产品
编 号：F610155
分子式：C57H86N2O14
分子量：1023.3
分子式：C57H86N2O14
分子量：1023.3
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CAS No: 892494-07-4
产品详情
生物活性：
ILS-920 is a nonimmunosuppressive Rapamycin analog with reduced immunosuppressive activity and potent neuroprotective activity. ILS-920 binds selectively to the immunophilin FKBP52 and to the β1-subunit of L-type voltage-gated calcium channels (VGCC). ILS-920 shows 200-fold selectivity for FKBP52 versus FKBP12.
体内研究：
In a transient middle cerebral artery occlusion (tMCAO) model of ischemic stroke, ILS-920, administered 4 h postocclusion at 10 and 30 mg/kg, significantly reduces infarct volume by 24% and 23% in 72 h, respectively, and robustly enhances functional recovery measured by improvement in neurological deficits.
体外研究：
ILS-920 promotes neuronal survival and stimulates neurite outgrowth with potent neurotrophic activities in cortical neuronal cultures.ILS-920 can inhibit L-type Ca2+ channels in rat hippocampal neurons and F-11 dorsal root ganglia (DRG)/neuroblastoma cells.ILS-920 can protect neurons from Ca2+-induced cell death by modulating Ca2+ channels and promote neurite outgrowth via FKBP52 binding.
ILS-920 is a nonimmunosuppressive Rapamycin analog with reduced immunosuppressive activity and potent neuroprotective activity. ILS-920 binds selectively to the immunophilin FKBP52 and to the β1-subunit of L-type voltage-gated calcium channels (VGCC). ILS-920 shows 200-fold selectivity for FKBP52 versus FKBP12.
体内研究：
In a transient middle cerebral artery occlusion (tMCAO) model of ischemic stroke, ILS-920, administered 4 h postocclusion at 10 and 30 mg/kg, significantly reduces infarct volume by 24% and 23% in 72 h, respectively, and robustly enhances functional recovery measured by improvement in neurological deficits.
体外研究：
ILS-920 promotes neuronal survival and stimulates neurite outgrowth with potent neurotrophic activities in cortical neuronal cultures.ILS-920 can inhibit L-type Ca2+ channels in rat hippocampal neurons and F-11 dorsal root ganglia (DRG)/neuroblastoma cells.ILS-920 can protect neurons from Ca2+-induced cell death by modulating Ca2+ channels and promote neurite outgrowth via FKBP52 binding.
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