EM-163
Based on 1 Customer Validation
EM-163 is a summative BB-Loop analog. EM-163 can alleviate inflammation and prevent death from toxic shock by targeting the TIR domain of MyD88. EM-163 can be used in the study of SEB poisoning (SEB: Staphylococcal enterotoxin B).
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 : 95.0%
- CAS 番号: 1206480-93-4
- 分子式: C44H60IN5O4
- 分子量:849.88
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保管条件:
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
生物活性
製品説明
体外実験
EM-163 (50-100 μg/mL) can target the TIR domain, binding to the protein of the TIR domain and inhibit the interaction of the TIR-TIR domain [1].
EM-163 (10-500 μM; 30 min) inhibits the production of TNF-α, IFN-γ, IL-2 and IL-1b induced by SEB (200 ng/mL) in human mononuclear cells (MNS) [1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
体内実験
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:SEB-induced BALB/c mice model [1]
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Dosage:0.21 mg/mouse, 0.42 mg/mouse, 0.86 mg/mouse
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Administration:Intraperitoneal injection (i.p.); Single dose. Before SEB treatment (0.5 μg/mouse, 5 μg/mouse; i.p.; single dose) and LPS treatment.
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Result:Delayed mouse death at a dose of 0.21 mg/mouse, and protected mice from death at either dose of 0.42 mg/mouse or 0.86 mg/mouse.
Delayed mouse death even at high doses of SEB (5 μg).
化学情報
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CAS 番号 1206480-93-4
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性状 Solid
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分子量 849.88
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分子式 C44H60IN5O4
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Color Brown to dark brown
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SMILES
O=C(N1CCCC1)[C@H](C(C)C)N(CCCC2=CC=CC=C2)C(C3=C[N+](C)=C(C=C3)C(N(CCCC4=CC=CC=C4)[C@@H](C(C)C)C(N5CCCC5)=O)=O)=O.[I-]
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
プロトコル
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
純度とドキュメンテーション
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データシート (274 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 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)