LQFM030 reduced Ehrlich ascites tumor cell proliferation and VEGF levels

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This study reports the biological properties of LQFM030 in vivo, a molecular simplification of the compound nutlin-1.

Main methods:

Ehrlich ascites tumor (EAT)-bearing mice were treated intraperitoneally with LQFM030 (50, 75 or 150 mg/kg) for 10 days to determine changes in ascites tumor volume, body weight, cytotoxicity and angiogenesis. Moreover, flow cytometric expression of p53 and p21 proteins and caspase-3/7, − 8 and − 9 activation were investigated in EAT cells from mice treated. Acute oral systemic toxicity potential of LQFM030 in mice was also investigated using an alternative method.

Key findings:

Treatment of EAT-bearing mice with LQFM030 resulted in a marked decline in tumor cell proliferation and the vascular endothelial growth factor (VEGF) levels along with enhanced survival of the mice. Apoptotic tumor cell death was detected through p53 and p21 modulation and increase of caspase-3/7, − 8 and − 9 activity. LQFM030 also showed orally well tolerated, being classified in the UN GHS category 5 (LD50 > 2000–5000 mg/Kg).


LQFM030 seems to be a promising antitumor candidate for combinatory therapy with typical cytotoxic compounds, reducing the toxicity burden while allowing a superior anticancer activity. Moreover, these data also open new perspectives for LQFM030 as an antiangiogenic agent for treatment of diseases involving VEGF overexpression.

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