen receptor. This compound binds a nuclear receptor in the lipid-sensing family, which is why the 2026 WADA Prohibited List files it at S4.4.1 under metabolic modulators, next to AMPK activators and Rev-erb agonists, while the SARMs sit at S1.2 under anabolic agents. Two sections apart, on purpose.

Where the mislabel comes from: retail listings, not chemistry. In a 2017 analysis of products sold online as SARMs, GW501516 was one of the unapproved drugs found inside products in that category (Van Wagoner, 2017).

Does cardarine cause cancer?

In rodents, on the published record, tumors were reported in both species tested after two years of daily dosing, and the developer stopped the program. The precise wording in the peer-reviewed literature is that the compound causes cancer in rats and in mice after 104 weeks of dosing, sourced to two 2009 toxicology meeting abstracts rather than to full papers.

In humans: there is no carcinogenicity data. People did receive the compound in six published studies, five of them measuring lipids and metabolism over 2 to 12 weeks and the sixth following one dose through the urine. That is far too short and far too small to detect a tumor signal, and none of the six was designed to look for one. Absence of human data is not reassurance, it is absence.

The honest summary: a rodent carcinogenicity signal strong enough to end a pharmaceutical program, documented in conference abstracts from the developer's own safety group, with no human evidence in either direction.

Why was GW501516 abandoned?

Because pre-clinical toxicity ended it. The World Anti-Doping Agency issued an alert on 21 March 2013 stating that the compound was withdrawn from research by the pharmaceutical company and terminated when serious toxicities were discovered in pre-clinical studies, and that clinical approval has not and will not be given for it. The alert points readers at the two 2009 carcinogenicity abstracts by page and number, which is how the document trail on this page was assembled.

Why an anti-doping agency issued a drug-safety alert: athletes were testing positive for it, the compound was circulating on a gray market, and the agency judged the health risk serious enough to warn people it was trying to catch.

Is cardarine legal?

There is no approved medicine containing it anywhere. The United States Anti-Doping Agency's published page on the compound states that GW1516 is not legally permitted in any medications, supplements, or foods, and that it is not available anywhere as an approved medication and has no recognized therapeutic uses. In sport it is prohibited at all times, in and out of competition, under S4.4.1 of the 2026 list, where the entry names it by its full chemical name and both code names.

What sellers rely on: the phrase "research use only", which describes an intention rather than a legal category. FDA has put the point in writing. In a warning letter of 12 December 2025 it told a seller that despite labeling calling the products a "RESEARCH COMPOUND" and "NOT FOR HUMAN CONSUMPTION", the evidence from the labeling and the website established that they were intended to be drugs for human use, and were therefore unapproved new drugs. That letter names LGD-4033, RAD-140, MK-677 and S-23 rather than GW501516, so it settles how the agency reads the disclaimer, not what has been written about this compound specifically.

Where the evidence runs out

Four limits on what the published record can tell you:

Tumor incidence. The two carcinogenicity studies are conference abstracts. They name the organs and the amount at which each finding appeared, but incidence counts, control comparisons and the full pathology are not in the retrievable record, and neither study reached full peer review.
Any human risk figure. We found no published human carcinogenicity study for this compound, and the anti-doping agency's 2013 alert states that clinical approval has not been and will not be given for it.
Duration in people. The longest published human exposure we found is 12 weeks (Olson, 2012).
Endurance in people. The endurance literature is rodent. We found no published human performance trial.

No approved product contains GW501516, in any jurisdiction we could check.

The safety picture, from the record

What the document trail holds: a two-year rodent carcinogenicity program in two species that ended clinical development, an anti-doping alert describing serious pre-clinical toxicities, and a peer-reviewed mouse model in which the compound drove metastatic tumors within two months after carcinogen exposure. Against that sits a human record of six published studies, five of them metabolic with favorable lipid readouts and the sixth a single-dose excretion study, the longest of them running twelve weeks. The lipid results are real and they are also the reason the compound got as far as it did. Anyone weighing this is weighing a twelve-week benefit signal against a two-year cancer signal in two other species, and that is a conversation for a doctor, not for a page.

How this page is sourced

Where each claim comes from: the pharmacology, the endurance claim and the human data come from the first seven papers below plus the 2012 excretion study at number 19, the carcinogenicity record from the two 2009 meeting abstracts themselves plus the peer-reviewed letter citing them and one full peer-reviewed animal paper, the retail mislabeling from a 2017 analysis, and the development history and legal status from four agency documents.

Nineteen sources: thirteen papers with DOIs and PubMed IDs, two Society of Toxicology meeting abstracts reproduced in full in that society's published abstract book, and four agency documents. The 2009 abstracts are named as abstracts, not as papers, because that is what they are.

Added 30 July 2026: the "research use only" paragraph in the legal section asserted that regulators had said something in writing and cited nothing, which left a reader no way to check it. Reference 16 is that document. It is quoted for what it actually says, and its scope is stated on the page, since it addresses a seller of products marketed as SARMs and never mentions this compound.

How the count of six was tested, because a count is a claim about a whole literature: on 30 July 2026 we searched PubMed for GW501516 across all fields, which returns 365 records, and narrowed that with PubMed's own Clinical Trial and Randomized Controlled Trial publication types, which returns six. That publication-type filter was the whole screen, and on its own it is wrong in both directions. Four of its six records are the human studies above. The other two, PMID 17500064 and PMID 22683888, carry the trial tag but dosed cultured human cells rather than people. Worse, a paper that gave the compound to people outside a trial design carries no trial tag at all, so the filter can never reach it: Christodoulides 2009 is one such paper, and so is PMID 22977012, an excretion study sitting inside the same 365 records. That second one is why this page said five until 3 August 2026, when we re-screened those 365 records for human administration rather than for trial type and found it. One database, those two queries, those dates, and every record they surfaced read rather than counted. We have not read all 365, so six is the count we can show the working for, not a proof that no seventh exists.

The standard: the full sourcing and citation-verification standard for this site, including who checks a page before it ships, lives on the methodology page.

Last reviewed: 27 July 2026.

1
Oliver WR Jr, Shenk JL, Snaith MR, et al. A selective peroxisome proliferator-activated receptor delta agonist promotes reverse cholesterol transport. Proc Natl Acad Sci U S A. 2001;98(9):5306-5311. doi:10.1073/pnas.091021198. PMID 11309497.
2
Sprecher DL, Massien C, Pearce G, et al. Triglyceride:high-density lipoprotein cholesterol effects in healthy subjects administered a peroxisome proliferator activated receptor delta agonist. Arterioscler Thromb Vasc Biol. 2007;27(2):359-365. doi:10.1161/01.ATV.0000252790.70572.0c. PMID 17110604.
3
Risérus U, Sprecher D, Johnson T, et al. Activation of peroxisome proliferator-activated receptor (PPAR)delta promotes reversal of multiple metabolic abnormalities, reduces oxidative stress, and increases fatty acid oxidation in moderately obese men. Diabetes. 2008;57(2):332-339. doi:10.2337/db07-1318. PMID 18024853.
4
Christodoulides C, Dyson P, Sprecher D, Tsintzas K, Karpe F. Circulating fibroblast growth factor 21 is induced by peroxisome proliferator-activated receptor agonists but not ketosis in man. J Clin Endocrinol Metab. 2009;94(9):3594-3601. doi:10.1210/jc.2009-0111. PMID 19531592. The PPAR-delta arm of its third group received 10 mg per day of GW501516 for two weeks.
5
Ooi EM, Watts GF, Sprecher DL, Chan DC, Barrett PH. Mechanism of action of a peroxisome proliferator-activated receptor (PPAR)-delta agonist on lipoprotein metabolism in dyslipidemic subjects with central obesity. J Clin Endocrinol Metab. 2011;96(10):E1568-E1576. doi:10.1210/jc.2011-1131. PMID 21816786.
6
Olson EJ, Pearce GL, Jones NP, Sprecher DL. Lipid effects of peroxisome proliferator-activated receptor-delta agonist GW501516 in subjects with low high-density lipoprotein cholesterol: characteristics of metabolic syndrome. Arterioscler Thromb Vasc Biol. 2012;32(9):2289-2294. doi:10.1161/ATVBAHA.112.247890. PMID 22814748. This is the largest published human study of the compound, and its 12-week treatment period is the longest continuous human exposure in the published record.
7
Narkar VA, Downes M, Yu RT, et al. AMPK and PPARdelta agonists are exercise mimetics. Cell. 2008;134(3):405-415. doi:10.1016/j.cell.2008.06.051. PMID 18674809.
8
Geiger LE, Dunsford WS, Lewis DJ, Brennan C, Liu KC, Newsholme SJ. Rat carcinogenicity study with GW501516, a PPAR delta agonist. The Toxicologist, Supplement to Toxicological Sciences. 2009;108(1):185, abstract 895. Society of Toxicology 48th Annual Meeting, Baltimore, 15 to 19 March 2009. Accessed 29 July 2026. toxicology.org, 2009 abstract book.
9
Newsholme SJ, Dunsford WS, Brodie T, Brennan C, Brown M, Geiger LE. Mouse carcinogenicity study with GW501516, a PPAR delta agonist. The Toxicologist, Supplement to Toxicological Sciences. 2009;108(1):185, abstract 896. Society of Toxicology 48th Annual Meeting, Baltimore, 15 to 19 March 2009. Accessed 29 July 2026. toxicology.org, 2009 abstract book.
10
Mitchell JA, Bishop-Bailey D. PPAR-beta/delta a potential target in pulmonary hypertension blighted by cancer risk. Pulm Circ. 2019;9(1):2045894018812053. doi:10.1177/2045894018812053. PMID 30351241. This letter is the peer-reviewed source of the 104-week statement, and it cites the two abstracts above.
11
Pollock CB, Rodriguez O, Martin PL, et al. Induction of metastatic gastric cancer by peroxisome proliferator-activated receptor delta activation. PPAR Res. 2010;2010:571783. doi:10.1155/2010/571783. PMID 21318167.
12
Van Wagoner RM, Eichner A, Bhasin S, Deuster PA, Eichner D. Chemical composition and labeling of substances marketed as selective androgen receptor modulators and sold via the internet. JAMA. 2017;318(20):2004-2010. doi:10.1001/jama.2017.17069. PMID 29183075.
13
World Anti-Doping Agency. WADA issues alert on GW501516. Released 21 March 2013. Accessed 29 July 2026. Re-checked 31 July 2026: an automated request returned HTTP 202 with an empty body, which is a bot challenge rather than a missing document, so this source could not be re-retrieved by script on that date. wada-ama.org, GW501516 alert.
14
World Anti-Doping Agency. World Anti-Doping Code International Standard: Prohibited List 2026, section S4.4.1, effective 1 January 2026. Accessed 29 July 2026. wada-ama.org, 2026 Prohibited List.
15
United States Anti-Doping Agency. What should tested athletes know about GW1516? Accessed 29 July 2026. usada.org, GW1516.
16
U.S. Food and Drug Administration, Center for Drug Evaluation and Research. Warning letter to Prime Sports Nutrition, MARCS-CMS 719433, 12 December 2025, on products marketed as LGD-4033, RAD-140, MK-677 and S-23, and stating that despite product labeling marketing some of them as a "RESEARCH COMPOUND" and "NOT FOR HUMAN CONSUMPTION", the evidence from the labeling and the website establishes that the products are intended to be drugs for human use. It does not name GW501516. Retrieved 30 July 2026, HTTP 200. fda.gov warning letter 719433.
17
Krämer DK, Al-Khalili L, Guigas B, Leng Y, Garcia-Roves PM, Krook A. Role of AMP kinase and PPARdelta in the regulation of lipid and glucose metabolism in human skeletal muscle. J Biol Chem. 2007;282(27):19313-19320. Primary cultured human muscle cells, not living subjects. doi:10.1074/jbc.M702329200. PMID 17500064.
18
Serrano-Marco L, Chacón MR, Maymó-Masip E, et al. TNF-alpha inhibits PPARbeta/delta activity and SIRT1 expression through NF-kappaB in human adipocytes. Biochim Biophys Acta. 2012;1821(9):1177-1185. Cultured human SGBS adipocytes, not living subjects. doi:10.1016/j.bbalip.2012.05.006. PMID 22683888.
19
Sobolevsky T, Dikunets M, Sukhanova I, Virus E, Rodchenkov G. Detection of PPARδ agonists GW1516 and GW0742 and their metabolites in human urine. Drug Test Anal. 2012;4(10):754-760. doi:10.1002/dta.1413. PMID 22977012. Its controlled excretion study gave a single oral dose of 15 mg, and reports the sulfone metabolite of GW1516 detectable in urine up to 40 days afterwards. Carries no clinical trial publication type, which is why a trial-type filter cannot surface it. Retrieved 3 August 2026.

Around this page: five neighboring pages on what a compound is and on what a test result covers.

Is MK-677 a SARM: the growth hormone secretagogue that shares this compound's retail shelf and none of its pharmacology.
Is ostarine a steroid: the androgen receptor side of the same three-way mix-up, with the statutory definition.
MOTS-c guide: another compound filed in the same S4.4.1 metabolic-modulator entry.
What an HPLC purity number misses: why a percentage on a certificate does not identify what is in a vial.
PT-141 and the Vyleesi approval: the opposite case, a compound that did reach approval, and exactly what that approval covers.

Next in the series: one compound gets taken apart each week in The Decadewise briefing.

The disclaimer

Every page is reviewed by medical professionals before it ships, and written with longtime biohackers who were doing this before it was a trend. Reviewed still does not mean prescribed: nothing here is medical advice. It is research, trial data, and reported use, with the numbers intact so you can check them. For decisions about your body, see a doctor who can look at your labs.