TAK 044
Based on 1 Customer Validation
TAK 044 is an antagonist of Endothelin Receptor. TAK 044 strongly inhibits ET-induced deterioration in various animal models. TAK 044 can be used in study ET-related diseases such as acute myocardial infarction,acute renal failure, acute hepatic malfunction, and subarachnoid hemorrhage.
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 : 96.94%
- CAS 番号: 157380-72-8
- 分子式: C45H51N9Na2O11S
- 分子量:971.98
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保管条件:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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生物活性
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化学情報
- プロトコル
- 純度とドキュメンテーション
- 参考文献
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Help & FAQs
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HY-P0202
Endothelin 1 (swine, human)Vasoconstrictor -
HY-15894A
BQ-788ETB Receptor Antagonist -
HY-12378
BQ-123ETA Receptor Antagonist -
HY-11103
Sitaxsentan sodiumEndothelin A Receptor Antagonist -
HY-15895
AprocitentanEndothelin Receptor Antagonist -
HY-15403
AtrasentanEndothelin Receptor Antagonist -
HY-17352
ClazosentanETA Receptor Antagonist -
HY-15894
BQ-788 sodium saltETB Receptor Antagonist -
HY-15403A
Atrasentan hydrochlorideETA Receptor Antagonist -
HY-17351
TezosentanET Receptor Antagonist -
HY-16465
IRL-1620ETB Agonist -
HY-A0013A
Bosentan hydrateET1 Receptor Antagonist
生物活性
製品説明
化学情報
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CAS 番号 157380-72-8
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性状 Solid
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分子量 971.98
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分子式 C45H51N9Na2O11S
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Color White to off-white
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配列
cyclo({d-Asp}-{α-amino-γ-oxo-4-phenyl-1-piperazinebutanoyl-Asp}-Asp-{d-(2-thienyl)glycine}-Leu-{d-Trp}) (disodium salt)
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シーケンスの短縮
cyclo({d-Asp}-{α-amino-γ-oxo-4-phenyl-1-piperazinebutanoyl-Asp}-D-{d-(2-thienyl)glycine}-L-{d-Trp}) (disodium salt)
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * 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 Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
純度とドキュメンテーション
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データシート (259 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)
TAK 044 関連分類
HY-105168 関連分類
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