Coelonin is a dihydrophenanthrene compound with anti-inflammatory activity. Coelonin can inhibit the phosphorylation of PTEN induced by LPS, and inhibit the activation of NF-κB and the degradation of p27^Kip1 by negatively regulating PI3K/AKT signaling pathway. Coelonin can also inhibit the phosphorylation and degradation of IκBα, thus up-regulating the level of IκBα protein.

PC3 cells:2.82 μg/mL (EC50), HCT8 cells:3.84 μg/mL (EC50), BV-2 cells:15.2 μM, A549 cells:5.05 μg/mL (EC50), DU-145 cells:4.79 μg/mL (EC50), KB:3.4 μg/mL (EC50), MCF7:1.8 μg/mL (EC50)

Coelonin (2.5 μg/mL) significantly reduced the phosphorylation levels of NF-κB p65 and p105/50 [1].
Coelonin (0-5 μg/mL, 1.5 h) decreased the increase of PTEN, AKT and IκBa phosphorylation induced by LPS in a dose-dependent manner [1].
Coelonin (10 and 20 μg/ml) can alleviate the inflammation induced by particulate matter 2.5 (PM2.5) by reducing the production of inflammatory factors, including interleukin-6 (IL-6) and tumor necrosis factor -α (TNF-α) [2].
Coelonin's inhibition on the expression of IL-1β, IL-6 and TNF-α has nothing to do with PTEN, but the inhibition on the degradation of p27Kip1 leads to the cell cycle stagnation in G1 phase, which depends on PTEN[1].