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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)
5mg电议
10mg电议
50mg电议

产品介绍
F16 是 neu 过表达细胞的有效生长抑制剂,还选择性地抑制乳腺上皮细胞以及多种小鼠乳腺肿瘤和人乳腺癌细胞系的增殖。
Cas No.36098-33-6
化学名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-]
分子式C16H15N2o I
分子量362.2
溶解度≤500μg/ml in ethanol;20mg/ml in DMSO;25mg/ml in dimethyl formamide
储存条件Store at -20℃
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
产品描述

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.