Enoxacin (AT 2266), a fluoroquinolone, interferes withDNA replicationand inhibitsbacterialDNA gyrase (IC₅₀=126 μg/ml) andtopoisomeraseIV (IC₅₀=26.5 μg/ml). Enoxacin is amiRNAprocessing activator and enhances siRNA-mediated mRNA degradation and promotes the biogenesis of endogenous miRNAs. Enoxacin has potent activities against gram-positive and -negative bacteria. Enoxacin is a cancer-specific growth inhibitor that acts by enhancing TAR RNA-binding protein 2 (TRBP)-mediatedmicroRNAprocessing^[1][2][3][4].

Enoxacin (AT 2266) increases siGFP-mediated gene knockdown mediated by siRNA against EGFP in HEK293 cells-based reporter system in a dose-dependent manner, with a median effective concentration (EC50) of ~30 μM, whereas it has no effect on the cells expressing GFP only. Enoxacin (50 μM) promotes the processing of miRNAs and the loading of siRNA duplexes onto RISCs in HEK293 cells^[3].
Enoxacin has no effect on the processing of pre-let-7 or pre-miR-30a by Dicer alone. However, the addition of Enoxacin can enhance the processing of let-7 or pre-miR-30a by Dicer and TRBP together^[3].
Enoxacin inhibits 90% Escherichia coli, Klebsiella sp., Aeromonas sp., Enterobacter spp., Serratia spp., Proteus mirabilis, and Morganella morganii at less than or equal to 0.8 micrograms/ml^[5].

Enoxacin (AT 2266; 100 μM; 2 μl; injected into ear once a day for 3 consecutive days (days 12, 13 and 14)) enhances the the GFP mRNA knockdown efficiency by Lv-siGFP (from 80% to 60%; 40% GFP mRNA level remained), whereas alone has no effect on GFP expression in GFP transgenic line C57BL/6-Tg(ACTB-EGFP)1Osb/J (10 d old) with lentivirus expressing shGFP (Lv-siGFP; injected into ear for 10 days)^[3].

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74011-58-8

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