產(chǎn)品屬性：
產(chǎn)品名稱 | Quinacrine dihydrochloride |
規(guī)格 | 10mM*1 mL in DMSO、100mg、500mg |
貨號(hào) | EY-01Y10133 |
Cas No.: 1969-5-6
別名: N/A
化學(xué)名: N/A
分子式: C23H32Cl3N3O
分子量: 472.88
溶解度: DMSO: ≥ 44 mg/mL (93.05 mM); H2O: 33.33 mg/mL (70.48 mM)
儲(chǔ)存條件: Store at -20°C
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
產(chǎn)品描述：
Quinacrine (Mepacrine) dihydrochloride is an orally bioavailable antimalarial agent, which possess anticancer effect both in vitro and vivo. Quinacrine dihydrochloride suppresses NF-κB and activate p53 signaling, which results in the induction of the apoptosis[1].Quinacrine (5-20 μM; 24 hours) inhibits the growth of SGC-7901 cells[1].Quinacrine (7.5 and 15 μM; 24 hours) induces apoptosis in SGC-7901 cells, which is associated with mitochondria-dependent signal pathway and involves p53 upregulation and caspase-3 activation pathway[1].Quinacrine (15 μM; 24 hours) treatment significantly increased the levels of proapoptotic proteins, including cytochrome c, Bax, and p53, and decreased the levels of antiapoptotic protein Bcl-2, thus shifting the ratio of Bax/Bcl-2 in favor of apoptosis [1]. Cell Viability Assay[1]Cell Line: SGC-7901 cellsQuinacrine (100 mg/kg three times per week for two consecutive weeks) significantly suppresses circulating blast cells at days 30/31 and increases the median survival time (MST). Quinacrine does not decrease the body weight of treated animals at the tested dose[2]. Animal Model:Female SCID mice with acute myeloid leukemia (AML)-PS model[2][1]. Xiaoyang Wu, et al. Quinacrine Inhibits Cell Growth and Induces Apoptosis in Human Gastric Cancer Cell Line SGC-7901. Curr Ther Res Clin Exp. 2012 Feb;73(1-2):52-64.[2]. Anna Eriksson, et al. Towards repositioning of quinacrine for treatment of acute myeloid leukemia - Promising synergies and in vivo effects. Leuk Res. 2017 Dec;63:41-46.
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