质量水平
检测方案
≥98% (HPLC)
形式
powder
颜色
white to beige
储存温度
2-8°C
SMILES字符串
Cc1onc(C(=O)N2CCN(CC2)C(c3ccc(Cl)cc3)c4ccc(Cl)cc4)c1[N+]([O-])=O
InChI
1S/C22H20Cl2N4O4/c1-14-20(28(30)31)19(25-32-14)22(29)27-12-10-26(11-13-27)21(15-2-6-17(23)7-3-15)16-4-8-18(24)9-5-16/h2-9,21H,10-13H2,1H3
InChI key
VIBHJPDPEVVDTB-UHFFFAOYSA-N
应用
ML 210 可用作含硒酶谷胱甘肽过氧化物酶 4（GPX4）的抑制剂，以诱导癌细胞的铁死亡。此外，还可作为 GPX4 抑制剂研究 GPX4 的药理性抑制功能是否改变了粘附 MCF10A 和 Hs578t 细胞中 prominin2 表达并影响铁死亡。
生化/生理作用
ML 210 可作为含硒酶谷胱甘肽过氧化物酶 4（GPX4）的抑制剂。它对少数卵巢癌细胞系表现出细胞毒性。
在表达 RAS 癌基因的肿瘤细胞中，ML 210 诱导非凋亡性细胞死亡。
警示用语：
Warning
危险声明
危险分类
Acute Tox. 4 Oral
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Amrita Basu et al.
Cell, 154(5), 1151-1161 (2013-09-03)
The high rate of clinical response to protein-kinase-targeting drugs matched to cancer patients with specific genomic alterations has prompted efforts to use cancer cell line (CCL) profiling to identify additional biomarkers of small-molecule sensitivities. We have quantitatively measured the sensitivity
Jianling Bi et al.
Cell death & disease, 10(10), 682-682 (2019-09-19)
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death driven by lipid hydroperoxides within biological membranes. Although therapy-resistant mesenchymal-high cancers are particularly vulnerable to ferroptosis inducers, especially phospholipid glutathione peroxidase 4 (GPx4) inhibitors, the underlying mechanism is yet to
Yinu Wang et al.
Cancer research, 81(2), 384-399 (2020-11-12)
Defining traits of platinum-tolerant cancer cells could expose new treatment vulnerabilities. Here, new markers associated with platinum-tolerant cells and tumors were identified using in vitro and in vivo ovarian cancer models treated repetitively with carboplatin and validated in human specimens.
Yilong Zou et al.
Nature, 585(7826), 603-608 (2020-09-18)
Ferroptosis-an iron-dependent, non-apoptotic cell death process-is involved in various degenerative diseases and represents a targetable susceptibility in certain cancers1. The ferroptosis-susceptible cell state can either pre-exist in cells that arise from certain lineages or be acquired during cell-state transitions2-5. However
Nobuaki Takahashi et al.
Molecular cell, 80(5), 828-844 (2020-11-01)
Cancer-associated mutations that stabilize NRF2, an oxidant defense transcription factor, are predicted to promote tumor development. Here, utilizing 3D cancer spheroid models coupled with CRISPR-Cas9 screens, we investigate the molecular pathogenesis mediated by NRF2 hyperactivation. NRF2 hyperactivation was necessary for
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