Name | KKL-35 |
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Synonyms |
4-Chloro-N-[5-(4-fluorophenyl)-1,3,4-oxadiazol-2-yl]benzamide
Benzamide, 4-chloro-N-[5-(4-fluorophenyl)-1,3,4-oxadiazol-2-yl]- |
Description | KKL-35 is a trans-translation tagging reaction inhibitor with an IC50 of 0.9 µM. |
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Related Catalog | |
Target |
IC50: 0.9 µM (trans-translation tagging reaction)[1] |
In Vitro | KKL-35 exhibits broad-spectrum antibiotic activity. KKL-35 prevents growth of B. anthracis and M. smegmatis with minimum inhibitory concentration (MIC) values of less than 6 µM. KKL-35 inhibit trans-translation at some step before proteolysis of tagged proteins. KKL-35 inhibits tagging of DHFR-ns. A large amount of untagged DHFR is produced in reactions with the highest concentrations of KKL-35, indicating that KKL-35 does not inhibit translation. KKL-35 prevents growth of WT S. flexneri with a MIC of 6 µM, and addition of KKL-35 to a growing culture of S. flexneri stops growth. In an S. flexneri strain expressing ArfA and deleted for ssrA, addition of KKL-35 has little effect on viability or growth rate. KKL-35 inhibits the growth of E. coli ∆tolC, which is deficient in small molecule efflux, with an MIC of 0.3 µM[1]. |
In Vivo | Evidence suggest that the in vivo effects of KKL-35 are caused by inhibition of the release of nonstop translation complexes by trans-translation. KKL-35 inhibits trans-translation and prevents growth of S. flexneri strains that require trans-translation. The correlation between inhibition of trans-translation and growth is supported by genetic and pharmacological experiments showing that alternative mechanisms to release nonstop translation complexes relieve the growth suppression of KKL-35[1]. |
References |
Density | 1.5±0.1 g/cm3 |
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Molecular Formula | C15H9ClFN3O2 |
Molecular Weight | 317.702 |
Exact Mass | 317.036743 |
LogP | 4.13 |
Index of Refraction | 1.639 |