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Merck
CN

SML2993

JH-RE-06

≥98% (HPLC)

Synonym(s):

8-Chloro-2-[(2,4-dichlorophenyl)amino]-3-(3-methyl-1-oxobutyl)-5-nitro-4(1H)-quinolinone

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About This Item

Empirical Formula (Hill Notation):
C20H16Cl3N3O4
CAS Number:
1361227-90-8
Molecular Weight:
468.72
MDL number:
MFCD32197217
UNSPSC Code:
12352200
NACRES:
NA.77

Key Documents

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Quality Level

100

Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

2-8°C

SMILES string

Clc1c(ccc(c1)Cl)Nc2[nH]c3c([c](c2C(=O)CC(C)C)=O)c(ccc3Cl)[N+](=O)[O-]

InChI

1S/C20H16Cl3N3O4/c1-9(2)7-15(27)17-19(28)16-14(26(29)30)6-4-11(22)18(16)25-20(17)24-13-5-3-10(21)8-12(13)23/h3-6,8-9H,7H2,1-2H3,(H2,24,25,28)

InChI key

LRTXIQCBQIKIOH-UHFFFAOYSA-N

Related Categories

Biochem/physiol Actions

JH-RE-06 is a potent and selective inhibitor of REV1-REV7 interaction that induces REV1 dimerization blocking the REV1-REV7 interaction and POL ϲ recruitment. JH-RE-06 potently inhibits translesion synthesis (TLS) and augments cisplatin effectiveness in cultured human and mouse cell lines. It improves effectiveness of cisplatin in A375 tumor xenograft mouse model.
potent and selective inhibitor of REV1-REV7 interaction blocking the REV1-REV7 interaction and POL ϲ recruitment

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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Certificates of Analysis (COA)

Lot/Batch Number
0000390128
0000390128
0000187034
0000187035
0000187034

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Kavi P M Mehta et al.
Cell reports, 31(9), 107705-107705 (2020-06-04)
5-Hydroxymethylcytosine (5hmC) binding, ES-cell-specific (HMCES) crosslinks to apurinic or apyrimidinic (AP, abasic) sites in single-strand DNA (ssDNA). To determine whether HMCES responds to the ssDNA abasic site in cells, we exploited the activity of apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like
Jessica L Wojtaszek et al.
Cell, 178(1), 152-159 (2019-06-11)
Intrinsic and acquired drug resistance and induction of secondary malignancies limit successful chemotherapy. Because mutagenic translesion synthesis (TLS) contributes to chemoresistance as well as treatment-induced mutations, targeting TLS is an attractive avenue for improving chemotherapeutics. However, development of small molecules with

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