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SML1797

Sigma-Aldrich

L67

≥98% (HPLC)

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Synonym(s):
LigI/III inhibitor L67, N-(3,5-Dibromo-4-methylphenyl)-glycine 2-[(2-hydroxy-5-nitrophenyl)methylene]hydrazide
Empirical Formula (Hill Notation):
C16H14Br2N4O4
CAS Number:
Molecular Weight:
486.11
MDL number:
PubChem Substance ID:

Quality Level

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

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1 of 4

This Item
SML2360SML2529SML0270
L67 ≥98% (HPLC)

SML1797

L67

LX-4 ≥98% (HPLC)

SML2360

LX-4

MDL-800 ≥98% (HPLC)

SML2529

MDL-800

NSC 632839 ≥98% (HPLC)

SML0270

NSC 632839

form

powder

form

powder

form

powder

form

powder

Quality Level

100

Quality Level

-

Quality Level

-

Quality Level

-

storage temp.

−20°C

storage temp.

2-8°C

storage temp.

2-8°C

storage temp.

2-8°C

solubility

DMSO: 10 mg/mL, clear

solubility

DMSO: 2 mg/mL, clear

solubility

DMSO: 2 mg/mL, clear

solubility

DMSO: ≥2 mg/mL (warmed)

color

white to beige

color

faint yellow to dark brown

color

white to beige

color

faintly yellow to dark yellow

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.

Hazard Statements

Precautionary Statements

Hazard Classifications

Aquatic Chronic 4

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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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
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
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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