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Cucurbitacin E inhibits actin depolymerization

Catalog No.N2791
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Sample solution is provided at 25 µL, 10mM.

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Chemical structure

Cucurbitacin E

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Chemical Properties

Cas No. 18444-66-1 SDF Download SDF
Chemical Name [(E,6R)-6-[(8S,9R,10R,13R,14S,16R,17R)-2,16-dihydroxy-4,4,9,13,14-pentamethyl-3,11-dioxo-8,10,12,15,16,17-hexahydro-7H-cyclopenta[a]phenanthren-17-yl]-6-hydroxy-2-methyl-5-oxohept-3-en-2-yl] acetate
Canonical SMILES CC(=O)OC(C)(C)C=CC(=O)C(C)(C1C(CC2(C1(CC(=O)C3(C2CC=C4C3C=C(C(=O)C4(C)C)O)C)C)C)O)O
Formula C32H44O8 M.Wt 556.69
Solubility Storage Store at -20°C
Shipping Condition Evaluation sample solution : ship with blue ice.All other available size: ship with RT , or blue ice upon request
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.


Cucurbitacin E, a widely available plant-derived natural product, is a useful tool to study actin dynamics in cells and actin-based processes such as cytokinesis [1].

In vitro: In assays using pure fluorescently labeled actin, Cucurbitacin E affected depolymerization without affecting the polymerization. It inhibited actin depolymerization at substoichiometric concentrations up to 1:6 cucurbitacin E:actin. Cucurbitacin E specifically bound to F-actin to form a covalent bond at residue Cys257, but not to monomeric actin (G-actin) [1]. In human leukemia HL-60 cells, Cucurbitacin E (3-50 nmol/l) inhibited the growth of HL-60 cells. At high concentrations (1-10 mol/l), Cucurbitacin E induced apoptosis of HL-60 cells and activation of caspase-3, 8 and 9. Jurkat leukemia cells with or without caspase-8 expression were nearly equally sensitive to cucurbitacin E-induced apoptosis[2]. Cucurbitacin E disrupted the actin cytoskeleton. In a series of cucurbitacin analogues, the anti-proliferative activity was correlated with the disruption of the F-actin cytoskeleton directly [3].

[1]. Sorensen P M, Iacob R E, Fritzsche M, et al. The natural product cucurbitacin E inhibits depolymerization of actin filaments[J]. ACS chemical biology, 2012, 7(9): 1502-1508.
[2]. Li Y, Wang R, Ma E, et al. The induction of G2/M cell-cycle arrest and apoptosis by cucurbitacin E is associated with increased phosphorylation of eIF2α in leukemia cells[J]. Anti-cancer drugs, 2010, 21(4): 389-400.
[3]. Duncan K L K, Duncan M D, Alley M C, et al. Cucurbitacin E-induced disruption of the actin and vimentin cytoskeleton in prostate carcinoma cells[J]. Biochemical pharmacology, 1996, 52(10): 1553-1560.