JH-RE-06

Research use only, not for human use.

JH-RE-06 disrupts mutagenic translesion synthesis (TLS) by preventing the recruitment of mutagenic POLζ. JH-RE-06 is an effective REV1-REV7 interface inhibitor (IC50=0.78 μM; Kd=0.42 μM), which targets REV1 that interacts with the REV7 subunit of POLζ. JH-RE-06 also improves chemotherapy.

JH-RE-06 disrupts mutagenic translesion synthesis (TLS) by preventing the recruitment of mutagenic POLζ. JH-RE-06 is an effective REV1-REV7 interface inhibitor (IC50=0.78 μM; Kd=0.42 μM), which targets REV1 that interacts with the REV7 subunit of POLζ. JH-RE-06 also improves chemotherapy. JH-RE-06 unexpectedly causes dimerization of the REV1 CTD at its REV7-binding surface. It also blocks the REV1-REV7 interaction. In mice, co-administration of JH-RE-06 with cisplatin inhibits the growth of xenograft human melanomas. JH-RE-06 suppresses mutagenic TLS and increases cisplatin-induced toxicity in cultured human and mouse cell lines.

JH-RE-06 unexpectedly induces dimerization of the REV1 CTD at its REV7-binding surface and blocks the REV1-REV7 interaction.

JH-RE-06 inhibits mutagenic TLS and enhances cisplatin-induced toxicity in cultured human and mouse cell lines. Co-administration of JH-RE-06 with cisplatin suppresses the growth of xenograft human melanomas in mice.

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Cell Cycle/DNA Damage

DNA/RNA Synthesis

REV1-REV7

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1361227-90-8

468.72

C20H16Cl3N3O4

>98% (HPLC)

DMSO:5 mg/mL (10.67 mM; Need ultrasonic)

O=C1C(C(CC(C)C)=O)=C(NC2=CC=C(Cl)C=C2Cl)NC3=C1C([N+]([O-])=O)=CC=C3Cl

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(-20℃)

With Ice Pack

≥ 2 years