K284-6111

K284-6111 is a high-affinity and orally active CHI3L1 inhibitor, and inhibits CHI3L1 expression. K284-6111 inhibits ERK and NF-κB pathway. K284-6111 suppresses nuclear translocation of p50 and p65, and phosphorylation of IκB. K284-6111 improves memory dysfunction by alleviating amyloidogenesis and neuroinflammation, with the reduction of inflammatory proteins (eg: iNOS, COX-2, GFAP, and Iba-1) . K284-6111 reduces atopic-like skin inflammation and inhibits LPS (HY-D1056) -induced liver injury. K284-6111 can be used for the study of Alzheimer's diseases and sepsis like hepatic injury[1][2][3][4].

Product Specifications

CAS Number

[702668-62-0]

UNSPSC

12352005

Target

Amyloid-β; COX; ERK; Glycosidase; Interleukin Related; NF-κB; NO Synthase

Type

Reference compound

Related Pathways

Immunology/Inflammation; MAPK/ERK Pathway; Metabolic Enzyme/Protease; Neuronal Signaling; NF-κB; Stem Cell/Wnt

Applications

Neuroscience-Neurodegeneration

Field of Research

Inflammation/Immunology; Neurological Disease

Assay Protocol

https://www.medchemexpress.com/k284-6111.html

Purity

99.94

Solubility

DMSO : 2 mg/mL (ultrasonic; warming; heat to 60°C)

Smiles

O=C1C2=C(N=C(N1CCC3=CCCCC3)SC(CC)C(NC4=CC=C(CC)C=C4)=O)C=C(OC)C(OC)=C2

Molecular Formula

C30H37N3O4S

Molecular Weight

535.70

References & Citations

[1]Ham HJ, et al. K284-6111 alleviates memory impairment and neuroinflammation in Tg2576 mice by inhibition of Chitinase-3-like 1 regulating ERK-dependent PTX3 pathway. J Neuroinflammation. 2020 Nov 22;17 (1) :350. |[2]Choi JY, et al. K284-6111 prevents the amyloid beta-induced neuroinflammation and impairment of recognition memory through inhibition of NF-κB-mediated CHI3L1 expression. J Neuroinflammation. 2018 Aug 11;15 (1) :224.|[3]Jeon SH, et al. Inhibition of Chitinase-3-like-1 by K284-6111 Reduces Atopic Skin Inflammation via Repressing Lactoferrin. Immune Netw. 2021 Jun 29;21 (3) :e22. |[4]Inhibition of Chitinase-3-like-1 expression by K284 ameliorates lipopolysaccharide-induced acute liver injury through down regulation of CXCL3.