| Bioactivity | 9-ING-41 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]. | ||||||||||||
| Invitro | 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]. Cell Viability Assay[2] Cell Line: | ||||||||||||
| Name | 9-ING-41 | ||||||||||||
| CAS | 1034895-42-5 | ||||||||||||
| Formula | C22H13FN2O5 | ||||||||||||
| Molar Mass | 404.35 | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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