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Cardarine

C
Animal replicated
Research chemicalPPARδ AgonistSmall MoleculeExercise Mimetic
RouteOralGray-market only
C
Evidence grade: Animal replicated

Effect demonstrated in multiple animal studies; human data sparse or extrapolated. Grades summarize evidence quality, not whether a compound is appropriate, legal, or risk-free.

At a glance
What it is
GW501516 / GW1516 / Endurobol — PPARδ Agonist — PPARδ Agonist, Small Molecule, Exercise Mimetic.
Why people use it
Endurance and Exercise Capacity · Lipid Profile Improvements · Fat Oxidation and Body Composition · Insulin Sensitivity and Metabolic Markers
What the evidence supports
GW501516 has Grade B evidence for its performance and metabolic benefits, Grade A evidence for its carcinogenicity in animal models, and the worst possible outcome at the intersection: the mechanism that produces the benefits (PPARδ activation) is the same mechanism that plausibly produces the cancer risk. This is not a case where the benefits and risks are from different biological systems that can be traded off. They are the same system.
Key risks
Key risks: Active malignancy or cancer history, Pregnancy, Children and adolescents, Tested athletes.
If you only read one thing

GW501516 (Cardarine) caused rapid tumor development in multiple organ systems in rats and mice at doses spanning 3-30x above typical community use in standard two-year carcinogenicity studies — the studies that pharmaceutical regulators require before any drug is approved for chronic human use. GlaxoSmithKline, the developer, terminated all development in 2007 based on this data. No human cancer cases have been specifically documented and attributed to cardarine use. Both of these statements are true simultaneously. The community's counterargument — 'it hasn't been proven to cause cancer in humans' — is technically accurate and deeply misleading, because the reason long-term human cancer data doesn't exist is that the preclinical carcinogenicity signal was so severe that long-term human studies were never conducted. This chapter covers cardarine's genuine performance benefits and its cancer risk with equal honesty. The chapter does not tell you what to do. It tells you what is known.

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Published literature
3human RCTs1human study5animal3in vitro

Human evidence is short-term oral metabolic/lipid/liver-fat controlled data; development was terminated after animal carcinogenicity findings, so no Phase 3 or long-term human safety evidence exists.

Evidence reality check
Human evidence
4 human studies
3 randomized; 1 observational.
Preclinical base
8 lab signals
5 animal; 3 in-vitro/mechanistic.
Evidence snapshot
GW501516 has Grade B evidence for its performance and metabolic benefits, Grade A evidence for its carcinogenicity in animal models, and the worst possible outcome at the intersection: the mechanism that produces the benefits (PPARδ activation) is the same mechanism that plausibly produces the cancer risk. This is not a case where the benefits and risks are from different biological systems that can be traded off. They are the same system.
From the chapter quick-reference block.
Indication map
Supported / plausible / speculative / avoid
Plausible
Endurance and Exercise Capacity · Lipid Profile Improvements · Fat Oxidation and Body Composition · Insulin Sensitivity and Metabolic Markers
GW501516 has Grade B evidence for its performance and metabolic benefits, Grade A evidence for its carcinogenicity in animal models, and the worst possible outcome at the intersection: the mechanism that produces the benefits (PPARδ activation) is the same mechanism that plausibly produces the cancer risk. This is not a case where the benefits and risks are from different biological systems that can be traded off. They are the same system.
Avoid
Active malignancy or cancer history
PPARδ activation supports tumor cell survival and immune evasion. This is not a theoretical concern — it is the documented mechanism of carcinogenicity. Active malignancy is an absolute contraindication.

Cardarine is the compound in this reference where the chapter has the most uncomfortable job to do. The performance benefits are real and well-documented. The cancer risk is real and documented by the developer themselves. There is no reassuring resolution of this tension.

The central tension resolved: GW501516 is one of the most effective exercise mimetics and endurance enhancers ever developed. The Salk Institute's independent endurance research is genuine. The short-term human lipid and liver fat data is genuine. The compound works. GlaxoSmithKline, a company with every financial incentive to bring it to market given those results, terminated their own program because the two-year carcinogenicity studies showed rapid multi-organ tumor development in multiple species at multiple doses. This was not a marginal safety signal. It was the kind of signal that terminates pharmaceutical programs. The community has assessed this differently: the benefits are observable, the cancer risk is long-latency and unconfirmed in humans, and the doses being used are below the animal study doses. Whether this risk assessment is correct will only be determinable 10-20 years from now, when the current cohort of cardarine users reaches the age where long-latency cancers would present. No community forum will tell you that data when it becomes available.

This chapter's position: the carcinogenicity data from GSK should be the primary frame for any decision about GW501516 use. It should not be minimized, rationalized, or contextualized away. The performance benefits do not change the biological reality of what happened in those animal studies. A compound that causes this kind of carcinogenicity finding belongs in a category of extreme caution, regardless of how good the acute performance benefits are or how mild the short-term side effects are.

Categories
Muscle & PerformanceWeight Loss & MetabolicMitochondrial & Energy
Properties
Active malignancy: hard stopWADA S4✓ Human RCTNot injectable
  • ⛔ Active malignancy or cancer history — PPARδ activation supports tumor cell survival and immune evasion. This is not a theoretical concern — it is the documented mechanism of carcinogenicity. Active malignancy is an absolute contraindication.
  • ⛔ Pregnancy — carcinogen exposure during pregnancy with potential transplacental exposure to the fetus. Absolute contraindication.
  • ⛔ Children and adolescents — rapidly proliferating cells are most sensitive to carcinogens. Absolute contraindication.
  • ⛔ Tested athletes — WADA S4.4 ban; supplement contamination risk adds violation exposure even without intentional use. Complete prohibition.
Half-life
Half-life in humans: approximately 16-24 hours, supporting once-daily dosing
Evidence
CAnimal replicated
NOT A SARM — Important Distinction
Cardarine is consistently mis-marketed and mis-categorized as a SARM (selective androgen receptor modulator). It has zero androgen receptor activity. It works through PPARδ, a nuclear receptor that regulates fat oxidation and energy metabolism — completely different mechanism from SARMs, steroids, or GH secretagogues.
Names / Aliases
GW501516 = GW1516 = GW-501,516 = GSK-516 = Cardarine = Endurobol. All the same compound.
Why It Was Developed
Developed in the 1990s as a potential treatment for metabolic syndrome, dyslipidemia, obesity, and cardiovascular disease. PPARδ activation was understood to improve fat oxidation and lipid profiles. The compound advanced to Phase 1 and Phase 2 clinical trials in humans.
What It Does — The Performance Reality
Dramatically increases fat oxidation in skeletal muscle. Switches muscle fiber composition toward oxidative (Type I/IIa). Dramatically improves endurance in animal models — Wang et al. (2003) showed 70% increase in running capacity. Raises HDL by up to 16.9% in short-term human trials. Reduces liver fat 20% in 2 weeks at 10 mg/day in humans. These effects are real and well-documented in controlled studies.
THE CANCER PROBLEM — READ THIS BEFORE ANYTHING ELSE
GlaxoSmithKline terminated all GW501516 development in 2007 after two-year carcinogenicity studies in rats and mice showed rapid tumor development in multiple organ systems — liver, stomach, skin, bladder, intestines — at multiple dose levels. This was not a marginal finding. Multi-organ tumor development in multiple species at doses spanning 3-30x above typical community use is what standard carcinogenicity testing is designed to detect. The protocol exists because if a drug fails here, it has unacceptable cancer risk for human chronic use. GW501516 failed catastrophically. The community continues to use it.
The Dose Argument — And Its Limits
Community doses: 10-20 mg/day. GSK carcinogenicity study doses in rats: 5 mg/kg/day and 40 mg/kg/day (approximately 50-400 mg/day human-equivalent by allometric scaling). The argument: community doses are 3-30x below animal study doses. The counterargument: two-year carcinogenicity studies are specifically calibrated to be sensitive to compounds that would cause only marginal cancer risk increases in humans. The fact that cardarine produced multi-organ tumors at these doses — not marginal increases, but rapid multi-organ tumor development — is among the most concerning carcinogenicity signals in pharmaceutical development history. 'Lower doses' is not reassurance when the compound causes this kind of signal at any dose studied.
WADA Status
BANNED — S4.4 Metabolic Modulators since 2009. Banned at all times, in and out of competition, with no TUE pathway. WADA acted before long-term human safety data was even available — a regulatory response to the carcinogenicity data. Zero tolerance; no detection threshold at WADA level (NCAA applies a 100 pg/mL threshold for atypical findings).
FDA Status
FDA classifies GW501516 as an unapproved new drug. Not legal to market as a medication, dietary supplement, or food ingredient. Not a research chemical in the conventional sense — GSK's terminated drug. Research chemical vendors sell it anyway.
Supplement Contamination
USADA has documented cardarine as a supplement contaminant — athletes have tested positive after taking supplements not labeled to contain it. This creates WADA violation risk even for athletes who have never intentionally used it.
Human Cancer Evidence
No documented human cancer cases specifically linked to cardarine use have been published. This is not proof of safety — it reflects: (1) the absence of long-term human follow-up studies; (2) the difficulty of attributing any individual's cancer to a specific compound; (3) typical 15-30 year latency between carcinogen exposure and cancer diagnosis. The absence of reported cases is not reassuring for a compound whose animal carcinogenicity signal was this severe.
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