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SML0364

Sigma-Aldrich

RAD51 Inhibitor B02

≥98% (HPLC)

Sinónimos:

3-(Phenylmethyl)-2-[(1E)-2-(3-pyridinyl)ethenyl]-4(3H)-quinazolinone

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About This Item

Fórmula empírica (notación de Hill):
C22H17N3O
Número de CAS:
1290541-46-6
Peso molecular:
339.39
Número MDL:
MFCD03294274
Código UNSPSC:
12352200
ID de la sustancia en PubChem:
329825366
NACRES:
NA.77

Nivel de calidad

100

Ensayo

≥98% (HPLC)

Formulario

powder

color

white to dark brown

solubilidad

DMSO: ≥5 mg/mL

temp. de almacenamiento

2-8°C

cadena SMILES

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+

Clave InChI

GEKDQXSPTHHANP-OUKQBFOZSA-N

Aplicación

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)

Acciones bioquímicas o fisiológicas

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.

Código de clase de almacenamiento

11 - Combustible Solids

Clase de riesgo para el agua (WGK)

WGK 3

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable

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Certificados de análisis (COA)

Lot/Batch Number
116M4607V
105M4615V
052M4618V

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Sigma-Aldrich

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Sigma-Aldrich

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Sigma-Aldrich

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AICAR

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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