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.
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- Pureté : 96.94%
- CAS No.: 157380-72-8
- Formule: C45H51N9Na2O11S
- Masse moléculaire:971.98
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Stockage:
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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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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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
Activité biologique
Description
Chemical Information
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CAS No. 157380-72-8
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Appearance Solid
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Masse moléculaire 971.98
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Formule C45H51N9Na2O11S
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Color White to off-white
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Sequence
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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Sequence Shortening
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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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
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)
Protocole
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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.
Pureté et documentation
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Fiche technique (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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Instruction de manipulation (2659 KB)
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
TAK 044 Related Classifications
HY-105168 Related Classifications
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