SU3327

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.

Product information

CAS Number: 40045-50-9

Molecular Weight: 261.30

Formula: C5H3N5O2S3

Chemical Name: 5-[(5-nitro-1, 3-thiazol-2-yl)sulfanyl]-1, 3, 4-thiadiazol-2-amine

Smiles: NC1=NN=C(S1)SC1=NC=C(S1)[N+]([O-])=O

InChiKey: NQQBNZBOOHHVQP-UHFFFAOYSA-N

InChi: InChI=1S/C5H3N5O2S3/c6-3-8-9-5(14-3)15-4-7-1-2(13-4)10(11)12/h1H,(H2,6,8)

Technical Data

Appearance: Solid Power

Purity: ≥98% (or refer to the Certificate of Analysis)

Solubility: DMSO : 62.5 mg/mL (239.19 mM; Need ultrasonic)

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis

Storage Condition: Dry, dark and -20 ^oC for 1 year or refer to the Certificate of Analysis.

Shelf Life: ≥360 days if stored properly.

Stock Solution Storage: 0 - 4 ^oC for 1 month or refer to the Certificate of Analysis.

Drug Formulation: To be determined

HS Tariff Code: 382200

How to use

In Vitro:

SU3327 (compound 9) is able to inhibit TNF-α stimulated phosphorylation of c-Jun in HeLa cells (EC50 = 6.23 μM). 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.

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. SU3327 (Compound 9) has favorable microsomal and plasma stability (T1/2 = 27 min).

References:

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.

Products are for research use only. Not for human use.