1228280-29-2

Basic information

• Product Name: KY 05009
• Synonyms: KY 05009;5-(4-methylbenzamido)-2-(phenylamino)thiazole-4-carboxamide;5-(4-methylbenzamido)-2-(phenylamino)thiazole-4-carboxamide(WXC06259)
• CAS NO: 1228280-29-2
• Molecular Formula: C₁₈H₁₆N₄O₂S
• Molecular Weight: 352.41024
• Mol File: 1228280-29-2.mol
• Article Data: 1

Chemical Properties

• Appearance: /
• Storage Temp.: 2-8°C
• CAS DataBase Reference: KY 05009(CAS DataBase Reference)
• NIST Chemistry Reference: KY 05009(1228280-29-2)
• EPA Substance Registry System: KY 05009(1228280-29-2)

Safety Data

• Hazardous Substances Data: 1228280-29-2(Hazardous Substances Data)

Usage

Biochem/physiol Actions

KY-05009 is a Traf2- and Nck-interacting kinase (TNIK) inhibitor that inhibits the epithelial-to-mesenchymal transition (EMT) in cancer cells.

Relevant articles and documents

A novel aminothiazole KY-05009 with potential to inhibit Traf2- And Nck-Interacting Kinase (TNIK) attenuates TGF-β1-mediated epithelial-to-mesenchymal transition in human lung adenocarcinoma A549 cells

Transforming growth factor (TGF)-β triggers the epithelial-to-mesenchymal transition (EMT) of cancer cells via wellorchestrated crosstalk between Smad and non-Smad signaling pathways, including Wnt/β-catenin. Since EMT-induced motility and invasion play a critical role in cancer metastasis, EMT-related molecules are emerging as novel targets of anticancer therapies. Traf2- and Nck-interacting kinase (TNIK) has recently been considered as a first-in-class anti-cancer target molecule to regulate Wnt signaling pathway, but pharmacologic inhibition of its EMT activity has not yet been studied. Here, using 5-(4-methylbenzamido)-2-(phenylamino)thiazole-4-carboxamide (KY-05009) with TNIK-inhibitory activity, its efficacy to inhibit EMT in cancer cells was validated. The molecular docking/binding study revealed the binding of KY-05009 in the hinge region of TNIK, and the inhibitory activity of KY-05009 against TNIK was confirmed by an ATP competition assay (Ki, 100 nM). In A549 cells, KY-05009 significantly and strongly inhibited the TGF-β-activated EMT through the attenuation of Smad and non-Smad signaling pathways, including the Wnt, NF-κB, FAK-Src-paxillin-related focal adhesion, and MAP kinases (ERK and JNK) signaling pathways. Continuing efforts to identify and validate potential therapeutic targets associated with EMT, such as TNIK, provide new and improved therapies for treating and/or preventing EMT-based disorders, such as cancer metastasis and fibrosis.