SU3327

Names

[ Name ]:
SU3327

[Synonym ]:
Loreclezole hydrochloride
2-amino-1,3,4-thiadiazole,9
SU 3327
5-[(5-nitro-1,3-thiazol-2-yl)thio]-1,3,4-thiadiazol-2-amine
5-(5-nitrothiazol-2-ylthio)-1,3,4-thiadiazol-2-amine
5-(5-nitro-thiazol-2-ylsulfanyl)-[1,3,4]thiadiazol-2-ylamine
(amino-5 thiadiazol-1,3,4-yl-2) thio-2 nitro-5 thiazole
2-Amino-5-(5-nitrothiazol-2-yl)mercapto-1,3,4-thiadiazole

Biological Activity

[Description]:

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].

[Related Catalog]:

Research Areas >> Inflammation/Immunology

Research Areas >> Metabolic Disease

Signaling Pathways >> MAPK/ERK Pathway >> JNK

[Target]

IC50: 0.7 μM (JNK); 239 nM (JNK-JIP interactions)[1]

[In Vitro]

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: Male BKS.Cg-+Leprdb/+Leprdb/OlaHsd db/db mice (11-week-old ) injected with insulin[1] Dosage: 25 mg/kg Administration: Intraperitoneal injection Result: Resulted in a statistically significant reduction in blood glucose levels.

[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.

Chemical & Physical Properties

[ Density]:
1.888g/cm3

[ Boiling Point ]:
549.841ºC at 760 mmHg

[ Melting Point ]:
160 °C(dec.)

[ Molecular Formula ]:
C₅H₃N₅O₂S₃

[ Molecular Weight ]:
261.30500

[ Flash Point ]:
286.334ºC

[ Exact Mass ]:
260.94500

[ PSA ]:
193.02000

[ LogP ]:
2.08950

[ Index of Refraction ]:
1.793

Synthetic Route

Click to get detail synthetic route

Precursor & DownStream

Precursor

DownStream

Related Compounds

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