Details
Stereochemistry | RACEMIC |
Molecular Formula | C19H19N3O6 |
Molecular Weight | 385.3714 |
Optical Activity | ( + / - ) |
Defined Stereocenters | 0 / 1 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
CC(C)OC(=O)C1=C(C)NC(=C(C1c2cccc(c2)N(=O)=O)C(=O)OC)C#N
InChI
InChIKey=FAIIFDPAEUKBEP-UHFFFAOYSA-N
InChI=1S/C19H19N3O6/c1-10(2)28-19(24)15-11(3)21-14(9-20)17(18(23)27-4)16(15)12-6-5-7-13(8-12)22(25)26/h5-8,10,16,21H,1-4H3
Molecular Formula | C19H19N3O6 |
Molecular Weight | 385.3714 |
Charge | 0 |
Count |
|
Stereochemistry | RACEMIC |
Additional Stereochemistry | No |
Defined Stereocenters | 0 / 1 |
E/Z Centers | 0 |
Optical Activity | ( + / - ) |
DescriptionSources: http://www.hmdb.ca/metabolites/HMDB15657Curator's Comment:: description was created based on several sources, including
https://www.ncbi.nlm.nih.gov/pubmed/7898101
Sources: http://www.hmdb.ca/metabolites/HMDB15657
Curator's Comment:: description was created based on several sources, including
https://www.ncbi.nlm.nih.gov/pubmed/7898101
Nilvadipine (NIVADIL®) is a L-type calcium channel blocker for treatment of hypertension. It inhibits the influx of extracellular calcium through myocardial and vascular membrane pores by physically plugging the channel. The decrease in intracellular calcium inhibits the contractile processes of smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload.
CNS Activity
Originator
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
---|---|---|---|
Target ID: CHEMBL2830 Sources: https://www.ncbi.nlm.nih.gov/pubmed/7898101 |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
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Primary | NIVADIL Approved UseNivadil is indicated for the treatment of essential hypertension. Launch Date8.3790719E11 |
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Primary | Nilvadipine Approved UseUnknown |
PubMed
Title | Date | PubMed |
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Tacrolimus (FK506)-induced nephrotoxicity in spontaneous hypertensive rats. | 1994 Nov |
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Effects of nilvadipine (a dihydropyridine-type calcium entry blocker) on cerebral blood flow in acute experimental brain ischemia in rats. | 1996 Aug |
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Angiotensin II regulation of vascular endothelial growth factor and receptors Flt-1 and KDR/Flk-1 in cyclosporine nephrotoxicity. | 2002 Aug |
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Interaction of digoxin with antihypertensive drugs via MDR1. | 2002 Feb 15 |
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Amlodipine and carvedilol prevent cytotoxicity in cortical neurons isolated from stroke-prone spontaneously hypertensive rats. | 2004 Apr |
Patents
Sample Use Guides
In Vivo Use Guide
Sources: http://www.medicines.ie/medicine/3202/SPC
The recommended dose is 1 NIVADIL® 8 mg prolonged release capsule per day in the morning as a starting dose. If after 2 - 4 weeks of therapy an adequate anti-hypertensive effect is not achieved, a daily dose of 16 mg nilvadipine (2 x 8 mg NIVADIL® prolonged release capsules, or 1 x 16 mg NIVADIL® prolonged release capsule, in the morning) may improve the blood pressure response.
Route of Administration:
Oral
In Vitro Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/6196557
The cardiovascular effect of nilvadipine (FR34235) with the effects of nifedipine, nicardipine, and diltiazem on the dog using in vitro arterial strip preparations was compared. FR34235 reduced the amplitude of coronary arterial contraction induced by K+ more so than that induced by norepinephrine in in vitro preparations. The ID50 values of FR34235 for various arterial strips contracted by K+ were smaller (1/5-1/426) than those of nifedipine and diltiazem, and almost the same as those of nicardipine.
Substance Class |
Chemical
Created
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admin
on
Edited
Sat Jun 26 13:46:26 UTC 2021
by
admin
on
Sat Jun 26 13:46:26 UTC 2021
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Record UNII |
0214FUT37J
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Record Status |
Validated (UNII)
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WHO-ATC |
C08CA10
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WHO-VATC |
QC08CA10
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NCI_THESAURUS |
C333
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75530-68-6
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1934
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4494
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M7900
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5459
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C84019
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0214FUT37J
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CHEMBL517427
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SUB09292MIG
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DB06712
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75530-68-6
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53692
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C035100
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