SML0364
RAD51抑制剂B02
≥98% (HPLC), RAD51 recombinase inhibitor, powder
别名:
3-（苯甲基）-2-[（1E）-2-（3-吡啶基）乙烯基]-4（3H）-喹唑啉酮
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关于此项目
经验公式（希尔记法）:
C22H17N3O
化学文摘社编号:
分子量:
339.39
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
产品名称
RAD51抑制剂B02, ≥98% (HPLC)
SMILES string
O=C1N(CC2=CC=CC=C2)C(/C=C/C3=CN=CC=C3)=NC4=C1C=CC=C4
InChI
1S/C22H17N3O/c26-22-19-10-4-5-11-20(19)24-21(13-12-17-9-6-14-23-15-17)25(22)16-18-7-2-1-3-8-18/h1-15H,16H2/b13-12+
InChI key
GEKDQXSPTHHANP-OUKQBFOZSA-N
assay
≥98% (HPLC)
form
powder
color
white to dark brown
solubility
DMSO: ≥5 mg/mL
storage temp.
2-8°C
Quality Level
Application
RAD51 抑制剂B02已被用于：
- 测试其对猪卵母细胞极体排放（PBE）率的影响
- 用于猪胚胎的RAD51抑制
- 作为RAD51 抑制剂并用于测试其对诱导多能干细胞 (iPSC) 中靶向氨基酸替换 (TNS) 的影响
Biochem/physiol Actions
B02 (3-（苯甲基）-2-[（1E）-2-（3-吡啶基）乙烯基]-4（3H）-喹唑啉酮是一种吡啶基乙烯基喹唑啉酮化合物，可以穿透细胞。B02抑制人RAD51重组酶及之后核线的形成。它可以中止癌细胞中的同源重组（HR）修复活动。B02促进多发性骨髓瘤中的细胞凋亡，同时也是敏化多柔比星的关键。
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
RAD51 maintains chromosome integrity and mitochondrial distribution during porcine oocyte maturation in vitro
Jin ZL and Kim NH
Journal of Reproduction and Development (2017)
Inhibition of DNA repair protein RAD51 affects porcine preimplantation embryo development
Jin ZL, et al.
Reproduction (Cambridge, England), 157(3) (2019)
Ivana Murfuni et al.
PLoS genetics, 9(10), e1003910-e1003910 (2013-11-10)
In checkpoint-deficient cells, DNA double-strand breaks (DSBs) are produced during replication by the structure-specific endonuclease MUS81. The mechanism underlying MUS81-dependent cleavage, and the effect on chromosome integrity and viability of checkpoint deficient cells is only partly understood, especially in human
A small-molecule inhibitor of RAD51 reduces homologous recombination and sensitizes multiple myeloma cells to doxorubicin
Alagpulinsa DA, et al.
Frontiers in Oncology, 4, 289-289 (2014)
Arthur Aubry et al.
Oncogene, 39(31), 5338-5357 (2020-06-24)
Local intravitreal or intra-arterial chemotherapy has improved therapeutic success for the pediatric cancer retinoblastoma (RB), but toxicity remains a major caveat. RB initiates primarily with RB1 loss or, rarely, MYCN amplification, but the critical downstream networks are incompletely understood. We
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