GW-501516 (Cardarine) Research Overview (also known as Cardarine, Endurobol, GW501516, GW1516)
GW-501516, commonly called Cardarine or Endurobol, is an experimental selective agonist of peroxisome proliferator-activated receptor delta (PPARδ), a nuclear receptor involved in fatty-acid metabolism, glucose handling, and skeletal-muscle energy use. It is often grouped with SARMs in research-compound discussions, but it is not a selective androgen receptor modulator because it does not act through the androgen receptor; development was abandoned after dose-dependent carcinogenicity findings in long-term rodent studies.
What Is GW-501516?
GW-501516, widely known as Cardarine, Endurobol, GW501516, or GW1516, is a synthetic small molecule that activates peroxisome proliferator-activated receptor delta, usually abbreviated PPARδ or PPAR-beta/delta. It was developed jointly by GlaxoSmithKline, commonly abbreviated GSK, and Ligand Pharmaceuticals during the 1990s as a pharmacological approach to metabolic syndrome, dyslipidemia, obesity-related insulin resistance, and cardiovascular disease. The compound attracted interest because PPARδ influences the expression of genes involved in fatty-acid transport, fatty-acid oxidation, glucose utilization, mitochondrial function, and energy expenditure. In animal models, activation of this receptor produced changes resembling some effects of endurance exercise, including enhanced oxidative metabolism in skeletal muscle.
GW-501516 is frequently listed alongside selective androgen receptor modulators, or SARMs, in online research-compound catalogs and performance-enhancement discussions. That classification is technically inaccurate. A SARM acts at the androgen receptor, whereas GW-501516 acts at PPARδ, a ligand-activated nuclear receptor that regulates transcription of metabolic genes. The distinction matters because GW-501516 is not expected to produce the androgen-receptor-mediated anabolic, virilizing, or suppressive effects associated with many SARMs. It also means that concepts such as post-cycle therapy do not translate directly from androgenic compounds to GW-501516.
GSK abandoned clinical development after extended toxicology studies in rodents identified dose-dependent increases in tumors across multiple tissues and in more than one rodent species. Public descriptions of the development program indicate that the findings occurred with prolonged administration and at exposures relevant to the safety assessment, creating an unacceptable risk-benefit profile for a nonessential metabolic drug. The company discontinued the program rather than pursuing approval for metabolic or cardiovascular indications. The rodent findings do not establish that every exposure in humans will cause cancer, and the precise relevance of the animal exposure levels to humans remains a scientific question. Nevertheless, the findings are a major safety signal, and there are no adequate long-term human data capable of ruling out carcinogenic risk. The compound therefore remains investigational and is not an approved treatment, dietary supplement, or established human performance aid.
Despite the termination of development, GW-501516 continues to be studied experimentally because it provides a useful tool for understanding PPARδ biology. Laboratory research has examined its effects on fat oxidation, skeletal-muscle fiber characteristics, glucose metabolism, lipid transport, hepatic metabolism, and exercise capacity. These findings are valuable for basic and translational research, but positive results in mice or short-term cell-based experiments do not translate automatically to safe or effective human use.
Research Indications
Lipid Metabolism
HDL and triglyceride modulation
Short human studies of GW-501516 reported dose-related increases in HDL cholesterol and reductions in triglycerides in subjects with dyslipidemia.
Reverse cholesterol transport
Preclinical work links PPARδ activation to macrophage cholesterol efflux and reverse cholesterol transport pathways.
Fatty-Acid Oxidation
Skeletal-muscle oxidative gene programs
Animal and cell studies show that PPARδ signaling can increase expression of genes involved in lipid uptake and oxidative metabolism.
Metabolic flexibility
The proposed shift toward fatty-acid utilization is mechanistically plausible, but long-term clinical metabolic outcomes remain unestablished.
Exercise Performance
Mouse endurance models
PPARδ agonism enhanced endurance-related phenotypes in mouse studies, including work combining pharmacologic activation with exercise.
Human performance uncertainty
Controlled evidence demonstrating improved athletic performance in healthy humans is limited; it is prohibited in sport by the World Anti-Doping Agency.
Glucose and Insulin Signaling
Insulin-sensitivity pathways
PPARδ is involved in energy homeostasis, but findings from experimental models do not establish a safe or effective treatment role for glucose disorders.
No approved therapeutic indication
GW-501516 is investigational and is not approved as a treatment for diabetes, obesity, dyslipidemia, or exercise enhancement.
Research Protocols
As reported in cited literature and research-community logs (see Research Citations below) — not a personal dosing recommendation.
| Research Application | Dose | Frequency | Route |
|---|
| Early human lipid research | 2.5 mg | Once daily | Oral |
| Clinical dose-ranging studies | 5 mg | Once daily | Oral |
| Clinical dose-ranging studies | 10 mg | Once daily | Oral |
| Highest reported short-term study arm | 20 mg | Once daily | Oral |
Timing
Published human studies used once-daily oral administration over short durations. There is no established safe timing strategy, cycle length, or long-term regimen; GW-501516 development was discontinued and it is not approved for human use.
Peptide Interactions
Both may affect lipid-management decisions and liver-enzyme monitoring. Clinical combination safety data are insufficient.
Fibrates are PPARα-directed lipid drugs; overlapping metabolic effects and absent combination studies warrant clinician oversight.
Potential effects on substrate metabolism could complicate glucose management; monitor for unexpected glycemic changes with a prescriber.
Unregulated stacking obscures causality, increases exposure uncertainty, and has no established safety basis.
Avoiding alcohol is prudent when using an unapproved compound with uncertain hepatic and systemic safety.
No specific pharmacologic interaction is established, though stimulant adverse effects can confound tolerability and exercise-related symptoms.
Reported Research Timeline
01First 1–3 days (reported in cited studies): no reliably established perceptible effect; acute subjective changes are not a validated marker of activity or safety.
02Week 1–2 (reported in cited studies): lipid changes, if present, are laboratory findings rather than dependable felt effects; baseline and follow-up testing are more informative than symptoms.
03Weeks 3–4 (reported in cited studies): short clinical studies reported lipid biomarker changes over this general timeframe; individual response and relevance to healthy users are uncertain.
04Weeks 4–8 (reported in cited studies): claims of improved endurance are largely extrapolated from animal research and anecdote; controlled healthy-human performance data are lacking.
05Beyond 8 weeks: safety uncertainty rises because long-duration human data are limited and preclinical toxicology raised serious concerns.
06After discontinuation (reported in cited studies): the time course for reversal of biomarker effects and long-term risk is not well characterized in independent human studies.
Safety Notes
Included for harm-reduction awareness only, in the event this compound is encountered outside its labeled research use. Inclusion here does not imply RUO Codes endorses, recommends, or instructs human use.
GW-501516 is an investigational PPARδ agonist, not a SARM in the pharmacologic sense, and is not approved for human therapeutic use.
Development was discontinued after long-term animal studies identified multiple cancer findings at exposures relevant to concern; human cancer risk is unknown.
Do not use during pregnancy, while breastfeeding, or when trying to conceive because reproductive and developmental safety data are inadequate.
Avoid use with active or prior malignancy, unexplained weight loss, gastrointestinal bleeding, or strong familial cancer syndromes unless specifically evaluated by an oncologist.
Products sold as research chemicals may be mislabeled, underdosed, contaminated, or substituted with unrelated substances.
GW-501516 is prohibited at all times under the World Anti-Doping Agency Prohibited List; athletes may face sanctions from a positive test.
Seek Medical Attention If:
You develop chest pain, shortness of breath, fainting, a new irregular heartbeat, or severe exercise intolerance.
You experience yellowing of the skin or eyes, dark urine, persistent vomiting, severe abdominal pain, or marked fatigue.
You notice blood in stool or urine, black tarry stools, unexplained rectal bleeding, or persistent changes in bowel habits.
You have facial swelling, hives, wheezing, confusion, or any severe or rapidly worsening reaction.
Quality Indicators
Verified Marker
Lot-specific third-party COA
A current certificate of analysis should identify the exact lot, test date, laboratory, method, analyte name, and quantitative result.
Verified Marker
HPLC or LC-MS identity confirmation
Prefer chromatographic identity testing with a readable chromatogram and retention-time comparison, ideally supported by mass-spectrometric confirmation.
Verified Marker
Oral-unit content verification
For capsules or tablets, seek assay results for mg content per unit and content-uniformity testing rather than bulk-powder purity alone.
Acceptable Range
Quantitative purity result reported
A stated HPLC purity value is useful only when it is linked to a traceable lot and an independent laboratory; purity alone does not confirm dose accuracy or absence of all contaminants.
Quality Concern
Vendor-generated or recycled certificates
Undated reports, identical COAs across multiple lots, missing laboratory contact details, or image-only certificates without raw data are significant red flags.
Research Citations
- A selective peroxisome proliferator-activated receptor delta agonist promotes reverse cholesterol transport.
Oliver, W. R., Jr., Shenk, J. L., Snaith, M. R., et al., 2001, Proceedings of the National Academy of Sciences of the United States of America - A PPARdelta agonist promotes reverse cholesterol transport in monkeys.
Barish, G. D., Atkins, A. R., Downes, M., et al., 2006, Journal of Clinical Investigation - Endurance exercise performance in mice is enhanced by pharmacological activation of PPARdelta.
Narkar, V. A., Downes, M., Yu, R. T., et al., 2008, Cell - Peroxisome proliferator-activated receptor delta is a nuclear target for the anti-inflammatory leukotriene B4.
Lee, C. H., Chawla, A., Urbiztondo, N., et al., 2003, Journal of Biological Chemistry - Activation of PPARdelta promotes lipid accumulation in human skeletal muscle.
Krämer, D. K., Al-Khalili, L., Guigas, B., et al., 2007, Cell Metabolism
Research Focus
endurance, fat oxidation, metabolic syndrome, cardiovascular health, PPARdelta
Frequently Asked Questions
What should researchers watch for with GW-501516 (Cardarine)?
Included for harm-reduction awareness only, in the event this compound is encountered outside its labeled research use. Inclusion here does not imply RUO Codes endorses, recommends, or instructs human use.
What should researchers expect over time with GW-501516 (Cardarine)?
First 1–3 days (reported in cited studies): no reliably established perceptible effect; acute subjective changes are not a validated marker of activity or safety.
How is GW-501516 (Cardarine) typically administered in research?
As reported in cited literature and research-community logs (see Research Citations below) — not a personal dosing recommendation.
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