The persister cells have the ability to communicate amongst themselves leading to virulence and the generation of resistance. Different quorum quenching agents have been explored in order to find adjuvant therapy. The bacterial QS inhibitory effect of subtilosin (9
), a cyclic lantibiotic formed by B. subtilis
KATMIRA1933, was assessed by Algburi et al. 
. Subtilosin shows its effect by targeting the surface receptor and binding to the bacterial cell membrane by electrostatic forces. The study revealed that at a concentration of 15.1 μg/mL an inhibition of 80% of L. monocytogenes
and about 60% of E. coli
biofilms was seen. Moreover, subtilosin decreased the autoinducer-2 formation in Gardnerella vaginalis
at a concentration of 3–4 μg/mL 
. Zhou et al. evaluated the QS inhibitory potential of hordenine (10
) isolated from sprouting barley towards P. aeruginosa.
It was found to inhibit the autoinducer AHLs at concentrations of 0.5 to 1.0 mg/ mL. Additionally, it also remarkably suppressed the QS associated genes lasR
and lasI 
. In another work by Zhao et al. the QS inhibitory effect of falcarindiol (11
) against P. aeruginosa
infestation was assessed. Biofilm formation and associated virulance factors were significantly inhibited at subinhibitory concentrations. Also, there was appreciable downregulation of the mRNA expression of QS associated genes lasI, lasB
, rhlR, phzH
and rhl I 
. QS and biofilm inhibitory effects of a few hordenine derivatives towards P.
aeruginosa and Serratia marcescens
was recently analysed by Liu et al. Derivatives 12a
exhibited superior QS inhibitory activity and biofilm inhibition towards P.
aeruginosa. Additionally, analogues 12a
displayed remarkable QS inhibition against S.
marcescens. SAR studies revealed essential factors involved in activity like alkyl chain length, presence or absence of amino or hydroxyl groups and unsaturation in the aromatic benzene ring 
. A thiolactone analog of AHL covalently linked to ciprofloxacin (QS0108) (13
) was developed by Ganguly et al. to assess them as inhibitors of AHL-2 in P. aeruginosa.
This system effectively disrupted dormant and mature biofilms compared to antibiotic treatment alone (Figure 6