naturally polyether ionophore antibiotic
CAS：22373-78-0
分子式：C36H61NaO11
分子量：692.85
纯度：98%
存储：Store at -20°C

Background:

Monensin sodium salt is an antibiotic secreted by the bacteria Streptomyces cinnamonensis.

Monensin sodium salt is an antibiotic secreted by the bacteria Streptomyces cinnamonensis. Untreated cells display 2.5% apoptosis; 48 hours treatment with 1 μM Monensin sodium salt shows 4.5% apoptosis whereas 5 μM Monensin sodium salt for 48 hours induces a greater apoptotic response (16.4%). Pretreatment with either 1 or 5 μM Monensin sodium salt for 24 hours followed by 10 μM erlotinib treatment for another 24 hours results in a marked increases in apoptotic events (14.6% and 38.7%, respectively) when compare with either Monensin sodium salt or erlotinib treatments alone. Combination of 5 μM Monensin sodium salt with 10 μM erlotinib shows the highest percentage of apoptosis (38.7%)[1].

Although the numbers of tumors do not change substantially, a significant (P=0.0144) reduction in the average size of lesions is observed in Monensin sodium salt-treated Apc+/Min mice when compare with control animals (mean 0.199 mm2 vs. 0.299 mm2). The total tumor area estimated in one animal is decreased in individuals receiving Monensin sodium salt (mean 10.16 mm2 vs. 16.46 mm2; P=0.0125). Monensin sodium salt treatment increases the numbers of apoptotic cells and cells expressing the p21 cell-cycle inhibitor at the surface area of the neoplastic outgrowths. No changes in the cell proliferation, differentiation, and tissue architecture in the healthy parts of mucosa are noted after exposure to Monensin sodium salt[2].

参考文献:
[1]. Dayekh K, et al. Monensin inhibits epidermal growth factor receptor trafficking and activation: synergistic cytotoxicity in combination with EGFR inhibitors. Mol Cancer Ther. 2014 Nov;13(11):2559-71.
[2]. Tumova L, et al. Monensin inhibits canonical Wnt signaling in human colorectal cancer cells and suppresses tumor growth in multiple intestinal neoplasia mice. Mol Cancer Ther. 2014 Apr;13(4):812-22.