产品
编 号：F366168
分子式：C15H19Cl2N3O2
分子量：344.24
分子式：C15H19Cl2N3O2
分子量：344.24
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CAS No: 478148-58-2
产品详情
生物活性：
PHA-543613 dihydrochloride is a potent, orally active, brain-penetrant and selective α7 nAChR agonist with a Ki value of 8.8 nM. PHA-543613 dihydrochloride displays selectivity for α7-nAChR over α3β4, α1β1γδ, α4β2 and 5-HT3 receptors. PHA-543613 dihydrochloride can be used for the cognitive deficits of Alzheimer's disease and schizophrenia research.
体内研究：
PHA-543613 dihydrochloride (0.3 mg/kg) successfully reverses Scopolamine-induced short-term memory deficits in rats.PHA-543613 dihydrochloride (4 and 12 mg/kg; i.p. once) reduces behavioral deficits and brain edema is dependent on the PI3K-Akt signaling pathway.Animal Model:Male CD-1 mice with (intracerebral hemorrhage) ICH-induction or sham surgery
Dosage:4 and 12 mg/kg
Administration:Intraperitoneal injection; 4 and 12 mg/kg; 1 hour after surgery
Result:Increased p-Akt and decreased p-GSK-3 and CC3 expressions in the ipsilateral hemisphere and reduced the neuronal cell death in the perihematomal area. Attenuated behavioral deficits andbrain edema at 72 hours after ICH.
PHA-543613 dihydrochloride is a potent, orally active, brain-penetrant and selective α7 nAChR agonist with a Ki value of 8.8 nM. PHA-543613 dihydrochloride displays selectivity for α7-nAChR over α3β4, α1β1γδ, α4β2 and 5-HT3 receptors. PHA-543613 dihydrochloride can be used for the cognitive deficits of Alzheimer's disease and schizophrenia research.
体内研究：
PHA-543613 dihydrochloride (0.3 mg/kg) successfully reverses Scopolamine-induced short-term memory deficits in rats.PHA-543613 dihydrochloride (4 and 12 mg/kg; i.p. once) reduces behavioral deficits and brain edema is dependent on the PI3K-Akt signaling pathway.Animal Model:Male CD-1 mice with (intracerebral hemorrhage) ICH-induction or sham surgery
Dosage:4 and 12 mg/kg
Administration:Intraperitoneal injection; 4 and 12 mg/kg; 1 hour after surgery
Result:Increased p-Akt and decreased p-GSK-3 and CC3 expressions in the ipsilateral hemisphere and reduced the neuronal cell death in the perihematomal area. Attenuated behavioral deficits andbrain edema at 72 hours after ICH.
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