Rubrofusarin gentiobioside

Rubrofusarin gentiobioside (Rrubrofusarin-6-β-gentiobioside) is an orally active weak inhibitor of PTP1B and MAO-A (IC₅₀ >100 μM), and its glycosylation modification results in lower biological activity than its aglycone Rubrofusarin (HY-130307). Rubrofusarin gentiobioside promotes AMPK phosphorylation in an LKB1-independent manner and inhibits the mTOR signaling pathway, thereby downregulating the expressions of PPARγ, C/EBPα, as well as FAS, LPL and aP2. Rubrofusarin gentiobioside inhibits lipid accumulation, reduces body weight and epididymal white adipose tissue volume, improves fatty liver, and shows no cytotoxicity to hepatocytes. Rubrofusarin gentiobioside is widely used in obesity-related studies^[1][2]. IC50 & Target:IC50: radical scavenger^[1] In Vitro: Rubrofusarin gentiobioside (200, 400 μM; 48 h) is non-cytotoxic to 3T3-L1 murine pre-adipocytes^[1].
Rubrofusarin gentiobioside (50, 100, 200 μM) activates AMPKα in an LKB1-independent manner, suppresses mTOR phosphorylation, and does not regulate the PI3K/AKT pathway in differentiated 3T3-L1 murine pre-adipocytes at concentrations of 50, 100, and 200 μM^[1].
Rubrofusarin gentiobioside (400 μM; 48 h) is non-cytotoxic to human adipose mesenchymal stem cells at concentrations up to 400 μM when incubated for 48 h^[1].
Rubrofusarin gentiobioside (25-100 μM) is non-toxic to HepG2 human hepatocarcinoma cells at concentrations up to 100 μM^[2].
Rubrofusarin gentiobioside has limited druglike properties per Lipinski’s rule and poor predicted ADME characteristics including low intestinal absorption and blood-brain barrier penetration^[2]. In Vivo: Rubrofusarin gentiobioside (50-100 mg/kg/day; p.o.; daily; 10 weeks) dose-dependently reduces weight gain, adipocyte size, hepatic steatosis, and dysregulated serum lipid levels in HFD-induced obese mice^[1].