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BAY 73-6691((R)-BAY 73-6691)
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
BAY 73-6691((R)-BAY 73-6691)图片
CAS NO:794568-92-6
规格:98%
分子量:356.73
包装与价格:
包装价格(元)
5mg电议
10mg电议
25mg电议
50mg电议
100mg电议

产品介绍
BAY73-6691是一种有效且有选择性的脑渗透PDE9A抑制剂。
CAS:794568-92-6
分子式:C15H12ClF3N4O
分子量:356.73
纯度:98%
存储:Store at -20°C

Background:

BAY 73-6691 is a potent, selective brain penetrant PDE9A inhibitor.


The BAY 73-6691 dose-dependently alleviates cell viability loss due to Aβ25-35 treatment. It is found that when SH-SY5Y cells are cultured by Aβ25-35, a high degree of cell apoptosis is observed, while additional stimulation with BAY 73-6691 causes attenuation of cell apoptosis. BAY 73-6691 dose-dependently attenuates oxidative stress induced by Aβ25-35, and BAY 73-6691 at 200 μg/mL almost neutralizes Aβ25-35-induced oxidative damage. The BAY 73-6691 attenuates Aβ25-35-induced increase of apoptosis cells[1].


BAY 73-6691 dose-dependently improves the acquisition performance in the Aβ25-35-injected mice on days 7 to 10 (day 7, F(5,54)=65.153; day 8, F(5,54)=62.340; day 9, F(5,54)=37.529; day 10, F(5,54)=38.624; P<0.001). BAY 73-6691 at 3 mg/kg can almost completely abolish the prolongation of escape-latency on days 9 to 10. BAY 73-6691 dose-dependently elevates the Aβ25-35-induced decrease of the dwell time on the 10th day post Aβ25-35 injection (day 10, F(5,54)=27.360, P<0.001). Results reveal that the Aβ25-35 injection and BAY 73-6691 treatment cause no influence on the swimming speed. Treatment with BAY 73-6691 does not cause detectable alteration of spatial memory in sham mice. BAY 73-6691 alleviates Aβ25-35-induced abnormalities of the above indices. The BAY 73-6691 causes no influence on the four indices mentioned above in sham mice. The BAY 73-6691 has no significant effect on the apoptosis of hippocampal neurons in sham mice[1].


[1]. Li J, et al. Protective effects of BAY 73-6691, a selective inhibitor of phosphodiesterase 9, on amyloid-β peptides-induced oxidative stress in in-vivo and in-vitro models of Alzheimer’s disease. Brain Res. 2016 Jul 1;1642:327-335.