Plumbagin

Biological Activity

Anticancer agent. Induces G₂/M cell cycle arrest and apoptosis in A549 cells through JNK-dependent p53 Ser15 phosphorylation; inhibits A549 and MDA-MD-231 tumour xenograft growth in nude mice. Promotes autophagic cell death in MDA-MB-231 and MCF-7 cells and inhibits Akt/mTOR signaling. Induces intracellular ROS generation in a PI 5-kinase-dependent manner. Also inhibits p300-mediated acetylation of p53.

Technical Data

The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.

Background References

1. Plumbagin (5-hydroxy-2-methyl-1,4-napthoquinone) induces apoptosis and cell cycle arrest in A549 cells through p53 accumulation via c-Jun NH₂-terminal kinase mediated phosphorylation at serine 15 in vitro and in vivo.
   Hsu et al.
   J.Pharmacol.Exp.Ther., 2006;318:484
2. Plumbagin induces G₂-M arrest and autophagy by inhibiting the AKT/mammalian target of rapamycin pathway in breast cancer cells.
   Kuo et al.
   Mol.Cancer Ther., 2006;5:3209
3. The natural anticancer agent plumbagin induces potent cytotoxicity in MCF-7 human breast cancer cells by inhibiting a PI-5 kinase for ROS generation.
   Lee et al.
   PLoS One., 2012;7:e45023
4. Inhibition of lysine acetyltransferase KAT3B/p300 activity by a naturally occurring hydroxynaphthoquinone, plumbagin.
   Ravindra et al.
   J.Biol.Chem., 2009;284:24453

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