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Merck

SML0142

Valsartan

≥98% (HPLC), Angiotensin II type 1 (AT1) receptor antagonist, powder

Synonyme(s) :

N-(1-Oxopentyl)-N-[[2′-(2H-tetrazol-5-yl)[1,1′-biphenyl]-4-yl]methyl]-L-valine

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A propos de cet article

Formule empirique (notation de Hill) :
C24H29N5O3
Numéro CAS:
137862-53-4
Poids moléculaire :
435.52
UNSPSC Code:
12352200
PubChem Substance ID:
329825190
NACRES:
NA.77
MDL number:
MFCD00865840

Principaux documents

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Nom du produit

Valsartan, ≥98% (HPLC)

SMILES string

CCCCC(=O)N(Cc1ccc(cc1)-c2ccccc2-c3nnn[nH]3)[C@@H](C(C)C)C(O)=O

InChI

1S/C24H29N5O3/c1-4-5-10-21(30)29(22(16(2)3)24(31)32)15-17-11-13-18(14-12-17)19-8-6-7-9-20(19)23-25-27-28-26-23/h6-9,11-14,16,22H,4-5,10,15H2,1-3H3,(H,31,32)(H,25,26,27,28)/t22-/m0/s1

InChI key

ACWBQPMHZXGDFX-QFIPXVFZSA-N

assay

≥98% (HPLC)

form

powder

optical activity

[α]/D -55 to -70°, c = 1 in methanol

storage condition

desiccated

color

white to tan

solubility

DMSO: ≥20 mg/mL

originator

Novartis

storage temp.

2-8°C

Quality Level

100

Gene Information

human ... AGTR1(185)

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Catégories apparentées

Application

Mice were treated with valsartan to study the role of Ang II-dependent pathway in aldosterone-related effects.

Biochem/physiol Actions

Valsartan is an Angiotensin II type 1 (AT1) receptor antagonist and anti-hypertensive. Valsartan renders protection against heart attack and stroke resulting from abrupt increase in blood pressure. Valsartan reduces myocardial-infarction-related complications in heart attack survivors.

Features and Benefits

This compound is a featured product for ADME Tox research. Click here to discover more featured ADME Tox products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.
This compound is featured on the Angiotensin Receptors page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.
This compound was developed by Novartis. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.

pictograms

Health hazardExclamation mark
GHS08,GHS07

signalword

Warning

Hazard Classifications

Repr. 2 - STOT SE 3

target_organs

Central nervous system

Classe de stockage

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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Certificats d'analyse (COA)

Lot/Batch Number
0000465081
0000294573
0000294573
0000294574
0000294574

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

Frédéric Michel et al.
Circulation, 109(16), 1933-1937 (2004-04-14)
We analyzed the role of aldosterone in ischemia-induced neovascularization and the involvement of angiotensin II (Ang II) signaling in this effect. Ischemia was induced by right femoral artery ligature in mice treated or not with aldosterone (4.5 microg/day), aldosterone plus
N M Kaplan
American family physician, 60(4), 1185-1190 (1999-10-03)
The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-VI) includes recommendations for the assessment of overall cardiovascular risk and the need for active antihypertensive drug therapy. Once the decision to
Bodh I Jugdutt
Vascular health and risk management, 2(2), 125-138 (2007-02-27)
Survivors of myocardial infarction (MI) are at high risk of disability and death. This is due to infarct-related complications such as heart failure, cardiac remodeling with progressive ventricular dilation, dysfunction, and hypertrophy, and arrhythmias including ventricular and atrial fibrillation. Angiotensin
Teun van der Bom et al.
Circulation, 127(3), 322-330 (2012-12-19)
The role of angiotensin II receptor blockers in patients with a systemic right ventricle has not been elucidated. We conducted a multicenter, double-blind, parallel, randomized controlled trial of angiotensin II receptor blocker valsartan 160 mg twice daily compared with placebo
Arjan J Kwakernaak et al.
Atherosclerosis, 226(2), 459-465 (2012-12-25)
LDL-receptor deficiency may provide a mechanism which contributes to atherogenic lipoprotein abnormalities in experimental nephrosis and in humans with glomerular proteinuria. The proprotein convertase subtilisin-kexin type 9 (PCSK9) pathway plays a key role in lipoprotein metabolism by promoting LDL-receptor degradation.
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