Damnacanthal possesses anti-cancer, immunomodulatory, antinociceptive and anti-inflammatory actions, it can treat or prevent hepatocellular carcinoma through its inhibitory effects on the HGF/c-Met axis.

Phosphorylation of exogenous substrates by p56lck:220 nM (IC50), p56lck autophosphorylation:46 nM (IC50)

Here we show that Damnacanthal has profound inhibitory activity on mast cell activation through this pathway. The release of the granule compounds beta-hexosaminidase and tryptase release was completely abrogated by Damnacanthal at doses that were non-toxic to mast cells. In addition, Damnacanthal inhibited activation-dependent pro-inflammatory gene induction, as well as cytokine/chemokine release in response to mast cell stimulation. The mechanism underlying Damnacanthal inhibition was linked to impaired phosphorylation of Syk and Akt. Furthermore, Damnacanthal inhibited mast cell activation in response to calcium ionophore A23187[1]