MBL-IN-8
MBL-IN-8 is a metallo-β-lactamase (MBL) inhibitor. MBL-IN-8 can be used in research on K. pneumoniae infection.
For research use only. We do not sell to patients.
- CAS No.: 3125906-48-8
- Formula: C19H18FNO4S2
- Molecular Weight:407.48
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
metallo-β-lactamase |
In Vitro
MBL-IN-8 (compound 57) (20 mM stock in DMSO; 10 min preincubation at room temperature) is a broad-spectrum inhibitor of recombinant NDM-1, IMP-1, VIM-1, and VIM-2 with IC50 values of 0.148, 0.478, 0.226, and 0.979 μM, respectively[1].
MBL-IN-8 (compound 57) (3-fold serial dilutions in DMSO; 15 min enzyme incubation at RT) is selective over MMP-1, MMP-2, MMP-8, and MMP-9, with IC50 values >50 μM[1].
MBL-IN-8 (compound 57) (10 μM; 10 min preincubation at 37 °C) weakly inhibits CYP450 isoforms 1A2, 2B6, 2C8, 2C9, 2C19, 2D6, and 3A4, with IC50 values >10 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Udea:ICR (female, 6 weeks old, 25-28 g)[1]
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Dosage:5 mg/kg ; 10 mg/kg
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Administration:i.p.; every 8 h; three doses
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Result:At 10 mg/kg in combination with Meropenem, it showed the most substantial reduction in bacterial burden among the groups.
A dose-dependent trend was observed for MBL-IN-8.
Chemical Information
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CAS No. 3125906-48-8
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Molecular Weight 407.48
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Formula C19H18FNO4S2
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SMILES
CC1=CC=C(S1)C2=C(C(C3=CC=C(C(F)=C3)CS(C)(=O)=O)=C(N2)C(O)=O)C
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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)