pqsr

HHQ (2-heptylquinolin-4(1H)-one) 是一种 PqsR 拮抗剂。

PqsR LasR-IN-3 (Compound 7a) 抑制 hERG，IC50值为 109.01 μM。它也是铜绿假单胞菌中PqsR 和LasR 系统的有效抑制剂。

PqsR-IN-1 (Compound 18) is a potent inhibitor of PqsR, which is a transcriptional regulator involved in the quorum sensing mechanism of Pseudomonas aeruginosa. This compound effectively reduces the production of pyocyanin and exhibits minimal cytotoxicity [1].

PqsR-IN-2 (Compound 19) is a highly potent inhibitor of PqsR, the transcriptional regulator responsible for quorum sensing in Pseudomonas aeruginosa. It effectively suppresses pyocyanin production without causing significant cytotoxicity, making it a promising compound for therapeutic applications [1].

PqsR LasR-IN-1 (Compound 2a) 是铜绿假单胞菌中LasR 和PqsR 系统的有效抑制剂。PqsR LasR-IN-1 也是 hERG 的抑制剂，IC50为 6.77 μM。

4-(tert-Butyl)-benzhydroxamic Acid is a PqsR antagonist with IC50s of 12.5 μM and 23.6 μM for E. coli and P. aeruginosa, respectively, and it reduces the production of the virulence factor pyocyanin in P. aeruginosa with an IC50 of 87.2 μM[1].

Quorum sensing-IN-9 (Compound 7d) 通过结合 PqsR 蛋白在 Pseudomonas aeruginosa 中阻断群体感应机制。它抑制 lasB、rhlA 和 pqsA 等群体感应相关基因的表达，从而阻止毒力因子如弹性蛋白酶 (elastase)、绿脓素 (pyocyanin) 和鼠李糖脂 (rhamnolipid) 的合成。该化合物削弱 P. aeruginosa 的运动能力，抑制生物膜的形成，降低其毒力及致病性。在大蜡螟 (Galleria mellonella) 幼虫模型中，Quorum sensing-IN-9 展现出抗感染活性。

RhlR antagonist 1 is a highly effective antagonist of the RhlR protein, showing an IC50 value of 26 μM. It exhibits selective antagonistic activity against RhlR, with minimal effect on LasR and PqsR. RhlR antagonist 1 strongly inhibits biofilm formation in both static and dynamic environments and reduces the production of virulence factors, such as rhamnolipid and pyocyanin, in P. aeruginosa. These characteristics make RhlR antagonist 1 a valuable tool for the development of molecules that modulate quorum sensing and control P. aeruginosa infections [1].

F-17 is a promising virulence factor inhibitor, displaying substantial inhibitory effects on biofilm formation, elastase activity, pyocyanin production, and swarming motility. Additionally, F-17 exhibits a strong binding affinity towards LasR and PqsR. Notably, F-17 does not exhibit any discernible cytotoxicity [1].

QZN34 is a PqsR inhibitor which prevents S. aureus biofilm formation, severely damaged established S. aureus biofilms, and perturbed P. aeruginosa biofilm development. The mechanism of action of QZN 34 toward Gram-positive bacteria is shown to involve membrane perturbation and dissipation of transmembrane potential.