Search Result
Results for "
virulence factors
" in MedChemExpress (MCE) Product Catalog:
3
Biochemical Assay Reagents
2
Isotope-Labeled Compounds
Cat. No. |
Product Name |
Target |
Research Areas |
Chemical Structure |
-
- HY-P2988
-
Exo-α-sialidase
|
Endogenous Metabolite
|
Infection
|
Neuraminidase, Microorganism (Exo-α-sialidase) is an exosialidase, is often used in biochemical studies. Neuraminidase cleaves α-ketosidic linkage between the sialic (N-acetylneuraminic) acid and an adjacent sugar residue. Neuraminidase, derived from mucosal pathogens, is a virulence factor that modifies the host's response to infection .
|
-
-
- HY-134215
-
|
Bacterial
Fungal
|
Infection
|
cis-11-Methyl-2-dodecenoic acid is a quorum sensing (QS) signal that acts as a diffusion signaling factor (DSF) in extracellular microbial and fungal communication systems. DSF is involved in the regulation of virulence and biofilm formation of a variety of bacterial pathogens .
|
-
-
- HY-115969
-
|
Bacterial
|
Infection
|
F-17 is a potential inhibitor of virulence factor. F-17 shows very significant inhibitory effect on biofilm, elastase, pyocyanin, and swarming motility. F-17 also shows a good binding effect on LasR and PqsR. F-17 has no obvious cytotoxicity .
|
-
-
- HY-115884
-
|
Bacterial
|
Infection
Inflammation/Immunology
|
PptT-IN-3 (compound 5p) is a potent inhibitor of with phosphopantetheinyl phosphoryl transferase (PptT) an IC50 of 3.5 μM. Phosphopantetheinyl transferase, an essential enzyme that plays a critical role in the biosynthesis of cellular lipids and virulence factors in Mycobacterium tuberculosis. PptT-IN-3 has the potential for the research of tuberculosis .
|
-
-
- HY-115883
-
|
Bacterial
|
Infection
Inflammation/Immunology
|
PptT-IN-2 (compound 5k) is a potent inhibitor of with phosphopantetheinyl phosphoryl transferase (PptT) an IC50 of 2.5 μM. Phosphopantetheinyl transferase, an essential enzyme that plays a critical role in the biosynthesis of cellular lipids and virulence factors in Mycobacterium tuberculosis. PptT-IN-2 has the potential for the research of tuberculosis .
|
-
-
- HY-115882
-
|
Bacterial
|
Infection
Inflammation/Immunology
|
PptT-IN-1 (compound 5j) is a potent inhibitor of with phosphopantetheinyl phosphoryl transferase (PptT) an IC50 of 2.8 μM. Phosphopantetheinyl transferase, an essential enzyme that plays a critical role in the biosynthesis of cellular lipids and virulence factors in Mycobacterium tuberculosis. PptT-IN-1 has the potential for the research of tuberculosis .
|
-
-
- HY-151376
-
|
Proteasome
|
Infection
|
SAP2-IN-1 is a secreted aspartic protease 2 (SAP2) inhibitor and has potent SAP2 inhibitory activity with an IC50 value of 0.92 μM. SAP2-IN-1 also is a virulence factor inhibitor and is inactive in vitro. SAP2-IN-1 can be used for the research of infection .
|
-
-
- HY-145741
-
|
Antibiotic
|
Infection
|
MptpB-IN-1 (Compound 13) is a potent and orally active inhibitor of MptpB. Mycobacterium tuberculosis protein-tyrosine-phosphatase B (MptpB) is a secreted virulence factor that subverts antimicrobial activity in the host. MptpB-IN-1 reduces multidrug-resistant mycobacterium tuberculosis survival and infection burden .
|
-
-
- HY-146304
-
|
Bacterial
|
Infection
|
YXL-13 is a potent Pseudomonas aeruginosa (PAO1) inhibitor with an IC50 value of 3.686 μM. YXL-13 can inhibit virulence factors and biofilm formation of PAO1. YXL-13 reduces the pathogenicity and agent resistance of PAO1 by inhibition of the quorum sensing (QS) system. YXL-13 can be used for researching anti-bacteria .
|
-
-
- HY-155479
-
|
Bacterial
|
Infection
|
PqsR-IN-3 (compound 16e) is a selective inhibitor of the pqs system (IC50=3.7 μM) and its associated virulence factor pyocyanin (IC50=2.7 μM). PqsR-IN-3 inhibits bacterial biofilm synthesis and is significantly cytotoxic against Pseudomonas aeruginosa. PqsR-IN-3 has synergistic effects with several antibiotics, such as Ciprofloxacin (HY-B0356) and Tobramycin (HY-B0441) .
|
-
-
- HY-131337
-
|
Bacterial
|
Infection
|
RhlR antagonist 1 is a potent RhlR antagonist with an IC50 of 26 μM. RhlR antagonist 1 displays selective RhlR antagonism over LasR and PqsR, strong inhibition of biofilm formation in static and dynamic settings, and reduces production of virulence factors such as rhamnolipid and pyocyanin in P. aeruginosa. RhlR antagonist 1 can be utilized for developing QS-modulating molecules in the control of P. aeruginosa infections . RhlR antagonist 1 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
|
-
-
- HY-W007390
-
|
Bacterial
|
Infection
|
Methyl 2-amino-5-bromobenzoate (compound 8/12) can be used for synthesis of 2-benzamidobenzoic acids, which are known FabH inhibitors. The derivates also inhibit PqsD, the pqs quorum sensing (QS) system of Pseudomonas aeruginosa, involving the production of a number of virulence factors and biofilm formation .
|
-
-
- HY-N7788
-
|
Bacterial
|
Infection
|
cis-2-Dodecenoic acid, originally discovered in Burkholderia cenocepacia, can interfere with the bacterial quorum sensing system and inhibit bacterial biofilm formation and virulence factor production .
|
-
-
- HY-149762
-
|
Bacterial
|
Infection
|
IMBI (compound 32) is an antibacterial agent that inhibits quorum sensing (QS) against drug-resistant pathogens. IMBI inhibits biofilm formation of Salmonella marcescens and restores or increases its susceptibility to antimicrobial drugs .
|
-
-
- HY-114818
-
|
Bacterial
|
Infection
|
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. 4-(tert-Butyl)-benzhydroxamic Acid reduces the production of the virulence factor pyocyanin in P. aeruginosa with an IC50 of 87.2 μM .
|
-
-
- HY-163542
-
|
Bacterial
|
Inflammation/Immunology
|
Pneumolysin-IN-1 (compound PB-3) is a targeted small molecule inhibitor of Pneumolysin (PLY) (IC50=3.1 µM). Pneumolysin-IN-1 is a pore blocking agent and an anti-virulence factor. Pneumolysin-IN-1 can be used to study the infection caused by Streptococcus pneumoniae .
|
-
-
- HY-158193
-
C10-CPA
|
Bacterial
|
Infection
|
N-Decanoyl cyclopentylamide (C10-CPA) is a potent inhibitor of quorum sensing in Pseudomonas aeruginosa. N-Decanoyl cyclopentylamide interferes with expression of Pseudomonas aeruginosa virulence factors regulated by the las and rhl quorum-sensing systems. N-Decanoyl cyclopentylamide inhibits production of elastase, pyocyanin, and rhamnolipid and biofilm formation .
|
-
-
- HY-149169
-
|
Others
|
Inflammation/Immunology
|
Phevamine A is a small molecule bacterial phytotoxin that can be isolated from Pseudomonas syringae. Phevamine promotes bacterial growth by suppressing plant immune responses .
|
-
-
- HY-152175
-
|
Bacterial
|
Infection
|
Antibacterial agent 130 is a 1,1-diarylthiogalactoside, used for targeting the Pseudomonas aeruginosa LecA. Antibacterial agent 130 shows high affinity toward LecA (Kd=1 μM). Antibacterial agent 130 has antibiofilm activity, but lacks bactericidal activity. LecA, a lectin and virulence factor from Pseudomonas aeruginosa involved in bacterial adhesion and biofilm formation .
|
-
-
- HY-144643
-
|
Fungal
HDAC
Cytochrome P450
|
Inflammation/Immunology
|
CYP51/HDAC-IN-1 is a potent, orally active CYP51/HDAC dual inhibitor. CYP51/HDAC-IN-1 inhibits important virulence factors and down-regulated resistance-associated genes. CYP51/HDAC-IN-1 exhibits potent therapeutic effects for both tropical candidiasis and cryptococcal meningitis .
|
-
-
- HY-N7118
-
|
Bacterial
Antibiotic
|
Infection
Cancer
|
Clindamycin hydrochloride monohydrate is an oral protein synthesis inhibitory agent that has the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin hydrochloride monohydrate resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin hydrochloride monohydrate decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla) .
|
-
-
- HY-P99583
-
MEDI4893
|
Bacterial
|
Infection
Inflammation/Immunology
|
Suvratoxumab (MEDI4893) is a long-acting, high-affinity human anti-α-toxin monoclonal antibody (IgG1κ type). Suvratoxumab potently neutralizes α-toxin, a key S. aureus virulence factor. Suvratoxumab improves survival and reduces lung injury in an immunocompromised mice model of pneumonia. Suvratoxumab also enhances the antibacterial activity of Vancomycin (HY-B0671) or Linezolid (HY-10394) .
|
-
-
- HY-124469
-
|
Bacterial
|
Infection
|
UM-C162, a benzimidazole derivative, can rescue nematodes from a S. aureus infection. UM-C162 prevents the formation of biofilm without interfering with bacterial viability. UM-C162 mediates the disruption of i>S. aureus hemolysins, proteases and clumping factors production. UM-C162 has the potential to be used as an anti-virulence agent to control i>S. aureus infections .
|
-
-
- HY-134922
-
|
Influenza Virus
|
Infection
|
NS1-IN-1 (compound 3) is a potent NS1 inhibitor. NS1 is a major influenza A virus virulence factor that inhibits host gene expression. NS1-IN-1 decreases viral protein levels, contributing to the reduction of virus replication. NS1-IN-1 shows antiviral activity by repressing the activity of mTORC1 in a TSC1-TSC2-dependent manner .
|
-
-
- HY-164173
-
|
Toll-like Receptor (TLR)
MyD88
|
Inflammation/Immunology
|
LPS-PG is a lipopolysaccharide from Porphyromonas gingivalis (P. gingivalis). LPS-PG is an important virulence factor in the pathogenesis of periodontal disease and activates immune cells via Toll-like receptor 2 (TLR2), rather than the receptor for Escherichia coli (E. coli), Toll-like receptor 4 (TLR4). A lipoprotein from LPS-PG has been shown to be the major component responsible for TLR2-mediated cell activation .
|
-
-
- HY-144694
-
|
HSP
HDAC
Fungal
|
Infection
|
HDAC/HSP90-IN-3 (compound J5) is a potent and selective fungal Hsp90 and HDAC dual inhibitor, with IC50 values of 0.83 and 0.91 μM, respectively. HDAC/HSP90-IN-3 shows antifungal activity against azole resistant C. albicans. HDAC/HSP90-IN-3 can suppress important virulence factors and down-regulate drug-resistant genes ERG11 and CDR1 .
|
-
-
- HY-N7118R
-
|
Bacterial
Antibiotic
|
Infection
Cancer
|
Clindamycin (hydrochloride monohydrate) (Standard) is the analytical standard of Clindamycin (hydrochloride monohydrate). This product is intended for research and analytical applications. Clindamycin hydrochloride monohydrate is an oral protein synthesis inhibitory agent that has the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin hydrochloride monohydrate resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin hydrochloride monohydrate decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla) .
|
-
-
- HY-B1455
-
Clindamycin
Maximum Cited Publications
7 Publications Verification
|
Bacterial
Antibiotic
Parasite
|
Infection
Cancer
|
Clindamycin is an orally active and broad-spectrum bacteriostatic lincosamide antibiotic. Clindamycin can inhibit bacterial protein synthesis, possessing the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla). Clindamycin also can be used for researching malaria .
|
-
-
- HY-B1455S
-
|
Bacterial
Antibiotic
Parasite
|
Infection
|
Clindamycin-d3 (hydrochloride) is the deuterium labeled Clindamycin. Clindamycin is an orally active and broad-spectrum bacteriostatic lincosamide antibiotic. Clindamycin can inhibit bacterial protein synthesis, possessing the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla). Clindamycin also can be used for researching malaria[1][2].
|
-
-
- HY-B1455R
-
|
Bacterial
Antibiotic
Parasite
|
Infection
Cancer
|
Clindamycin (Standard) is the analytical standard of Clindamycin. This product is intended for research and analytical applications. Clindamycin is an orally active and broad-spectrum bacteriostatic lincosamide antibiotic. Clindamycin can inhibit bacterial protein synthesis, possessing the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla). Clindamycin also can be used for researching malaria .
|
-
-
- HY-B1455S1
-
|
Isotope-Labeled Compounds
Bacterial
Antibiotic
Parasite
|
Infection
|
Clindamycin- 13C,d3 is the 13C- and deuterium labeled Clindamycin. Clindamycin is an orally active and broad-spectrum bacteriostatic lincosamide antibiotic. Clindamycin can inhibit bacterial protein synthesis, possessing the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla). Clindamycin also can be used for researching malaria[1][2][3].
|
-
-
- HY-114773
-
|
Biochemical Assay Reagents
|
Others
|
Quorum sensing is a regulatory system used by bacteria to control gene expression in response to increased cell density. This regulatory process manifests itself in a variety of phenotypes, including biofilm formation and virulence factor production. Coordinated gene expression is achieved through the production, release and detection of small diffusible signaling molecules called autoinducers. N-acylated homoserine lactones (AHLs) comprise a class of such autoinducers, each of which generally consists of a fatty acid coupled to a homoserine lactone (HSL). Modulation of bacterial quorum-sensing signaling systems to suppress pathogenesis represents a new approach to antimicrobial research for infectious diseases. AHLs differ in acyl length (C4-C18), C3 substitution (hydrogen, hydroxyl, or oxo group), and the presence or absence of one or more carbon-carbon double bonds in the fatty acid chain. These differences confer signaling specificity through the affinity of the LuxR family of transcriptional regulators. C11-HSL has a rare odd-numbered acyl carbon chain and may be a minor quorum-sensing signaling molecule in Pseudomonas aeruginosa strains.
|
-
-
- HY-W127393
-
|
Biochemical Assay Reagents
|
Others
|
Quorum sensing is a regulatory system used by bacteria to control gene expression in response to increased cell density. This regulatory process manifests itself in a variety of phenotypes, including biofilm formation and virulence factor production. Coordinated gene expression is achieved through the production, release and detection of small diffusible signaling molecules called autoinducers. N-acylated homoserine lactones (AHLs) comprise a class of such autoinducers, each of which generally consists of a fatty acid coupled to a homoserine lactone (HSL). Modulation of bacterial quorum-sensing signaling systems to suppress pathogenesis represents a new approach to antimicrobial research for infectious diseases. AHLs differ in acyl length (C4-C18), C3 substitution (hydrogen, hydroxyl, or oxo group), and the presence or absence of one or more carbon-carbon double bonds in the fatty acid chain. These differences confer signaling specificity through the affinity of the LuxR family of transcriptional regulators. C9-HSL is a rare odd-numbered acyl carbon chain produced by wild-type Erwinia carotovora strain SCC 3193 grown in nutrient-rich Luria-Bertani broth (LB) medium.
|
-
-
- HY-W127487
-
|
Biochemical Assay Reagents
|
Others
|
Quorum sensing is a regulatory system used by bacteria to control gene expression in response to increased cell density. This regulatory process manifests itself in a variety of phenotypes, including biofilm formation and virulence factor production. Coordinated gene expression is achieved through the production, release and detection of small diffusible signaling molecules called autoinducers. N-acylated homoserine lactones (AHLs) comprise a class of such autoinducers, each of which generally consists of a fatty acid coupled to a homoserine lactone (HSL). Modulation of bacterial quorum-sensing signaling systems to suppress pathogenesis represents a new approach to antimicrobial research for infectious diseases. AHLs differ in acyl length (C4-C18), C3 substitution (hydrogen, hydroxyl, or oxo group), and the presence or absence of one or more carbon-carbon double bonds in the fatty acid chain. These differences confer signaling specificity through the affinity of the LuxR family of transcriptional regulators. C18-HSL, one of four lipophilic long acyl side chain AHLs produced by the LuxI AHL synthase homolog SinI, is involved in quorum-sensing signaling in strains of Rhizobium meliloti (a nitrogen-fixing bacterial symbiont of the legume M. sativa) . C18-HSL and other hydrophobic AHLs tend to localize in the relatively lipophilic environment of bacterial cells and cannot diffuse freely across the cell membrane. Long-chain N-acyl homoserine lactones can be exported from cells by efflux pumps, or can be transported between communicating cells by extracellular outer membrane vesicles.
|
-
Cat. No. |
Product Name |
Type |
-
- HY-114773
-
|
Microbial Culture
|
Quorum sensing is a regulatory system used by bacteria to control gene expression in response to increased cell density. This regulatory process manifests itself in a variety of phenotypes, including biofilm formation and virulence factor production. Coordinated gene expression is achieved through the production, release and detection of small diffusible signaling molecules called autoinducers. N-acylated homoserine lactones (AHLs) comprise a class of such autoinducers, each of which generally consists of a fatty acid coupled to a homoserine lactone (HSL). Modulation of bacterial quorum-sensing signaling systems to suppress pathogenesis represents a new approach to antimicrobial research for infectious diseases. AHLs differ in acyl length (C4-C18), C3 substitution (hydrogen, hydroxyl, or oxo group), and the presence or absence of one or more carbon-carbon double bonds in the fatty acid chain. These differences confer signaling specificity through the affinity of the LuxR family of transcriptional regulators. C11-HSL has a rare odd-numbered acyl carbon chain and may be a minor quorum-sensing signaling molecule in Pseudomonas aeruginosa strains.
|
-
- HY-W127393
-
|
Biochemical Assay Reagents
|
Quorum sensing is a regulatory system used by bacteria to control gene expression in response to increased cell density. This regulatory process manifests itself in a variety of phenotypes, including biofilm formation and virulence factor production. Coordinated gene expression is achieved through the production, release and detection of small diffusible signaling molecules called autoinducers. N-acylated homoserine lactones (AHLs) comprise a class of such autoinducers, each of which generally consists of a fatty acid coupled to a homoserine lactone (HSL). Modulation of bacterial quorum-sensing signaling systems to suppress pathogenesis represents a new approach to antimicrobial research for infectious diseases. AHLs differ in acyl length (C4-C18), C3 substitution (hydrogen, hydroxyl, or oxo group), and the presence or absence of one or more carbon-carbon double bonds in the fatty acid chain. These differences confer signaling specificity through the affinity of the LuxR family of transcriptional regulators. C9-HSL is a rare odd-numbered acyl carbon chain produced by wild-type Erwinia carotovora strain SCC 3193 grown in nutrient-rich Luria-Bertani broth (LB) medium.
|
-
- HY-W127487
-
|
Drug Delivery
|
Quorum sensing is a regulatory system used by bacteria to control gene expression in response to increased cell density. This regulatory process manifests itself in a variety of phenotypes, including biofilm formation and virulence factor production. Coordinated gene expression is achieved through the production, release and detection of small diffusible signaling molecules called autoinducers. N-acylated homoserine lactones (AHLs) comprise a class of such autoinducers, each of which generally consists of a fatty acid coupled to a homoserine lactone (HSL). Modulation of bacterial quorum-sensing signaling systems to suppress pathogenesis represents a new approach to antimicrobial research for infectious diseases. AHLs differ in acyl length (C4-C18), C3 substitution (hydrogen, hydroxyl, or oxo group), and the presence or absence of one or more carbon-carbon double bonds in the fatty acid chain. These differences confer signaling specificity through the affinity of the LuxR family of transcriptional regulators. C18-HSL, one of four lipophilic long acyl side chain AHLs produced by the LuxI AHL synthase homolog SinI, is involved in quorum-sensing signaling in strains of Rhizobium meliloti (a nitrogen-fixing bacterial symbiont of the legume M. sativa) . C18-HSL and other hydrophobic AHLs tend to localize in the relatively lipophilic environment of bacterial cells and cannot diffuse freely across the cell membrane. Long-chain N-acyl homoserine lactones can be exported from cells by efflux pumps, or can be transported between communicating cells by extracellular outer membrane vesicles.
|
Cat. No. |
Product Name |
Target |
Research Area |
-
- HY-W141788
-
|
Peptides
|
Infection
|
N-Butyryl-DL-homocysteine thiolactone is an N-acyl homoserine lactone (AHL) analogue. AHLs are potent inhibitors of biofilm formation and virulence factors, and has been used for degrading microbial communities, reducing bacterial pathogenicity .
|
-
- HY-P5481
-
|
Peptides
|
Others
|
DABCYL-LPETG-EDANS is a biological active peptide. (This 5-amino acid peptide is a sortase substrate, C-terminal sorting signal. Sortase cleaves surface proteins at the LPXTG motif and catalyzes the formation of an amide bond between the carboxyl group of threonine and the amino group of cell-wall crossbridges. Sortases are a family of Gram-positive transpeptidases responsible for anchoring surface protein virulence factors to the peptidoglycan cell wall layer. Cleavage of this FRET substrate by sortase reveals the fluorescent signal, Abs/Em = 340/490 nm.)
|
Cat. No. |
Product Name |
Target |
Research Area |
-
- HY-P99583
-
MEDI4893
|
Bacterial
|
Infection
Inflammation/Immunology
|
Suvratoxumab (MEDI4893) is a long-acting, high-affinity human anti-α-toxin monoclonal antibody (IgG1κ type). Suvratoxumab potently neutralizes α-toxin, a key S. aureus virulence factor. Suvratoxumab improves survival and reduces lung injury in an immunocompromised mice model of pneumonia. Suvratoxumab also enhances the antibacterial activity of Vancomycin (HY-B0671) or Linezolid (HY-10394) .
|
Cat. No. |
Product Name |
Category |
Target |
Chemical Structure |
Cat. No. |
Product Name |
Chemical Structure |
-
- HY-B1455S1
-
|
Clindamycin- 13C,d3 is the 13C- and deuterium labeled Clindamycin. Clindamycin is an orally active and broad-spectrum bacteriostatic lincosamide antibiotic. Clindamycin can inhibit bacterial protein synthesis, possessing the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla). Clindamycin also can be used for researching malaria[1][2][3].
|
-
-
- HY-B1455S
-
|
Clindamycin-d3 (hydrochloride) is the deuterium labeled Clindamycin. Clindamycin is an orally active and broad-spectrum bacteriostatic lincosamide antibiotic. Clindamycin can inhibit bacterial protein synthesis, possessing the ability to suppress the expression of virulence factors in Staphylococcus aureus at sub-inhibitory concentrations (sub-MICs). Clindamycin resistance results from enzymatic methylation of the antibiotic binding site in the 50S ribosomal subunit (23S rRNA). Clindamycin decreases the production of Panton-Valentine leucocidin (PVL), toxic-shock-staphylococcal toxin (TSST-1) or alpha-haemolysin (Hla). Clindamycin also can be used for researching malaria[1][2].
|
-
Your information is safe with us. * Required Fields.
Inquiry Information
- Product Name:
- Cat. No.:
- Quantity:
- MCE Japan Authorized Agent: