MGB-BP-3

MGB-BP-3 (0.1-100 μM; 20 h) potently inhibits the growth of Staphylococcus aureus ATCC 43300, Enterococcus faecalis ATCC 51299, and an expanded panel of Gram-positive strains with MIC values ranging from 0.1-0.78 μM, but shows no activity against tested Gram-negative ESKAPE pathogens up to 100 μM^[1].
MGB-BP-3 (in combination with 100 μg/mL PAβN; 20 h) acts synergistically with PAβN to inhibit the growth of Gram-negative ESKAPE pathogens and multidrug-resistant clinical isolates of E. coli and K. pneumoniae, with FICI values ranging from ≤0.03 to 0.47 and MIC₈₀ values as low as 0.05 μM^[1].
MGB-BP-3 (20 μM) binds strongly to genomic DNA from both Gram-positive (S. aureus, E. faecalis) and Gram-negative (E. coli, P. aeruginosa, A. baumannii, K. pneumoniae) bacteria, as well as salmon genomic DNA, as shown by consistent SYBR Safe displacement with remaining fluorescence ranging from 19-28%^[1].
MGB-BP-3 (0.01-500 μM; 30 min) interferes with the supercoiling activity of S. aureus and E. coli gyrase (IC₅₀ 1.94-8.17 μM) and the decatenation and relaxation activities of S. aureus and E. coli topoisomerase IV (IC₅₀ 1.93-2.50 μM) without stabilizing enzyme-DNA cleavage complexes, unlike fluoroquinolones^[1].
MGB-BP-3 (1.5625 μM; 20 h) does not induce the SOS response in E. coli K12 MG1655 reporter strains at 0.5× MIC, confirming it does not cause double-strand DNA breaks like fluoroquinolones^[1].
MGB-BP-3 potently inhibits Staphylococcus aureus growth with an MIC₈₀ of less than 0.2 μM^[2].
MGB-BP-3 (sub-MIC₈₀ concentrations; 80 generations) shows intrinsic resilience to resistance development in Staphylococcus aureus after 80 generations of sub-MIC₈₀ exposure^[2].
MGB-BP-3 (0.25 µg/mL) potently kills the Clostridioides difficile NAP1/027 strain with an MIC of 0.25 µg/mL, acting faster than vancomycin^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.