HIV-1 inhibitor-55
HIV-1 inhibitor-55 (compound 4d) inhibits WT HIV-1 with an EC50 value of 8.6 nM. HIV-1 inhibitor-55 also shows inhibitory potency against single and double HIV-1 mutants. HIV-1 inhibitor-55 can be used for the research of virus infection.
For research use only. We do not sell to patients.
- CAS No.: 2771211-73-3
- Formula: C28H32N6O4S
- Molecular Weight:548.66
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| MT4 | CC50 |
19 μM
Compound: 4d
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Cytotoxicity against human MT4 cells assessed as reduction in cell viability incubated for 5 days by MTT spectrophotometric assay
Cytotoxicity against human MT4 cells assessed as reduction in cell viability incubated for 5 days by MTT spectrophotometric assay
|
[PMID: 36640458] |
In Vitro
HIV-1 inhibitor-55 shows inhibitory potency against WT HIV-1 with an EC50 value of 8.6 nM[1]. HIV-1 inhibitor-55 shows potent activities against reverse transcriptase (RT) HIV-1 mutants L100I, K103N, Y181C, Y188L, E138K and F227L + V106A with EC50 values of 1.1, 0.12, 0.36, 0.75, 0.033 and 3.06 μM, respectively[1]. HIV-1 inhibitor-55 inhibits WT HIV-1 RT activity with an IC50 value of 0.11 μM[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. 2771211-73-3
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Molecular Weight 548.66
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Formula C28H32N6O4S
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SMILES
CC1=CC(C)=C(C(C)=C1)OC2=CC=NC(NC3CCN(CC3)C(C4=CC5=C(N4)C=CC(NS(C)(=O)=O)=C5)=O)=N2
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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)