生物活性 | |||
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描述 | Tramiprosate targets soluble Aβ, interacts with Aβ peptide and prevents its aggregation. Tramiprosate favours tau aggregation, in tau transfected non-neuronal cells, and in neuronal cells. It does not affect the binding of tau to microtubules but may prevent the formation of tau-actin aggregates[4]. Tramiprosate was found to maintain Aβ in a non-fibrillar form, to decrease Aβ42-induced cell death in neuronal cell cultures, and to inhibit amyloid deposition. It can cross the murine blood-brain barrier (BBB) to exert its activity. Treatment of TgCRND8 mice with Tramiprosate resulted in significant reduction (∼30%) in the brain amyloid plaque load and a significant decrease in the cerebral levels of soluble and insoluble Aβ40 and Aβ42 (∼20–30%). Tramiprosate influenced the central pool of Aβ, changing either its efflux or its metabolism in the brain, as a reduction up to 60% of plasma Aβ levels was observed[5]. | ||
作用机制 | Tramiprosate is a sulfated glycosaminoglycan mimetic which can interact with Aβ peptide, preventing its aggregation.[4] |
实验方案 | |||
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1mg | 5mg | 10mg | |
1 mM 5 mM 10 mM |
7.19mL 1.44mL 0.72mL |
35.93mL 7.19mL 3.59mL |
71.85mL 14.37mL 7.19mL |
参考文献 |
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