Drug development targeting for regeneration of neurovascular units in neurodegenerative disorders

ST 101刺激海马中的记忆分子，Ca 2 +/钙调蛋白依赖性蛋白激酶II（CaMKII）。在本研究中，我们研究了神经血管再生化合物ST 101的长期给药是否对脑功能具有持久的改善作用，并确定了其在神经退行性疾病中治疗作用的分子机制。ST 101目前正在美国进行II期临床试验，我们将T型电压门控钙通道确定为ST 101的分子靶点。接下来，我们通过使用过表达T型电压门控钙通道的neuro 2A细胞引入了新的和有效的衍生物SAK 3。这是世界上首次发现T型电压门控钙通道激活剂。我们的研究最有希望的证据是，T型钙通道是阿尔茨海默病治疗的新的治疗靶点，以恢复神经退行性疾病的神经网络。

ST101 stimulates memory molecule, Ca2+/calmodulin-dependent protein kinase II (CaMKII) in the hippocampus. In the present study, we investigated whether chronic administration of the neurovascular regenerative compound, ST101 elicits long lasting ameliorating effects on brain functions and defined the molecular mechanism underlying their therapeutic effects in the neurodegenerative disorders. ST101 was now under investigation in Phase II clinical trial of U.S.A. We defined T type voltage-gated calcium channel as molecular target of ST101. We next introduced novel and potent derivative, SAK3 by using neuro2A cells overexpressing T type voltage-gated calcium channel. This is the first discovery of activators of T type voltage-gated calcium channel in the world. The most promising evidence in our studies is that T type calcium channel is novel therapeutic target of Alzheimer therapy to restore the neural networks in the neurodegenerative disorders.