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N2540

Sigma-Aldrich

NS5806

≥98% (HPLC)

Synonym(s):

N-[3,5-bis(trifluoromethyl)phenyl]-N′-[2,4-dibromo-6-(1H-tetrazol-5-yl)phenyl]-urea

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About This Item

Empirical Formula (Hill Notation):
C16H8Br2F6N6O
CAS Number:
426834-69-7
Molecular Weight:
574.07
MDL number:
MFCD18432708
UNSPSC Code:
12352200
PubChem Substance ID:
329818416
NACRES:
NA.77

Quality Level

100

Assay

≥98% (HPLC)

form

powder

color

white to faint yellow

solubility

DMSO: >30 mg/mL

storage temp.

2-8°C

SMILES string

FC(F)(F)c1cc(NC(=O)Nc2c(Br)cc(Br)cc2-c3nnn[nH]3)cc(c1)C(F)(F)F

InChI

1S/C16H8Br2F6N6O/c17-8-4-10(13-27-29-30-28-13)12(11(18)5-8)26-14(31)25-9-2-6(15(19,20)21)1-7(3-9)16(22,23)24/h1-5H,(H2,25,26,31)(H,27,28,29,30)

InChI key

UZWJWROOLOOCPQ-UHFFFAOYSA-N

Biochem/physiol Actions

NS5806 increases peak current amplitude of the potassium channel Kv4.3 (EC50 = 5.3 uM). NS5806 also slows Kv4.3 and Kv4.2 current dacay in channel complexes containing KChIP2. In ventricular cardiomycytes, NS5806 increases transient outward current and reproduces the electrocardiographic profile of Brugada syndrome.

Pictograms

Skull and crossbones
GHS06

Signal Word

Danger

Hazard Statements

H301,H413

Hazard Classifications

Acute Tox. 3 Oral - Aquatic Chronic 4

Storage Class Code

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

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Sufen Wang et al.
Frontiers in physiology, 10, 1509-1509 (2020-01-11)
Background: NS5806 activates the transient outward potassium current Ito, and has been claimed to reproduce Brugada Syndrome (BrS) in ventricular wedge preparations. Ito modulates excitation-contraction coupling, which is critical in alternans dynamics. We explored NS5806-arrhythmogenic effects in the intact whole
José M Di Diego et al.
PloS one, 15(11), e0242747-e0242747 (2020-11-25)
J wave syndromes (JWS), including Brugada (BrS) and early repolarization syndromes (ERS), are associated with increased risk for life-threatening ventricular arrhythmias. Pharmacologic approaches to therapy are currently very limited. Here, we evaluate the effects of the natural flavone acacetin. The
Jinjing Yao et al.
Cell reports, 32(12), 108169-108169 (2020-09-24)
Neuronal hyperactivity is an early primary dysfunction in Alzheimer's disease (AD) in humans and animal models, but effective neuronal hyperactivity-directed anti-AD therapeutic agents are lacking. Here we define a previously unknown mode of ryanodine receptor 2 (RyR2) control of neuronal

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