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Gw53.0
Cardarine (GW501516) – Forschung
Überwiegend Mechanismus / Beobachtung
6 begutachtete Studien
Was die Evidenz sagt
Überwiegend Mechanismus / Beobachtung
Die meisten Studien zu Cardarine (GW501516) sind mechanistisch oder beobachtend statt RCTs, die einen klinischen Effekt messen — betrachte die Ergebnisse als vorläufig.
Die meiste Evidenz stammt aus gemischt-qualitativen randomisierten Studien, veröffentlicht 2004–2019 mit einer typischen Studiengröße von 24 Teilnehmenden.
Basierend auf 6 Studien · 1 RCT · 24 Teilnehmende insgesamt
Konfidenz
Geringe Konfidenz
Nach Outcome
Endurance (preclinical)Der Ruf für Ausdauer beruht auf einer einzigen Laufband-Studie an Mäusen; keine Wirksamkeitsstudien am Menschen. Die Entwicklung wurde wegen Krebs an mehreren Organen bei Tieren eingestellt, und es ist von der WADA verboten. · Nicht etabliert (keine Wirksamkeitsdaten am Menschen)
Überwiegend Mechanismus / Beobachtung3 Studien
Safety profile
Überwiegend Mechanismus / Beobachtung3 Studien
Cholesterol & lipids
Zu wenige bewertete Studien1 Studie
Ältere Forschungsbasis
Neueste Studie von 2019
200420112019
1Tierstudie2008
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