| Description |
Yonkenafil (Tunodafil), a novel phosphodiesterase 5 (PDE5) inhibitor, is effective in reducing cerebral infarction, neurological deficits, edema, and neuronal damage in the infarcted area. Yonkenafil may improve cognitive function by modulating neurogenesis and has a potential therapeutic effect on Alzheimer's disease[1].
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| Related Catalog |
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| In Vivo |
Yonkenafil (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[1]。 Animal Model: Male Sprague-Dawley (SD) Rat[1] 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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| References |
[1]. Xuemei Chen, et al. Yonkenafil: a novel phosphodiesterase type 5 inhibitor induces neuronal network potentiation by a cGMP-dependent Nogo-R axis in acute experimental stroke. Exp Neurol. 2014 Nov;261:267-77.
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