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.
Quick Reference
Member reference tables summarize the compound's research parameters.
Research Indications
Research Protocols
As reported in cited literature and research-community logs (see Research Citations below), not a personal dosing recommendation.
This member section describes parameters reported in the research literature.
Peptide Interactions
This member section summarizes reported compound interactions and evidence limitations.
Reported Research Time Points
This member section summarizes reported research time points.
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.
This member section discusses research safety considerations and uncertainties.
Quality Indicators
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