260961
DNA-PK Inhibitor II
The DNA-PK Inhibitor II, also referenced under CAS 154447-35-5, controls the biological activity of DNA-PK. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.
别名:
DNA-PK Inhibitor II, NU7026, DNA-Dependent Protein Kinase Inhibitor II, 2-(Morpholin-4-yl)-benzo[h]chromen-4-one, LY293646
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About This Item
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质量水平
方案
≥95% (HPLC)
表单
crystalline solid
制造商/商品名称
Calbiochem®
储存条件
OK to freeze
protect from light
溶解性
DMSO: 2 mg/mL
methanol: 700 μg/mL
运输
ambient
储存温度
2-8°C
InChI
1S/C17H15NO3/c19-15-11-16(18-7-9-20-10-8-18)21-17-13-4-2-1-3-12(13)5-6-14(15)17/h1-6,11H,7-10H2
InChI key
KKTZALUTXUZPSN-UHFFFAOYSA-N
一般描述
A cell-permeable benzochromenone compound that acts as a potent, specific, reversible, and ATP-competitive inhibitor of DNA-PK with an IC50 of 0.23 µM. It is highly selective towards DNA-PK over PI3K-related kinases (IC50 = 13 µM for PI 3-K and >100 µM for ATM and ATR) and has no effect on PARP-1. Inhibits DNA-PK-mediated, but not PARP-1-mediated, cellular DNA DSB (double strand break) repair and PLDR (potentially lethal damage recovery) following IR (ionizing radiation). Shown to sensitize both proliferating and quiescent cells to IR.
A cell-permeable, potent, specific, reversible, and ATP-competitive inhibitor of DNA-PK (IC50 = 230 nM). Reported to be highly selective for DNA-PK compared to PI3 K-related kinases (IC50 = 13 µM for PI 3-K and >100 µM for ATM and ATR). Exhibits no inhibitory effect on PARP-1. Shown to inhibit DNA-PK-mediated, but not PARP-1-mediated, cellular DNA double strand break (DSB) repair and potentially lethal damage recovery (PLDR) following ionizing radiation (IR). Also shown to sensitize both proliferating and quiescent cells to IR.
生化/生理作用
Cell permeable: yes
Primary Target
DNA-PK
DNA-PK
Product competes with ATP.
Reversible: yes
Target IC50: 0.23 µM against DNA-PK
包装
Packaged under inert gas
警告
Toxicity: Carcinogenic / Teratogenic (D)
重悬
Following reconstitution aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
其他说明
Willmore, E., et al. 2004. Blood,103, 4659.
Hollick, J.J., et al. 2003. Bioorg. Med. Chem. Lett.13, 3083.
Veuger, S.J., et al. 2003. Cancer Res.63, 6008.
Vlahos, C.J., et al. 1994. J. Biol. Chem.269, 5241.
Hollick, J.J., et al. 2003. Bioorg. Med. Chem. Lett.13, 3083.
Veuger, S.J., et al. 2003. Cancer Res.63, 6008.
Vlahos, C.J., et al. 1994. J. Biol. Chem.269, 5241.
法律信息
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
储存分类代码
11 - Combustible Solids
WGK
WGK 3
Ceylan Sonmez et al.
Nucleic acids research, 52(8), 4313-4327 (2024-02-26)
The complex formed by Ku70/80 and DNA-PKcs (DNA-PK) promotes the synapsis and the joining of double strand breaks (DSBs) during canonical non-homologous end joining (c-NHEJ). In c-NHEJ during V(D)J recombination, DNA-PK promotes the processing of the ends and the opening
Casey Krawic et al.
The Journal of biological chemistry, 299(12), 105385-105385 (2023-10-28)
Cancer is a genetic disease requiring multiple mutations for its development. However, many carcinogens are DNA-unreactive and nonmutagenic and consequently described as nongenotoxic. One of such carcinogens is nickel, a global environmental pollutant abundantly emitted by burning of coal. We
Sara H Small et al.
Science signaling, 14(714), eaba2611-eaba2611 (2021-12-22)
Cytokine production is a critical component of cell-extrinsic responses to DNA damage and cellular senescence. Here, we demonstrated that expression of the gene encoding interleukin-19 (IL-19) was enhanced by DNA damage through pathways mediated by c-Jun amino-terminal kinase (JNK) and
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