KSK120
KSK120 is a potent inhibitor of drug-resistant infections with specific activity against Chlamydia trachomatis (C. trachomatis). KSK120 inhibits the developmental cycle of C. trachomatis, thereby reducing the infectivity of progeny bacteria. KSK120 targets the glucose-6-phosphate (G-6P) metabolic pathway of C. trachomatis, showing its potential application in antimicrobial inhibition. The mechanism of KSK120 may involve inhibition of the transcriptional machinery, which provides new ideas for the development of specific drugs against C. trachomatis infection.
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- CAS No.: 1638100-63-6
- 화학식: C28H22N2O2S
- 분자량:450.55
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HeLa | EC50 |
1.25 μM
Compound: 1; KSK 120
|
Antimicrobial activity against Chlamydia trachomatis serovar LGV-L2 infected in human HeLa cells measured 44 to 48 hrs post infection by DAPI staining-based assay
Antimicrobial activity against Chlamydia trachomatis serovar LGV-L2 infected in human HeLa cells measured 44 to 48 hrs post infection by DAPI staining-based assay
|
[PMID: 26849778] |
| HeLa | EC50 |
254 nM
Compound: 1; KSK 120
|
Antimicrobial activity against Chlamydia trachomatis serovar LGV-L2 infected in human HeLa cells assessed as decrease in relative inclusion forming units measured 44 to 48 hrs post infection by DAPI staining-based assay
Antimicrobial activity against Chlamydia trachomatis serovar LGV-L2 infected in human HeLa cells assessed as decrease in relative inclusion forming units measured 44 to 48 hrs post infection by DAPI staining-based assay
|
[PMID: 26849778] |
Chemical Information
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CAS No. 1638100-63-6
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분자량 450.55
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화학식 C28H22N2O2S
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SMILES
O=C(C=C1CC2=CC=CC3=C2C=CC=C3)N4C(C(NC5=CC=CC=C5)=O)=CSC4=C1C6CC6
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)