N2540
NS5806
≥98% (HPLC)
别名:
N-[3,5-bis(trifluoromethyl)phenyl]-N′-[2,4-dibromo-6-(1H-tetrazol-5-yl)phenyl]-urea
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关于此项目
经验公式（希尔记法）:
C16H8Br2F6N6O
化学文摘社编号:
分子量:
574.07
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
InChI key
UZWJWROOLOOCPQ-UHFFFAOYSA-N
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)
assay
≥98% (HPLC)
form
powder
color
white to faint yellow
solubility
DMSO: >30 mg/mL
storage temp.
2-8°C
Quality Level
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.
NS5806 is an activator or transient outward potassium current (Ito).
signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 3 Oral - Aquatic Chronic 4
存储类别
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
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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