3-Deoxyanguibactin
3-Deoxyanguibactin is a siderophore and Fe(III) chelator/iron delivery agent. 3-Deoxyanguibactin binds Fe(III) with 2:1 stoichiometry in liquid phase, delivers iron into Acinetobacter baumannii cells, and relies on the BauA outer membrane receptor and bau transport system for cellular entry. 3-Deoxyanguibactin can be used for the research of acinetobacter baumannii infection.
Nos produits utilisent uniquement pour la recherche. Nous ne vendons pas aux patients.
- CAS No.: 2247437-94-9
- Formule: C15H16N4O3S
- Masse moléculaire:332.38
-
Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
In Vitro
3-Deoxyanguibactin (100 μM) forms a Fe3+-complex that induces characteristic absorption and fluorescence spectral changes, with efficient fluorescence quenching observed upon Fe3+ binding[1].
3-Deoxyanguibactin (0.1-25 μM) stimulates growth of iron-deficient Acinetobacter baumannii ΔbasD, with moderate activity retained at single-digit micromolar ranges[1].
3-Deoxyanguibactin (0.1-25 μM) does not stimulate growth of iron-deficient Acinetobacter baumannii ΔbauA, demonstrating iron delivery dependence on the BauA outer membrane receptor[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
-
CAS No. 2247437-94-9
-
Masse moléculaire 332.38
-
Formule C15H16N4O3S
-
SMILES
OC1=C(C=CC=C1)C2=N[C@@H](CS2)C(N(O)CCC3=CN=CN3)=O
-
Livraison
Room temperature in continental US; may vary elsewhere.
-
Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
-
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.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)