JAK2-IN-7 is a selective JAK2 inhibitor with IC 50 s of 3, 11.7, and 41 nM for JAK2 , SET-2, and Ba/F3 V617F cells, respectively. JAK2-IN-7 possesses >14-fold selectivity over JAK1 , JAK3 , FLT3 . JAK2-IN-7 stimulates cell cycle arrest in the G0/G1 phase and induces tumor cell apoptosis . Antitumor activities In Vitro JAK2-IN-7 (compound 13ac) (0-1000 nM; 2 hours) inhibits JAK2 and STAT5 phosphorylation in a dose-dependent manner in SET-2 and Ba/F3-JAK2 V617F cells. JAK2-IN-7 (10-160 nM; 24 hours) induces cell arrest in the G0/G1 phase. JAK2-IN-7 (0.05-1.6 μM; 2 hours) induces apoptosis in SET-2 cells. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Cycle AnalysisCell Line: SET-2 cells Concentration: 10-160 nM Incubation Time: 24 hours Result: Induced cell arrest in the G0/G1 phase in a concentration-dependent manner. Apoptosis AnalysisCell Line: SET-2 cells Concentration: 0.05-1.6 μM Incubation Time: 2 hours Result: Induced apoptosis in SET-2 cells. In Vivo JAK2-IN-7 (15-60 mg/kg; p.o.; daily for 16 days) shows potent in vivo antitumor efficacy with 82.3% tumor growth inhibition in the SET-2 xenograft model . JAK2-IN-7 (30-60 mg/kg; p.o.; q.d. for 16 day) significantly ameliorates the disease symptoms in a Ba/F3-JAK2V617F allograft model, with 77.1% normalization of spleen weight, which was more potent than Ruxolitinib . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: SET-2 cell-inoculated xenograft NOD/SCID mouse model Dosage: 15, 30, and 60 mg/kg Administration: Orally daily for 16 days Result: Exhibited a significant tumor growth inhibition of 82.3% without obvious weight change. Form:Solid IC50& Target:JAK1 42 nM (IC 50 ) JAK2 3 nM (IC 50 ) JAK3 94 nM (IC 50 ) Tyk2 75 nM (IC 50 ) FLT3 62 nM (IC 50 )