Piperazinomycin
Piperazinomycin is an antifungal and antibacterial antibiotic. Piperazinomycin is isolated from the culture broth of Streptoverticillium olivoreticuli subsp. neoenacticus. Piperazinomycin inhibits the growth of fungi, yeasts and some Mycobacterium species. Piperazinomycin exhibits inhibitory activity against Trichophyton species.
For research use only. We do not sell to patients.
- CAS No.: 83858-82-6
- Formula: C18H20N2O2
- Molecular Weight:296.36
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Antibiotic Isoforms
More
Biological Activity
Description
In Vitro
Piperazinomycin inhibits the growth of certain fungi, yeasts and bacteria, with an MIC of 3.12 μg/mL against Trichophyton mentagrophytes 833 and an MIC of 6.25 μg/mL against Trichophyton asteroides 429[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. 83858-82-6
-
Molecular Weight 296.36
-
Formula C18H20N2O2
-
SMILES
OC1=CC=C2C=C1OC3=CC=C(C=C3)C[C@](CN4)([H])NC[C@]4([H])C2
-
Structure Classification
-
Initial Source
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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)