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Merck
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SML1797

Sigma-Aldrich

L67

≥98% (HPLC)

Sinónimos:

LigI/III inhibitor L67, N-(3,5-Dibromo-4-methylphenyl)-glycine 2-[(2-hydroxy-5-nitrophenyl)methylene]hydrazide

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About This Item

Fórmula empírica (notación de Hill):
C16H14Br2N4O4
Número de CAS:
325970-71-6
Peso molecular:
486.11
MDL number:
MFCD00363966
UNSPSC Code:
12352200
PubChem Substance ID:
329826071
NACRES:
NA.77

Quality Level

100

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 10 mg/mL, clear

storage temp.

−20°C

SMILES string

O=C(N/N=C/C1=CC([N+]([O-])=O)=CC=C1O)CNC2=CC(Br)=C(C)C(Br)=C2

Biochem/physiol Actions

L67 is a potent and specific inhibitor of DNA ligase IIIα (LigIIIα) that preferentially targets mitochondrial LigIIIα resulting in mitochondrial dysfunction. L67 preferentially targets cancer cell mitochondria resulting in enhanced ROS production and caspase 1-dependent apoptosis. L67 in combination with PARP inhibitors decreases survival rate of therapy resistant breast cancer and leukemia cells.

hcodes

H413

Hazard Classifications

Aquatic Chronic 4

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Annahita Sallmyr et al.
Cancer research, 76(18), 5431-5441 (2016-08-10)
Elevated levels of DNA ligase IIIα (LigIIIα) have been identified as a biomarker of an alteration in DNA repair in cancer cells that confers hypersensitivity to a LigIIIα inhibitor, L67, in combination with a poly (ADP-ribose) polymerase inhibitor. Because LigIIIα
Xi Chen et al.
Cancer research, 68(9), 3169-3177 (2008-05-03)
Based on the crystal structure of human DNA ligase I complexed with nicked DNA, computer-aided drug design was used to identify compounds in a database of 1.5 million commercially available low molecular weight chemicals that were predicted to bind to
L A Tobin et al.
Oncogene, 32(14), 1784-1793 (2012-05-30)
Resistance to imatinib (IM) and other tyrosine kinase inhibitors (TKI)s is an increasing problem in leukemias caused by expression of BCR-ABL1. As chronic myeloid leukemia (CML) cell lines expressing BCR-ABL1 utilize an alternative non-homologous end-joining pathway (ALT NHEJ) to repair
Rajeswari Jayavaradhan et al.
Journal of molecular biology, 431(1), 102-110 (2018-05-12)
The efficient site-specific DNA double-strand breaks (DSB) created by CRISPR/Cas9 has revolutionized genome engineering and has great potential for editing hematopoietic stem/progenitor cells (HSPCs). However, detailed understanding of the variables that influence choice of DNA-DSB repair (DDR) pathways by HSPC

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