CAS NO: | 36098-33-6 |
包装 | 价格(元) |
10mg | 电议 |
50mg | 电议 |
Physical Appearance | A crystalline solid |
Storage | Store at -20°C |
M.Wt | 362.2 |
Cas No. | 36098-33-6 |
Formula | C16H15N2·I |
Solubility | ≤500μg/ml in ethanol;20mg/ml in DMSO;25mg/ml in dimethyl formamide |
Chemical Name | 4-[(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。 |
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.