产品
编 号：F320606
分子式：C17H15N7
分子量：317.35
分子式：C17H15N7
分子量：317.35
产品类型
规格
价格
是否有货
5mg
询价
询价
10mg
询价
询价
25mg
询价
询价
50mg
询价
询价
100mg
询价
询价
结构图
CAS No: 327031-55-0
产品详情
生物活性：
VLX600 is an iron-chelating inhibitor of oxidative phosphorylation (OXPHOS). VLX600 causes mitochondrial dysfunction and induces a strong shift to glycolysis. VLX600 displays selective cytotoxic activity against malignant cell and induces autophagy. Anticancer activity.
体内研究：
VLX600 (16?mg/kg; i.v.; every third day for 16 days) shows anti-tumor activity in human tumor xenografts.Animal Model:NMRI nu/nu mice (HCT116 and HT29 colon cancer xenografts)
Dosage:16?mg/kg
Administration:Intravenously; every third day for 16 days
Result:Anti-tumor activity was observed in both HCT116 and HT29 colon cancer xenografts.
体外研究：
VLX600 (6?μM; 72 hours) induces an autophagic response.VLX600 is cytotoxic to HCT116 spheroids. VLX600 induces a HIF-1α-dependent glycolytic response. VLX600 inhibits oxygen consumption in HCT116 cells. VLX600 inhibits phosphorylation of the mTOR downstream effectors 4EBP1 and p70-S6K by an HIF-1α-independent mechanism. VLX600 preferentially leads to decreased ATP levels in cancer but not normal cells.
VLX600 is an iron-chelating inhibitor of oxidative phosphorylation (OXPHOS). VLX600 causes mitochondrial dysfunction and induces a strong shift to glycolysis. VLX600 displays selective cytotoxic activity against malignant cell and induces autophagy. Anticancer activity.
体内研究：
VLX600 (16?mg/kg; i.v.; every third day for 16 days) shows anti-tumor activity in human tumor xenografts.Animal Model:NMRI nu/nu mice (HCT116 and HT29 colon cancer xenografts)
Dosage:16?mg/kg
Administration:Intravenously; every third day for 16 days
Result:Anti-tumor activity was observed in both HCT116 and HT29 colon cancer xenografts.
体外研究：
VLX600 (6?μM; 72 hours) induces an autophagic response.VLX600 is cytotoxic to HCT116 spheroids. VLX600 induces a HIF-1α-dependent glycolytic response. VLX600 inhibits oxygen consumption in HCT116 cells. VLX600 inhibits phosphorylation of the mTOR downstream effectors 4EBP1 and p70-S6K by an HIF-1α-independent mechanism. VLX600 preferentially leads to decreased ATP levels in cancer but not normal cells.
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