Kazinol B, a prenylated flavan with a dimethyl pyrane ring, is an inhibitor ofnitric oxide (NO)production. Kazinol B improvesinsulinsensitivity by enhancing glucose uptake via the insulin-Akt signaling pathway andAMPKactivation. Kazinol B has the potential for diabetes mellitus research^[1][2].

Kazinol B (2, 10 and 20 μM; 72 hours) shows no toxicity to adipocytes in 3T3-L1 cells^[1].
Kazinol B (2-20 μM; 72 hours) dose-dependently increases lipid accumulation by 2.4-fold (at 20 μM) treatment as compared with MDI-treated cells^[1].
Kazinol B (2-20 μM; 5 days) dose-dependently increases PPARγ and C/EBPα protein and mRNA levels in MDI-treated 3T3-L1 adipocytes. Kazinol B increases the mRNA level of adiponectin in a dose-dependent manner^[1].
Kazinol B (2-20 μM; 24 hours) increases the retained 2′NBDG-fluorescence in cells in a dose-dependent manner in differentiated 3T3-L1 adipocytes and C2C12 myoblasts. Kazinol B dependently increases the MDI-stimulated GLUT4 mRNA level up to 4.7-fold as compared with MDI-only treated cells^[1].
Kazinol B (10-20 μM; pre-treated for 1 h followed by 1 h insulin) dose-dependently increases insulin-dependent Akt phosphorylation. Kazinol B alone strongly induces Akt phosphorylation compared with untreated cells. Kazinol B also increased insulin-stimulated AMPK phosphorylation^[1].
Kazinol B (6.25, 12.5, 25, 50 μM; 18 hours) dose-dependently reduces amounts of iNOS protein in macrophages (RAW 264.7 cells) activated by LPS (1 ug/mL)^[2].

392.49

C₂₅H₂₈O₄

99624-27-8

小构树醇B

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