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编 号：F205771
分子式：C36H62O11
分子量：670.87
分子式：C36H62O11
分子量：670.87
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CAS No: 17090-79-8
产品详情
生物活性：
Monensin (Monensin A), an orally active antibiotic, is an ionophore that mediates Na+/H+ exchange. Monensin is a potent Wnt signaling inhibitor. Monensin causes a marked enlargement of the multivesicular bodies (MVBs) and regulates exosome secretion. Monensin can be used for bacterial, fungal, and parasitic infections research, and shows anticancer effects.
体内研究：
Monensin（10 mg/kg；口服；每日；持续 6 周）可抑制多发性肠道肿瘤 (Min) 小鼠肠道肿瘤的进展，且对正常粘膜没有任何毒性迹象。Animal Model:Multiple intestinal neoplasia (Min) mice (four-week-old)
Dosage:10 mg/kg
Administration:Orally application; daily; for 6 weeks
Result:Suppressed progression of the intestinal tumors without any sign of toxicity on normal mucosa.
体外研究：
Monensin（1-5 μM；48 小时）会导致活力显着下降，且呈剂量依赖性。Monensin（1-5 μM；24 小时）显示出统计显着的细胞凋亡诱导作用。Monensin（0.1-1 μM；24 小时）抑制 pEGFR 及其下游靶点 pAKT 和 pERK。SCC25 cells1 μM, or 5 μM 24 hours Induced a potent apoptotic response.SCC9 and SCC25 cells0.1 μM, or 1 μM24 hours Induced approximately a 50% inhibition of EGF-treated SCC9 cells with respect to pEGFR and its downstream targets pAKT and pERK.
Monensin (Monensin A), an orally active antibiotic, is an ionophore that mediates Na+/H+ exchange. Monensin is a potent Wnt signaling inhibitor. Monensin causes a marked enlargement of the multivesicular bodies (MVBs) and regulates exosome secretion. Monensin can be used for bacterial, fungal, and parasitic infections research, and shows anticancer effects.
体内研究：
Monensin（10 mg/kg；口服；每日；持续 6 周）可抑制多发性肠道肿瘤 (Min) 小鼠肠道肿瘤的进展，且对正常粘膜没有任何毒性迹象。Animal Model:Multiple intestinal neoplasia (Min) mice (four-week-old)
Dosage:10 mg/kg
Administration:Orally application; daily; for 6 weeks
Result:Suppressed progression of the intestinal tumors without any sign of toxicity on normal mucosa.
体外研究：
Monensin（1-5 μM；48 小时）会导致活力显着下降，且呈剂量依赖性。Monensin（1-5 μM；24 小时）显示出统计显着的细胞凋亡诱导作用。Monensin（0.1-1 μM；24 小时）抑制 pEGFR 及其下游靶点 pAKT 和 pERK。SCC25 cells1 μM, or 5 μM 24 hours Induced a potent apoptotic response.SCC9 and SCC25 cells0.1 μM, or 1 μM24 hours Induced approximately a 50% inhibition of EGF-treated SCC9 cells with respect to pEGFR and its downstream targets pAKT and pERK.
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