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F16
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
F16图片
CAS NO:36098-33-6
包装与价格:
包装价格(元)
10mg电议
50mg电议

产品介绍

化学性质

Physical AppearanceA crystalline solid
StorageStore at -20°C
M.Wt362.2
Cas No.36098-33-6
FormulaC16H15N2·I
Solubility≤500μg/ml in ethanol;20mg/ml in DMSO;25mg/ml in dimethyl formamide
Chemical Name4-[(1E)-2-(1H-indol-3-yl)ethenyl]-1-methyl-pyridinium iodide
Canonical SMILES[H]N1C=C(/C=C/C2=CC=[N+](C)C=C2)C3=CC=CC=C31.[I-]
运输条件蓝冰运输或根据您的需求运输。
一般建议为了使其更好的溶解,请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存,请尽快用完。

资料参考

F16 is a small, cationic, lipophilic, and fluorescent molecule capable of binding preferentially to mitochondrial membranes and disrupts their function. F16 is a potential antitumor agent.

F16 affected growth in some mouse and human breast cancer cell lines. F16 resulted in a dramatic decrease in the number of cells in S phase and an increase in the percentage of cells in G1 phase [1]. Prolonged incubation with 3 μM F16 led to increased cell death of F16-sensitive cells but not of F16-resistant ones. F16 accumulation in mitochondria induced mitochondrial damage characterized by imbalance of volumetric homeostasis, failure to synthesize ATP, cytochrome c release and increased production of reactive oxy gen species [1]. F16 incubation decreased the cellular ATP pool in both parental EpH4-A6 and Bcl-2-overexpressing EpH4-A6.C13 and EpH4-A6.C18 cells in a time-dependent manner [1]. Treatment with F16 promoted early release of cytochrome c in transformed EpH4-A6 cells. Treatment with F16 (0.3-3 μM) resulted in the characteristic apoptotic DNA laddering in the EpH4-A6 cells. F16-Induced mitochondrial dysfunction triggers apoptosis or necrosis. F16 induced necrosis in various cell lines resistant to apoptosis [2].

References:
[1] Fantin V R, Berardi M J, Scorrano L, et al.  A novel mitochondriotoxic small molecule that selectively inhibits tumor cell growth[J]. Cancer cell, 2002, 2(1): 29-42.
[2] Fantin V R, Leder P.  F16, a mitochondriotoxic compound, triggers apoptosis or necrosis depending on the genetic background of the target carcinoma cell[J]. Cancer research, 2004, 64(1): 329-336.