GW501516 — commonly referred to as Cardarine, and also by the designation GW-501,516 or Endurobol — is a synthetic PPARδ (Peroxisome Proliferator-Activated Receptor delta) agonist originally developed in a collaboration between GlaxoSmithKline and Ligand Pharmaceuticals in the early 1990s. Despite often being grouped with SARMs in research communities, GW501516 does not bind to androgen receptors. It operates through an entirely separate molecular pathway.
GW501516’s primary research interest has centered on lipid metabolism, fatty acid oxidation, and preclinical endurance outcomes. It has also been the subject of significant safety scrutiny following GlaxoSmithKline’s internal carcinogenicity findings that led to termination of their development program. Both the metabolic findings and the safety data are documented in the published literature and are essential context for any researcher working with this compound.
What Is GW501516? (It Is Not a SARM)
GW501516 is a PPARδ agonist — it activates Peroxisome Proliferator-Activated Receptor delta, a nuclear receptor expressed predominantly in skeletal muscle, heart muscle, and adipose tissue that regulates genes involved in fatty acid metabolism and energy expenditure. SARMs target androgen receptors. GW501516 does not bind to androgen receptors at physiologically relevant concentrations. The two compound classes work through unrelated receptor systems.
For foundational context on how SARMs work, see our Complete Guide to SARMs.
Mechanism of Action: PPARδ Agonism
PPARδ is a ligand-activated transcription factor. When a compound binds to its ligand-binding domain, the receptor forms a heterodimer with RXR (Retinoid X Receptor) and binds to PPAR response elements (PPREs) in the promoter regions of target genes.
Fatty acid oxidation: PPARδ activation upregulates genes encoding enzymes in the β-oxidation pathway, increasing the rate at which cells metabolize fatty acids for energy. In skeletal muscle, this shifts fuel utilization toward fat and away from glucose and glycogen.
Mitochondrial biogenesis: PPARδ agonism in muscle tissue has been associated with increased expression of genes related to mitochondrial proliferation and oxidative phosphorylation capacity — the basis of research interest in GW501516’s effects on aerobic capacity.
Lipid transport and storage: In adipose tissue and the liver, PPARδ activation influences lipid handling, including effects on HDL cholesterol, triglyceride levels, and fatty acid storage pathways.
Preclinical Research Findings
Metabolic effects in rodent models: Studies in diet-induced obese mice reported that GW501516 administration reduced adiposity, improved insulin sensitivity, and altered lipid profiles — including increases in HDL and decreases in LDL and triglycerides — at doses in the range of 3–10 mg/kg/day.
Skeletal muscle fiber type shift: PPARδ activation in skeletal muscle has been associated with a shift toward Type I (slow-twitch, oxidative) muscle fiber composition. Studies in transgenic mice overexpressing PPARδ demonstrated markedly increased running endurance. GW501516 treatment produced similar directional findings at pharmacological doses.
Endurance in sedentary vs. trained models: A widely referenced 2008 study by Narkar et al. (Cell) demonstrated that GW501516 treatment enhanced endurance in both sedentary and exercise-trained mice, generating substantial research interest in GW501516 as a tool for studying PPARδ’s role in exercise adaptation biology.
The Carcinogenicity Data — Critical Research Context
Any researcher working with GW501516 must be aware of the carcinogenicity findings that led GlaxoSmithKline to terminate the compound’s clinical development program.
In preclinical safety studies, GSK researchers observed that GW501516 treatment in rodents produced rapid and multi-tissue tumor growth. The tumors appeared in multiple tissue types including the colon, liver, tongue, testes, ovaries, and skin. The proposed mechanism was not genotoxic but rather proliferative — PPARδ activation may accelerate the growth of pre-existing or latent cancer cells.
These findings were sufficient for GSK to halt all clinical development of GW501516 by approximately 2007. No clinical efficacy data from human trials was published because the program did not advance past preclinical safety review.
Researchers using GW501516 as a tool compound to study PPARδ biology should account for these proliferative findings when designing studies, interpreting results involving cell viability or proliferation endpoints, and selecting appropriate animal models.
GW501516 vs. SR9009 (Stenabolic)
Researchers frequently compare GW501516 and SR9009 because both are studied in the context of metabolic activity and endurance, and both are grouped with SARMs despite neither being androgen receptor modulators.
GW501516 acts on PPARδ — a metabolic transcription factor regulating fatty acid oxidation and mitochondrial gene expression in muscle and adipose tissue.
SR9009 acts on Rev-Erb nuclear receptors, which regulate circadian rhythm biology, mitochondrial biogenesis, and metabolic gene expression.
Both compounds affect mitochondrial activity and lipid metabolism through entirely different upstream mechanisms. SR9009 (Stenabolic) represents a complementary research tool for researchers studying the interface between circadian biology and metabolism.
Pharmacokinetics
Published pharmacokinetic data for GW501516 is primarily from rodent studies, with limited human data due to the termination of clinical development. GW501516 demonstrates good oral bioavailability in rodent models. Its elimination half-life in rodent studies is approximately 16–24 hours, supporting once-daily dosing in research protocols. It is highly protein-bound in plasma and highly lipophilic, partitioning preferentially into fatty tissues.
Sourcing GW501516 for Research
Given the carcinogenicity findings in the literature, purity and identity verification are critically important when sourcing GW501516. Chemyo Sarms supplies GW501516 as a research-grade compound with independent third-party COA documentation confirming identity by HPLC, purity percentage, and concentration.
→ View GW501516 (Cardarine) research compound
Frequently Asked Questions
Is GW501516 a SARM?
No. GW501516 (Cardarine) is a PPARδ agonist, not a Selective Androgen Receptor Modulator. It does not bind to androgen receptors. It is grouped with SARMs in research communities because it is commonly studied alongside them, but mechanistically it belongs to a different compound class.
Why did GlaxoSmithKline stop developing GW501516?
GSK terminated GW501516’s development program following internal preclinical carcinogenicity studies that showed rapid tumor growth in multiple tissue types in rodents. The proposed mechanism is PPARδ-mediated proliferative activity rather than genotoxicity.
Does GW501516 suppress testosterone?
No. GW501516 does not act on androgen receptors or the HPG axis. It has no direct mechanism for suppressing LH, FSH, or testosterone production.
What is Endurobol?
Endurobol is a colloquial name sometimes used for GW501516, derived from its studied effects on endurance in preclinical models. It is the same compound as GW501516/Cardarine.
Where can I find the primary research on GW501516?
Key references include Narkar et al. (2008) “AMPK and PPARδ Agonists Are Exercise Mimetics” (Cell). For carcinogenicity context, academic reviews of PPARδ agonist safety data are available via PubMed.
GW501516 is sold by Chemyo Sarms strictly as a research compound. Researchers should review the published carcinogenicity literature before designing protocols involving this compound. For educational reference only.