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Merck
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SML2185

Sigma-Aldrich

PA-6

≥98% (HPLC)

别名:

1,5-Bis[4-[[imino(phenyl)methyl]amino]phenoxy]pentane, N,N′-[1,5-Pentanediylbis(oxy-4,1-phenylene)]bis-benzenecarboximidamide, Pentamidine-Analogue 6

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About This Item

经验公式（希尔记法）:
C31H32N4O2
CAS号:
500715-03-7
分子量:
492.61
分類程式碼代碼:
12352200
NACRES:
NA.77

化驗

≥98% (HPLC)

形狀

powder

顏色

white to beige

溶解度

DMSO: 2 mg/mL, clear

儲存溫度

2-8°C

SMILES 字串

N=C(C1=CC=CC=C1)NC(C=C2)=CC=C2OCCCCCOC3=CC=C(NC(C4=CC=CC=C4)=N)C=C3

生化／生理作用

PA-6 (Pentamidine-Analogue 6) is a selective and potent IK1 (inward rectifier potassium current) inhibitor that terminates atrial fibrillation and does not cause ventricular arrhythmias in goat and dog models. PA-6 interacts with the cytoplasmic pore region of the KIR2.1 (KCNJ2) ion channel.

儲存類別代碼

11 - Combustible Solids

水污染物質分類（WGK）

WGK 3

閃點（°F）

Not applicable

閃點（°C）

Not applicable

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Yuan Ji et al.
British journal of pharmacology, 174(15), 2576-2590 (2017-05-26)
The density of the inward rectifier current (IK1 ) increases in atrial fibrillation (AF), shortening effective refractory period and thus promoting atrial re-entry. The synthetic compound pentamidine analogue 6 (PA-6) is a selective and potent IK1 inhibitor. We tested PA-6
Hiroki Takanari et al.
Cardiovascular research, 99(1), 203-214 (2013-04-30)
In excitable cells, KIR2.x ion-channel-carried inward rectifier current (IK₁) is thought to set the negative and stable resting membrane potential, and contributes to action potential repolarization. Loss- or gain-of-function mutations correlate with cardiac arrhythmias and pathological remodelling affects normal KIR2.x
Yuan Ji et al.
Journal of biomedical science, 24(1), 44-44 (2017-07-18)
The inward rectifier potassium current IK1 contributes to a stable resting membrane potential and phase 3 repolarization of the cardiac action potential. KCNJ2 gain-of-function mutations V93I and D172N associate with increased IK1, short QT syndrome type 3 and congenital atrial
Christophe Gattlen et al.
Glia, 68(10), 2119-2135 (2020-03-29)
Spinal microglia change their phenotype and proliferate after nerve injury, contributing to neuropathic pain. For the first time, we have characterized the electrophysiological properties of microglia and the potential role of microglial potassium channels in the spared nerve injury (SNI)

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