2. Stem Cell/Wnt Metabolic Enzyme/Protease Neuronal Signaling
  3. Wnt LDLR Amyloid-β
  4. SJ-300

SJ-300 是一种具有选择性，口服活性且可透过血脑屏障 DKK3-LRP1 抑制剂。 SJ 300 以 Kd = 7.9 μM 的结合力与 mLRPIV 结合，能够以 IC50 = 3.2 μM 的效力抑制 DKK3 mLRPIV 复合物，且不干扰 Aβ 与 LRP1 的结合。SJ-300 可在阿尔茨海默病模型中恢复 Aβ 清除功能，并在体内挽救认知功能、改善神经病理 (Aβ 斑块减少约 73.3%) 。SJ 300 可用于阿尔茨海默病的相关研究。

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SJ-300

SJ-300 Chemical Structure

CAS No. : 1210357-06-4

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SJ-300 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

SJ-300 is a potent and selective, orally active and brain-penetrat DKK3-LRP1 interaction inhibitor. SJ-300 restores Aβ clearance in AD models. SJ 300 binds to mLRPIV with a Kd of 7.9 μM, inhibits the DKK3 mLRPIV complex with an IC50 of 3.2 μM, and does not disrupt the binding of Aβ to LRP1. SJ 300 rescues cognitive function and ameliorates neuropathology (Aβ plaque reduction ≈ 73.3 %) in vivo. SJ 300 can be employed for research in Alzheimer’s disease[1].

体外研究
(In Vitro)

SJ-300 (0-5 μM) 在 SH-SY5Y 细胞中显著降低 DKK3-mLRPIV 相互作用[1]。
SJ-300 (1 μM, 2 小时) 在 AD-NSC 细胞中恢复 Aβ 的内化[1]。
SJ-300 (10 μM) 对 SH-SY5Y 细胞中的经典 Wnt/β-catenin 信号通路没有直接影响[1]。
SJ-300 (50 μM， 于 2 μL中， 0-60 分钟) 在小鼠和人肝微粒体中具有优异的代谢稳定性[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

SJ-300 相关抗体:

Immunofluorescence[1]

Cell Line: AD-NSC cell
Concentration: 1 μM
Incubation Time: 2 h
Result: Restored Aβ internalization in cells treated with DKK3 but in treated with DKK1.
体内研究
(In Vivo)

SJ-300 (单次静脉注射 2 mg/kg，单次口服 10 mg/kg) 在 C57 小鼠研究中，在整个观察时间段内均表现出稳定的血浆浓度[1]。
SJ-300 (灌胃给药，10 mg/kg，单次) 表现出脑渗透能力脑/血浆浓度比 (B/P比) 达到 5732%[1]。
SJ-300 (单次口服 10 mg/kg) 在 C57 小鼠中显示出极强的血脑屏障穿透能力，其脑、血浆浓度比高达5732%[1]。
SJ-300 (口服，5 mg/kg，每日一次，持续 8 周) 改善了 5×FAD 转基因 AD 模型小鼠的认知功能，且这些改善与 Aβ 病理的相关性较小[1]。
SJ-300 (口服，5 mg/kg，每日一次，持续 8 周) 通过增强 Aβ 清除，减轻了 6 月龄 5×FAD 小鼠的认知缺陷与 AD 病理[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: 5×FAD transgenic mouse model of AD (16 weeks)[1]
Dosage: 5 mg/kg
Administration: i.g., once daily for 8 weeks
Result: Reduced escape latencies during the 5-day acquisition phase.
Increased time spent in the target quadrant, and number of platform crossings during the probe trials.
Enhanced spatial working memory in the Y-maze test.
Reduced the number of Aβ plaques of various diameters in both brain regions.
Decreased the total number of Aβ plaques by approximately 73.3%.
Decreased the clustering of astrocytes by 64.1 % and microglia around the plaques.
Reduced both soluble and insoluble Aβ levels.
Did not affect APP cleavage or Aβ production.
Animal Model: 5×FAD transgenic mouse model of AD (6 months)[1]
Dosage: 5 mg/kg
Administration: i.g., once daily for 8 weeks
Result: Did not alter LRP1 expression but reduced colocalized Aβ on brain vascular basement membranes and endothelium.
Reduced the levels of both Aβ40 and Aβ42 in the plasma and liver of treated mice.
Did not alter the circulating concentrations of soluble LRP1.
Inhibited the association between soluble LRP1 (sLRP1) and DKK3.
分子量

342.45

Formula

C20H27FN4
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

SJ-300 相关分类

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Keywords:

SJ-3001210357-06-4SJ300SJ 300WntLDLRAmyloid-βLow-density lipoprotein receptorβ-amyloid peptideAβAbetaAlzheimer’s diseasecognitive functionDKK3LRP1,AβInhibitorinhibitorinhibit

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