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KCC009 is an inhibitor of transglutaminase 2 (TG2; Ki = 0.068 mM).1 It reduces radiation-induced increases in the expression of TGM2, the gene encoding TG2, in wild-type H1299 and p53-mutant H1299 (H1299/M175H-p53) cells when used at a concentration of 3.91 µM.2 KCC009 sensitizes wild-type H1299 and H1299/M175H-p53 cells to radiation and induces cell cycle arrest at the G0/G1 and G2/M phases, respectively. It inhibits fibronectin remodeling in U87MG glioblastoma cells when used at a concentration of 1 mM.3 KCC009 (50 mg/kg) sensitizes tumors to N,N’-bis(2-chloroethyl)-N-nitrosourea (carmustine; Item No. 15775) and increases survival in an orthotopic mouse model of DBT-FG glioblastoma when administered in combination with N,N’-bis(2-chloroethyl)-N-nitrosourea. It also reverses warfarin-induced arterial calcification in rats and prevents relapse in a rat model of experimental autoimmune encephalomyelitis (EAE).4,5
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1. Structure-
2. Transglutaminase 2 inhibitor KCC009 induces p53-
3. Transglutaminase 2 inhibitor, KCC009, disrupts fibronectin assembly in the extracellular matrix and sensitizes orthotopic glioblastomas to chemotherapy. Oncogene 26(18), 2563-2573 (2007).
4. Transglutaminase inhibitors attenuate vascular calcification in a preclinical model. Arterioscler. Thromb. Vasc. Biol. 33(1), 43-51 (2012).
5. Tissue transglutaminase contributes to experimental multiple sclerosis pathogenesis and clinical outcome by promoting macrophage migration. Brain Behav. Immun. 50, 141-154 (2015).