SML0364
RAD51 Inhibitor B02
≥98% (HPLC), RAD51 recombinase inhibitor, powder
동의어(들):
3-(Phenylmethyl)-2-[(1E)-2-(3-pyridinyl)ethenyl]-4(3H)-quinazolinone
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크기 선택
제품정보 (DICE 배송 시 비용 별도)
실험식(Hill 표기법):
C22H17N3O
CAS 번호:
Molecular Weight:
339.39
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
제품 이름
RAD51 Inhibitor 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
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Application
RAD51 Inhibitor B02 has been used:
- to test its effect on the polar body extrusion (PBE) rate in porcine oocytes
- for RAD51 inhibition in porcine embryos
- as RAD51 inhibitor and to test its effect on targeted nucleotide substitution (TNS) in induced pluripotent stem cells (iPSCs)
Biochem/physiol Actions
B02 (3-(Phenylmethyl)-2-[(1E)-2-(3-pyridinyl)ethenyl]-4(3H)-quinazolinone), a pyridinylvinyl-quinazolinone compound is cell-permeable. B02 inhibits human RAD51 recombinase and subsequent nucleofilaments formation. It halts homologous recombination (HR) repair events in cancer cells. B02 favors apoptosis in multiple myeloma and is crucial for sensitizing them to doxorubicin.
저장 등급
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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)
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
Giandomenico Turchiano et al.
Cell stem cell, 28(6), 1136-1147 (2021-02-25)
Genome editing has shown great promise for clinical translation but also revealed the risk of genotoxicity caused by off-target effects of programmable nucleases. Here we describe chromosomal aberrations analysis by single targeted linker-mediated PCR sequencing (CAST-Seq), a preclinical assay to
Chengkun Wang et al.
Nature cell biology, 24(2), 268-278 (2022-02-12)
Gene editing is a powerful tool for genome and cell engineering. Exemplified by CRISPR-Cas, gene editing could cause DNA damage and trigger DNA repair processes that are often error-prone. Such unwanted mutations and safety concerns can be exacerbated when altering
Zhe-Long Jin et al.
Reproduction (Cambridge, England), 157(3), 223-234 (2019-03-01)
Homologous recombination (HR) plays a critical role in facilitating replication fork progression when the polymerase complex encounters a blocking DNA lesion, and it also serves as the primary mechanism for error-free DNA repair of double-stranded breaks. DNA repair protein RAD51
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