JH-RE-06 |
| Catalog No.GC36367 |
JH-RE-06, un puissant inhibiteur de l'interface REV1-REV7 (IC50=0,78 μM ; Kd=0,42 μM), cible REV1 qui interagit avec la sous-unité REV7 de POLζ. JH-RE-06 perturbe la synthèse de la translésion mutagène (TLS) en empêchant le recrutement de POLζ mutagène. JH-RE-06 améliore la chimiothérapie.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 1361227-90-8
Sample solution is provided at 25 µL, 10mM.
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JH-RE-06, a potent REV1-REV7 interface inhibitor (IC50=0.78 μM; Kd=0.42 μM), targets REV1 that interacts with the REV7 subunit of POLζ. JH-RE-06 disrupts mutagenic translesion synthesis (TLS) by preventing recruitment of mutagenic POLζ. JH-RE-06 enhances Cisplatin-induced cytotoxicity and improves chemotherapy[1][2]. IC50: 0.78 μM (REV1-REV7)[1]Kd: 0.42 μM (REV1-REV7)[1]
JH-RE-06 unexpectedly induces dimerization of the REV1 CTD at its REV7-binding surface and blocks the REV1-REV7 interaction[1].
JH-RE-06 inhibits mutagenic TLS and enhances cisplatin-induced toxicity in cultured human and mouse cell lines[1]. Co-administration of JH-RE-06 with cisplatin suppresses the growth of xenograft human melanomas in mice[1].
[1]. Wojtaszek JL, et al. A Small Molecule Targeting Mutagenic Translesion Synthesis Improves Chemotherapy. Cell. 2019 Jun 27;178(1):152-159.e11. [2]. REV1-POLς Inhibition Enhances Cisplatin-Induced Cytotoxicity. Cancer Discov. 2019 Aug;9(8):OF17.
Average Rating: 5 (Based on Reviews and 17 reference(s) in Google Scholar.)
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