Macrocarpal A
Based on 1 Customer Validation
Macrocarpal A (10-epi-Eucarobustol F) is an antibacterial agent, which can be isolated from the leaves of Eucalyptus macrocarpa. Macrocarpal A inhibits the growth of Bacillus subtilis PCI219 (minimum inhibitory concentration below 0.2 µM) and Staphylococcus aureus FDA209P (minimum inhibitory concentration is 0.4 µM).
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。
- 純度 : 99.71%
- CAS 番号: 132951-90-7
- 分子式: C28H40O6
- 分子量:472.61
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保管条件:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
生物活性
製品説明
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| A549 | IC50 |
<10 μM
Compound: Macrocarpal A
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Cytotoxicity against human A549 cells assessed as reduction in cell viability incubated for 72 hrs by SRB assay
Cytotoxicity against human A549 cells assessed as reduction in cell viability incubated for 72 hrs by SRB assay
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[PMID: 27142786] |
| HL-60 | IC50 |
<10 μM
Compound: Macrocarpal A
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Cytotoxicity against human HL60 cells assessed as reduction in cell viability after 72 hrs by MTT assay
Cytotoxicity against human HL60 cells assessed as reduction in cell viability after 72 hrs by MTT assay
|
[PMID: 27142786] |
化学情報
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CAS 番号 132951-90-7
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性状 Solid
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分子量 472.61
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分子式 C28H40O6
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Color White to off-white
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SMILES
CC(C)C[C@@H](C1=C(C(C=O)=C(C(C=O)=C1O)O)O)[C@@]2([C@@]3([H])[C@@]4([H])[C@](CC[C@@](O)([C@]3([H])CC2)C)([H])C4(C)C)C
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別名
10-epi-Eucarobustol F
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Structure Classification
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Initial Source
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
プロトコル
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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.
純度とドキュメンテーション
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データシート (278 KB)
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SDS (254 KB)
- English - EN (254 KB)
- Français - FR (254 KB)
- Deutsch - DE (254 KB)
- Norwegian - NO (254 KB)
- Español - ES (254 KB)
- Swedish - SV (254 KB)
- Italian - IT (254 KB)
- Korean - KR (254 KB)
- Portuguese - PT (254 KB)
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取扱説明書 (2659 KB)
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)