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SU3327

SU3327 (halicin) 是具有底物竞争性的 JNK 选择性抑制剂，IC50为 0.7 μM。它还抑制 JNK 和 JIP 之间的蛋白相互作用，IC50值为 239 nM。

CAS号

40045-50-9

分子式

C5H3N5O2S3

主要靶点

JNK

仅限科研使用

Cat No : CM04927

Print datasheet

Synonyms

halicin

验证数据展示

  • CAS No.: 40045-50-9

    SU3327
    CAS#: 40045-50-9

产品信息

SU3327 is a potent, selective and substrate-competitive inhibitor of JNK(IC50 of 0.7 μM).

CAS号 40045-50-9
分子式 C5H3N5O2S3
主要靶点 JNK
主要通路 MAPK信号通路
分子量 261.3
纯度 97.13%， 此纯度可做参考，具体纯度与批次有关系，可咨询客服
储存条件 Powder: -20°C for 3 years | In solvent: -80°C for 1 year
别名 halicin

靶点活性

JNK-JIP interactions:239 nM |JNK:0.7 μM

体内活性

In male BKS.Cg-+Leprdb/+Leprdb/OlaHsd db/db mice, SU3327 (25 mg/kg; intraperitoneal injection; ) treatment possesses the ability to restore insulin sensitivity in mice models of diabetes[1]. SU3327 has favorable microsomal and plasma stability (T1/2 = 27 min)[1].

体外活性

TNF-α stimulated phosphorylation of c-Jun in HeLa cells inhibited by SU3327 with EC50 of 6.23 μM[1]. SU3327 (25 nM) pretreatment of human-derived cerebral microvascular endothelial cells (hCMEC/D3) effectively reduces LPS-induced polymorphonuclear leukocytes (PMN) rolling/adhesion to hCMEC/D3, prevents activation of AP-1, and significantly reduces expression of VCAM-1[3].

溶解度

DMSO:62.5 mg/mL (239.19 mM),Sonification is recommended.

参考文献

1.De SK, et al. Design, synthesis, and structure-activity relationship of substrate competitive, selective, and in vivo active triazole and thiadiazole inhibitors of the c-Jun N-terminal kinase. J Med Chem. 2009 Apr 9;52(7):1943-52.
2.Augustine C, et al. Traumatic injury elicits JNK-mediated human astrocyte retraction in vitro. Neuroscience. 2014 Aug 22;274:1-10.
3.Serizawa F, et al. Pretreatment of human cerebrovascular endothelial cells with CO-releasing molecule-3 interferes with JNK/AP-1 signaling and suppresses LPS-induced proadhesive phenotype. Microcirculation. 2015 Jan;22(1):28-36.

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