(R)-Niguldipine
(R)-Niguldipine, a R-epimer of Niguldipine (HY-101390B), is a calcium channel antagonist. (R)-Niguldipine exerts a vasodilatory effect by blocking calcium channels and reducing the transmembrane influx of calcium ions. (R)-Niguldipine can inhibit U-46619 (HY-108566)-induced coronary artery contraction in guinea pig Langendorff hearts (pID50 of 9.93), has high affinity for calcium channel binding sites on guinea pig skeletal muscle membranes (Ki of 8.10), and lowers blood pressure in spontaneously hypertensive rats (pED30 of 5.55). (R)-Niguldipine can improve cardiovascular diseases such as hypertension, angina pectoris, and arrhythmias.
For research use only. We do not sell to patients.
- CAS No.: 120054-86-6
- Formula: C36H39N3O6
- Molecular Weight:609.71
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
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Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| CCRF-CEM | EC50 |
0.06 μM
Compound: niguldipine
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Compound was tested for inhibition of daunomycin efflux in the resistant human T-lymphoblast cell line CEM vcr1000.
Compound was tested for inhibition of daunomycin efflux in the resistant human T-lymphoblast cell line CEM vcr1000.
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[PMID: 9767638] |
Chemical Information
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CAS No. 120054-86-6
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Molecular Weight 609.71
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Formula C36H39N3O6
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SMILES
O=C(C1=C(C)NC(C)=C(C(OC)=O)[C@H]1C2=CC([N+]([O-])=O)=CC=C2)OCCCN3CCC(C4=CC=CC=C4)(C5=CC=CC=C5)CC3
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
(R)-Niguldipine Related Classifications
HY-101390D Related Classifications
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