RB-105
RB-105 is an inhibitor of angiotensin-converting enzyme (ACE) (Ki = 4.2 nM) and neutral endopeptidase (NEP) (Ki = 1.7 nM). RB-105 after inhibiting ACE reduces the production of Ang II and increase the level of bradykinin. RB-105 after inhibiting NEP increases the level of natriuretic peptide and further increases the level of bradykinin, thereby generating a powerful synergistic effect. RB-105 has significant antihypertensive and natriuretic effects in both spontaneously hypertensive rats and normal blood pressure rats. RB-105 can be used for research on hypertension.
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- CAS No.: 155895-89-9
- Formule: C14H19NO3S
- Masse moléculaire:281.37
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
IC50 & Target
[1]|
ACE 4.2 nM (Ki) |
Chemical Information
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CAS No. 155895-89-9
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Masse moléculaire 281.37
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Formule C14H19NO3S
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SMILES
C[C@@H](C(O)=O)NC([C@@H](CS)[C@H](C1=CC=CC=C1)C)=O
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
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
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)