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SML0142

Sigma-Aldrich

Valsartan

≥98% (HPLC)

Synonyme(s) :

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

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About This Item

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

Niveau de qualité

100

Essai

≥98% (HPLC)

Forme

powder

Activité optique

[α]/D -55 to -70°, c = 1 in methanol

Conditions de stockage

desiccated

Couleur

white to tan

Solubilité

DMSO: ≥20 mg/mL

Auteur

Novartis

Température de stockage

2-8°C

Chaîne SMILES 

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

Clé InChI

ACWBQPMHZXGDFX-QFIPXVFZSA-N

Informations sur le gène

human ... AGTR1(185)

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Application

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

Actions biochimiques/physiologiques

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.

Caractéristiques et avantages

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.

Pictogrammes

Health hazardExclamation mark
GHS08,GHS07

Mention d'avertissement

Warning

Mentions de danger

H336,H361d

Conseils de prudence

P201 - P308 + P313

Classification des risques

Repr. 2 - STOT SE 3

Organes cibles

Central nervous system

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

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Certificats d'analyse (COA)

Lot/Batch Number
0000294574
0000294574
0000223492
0000223491
0000128000

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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
Jacob A Udell et al.
Clinical chemistry, 59(6), 959-967 (2013-03-20)
Acute coronary syndrome (ACS) activates neurohormonal pathways, including elevations in circulating aldosterone, with deleterious cardiovascular effects. We aimed to determine if early, more complete renin-angiotensin-aldosterone system inhibition (RAASI) in post-ACS patients without ventricular dysfunction or heart failure would result in
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