Monocillin IV
Monocillin IV is a macrolide with antibacterial and anti-HIV-1 activities, originally isolated and identified from the metabolites of Monocillium nordinii. Monocillin IV is an inhibitor of HIV-1 Tat protein transactivation, with an IC50 of 5.0 µM. Monocillin IV inhibits HIV-1 viral replication by blocking the Tat transactivation pathway. Monocillin IV exhibits moderate antibacterial activity, with an MIC of 25.6 µg/mL against Xanthomonas campestris pv. campestris . Monocillin IV can be used for research on black rot and HIV-1 infection.
For research use only. We do not sell to patients.
- CAS No.: 75207-14-6
- Formula: C18H22O5
- Molecular Weight:318.36
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Endogenous Metabolite Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
HIV-1 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| Jurkat | IC50 |
5.0 μM
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Inhibition of HIV-1 Tat-dependent transactivation in Jurkat-derived 63A9 cells harboring integrated HIV-1 provirus luciferase reporter incubated 24 hrs by luciferase assay.
Inhibition of HIV-1 Tat-dependent transactivation in Jurkat-derived 63A9 cells harboring integrated HIV-1 provirus luciferase reporter incubated 24 hrs by luciferase assay.
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17191924 |
| Jurkat | IC50 |
>100 μM
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Cytotoxicity against human Jurkat cells assessed as viability reduction by MTS assay.
Cytotoxicity against human Jurkat cells assessed as viability reduction by MTS assay.
|
17191924 |
| HeLa | IC50 |
6.2 μM
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Antiviral activity against HIV H9IIIb in P4/P5 HeLa cells containing integrated LTR-LacZ reporter assessed by β-gal substrate after 48 hrs incubation.
Antiviral activity against HIV H9IIIb in P4/P5 HeLa cells containing integrated LTR-LacZ reporter assessed by β-gal substrate after 48 hrs incubation.
|
17191924 |
In Vitro
Monocillin IV (0.4-204.8 µg/mL; 24 h) inhibits the growth of Xanthomonas campestris pv. campestris, with an MIC of 25.6 µg/mL[1].
Monocillin IV (1.25-10 mg/mL; 24 h) shows no activity against Meloidogyne incognita J2s and exhibited no nematicidal effect above 1,000 μg/mL[2].
Monocillin IV (up to 100 μM; 24 h) inhibits HIV-1 Tat-dependent transactivation in Jurkat-derived 63A9 cells with an IC50 of 5 µM[4].
Monocillin IV (up to 100 μM) exhibits no significant cytotoxicity in the Jurkat-derived cell line (63A9) (IC50 >100 µM)[4].
Monocillin IV (48 h) exhibits antiviral activity against single-cycle HIV viral replication in P4/P5 Hela cells expressing CD4 and CCR5, with an IC50 of 6.2 µM[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Xanthomonas campestris pv. campestris
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Concentration:Two-fold serial dilution concentration gradient from 204.8 µg/mL to 0.4 µg/mL
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Incubation Time:24 h
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Result:Exhibited modest inhibitory effects against Xanthomonas campestris, with MIC of 25.6 µg/mL.
Chemical Information
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CAS No. 75207-14-6
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Molecular Weight 318.36
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Formula C18H22O5
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SMILES
OC1=C2C(CC(CCCC/C=C/C[C@H](OC2=O)C)=O)=CC(O)=C1
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Structure Classification
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Initial Source
Monocillium nordinii
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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.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)