9-ING-41

9-ING-41 (Elraglusib) is a maleimide-based ATP-competitive and selective glycogen synthase kinase-3β (GSK-3β) inhibitor with an IC₅₀ of 0.71 μM. 9-ING-41 significantly leads to cell cycle arrest, autophagy and apoptosis in cancer cells. 9-ING-41 has anticancer activity and has the potential for enhancing the antitumor effects of chemotherapeutic drugs^[1][2][3][4]. In Vitro:9-ING-41 (2, 4 μM; 48 hours) decreases neuroblastoma cell viability induces apoptosis^[2].
9-ING-41 (1, 2 μM; 24 hours) is a potent cell cycle-blocking agent for lymphoma cells^[2].
9-ING-41 (10 μM; for 72 hours) increases the expression of LC3, an autophagy marker^[3].
9-ING-41 (compound 26; 5 μM; for 6, 12, 24, 36 h) results in a pronounced decrease in NFκB-mediated expression of XIAP, the most potent antiapoptotic protein, leading to subsequent apoptosis in BXPC3 pancreatic cancer cells^[1].
9-ING-41 (0.5, 1.0, 1.5, 2.0 μM) inhibits the proliferation rate of all TCL and MCL lines with concentrations as low as 1.0 mM^[2].
9-ING-41 (10 μM; for 72 hours) causes cell cycle blockage at G2/M after 24 hours. 9-ING-41 treatment induces apoptotic cell death in bladder cancer cells^[3].
9-ING-41 (25 μM; for 96 hours) significantly decreases expression of Cdk1 and Cyclin B1 proteins and leads to a decreased expression of antiapoptotic molecules, Bcl-2 and XIAP^[3].
9-ING-41 (0.1-1 µM) inhibits GSK-3 leading to a decreased expression of the NF-κB target XIAP and significant apoptosis in neuroblastoma cells as shown by PARP cleavage, an apoptosis marker^[4].
In Vivo:9-ING-41 (40 mg/kg/every other day; for 17 days) has single-agent antitumor activity in a mouse model of MCL^[2].