所有图片(1)
别名:
1-(2-(Diethylamino)ethyl)-3-(2-(4-ethylpiperazin-1-yl)-4-methylquinolin-6-yl)thiourea, N-[2-(Diethylamino)ethyl]-N′-[2-(4-ethyl-1-piperazinyl)-4-methyl-6-quinolinyl]-thiourea
经验公式（希尔记法）:
C23H36N6S
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检测方案
≥98% (HPLC)
形式
powder
颜色
white to beige
溶解性
DMSO: 2 mg/mL, clear
储存温度
2-8°C
SMILES字符串
S=C(NCCN(CC)CC)NC1=CC2=C(C=C1)N=C(N3CCN(CC)CC3)C=C2C
生化/生理作用
D-I03 is a selective RAD52 inhibitor (IC50 = 5 and 8 μM, respectively, by SSA and DNA pairing (D-loop formation) assay; <5% RAD51 inhibition at 80 μM) that blocks single-strand DNA (ssDNA) annealing (SSA)-, but not homology dependent recombination (HDR)-, mediated double-strand break (DSB) repair (5-30 μM using respective U2OS reporter cells) and reduces nuclear RAD52, but not RAD51, foci formation (2.5 μM) upon DNA damage by cisplatin. D-I03 selectively suppresses BRCA1-deficient over BRCA1-proficient cancer cells and exerts synergistic activity with PARP1 inhibitors against BRCA1-deficient cancer both in cultures (1 & 2.5 μM) and in mice (50 mg/kg/day i.p.) in vivo.
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Fei Huang et al.
Nucleic acids research, 44(9), 4189-4199 (2016-02-14)
RAD52 is a member of the homologous recombination (HR) pathway that is important for maintenance of genome integrity. While single RAD52 mutations show no significant phenotype in mammals, their combination with mutations in genes that cause hereditary breast cancer and
Katherine Sullivan-Reed et al.
Cell reports, 23(11), 3127-3136 (2018-06-14)
PARP inhibitors (PARPis) have been used to induce synthetic lethality in BRCA-deficient tumors in clinical trials with limited success. We hypothesized that RAD52-mediated DNA repair remains active in PARPi-treated BRCA-deficient tumor cells and that targeting RAD52 should enhance the synthetic
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