Cardarine

An abandoned GlaxoSmithKline drug candidate that shifts muscle fuel metabolism toward fat oxidation — known for rodent endurance findings, and for why development stopped. GW-0742 is a closely related compound from the same program.

Cardarine (GW501516) activates PPAR-delta, a nuclear receptor that switches on genes governing how cells use fat for fuel. In animals that shifts muscle toward fat oxidation and raises endurance, which is the entire basis of its reputation as "exercise in a pill". What ended its development was rodent carcinogenicity — tumours at multiple sites. Whether PPAR-delta activation is itself the causal pathway is NOT settled: the developer's own abstracts say some tumours may reflect it while noting conflicting proliferation findings elsewhere.

Early human trials showed lipid changes; the endurance results the marketing quotes are rodent data. Development was terminated after long-term rodent studies produced tumors at multiple sites; human relevance and any safe exposure threshold are unknown.

• NONE SHOWN for the endurance and fat-loss use it is sold for, and no clinical outcome benefit was ever demonstrated. That is narrower than "no human evidence": the trials did establish statistically significant changes in HDL, LDL, triglycerides and apolipoproteins.
• The human programme was not trivial: a randomised double-blind trial enrolled 268 participants with fasting HDL change at 12 weeks as its prespecified primary outcome, alongside a 37-participant exploratory study and an earlier 24-participant healthy-volunteer study. Those measured lipid markers, not endurance or fat loss.
• The decisive evidence is preclinical toxicology. The developer's published abstracts reported treatment-related tumours at multiple sites and at all tested dose levels in rats, and liver, stomach and combined squamous tumours in mice. Note these are conference abstracts rather than full public study reports, and the exact causal pathway and its human relevance remain unresolved — the developer's own abstracts describe conflicting proliferation findings.
• Development was halted or placed on hold across 2006-07 following preclinical toxicity findings. WADA has issued a rare direct public warning to athletes about it, citing serious toxicities in the plural — carcinogenicity is the dominant publicly known concern but not the only preclinical one; skeletal-muscle lesions were also reported in rats.
• Short-term human exposure and adverse-event data do exist from the clinical programme. What does not exist is any adequate long-term human safety dataset, and short trials cannot bound a long-latency carcinogenic risk.

Orally active. Human pharmacokinetics are poorly characterised because development stopped early. It is prohibited in sport. What is sold is research-chemical supply of unverified identity and purity, and analytical work on this category routinely finds products that are not what the label says.

The carcinogenicity finding is THE risk: multi-site tumors in both sexes of both rodent species, with no human long-term data to bound it. Community reassurance about doses and durations is exposure math without a human dataset behind it. WADA-prohibited.

• Everyone — a compound whose development was halted over rodent tumours at multiple sites, with no adequate long-term human safety data
• No human data identifies any lower-risk group, so an absent family history is not reassurance
• Anyone in tested sport, where WADA has issued a direct warning

• No characterised human interaction profile exists.
• Any tested sport, where it is prohibited and WADA has warned about it directly.

• There is no validated surveillance test that can quantify or exclude a future GW501516-related cancer risk, and presenting a lab panel here would imply a safety that does not exist. That is NOT a reason to skip ordinary cancer screening or to ignore symptoms — routine screening and prompt evaluation of anything new still matter, and matter more rather than less.
• The honest framing: this is a compound whose development was halted by rodent tumours at multiple sites, being used without adequate long-term human safety data.

No withdrawal syndrome has been established — the human trials were short and were not designed to look for one. The concern is not a reversible physiological effect: a long-latency carcinogenic risk would not announce itself on stopping, and no validated test can quantify or exclude it afterwards. Ordinary cancer screening and prompt evaluation of new symptoms still apply.

US: not FDA-approved for human use; unscheduled. The FDA has warned about this product category, and marketing it for human use may violate the FD&C Act.

Papers about this compound, not proof of the claims above. A title says what was studied, which is sometimes a negative result or a different question entirely.

• GW501516 facilitated tumor immune escape by inhibiting phagocytosis
  Eur J Pharmacol, 2025

• Roles of the peroxisome proliferator-activated receptors (PPARs) in the pathogenesis of nonalcoholic fatty liver disease (NAFLD)Pharmacol Res · 2023
• GW-501516 GlaxoSmithKline/LigandCurr Opin Investig Drugs · 2006
• Differential effects of selective- and pan-PPAR agonists on experimental steatohepatitis and hepatic macrophages(☆)J Hepatol · 2020
• Anti-inflammatory effects and improved metabolic derangements in ob/ob mice by a newly synthesized prenylated benzopyran with pan-PPAR activityPharmacol Res · 2023
• PPARdelta activator GW-501516 has no acute effect on glucose transport in skeletal muscleAm J Physiol Endocrinol Metab · 2006
• Testing for GW501516 (cardarine) in human hair using LC/MS-MS and confirmation by LC/HRMSDrug Test Anal · 2020
• Effects of the PPAR-beta agonist GW501516 in an in vitro model of brain inflammation and antibody-induced demyelinationJ Neuroinflammation · 2009
• PPARδ agonist enhances colitis-associated colorectal cancerEur J Pharmacol · 2019
• GW501516 facilitated tumor immune escape by inhibiting phagocytosisEur J Pharmacol · 2025
• Exercise Pills: At the Starting LineTrends Pharmacol Sci · 2015
• Recent Updates on Peroxisome Proliferator-Activated Receptor δ Agonists for the Treatment of Metabolic SyndromeMed Chem · 2016
• GLP-1 receptor agonist protects glucose-stimulated insulin secretion in pancreatic β-cells against lipotoxicity via PPARδ/UCP2 pathwayCell Mol Life Sci · 2025