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Merck
CN

PZ0311

Sigma-Aldrich

PF-05089771

≥98% (HPLC)

别名:

4-[2-(3-Amino-1H-pyrazol-4-yl)-4-chlorophenoxy]-5-chloro-2-fluoro-N-4-thiazolyl-benzenesulfonamide 4-methylbenzenesulfonate (1:1), 4-[2-(5-Amino-1H-pyrazol-4-yl)-4-chloro-phenoxy]-5-chloro-2-fluoro-N-thiazol-4-yl-benzenesulfonamide p-toluene sulfonate salt, PF-05089771 p-toluene sulfonate salt

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About This Item

经验公式(希尔记法):
C18H12Cl2FN5O3S2 · C7H8O3S
分子量:
672.56
UNSPSC代码:
12352200
PubChem化学物质编号:
NACRES:
NA.77

质量水平

方案

≥98% (HPLC)

表单

powder

颜色

white to beige

溶解性

DMSO: 30 mg/mL, clear

储存温度

room temp

SMILES字符串

ClC1=CC(C2=C(N)NN=C2)=C(OC3=C(Cl)C=C(S(NC4=CSC=N4)(=O)=O)C(F)=C3)C=C1.CC5=CC=C(S(=O)(O)=O)C=C5

InChI

1S/C18H12Cl2FN5O3S2.C7H8O3S/c19-9-1-2-14(10(3-9)11-6-24-25-18(11)22)29-15-5-13(21)16(4-12(15)20)31(27,28)26-17-7-30-8-23-17;1-6-2-4-7(5-3-6)11(8,9)10/h1-8,26H,(H3,22,24,25);2-5H,1H3,(H,8,9,10)

InChI key

NVKBPDYKPNYMDR-UHFFFAOYSA-N

生化/生理作用

PF-05089771 is a selective and potent inhibitor of the human voltage-gated sodium ion channel Nav1.7 with an IC50 value of 11 nM. PF-05089771 targets the voltage-sensing domain, preferentially interacting with, and stabilizing, inactivated channel conformations by interaction with the voltage-sensor domain (VSD) of Domain 4. Nav1.7 is expressed in sensory neurons and is critical for pain processing. PF-05089771 is being investigated for the treatment of chronic neuropathic pain.

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Sooyeon Jo et al.
Molecular pharmacology, 97(6), 377-383 (2020-03-21)
PF-05089771 is an aryl sulfonamide Nav1.7 channel blocker that binds to the inactivated state of Nav1.7 channels with high affinity but binds only weakly to channels in the resting state. Such aryl sulfonamide Nav1.7 channel blockers bind to the extracellular
Aristos J Alexandrou et al.
PloS one, 11(4), e0152405-e0152405 (2016-04-07)
Human genetic studies show that the voltage gated sodium channel 1.7 (Nav1.7) is a key molecular determinant of pain sensation. However, defining the Nav1.7 contribution to nociceptive signalling has been hampered by a lack of selective inhibitors. Here we report

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