产品
编 号：F465344
分子式：C24H34ClN5O4S
分子量：524.08
分子式：C24H34ClN5O4S
分子量：524.08
产品类型
规格
价格
是否有货
1mg
询价
询价
5mg
询价
询价
10mg
询价
询价
结构图
CAS No: 804519-64-0
产品详情
生物活性：
Yonkenafil (Tunodafil) hydrochloride, a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil (Tunodafil) hydrochloride may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer's disease.
体内研究：
Yonkenafil (Tunodafil) hydrochloride (4-32 mg/kg, i.v. daily for 7?days) 能够改善中风后的行为结果并减少脑梗塞体积，抑制神经元凋亡，并通过调节 BDNF/TrkB 和 NGF/TrkA 的表达显着增强缺血脑中的突触功能。Animal Model:Male Sprague-Dawley (SD) Rat
Dosage:4, 8, 16 and 32??mg/kg
Administration:i.v. daily for 7?days
Result:Induced a dose-dependent decrease in infarct volume, with an ED50 of 12.27 mg/kg.Increased hsp70 expression, decreased apaf-1 expression, and inhibited caspase-3 and caspase-9 cleavage.Significantly prevented neuronal damage and increases the number of surviving neurons after stroke.Prevented decrease in synaptophysin levels and increase in PSD-95 and nNOS levels.
Yonkenafil (Tunodafil) hydrochloride, a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil (Tunodafil) hydrochloride may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer's disease.
体内研究：
Yonkenafil (Tunodafil) hydrochloride (4-32 mg/kg, i.v. daily for 7?days) 能够改善中风后的行为结果并减少脑梗塞体积，抑制神经元凋亡，并通过调节 BDNF/TrkB 和 NGF/TrkA 的表达显着增强缺血脑中的突触功能。Animal Model:Male Sprague-Dawley (SD) Rat
Dosage:4, 8, 16 and 32??mg/kg
Administration:i.v. daily for 7?days
Result:Induced a dose-dependent decrease in infarct volume, with an ED50 of 12.27 mg/kg.Increased hsp70 expression, decreased apaf-1 expression, and inhibited caspase-3 and caspase-9 cleavage.Significantly prevented neuronal damage and increases the number of surviving neurons after stroke.Prevented decrease in synaptophysin levels and increase in PSD-95 and nNOS levels.
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