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.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- CAS 番号: 612547-11-2
- 分子式: C33H44N4O6S
- 分子量:624.79
-
保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
生物活性
製品説明
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] |
化学情報
-
CAS 番号 612547-11-2
-
分子量 624.79
-
分子式 C33H44N4O6S
-
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
-
輸送条件
Room temperature in continental US; may vary elsewhere.
-
保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
-
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.
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)