| Bioactivity | SU3327 is a potent, selective and substrate-competitive JNK inhibitor with an IC50 of 0.7 μM. SU3327 also inhibits protein-protein interactions between JNK and JNK Interacting Protein (JIP) with an IC50 of 239 nM. SU3327 shows less active against p38α and Akt kinase[1][2]. | ||||||||||||
| Target | IC50: 0.7 μM (JNK); 239 nM (JNK-JIP interactions) | ||||||||||||
| Invitro | SU3327 (compound 9) is able to inhibit TNF-α stimulated phosphorylation of c-Jun in HeLa cells (EC50 = 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]. | ||||||||||||
| In Vivo | SU3327 (Compound 9; 25 mg/kg; intraperitoneal injection; male BKS.Cg-+Leprdb/+Leprdb/OlaHsd db/db mice) treatment possesses the ability to restore insulin sensitivity in mice models of diabetes[1].SU3327 (Compound 9) has favorable microsomal and plasma stability (T1/2 = 27 min)[1]. Animal Model: | ||||||||||||
| Name | SU3327 | ||||||||||||
| CAS | 40045-50-9 | ||||||||||||
| Formula | C5H3N5O2S3 | ||||||||||||
| Molar Mass | 261.30 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
|
||||||||||||
| Reference | [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. |