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SML2257

Sigma-Aldrich

IBR2

≥98% (HPLC)

Synonym(e):

(1R)-1,2-Dihydro-1-(1H-indol-3-yl)-2-[(phenylmethyl)sulfonyl]isoquinoline, (R)-2-(benzylsulfonyl)-1-(1H-indol-3-yl)-1,2-dihydroisoquinoline, Isoquinoline, 1,2-dihydro-1-(1H-indol-3-yl)-2-[(phenylmethyl)sulfonyl]-, (1R)-

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About This Item

Empirische Formel (Hill-System):
C24H20N2O2S
CAS-Nummer:
952739-54-7
Molekulargewicht:
400.49
UNSPSC-Code:
12352200
NACRES:
NA.77

Assay

≥98% (HPLC)

Form

powder

Farbe

white to beige

Löslichkeit

DMSO: 2 mg/mL, clear

Lagertemp.

2-8°C

SMILES String

O=S(N1[C@@H](C2=CNC3=C2C=CC=C3)C4=CC=CC=C4C=C1)(CC5=CC=CC=C5)=O

Biochem./physiol. Wirkung

IBR2 is a cell penetrant, potent and specific RAD51 inhibitor that inhibits RAD51-mediated DNA double-strand break repair and enhances cytotoxicity of multiple anticancer agents with disparate biochemical targets including the Bcr-Abl inhibitor imatinib and multiple kinase inhibitor regorafenib. IBR2 disrupts RAD51 multimerization, accelerates proteasome-mediated RAD51 protein degradation, reduces ionizing radiation-induced RAD51 foci formation, inhibits cancer cell growth and induces apoptosis.

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Analysenzertifikate (COA)

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Jiewen Zhu et al.
European journal of medicinal chemistry, 96, 196-208 (2015-04-16)
RAD51 recombinase plays a critical role for cancer cell proliferation and survival. Targeting RAD51 is therefore an attractive strategy for treating difficult-to-treat cancers, e.g. triple negative breast cancers which are often resistant to existing therapeutics. To this end, we have
Jiewen Zhu et al.
EMBO molecular medicine, 5(3), 353-365 (2013-01-24)
RAD51 recombinase activity plays a critical role for cancer cell proliferation and survival, and often contributes to drug-resistance. Abnormally elevated RAD51 function and hyperactive homologous recombination (HR) rates have been found in a panel of cancers, including breast cancer and
Peter J Ferguson et al.
The Journal of pharmacology and experimental therapeutics, 364(1), 46-54 (2017-10-25)
Although cancer cell genetic instability contributes to characteristics that mediate tumorigenicity, it also contributes to the tumor-selective toxicity of some chemotherapy drugs. This synthetic lethality can be enhanced by inhibitors of DNA repair. To exploit this potential Achilles heel, we

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