JNJ-2901
JNJ-2901 is an inhibitor of M. tuberculosis cytochrome bc1:aa3. JNJ-2901 reduces bacterial load in the acute/chronic mouse infection models of M. tuberculosis H37Rv-ΔcydAB. JNJ-2901 can be used in tuberculosis (TB) research.
For research use only. We do not sell to patients.
- CAS No.: 2059985-55-4
- Formula: C24H24ClF3N4O3S
- Molecular Weight:540.99
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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
JNJ-2901 (0.005 µM-5 mM, 5 d) inhibits the growth of M. tuberculosis H37Rv-ΔcydAB in 7H9 medium (MIC50: 2.5 nM)[1].
JNJ-2901 inhibits oxygen consumption by the wild-type strain (IC50: 89 nM) and the cytochrome bd knockout strain (ΔcydAB) (IC50: 60 nM) of M. smegmatis, but has no significant effect on the cytochrome bc knockout strain (ΔqcrCAB)[1].
JNJ-2901 inhibits oxygen consumption by M. smegmatis cytochrome bcMtb-like (IC50: 17.4 nM)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Acute/chronic mouse model infected with M. tuberculosis H37Rv-ΔcydAB, 6-8 weeks old female Balb/cBy mice[1].
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Dosage:10 mg/kg
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Administration:Subcutaneous injection (s.c.), 12 d for acute infection and 8 weeks for chronic infection
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Result:Reduced bacterial load in an acute infection model in mice (3.6-log) and in a chronic infection model (4.0-log).
Chemical Information
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CAS No. 2059985-55-4
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Molecular Weight 540.99
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Formula C24H24ClF3N4O3S
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SMILES
CCC1=C(N2C=C(C=CC2=N1)Cl)C(NCC3=CC=C(C=C3)C4CC5(CN(C5)S(=O)(C(F)(F)F)=O)C4)=O
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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)
JNJ-2901 Related Classifications
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