Verrucarin A (Muconomycin A), a Type D macrocyclic mycotoxin derived from the pathogen fungus Myrothecium verrucaria, is an inhibitor of protein synthesis. Verrucarin A inhibits growth of leukemia cell lines and activates caspases and apoptosis and inflammatory signaling in macrophages. Verrucarin A effectively increased the phosphorylation of p38 MAPK and diminished the phosphorylation of ERK/Akt. Verrucarin A caused cell cycle deregulation through the induction of p21 and p53^{[1] [2]} .

Verrucarin A (0-0.6 μM/ml; 24-48 hours)-induces time- and dose-dependent growth inhibition in MCF-7 cells^[1] .
Verrucarin A increases the levels of reactive oxygen species (ROS), and subsequently induces mitochondrial membrane potential (Δψm) loss, leading to the increase of Bax/Bcl-2 ratio, cytochrome c release, caspase activation, PARP degradation, and apoptosis^[1] .

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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• [1]. Palanivel K, et al. Verrucarin A alters cell-cycle regulatory proteins and induces apoptosis through reactive oxygen species-dependent p38MAPK activation in the human breast cancer cell line MCF-7. Tumour Biol. 2014;35(10):10159-10167.

  [2]. Palanivel K, et al. Verrucarin A, a protein synthesis inhibitor, induces growth inhibition and apoptosis in breast cancer cell lines MDA-MB-231 and T47D. Biotechnol Lett. 2013;35(9):1395-1403.