Fitorine (GW-0742) 10mg – 60 capsules (preorder) Product Information
Fitorine — GW-0742 10 mg — 60 oral research capsules. GW-0742 is a high-potency, selective PPARδ agonist (EC₅₀ ≈ 1 nM, > 1,000-fold selectivity over PPARα and PPARγ) and the cleanest pharmacological tool available for studying the PPARδ-driven oxidative metabolism program in skeletal muscle, liver and macrophages. In landmark experiments by Narkar et al. (Cell, 2008), four-week PPARδ activation reprogrammed sedentary mouse muscle toward an oxidative, type-I-fiber-rich phenotype and dramatically extended endurance — placing GW-0742 alongside its sister molecule GW-501516 as a cornerstone tool of metabolic and exercise-mimetic research. RESEARCH USE ONLY · Not for human or veterinary use. For laboratory and collector purposes only. Purity ≥ 99 % (HPLC) — third-party tested, CoA on file Form Research capsules Content 10 mg GW-0742 per capsule Total 60 capsules per bottle (600 mg total) Packaging Sealed bottle with tamper-evident closure Storage Room temperature, dry, protected from light Molecular formula C₂₁H₁₇F₄NO₃S₂ Molecular weight ≈ 471.49 g·mol⁻¹ IUPAC name {4-[({4-methyl-2-[4-(trifluoromethyl)phenyl]-1,3-thiazol-5-yl}methyl)sulfanyl]-2-methylphenoxy}acetic acid CAS number 317318-84-6 Synonyms GW-0742X; selective PPARδ agonist Research Overview GW-0742 is the most selective PPARδ-targeted small molecule in routine research use, originally developed by GlaxoSmithKline as part of the program that produced GW-501516 [1]. PPARδ (peroxisome proliferator-activated receptor delta) is a nuclear receptor that, when activated, drives a transcriptional program centred on fatty-acid β-oxidation, mitochondrial biogenesis, oxidative-fiber-type specification, and cholesterol efflux via reverse cholesterol transport [1,2]. In the now-classic Narkar et al. study, GW-501516-treated sedentary mice showed expansion of oxidative type-I muscle fibers, marked endurance enhancement, and synergy with AMPK activation — providing the molecular blueprint for what is now an entire field of “exercise-mimetic” pharmacology [2]. GW-0742 produces the same core phenotype with even greater PPARδ selectivity, making it the preferred research tool when off-target PPARα/γ activity must be excluded. The molecule is also widely used in inflammation research (macrophage M2 polarization), atherosclerosis models (HDL elevation), and Duchenne muscular dystrophy preclinical work. Primary Research Areas PPARδ-selective pharmacology — the cleanest tool molecule available for dissecting PPARδ biology, with > 1,000-fold selectivity over PPARα and PPARγ [1]. Mitochondrial biogenesis and fatty-acid oxidation — drives the canonical PGC-1α / PPARδ-coordinated upregulation of β-oxidation enzymes, ETC components and oxidative-fiber-type genes [1,2]. Endurance and exercise-mimetic phenotypes — alongside GW-501516, the original compound class to demonstrate “trained muscle” gene programming in sedentary animals [2]. Lipid metabolism and atherosclerosis research — robust HDL elevation, ApoA1 upregulation and reverse-cholesterol-transport enhancement in rodent and primate models [1]. Macrophage polarization and inflammation — shifts macrophages toward the resolving M2 phenotype, of interest in atherosclerosis and chronic inflammation models [2]. References Sznaidman ML, Haffner CD, Maloney PR, et al. Novel selective small molecule agonists for peroxisome proliferator-activated receptor δ (PPARδ). Bioorg Med Chem Lett. 2003;13(9):1517–1521. Narkar VA, Downes M, Yu RT, et al. AMPK and PPARδ agonists are exercise mimetics. Cell. 2008;134(3):405–415. Bishop-Bailey D, Bystrom J. Emerging roles of peroxisome proliferator-activated receptor-β/δ in inflammation. Pharmacol Ther. 2009;124(2):141–150.
