PBT434 methanesulfonate structure
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Common Name | PBT434 methanesulfonate | ||
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| CAS Number | 2387898-69-1 | Molecular Weight | 398.26 | |
| Density | N/A | Boiling Point | N/A | |
| Molecular Formula | C13H17Cl2N3O5S | Melting Point | N/A | |
| MSDS | N/A | Flash Point | N/A | |
Use of PBT434 methanesulfonatePBT434 methanesulfonate is a potent, orally active and cross the blood-brain barrier α-synuclein aggregation inhibitor. PBT434 methanesulfonate can be used as a iron chelator and modulates transcellular iron trafficking. PBT434 methanesulfonate inhibits iron-mediated redox activity and iron-mediated aggregation of α-synuclein. PBT434 methanesulfonate prevents the loss of substantia nigra pars compacta neurons (SNpc). PBT434 methanesulfonate has the potential for the research of Parkinson’s disease (PD)[1][2]. |
| Name | PBT434 methanesulfonate |
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| Description | PBT434 methanesulfonate is a potent, orally active and cross the blood-brain barrier α-synuclein aggregation inhibitor. PBT434 methanesulfonate can be used as a iron chelator and modulates transcellular iron trafficking. PBT434 methanesulfonate inhibits iron-mediated redox activity and iron-mediated aggregation of α-synuclein. PBT434 methanesulfonate prevents the loss of substantia nigra pars compacta neurons (SNpc). PBT434 methanesulfonate has the potential for the research of Parkinson’s disease (PD)[1][2]. |
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| Related Catalog | |
| In Vitro | PBT434 methanesulfonate (0-20 µM;3 小时) 显着抑制铁产生的 H2O2,并显着降低 Fe 介导的 α-突触核蛋白聚集速率[1]。 PBT434 methanesulfonate (0-100 µM; 24 h) 对脑微血管内皮细胞没有细胞毒性作用[2]。 PBT434 methanesulfonate (20 µM; 24 h) 增加 hBMVEC 中总 TfR、Cp 蛋白水平的表达[2]。 Cell Cytotoxicity Assay[2] Cell Line: hBMVEC Concentration: 1, 10, 20, 50, 100 µM Incubation Time: 24 h Result: Showed no cytotoxic effects on brain microvascular endothelial cells. Western Blot Analysis[2] Cell Line: hBMVEC Concentration: 20 μM Incubation Time: 24 h Result: Increased the expression of total TfR, Cp protein level. |
| In Vivo | PBT434 methanesulfonate (30 mg/kg;口服;每日一次,持续 21 天) 显着保留了 6-OHDA 毒模型中的神经元数量,并在 L-DOPA 模型中显示出明显更少的旋转,显着减少了 MPTP 模型中的 SNpc 神经元损失[ 1]。 Animal Model: 12 weeks, 25 g, Male C57BL/6 J mice (6-OHDA intoxication model)[1] Dosage: 30 mg/kg Administration: P.o.; daily for 21 days (commencing 3 days following induction of lesion) Result: Prevented neuronal loss following 6-OHDA, preserving up to 75% of the SNpc neurons remaining (both Nissl and tyrosine hydroxylase (TH) positive neurons) after the initial phase of cell death. Animal Model: 12 weeks, 25 g, Male C57BL/6 J mice (MPTP model)[1] Dosage: 1, 3, 10, 30, 80 mg/kg Administration: P.o.; daily for 21 days (commenced 24 h after induction of lesion) Result: Increased the proportion of SNpc cells rescued, increased there was a trend to improved turning behavior, significantly increased varicosity abundance, prevented the decline in levels of the presynaptic marker synaptophysin (SYNP) in a dose-dependent manner. |
| References |
| Molecular Formula | C13H17Cl2N3O5S |
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| Molecular Weight | 398.26 |