BSc3094
目录号 : GC63697BSc3094 是一种 Tau aggregation 抑制剂。BSc3094 可用于阿尔茨海默病 (AD) 的研究。
Cas No.:946857-84-7
Sample solution is provided at 25 µL, 10mM.
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BSc3094 is a Tau aggregation inhibitor. BSc3094 can be used for the research of Alzheimer’s disease (AD)[1].
BSc3094 (3 mg/kg; i.v.) direct intraventricular administration reduces sarkosyl-insoluble Tau[1].BSc3094 (0.075~1.5 mM; intraventricular administration) reduces the levels of sarkosyl-insoluble Tau in cortical extracts by ≈70%[1].BSc3094 reverses the pre-synaptic impairment in organotypic hippocampal slices from pro-aggregant mice, by reversing the pairedpulse depression observed in non-treated pro-aggregant Tau slices after applying a paired-pulse stimulus of the Schaffer collaterals. BSc3094 reverses the increase in Tau phosphorylation levels in rTg4510 mice down to control level. BSc3094 partially reversed the memory deficits in rTg4510 mice[1].
[1]. Anglada-Huguet M, et al. Inhibition of Tau aggregation with BSc3094 reduces Tau and decreases cognitive deficits in rTg4510 mice. Alzheimers Dement (N Y). 2021;7(1):e12170. Published 2021 Jun 1.
Cas No. | 946857-84-7 | SDF | |
分子式 | C17H12N6O3S | 分子量 | 380.38 |
溶解度 | DMSO : 33.33 mg/mL (87.62 mM; Need ultrasonic) | 储存条件 | 4°C, protect from light |
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1 mg | 5 mg | 10 mg | |
1 mM | 2.6289 mL | 13.1447 mL | 26.2895 mL |
5 mM | 0.5258 mL | 2.6289 mL | 5.2579 mL |
10 mM | 0.2629 mL | 1.3145 mL | 2.6289 mL |
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2.
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Inhibition of Tau aggregation with BSc3094 reduces Tau and decreases cognitive deficits in rTg4510 mice
Alzheimers Dement (N Y) 2021 Jun 1;7(1):e12170.PMID:34095439DOI:10.1002/trc2.12170.
Background: One of the major hallmarks of Alzheimer's disease (AD)is the aberrant modification and aggregation of the microtubule-associated protein Tau . The extent of Tau pathology correlates with cognitive decline, strongly implicating Tau in the pathogenesis of the disease. Because the inhibition of Tau aggregation may be a promising therapeutic target, we tested the efficacy of BSc3094, an inhibitor of Tau aggregation, in reducing Tau pathology and ameliorating the disease symptoms in transgenic mice. Methods: Mice expressing human Tau with the P301L mutation (line rTg4510) were infused with BSc3094 into the lateral ventricle using Alzet osmotic pumps connected to a cannula that was placed on the skull of the mice, thus bypassing the blood-brain barrier (BBB) . The drug treatment lasted for 2 months, and the effect of BSc3094 on cognition and on reversing hallmarks of Tau pathology was assessed. Results: BSc3094 significantly reduced the levels of Tau phosphorylation and sarkosyl-insoluble Tau. In addition, the drug improved cognition in different behavioral tasks and reduced anxiety-like behavior in the transgenic mice used in the study. Conclusions: Our in vivo investigations demonstrated that BSc3094 is capable of partially reducing the pathological hallmarks typically observed in Tau transgenic mice, highlighting BSc3094 as a promising compound for a future therapeutic approach for AD.