推荐产品
方案
≥98% (HPLC)
表单
powder
颜色
white to beige
溶解性
DMSO: 2 mg/mL, clear
储存温度
2-8°C
SMILES字符串
N=C(C1=CC=CC=C1)NC(C=C2)=CC=C2OCCCCCOC3=CC=C(NC(C4=CC=CC=C4)=N)C=C3
InChI
1S/C31H32N4O2/c32-30(24-10-4-1-5-11-24)34-26-14-18-28(19-15-26)36-22-8-3-9-23-37-29-20-16-27(17-21-29)35-31(33)25-12-6-2-7-13-25/h1-2,4-7,10-21H,3,8-9,22-23H2,(H2,32,34)(H2,33,35)
InChI key
PETGITKEGWIZEL-UHFFFAOYSA-N
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.
selective and potent IK1 (inward rectifier potassium current) inhibitor that terminates atrial fibrillation
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
新产品
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
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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