Dehydrocostus Lactone

＞98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

去氢木香内酯

白色结晶性粉末

DMSO : ≥ 62.5 mg/mL (271.39 mM)

IKKβ ,COX2

Dehydrocostus lactone can inhibit PGE2 synthesis in vitro. It significantly decreases the expression of COX-2, but not that of COX-1. After treatment with DHE, the glioblastoma (U118, U251 or U87) cells are significantly inhibited in their viability, proliferation and migration. At the meantime, DHE also induces mitochondria-mediated apoptosis by promoting the release of cytochrome c into cytosol, which activating caspase signaling pathway. DHE significantly suppresses COX-2 expression by inhibiting the phosphorylation of IKKβ via targeting the ATP-binding site, thereby abrogating NF-κB binding and p300 recruitment to COX-2 promoter. DHE suppresses clonogenic and migratory ability of glioblastoma cells and induces apoptosis through mitochondrial pathway.

Dehydrocostus lactone suppresses the growth of colorecral cancer xenografts transplanted by colon cancer cell line colo205 in athymic mice. The inhibition effect is dose dependent. DHE can cross blood-brain barrier (BBB). Treatment with DHE markedly inhibits neoplastic weight and volume without the notable adverse effects in the xenograft nude mice model, and these effects may be mediated through inhibition of the IKKβ/NF-κB/COX-2 signaling pathway.

1. Dong GZ, et al. Phytother Res. 2015 May;29(5):680-6.

2. Rao Vadaparthi PR, et al. Pharmacogn Mag. 2015 Jan-Mar;11(41):180-90.