(R)-(+)-Nor Verapamil Hydrochloride - CAS 123932-43-4
Not Intended for Therapeutic Use. For research use only.
Category:
Inhibitor
Product Name:
(R)-(+)-Nor Verapamil Hydrochloride
Catalog Number:
123932-43-4
Synonyms:
(αR)-α-[3-[[2-(3,4-Dimethoxyphenyl)ethyl]amino]propyl]-3,4-dimethoxy-α-(1-methylethyl)-benzeneacetonitrile Hydrochloride; (R)-Norverapamil Hydrochloride;
CAS Number:
123932-43-4
Description:
This active molecular is a chiral metabolite of Verapamil which is a calcium channel blocker applicated in the treatment of hypertension, angina pectoris, cardiac arrhythmia, and cluster headaches recently.
Molecular Weight:
447.04
Molecular Formula:
C₂₆H₃₇ClN₂O₄
Quantity:
Milligrams-Grams
Quality Standard:
In-house standard
COA:
Inquire
MSDS:
Inquire
Canonical SMILES:
CC(C)C(CCCNCCC1=CC(=C(C=C1)OC)OC)(C#N)C2=CC(=C(C=C2)OC)OC.Cl
InChI:
InChI=1S/C26H36N2O4.ClH/c1-19(2)26(18-27,21-9-11-23(30-4)25(17-21)32-6)13-7-14-28-15-12-20-8-10-22(29-3)24(16-20)31-5;/h8-11,16-17,19,28H,7,12-15H2,1-6H3;1H/t26-;/m1./s1
InChIKey:
OEAFTRIDBHSJDC-UFTMZEDQSA-N
Targets:
Calcium Channel
Chemical Structure
CAS 123932-43-4 (R)-(+)-Nor Verapamil Hydrochloride

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Reference Reading


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Wyles SP1,2, Hrstka SC3,4, Reyes S3,4, Terzic A2,3,5,6, Olson TM5,7,8, Nelson TJ1,2,4,5,9. Clin Transl Sci. 2016 Apr 22. doi: 10.1111/cts.12393. [Epub ahead of print]
For inherited cardiomyopathies, abnormal sensitivity to intracellular calcium (Ca2+ ), incurred from genetic mutations, initiates subsequent molecular events leading to pathological remodeling. Here, we characterized the effect of β-adrenergic stress in familial dilated cardiomyopathy (DCM) using human-induced pluripotent stem cell (hiPSC)-derived cardiomyocytes (CMs) from a patient with RBM20 DCM. Our findings suggest that β-adrenergic stimulation accelerated defective Ca2+ homeostasis, apoptotic changes, and sarcomeric disarray in familial DCM hiPSC-CMs. Furthermore, pharmacological modulation of abnormal Ca2+ handling by pretreatment with β-blocker, carvedilol, or Ca2+ -channel blocker, verapamil, significantly decreased the area under curve, reduced percentage of disorganized cells, and decreased terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)-positive apoptotic loci in familial DCM hiPSC-CMs after β-adrenergic stimulation.
2.An improved substrate cocktail for assessing direct inhibition and time-dependent inhibition of multiple cytochrome P450s.
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AIM: The substrate cocktail is frequently used to evaluate cytochrome P450 (CYP) enzyme-mediated drug interactions and potential interactions among the probe substrates. Here, we re-optimized the substrate cocktail method to increase the reliability and accuracy of screening for candidate compounds and expanded the method from a direct CYP inhibition assay to a time-dependent inhibition (TDI) assay.
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Somatic and germline mutations in the inward rectifying K+channel (KCNJ5) are a common cause of primary aldosteronism (PA) in aldosterone producing adenoma and familial hyperaldosteronism type III, respectively. Dysregulation of adrenal cell calcium signaling represents one mechanism for mutated KCNJ5 stimulation of aldosterone synthase (CYP11B2) expression and aldosterone production. However, the mechanisms stimulating acute and chronic production of aldosterone by mutantKCNJ5have not been fully characterized. Herein, we defined the effects of the T158A KCNJ5 mutation (KCNJ5T158A) on acute and chronic regulation of aldosterone production using an adrenal cell line with a doxycycline inducibleKCNJ5T158Agene (HAC15-TRE-KCNJ5T158A). Doxycycline incubation caused a time-dependent increase inKCNJ5T158AandCYP11B2mRNA and protein levels. Electrophysiological analyses confirm the loss of inward rectification and increased Na+permeability inKCNJ5T158A-expressing cells.
4.Calcium channel blockers ameliorate iron overload-associated hepatic fibrosis by altering iron transport and stellate cell apoptosis.
Zhang Y1, Zhao X2, Chang Y3, Zhang Y4, Chu X5, Zhang X4, Liu Z6, Guo H6, Wang N7, Gao Y4, Zhang J8, Chu L9. Toxicol Appl Pharmacol. 2016 Apr 16. pii: S0041-008X(16)30074-6. doi: 10.1016/j.taap.2016.04.008. [Epub ahead of print]
Liver fibrosis is the principal cause of morbidity and mortality in patients with iron overload. Calcium channel blockers (CCBs) can antagonize divalent cation entry into renal and myocardial cells and inhibit fibrogenic gene expression. We investigated the potential of CCBs to resolve iron overload-associated hepatic fibrosis. Kunming mice were assigned to nine groups (n=8 per group): control, iron overload, deferoxamine, high and low dose verapamil, high and low dose nimodipine, and high and low dose diltiazem. Iron deposition and hepatic fibrosis were measured in mouse livers. Expression levels of molecules associated with transmembrane iron transport were determined by molecular biology approaches. In vitro HSC-T6 cells were randomized into nine groups (the same groups as the mice). Changes in proliferation, apoptosis, and metalloproteinase expression in cells were detected to assess the anti-fibrotic effects of CCBs during iron overload conditions.