JH-RE-06 |
| Katalog-Nr.GC36367 |
JH-RE-06, ein potenter REV1-REV7-Schnittstelleninhibitor (IC50=0,78 μM; Kd=0,42 μM), zielt auf REV1 ab, das mit der REV7-Untereinheit von POLζ interagiert. JH-RE-06 unterbricht die mutagene Translesionssynthese (TLS), indem es die Rekrutierung von mutagenem POLζ verhindert. JH-RE-06 verbessert die Chemotherapie.
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.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
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.)
GLPBIO products are for RESEARCH USE ONLY. Please make sure your review or question is research based.
Required fields are marked with *