GW-501516 (Cardarine): 2-[2-methyl-4-[[4-methyl-2-[4-(trifluoromethyl)phenyl] -1,3-thiazol-5-yl]methylsulfanyl]phenoxy]acetic acid
Molecular Formula: C21H18F3NO3S2
Molecular Weight: 453.498 g/mol
CAS number: 317318-70-0
Purity: Greater than 99%
Other details: No DMSO or other harmful solvents
Storage: This product must be stored at 4°C. Not suitable for freezing.
Shake well before use.
Possible therapy for dyslipidemia is the peroxisome proliferator-activated receptor delta (PPARδ) agonist GW-501516. It has been researched to treat cardiovascular disease, lipid disorders, and obesity. The drug GW-501516 showed a markedly favourable decrease in triglycerides, fatty acids, VLDL, and LDL with a concurrent rise in HDL (the "good cholesterol"). GW-501516 binds to PPARδ and activates the coactivator PGC-1α with great potency and affinity for the peroxisome proliferator-activated receptor delta. The liver converts fatty acids into its primary energy source by activating PPARδ, which may lower blood sugar levels.
In turn, this enhances insulin sensitivity and body composition, upregulates the body's production of proteins involved in energy expenditure, and may reduce the prevalence of type II diabetes and cardiovascular disease. The most prominent advantages that GW-501516 has shown in trials via its specific activation of PPARδ include increased energy, the capacity to grow muscle, insulin sensitivity, the capacity to burn fat, endurance, and better lipid profiles.
The following advantages of GW-501516 have been shown through research:
- Mice's inflammation is reduced
- Mice with better blood flow by increasing nitric oxide levels
- Activation of PPARδ in white adipose tissue to increase total oxidative metabolism and reverse obesity and diabetes
- Insulin sensitivity, a key risk factor for diabetes, obesity, heart disease, and cancer, significantly improved in mice.
Two early studies in healthy people showed that GW-501516 was effective in lowering levels of Triglycerides, LDL cholesterol, apoB, and insulin while raising HDL cholesterol and enhancing insulin sensitivity. 24 healthy males participated in the first clinical study, which lasted two weeks. Each participant received either a placebo, 2.5 mg, or 10 mg of GW-501516 daily. GW-501516 substantially decreased Triglycerides and raised HDL cholesterol levels.
Due to GW-501516's capacity to promote the upregulation of human skeletal muscle fat consumption, ABCA1 expression, and increased serum fat clearance rates, the lipid profile has improved. When the lipolytic activity was measured to compare GW-501516's effectiveness to a placebo, the results showed that even in the presence of high-fat meals, the 2.5 mg and 10 mg treated groups dramatically decreased Triglyceride levels. During this experiment, it was shown that GW-501516 was secure and well-tolerated. No notable negative side effects, including liver and muscle reactions, were seen in subjects receiving treatment with GW-501516.
GW-501516 inhibits glucose catabolism and promotes fatty acid metabolism without impairing mitochondrial composition or muscle fibre type. By preserving glucose in the body, GW-501516 significantly increases running times and overall endurance while delaying the onset of hypoglycemia during exercise. The most stated advantage of GW-501516 is, without a doubt, the enormous increase in endurance, and users often gush about how they feel as if their endurance has increased by 25–30% right away after taking it. Expectedly, athletes who use GW-501516 in endurance sports have extremely positive results in their performance.
PCT (post-cycle therapy): GW-501516 does not decrease the endocrine system, diminish natural testosterone levels, or block LH, FSH, or SHBG. Additionally, it does not raise estrogen levels, which indirectly reduces testosterone. GW-501516 suppresses no sex hormones, and no antagonistic hormones are increased. Hence a PCT phase is unnecessary since GW-501516 does not cause any hormone suppression.
W. Chen et al., "A metabolomic study of the PPARδ agonist GW501516 for enhancing running endurance in Kunming mice" [PubMed]
U. Dressel et al., "The peroxisome proliferator-activated receptor beta/delta agonist, GW501516, regulates the expression of genes involved in lipid catabolism and energy uncoupling in skeletal muscle cells" [PubMed]
P. Kintz et al., "Testing for GW501516 (cardarine) in human hair using LC/MS-MS and confirmation by LC/HRMS" [PubMed]
M. Idrees et al., "The PPARδ Agonist GW501516 Improves Lipolytic/Lipogenic Balance through CPT1 and PEPCK during the Development of Pre-Implantation Bovine Embryos" [PubMed]
N. Dimopoulos et al., "The PPARdelta agonist, GW501516, promotes fatty acid oxidation but has no direct effect on glucose utilisation or insulin sensitivity in rat L6 skeletal muscle cells" [PubMed]
M.P. Mosti et al., "Effects of the peroxisome proliferator-activated receptor (PPAR)-δ agonist GW501516 on bone and muscle in ovariectomized rats" [PubMed]
E. Barroso et al., "The PPARβ/δ activator GW501516 prevents the down-regulation of AMPK caused by a high-fat diet in liver and amplifies the PGC-1α-Lipin 1-PPARα pathway leading to increased fatty acid oxidation" [PubMed]
D'angelo C. Magliano et al., "Short-term administration of GW501516 improves inflammatory state in white adipose tissue and liver damage in high-fructose-fed mice through modulation of the renin-angiotensin system" [PubMed]
S. Trevisiol et al., "Comprehensive characterization of the peroxisome proliferator activated receptor-δ agonist GW501516 for horse doping control analysis" [PubMed]
This product is intendend for lab research and development use only. These studies are performed outside of the body. This product is not medicines or drugs and has not been approved by the FDA or EMA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law. This product should only be handled by licensed, qualified professionals.
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