For research use only. Not for therapeutic Use.
ML328 is a selective inhibitor of bacterial AddAB and RecBCD helicase-nucleases with IC50 values of 26 and 5.1 μM, respectively. ML328 is a gyrase inhibitor. ML328 strongly inhibits the growth of E. coli in the presence of phage. ML328 can be used for the research of bacterial infection[1][2].
ML328 (0.1-1000 μM) shows AddAB and RecBCD nuclease inhibitory activities with IC50 values of 26 and 5.1 μM, respectively[1].
ML328 pathway-specifically inhibits of (high-frequency recombination) Hfr for RecBCD, RecF and RecE pathways[1].
ML328 shows RecBCD inhibitory effects with IC50 values of 3 μΜ for nuclease and Chi-cutting with purified enzyme, 0.3 μΜ for Hfr recombination and 5 μΜ for phage λ recombination promoted by RecBCD[2].
ML328 inhibits E. coli RecBCD, H. pylori AddAB, M. smeg AddAB and M. smeg RecBCD with IC50 values of 4.6, 16, 2.4 and 5.5 μM, respectively[2].
ML328 (25 μΜ; 2 h) reduces the frequency of H2O2-induced mutation in E. coli[2].
ML328 (25 μΜ; 1 h) reduces the requency of H2O2-induced mutation to valine-resistance (valineR) in E. coli[2].
ML328 (50 μΜ) slightly inhibits E. coli growth but strongly inhibits E. coli at the presence of phage[2].
Catalog Number | I012408 |
CAS Number | 634175-34-1 |
Synonyms | 8-ethyl-5-oxo-2-[4-[[3-(trifluoromethyl)phenyl]carbamothioyl]piperazin-1-yl]pyrido[2,3-d]pyrimidine-6-carboxylic acid |
Molecular Formula | C22H21F3N6O3S |
Purity | ≥95% |
InChI | InChI=1S/C22H21F3N6O3S/c1-2-29-12-16(19(33)34)17(32)15-11-26-20(28-18(15)29)30-6-8-31(9-7-30)21(35)27-14-5-3-4-13(10-14)22(23,24)25/h3-5,10-12H,2,6-9H2,1H3,(H,27,35)(H,33,34) |
InChIKey | USYVBPXJSBDUTJ-UHFFFAOYSA-N |
SMILES | CCN1C=C(C(=O)C2=CN=C(N=C21)N3CCN(CC3)C(=S)NC4=CC=CC(=C4)C(F)(F)F)C(=O)O |
Reference | [1]. Amundsen SK, et al. Small-molecule inhibitors of bacterial AddAB and RecBCD helicase-nuclease DNA repair enzymes. ACS Chem Biol. 2012 May 18;7(5):879-91. [2]. SMITH GERALD R, et al. ANTIBIOTIC COMPOUNDS AND COMPOSITIONS, AND METHODS FOR IDENTIFICATION THEREOF. WO/2013/142628. 2014. |