SML4192
DNA2 Inhibitor C5
≥95% (HPLC)
别名:
4-Hydroxy-8-nitroquinoline-3-carboxylic acid, 4-Hydroxy-8-nitro-3-quinolinecarboxylic acid, DNA2i-C5, NSC 15765
质量水平
方案
≥95% (HPLC)
表单
powder
颜色
white to beige
溶解性
DMSO: 2 mg/mL, clear (warmed)
储存温度
2-8°C
SMILES字符串
O=C(C1=CN=C2C(C=CC=C2[N+]([O-])=O)=C1O)O
生化/生理作用
Suppresses nuclease/helicase activities, impairs DNA repair/replication, causes cell cycle arrest, and shows synergistic cancer cell killing with DNA-damaging agents and PARP/ATR inhibitors.
The DNA2 inhibitor C5 (DNA2i-C5) binds to a pocket near the DNA binding site in the helicase domain of DNA2 with an IC50 of 20-30 μM for inhibiting nuclease activity and DNA binding. C5 effectively suppresses both the nuclease and helicase activities of DNA2, impairing DNA end resection, homologous recombination, single-strand annealing repair, and replication fork restart after stalling. In cells, C5 mimics genetic knockout of DNA2, causing cell cycle arrest in late S/G2 phase, reducing mitotic entry, and leading to chromosomal segregation defects, particularly affecting centromeric DNA replication and integrity. Importantly, C5 shows synergistic killing of various cancer cell types when combined with DNA damaging agents like camptothecin or inhibitors of PARP and ATR, highlighting its potential as a cancer therapeutic strategy.
The DNA2 inhibitor C5 (DNA2i-C5) binds to a pocket near the DNA binding site in the helicase domain of DNA2 with an IC50 of 20-30 μM for inhibiting nuclease activity and DNA binding. C5 effectively suppresses both the nuclease and helicase activities of DNA2, impairing DNA end resection, homologous recombination, single-strand annealing repair, and replication fork restart after stalling. In cells, C5 mimics genetic knockout of DNA2, causing cell cycle arrest in late S/G2 phase, reducing mitotic entry, and leading to chromosomal segregation defects, particularly affecting centromeric DNA replication and integrity. Importantly, C5 shows synergistic killing of various cancer cell types when combined with DNA damaging agents like camptothecin or inhibitors of PARP and ATR, highlighting its potential as a cancer therapeutic strategy.
法规信息
新产品
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
Wenpeng Liu et al.
EBioMedicine, 6, 73-86 (2016-05-24)
Cancer cells frequently up-regulate DNA replication and repair proteins such as the multifunctional DNA2 nuclease/helicase, counteracting DNA damage due to replication stress and promoting survival. Therefore, we hypothesized that blocking both DNA replication and repair by inhibiting the bifunctional DNA2
Zhengke Li et al.
The EMBO journal, 37(14) (2018-05-19)
DNA2 is a nuclease/helicase that is involved in Okazaki fragment maturation, replication fork processing, and end resection of DNA double-strand breaks. Similar such helicase activity for resolving secondary structures and structure-specific nuclease activity are needed during DNA replication to process
Ilaria Ceppi et al.
Nature, 634(8033), 492-500 (2024-09-12)
DNA double-strand break (DSB) repair by homologous recombination is initiated by DNA end resection, a process involving the controlled degradation of the 5'-terminated strands at DSB sites1,2. The breast cancer suppressor BRCA1-BARD1 not only promotes resection and homologous recombination, but
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