Lydimycin
Lydimycin (α-DHB; α-Dehydrobiotin) is an antibiotic produced by Streptomyces lydicus, with antibacterial, antifungal and antiviral activities. Lydimycin inhibits the binding of SARS-CoV-2 S-614G spike protein to human ACE2. The antibacterial activity of Lydimycin can be reversed by Biotin (HY-B0511) in the culture medium. Lydimycin is applicable to infection-related research.
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- CAS. Nr.: 10118-85-1
- Formel: C10H14N2O3S
- Molecular Weight:242.29
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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
IC50 & Target
Bacterial[1]
In Vitro
Lydimycin (compound Ⅰ) displays broad-spectrum in vitro antimicrobial activity against diverse gram-positive bacteria, gram-negative bacteria, and fungi[1].
Lydimycin (1.25-20.0 μg) inhibits Escherichia coli growth in a synthetic medium in a dose-dependent manner, with its antibacterial activity reversed by increasing concentrations of biotin, showing no inhibition at 0.100 μg/mL Biotin (HY-B0511) across all tested doses[1].
Lydimycin (0-200 μM) inhibits the binding of SARS-CoV-2 S-614G-Strep spike protein to human ACE2-Fc with an IC50 of 1.6 μM, without non-specific Alpha signal interference[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS. Nr. 10118-85-1
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Molecular Weight 242.29
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Formel C10H14N2O3S
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SMILES
C(C/C=C/C(O)=O)[C@H]1[C@@]2([C@@](NC(=O)N2)(CS1)[H])[H]
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Synonyms
α-DHB; α-Dehydrobiotin
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Structure Classification
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Initial Source
Streptomyces lydicus
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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.
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Bacterial live/dead nucleic-acid viability staining
The LIVE/DEAD bacterial viability staining method is based on differential permeability of nucleic-acid-binding fluorescent dyes, most commonly SYTO 9 and propidium iodide (PI), which enables discrimination of bacterial populations with intact versus compromised cytoplasmic membranes. SYTO 9 penetrates both intact and damaged bacterial membranes and binds nucleic acids to produce green fluorescence, whereas propidium iodide penetrates only cells with compromised membranes and fluoresces red while also reducing SYTO 9 signal through competitive binding and fluorescence interactions. The resulting fluorescence pattern is interpreted as a proxy for membrane integrity, which is widely used as an indicator of bacterial viability in microscopy, flow cytometry, and spectroscopic platforms. However, mechanistic studies show that SYTO 9 and PI interactions involve displacement and fluorescence resonance energy transfer effects, which can influence signal interpretation depending on dye ratios a
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)