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SIS3 HCl

SIS3HCl 是一种有效的选择性 Smad3 抑制剂，对 Smad3 磷酸化的 IC50 为 3 μM。

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SIS3 HCl的二维码
  • 库存: 现货
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  • 2mg
    ￥600.00
    480.00
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  • 5mg
    ￥887.00
    710.00
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  • 25mg
    ￥2737.00
    2190.00
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    ￥25800.00
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  • 1g
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使用我司产品发表的文章

  • 货号: ajci18624
  • CAS: 521984-48-5
  • 别名: SIS3 盐酸盐
  • 分子式: C28H28ClN3O3
  • 分子量: 489.99
  • 纯度: >98%
  • 溶解度: ≥ 49 mg/mL in DMSO, ≥ 11 mg/mL in EtOH with ultrasonic and warming
  • 储存: Store at -20°C
  • 库存: 现货

Background

IC50: 3 μM


SIS3 HCI?is an inhibitor of Smad3.


The receptor-associated Smads, such as Smad2 and Smad3, directly interact with activated TGF-receptor type I. Smads form heteromeric complexes with Smad4, which is a common mediator for all Smad pathways.


In vitro: In the reporter assay, it was found that the increased luciferase activity of p3TP-lux could be abrogated by the?SIS3 HCI treatment in a dosedependent manner. Immunoprecipitation revealed?SIS3 HCI attenuated the TGF-1-induced phosphorylation of Smad3 and interaction of Smad3 with Smad4. Whereas, SIS3 did not affect the phosphorylation of Smad2. In addition, it was found that SIS3 HCI attenuated the effects of TGF-1 by reducing the transcriptional activity.?SIS3 HCI could also inhibit the myofibroblast differentiation of fibroblasts by TGF-1. Moreover,?SIS3 HCI diminished the constitutive phosphorylation of Smad3 completely [1].


In vivo: Animal study showed that, in Tie2-Cre;Loxp-EGFP mice, AGEs could induce EndoMT. Immunoprecipitation and Western blotting showed that Smad3 could be activated by AGEs but was inhibited by?SIS3 HCI in both MMECs and in STZ-induced diabetic nephropathy. Furthermore, confocal microscopy and real-time PCR showed that SIS3 HCI could abrogate EndoMT, reduce renal fibrosis, as well as retard nephropathy progression [2].


Clinical trial: Up to now, SIS3 HCI is still in the preclinical development stage.


IC50: 3 μM


SIS3 HCI 是一种Smad3抑制剂。


受体相关Smads，如Smad2和Smad3，直接与活化的TGF-受体I相互作用。Smads与Smad4形成异源二聚体，后者是所有Smad通路的共同介质。


体外：在报告基因实验中，发现SIS3 HCI治疗可剂量依赖性地消除p3TP-lux的增强荧光素活性。免疫共沉淀发现，SIS3 HCI减弱了TGF-1诱导的Smad3磷酸化和Smad3与Smad4的相互作用。而SIS3并不影响Smad2的磷酸化。此外，研究发现SIS3 HCI通过减少转录活性来减轻TGF-1的作用。SIS3 HCI还可以通过TGF-1抑制成肌成纤维细胞的分化。此外，SIS3 HCI完全减弱了Smad3的非瘤细胞的构成性磷酸化[1]。


体内：动物研究表明，对Tie2-Cre;Loxp-EGFP小鼠的研究发现，AGEs可以诱导内皮间质转化。免疫共沉淀和Western blotting显示Smad3可以被AGEs激活，但在MMECs和STZ诱导的糖尿病性肾病中被SIS3 HCI抑制。此外，共聚焦显微镜和实时PCR显示，SIS3 HCI可以消除内皮间质转化，减少肾脏纤维化，并减缓肾病的进展[2]。


临床试验：截至目前，SIS3 HCI仍处于临床前开发阶段。

参考文献:
[1] Jinnin M et al.? Characterization of SIS3, a novel specific inhibitor of Smad3, and its effect on transforming growth factor-beta1-induced extracellular matrix expression. Mol Pharmacol. 2006 Feb;69(2):597-607.
[2] Li J et al.? Blockade of endothelial-mesenchymal transition by a Smad3 inhibitor delays the early development of streptozotocin-induced diabetic nephropathy. Diabetes.2010 Oct;59(10):2612-24.

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