Cucurbitacin E

Cucurbitacin E is a plant-derived triterpene that has diverse biological activities. At a concentration of 10 pM, it reduces MPP⁺-induced death of neuronal PC12 cells through inhibition of autophagy in vitro. Cucurbitacin E inhibits growth of T24 bladder, MDA-MB-468 and MCF-7 breast, PC3 prostate, and colorectal cancer cell lines (IC₅₀s = 50-1,000 nM) through induction of G₂/M arrest and apoptosis. It increases bilirubin binding to human serum albumin (HSA) in human plasma in a dose-dependent manner. Cucurbitacin E also inhibits depolymerization of actin filaments isolated from rabbit skeletal muscle actin and in HeLa cells.

white to beige powder

Cucurbitacin E has been used as a cofilin inhibitor. It is also used as a F-actin stabilizer to prevent membrane-associated periodic skeleton (MPS) loss and protect from axonal fragmentation.

Cucurbitacin E is a biochemical compound from the family of Cucurbitacins. Cucurbitacin E is a highly oxidated steroid consisting of a tetracyclic triterpene. Cucurbitacin E is known to possess broad spectrum of potential anti-inflammatory, antitumor andantioxidant effects.

ChEBI: A cucurbitacin in which a lanostane skeleton is multi-substituted with hydroxy, methyl and oxo substituents, with unsaturation at positions 1, 5 and 23.

This substance is a primary reference substance with assigned absolute purity (considering chromatographic purity, water, residual solvents, inorganic impurities). The exact value can be found on the certificate. Produced by PhytoLab GmbH & Co. KG.

Cucurbitacin E is a potent inhibitor of actin depolymerization. Cucurbitacin E is more active than jasplakinolide, and has a different mechanism of action, binding to a different site. Cucurbitacin E binds specifically to filamentous actin (F-actin) forming a covalent bond at residue Cys257, but not to monomeric actin (G-actin), stabilizing F-actin, without affecting actin polymerization or nucleation.

[1] ANNE-MARIE AREL-DUBEAU. Cucurbitacin E has neuroprotective properties and autophagic modulating activities on dopaminergic neurons.[J]. Oxidative Medicine and Cellular Longevity, 2014, 2014: 425496. DOI: 10.1155/2014/425496
[2] Y-C HSU  M J C  T Y Huang. Therapeutic ROS targeting of GADD45γ in the induction of G2/M arrest in primary human colorectal cancer cell lines by cucurbitacin E[J]. Cell Death & Disease, 2014, 5 4: e1198-e1198. DOI: 10.1038/cddis.2014.151
[3] YANJIE KONG. Cucurbitacin E induces cell cycle G2/M phase arrest and apoptosis in triple negative breast cancer.[J]. PLoS ONE, 2014: e103760. DOI: 10.1371/journal.pone.0103760
[4] WEN-WEN HUANG. Cucurbitacin E Induces G(2)/M Phase Arrest through STAT3/p53/p21 Signaling and Provokes Apoptosis via Fas/CD95 and Mitochondria-Dependent Pathways in Human Bladder Cancer T24 Cells.[J]. Evidence-based Complementary and Alternative Medicine, 2012: 952762. DOI: 10.1155/2012/952762
[5] H. GREIGE-GERGES . Effect of cucurbitacins on bilirubin–albumin binding in human plasma[J]. Life sciences, 2007, 80 6: Pages 579-585. DOI: 10.1016/j.lfs.2006.10.005
[6] PIA M. SRENSEN. The Natural Product Cucurbitacin E Inhibits Depolymerization of Actin Filaments[J]. ACS Chemical Biology, 2012, 7 9: 1502-1508. DOI: 10.1021/cb300254s