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SML0142

Sigma-Aldrich

Valsartan

≥98% (HPLC)

Synonym(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

Empirical Formula (Hill Notation):
C24H29N5O3
CAS Number:
Molecular Weight:
435.52
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77

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

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

Gene Information

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.

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

Signal Word

Warning

Hazard Statements

Precautionary Statements

Hazard Classifications

Repr. 2 - STOT SE 3

Target Organs

Central nervous system

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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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