JAK2-IN-7 是一种选择性JAK2抑制剂，对 JAK2，SET-2 和 Ba/F3V617F细胞的IC50为 3、11.7 和 41 nM。 JAK2-IN-7 的选择性是 JAK1, JAK3，FLT3 的 14 倍以上。JAK2-IN-7 刺激细胞周期停滞在 G0/G1 期，并诱导肿瘤细胞Apoptosis" style="display: inline; color: #c13a36">凋亡 (Apoptosis)，具有抗肿瘤活性。

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 over 14-fold selectivity over JAK1, JAK3, FLT3. JAK2-IN-7 stimulates cell cycle arrest in the G0/G1 phase and induces tumor cell apoptosis that has antitumor activities [1].

JAK2-IN-7 (compound 13ac) (0-1000 nM; 2 hours) inhibits phosphorylation of JAK2 and STAT5 in a dose-dependent manner in SET-2 and Ba/F3-JAK2 V617F cells [1]. JAK2-IN-7 (10-160 nM; 24 hours) induces cell arrest in the G0/G1 phase [1]. JAK2-IN-7 (0.05-1.6 μM; 2 hours) induces apoptosis in SET-2 cells [1]. Cell Cycle Analysis [1] Cell 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 Analysis [1] Cell Line: SET-2 cells Concentration: 0.05-1.6 μM Incubation Time: 2 hours Result: Induced apoptosis in SET-2 cells.

JAK2-IN-7 (15-60 mg/kg; p.o.; daily for 16 days) exhibits potent in vivo antitumor efficacy with 82.3% tumor growth inhibition in the SET-2 xenograft model [1]. 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 [1]. Animal Model: SET-2 cell-inoculated xenograft NOD/SCID mouse model [1] 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.

2593402-36-7

JAK2-IN-7

DMSO:250 mg/mL (543.96 mM),Need ultrasonic
Powder: -20°C for 3 years
In solvent: -80°C for 2 years