PL-100
PL-100 is a potent HIV-1 protease inhibitor with a Ki of 36 pM and an EC50 of 16 nM. PL-100 inhibits viral replication by suppressing HIV-1 protease activity and demonstrates excellent antiviral efficacy against drug-resistant HIV strains. PL-100 can be used in research on drug-resistant HIV disease.
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- CAS No.: 612547-11-2
- 화학식: C33H44N4O6S
- 분자량:624.79
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
Cellular Effect
|
Cell Line
|
Type | Value | Description | References |
|---|---|---|---|---|
| HEK293 | EC50 |
5.3 nM
Compound: PL-100
|
Antiviral activity against wild type HIV1 NL4-3 in HEK293 cells after 48 hrs by replication-deffective luciferase reporter gene-based phenotypic assay
Antiviral activity against wild type HIV1 NL4-3 in HEK293 cells after 48 hrs by replication-deffective luciferase reporter gene-based phenotypic assay
|
[PMID: 17638694] |
| MT4 | CC50 |
37 μM
Compound: PL-100
|
Cytotoxicity against human MT4 cells after 6 days by MTT assay
Cytotoxicity against human MT4 cells after 6 days by MTT assay
|
[PMID: 17638694] |
| MT4 | EC50 |
0.016 μM
Compound: PL-100
|
Antiviral activity against wild type HIV1 NL4-3 infected in MT4 cells after 6 days by MTT assay
Antiviral activity against wild type HIV1 NL4-3 infected in MT4 cells after 6 days by MTT assay
|
[PMID: 17638694] |
| MT4 | EC50 |
16 nM
Compound: 13
|
Antiviral activity against HIV1 NL4-3 in MT4 cells
Antiviral activity against HIV1 NL4-3 in MT4 cells
|
[PMID: 16644213] |
Chemical Information
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CAS No. 612547-11-2
-
분자량 624.79
-
화학식 C33H44N4O6S
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SMILES
O=S(N(CC(C)C)[C@H](CO)CCCCNC([C@@H](NC(OC)=O)C(C1=CC=CC=C1)C2=CC=CC=C2)=O)(C3=CC=C(C=C3)N)=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)