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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
G-749 is a selective inhibitor of Fms-like tyrosine receptor kinase-3 (FLT3) with IC50 value of 0.4 nM for wild-type FLT31.
G-749 is a synthesized and ATP-competitive inhibitor of wild-type FLT3 with high potency. It inhibited the autophosphorylation of FLT3 with IC50 value of ≤ 8 nM in RS4-11 leukemia cells. It also has inhibitory activity against various FLT3 mutants. In BaF3 cell lines that stably express FLT3-ITD/N676D, -ITD/F691L, -D835Y or -D835Y/N676D, G-749 showed strong potency against autophosphorylation of all tested FLT3 mutants with IC50 of < 10 nM. In MV4-11 and Molm-14 cell lines addicted to FLT3-ITD, G-749 significantly suppressed cell proliferation as well as increased active caspase 3/7 level and cleaved PARP in a dose-dependent manner. Besides that, G-749 showed high potency against p-FLT3, p-ERK1/2 and p-AKT even in high FLT3 ligand milieu1.
References:1. Lee H K, Kim H W, Lee I Y, et al. G-749, a novel FLT3 kinase inhibitor, can overcome drug resistance for the treatment of acute myeloid leukemia. Blood, 2014, 123(14): 2209-2219.