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Gw53.0
Cardarine (GW501516) Research
Mostly mechanism / observationalLimited safety
6 peer-reviewed studies
What the evidence says
Mostly mechanism / observational
Most Cardarine (GW501516) studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality randomised trials published 2004–2019 with a typical study size of 24 participants.
Based on 6 studies · 1 RCT · 24 total participants
Confidence
Low
By outcome
Endurance (preclinical)
Mostly mechanism / observational3 studies
Safety profile
Mostly mechanism / observational3 studies
Cholesterol & lipids
Too few graded studies1 study
Older research base
Newest study from 2019
200420112019
1Animal2008
Even in sedentary mice, 4 weeks of AICAR treatment alone induced metabolic genes and enhanced running endurance by 44%.
Narkar VA, Downes M, Yu RT, Embler E, Wang YX, Banayo E, et al. · Cell (2008)
The foundational 'exercise mimetic' study — but entirely in mice: a treadmill running test, not a human trial
The orally active AMPK agonist AICAR, given for 4 weeks to SEDENTARY mice, increased running endurance by 44% with no exercise
AICAR and a PPARβ/δ agonist induced oxidative myofibers and metabolic genes via the AMPK–PGC-1α pathway
This is the first report of a PPARdelta agonist administered to man ... GW501516 significantly influenced HDLc and TGs in healthy volunteers.
Sprecher DL, Massien C, Pearce G, Billin AN, Perlstein I, Willson TM, et al. · Arteriosclerosis, thrombosis, and vascular biology (2007)
The only published human study of GW501516 — a 2-week randomised trial in 24 healthy, sedentary, hospitalised volunteers (placebo vs 2.5 mg vs 10 mg once daily)
GW501516 raised HDL cholesterol in both dose groups and improved post-fat-feeding triglyceride clearance; in vitro it upregulated fatty-acid oxidation, CPT1, CD36 and ABCA1 in human muscle cells
A lipid/biomarker pharmacology signal — NOT a demonstrated clinical outcome, and not an endurance or performance study
PPARdelta is a key regulator of fatty acid catabolism and oxidative metabolism in skeletal muscle, positioning it as a target for the treatment of metabolic syndrome.
Luquet S, Lopez-Soriano J, Holst D, Gaudel C, Jehl-Pietri C, Fredenrich A, et al. · Biochimie (2004)
Mechanistic review of PPARδ as the master regulator of fatty-acid oxidation and oxidative-fibre metabolism in skeletal muscle
Explains the molecular rationale GW501516 exploits: PPARδ activation drives fatty-acid uptake and β-oxidation and an oxidative fibre-type shift
Frames PPARδ as a candidate target for metabolic syndrome — the original therapeutic hypothesis behind the compound
GW501516 significantly enhanced colitis-associated colorectal cancer in AOM/DSS-induced mice.
Zhou D, Jin J, Liu Q, Shi J, Hou Y · European journal of pharmacology (2019)
Mandatory counter-evidence: the PPARδ agonist GW501516 itself significantly enhanced colitis-associated colorectal cancer in AOM/DSS-induced mice
GW501516 raised pro-inflammatory gene expression (COX-2, IL-6, IL-8, MCP-1) in inflamed colon and increased Glut1/SLC1A5 in colon cancer cells and tumours
Mechanistically links the compound's PPARδ activation to tumour promotion — coherent with the carcinogenicity that ended its development
Since January 2009, the list of prohibited substances and methods of doping ... includes ... the PPAR-delta agonist GW1516, which is categorized as a gene doping substance.
Thevis M, Möller I, Thomas A, Beuck S, Rodchenkov G, Bornatsch W, et al. · Analytical and bioanalytical chemistry (2010)
Documents that GW501516 (GW1516) has been on the World Anti-Doping Agency prohibited list since January 2009 as a gene-doping agent
Characterised two major urinary metabolites (sulfoxide and sulfone) and implemented a validated LC-MS/MS urine assay for routine doping control (limit of detection 0.1 ng/ml)
Confirms cardarine is a banned doping substance with established detection in sport, not an approved therapeutic
These findings were confirmed with an additional high-affinity PPARdelta agonist, GW501516 ... activation of PPARdelta can result in increased growth in breast and prostate cancer cell lines.
Stephen RL, Gustafsson MC, Jarvis M, Tatoud R, Marshall BR, Knight D, et al. · Cancer research (2004)
Additional counter-evidence: the high-affinity PPARδ agonist GW501516 stimulated proliferation of human breast (T47D, MCF7) and prostate (LNCaP) cancer cell lines
GW501516 increased the proliferation marker Cdk2 and VEGFα/FLT-1, suggesting an autocrine proliferative and pro-angiogenic loop
Pro-proliferative effects extended to human endothelial cells, consistent with tumour angiogenesis