L-731988
L-731988 is an inhibitor targeting HIV-1 integrase. L-731988 inhibits HIV-1 replication by blocking integrase function. L-731988 exhibits ED50 values ranging from 0.5 μM to 3.14 μM against various HIV-1 isolates. L-731988 can be used for the research of human immunodeficiency virus type 1 (HIV-1) infection.
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- CAS No.: 251922-77-7
- 화학식: C15H12FNO4
- 분자량:289.26
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocol
- 순도&문서
- References
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Help & FAQs
Biological Activity
제품 설명
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HCT-116 | CC50 |
10 μM
Compound: L-731988
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Cytotoxicity against human HCT116 cells expressing p53 after 72 hrs by MTT assay
Cytotoxicity against human HCT116 cells expressing p53 after 72 hrs by MTT assay
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[PMID: 19026554] |
In Vitro
L-731988 (0.5-5.0 μM) suppresses RT activity of HIV-1 primary isolates in PBLs in a dose-dependent manner[1].
L-731988 inhibits replication of diverse primary HIV-1 isolates in PBLs, with ED50 values ranging from 0.544 to 3.14 μM; most isolates show less-than-twofold differences in susceptibility relative to HIVLAI, while HIV92RW009 exhibits a sixfold reduction in susceptibility[1].
L-731988 inhibits HIV-1 replication in MT-2 cells with ED50 values ranging from 0.505 to 1.6 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. 251922-77-7
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분자량 289.26
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화학식 C15H12FNO4
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SMILES
O=C(C(CC(C1=CC=CN1CC2=CC=C(C=C2)F)=O)=O)O
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
L-731988 Related Classifications
HY-182678 Related Classifications
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