CppA-IN-1
CppA-IN-1 is a CppA inhibitor specific to Chlamydia trachomatis, which inhibits the growth of Chlamydia trachomatis. CppA-IN-1 shows no activity against recombinant CppA in vitro. CppA-IN-1 can be used in studies related to Chlamydia trachomatis infection.
For research use only. We do not sell to patients.
- CAS No.: 28505-57-9
- Formula: C17H16O6
- Molecular Weight:316.31
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
CppA-IN-1 (compound 3) (18.2 μM) does not inhibit the phosphatase activity of purified recombinant Chlamydia trachomatis CppA[1].
CppA-IN-1 (50 μM) does not inhibit Chlamydia trachomatis infection in HeLa cells, as measured by inclusion forming unit production[1].
CppA-IN-1 does not form critical interactions with residues R166 and/or N167 of the Chlamydia trachomatis CppA homology model, correlating with its lack of in vitro CppA inhibitory activity[1].
CppA-IN-1 (50 μM) is non-cytotoxic to HeLa human cervical cancer cells, with >90% cell viability maintained[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 28505-57-9
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Molecular Weight 316.31
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Formula C17H16O6
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SMILES
O=C(OC)C1=CC(CC2=CC=C(O)C(C(OC)=O)=C2)=CC=C1O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
CppA-IN-1 Related Classifications
HY-181614 Related Classifications
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