G-749 是一种高效的, ATP 竞争性的 FLT3 抑制剂，对野生型 FLT3 和突变型 FLT3-D835Y 作用的 IC₅₀ 值分别为 0.4 nM 和 0.6 nM。G-749 可用于急性髓系白血病 (AML) 的耐药研究。

G-749 is a potent, oral active and ATP competitive FLT3 inhibitor, with IC 50 s of 0.4 nM and 0.6 nM for FLT3 wild type and FLT3-D835Y, respectively. G-749 can be used for the research of drug resistance for acute myeloid leukemia (AML).

Solid

IC50: 0.4 nM (FLT3-WT), 0.6 nM (FLT3-D835Y)

G-749 shows potent and sustained inhibition of the FLT3 wild type and mutants including FLT3-ITD, FLT3-D835Y, FLT3-ITD/N676D, and FLT3-ITD/F691L in cellular assays.
G-749 inhibits autophosphorylation of FLT3 with an IC50 value of ≤8 nM in FLT3-WT bearing RS4-11 and in FLT3-ITD harboring MV4-11 and Molm-14 cells.
G-749 (0.0001-10 nM; 72 hours) shows strong antiproliferation of leukemia cells addicted to FLT3-ITD (MV4-11 and Molm-14) in a dose-dependent manner.
G-749 (25-100 nM; 36 hours) causes antiproliferative activity through apoptosis.
G-749 (1.6-1000 nM; 2 hours) shows more potent inhibition of p-FLT3, p-ERK1/2, and p-AKT than AC220 and PKC412.
has not independently confirmed the accuracy of these methods. They are for reference only.

G-749 (3-30 mg/kg; p.o.; daily; for 28 days) shows effective antitumor activity in mouse models.
has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Athymic nu/nu mice, subcutaneous

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[1]. Lee HK, et al. G-749, a novel FLT3 kinase inhibitor, can overcome drug resistance for the treatment of acute myeloid leukemia. Blood. 2014 Apr 3;123(14):2209-19.

In Vitro: DMSO : 25 mg/mL (47.95 mM; Need ultrasonic)配制储备液