Carmaphycin-17
Carmaphycin-17 (CP-17) is a selective 20S proteasome inhibitor with an EC50 of 217 ?nM. Carmaphycin-17 has potent antimicrobial activity against Trichomonas vaginalis. Carmaphycin-17 overcomes Metronidazole (HY-B0318) resistance and significantly reduces parasite burden upon topical treatment without any apparent adverse effects in vaginal trichomonad infection mice model. Carmaphycin-17 can be used for sexually transmitted disease like trichomoniasis research.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 2143080-91-3
- Formel: C40H45N5O5
- Molecular Weight:675.82
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
Beschreibung
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HepG2 | IC50 |
346 nM
Compound: 17
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Cytotoxicity against human HepG2 cells harboring A16-CD81EGFP assessed as cell viability after 48 hrs by bioluminescence assay
Cytotoxicity against human HepG2 cells harboring A16-CD81EGFP assessed as cell viability after 48 hrs by bioluminescence assay
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[PMID: 28696697] |
Chemical Information
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CAS. Nr. 2143080-91-3
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Molecular Weight 675.82
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Formel C40H45N5O5
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SMILES
O=C([C@]1(CO1)C)[C@H](CC2=CC=CC=C2)NC([C@@H](NC([C@@H](NC(CCCCC)=O)CC3=CNC4=CC=CC=C34)=O)CC5=CNC6=CC=CC=C56)=O
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)