C16G2

C16G2 selectively kills Streptococcus mutans in saliva-derived oral bacterial communities and depletes dependent community members, reducing the community to an avirulent state^[1].
C16G2 (100 μM; 5 min-16 h) specifically eliminates S. mutans in saliva-derived mixtures containing S. mutans and renders the biofilms it forms resistant to subsequent recolonization by S. mutans^[2].
C16G2 specifically eradicates S. mutans in planktonic state and saliva-derived biofilms without affecting other oral streptococci, and kills S. mutans within one minute of exposure^[3].
C16G2 (0.625-64 μM; 16-20 h) potently inhibits S. mutans UA140 and S. mutans ATCC 104495, with MICs of 5.2 μM and 4.2 μM, respectively, and an MBC of 20 μM^[4].
C16G2 (6.25 μM) rapidly reduces the CFU/mL of S. mutans JM11 by approximately 2 log10 within 10 min, whereas non-mutans streptococci decrease by only 47%^[4].
C16G2 (3.125 μM; 10 min) permeabilizes S. mutans biofilms but does not affect S. sanguinis or S. salivarius biofilms^[4].
C16G2 (6.25 μM; 5 min) induces ATP efflux in S. mutans UA140 and S. mutans ATCC 104495^[4].
C16G2 (3.125 μM; > 40 min) depolarizes the S. mutans membrane but does not affect the S. gordonii or S. salivarius membrane^[4].
C16G2 (approximately 24 h) exhibits the strongest potency against planktonic S. mutans strains UA159, ATCC 25175, T8, and comD, with MICs of 3.0-5.1 μM, whereas non-S. mutans streptococci require 19.1-23.5 μM^[5].