CI-39
CI-39 is an antiviral natural product. CI-39 is an NNRTI (non-nucleoside reverse transcriptase inhibit) antiviral agent with an EC50 of 3.40 μM and an CC50 of >30 μM for wild type HIV-1. CI-39 inhibits HIV-1 RT DNA polymerase and ribonuclease H activitiessup.
For research use only. We do not sell to patients.
- CAS No.: 2132412-25-8
- Formula: C19H18N2O4
- Molecular Weight:338.36
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All DNA/RNA Synthesis Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
HIV-1 (WT) 3.40 μM (EC50) |
DNA Polymerase |
HIV-1 (WT) >30 μM (CC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| HEK-293T | CC50 |
>30 μM
Compound: Cl-39
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Cytotoxicity against human HEK 293T cells assessed as reduction in cell viability measured after 48 hrs by Celltiter-glo assay
Cytotoxicity against human HEK 293T cells assessed as reduction in cell viability measured after 48 hrs by Celltiter-glo assay
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[PMID: 32004936] |
In Vitro
CI-39 (0-100 μM) inhibits HIV-1 RT DNA polymerase and ribonuclease H activities with EC50s of 7.20, >30 μM, respectively[1].
CI-39 shows antiviral activities with EC50s of 3.37, 3.00, 2.41, 3.08, 2.14, 3.27, 3.19, 4.07 μM for VSVG/HIV-1wt, VSVG/HIV-1RT-K103N, VSVG/HIV-1wtRT-K103N, VSVG/HIV-1RT-K1RT-Y181C, VSVG/HIV-1RT-K1RT-K103N,Y181C, VSVG/HIV-1RT-K103N,Y181C, VSVG/HIV-1RT-L100I,K103N, VSVG/HIV-1RT-Y188L, VSVG/HIV-1RT-K103N,G190A, VSVG/HIV-1RT-K103N,V108I, respectively[1].
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 No. 2132412-25-8
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Molecular Weight 338.36
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Formula C19H18N2O4
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SMILES
O=C(CC1=CN(C2=C1C=CC=C2)OC)NC3=C(C(OC)=O)C=CC=C3
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Structure Classification
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Initial Source
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)