Cucurbitacin B (Cuc B) has profound in vitro and in vivo antiproliferative effects against human pancreatic Y cells. It inhibited AKT signaling activation through up-regulation of PTEN. Cucurbitacin B is an effective inhibitor of HIF-1 and provide new perspectives into the mechanism of its anticancer activity. Cucurbitacin B inhibits proliferation and induces apoptosis via STAT3 pathway inhibition in A549 lung Y cells.

Cucurbitacin B inhibits the growth of 5 GBM cell lines: U87, U118, U343, U373 and T98 g by affecting the cytoskeleton and the JNK pathway, with ED50 ranged from 5 nM to 100 nM. Cucurbitacin B also causes cell cycle arrest at the G2/M phase, decreases cell migration and induces apoptosis of GBM cells. [1] In human breast cancer cell lines, Cucurbitacin B also inhibits cell growth with ED50 varied from 30.3 nM to 418 nM, and rapidly induces cytoskeletal disruption. [2] In addition, Cucurbitacin B possesses immunomodulatory and anti-inflammatory effects, depending on the induction of heme oxygenase-1 expression via Nrf2 activation. [3]

In nude mice bearing MDA-MB-231 tumors, Cucurbitacin B (1 mg/kg, i.p.) inhibits tumor growth by 55 %, and causes lower serum glucose levels. [2]

For proliferation measurements, the cells are placed into 96 well plates, and cell growth is measured at various times by MTT assay according to the protocol.(Only for Reference)

DMSO: 144.00 mg/mL (257.74 mM), Sonication is recommended.

Chloroform, Dichloromethane, Ethyl Acetate: Soluble

Ethanol: 50.00 mg/mL (89.49 mM), Sonication is recommended.

10% DMSO+40% PEG300+5% Tween 80+45% Saline: 4.00 mg/mL (7.16 mM), Sonication is recommended.