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编 号：F755388
分子式：C17H19N5O
分子量：309.37
分子式：C17H19N5O
分子量：309.37
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CAS No: 2755454-90-9
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生物活性：
Autophagy-IN-2 (Compound 7h) is an autophagic flux inhibitor. Autophagy-IN-2 induces cancer cell apoptosis and can be used for triple-negative breast cancer research.
体内研究：
Autophagy-IN-2 (Compound 7h) (5 and 15 mg/kg; i.p.; every 3 days for 3 weeks) suppresses tumor growth in a dose-dependent manner.Animal Model:Six-week-old female NOD/SCID mice, MDA-MB-231 xenograft
Dosage:5 mg/kg, 15 mg/kg
Administration:Intraperitoneal injection, every 3 days for 3 weeks
Result:Suppressed human TNBC tumor growth in a dose-dependent manner and resulted in a concentration-dependent upregulation of LC3B-II, p62, γH2AX and PARP.
体外研究：
Autophagy-IN-2 (Compound 7h) (0-200 μM, 48 h) shows anti-viability activities against various cancer cells.Autophagy-IN-2 (0-20 μM, 0-48 h) suppresses autophagic flux and impairs DNA repair through down-regulating chromatin ubiquitination in a p62-dependent manner.Autophagy-IN-2 (0-20 μM, 48 h) induces cell cycle arrest at S-phase and mitochondria-dependent intrinsic apoptosis.
Autophagy-IN-2 (Compound 7h) is an autophagic flux inhibitor. Autophagy-IN-2 induces cancer cell apoptosis and can be used for triple-negative breast cancer research.
体内研究：
Autophagy-IN-2 (Compound 7h) (5 and 15 mg/kg; i.p.; every 3 days for 3 weeks) suppresses tumor growth in a dose-dependent manner.Animal Model:Six-week-old female NOD/SCID mice, MDA-MB-231 xenograft
Dosage:5 mg/kg, 15 mg/kg
Administration:Intraperitoneal injection, every 3 days for 3 weeks
Result:Suppressed human TNBC tumor growth in a dose-dependent manner and resulted in a concentration-dependent upregulation of LC3B-II, p62, γH2AX and PARP.
体外研究：
Autophagy-IN-2 (Compound 7h) (0-200 μM, 48 h) shows anti-viability activities against various cancer cells.Autophagy-IN-2 (0-20 μM, 0-48 h) suppresses autophagic flux and impairs DNA repair through down-regulating chromatin ubiquitination in a p62-dependent manner.Autophagy-IN-2 (0-20 μM, 48 h) induces cell cycle arrest at S-phase and mitochondria-dependent intrinsic apoptosis.
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