quorum-sensing

Quorum Sensing-IN-3 (QS-IN-1) is a compound with inhibitory effects on bacterial community sensing, which inhibits the exchange of information between bacteria and inhibits biofilm formation.

Quorum Sensing-IN-1 [QSI-1] is a small-molecule inhibitor targeting quorum sensing.

Quorum Sensing-IN-2 (compound 23e) is a quorum sensing inhibitor that reduces bacterial pathogenicity without affecting growth, exhibits minimal hemolytic activity, effectively inhibits bacterial infections, and shows a synergistic effect when combined with Ciprofloxacin in a P. aeruginosa PAO1-infected bacteremia model [1].

Methyl anthranilate is a natural product. Methyl anthranilate is a novel quorum sensing inhibitor and anti-biofilm agent against Aeromonas sobria

N-dodecanoyl-L-Homoserine lactone (C12-HSL) is a quorum sensing (QS) signaling molecule that impacts biofilm formation in bioreactors through acyl homoserine lactone (AHL) mediated microbial communication.

QStatin, a Selective Inhibitor of Quorum Sensing in Vibrio Species( SmcR with an EC50 of 208.9 nM).

N-hexanoyl-L-Homoserine lactone (C6-HSL), a small diffusible signaling molecule, is involved in controlling gene expression, affecting cellular metabolism, and quorum sensing.

N-acetyltyramine is a metabolite of the biogenic amine tyramine . It enhances cytotoxicity of doxorubicin in resistant P388 murine leukemia cells with an IC50 value of 0.13 μg ml compared with an IC50 value of 0.48 μg ml for doxorubicin alone.

N-(3-Oxodecanoyl)-L-homoserine lactone (3-Oxo-C10-HSL) functions as a bacterial quorum-sensing signal autoinducer [1].

CAI-1 is a vibrio cholerae quorum-sensing autoinducer.

Cis-11-Methyl-2-dodecenoic acid functions as a quorum sensing (QS) signal and a diffusion signaling factor (DSF) within extracellular microbial and fungal communication systems. It plays a pivotal role in regulating virulence and biofilm formation among diverse bacterial pathogens [1].

V-06-018 is a quorum-sensing modulator. It also acts as a LasR antagonist.

Quorum sensing is a regulatory system used by bacteria for controlling gene expression in response to increasing cell density. This regulatory process manifests itself with a variety of phenotypes including biofilm formation and virulence factor production. Coordinated gene expression is achieved by the production, release, and detection of small diffusible signal molecules called autoinducers. The N-acylated homoserine lactones (AHLs) comprise one such class of autoinducers, each of which generally consists of a fatty acid coupled with homoserine lactone (HSL). Regulation of bacterial quorum sensing signaling systems to inhibit pathogenesis represents a new approach to antimicrobial therapy in the treatment of infectious diseases. AHLs vary in acyl group length (C4-C18), in the substitution of C3 (hydrogen, hydroxyl, or oxo group), and in the presence or absence of one or more carbon-carbon double bonds in the fatty acid chain. These differences confer signal specificity through the affinity of transcriptional regulators of the LuxR family. C15-HSL is a product of Y. pseudituberculosis.

Quorum sensing is a regulatory process used by bacteria for controlling gene expression in response to increasing cell density. This regulatory process manifests itself with a variety of phenotypes including biofilm formation and virulence factor production. Coordinated gene expression is achieved by the production, release, and detection of small diffusible signal molecules called autoinducers. The N-acylated homoserine lactones (AHLs) comprise one such class of autoinducers, each of which generally consists of a fatty acid coupled with homoserine lactone (HSL). AHLs vary in acyl group length (C4-C18), in the substitution of C3 (hydrogen, hydroxyl, or oxo group) and in the presence or absence of one or more carbon-carbon double bonds in the fatty acid chain. These differences confer signal specificity through the affinity of transcriptional regulators of the LuxR family. C14:1-δ9-cis-(L)-HSL is a long-chain AHL that functions as a signaling molecule in the quorum sensing of A. vitis. Regulating bacterial quorum sensing signaling can be used to inhibit pathogenesis and thus, represents a new approach to antimicrobial therpy in the treatment of infectious diseases.

QS inhibitor 2 is a novel potent inhibitor of quorum sensing (QS) pathways.

QS inhibitor 1 is a novel potent inhibitor of quorum sensing (QS) pathways.

N-(3-Oxotetradecanoyl)-DL-homoserine lactone, part of the N-Acyl homoserine lactone (AHL) family derived from gram-negative bacteria, serves as a quorum sensing (QS) signaling molecule.

Hamamelitannin has cytotoxic, and antibiofilm activities. It increases the susceptibility of S. aureus to antibiotic treatment in in vivo Caenorhabditis elegans and mouse mammary gland infection models. It also has a high protective activity on cell damag

CSP1 is a highly potent and selective agonist of the ComD1 receptor, exhibiting an IC50 value of 10.3 nM. It represents a major variant of competence-stimulating peptide (CSP) and plays a crucial role in regulating the genetic transformation of S. pneumoniae through modulation of quorum sensing (QS). Additionally, CSP1 possesses antibacterial activity, further enhancing its potential as an effective antibacterial agent.

AIP-II is a macrocyclic peptide signaling molecule produced by Staphylococcus aureus for quorum sensing. It binds to the AgrC-II receptor, regulating the expression of virulence genes within Staphylococcus aureus. Additionally, AIP-II acts as an antagonist to the AgrC-I receptor.

Quorum sensing is a regulatory system used by bacteria for controlling gene expression in response to increasing cell density. Controlling bacterial infections by quenching their quorum sensing systems is a promising field of study. The expression of specific target genes, such as transcriptional regulators belonging to the LuxIR family of proteins, is coordinated by the synthesis of diffusible acylhomoserine lactone (AHL) molecules. N-3-oxo-tetradecanoyl-L-homoserine lactone (3-oxo-C14-HSL) is a small diffusible signaling molecule involved in quorum sensing, thereby controlling gene expression and affecting cellular metabolism in bacteria.[1] [2] [3] It appears later than shorter acyl chain AHLs in developing biofilms [4] and, like other long chain 3-oxo-AHLs, stimulates the production of putisolvin, [5] which in turn, inhibits biofilm formation.

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

3-hydroxy Palmitic acid methyl ester (3-hydroxy PAME) is an esterized long-chain fatty acid involved in quorum sensing in R. solanacearum, a bacteria that causes lethal wilting in plants. 3-hydroxy-PAME (175 nM) increases levels of PhcA-regulated virulence factors, greater than 20-, 30-, and 25-fold for EPS I, EGL, and PME, respectively, in the AW1-83 strain of R. solanacearum.

YXL-13 is a highly effective inhibitor of Pseudomonas aeruginosa (PAO1), with an IC50 value of 3.686 μM. It effectively hinders the expression of virulence factors and inhibits biofilm formation in PAO1. Moreover, YXL-13 significantly diminishes both the pathogenicity and drug resistance of PAO1 by inhibiting the quorum sensing (QS) system. Thus, YXL-13 holds great potential for studying antibacterial properties [1].

Hordenine hydrochloride is a biochemical that inhibits the activity of PDK3, inhibits quorum sensing, and acts as an antibiofilm agent against bacteria.

Quorum sensing is a regulatory process used by bacteria for controlling gene expression in response to increasing cell density. This regulatory process manifests itself with a variety of phenotypes including biofilm formation and virulence factor production. Coordinated gene expression is achieved by the production, release, and detection of small diffusible signal molecules called autoinducers. The N-acylated homoserine lactones (AHLs) comprise one such class of autoinducers, each of which generally consists of a fatty acid coupled with homoserine lactone (HSL). AHLs vary in acyl group length (C4-C18), in the substitution of C3 (hydrogen, hydroxyl, or oxo group) and in the presence or absence of one or more carbon-carbon double bonds in the fatty acid chain. These differences confer signal specificity through the affinity of transcriptional regulators of the LuxR family. C18:1-δ9 cis-(L)-HSL is a long-chain AHL that may have antimicrobial activity and thus, might be used to inhibit pathogenesis by regulating bacerial quorum sensing signaling.

ML366 is a Vibrio cholerae Quorum Sensing inhibitor Acting via the LuxO response regulator.

P516-0475 is a novel chemical inducer of Streptococcus quorum sensing acts by inhibiting the pheromone-degrading endopeptidase PepO. This compound induces quorum sensing by stabilizing SHP pheromones in culture.

L-Homoserine lactone is a synthetic intermediate.1,2It has been used in the synthesis of organoselenium chemistry intermediates and analogs of bacterial quorum-sensing signaling molecules. 1.Koch, T., and Buchardt, O.Synthesis of L-(+)-selenomethionineSynthesis1065-1067(1993) 2.Chhabra, S.R., Harty, C., Hooi, D.S.W., et al.Synthetic analogues of the bacterial signal (quorum seensing) molecule N-(3-oxododecanoyl)-L-homoserine lactone as immune modulatorsJ. Med. Chem.46(1)97-104(2003)

N-(Ketocaproyl)-DL-homoserine lactone is a quorum sensing (QS) autoinducer and a natural, active ligand of LuxR.

N-(beta-Ketocaproyl)-L-hoMoserine lactone (N-(Ketocaproyl)-L-homoserine lactone) is a component of quorum regulatory sensing and an autoinducer of P. fischeri luciferase.

2-heptyl-3-hydroxy-4(1H)-Quinolone (Pseudomonas Quinolone Signal) is a quorum-sensing signalling molecule produced by Pseudomonas aeruginosa in response to increased cell density. It increases the expression of the lasB gene in P. aeruginosa, the secretion of the metabolites pyocyanin and the lectin PA-IL, as well as increasing biofilm production in P. aeruginosa populations. It also reduces the iron content of the P. aeruginosa growth medium when used at a concentration of 40 μM and acts as an iron chelator in iron sulphate solutions.

Competence-Stimulating Peptide-2 (CSP-2) is a quorum sensing signal peptide synthesized by Streptococcus pneumoniae. Its compatible receptor, ComD2, exhibits an EC50 value of 50.7 nM.

N-Decanoyl cyclopentylamide (C10-CPA) serves as a potent quorum sensing inhibitor in Pseudomonas aeruginosa, disrupting the expression of virulence factors governed by both the las and rhl systems. It effectively suppresses the production of elastase, pyocyanin, rhamnolipid, and hinders biofilm formation.

Programmed cell death in bacteria is dependent on a system of cell-to-cell communication termed quorum sensing. Extracellular death factor (EDF) is a linear pentapeptide that communicating cells produce and release, which upon reaching a sufficient concentration activates the cell death pathway in a subset of cells. It is sensitive to extreme pH, high temperatures, and other stressful conditions. At 2.5 ng/ml, EDF has been shown to facilitate mazEF-mediated cell death, significantly reducing population size in E. coli cultures.

Nifuroxazide-d4 is intended for use as an internal standard for the quantification of nifuroxazide by GC- or LC-MS. Nifuroxazide is a nitrofuran antibiotic. It is active against strains of the enteropathogenic bacteria C. jejuni, Salmonella, Y. enterocolitica, Shigella, and E. coli. It inhibits quorum sensing and virulence factor production in P. aeruginosa. Nifuroxazide inhibits STAT3 activity in a reporter assay and decreases viability of U266 and INA-6 myeloma cells, which have constitutive STAT3 phosphorylation, with EC50 values of approximately 4.5 µM for both. It also decreases viability, migration, and invasion of, and induces apoptosis in, MCF-7, 4T1, and MDA-MB-231 breast cancer cells. Nifuroxazide reduces tumor growth and prevents pulmonary metastasis in a 4T1 murine mammary carcinoma model. It also reduces diarrhea, weight loss, and colon inflammation in a rat model of acetic acid-induced ulcerative colitis.

Quorum sensing is a regulatory process used by bacteria for controlling gene expression in response to increasing cell density.[1] This regulatory process manifests itself with a variety of phenotypes including biofilm formation and virulence factor production.[2] Coordinated gene expression is achieved by the production, release, and detection of small diffusible signal molecules called autoinducers. The N-acylated homoserine lactones (AHLs) comprise one such class of autoinducers, each of which generally consists of a fatty acid coupled with homoserine lactone (HSL). AHLs vary in acyl group length (C4-C18), in the substitution of C3 (hydrogen, hydroxyl, or oxo group) and in the presence or absence of one or more carbon-carbon double bonds in the fatty acid chain. These differences confer signal specificity through the affinity of transcriptional regulators of the LuxR family.[3] C16:1-Δ9-(L)-HSL is a long-chain AHL that functions as a quorum sensing signaling molecule in strains of S. meliloti.[4],[5],[6],[7] Regulating bacterial quorum sensing signaling can be used to inhibit pathogenesis and thus, represents a new approach to antimicrobial therapy in the treatment of infectious diseases.[8] Reference：[1]. González, J.E., and Keshavan, N.D. Messing with bacterial quorum sensing. Microbiol. Mol. Biol. Rev. 70(4), 859-875 (2006).[2]. Gould, T.A., Herman, J., Krank, J., et al. Specificity of acyl-homoserine lactone syntheses examined by mass spectrometry. J. Bacteriol. 188(2), 773-783 (2006).[3]. Penalver, C.G.N., Morin, D., Cantet, F., et al. Methylobacterium extorquens AM1 produces a novel type of acyl-homoserine lactone with a double unsaturated side chain under methylotrophic growth conditions. FEBS Lett. 580(2), 561-567 (2006).[4]. Teplitski, M., Eberhard, A., Gronquist, M.R., et al. Chemical identification of N-acyl homoserine lactone quorum-sensing signals produced by Sinorhizobium meliloti strains in defined medium. Archives of Microbiology 180, 494-497 (2003).[5]. Gao, M., Chen, H., Eberhard, A., et al. sinI- and expR-dependent quorum sensing in Sinorhizobium meliloti. Journal of Bacteriology 187(23), 7931-7944 (2005).[6]. Marketon, M.M., Glenn, S.A., Eberhard, A., et al. Quorum sensing controls exopolysaccharide production in Sinorhizobium meliloti. Journal of Bacteriology 185(1), 325-331 (2003).[7]. Marketon, M., Gronquist, M.R., Eberhard, A., et al. Characterization of the Sinorhizobium meliloti sinR/sinI locus and the production of novel N-Acyl homoserine lactones. Journal of Bacteriology 184(20), 5686-5695 (2002).[8]. Cegelski, L., Marshall, G.R., Eldridge, G.R., et al. The biology and future prospects of antivirulence therapies. Nat. Rev. Microbiol. 6(1), 17-27 (2008).

RhlR antagonist E22 is a quorum sensing modulator as an RhlR antagonist.

Aculene D, a fungal metabolite, exhibits quorum sensing (QS) inhibitory effects on Chromobacterium violaceum CV026, significantly reducing violacein production in N-hexanoyl-l-homoserine lactone (C6-HSL) induced cultures of C. violaceum CV026 at sub-inhibitory concentrations [1].

Quorum sensing is a regulatory system used by bacteria for controlling gene expression in response to increasing cell density. This regulatory process manifests itself with a variety of phenotypes including biofilm formation and virulence factor production. Coordinated gene expression is achieved by the production, release, and detection of small diffusible signal molecules called autoinducers. The N-acylated homoserine lactones (AHLs) comprise one such class of autoinducers, each of which generally consists of a fatty acid coupled with homoserine lactone (HSL). Regulation of bacterial quorum sensing signaling systems to inhibit pathogenesis represents a new approach to antimicrobial therapy in the treatment of infectious diseases. AHLs vary in acyl group length (C4-C18), in the substitution of C3 (hydrogen, hydroxyl, or oxo group), and in the presence or absence of one or more carbon-carbon double bonds in the fatty acid chain. These differences confer signal specificity through the affinity of transcriptional regulators of the LuxR family. N-tridecanoyl-L-Homoserine lactone (C13-HSL) possesses a rare odd-numbered acyl carbon chain and is produced by wild-type and mutant strains of Y. pseudotuberculosis in trace amounts.

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

N-butyryl-L-Homocysteine thio-lactone, an analog of N-butyryl-L-homoserine lactone, is a small diffusible signaling molecule involved in quorum sensing for controlling gene expression and cellular metabolism. It induces violacein expression in C. violaceum mutants usually not able to produce acylhomoserine lactone (AHL), regulating genes like LuxIR family transcriptional regulators.

Synthetic furanone bacterial quorum sensing inhibitor. Inhibits virulence factor expression in Pseudomonas aeruginosa and increases bacterial susceptibility to antibiotics in vitro. Also inhibits bacterial quorum sensing in vivo and promotes bacterial clearance in a mouse pulmonary infection model. Hentzer et al (2003) Attenuation of Pseudomonas aeruginosa virulence by quorum sensing inhibitors. EMBO J. 22 3803 PMID:12881415

N-acylated homoserine lactones (AHLs) are a class of autoinducers used in bacterial quorum sensing to control gene expression in response to cell density. These molecules, comprising a fatty acid coupled with homoserine lactone (HSL), vary in acyl group length (C4-C18), C3 substitution (hydrogen, hydroxyl, or oxo group), and the presence of carbon-carbon double bonds, determining signal specificity through LuxR family transcriptional regulators. C11-HSL, with its rare odd-numbered acyl carbon chain, may act as a minor quorum-sensing signaling molecule in P. aeruginosa strains. Regulating bacterial quorum sensing can inhibit pathogenesis and represents a novel antimicrobial therapy approach for infectious diseases.

N-(3-hydroxy-7-cis tetradecenoyl)-L-Homoserine lactone is a long-chain N-acyl-homoserine lactone (AHL) produced by some Gram-negative bacteria and is involved in quorum sensing. Quorum sensing enables bacteria to change gene expression based on cues from nearby bacteria and from eukaryotic hosts about nutrients, environmental conditions, or threats. Due to the benefit of quorum sensing for bacterial survival, quorum sensing molecules are potential targets for controlling bacterial infections. In mouse and human leukocyte immunoassays using LPS-stimulated macrophages, N-(3-hydroxy-7-cis tetradecenoyl)-L-homoserine lactone did not have an effect on cytokine or antibody production.

Hordenine sulfate inhibits the activity of PDK3, inhibits quorum sensing, and acts as an antibiofilm agent against bacteria.

3-hydroxy Palmitic acid is a form of the 16:0 lipid palmitic acid . The lipid A part of lipopolysaccharides contain various 3-hydroxy fatty acids, making oxylipins such as 3-hydroxy palmitic acid useful as chemical markers of endotoxins. In R. solanacearum, 3-hydroxy palmitic acid is converted by an S-adenosyl methionine-dependent methyltransferase to 3-hydroxy palmitic acid methyl ester, which acts as a quorum sensing signal molecule for post-transcriptional modulation of genes involved in virulence. Long-chain 3-hydroxy fatty acids, such as 3-hydroxy palmitic acid, are also known to accumulate during long-chain 3-hydroxy-acyl-CoA dehydrogenase and mitochondrial trifunctional protein deficiencies. Such accumulation induces oxidative stress, leading to mitochondrial bioenergetics deregulation and eventual multi-organ dysfunction.

N-3-oxo-dodecanoyl-L-Homoserine lactone (3-oxo-C12-HSL), a quorum-sensing signaling molecule synthesized by P. aeruginosa and specific B. cepacia complex strains [1][2], facilitates bacterial gene expression modulation in response to cell density escalation and triggers IL-8 production in 16HBE human bronchial epithelial cells [3].

Nifuroxazide (Diarlidan) is an orally available and cell-permeable nitrofuran-based antidiarrheal agent. It has the inhibitory effect against the activation of cellular STAT1 3 5 transcription.