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Details

Stereochemistry ABSOLUTE
Molecular Formula C32H46O8
Molecular Weight 558.7028
Optical Activity UNSPECIFIED
Defined Stereocenters 9 / 9
E/Z Centers 1
Charge 0

SHOW SMILES / InChI
Structure of CUCURBITACIN B

SMILES

[H][C@@]1([C@H](O)C[C@@]2(C)[C@]3([H])CC=C4[C@@]([H])(C[C@H](O)C(=O)C4(C)C)[C@]3(C)C(=O)C[C@]12C)[C@@](C)(O)C(=O)\C=C\C(C)(C)OC(C)=O

InChI

InChIKey=IXQKXEUSCPEQRD-DKRGWESNSA-N
InChI=1S/C32H46O8/c1-17(33)40-27(2,3)13-12-23(36)32(9,39)25-21(35)15-29(6)22-11-10-18-19(14-20(34)26(38)28(18,4)5)31(22,8)24(37)16-30(25,29)7/h10,12-13,19-22,25,34-35,39H,11,14-16H2,1-9H3/b13-12+/t19-,20+,21-,22+,25+,29+,30-,31+,32+/m1/s1

HIDE SMILES / InChI

Description

Cucurbitacin B (CuB), an oxygenated tetracyclic triterpenoid compound extracted from Cucurbitaceae plant species, is a long-term anticancer agent by disruption of microtubule polymerization. Cucurbitacin B is a naturally occurring compound that is found abundantly in cucumbers and other vegetables, and it is known to exert anti-cancer activities (primarily via apoptosis-induction) in several human cancers. Cucurbitacin B also protects against cardiac hypertrophy through increasing the autophagy level in cardiomyocytes, which is associated with the inhibition of Akt/mTOR/FoxO3a signal axis. ACLY over-expression abrogated CuB's apoptotic effects in prostate cancer cells, confirming ACLY as a direct target of CuB. Thus, CuB harbors potent chemopreventive activity for prostate cancer, and we revealed a novel anti-tumor mechanism of CuB via inhibition of ACLY signaling in human cancer. It has being suggested that cucurbitacin B exerts an anticancer effect by inhibiting telomerase via down regulating both the hTERT and c-Myc expression in breast cancer cells.

Approval Year

Targets

Primary TargetPharmacologyConditionPotency

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
Unknown
Primary
Unknown
Primary
Unknown
Primary
Unknown
Primary
Unknown

PubMed

Sample Use Guides

In Vivo Use Guide
Mice: When the BEL-7402 tumor size reached 30–50 mm3, the mice were dosed with cucurbitacin B at 0.1, 0.5, 1.0 and 3.0 mg/kg twice a day through oral administration. Oral administration of cucurbitacin B at 0.5 and 1 mg/kg obviously inhibited tumor growth in more than half of the treated mice. The tumor weight of the 0.5 mg/kg and 1 mg/kg treated groups was 0.42 ± 0.19 g and 0.34 ± 0.16 g, respectively. When compared to the control group (0.69 ± 0.22 g), the inhibition rate was 40.03% at 0.5 mg/kg (P < 0.05) and 50.43% at 1 mg/kg (P < 0.01).
Route of Administration: Oral
In Vitro Use Guide
Cucurbitacin B (CuB) inhibited the growth of various breast cancer cells with an IC50 ranging from 18-50nM after 48 and 72 h of treatment.